The List

Candida albicans

-Candida albicans is an opportunistic pathogenic yeast [4] that is a common member of the human gut flora. It does not proliferate outside the human body.[5] It is detected in the gastrointestinal tract and mouth in 40-60% of healthy adults.[6][7] It is usually a commensal organism, but can become pathogenic in immunocompromised individuals under a variety of conditions.[7][8] It is one of the few species of the Candida genus that causes the human infection candidiasis, which results from an overgrowth of the fungus.[7][8] Candidiasis is for example often observed in HIV-infected patients.[9] C. albicans is the most common fungal species isolated from biofilms either formed on (permanent) implanted medical devices or on human tissue.[10][11] C. albicans, C. tropicalis, C. parapsilosis, and C. glabrata, are together responsible for 50-90% of all cases of candidiasis in humans.[8][12][13] A mortality rate of 40% has been reported for patients with systemic candidiasis due to C. albicans.[14] By one estimate, invasive candidiasis contracted in a hospital causes 2800 to 11200 deaths yearly in the US. -Candida is found worldwide but most commonly compromises immunocompromised individuals diagnosed with serious diseases such as HIV and cancer. Candida are ranked as one of the most common groups of organisms that cause nosocomial infections. Especially high risk individuals are patients that have recently undergone surgery, a transplant or are in the Intensive Care Units (ICU),[64] Candida albicans infections is the top source of fungal infections in critically ill or otherwise immuncompromised patients.[65] These patients predominantly develop oropharyngeal or thrush candidiasis, which can lead to malnutrition and interfere with the absorption of medication.[66] Methods of transmission include mother to infant through childbirth, people-to-people acquired infections that most commonly occur in hospital settings where immunocompromised patients acquire the yeast from healthcare workers and has a 40% incident rate. Men can become infected after having sex with a woman that has an existing vaginal yeast infection.[64] Parts of the body that are commonly infected include the skin, genitals, throat, mouth, and blood.[67] Distinguishing features of vaginal infection include discharge, and dry and red appearance of vaginal mucosa or skin. Candida continues to be the fourth most commonly isolated organism in bloodstream infections.[68] Healthy people usually do not suffer (severely) from superficial infections caused by a local alteration in cellular immunity as seen by asthma patients that use oral corticosteroids. -Given the fact that candidiasis is the fourth (to third) most frequent hospital acquired infection worldwide it leads to immense financial implications. Approximately 60000 cases of systemic candidiasis each year in the USA alone lead up to a cost to be between $2-4 billion.[81] The total costs for candidiasis are among the highest compared to other fungal infections due to the high prevalence.[82] The immense costs are partly explained by a longer stay in the intensive care unit or hospital in general. An extended stay for up to 21 more days compared to non infected patients is not uncommon

Coccidioides immitis

-Coccidioides immitis is a pathogenic fungus that resides in the soil in certain parts of the southwestern United States, northern Mexico, and a few other areas in the Western Hemisphere. -C. immitis, along with its relative C. posadasii,[3] is most commonly seen in the desert regions of the southwestern United States, including certain areas of Arizona, California, New Mexico, Nevada, Texas, and Utah; and in Central and South America in Argentina, Brazil, Colombia, Guatemala, Honduras, Mexico, Nicaragua, Paraguay, and Venezuela -C. immitis can cause a disease called coccidioidomycosis (valley fever).[8][9][10] Its incubation period varies from 7 to 21 days.[11] Coccidioidomycosis is not easily diagnosed on the basis of vital signs and symptoms, which are usually vague and nonspecific. Even a chest X-ray or CT scan cannot reliably distinguish it from other lung diseases, including lung cancer. Blood or urine tests are administered, which aim to discover Coccidioides antigens. However, because the Coccidioides creates a mass that can mimic a lung tumor, the correct diagnosis may require a tissue sample (biopsy). A Gomori methenamine silver stain can then confirm the presence of the Coccidioides organism's characteristic spherules within the tissue. The C. immitis fungus can be cultured from a patient sample, but the culture can take weeks to grow and requires special precautions on a part of the laboratory staff while handling it (screw cap vials and sterile transfer hoods are recommended.[12] It is reported as the tenth-most often acquired infection in the laboratory conditions with two documented deaths.[2] Until October 2012, C. immitis had been listed as a select agent by both the U.S. Department of Health and Human Services and the U.S. Department of Agriculture, and was considered a biosafety level 3 pathogen. -The introduction of azoles revolutionized treatment for coccidioidomycosis,[14] and these agents are usually the first line of therapy. However, none of the azoles is safe to use in pregnancy and lactation because they have shown teratogenicity in animal studies.

Burkholderia mallei

-gram-negative, bipolar, aerobic bacterium -is nonmotile; its shape is something between a rod and a coccus -human and animal pathogen causing glanders diseases -an obligate mammalian pathogen, it must infect a host mammal t live and to be transmitted from one host to another -when grown in culture, it grows in smooth, grey, translucent colonies -is susceptible to numerous disinfectants including iodine and ethanol -can be destroyed by heating or ultraviolet light -is resistant to a number of antibiotics including aminoglycoside, polymyxins, and beta-lactams -no vaccine is currently available for humans or animals to protect against B. mallei infection -is responsible for causing glanders disease, which historically mostly affected animals, such as horses, mules, and donkeys, and rarely humans -horses are considered the natural host for infection and are highly susceptible to it -symptoms in horses include: mucus-containing nasal discharge, lung lesions, and nodules around the liver or spleen -acute infection in horses results in a high fever, loss of fat or muscle, erosion of the surface of the nasal septum, hemorrhaging or mucus discharge -the bacterium mostly affects the lungs and airways -human infections are rare, although it occasionally occurs among lab workers dealing with the bacteria or those who are frequently near infected animals -the bacteria usually infect a person through their eyes, nose, mouth, or cuts in the skin -once people are infected, they develop a fever and rigors -eventually, they get pneumonia, pustules, and abscesses, which prove fatal within a week to 10 days if left untreated by antibiotics -the way someone is infected by the bacteria also affects the type of symptoms that will result -it has been eradicated in the US and most Western countries, but still affects animals in Africa, Asia, the middle East, Central America, and South America -it has a history of being on a list of potential biological warfare agents -was used as a weapon in WWI

Aspergillus spp.

-is a genus consisting of a few hundred mold species found in various climates worldwide. -Aspergillus was first catalogued in 1729 by the Italian priest and biologist Pier Antonio Micheli. Viewing the fungi under a microscope, Micheli was reminded of the shape of an aspergillum (holy water sprinkler), from Latin spargere (to sprinkle), and named the genus accordingly.[1] Aspergillum is an asexual spore-forming structure common to all Aspergillus species; around one-third of species are also known to have a sexual stage. -Members of the genus possess the ability to grow where a high osmotic pressure exists (high concentration of sugar, salt, etc.). Aspergillus species are highly aerobic and are found in almost all oxygen-rich environments, where they commonly grow as molds on the surface of a substrate, as a result of the high oxygen tension. Commonly, fungi grow on carbon-rich substrates like monosaccharides (such as glucose) and polysaccharides (such as amylose). Aspergillus species are common contaminants of starchy foods (such as bread and potatoes), and grow in or on many plants and trees. -In addition to growth on carbon sources, many species of Aspergillus demonstrate oligotrophy where they are capable of growing in nutrient-depleted environments, or environments with a complete lack of key nutrients. A. niger is a prime example of this; it can be found growing on damp walls, as a major component of mildew. -are found in millions in pillows -Species of Aspergillus are important medically and commercially. Some species can cause infection in humans and other animals. Some infections found in animals have been studied for years, while other species found in animals have been described as new and specific to the investigated disease, and others have been known as names already in use for organisms such as saprophytes. More than 60 Aspergillus species are medically relevant pathogens.[4] For humans, a range of diseases such as infection to the external ear, skin lesions, and ulcers classed as mycetomas are found. -Other species are important in commercial microbial fermentations -Members of the genus are also sources of natural products that can be used in the development of medications to treat human disease. -Some Aspergillus species cause serious disease in humans and animals -The symptoms include fever, cough, chest pain, or breathlessness, which also occur in many other illnesses, so diagnosis can be difficult. Usually, only patients with already weakened immune systems or who suffer other lung conditions are susceptible -In humans, the major forms of disease are: Allergic bronchopulmonary aspergillosis, which affects patients with respiratory diseases such as asthma, cystic fibrosis, and sinusitis Acute invasive aspergillosis, a form that grows into surrounding tissue, more common in those with weakened immune systems such as AIDS or chemotherapy patients Disseminated invasive aspergillosis, an infection spread widely through the body Aspergilloma, a "fungus ball" that can form within cavities such as the lung Aspergillosis of the air passages is also frequently reported in birds, and certain species of Aspergillus have been known to infect insects.

Campylobacter jejuni

Campylobacter jejuni (/ˈkæmpɪloʊˌbæktər dʒəˈdʒuːni/) is one of the most common causes of food poisoning in the United States and in Europe. The vast majority of cases occur as isolated events, not as part of recognized outbreaks.[1] Active surveillance through the Foodborne Diseases Active Surveillance Network (FoodNet) indicates that about 14 cases are diagnosed each year for each 100,000 persons in the population.[2] The European Food Safety Authority estimated in 2011 that there are approximately nine million cases of human campylobacteriosis per year in the European Union.[3] Campylobacter jejuni is in a genus of bacteria that is among the most common causes of bacterial infections in humans worldwide. Campylobacter means "curved rod", deriving from the Greek campylos (curved) and baktron (rod). It has been noted that there "is wide diversity in the genus. The species are metabolically and genetically different to the extent that one can question whether one genus is adequate to house all of the species." Of its many species, C. jejuni is considered one of the most important from both a microbiological and public health perspective.[4] C. jejuni is also commonly found in animal feces. Campylobacter is a helical-shaped, nonspore-forming, Gram-negative, microaerophilic, nonfermenting bacterium forming motile rods with a single polar flagellum, which are also oxidase-positive and grow optimally at 37 to 42 °C.[5][6][7][8] When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form.[9] This species of pathogenic bacteria is one of the most common causes of human gastroenteritis in the world. Food poisoning caused by Campylobacter species can be severely debilitating, but is rarely life-threatening. It has been linked with subsequent development of Guillain-Barré syndrome, which usually develops two to three weeks after the initial illness.[10] Individuals with recent C. jejuni infections develop Guillain-Barré syndrome at a rate of 0.3 per 1000 infections, about 100 times more often than the general population Campylobacteriosis is an infectious disease caused by bacteria of the genus Campylobacter. In most people who become ill with campylobacteriosis, symptoms develop within two to five days of exposure to the organism and illness typically lasts seven days following onset.[2] Infection with C. jejuni usually results in enteritis, which is characterised by abdominal pain, diarrhea, fever, and malaise. Diarrhea itself can vary in severity from loose to bloody stools. The disease is usually self-limiting. However, it does respond to antibiotics. Severe (accompanying fevers, blood in stools) or prolonged cases may require erythromycin, azithromycin, ciprofloxacin, or norfloxacin. Fluid replacement via Oral Rehydration Salts may be needed and intravenous fluid may be required for serious cases.[2] Studies on the pathogenesis of C. jejuni show that for this organism to cause disease, the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection, the organism must penetrate the gastrointestinal mucus, which it does using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and can then induce diarrhea by toxin release. C. jejuni releases several different toxins, mainly enterotoxin and cytotoxins, which vary from strain to strain and correlate with the severity of the enteritis. During infection, levels of all immunoglobulin classes rise. Of these, IgA is the most important because it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism.[13] The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever. Stools contain leukocytes and blood. The role of toxins in pathogenesis is unclear. C jejuni antigens that cross-react with one or more neural structures may be responsible for triggering the Guillain-Barré syndrome.[8] Campylobacter causes an estimated 1.3 million illnesses each year in the United States. Most illnesses likely occur due to eating raw or undercooked poultry, or to eating something that touched it. Some are due to contaminated water, contact with animals, or drinking raw (unpasteurized) milk. Although people with Campylobacter infection usually recover on their own, some need medical treatment.

Echinococcus granulosus

Echinococcus granulosus, also called the hydatid worm, hyper tape-worm or dog tapeworm, is a cyclophyllid cestode that parasitizes the small intestine of canids as an adult, but which has important intermediate hosts such as livestock and humans, where it causes cystic echinococcosis, also known as hydatid disease. The adult tapeworm ranges in length from 3 mm to 6 mm and has three proglottids ("segments") when intact—an immature proglottid, mature proglottid and a gravid proglottid.[1] The average number of eggs per gravid proglottid is 823. Like all cyclophyllideans, E. granulosus has four suckers on its scolex ("head"), and E. granulosus also has a rostellum with hooks. Several strains of E. granulosus have been identified, and all but two are noted to be infective in humans.[2] The lifecycle of E. granulosus involves dogs and wild carnivores as a definitive host for the adult tapeworm.[3] Definitive hosts are where parasites reach maturity and reproduce. Wild or domesticated ungulates, such as sheep, serve as an intermediate host.[3] Transitions between life stages occur in intermediate hosts. The larval stage results in the formation of echinococcal cysts in intermediate hosts.[3] Echinococcal cysts are slow growing,[3] but can cause clinical symptoms in humans and be life-threatening.[4] Cysts may not initially cause symptoms, in some cases for many years.[3] Symptoms developed depend on location of the cyst, but most occur in the liver, lungs, or both.[4] E. granulosus was first documented in Alaska but is distributed worldwide. It is especially prevalent in parts of Eurasia, north and east Africa, Australia, and South America.[4] Communities that practice sheep farming experience the highest risk to humans,[4] but wild animals can also serve as an avenue for transmission. For example, dingoes serve as a definitive host before larvae infect sheep in the mainland of Australia.[4] Sled dogs may expose moose or reindeer to E. granulosus in parts of North America and Eurasia E. granulosus requires two host types, a definitive host and an intermediate host. The definitive host of this parasite are dogs and the intermediate host are most commonly sheep, however, cattle, horses, pigs, goats, and camels are also potential intermediate hosts.[5] Humans can also be an intermediate host for E. granulosus, however this is uncommon and therefore humans are considered an aberrant intermediate host. E. granulosus is ingested and attaches to the mucosa of the intestines in the definitive host and there the parasite will grow into the adult stages.[6] Adult E. granulosus release eggs within the intestine which will be transported out of the body via feces.[6] When contaminated waste is excreted into the environment, intermediate host has the potential to contract the parasite by grazing in contaminated pasture, perpetuating the cycle.[5][7] E. granulosus is transmitted from the intermediate host (sheep) to the definitive host (dogs) by frequent feeding of offal, also referred to as "variety meat" or "organ meat". Consuming offal containing E. granulosus can lead to infection; however, infection is dependent on many factors.[4] The frequency of offal feedings, the prevalence of the parasites within the offal, and the age of the intermediate host are factors that affect infection pressure within the definitive host.[6] The immunity of both the definitive and intermediate host plays a large role in the transmission of the parasite, as well as the contact rate between the intermediate and the definitive host (such as herding dogs and pasture animals being kept in close proximity where dogs can contaminate grazing areas with fecal matter).[4] The life expectancy of the parasite, coupled with the frequency of anthelminthic treatments, will also play a role in the rate of infection within a host. The temperature and humidity of the environment can affect the survival of E. granulosus.[4] Once sheep are infected, the infection typically remains within the sheep for life. However, in other hosts, such as dogs, treatment for annihilating the parasite is possible. However, the intermediate host is assumed to retain a greater life expectancy than the definitive host Humans should avoid handling stool of dogs and avoid eating infected animals and home slaughtering animals. If a human becomes infected there are a variety of methods for treatment.[2][10] The most common treatment in the past years has been surgical removal of the hydatid cysts.[10] The fluid in the cysts contain antigens that can immunologically sensitize the host, so cyst manipulation should be performed with caution, as spilling of cyst contents can cause anaphylactic shock. However, in recent years, less invasive treatments have been developed such as cyst puncture, aspiration of the liquids, the injection of chemicals, and then re-aspiration.[2] Benzimidazole-based chemotherapy is also a new treatment option for humans In order to prevent transmission to dogs from intermediate hosts, dogs can be given anthelminthic vaccinations.[3][10] In the case of intermediate hosts, especially sheep, these anthelminthic vaccinations do cause an antigenic response—meaning the body produces antibodi avinash response—however it does not prevent infection in the host.[3][10] Clean slaughter and high surveillance of potential intermediate host during slaughter is key in preventing the spread this cestode to its definitive host. It is vital to keep dogs and potential intermediate host as separated as possible to avoid perpetuating infection.[3][11] According to mathematical modeling, vaccination of intermediate hosts, coupled with dosing definitive hosts with anthelminths is the most effect method for intervening with infection rates.[3] Proper disposal of carcasses and offal after home slaughter is difficult in poor and remote communities and therefore dogs readily have access to offal from livestock, thus completing the parasite cycle of Echinococcus granulosus and putting communities at risk of cystic echinococcosis. Boiling livers and lungs which contain hydatid cysts for 30 minutes has been proposed as a simple, efficient and energy- and time-saving way to kill the infectious larvae.

Hepatitis B virus

Hepatitis B virus, abbreviated HBV, is a double stranded DNA virus,[1] a species of the genus Orthohepadnavirus, and a member of the Hepadnaviridae family of viruses.[2] This virus causes the disease hepatitis B In addition to causing hepatitis, infection with HBV can lead to cirrhosis and hepatocellular carcinoma.[4] It has also been suggested that it may increase the risk of pancreatic cancer Hepatitis B is a serious liver infection caused by the hepatitis B virus (HBV). For some people, hepatitis B infection becomes chronic, meaning it lasts more than six months. Having chronic hepatitis B increases your risk of developing liver failure, liver cancer or cirrhosis — a condition that permanently scars of the liver. Most adults with hepatitis B recover fully, even if their signs and symptoms are severe. Infants and children are more likely to develop a chronic (long-lasting) hepatitis B infection. A vaccine can prevent hepatitis B, but there's no cure if you have the condition. If you're infected, taking certain precautions can help prevent spreading the virus to others. Signs and symptoms of hepatitis B range from mild to severe. They usually appear about one to four months after you've been infected, although you could see them as early as two weeks post-infection. Some people, usually young children, may not have any symptoms. Hepatitis B signs and symptoms may include: Abdominal pain Dark urine Fever Joint pain Loss of appetite Nausea and vomiting Weakness and fatigue Yellowing of your skin and the whites of your eyes (jaundice) Hepatitis B infection is caused by the hepatitis B virus (HBV). The virus is passed from person to person through blood, semen or other body fluids. It does not spread by sneezing or coughing. Common ways that HBV can spread are: Sexual contact. You may get hepatitis B if you have unprotected sex with someone who is infected. The virus can pass to you if the person's blood, saliva, semen or vaginal secretions enter your body. Sharing of needles. HBV easily spreads through needles and syringes contaminated with infected blood. Sharing IV drug paraphernalia puts you at high risk of hepatitis B. Accidental needle sticks. Hepatitis B is a concern for health care workers and anyone else who comes in contact with human blood. Mother to child. Pregnant women infected with HBV can pass the virus to their babies during childbirth. However, the newborn can be vaccinated to avoid getting infected in almost all cases. Talk to your doctor about being tested for hepatitis B if you are pregnant or want to become pregnant. Hepatitis B infection may be either short-lived (acute) or long lasting (chronic). Acute hepatitis B infection lasts less than six months. Your immune system likely can clear acute hepatitis B from your body, and you should recover completely within a few months. Most people who get hepatitis B as adults have an acute infection, but it can lead to chronic infection. Chronic hepatitis B infection lasts six months or longer. It lingers because your immune system can't fight off the infection. Chronic hepatitis B infection may last a lifetime, possibly leading to serious illnesses such as cirrhosis and liver cancer. The younger you are when you get hepatitis B — particularly newborns or children younger than 5 — the higher your risk of the infection becoming chronic. Chronic infection may go undetected for decades until a person becomes seriously ill from liver disease. Hepatitis B spreads through contact with blood, semen or other body fluids from an infected person. Your risk of hepatitis B infection increases if you: Have unprotected sex with multiple sex partners or with someone who's infected with HBV Share needles during IV drug use Are a man who has sex with other men Live with someone who has a chronic HBV infection Are an infant born to an infected mother Have a job that exposes you to human blood Travel to regions with high infection rates of HBV, such as Asia, the Pacific Islands, Africa and Eastern Europe Having a chronic HBV infection can lead to serious complications, such as: Scarring of the liver (cirrhosis). The inflammation associated with a hepatitis B infection can lead to extensive liver scarring (cirrhosis), which may impair the liver's ability to function. Liver cancer. People with chronic hepatitis B infection have an increased risk of liver cancer. Liver failure. Acute liver failure is a condition in which the vital functions of the liver shut down. When that occurs, a liver transplant is necessary to sustain life. Other conditions. People with chronic hepatitis B may develop kidney disease or inflammation of blood vessels. The hepatitis B vaccine is typically given as three or four injections over six months. You can't get hepatitis B from the vaccine. The hepatitis B vaccine is recommended for: Newborns Children and adolescents not vaccinated at birth Those who work or live in a center for people who are developmentally disabled People who live with someone who has hepatitis B Health care workers, emergency workers and other people who come into contact with blood Anyone who has a sexually transmitted infection, including HIV Men who have sex with men People who have multiple sexual partners Sexual partners of someone who has hepatitis B People who inject illegal drugs or share needles and syringes People with chronic liver disease People with end-stage kidney disease Travelers planning to go to an area of the world with a high hepatitis B infection rate

Influenza virus

Influenza, commonly known as "the flu", is an infectious disease caused by an influenza virus.[1] Symptoms can be mild to severe.[4] The most common symptoms include: a high fever, runny nose, sore throat, muscle pains, headache, coughing, and feeling tired.[1] These symptoms typically begin two days after exposure to the virus and most last less than a week.[1] The cough, however, may last for more than two weeks.[1] In children, there may be nausea and vomiting, but these are not common in adults.[5] Nausea and vomiting occur more commonly in the unrelated infection gastroenteritis, which is sometimes inaccurately referred to as "stomach flu" or the "24-hour flu".[5] Complications of influenza may include viral pneumonia, secondary bacterial pneumonia, sinus infections, and worsening of previous health problems such as asthma or heart failure.[2][4] ssRNA virus Three types of influenza viruses affect people, called Type A, Type B, and Type C.[2] Usually, the virus is spread through the air from coughs or sneezes.[1] This is believed to occur mostly over relatively short distances.[6] It can also be spread by touching surfaces contaminated by the virus and then touching the mouth or eyes.[4][6] A person may be infectious to others both before and during the time they are showing symptoms.[4] The infection may be confirmed by testing the throat, sputum, or nose for the virus.[2] A number of rapid tests are available; however, people may still have the infection if the results are negative.[2] A type of polymerase chain reaction that detects the virus's RNA is more accurate.[2] Frequent hand washing reduces the risk of viral spread.[3] Wearing a surgical mask is also useful.[3] Yearly vaccinations against influenza are recommended by the World Health Organization for those at high risk.[1] The vaccine is usually effective against three or four types of influenza.[1] It is usually well tolerated.[1] A vaccine made for one year may not be useful in the following year, since the virus evolves rapidly.[1] Antiviral drugs such as the neuraminidase inhibitor oseltamivir, among others, have been used to treat influenza.[1] Their benefits in those who are otherwise healthy do not appear to be greater than their risks.[7] No benefit has been found in those with other health problems.[7][8] Influenza spreads around the world in a yearly outbreak, resulting in about three to five million cases of severe illness and about 250,000 to 500,000 deaths.[1] In the Northern and Southern parts of the world, outbreaks occur mainly in winter while in areas around the equator outbreaks may occur at any time of the year.[1] Death occurs mostly in the young, the old and those with other health problems.[1] Larger outbreaks known as pandemics are less frequent.[2] In the 20th century, three influenza pandemics occurred: Spanish influenza in 1918 (~50 million deaths), Asian influenza in 1957 (two million deaths), and Hong Kong influenza in 1968 (one million deaths).[9] The World Health Organization declared an outbreak of a new type of influenza A/H1N1 to be a pandemic in June 2009.[10] Influenza may also affect other animals, including pigs, horses, and birds. Approximately 33% of people with influenza are asymptomatic.[14] Symptoms of influenza can start quite suddenly one to two days after infection. Usually the first symptoms are chills and body aches, but fever is also common early in the infection, with body temperatures ranging from 38 to 39 °C (approximately 100 to 103 °F).[15] Many people are so ill that they are confined to bed for several days, with aches and pains throughout their bodies, which are worse in their backs and legs.[16] Symptoms of influenza Fever and chills Cough Nasal congestion Runny nose Sneezing Sore throat Hoarseness Ear pressure Earache Muscle aches Fatigue Headache Irritated, watering eyes Reddened eyes, skin (especially face), mouth, throat and nose Petechial rash[17] In children, gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain,[18][19] (may be severe in children with influenza B)[20] It can be difficult to distinguish between the common cold and influenza in the early stages of these infections.[21] Influenza is a mixture of symptoms of common cold and pneumonia, body ache, headache, and fatigue. Diarrhea is not normally a symptom of influenza in adults,[12] although it has been seen in some human cases of the H5N1 "bird flu"[22] and can be a symptom in children.[18] The symptoms most reliably seen in influenza are shown in the adjacent table.[12] Since antiviral drugs are effective in treating influenza if given early (see treatment section, below), it can be important to identify cases early. Of the symptoms listed above, the combinations of fever with cough, sore throat and/or nasal congestion can improve diagnostic accuracy.[23] Two decision analysis studies[24][25] suggest that during local outbreaks of influenza, the prevalence will be over 70%,[25] and thus patients with any of these combinations of symptoms may be treated with neuraminidase inhibitors without testing. Even in the absence of a local outbreak, treatment may be justified in the elderly during the influenza season as long as the prevalence is over 15%.[25] The available laboratory tests for influenza continue to improve. The United States Centers for Disease Control and Prevention (CDC) maintains an up-to-date summary of available laboratory tests.[26] According to the CDC, rapid diagnostic tests have a sensitivity of 50-75% and specificity of 90-95% when compared with viral culture.[27] These tests may be especially useful during the influenza season (prevalence=25%) but in the absence of a local outbreak, or peri-influenza season (prevalence=10%[25]). Occasionally, influenza can cause severe illness including primary viral pneumonia or secondary bacterial pneumonia.[28][29] The obvious symptom is trouble breathing. In addition, if a child (or presumably an adult) seems to be getting better and then relapses with a high fever, that is a danger sign since this relapse can be bacterial pneumonia.[30] Sometimes, influenza may have abnormal presentations, like confusion in the elderly and a sepsis-like syndrome in the young[31]. Encephalitis due to the flu is rare but not unheard of. One patient and his sibling had a fever, severe diarrhea, and lowering consciousness, followed by seizures and a coma and eventually death without any respiratory disease.[32] One elderly man had confusion, a steadily lowering Glasgow Coma Scale, and soon a coma. He survived, but he had residual neurological symptoms like paraplegia and urinary incontinence.[33] Emergency warning signs Shortness of breath Chest pain Dizziness Confusion Extreme vomiting Flu symptoms that improve but then relapse with a high fever and severe cough (can be bacterial pneumonia) Cyanosis Fever and a rash. Not drinking fluids Signs of dehydration (in infants) Far fewer wet diapers than regularly[34] Cannot keep down fluids (in infants) No tears when crying. Types of virus Structure of the influenza virion. The hemagglutinin (HA) and neuraminidase (NA) proteins are shown on the surface of the particle. The viral RNAs that make up the genome are shown as red coils inside the particle and bound to ribonuclearproteins (RNP). In virus classification influenza viruses are RNA viruses that make up three of the five genera of the family Orthomyxoviridae:[35] Influenzavirus A Influenzavirus B Influenzavirus C These viruses are only distantly related to the human parainfluenza viruses, which are RNA viruses belonging to the paramyxovirus family that are a common cause of respiratory infections in children such as croup,[36] but can also cause a disease similar to influenza in adults.[37] A fourth family of influenza viruses has been proposed - influenza D.[38][39][40][41][42][43][44] The type species for this family is Bovine Influenza D virus which was first isolated in 2012.

Mumps virus

Mumps is a contagious disease caused by a virus. It typically starts with a few days of fever, headache, muscle aches, tiredness, and loss of appetite, followed by swollen salivary glands. You can protect yourself and your family against mumps with vaccination. Mumps is a contagious disease caused by a virus. It spreads through saliva or mucus from the mouth, nose, or throat. An infected person can spread the virus by coughing, sneezing, or talking, sharing items, such as cups or eating utensils, with others, and touching objects or surfaces with unwashed hands that are then touched by others. Mumps likely spreads before the salivary glands begin to swell and up to five days after the swelling begins. Mumps is best known for the puffy cheeks and swollen jaw that it causes. This is a result of swollen salivary glands. The most common symptoms include: Fever Headache Muscle aches Tiredness Loss of appetite Swollen and tender salivary glands under the ears on one or both sides (parotitis) Symptoms typically appear 16-18 days after infection, but this period can range from 12-25 days after infection. Some people who get mumps have very mild or no symptoms, and often they do not know they have the disease. Most people with mumps recover completely in a few weeks.

Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8)

Kaposi's sarcoma-associated herpesvirus (KSHV) is the eighth human herpesvirus; its formal name according to the International Committee on Taxonomy of Viruses (ICTV) is HHV-8. Like other herpesviruses, its informal name (KSHV) is used interchangeably with its more formal ICTV name. This virus causes Kaposi's sarcoma, a cancer commonly occurring in AIDS patients,[1] as well as primary effusion lymphoma,[2] some types of multicentric Castleman's disease and KSHV inflammatory cytokine syndrome.[3] It is one of seven currently known human cancer viruses, or oncoviruses. dsDNA virus HHV-8 is transmitted through saliva, but infection may also be acquired through sexual intercourse, blood transfusion, and organ transplantation [141]. HHV-8 causes Kaposi sarcoma (KS) and is linked with primary effusion lymphoma and multicentric Castleman disease (Table 8.4) [142]. HHV-8 has also been reported to cause fever and other constitutional symptoms, bone marrow suppression, hemophagocytic syndrome, and clonal gammopathy after transplantation [143-145]. Diagnosis of KS and other HHV-8-associated malignancies requires histopathologic evaluation of biopsied tissue. HHV-8 testing with IHC or PCR of biopsied tissue is not essential, but can be helpful if the diagnosis is unclear. Detection and quantitation of HHV-8 DNA in PBMCs and plasma can aid in predicting the development of KS and treatment outcomes. In one study, KS incidence was 10-fold higher in HIV-positive patients with detectable PBMC-associated HHV-8 DNA (30.3 per 100 person years vs 3.4 per 100 person years) compared to those without detectable HHV-8 DNA [146]. Pretreatment HHV-8 DNA levels in plasma in patients with KS have also been associated with decreased survival and poor clinical response to treatment, and thus may be useful in risk stratification, selection of treatment strategy, and monitoring treatment response [147-149]. A study comparing simultaneously collected plasma and PBMCs from patients with different HHV-8-related lymphoproliferative diseases found comparable plasma and PBMC HHV-8 levels, suggesting that either specimen type may be suitable for HHV-8 testing [150]. Regardless of which blood compartment is evaluated, more studies are needed to further determine the clinical utility of HHV-8 quantitation in patients at risk for KS, as well as those patients that have already developed disease.

Norovirus

Norovirus, sometimes referred to as the winter vomiting bug, is the most common cause of gastroenteritis.[5] Infection is characterized by diarrhea, vomiting, and stomach pain.[1] Blood is not usually present.[2] Fever or headaches may also occur.[1] This usually develops 12 to 48 hours after being exposed.[1] Recovery typically occurs within 1 to 3 days.[1] Complications may include dehydration.[1] The virus is usually spread by the fecal-oral route.[2] This may be by contaminated food or water or person-to-person contact.[2] It may also spread via contaminated surfaces or through the air.[2] Risk factors include unsanitary food preparation.[2] Diagnosis is generally based on symptoms.[2] Confirmatory testing may be done for public health purposes.[2] Prevention involves proper hand washing and disinfection of contaminated surfaces.[3] Alcohol-based hand sanitizers are less effective.[3] A vaccine does not exist.[3] There is no specific treatment.[4] Efforts involve supportive care such as drinking sufficient fluids or intravenous fluids.[4] Norovirus results in about 685 million cases of disease and 200,000 deaths globally a year.[5][6] It is common both in the developed and developing world.[2][7] Those under the age of five are most often affected and in this group it results in about 50,000 deaths in the developing world.[5] Disease more commonly occurs in winter months.[5] It often occurs in outbreaks, especially among those living in close quarters.[2] In the United States it is the cause of about half of food-borne disease outbreaks.[2] The disease is named after Norwalk, Ohio, where an outbreak occurred in 1972 Norovirus infection is characterized by nausea, vomiting, watery diarrhea, abdominal pain, and in some cases, loss of taste. A person usually develops symptoms of gastroenteritis 12 to 48 hours after being exposed to norovirus.[9] General lethargy, weakness, muscle aches, headaches, and low-grade fevers may occur. The disease is usually self-limiting, and severe illness is rare. Although having norovirus can be unpleasant, it is not usually dangerous and most who contract it make a full recovery within two to three days Noroviruses are transmitted directly from person to person (62-84% of all reported outbreaks)[11] and indirectly via contaminated water and food. They are extremely contagious, and fewer than twenty virus particles can cause an infection[12] (some research suggests as few as five).[13] Transmission can be aerosolized when those stricken with the illness vomit, and can be aerosolized by a toilet flush when vomit or diarrhea is present; infection can follow eating food or breathing air near an episode of vomiting, even if cleaned up.[14] The viruses continue to be shed after symptoms have subsided and shedding can still be detected many weeks after infection.[15] Vomiting, in particular, transmits infection effectively, and appears to allow airborne transmission. In one incident, a person who vomited spread infection across a restaurant, suggesting that many unexplained cases of food poisoning may have their source in vomit.[16] In December 1998, 126 people were dining at six tables; one woman vomited onto the floor. Staff quickly cleaned up, and people continued eating. Three days later others started falling ill; 52 people reported a range of symptoms, from fever and nausea to vomiting and diarrhea. The cause was not immediately identified. Researchers plotted the seating arrangement: more than 90% of the people at the same table as the sick woman later reported becoming ill. There was a direct correlation between the risk of infection of people at other tables and how close they were to the sick woman. More than 70% of the diners at an adjacent table fell ill; at a table on the other side of the restaurant, the attack rate was still 25%. The outbreak was attributed to a Norwalk-like virus (norovirus). Other cases of transmission by vomit were later identified.[17] In one outbreak at an international scout jamboree in the Netherlands, each person with gastroenteritis infected an average of 14 people before increased hygiene measures were put in place. Even after these new measures were enacted, an ill person still infected an average of 2.1 other people.[18] A US CDC study of 11 outbreaks in New York State lists the suspected mode of transmission as person-to-person in seven outbreaks, foodborne in two, waterborne in one, and one unknown. The source of waterborne outbreaks may include water from municipal supplies, wells, recreational lakes, swimming pools and ice machines.[19] Shellfish and salad ingredients are the foods most often implicated in norovirus outbreaks. Ingestion of shellfish that have not been sufficiently heated - under 75 °C (167 °F) - poses a high risk for norovirus infection.[20][21] Foods other than shellfish may be contaminated by infected food handlers.[22] Many norovirus outbreaks have been traced to food that was handled by one infected person Noroviruses (NoV) are a genetically diverse group of single-stranded positive-sense RNA, non-enveloped viruses belonging to the family Caliciviridae. When a person becomes infected with norovirus, the virus is replicated within the small intestine. After approximately one to two days, norovirus infection symptoms can appear. The principal symptom is acute gastroenteritis that develops between 12 and 48 hours after exposure, and lasts for 24-72 hours.[45] The disease is usually self-limiting, and characterized by nausea, forceful vomiting, watery diarrhea, and abdominal pain, and in some cases, loss of taste. General lethargy, weakness, muscle aches, headache, coughs, and low-grade fever may occur. Severe illness is rare; although people are frequently treated at the emergency ward, they are rarely admitted to the hospital. The number of deaths from norovirus in the United States is estimated to be around 300 each year, with most of these occurring in the very young, the elderly, and persons with weakened immune systems. Symptoms may become life-threatening in these groups if dehydration or electrolyte imbalance is ignored or not treated There is no specific medicine to treat people with norovirus illness. Norovirus infection cannot be treated with antibiotics because it is not a bacterial infection. Treatments aim to avoid complications by measures such as the management of dehydration caused by fluid loss in vomiting and diarrhea,[4] and to mitigate symptoms using antiemetics and antidiarrheals.

Rotavirus

Rotavirus is a contagious virus that can cause gastroenteritis (inflammation of the stomach and intestines). Symptoms include severe watery diarrhea, often with vomiting, fever, and abdominal pain. Infants and young children are most likely to get rotavirus disease. They can become severely dehydrated and need to be hospitalized and can even die. Rotavirus vaccines are very effective at preventing rotavirus disease. Children should get either of the two available rotavirus vaccines: RotaTeq® (RV5) is given in 3 doses at ages 2 months, 4 months, and 6 months Rotarix® (RV1) is given in 2 doses at ages 2 months and 4 months. People who are infected with rotavirus shed the virus in their feces (poop). If you accidently get poop in your mouth, you can get infected with rotavirus. This can happen by having contact with someone who is infected with rotavirus touching contaminated objects or surfaces then putting your fingers in your mouth consuming contaminated food and liquids Rotavirus is the most common cause of diarrhoeal disease among infants and young children.[1] It is a genus of double-stranded RNA viruses in the family Reoviridae. Nearly every child in the world is infected with rotavirus at least once by the age of five.[2] Immunity develops with each infection, so subsequent infections are less severe; adults are rarely affected.[3] There are eight species of this virus, referred to as A, B, C, D, E, F, G and H. Rotavirus A, the most common species, causes more than 90% of rotavirus infections in humans. The virus is transmitted by the faecal-oral route. It infects and damages the cells that line the small intestine and causes gastroenteritis (which is often called "stomach flu" despite having no relation to influenza). Although rotavirus was discovered in 1973 by Ruth Bishop and her colleagues by electron micrograph images[4] and accounts for approximately one third of hospitalisations for severe diarrhoea in infants and children,[5] its importance has historically been underestimated within the public health community, particularly in developing countries.[6] In addition to its impact on human health, rotavirus also infects animals, and is a pathogen of livestock.[7] Rotavirus is usually an easily managed disease of childhood, but in 2013, rotavirus caused 37 percent of deaths of children from diarrhoea and 215,000 deaths worldwide,[8] and almost two million more become severely ill.[6] Most of these deaths occurred in developing countries.[9] In the United States, before initiation of the rotavirus vaccination programme, rotavirus caused about 2.7 million cases of severe gastroenteritis in children, almost 60,000 hospitalisations, and around 37 deaths each year.[10] Following rotavirus vaccine introduction in the United States, hospitalisation rates have fallen significantly.[11][12] Public health campaigns to combat rotavirus focus on providing oral rehydration therapy for infected children and vaccination to prevent the disease.[13] The incidence and severity of rotavirus infections has declined significantly in countries that have added rotavirus vaccine to their routine childhood immunisation policies.

Rhinovirus

The rhinovirus (from the Greek ῥίς rhis "nose", gen ῥινός rhinos "of the nose", and the Latin vīrus) is the most common viral infectious agent in humans and is the predominant cause of the common cold. Rhinovirus infection proliferates in temperatures between 33-35 °C (91-95 °F), the temperatures found in the nose. Rhinoviruses is a genus within the Picornaviridae family of viruses. There are currently around 160 recognized types of human rhinoviruses that differ according to their surface proteins (serotypes).[1] They are lytic in nature and are among the smallest viruses, with diameters of about 30 nanometers. By comparison, other viruses, such as smallpox and vaccinia, are around 10 times larger at about 300 nanometers; while flu viruses are around 80-120 nm. There are two modes of transmission: via aerosols of respiratory droplets and from fomites (contaminated surfaces), including direct person-to-person contact. Rhinoviruses are spread worldwide and are the primary cause of the common cold. Symptoms include sore throat, runny nose, nasal congestion, sneezing and cough; sometimes accompanied by muscle aches, fatigue, malaise, headache, muscle weakness, or loss of appetite. Fever and extreme exhaustion are more usual in influenza. Children may have six to twelve colds a year. In the United States, the incidence of colds is higher in the autumn and winter, with most infections occurring between September to April. The seasonality may be due to the start of the school year[citation needed] and to people spending more time indoors (thus in proximity with each other)[citation needed], thereby increasing the chance of transmission of the virus. Lower ambient, especially outdoor, temperatures may also be factor [2] given that rhinoviruses preferentially replicate at 32 °C (89 °F) as opposed to 37 °C (98 °F) - see following section. Variant pollens, grasses, hays and agricultural practices may be factors in the seasonality as well as the use of chemical controls of lawn, paddock and sportsfields within schools and communities. The changes in temperature, humidity and wind patterns seem to be factors. It is also postulated that poor housing, overcrowding and insanitary conditions related to poverty are relevant factors in the transmission of 'common cold'. Those most affected by rhinoviruses are infants, the elderly, and immunocompromised people The primary route of entry for human rhinoviruses is the upper respiratory tract (mouth and nose). Rhinovirus A and B bind to ICAM-1 (Inter-Cellular Adhesion Molecule 1) also known as CD54 (Cluster of Differentiation 54) receptors on respiratory epithelial cells while rhinovirus C uses cadherin-related family member 3 (CDHR3) to mediate cellular entry.[4] As the virus replicates and spreads, infected cells release distress signals known as chemokines and cytokines (which in turn activate inflammatory mediators). Cell lysis occurs at the upper respiratory epithelium. Infection occurs rapidly, with the virus adhering to surface receptors within 15 minutes of entering the respiratory tract. High-risk individuals include children and the elderly. Just over 50% of individuals will experience symptoms within 2 days of infection. Only about 5% of cases will have an incubation period of less than 20 hours, and, at the other extreme, it is expected that 5% of cases would have an incubation period of greater than four and a half days.[5] Human rhinoviruses preferentially grow at 32 °C (89 °F), notably colder than the average human body temperature of 37 °C (98 °F); hence the virus's tendency to infect the upper respiratory tract, where respiratory airflow is in continual contact with the (colder) extrasomatic environment. Rhinovirus C, unlike the A and B species, may be able to cause severe infections.[6] This association disappears after controlling for confounders Single-stranded positive sense RNA Interferon-alpha used intranasally was shown to be effective against Human rhinovirus infections. However, volunteers treated with this drug experienced some side effects, such as nasal bleeding, and began developing resistance to the drug. Subsequently, research into the treatment was abandoned There are no vaccines against these viruses as there is little-to-no cross-protection between serotypes. At least 99 serotypes of Human rhinoviruses affecting humans have been sequenced.[16][17] However, a study of the VP4 protein has shown it to be highly conserved among many serotypes of Human rhinovirus,[18] opening up the potential for a future pan-serotype Human rhinovirus vaccine. Human rhinovirus is most contagious during the fall and winter months. The virus can live up to 3 hours outside of a human host. Once contracted, a person is most contagious within the first 3 days. Preventative measures such as regular vigorous hand washing with soap and water may aid in avoiding the virus. Avoiding touching the mouth, eyes and nose, the most common entry points for rhinovirus, may also aid in prevention. Droplet precautions, which is a surgical mask and gloves, is the method used in major hospitals.

Trypanosoma brucei

Trypanosoma brucei is a species of parasitic kinetoplastid belonging to the genus Trypanosoma. The parasite is the cause of a vector-borne disease of vertebrate animals, including humans, carried by genera of tsetse fly in sub-Saharan Africa. In humans T. brucei causes African trypanosomiasis, or sleeping sickness. In animals it causes animal trypanosomiasis, also called nagana in cattle and horses. T. brucei has traditionally been grouped into three subspecies: T. b. brucei, T. b. gambiense and T. b. rhodesiense.[1] The first is a parasite of non-human vertebrates, while the latter two are the known parasites of humans. Only rarely can the T. b. brucei infect a human.[2] T. brucei is transmitted between mammal hosts by an insect vector belonging to different species of tsetse fly (Glossina). Transmission occurs by biting during the insect's blood meal. The parasites undergo complex morphological changes as they move between insect and mammal over the course of their life cycle. The mammalian bloodstream forms are notable for their cell surface proteins, variant surface glycoproteins, which undergo remarkable antigenic variation, enabling persistent evasion of host adaptive immunity leading to chronic infection. T. brucei is one of only a few pathogens known to cross the blood brain barrier.[3] There is an urgent need for the development of new drug therapies, as current treatments can have severe side effects and can prove fatal to the patient.[4] Whilst not historically regarded as T. brucei subspecies due to their different means of transmission, clinical presentation, and loss of kinetoplast DNA, genetic analyses reveal that T. equiperdum and T. evansi are evolved from parasites very similar to T. b. brucei, and are thought to be members of the brucei clade.[5] The parasite was discovered in 1894 by Sir David Bruce, after whom the scientific name was given in 1899. T. brucei is a typical unicellular eukaryotic cell, and measures 8 to 50 μm in length. T. brucei completes its life cycle between tsetsefly (of the genus Glossina) and mammalian hosts, including humans, cattle, horses, and wild animals. wild animals. In mammalian host Infection occurs when a vector tsetse fly bites a mammalian host. The fly injects the metacyclic trypomastigotes into the skin tissue. The trypomastigotes enter the lymphatic system and into the bloodstream. The initial trypomastigotes are short and stumpy. Once inside the bloodstream, they grow into long and slender forms. Then, they multiply by binary fission. The daughter cells then become short and stumpy again.[13][14] The long slender forms are able to penetrate the blood vessel endothelium and invade extravascular tissues, including the central nervous system (CNS).[12] Sometimes, wild animals can be infected by the tsetse fly and they act as reservoirs. In these animals, they do not produce the disease, but the live parasite can be transmitted back to the normal hosts. The short and stumpy trypomastigotes are taken up by tsetse fly during blood meal. The trypomastigotes enter the midgut of the fly where they become procyclic trypomastigotes. These rapidly divide to become epimastigotes. The epimastigotes migrate from the gut via the proventriculus to the salivary glands where they get attached to the salivary gland epithelium. In the salivary glands, some parasites detach and undergo transformation into short and stumpy trypomastigotes. These become the infective metacyclic trypomastigotes. They are injected into the mammalian host along with the saliva on biting. Complete development in the fly takes about 20 days. Reproduces through binary fission In later stages of a T. brucei infection of a mammalian host the parasite may migrate from the bloodstream to also infect the lymph and cerebrospinal fluids. It is under this tissue invasion that the parasites produce the sleeping sickness.[13] In addition to the major form of transmission via the tsetse fly T. brucei, may be transferred between mammals via bodily fluid exchange, such as by blood transfusion or sexual contact, although this is thought to be rare. T. brucei is found where the tsetse fly vectors are prevalent. It is present in tropical and subtropical areas of Africa north of the equator, covering East, Central and West Africa.[10] Hence, the equatorial region of Africa is called the "sleeping sickness" belt. However, the specific type of the trypanosome differs according to geography. T. b. rhodesiense is found primarily in East Africa (Botswana, Ethiopia, Kenya, Malawi, Tanzania, Uganda, Zaire, and Zimbabwe), while T. b. gambiense is found in Central and West Africa

West Nile virus

West Nile is a virus most commonly spread to people by mosquito bites. In North America, cases of West Nile virus (WNV) occur during mosquito season, which starts in the summer and continues through fall. WNV cases have been reported in all of the continental United States. There are no vaccines to prevent or medications to treat WNV. Fortunately, most people infected with WNV do not have symptoms. About 1 in 5 people who are infected develop a fever and other symptoms. About 1 out of 150 infected people develop a serious, sometimes fatal, illness. You can reduce your risk of WNV by using insect repellent and wearing long-sleeved shirts and long pants to prevent mosquito bites. Prevention: insect repelent West Nile virus is most commonly spread to people by the bite of an infected mosquito. Mosquitoes become infected when they feed on infected birds. Infected mosquitoes then spread West Nile virus to people and other animals by biting them. In a very small number of cases, West Nile virus has been spread through: Exposure in a laboratory setting Blood transfusion and organ donation Mother to baby, during pregnancy, delivery, or breast feeding West Nile virus is not spread: Through coughing, sneezing, or touching By touching live animals From handling live or dead infected birds. Avoid bare-handed contact when handling any dead animal. If you are disposing of a dead bird, use gloves or double plastic bags to place the carcass in a garbage can. Through eating infected birds or animals. Always follow instructions for fully cooking meat from either birds or mammals. No symptoms in most people. Most people (8 out of 10) infected with West Nile virus do not develop any symptoms. Febrile illness (fever) in some people. About 1 in 5 people who are infected develop a fever with other symptoms such as headache, body aches, joint pains, vomiting, diarrhea, or rash. Most people with this type of West Nile virus disease recover completely, but fatigue and weakness can last for weeks or months. Serious symptoms in a few people. About 1 in 150 people who are infected develop a severe illness affecting the central nervous system such as encephalitis (inflammation of the brain) or meningitis (inflammation of the membranes that surround the brain and spinal cord). Symptoms of severe illness include high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness and paralysis. Severe illness can occur in people of any age; however, people over 60 years of age are at greater risk. People with certain medical conditions, such as cancer, diabetes, hypertension, kidney disease, and people who have received organ transplants, are also at greater risk. Recovery from severe illness might take several weeks or months. Some effects to the central nervous system might be permanent. About 1 out of 10 people who develop severe illness affecting the central nervous system die. Diagnosis See your healthcare provider if you develop the symptoms described above. Your healthcare provider can order tests to look for West Nile virus infection. To learn more about testing, visit our Healthcare Providers page. Treatment No vaccine or specific antiviral treatments for West Nile virus infection are available. Over-the-counter pain relievers can be used to reduce fever and relieve some symptoms In severe cases, patients often need to be hospitalized to receive supportive treatment, such as intravenous fluids, pain medication, and nursing care. If you think you or a family member might have West Nile virus disease, talk with your health care provider.

Enterovirus D68

What is enterovirus D68? Enterovirus D68 (EV-D68) is one of more than 100 non-polio enteroviruses. This virus was first identified in California in 1962. How common is EV-D68 in the United States? Small numbers of EV-D68 have been reported regularly to CDC since 1987. However, during 2014 the number of people reported with confirmed EV-D68 infection was much greater than that reported in previous years. We can't predict whether EV-D68 will be a common type of enterovirus detected this year or in future seasons. That's because a mix of enteroviruses circulates every year, and different types of enteroviruses can be common in different years. What time of the year are people most likely to get infected? In the United States, you are more likely to get infected with enteroviruses in the summer and fall. However, you can get infected year round. A large outbreak of EV-D68 occurred in 2014. How many people got sick ? In summer and fall 2014, the United States experienced a nationwide outbreak of EV-D68 associated with severe respiratory illness. From mid-August 2014 to January 15, 2015, CDC or state public health laboratories confirmed a total of 1,153 people in 49 states and the District of Columbia with respiratory illness caused by EV-D68. Almost all of the confirmed cases were among children, many whom had asthma or a history of wheezing. Additionally, there were likely many thousands of mild EV-D68 infections for which people did not seek medical treatment and/or get tested. This was the first documented nationwide outbreak of EV-D68. EV-D68 cases in years since 2014 have been reported more sporadically, which is considered typical. CDC received about 2,600 specimens for enterovirus testing during 2014, which was substantially more than usual. About 36% of those tested positive for EV-D68. About 33% tested positive for an enterovirus or rhinovirus other than EV-D68. What are the symptoms of EV-D68 infection? EV-D68 can cause mild to severe respiratory illness, or no symptoms at all. Mild symptoms may include runny nose, sneezing, cough, body aches, and muscle aches. Severe symptoms may include wheezing and difficulty breathing. Anyone with respiratory illness should contact their doctor if they are having difficulty breathing or if their symptoms are getting worse. How does the virus spread? Since EV-D68 causes respiratory illness, the virus can be found in an infected person's respiratory secretions, such as saliva, nasal mucus, or sputum. EV-D68 likely spreads from person to person when an infected person coughs, sneezes, or touches a surface that is then touched by others. Who is at risk? In general, infants, children, and teenagers are most likely to get infected with enteroviruses and become ill. That's because they do not yet have immunity (protection) from previous exposures to these viruses. We believe this is also true for EV-D68. Adults can get infected with enteroviruses, but they are more likely to have no symptoms or mild symptoms. Children with asthma may have a higher risk for severe respiratory illness caused by EV-D68 infection. How is it diagnosed? EV-D68 can only be diagnosed by doing specific lab tests on specimens from a person's nose and throat, or blood. Many hospitals and some doctor's offices can test ill patients to see if they have enterovirus infection. However, most cannot do specific testing to determine the type of enterovirus, like EV-D68. CDC and some state health departments can do this sort of testing using a real-time reverse transcription polymerase chain reaction (rRT-PCR) lab test, which allows testing and reporting of results within a few days of receiving specimens. Health departments may contact CDC for further enterovirus typing. What are the treatments? There is no specific treatment for people with respiratory illness caused by EV-D68. Talk to a doctor about your symptoms and the best way to control them. Some people with severe respiratory illness may need to be hospitalized and receive intensive supportive therapy. There are no antiviral medications currently available for people who become infected with EV-D68.

Plasmodium falciparum

-a protozoan parasite that causes an infectious disease known as malaria. P. falciparum is the most severe strain of the malaria species correlated with almost every malarial death.[1] The other 3 species that cause malaria include: P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which, transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to adhere to blood vessels, cytoadherence, as well as to other red blood cells.[2] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. -Transmission of P. falciparum occurs between humans and Anopheles mosquitoes. Mosquito vectors pass malaria from host to host. The parasite can infect the mosquitoes through the in take of human blood or a human may be infected by the mosquito's injection of saliva. [1] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [4] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. -continues to increase in drug-resistant populations and insecticide-resistant mosquitoes leading to the prediction that the disease will only worsen over time. -sickle cell resistance -normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise -In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum. [1] Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth. Young children are also at higher risk for more severe infections due to the immaturity of their immune systems. -Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P.falciparumare seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots -The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite.

Coxiella burnetii

Coxiella burnetii is an obligate intracellular bacterial pathogen, and is the causative agent of Q fever. The genus Coxiella is morphologically similar to Rickettsia, but with a variety of genetic and physiological differences. C. burnetii is a small Gram-negative bacterium that is highly resistant to environmental stresses such as high temperature, osmotic pressure, and ultraviolet light. These characteristics are attributed to a small cell variant form of the organism that is part of a biphasic developmental cycle, including a more metabolically and replicatively active large cell variant form.[1] It can survive standard disinfectants, and is resistant to many other environmental changes like those presented in the phagolysosome. Coxiella burnetii is an obligate intracellular Gram-negative coccobacillus bacterium that is known to be the main pathogen that causes Q fever in mammals and humans. (3) Harold Cox and MacFarlane Burnet initially identified Q fever as "query fever" in 1935 when a number of infections were found to be from an Australian slaughterhouse. Once this disease was elucidated to be a human pathogen, the name was properly changed to Q fever. (4) Its global pathogenic effect demonstrates the need for preventive measures to control the rate of infection worldwide and its potential use for bioterrorism. The significance of a completed sequenced genome is the benefit of being able to further understand the mechanisms of pathogenesis and use this knowledge to fight against this infectious disease. Sheep, cattle, and goats are major sources of Coxiella burnetii that can potentially help spread the disease to other organisms. The most common mode of transmission to humans is primarily through external waste excretions from infected animals. The aerosol route to infection is frequent by inhalation of contaminated air that contains many of these organisms or through an insect vector. (5) Coxiella burnetii live in a wildlife livestock environment and can withstand heat, dryness, and antibacterial compounds, allowing this bacterium to persist outside the host for an extensively long period of time. It is an acidophile, meaning it tends to surround itself in an environment with low pH. Uniquely enough, it can be endocytosed by a macrophage and complete replication inside the phagolysozyme during its life cycle.

T4 phage

Enterobacteria phage T4 is a bacteriophage that infects Escherichia coli bacteria. The T4 phage is a member of the T-even phages, a group including enterobacteriophages T2 and T6. T4 is capable of undergoing only a lytic lifecycle and not the lysogenic lifecycle. dsDNA Bacteriophage T4 is a double-stranded DNA (dsDNA) contractile-tailed virus that infects the Escherichia coli strains. The T4-like subgroup of Myoviridae (Ackermann, 1999) is widely spread, propagates on a broad range of bacterial hosts that grow in diverse environments, and represents one of the most numerically abundant genetic domains in the biosphere (Brussow and Hendrix, 2002). Studies of the evolution of the phages and their impact in natural ecosystems are now flourishing (Hendrix, 2002; Hendrix et al., 1999; Wommack and Colwell, 2000). During the past five decades, bacteriophage T4 has provided an experimental model system for combining genetic, biochemical, and structural research to understand the mechanisms controlling assembly and morphogenesis of complex biologic systems and viruses (Kellenberger, 1966, 1980, 1990; Wood, 1980). The principles realized in the T4 assembly can be encountered in a broader range of cell biology processes, including cytoskeleton biology, signaling pathways, transcription, protein trafficking, and assembly of other viruses. The AT-rich (65.5%) T4 genome of 168,903 bps has 289 open reading frame encoded proteins, 8 t-RNA genes, and at least 2 other genes that encode small but stable RNAs of unknown function (Kutter et al., 1993; Miller et al., 2003). More than 150 T4 genes have been characterized by genetic analysis or by the analysis of cloned gene products, but only 62 genes are "essential" under standard laboratory conditions. Among known viruses studied on the molecular level, the virion of bacteriophage T4 is extremely structurally complex (Fig. 1). The T4 virion is built by more than 1500 protein subunits that represent about 50 different gene products. Of these, 24 gene products are involved in the head assembly, 22 in the tail assembly, and 6 in formation of the tail fibers. More than 10 other genes code for scaffolding, which involves catalytic and chaperone-like proteins that assist in protein folding and protein assembly but that are not present in the assembled infectious virion particle. The mature T4 particle consists of a 1150-Å long and 850-Å wide prolate head encapsidating a single molecule of genomic dsDNA; a 1000-Å long and 210-Å diameter contractile tail formed on a 500-Å diameter baseplate; and six long tail fibers (LTFs) of 1450 Å attached to the baseplate (Eiserling and Black, 1994). Bacteriophage T4 assembly occurs by one of the most complex processes so far extensively characterized at the molecular level using a combination of electron microscopy, genetics, and biochemical approaches. As was established a long time ago, a T4 head, a tail, LTFs, and whiskers are assembled via four independent pathways and joined together to form a mature infectious virion (Edgar and Lielausis, 1968; Wood et al., 1968). Many of the steps in the T4 assembly could proceed by complementation in vitro, with production of infectious particles when extracts of the mutant-infected cells that produce different phage components are incubated together (Edgar and Lielausis, 1968; Edgar and Wood, 1966). In addition, phage components isolated from one mutant could be assayed for ability to complement each other to correct the defective function. Most of the T4 genes that code structural proteins are expressed during the latter half of the infectious cycle, and they are largely clustered. Because all proteins of the T4 particle are synthesized simultaneously, the order of their assembly cannot result from the temporal regulation of gene products synthesis but must be controlled at the level of protein interaction (Kellenberger, 1976). The level of finished T4 parts does not appear to exert feedback controls on their production level or on the production of other components. Instead, the T4 genetic system appears to be settled to produce components in fixed relative amounts with tails and tail fibers in excess over heads, presumably maximizing the probability that assembled heads containing the genomic DNA will become converted to infectious particles (Wood, 1980). Recent breakthroughs in X-ray crystallography and cryo-electron microscopy (Adrian et al., 1984; Dubochet et al., 1988; Rossmann et al., 2001) have made it possible to extend the structural knowledge of T4 to a higher resolution. Success of Michael Rossmann's laboratory in determining the atomic structures of a number of T4 virion proteins, such as gene product (gp) whiskers antigen control (wac) or fibritin (Strelkov et al., 1997, 1998; Tao et al., 1997), gp8 (Leiman et al., 2003), gp9 (Kostyuchenko et al., 1999), gp11 (Leiman et al., 2000), gp5-gp27 complex (Kanamaru et al., 2002), and Mark van Raaij's group success in solving the gp12 structure (Thomassen et al., 2003; van Raaij et al., 2001) provided insight into the processes that link the initial recognition of the tail fibers of the host receptors with the subsequent injection of the viral DNA into the host. Latest developments in cryo-electron microscopy and three-dimensional (3-D) image reconstruction (Kostyuchenko et al., 2003) have explained further the regulation of the T4 assembly pathways and the functioning of infection machinery. The stepping stones for this review are the chapters of Kellenberger (1990), Black et al. (1994), Coombs and Arisaka (1994), Wood et al. (1994), and Leiman et al. (2003), and Rossmann et al. (2004). This review aims to summarize briefly the current knowledge of the T4 structure and assembly pathways and to point out the most significant recent results in this area. Furthermore, as the chapter author, I will concentrate on the T4 head structure present data on the individual T4 proteins whose spatial structures were successfully solved recently by X-ray crystallography at atomic resolution. Finally, I attempt to describe the quasi-atomic structure of the T4 baseplate, a multiprotein nanomachine, which controls host-cell recognition and attachment, tail sheath contraction, and viral DNA ejection into cell. The T4 baseplate employs a novel structural element, a rigid molecular cell-puncturing device that contains a lysozyme domain. Its functions are to penetrate the outer cell membrane and to disrupt the peptidoglycan layer for subsequent injection of viral DNA into the host cell.

Lambda phage

Enterobacteria phage λ (lambda phage, coliphage λ) is a bacterial virus, or bacteriophage, that infects the bacterial species Escherichia coli (E. coli). It was discovered by Esther Lederberg in 1950 when she noticed that streaks of mixtures of two E. coli strains, one of which treated with ultraviolet light, was "nibbled and plaqued".[1][2] The wild type of this virus has a temperate lifecycle that allows it to either reside within the genome of its host through lysogeny or enter into a lytic phase (during which it kills and lyses the cell to produce offspring); mutant strains are unable to lysogenize cells - instead, they grow and enter the lytic cycle after superinfecting an already lysogenized cell.[3] The phage particle consists of a head (also known as a capsid), a tail, and tail fibers (see image of virus below). The head contains the phage's double-strand linear DNA genome. During infection, the phage particle recognizes and binds to its host, E. coli, causing DNA in the head of the phage to be ejected through the tail into the cytoplasm of the bacterial cell. Usually, a "lytic cycle" ensues, where the lambda DNA is replicated and new phage particles are produced within the cell. This is followed by cell lysis, releasing the cell contents, including virions that have been assembled, into the environment. However, under certain conditions, the phage DNA may integrate itself into the host cell chromosome in the lysogenic pathway. In this state, the λ DNA is called a prophage and stays resident within the host's genome without apparent harm to the host. The host is termed a lysogen when a prophage is present. This prophage may enter the lytic cycle when the lysogen enters a stressed condition. Bacteriophage lambda Vectors Bacteriophage lambda is a virus that infects E. coli. The typical infection cycle results in the lysis of the E. coli cell and the release of about 100 progeny phage particles, each capable of infecting another cell. When lambda is plated at low density on a lawn of E. coli cells on agar medium, the resulting pattern of clearings (plaques) in the lawn caused by the lysed cells identify the location of individual lambda clones. Harvesting the phage particles from a plaque (picking a plaque) provides a stock of the phage clones for subsequent rounds of propagation. Like the plasmid vectors, wild-type lambda has been extensively engineered for use as a vector. Genes not essential for the lambda life cycle described above have been removed to make room for carrying exogenous insert DNA. The early popularity of lambda as a cloning vector for genomic library construction is a consequence of the very efficient pathway for getting lambda DNA into E. coli cells. This was in contrast to the inefficient chemical transformation used for plasmids, particularly for larger constructs. The bacteriophage lambda DNA or recombinant lambda DNA-containing inserts is packaged into infectious phage particles using an efficient in vitro packaging reaction. Once the particles are formed, each one can inject its DNA into an E. coli cell. The limit on how much exogenous DNA can be propagated in a lambda vector results from the packaging capacity of the phage particle, approximately 35-50 kb of DNA. Because of the requirement for lambda genes for a productive infection, the amount of insert DNA is restricted to 10-20 kb depending on the specific vector. Figure 2 illustrates the process of constructing a genomic library in a lambda vector.

Hepatitis A virus

Hepatitis A is an infectious disease of the liver caused by the hepatitis A virus (HAV).[6] Many cases have few or no symptoms, especially in the young.[1] The time between infection and symptoms, in those who develop them, is between two and six weeks.[2] When symptoms occur, they typically last eight weeks and may include nausea, vomiting, diarrhea, jaundice, fever, and abdominal pain.[1] Around 10-15% of people experience a recurrence of symptoms during the six months after the initial infection.[1] Acute liver failure may rarely occur, with this being more common in the elderly.[1] It is usually spread by eating food or drinking water contaminated with infected feces.[1] Shellfish which have not been sufficiently cooked are a relatively common source.[7] It may also be spread through close contact with an infectious person.[1] While children often do not have symptoms when infected, they are still able to infect others.[1] After a single infection, a person is immune for the rest of his or her life.[8] Diagnosis requires blood testing, as the symptoms are similar to those of a number of other diseases.[1] It is one of five known hepatitis viruses: A, B, C, D, and E. The hepatitis A vaccine is effective for prevention.[1][3] Some countries recommend it routinely for children and those at higher risk who have not previously been vaccinated.[1][9] It appears to be effective for life.[1] Other preventive measures include hand washing and properly cooking food.[1] No specific treatment is available, with rest and medications for nausea or diarrhea recommended on an as-needed basis.[1] Infections usually resolve completely and without ongoing liver disease.[1] Treatment of acute liver failure, if it occurs, is with liver transplantation.[1] Globally, around 1.4 million symptomatic cases occur each year[1] and about 114 million infections (symptomatic and asymptomatic).[4] It is more common in regions of the world with poor sanitation and not enough safe water.[9] In the developing world, about 90% of children have been infected by age 10, thus are immune by adulthood.[9] It often occurs in outbreaks in moderately developed countries where children are not exposed when young and vaccination is not widespread.[9] Acute hepatitis A resulted in 11,200 deaths in 2015.[5] World Hepatitis Day occurs each year on July 28 to bring awareness to viral hepatitis.

Hepatitis C virus

Hepatitis C virus (HCV) is a small (55-65 nm in size), enveloped, positive-sense single-stranded RNA virus of the family Flaviviridae. Hepatitis C virus is the cause of hepatitis C and some cancers such as liver cancer (hepatocellular carcinoma, abbreviated HCC) and lymphomas in humans. The hepatitis C virus belongs to the genus Hepacivirus, a member of the family Flaviviridae. Until recently it was considered to be the only member of this genus. However a member of this genus has been discovered in dogs: canine hepacivirus.[3] There is also at least one virus in this genus that infects horses.[4] Several additional viruses in the genus have been described in bats and rodents.[5][6] The hepatitis C virus particle consists of a core of genetic material (RNA), surrounded by an icosahedral protective shell of protein, and further encased in a lipid (fatty) envelope of cellular origin. Two viral envelope glycoproteins, E1 and E2, are embedded in the lipid envelope.[7] ssRNA Unlike hepatitis A and B, there is currently no vaccine to prevent hepatitis C infection.[52] Hepatitis C is a liver disease caused by the hepatitis C virus: the virus can cause both acute and chronic hepatitis, ranging in severity from a mild illness lasting a few weeks to a serious, lifelong illness. The hepatitis C virus is a bloodborne virus and the most common modes of infection are through exposure to small quantities of blood. This may happen through injection drug use, unsafe injection practices, unsafe health care, and the transfusion of unscreened blood and blood products. Globally, an estimated 71 million people have chronic hepatitis C infection. A significant number of those who are chronically infected will develop cirrhosis or liver cancer. Approximately 399 000 people die each year from hepatitis C, mostly from cirrhosis and hepatocellular carcinoma. Antiviral medicines can cure more than 95% of persons with hepatitis C infection, thereby reducing the risk of death from liver cancer and cirrhosis, but access to diagnosis and treatment is low. There is currently no vaccine for hepatitis C; however research in this area is ongoing.

Nipah virus

Nipah virus (NiV) is a member of the family Paramyxoviridae, genus Henipavirus. NiV was initially isolated and identified in 1999 during an outbreak of encephalitis and respiratory illness among pig farmers and people with close contact with pigs in Malaysia and Singapore. Its name originated from Sungai Nipah, a village in the Malaysian Peninsula where pig farmers became ill with encephalitis. Given the relatedness of NiV to Hendra virus, bat species were quickly singled out for investigation and flying foxes of the genus Pteropus were subsequently identified as the reservoir for NiV (Distribution Map). In the 1999 outbreak, Nipah virus caused a relatively mild disease in pigs, but nearly 300 human cases with over 100 deaths were reported. In order to stop the outbreak, more than a million pigs were euthanized, causing tremendous trade loss for Malaysia. Since this outbreak, no subsequent cases (in neither swine nor human) have been reported in either Malaysia or Singapore. In 2001, NiV was again identified as the causative agent in an outbreak of human disease occurring in Bangladesh. Genetic sequencing confirmed this virus as Nipah virus, but a strain different from the one identified in 1999. In the same year, another outbreak was identified retrospectively in Siliguri, India with reports of person-to-person transmission in hospital settings (nosocomial transmission). Unlike the Malaysian NiV outbreak, outbreaks occur almost annually in Bangladesh and have been reported several times in India. Transmission of Nipah virus to humans may occur after direct contact with infected bats, infected pigs, or from other NiV infected people. In Malaysia and Singapore, humans were apparently infected with Nipah virus only through close contact with infected pigs. The NiV strain identified in this outbreak appeared to have been transmitted initially from bats to pigs, with subsequent spread within pig populations. Incidental human infections resulted after exposure to infected pigs. No occurrence of person-to-person transmission was reported in this outbreak. Conversely, person-to-person transmission of Nipah virus in Bangladesh and India is regularly reported. This is most commonly seen in the family and caregivers of Nipah virus-infected patients. Transmission also occurs from direct exposure to infected bats. A common example is consumption of raw date palm sap contaminated with infectious bat excretions. Infection with Nipah virus is associated with encephalitis (inflammation of the brain). After exposure and an incubation period of 5 to 14 days,illness presents with 3-14 days of fever and headache, followed by drowsiness, disorientation and mental confusion. These signs and symptoms can progress to coma within 24-48 hours. Some patients have a respiratory illness during the early part of their infections, and half of the patients showing severe neurological signs showed also pulmonary signs. During the Nipah virus disease outbreak in 1998-99, 265 patients were infected with the virus. About 40% of those patients who entered hospitals with serious nervous disease died from the illness. Long-term sequelae following Nipah virus infection have been noted, including persistent convulsions and personality changes. Latent infections with subsequent reactivation of Nipah virus and death have also been reported months and even years after exposure.

Rubella virus

Rubella, or German measles, is an infection caused by the rubella virus. Symptoms are often mild, but if infection occurs during pregnancy, it can cause severe harm to the unborn child, including deafness. Rubella is a preventable disease. Since 1969, vaccination programs have led to a dramatic fall in the number of cases, and it was declared eliminated from the United States in 2004. However, it is important to continue vaccinating as rubella can enter the U.S. from other countries. Between 25 and 50 percent of those who have rubella do not notice that they have it. This means that a person can come into contact with rubella and become infected without realizing it. However, if infection occurs during early pregnancy, it can cause congenital rubella syndrome, and this can have a long-term impact on the fetus. Rubella is viral and predominantly transmitted by coughs. The virus can pass across the placenta and affect the fetus. In around half of rubella cases there are very few symptoms, but symptoms include a rash, a runny nose, a headache, and fever. During pregnancy, rubella can cause congenital rubella syndrome, a leading cause of deafness, in the unborn child. Vaccination is the only way to prevent the disease. Rubella virus (RuV) is the pathogenic agent of the disease rubella, and is the cause of congenital rubella syndrome when infection occurs during the first weeks of pregnancy. Rubella virus is the only member of the genus Rubivirus and belongs to the family of Togaviridae, whose members commonly have a genome of single-stranded RNA of positive polarity which is enclosed by an icosahedral capsid. The molecular basis for the causation of congenital rubella syndrome are not yet completely clear, but in vitro studies with cell lines showed that rubella virus has an apoptotic effect on certain cell types. There is evidence for a p53-dependent mechanism.

Severe acute respiratory syndrome (SARS) virus

Severe acute respiratory syndrome (SARS) is a viral respiratory illness caused by a coronavirus called SARS-associated coronavirus (SARS-CoV). SARS was first reported in Asia in February 2003. The illness spread to more than two dozen countries in North America, South America, Europe, and Asia before the SARS global outbreak of 2003 was contained. Since 2004, there have not been any known cases of SARS reported anywhere in the world. The content in this website was developed for the 2003 SARS epidemic. But some guidelines are still being used. Any new SARS updates will be posted on this website. Severe acute respiratory syndrome (SARS) is a viral respiratory disease of zoonotic origin caused by the SARS coronavirus (SARS-CoV). Between November 2002 and July 2003, an outbreak of SARS in southern China caused an eventual 8,098 cases, resulting in 774 deaths reported in 37 countries,[1] with the majority of cases in China[2] (9.6% fatality rate) according to the World Health Organization (WHO).[2] No cases of SARS have been reported worldwide since 2004.[3] In late 2017, Chinese scientists traced the virus to cave-dwelling Horseshoe bats in Yunnan province. Initial symptoms are flu-like and may include fever, myalgia, lethargy symptoms, cough, sore throat, and other nonspecific symptoms. The only symptom common to all patients appears to be a fever above 38 °C (100 °F). SARS may eventually lead to shortness of breath and/or pneumonia; either direct viral pneumonia or secondary bacterial pneumonia.[citation needed] The average incubation period for SARS is 4-6 days, although rarely it could be as short as 1 day or as long as 14 days. The primary route of transmission for SARS is contact of the mucous membranes with respiratory droplets or fomites. Whilst diarrhea is common in people with SARS, the fecal-oral route does not appear to be a common mode of transmission.[5] The basic reproduction number of SARS, R0, range for 2-4 depending on different analyses. Control measures introduced in April 2003 reduced this down to .4. There is no vaccine for SARS. Isolation and quarantine remain the most effective means to prevent the spread of SARS. Other preventative measures include: Handwashing Disinfection of surfaces for fomites Wearing a surgical mask Avoiding contact with bodily fluids Washing the personal items of someone with SARS in hot, soapy water (eating utensils, dishes, bedding, etc.)[8] Keeping children with symptoms home from school Award to the staff of the Hôspital Français de Hanoï for their dedication during the SARS crisis Antibiotics are ineffective, as SARS is a viral disease. Treatment of SARS is largely supportive with antipyretics, supplemental oxygen and mechanical ventilation as needed. People with SARS must be isolated, preferably in negative pressure rooms, with complete barrier nursing precautions taken for any necessary contact with these patients.

Smallpox virus

Smallpox was an infectious disease caused by one of two virus variants, Variola major and Variola minor.[7] The last naturally occurring case was diagnosed in October 1977 and the World Health Organization certified the global eradication of the disease in 1980.[10] The risk of death following contracting the disease was about 30%, with higher rates among babies.[6][11] Often those who survive have extensive scarring of their skin and some are left blind.[6] The initial symptoms of the disease include fever and vomiting.[5] This is then followed by formation of sores in the mouth and a skin rash.[5] Over a number of days the skin rash turns into characteristic fluid filled bumps with a dent in the center.[5] The bumps then scab over and fall off leaving scars.[5] The disease used to spread between people or via contaminated objects.[6][12] Prevention is by the smallpox vaccine.[9] Once the disease has developed certain antiviral medication may help.[9] The origin of smallpox is unknown.[13] The earliest evidence of the disease dates back to the 3rd century BC in Egyptian mummies.[13] The disease historically occurred in outbreaks.[10] In 18th century Europe it is estimated 400,000 people per year died from the disease, and one-third of the cases resulted in blindness.[14][10] These deaths included those of at least five reigning monarchs.[14][10] In the 20th century it is estimated that smallpox resulted in 300-500 million deaths.[12][15] As recently as 1967, 15 million cases occurred a year.[10] Edward Jenner discovered in 1798 that vaccination could prevent smallpox.[10] In 1967, the World Health Organization intensified efforts to eliminate the disease.[10] Smallpox is one of two infectious diseases to have been eradicated, the other being rinderpest in 2011.[16][17] The term "smallpox" was first used in Britain in the 15th century to distinguish the disease from syphilis, which was then known as the "great pox".[18] Other historical names for the disease include pox, speckled monster, and red plague There were two clinical forms of smallpox. Variola major was the severe and most common form, with a more extensive rash and higher fever. Variola minor was a less common presentation, and a much less severe disease, with historical death rates of 1 percent or less.[19] Subclinical (asymptomatic) infections with variola virus were noted but were not common.[20] In addition, a form called variola sine eruptione (smallpox without rash) was seen generally in vaccinated persons. This form was marked by a fever that occurred after the usual incubation period and could be confirmed only by antibody studies or, rarely, by virus isolation The incubation period between contraction and the first obvious symptoms of the disease is around 12 days. Once inhaled, variola major virus invades the oropharyngeal (mouth and throat) or the respiratory mucosa, migrates to regional lymph nodes, and begins to multiply. In the initial growth phase the virus seems to move from cell to cell, but around the 12th day, lysis of many infected cells occurs and the virus is found in the bloodstream in large numbers (this is called viremia), and a second wave of multiplication occurs in the spleen, bone marrow, and lymph nodes. The initial symptoms are similar to other viral diseases such as influenza and the common cold: fever of at least 38.3 °C (101 °F), muscle pain, malaise, headache and prostration. As the digestive tract is commonly involved, nausea and vomiting and backache often occur. The prodrome, or preeruptive stage, usually lasts 2-4 days. By days 12-15 the first visible lesions—small reddish spots called enanthem—appear on mucous membranes of the mouth, tongue, palate, and throat, and temperature falls to near normal. These lesions rapidly enlarge and rupture, releasing large amounts of virus into the saliva.[21] Smallpox virus preferentially attacks skin cells, causing the characteristic pimples (called macules) associated with the disease. A rash develops on the skin 24 to 48 hours after lesions on the mucous membranes appear. Typically the macules first appear on the forehead, then rapidly spread to the whole face, proximal portions of extremities, the trunk, and lastly to distal portions of extremities. The process takes no more than 24 to 36 hours, after which no new lesions appear.[21] At this point variola major infection can take several very different courses, resulting in four types of smallpox disease based on the Rao classification:[22] ordinary, modified, malignant (or flat), and hemorrhagic. Historically, smallpox has an overall fatality rate of about 30 percent; the malignant and hemorrhagic forms are usually fatal Variola is a large brick-shaped virus measuring approximately 302 to 350 nanometers by 244 to 270 nm,[31] with a single linear double stranded DNA genome 186 kilobase pairs (kbp) in size and containing a hairpin loop at each end.[32][33] The two classic varieties of smallpox are variola major and variola minor. Transmission occurs through inhalation of airborne variola virus, usually droplets expressed from the oral, nasal, or pharyngeal mucosa of an infected person. It is transmitted from one person to another primarily through prolonged face-to-face contact with an infected person, usually within a distance of 6 feet (1.8 m), but can also be spread through direct contact with infected bodily fluids or contaminated objects (fomites) such as bedding or clothing. Rarely, smallpox has been spread by virus carried in the air in enclosed settings such as buildings, buses, and trains.[19] The virus can cross the placenta, but the incidence of congenital smallpox is relatively low.[21] Smallpox is not notably infectious in the prodromal period and viral shedding is usually delayed until the appearance of the rash, which is often accompanied by lesions in the mouth and pharynx. The virus can be transmitted throughout the course of the illness, but is most frequent during the first week of the rash, when most of the skin lesions are intact.[20] Infectivity wanes in 7 to 10 days when scabs form over the lesions, but the infected person is contagious until the last smallpox scab falls off.[34] Smallpox is highly contagious, but generally spreads more slowly and less widely than some other viral diseases, perhaps because transmission requires close contact and occurs after the onset of the rash. The overall rate of infection is also affected by the short duration of the infectious stage. In temperate areas, the number of smallpox infections were highest during the winter and spring. In tropical areas, seasonal variation was less evident and the disease was present throughout the year.[20] Age distribution of smallpox infections depends on acquired immunity. Vaccination immunity declines over time and is probably lost within thirty years.[21] Smallpox is not known to be transmitted by insects or animals and there is no asymptomatic carrier state

Phi X 174

The phi X 174 (or ΦX174) bacteriophage is a single-stranded DNA (ssDNA) virus and the first DNA-based genome to be sequenced. This work was completed by Fred Sanger and his team in 1977.[2] In 1962, Walter Fiers and Robert Sinsheimer had already demonstrated the physical, covalently closed circularity of ΦX174 DNA.[3] Nobel prize winner Arthur Kornberg used ΦX174 as a model to first prove that DNA synthesized in a test tube by purified enzymes could produce all the features of a natural virus, ushering in the age of synthetic biology.[4][5] In 2003, it was reported by Craig Venter's group that the genome of ΦX174 was the first to be completely assembled in vitro from synthesized oligonucleotides.[6] The ΦX174 virus particle has also been successfully assembled in vitro.[7] Recently, it was shown how its highly overlapping genome can be fully decompressed and still remain functional. Microviridae Bacteriophages The structures of ssDNA bacteriophages φX174 and G4 have been reported in mature and provirus forms (Dokland et al., 1997; McKenna et al., 1992b, 1996). The mature viruses are T=1 with 60 copies each of the F, G, and (small J) proteins, and 12 copies of the H protein. Both the F and G proteins are classic viral jelly-roll structures. It is the F protein that occupies the positions homologous to the (+)ssRNA capsids. At 430 residues, the F protein is closest in size to the parvoviral capsids, and achieves its size through large loop insertions, primarily in the EF and HI loops. It is these loops that form the primary inter subunit contacts rather than direct barrel contacts as in the (+)ssRNA viruses. The G proteins form large pentameric protrusions that decorate the surface of the F-protein assembly. The barrels of the G proteins are oriented with strands radial with respect to the virus center. The H protein is not seen in the mature virus crystal structure. The structure of the procapsid has now been refined (Dokland et al., 1999), and there are several interesting findings relevant to assembly. The external "D" scaffolding protein forms a T=4 lattice that is therefore mismatched with the T=1 structure of F and G proteins. It forms a shell surrounding, but only loosely associated with, the F-protein shell, filling and leveling the surface between the G-protein spikes. The D protein has a compact globular structure and has 7 α helices connected by short loops, one of which has a β strand. About half the internal "B" scaffolding protein is seen, and it is also helical.

Vaccinia virus (cowpox)

Vaccinia virus (VACV or VV) is a large, complex, enveloped virus belonging to the poxvirus family.[1] It has a linear, double-stranded DNA genome approximately 190 kbp in length, and which encodes approximately 250 genes. The dimensions of the virion are roughly 360 × 270 × 250 nm, with a mass of approximately 5-10 fg.[2] Smallpox was the first disease to be widely prevented by vaccination due to pioneering work by the English physician and scientist Edward Jenner in the eighteenth century using cowpox virus. Vaccinia virus is the active constituent of the vaccine that eradicated smallpox, making it the first human disease to be eradicated. This endeavour was carried out by the World Health Organization under the Smallpox Eradication Program. Post eradication of smallpox, scientists study vaccinia virus to use as a tool for delivering genes into biological tissues (gene therapy and genetic engineering) and because of concerns about smallpox being used as an agent for bioterrorism. Vaccinia virus is closely related to the virus that causes cowpox; historically the two were often considered to be one and the same.[4] The precise origin of vaccinia virus is unknown due to the lack of record-keeping as the virus was repeatedly cultivated and passaged in research laboratories for many decades.[5] The most common notion is that vaccinia virus, cowpox virus, and variola virus (the causative agent of smallpox) were all derived from a common ancestral virus. There is also speculation that vaccinia virus was originally isolated from horses,[4] and analysis of DNA from an early (1902) sample of smallpox vaccine was 99.7% similar to horsepox virus. A Vaccinia virus infection is very mild and is typically asymptomatic in healthy individuals, but it may cause a mild rash and fever. Immune responses generated from a Vaccinia virus infection protects the person against a lethal smallpox infection. For this reason, Vaccinia virus was, and is still being used as a live-virus vaccine against smallpox. Unlike vaccines that use weakened forms of the virus being vaccinated against, the Vaccinia virus vaccine cannot cause a smallpox infection because it does not contain the smallpox virus. However, certain complications and/or vaccine adverse effects occasionally arise. The chance of this happening is significantly increased in people who are immunocompromised. Approximately one in one million individuals will develop a fatal response to the vaccination. Currently, the vaccine is only administered to health care workers or research personnel who have a high risk of contracting the variola virus, and to the military personnel of the United States of America. Due to the threat of smallpox bioterrorism, there is a possibility the vaccine may have to be widely administered again in the future. Therefore, scientists are currently developing novel vaccine strategies against smallpox which are safer and much faster to deploy during a bioterrorism event.

Zika virus

Zika is spread mostly by the bite of an infected Aedes species mosquito (Ae. aegypti and Ae. albopictus). These mosquitoes bite during the day and night. Zika can be passed from a pregnant woman to her fetus. Infection during pregnancy can cause certain birth defects. There is no vaccine or medicine for Zika. Local mosquito-borne Zika virus transmission has been reported in the continental United How Zika spreads Zika can be transmitted Through mosquito bites From a pregnant woman to her fetus Through sex Through blood transfusion (very likely but not confirmed) Zika symptoms most common symptoms Many people infected with Zika virus won't have symptoms or will only have mild symptoms. The most common symptoms of Zika are Fever Rash Headache Joint pain Red eyes Muscle pain Symptoms can last for several days to a week. People usually don't get sick enough to go to the hospital, and they very rarely die of Zika. Once a person has been infected with Zika, they are likely to be protected from future infections. Zika infection during pregnancy can cause a birth defect of the brain called microcephaly and other severe brain defects. It is also linked to other problems, such as miscarriage, stillbirth, and other birth defects. There have also been increased reports of Guillain-Barré syndrome, an uncommon sickness of the nervous system, in areas affected by Zika. There is no vaccine to prevent Zika. The best way to prevent diseases spread by mosquitoes is to protect yourself and your family from mosquito bites. Wear long-sleeved shirts and long pants. Treat your clothing and gear with permethrin or buy pre-treated items. Prevent sexual transmission of Zika by using condoms or not having sex. Zika virus was first discovered in 1947 and is named after the Zika Forest in Uganda. In 1952, the first human cases of Zika were detected and since then, outbreaks of Zika have been reported in tropical Africa, Southeast Asia, and the Pacific Islands. Zika outbreaks have probably occurred in many locations. Before 2007, at least 14 cases of Zika had been documented, although other cases were likely to have occurred and were not reported. Because the symptoms of Zika are similar to those of many other diseases, many cases may not have been recognized.

Middle East Respiratory Syndrome (MERS) virus

-Middle East respiratory syndrome (MERS), also known as camel flu,[1] is a viral respiratory infection caused by the MERS-coronavirus (MERS-CoV).[2] Symptoms may range from mild to severe.[3] They include fever, cough, diarrhea, and shortness of breath.[2] Disease is typically more severe in those with other health problems.[3] MERS-CoV is a betacoronavirus derived from bats.[2] Camels have been shown to have antibodies to MERS-CoV but the exact source of infection in camels has not been identified. Camels are believed to be involved in its spread to humans but it is unclear how.[3] Spread between humans typically requires close contact with an infected person.[2] Its spread is uncommon outside of hospitals.[3] Thus, its risk to the global population is currently deemed to be fairly low.[3] As of 2016 there is no specific vaccine or treatment for the disease.[4][3] However, a number of antiviral medications are currently being studied.[3] The World Health Organization recommends that those who come in contact with camels wash their hands frequently and do not touch sick camels.[2] They also recommend that camel products be appropriately cooked.[2] Among those who are infected treatments that help with the symptoms may be given.[2] Just under 2000 cases have been reported as of April 4, 2017.[5] About 36% of those who are diagnosed with the disease die from it.[5] The overall risk of death may be lower as those with mild symptoms may be undiagnosed.[5][6] The first identified case occurred in 2012 in Saudi Arabia and most cases have occurred in the Arabian Peninsula.[2][3] A strain of MERS-CoV known as HCoV-EMC/2012 found in the first infected person in London in 2012 was found to have a 100% match to Egyptian tomb bats. A large outbreak occurred in the Republic of Korea in 2015. -Early reports[7] compared the virus to severe acute respiratory syndrome (SARS), and it has been referred to as Saudi Arabia's SARS-like virus.[8] The first person, in June 2012, had a "seven-day history of fever, cough, expectoration, and shortness of breath."[7] One review of 47 laboratory confirmed cases in Saudi Arabia gave the most common presenting symptoms as fever in 98%, cough in 83%, shortness of breath in 72% and myalgia in 32% of people. There were also frequent gastrointestinal symptoms with diarrhea in 26%, vomiting in 21%, abdominal pain in 17% of people. 72% of people required mechanical ventilation. There were also 3.3 males for every female.[9] One study of a hospital-based outbreak of MERS had an estimated incubation period of 5.5 days (95% confidence interval 1.9 to 14.7 days).[10] MERS can range from asymptomatic disease to severe pneumonia leading to acute respiratory distress syndrome (ARDS).[9] Kidney failure, disseminated intravascular coagulation (DIC), and pericarditis have also been reported. -Middle East respiratory syndrome is caused by the newly identified MERS coronavirus (MERS-CoV), a species with single-stranded RNA belonging to the genus betacoronavirus which is distinct from SARS coronavirus and the common-cold coronavirus. -A study performed between 2010 and 2013, in which the incidence of MERS was evaluated in 310 dromedary camels, revealed high titers of neutralizing antibodies to MERS-CoV in the blood serum of these animals.[15] A further study sequenced MERS-CoV from nasal swabs of dromedary camels in Saudi Arabia and found they had sequences identical to previously sequenced human isolates. Some individual camels were also found to have more than one genomic variant in their nasopharynx.[16] There is also a report of a Saudi Arabian man who became ill seven days after applying topical medicine to the noses of several sick camels and later he and one of the camels were found to have identical strains of MERS-CoV.[17][18] It is still unclear how the virus is transmitted from camels to humans. The World Health Organization advises avoiding contact with camels and to eat only fully cooked camel meat, pasteurized camel milk, and to avoid drinking camel urine. Camel urine is considered a medicine for various illnesses in the Middle East.[19] The Saudi Ministry of Agriculture has advised people to avoid contact with camels or wear breathing masks when around them.[20] In response "some people have refused to listen to the government's advice"[21] and kiss their camels in defiance of their government's advice. -There has been evidence of limited, but not sustained spread of MERS-CoV from person to person, both in households as well as in health care settings like hospitals.[10][22] Most transmission has occurred "in the circumstances of close contact with severely ill persons in healthcare or household settings" and there is no evidence of transmission from asymptomatic cases.[23] Cluster sizes have ranged from 1 to 26 people, with an average of 2.7 -Chest X-ray findings tend to show bilateral patchy infiltrates consistent with viral pneumonitis and ARDS. Lower lobes tend to be more involved. CT scans show interstitial infiltrates

Streptococcus pneumoniae

Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic (under aerobic conditions) or beta-hemolytic (under anaerobic conditions), facultative anaerobic member of the genus Streptococcus.[1] They are usually found in pairs (diplococci) and do not form spores and are non-motile.[2] As a significant human pathogenic bacterium S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century, and is the subject of many humoral immunity studies. S. pneumoniae resides asymptomatically in healthy carriers typically colonizing the respiratory tract, sinuses, and nasal cavity. However, in susceptible individuals with weaker immune systems, such as the elderly and young children, the bacterium may become pathogenic and spread to other locations to cause disease. It spreads by direct person-to-person contact via respiratory droplets and by autoinoculation in persons carrying the bacteria in their upper respiratory tract.[3] It can be a cause of neonatal infections.[4] S. pneumoniae is the main cause of community acquired pneumonia and meningitis in children and the elderly,[5] and of septicemia in those infected with HIV. The organism also causes many types of pneumococcal infections other than pneumonia. These invasive pneumococcal diseases include bronchitis, rhinitis, acute sinusitis, otitis media, conjunctivitis, meningitis, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.[6] S. pneumoniae can be differentiated from the viridans streptococci, some of which are also alpha-hemolytic, using an optochin test, as S. pneumoniae is optochin-sensitive. S. pneumoniae can also be distinguished based on its sensitivity to lysis by bile, the so-called "bile solubility test". The encapsulated, Gram-positive coccoid bacteria have a distinctive morphology on Gram stain, lancet-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism; more than 90 different serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance. S. pneumoniae is part of the normal upper respiratory tract flora. As with many natural flora it can become pathogenic under the right conditions, typically when the immune system of the host is suppressed. Invasins, such as pneumolysin, an anti-phagocytic capsule, various adhesins, and immunogenic cell wall components are all major virulence factors. After S. pneumoniae colonizes the air sacs of the lungs, the body responds by stimulating the inflammatory response causing plasma, blood, and white blood cells to fill the alveoli. This condition is called pneumonia.[20] It is susceptible to clindamycin. Pneumonia is the most common and most serious of the S. pneumoniae diseases which include symptoms like fever and chills, cough, rapid breathing, difficulty breathing, chest pain. For the elderly they may include confusion, low alertness, and less of the former listed symptoms. Pneumococcal meningitis is an infection of the tissue covering the brain and spinal cord. Symptoms include: stiff neck, fever, headache, confusion and photophobia. Sepsis is caused by overwhleming response to an infection and leads to tissue damage, organ failure, and even death. The symptoms include: confusion, shortness of breath, elevated heart rate, pain or discomfort, over-perspiration, fever, shivering, or feeling cold. Due to the importance of disease caused by S. pneumoniae several vaccines have been developed to protect against invasive infection. The World Health Organization recommend routine childhood pneumococcal vaccination;[23] it is incorporated into the childhood immunization schedule in a number of countries including the United Kingdom,[24] United States,[25] and South Africa.

Taenia solium

-Taenia solium is the pork tapeworm belonging to cyclophyllid cestodes in the family Taeniidae. It is an intestinal zoonotic parasite found throughout the world, and is most prevalent in countries where pork is eaten. The adult worm is found in humans and has a flat, ribbon-like body, which is white in color and measures 2 to 3 m in length. Its distinct head, the scolex, contains suckers and a rostellum as organs of attachment. The main body, the strobila, consists of a chain of segments known as proglottids. Each proglottid is a complete reproductive unit; hence, the tapeworm is a hermaphrodite. It completes its life cycle in humans as the definitive host and pigs as intermediate host. It is transmitted to pigs through human feces or contaminated fodder, and to humans through uncooked or undercooked pork. Pigs ingest embryonated eggs called morula, which develop into larvae, the oncospheres, and ultimately into infective larvae, cysticerci. A cysticercus grows into an adult worm in human small intestines. Infection is generally harmless and asymptomatic. However, accidental infection in humans by the larval stage causes cysticercosis. The most severe form is neurocysticercosis, which affects the brain and is a major cause of epilepsy. Human infection is diagnosed by the parasite eggs in the faeces. For complicated cysticercosis, imaging techniques such as computed tomography and nuclear magnetic resonance are employed. Blood samples can also be tested using antibody reaction of enzyme-linked immunosorbent assay. Broad-spectrum anthelmintics such as praziquantel and albendazole are the most effective medications. -The life cycle of T. solium is indirect. It passes through pigs, as intermediate hosts, into humans, as definitive hosts. From humans, the eggs are released in the environment where they await ingestion by another host. Humans as the definitive hosts are directly infected from contaminated meat. -Intestinal infection of T. solium is called taeniasis which is quite asymptomatic. Only in severe cases, conditions of intestinal irritation, anaemia, and indigestion occur, which can lead to loss of appetite and emaciation. Cysticercus is clinically pathogenic. Ingestion of T. solium eggs or proglottids which rupture within the host intestines can cause larvae to migrate into host tissue to cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed, including headaches, dizziness, and occasional seizures. In more severe cases, dementia or hypertension can occur due to perturbation of the normal circulation of cerebrospinal fluid. (Any increase in intracranial pressure will result in a corresponding increase in arterial blood pressure, as the body seeks to maintain circulation to the brain.) The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements, and brain system dysfunction. In children, ocular location of cysts is more common than cystation in other locations of the body.[8] In many cases, cysticercosis in the brain can lead to epilepsy, seizures, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels. It is the cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions, and even death -The best way to avoid getting tapeworms is to not eat undercooked pork. Moreover, a high level of sanitation and prevention of faecal contamination of pig feeds also plays a major role in prevention. Infection can be prevented with proper disposal of human faeces around pigs, cooking meat thoroughly and/or freezing the meat at −10 °C for 5 days. For human cysticercosis, dirty hands are attributed to be the primary cause, and especially common among food handlers.[7] Therefore, personal hygiene such as washing one's hands before eating is an effective measure. -T. solium is found worldwide, but is more common in cosmopolitan areas. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Therefore, high prevalences are reported in Mexico, Latin America, West Africa, Russia, India, Pakistan, Manchuria, and Southeast Asia.[11] In Europe it is most widespread among Slavic countries.

Streptococcus pyogenes (GAS)

-gram-positive bacterium -usually grows in pairs or chains -when cultured on a blood agar plate, all the red blood cells are ruptured by the bacteria -flesh-eating bacteria -mild illnesses (strep throat) to serious diseases (scarlet fever) -untreated strep throat leads to rheumatic fever -fever, severe pain, dizziness, and a red rash at wound site

Human Immunodeficiency Virus (HIV)

The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[3] In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids. Non-sexual transmission can occur from an infected mother to her infant through breast milk.[4][5][6] An HIV-positive mother can transmit HIV to her baby both during pregnancy and childbirth due to exposure to her blood or vaginal fluid.[7] Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[8] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[9] apoptosis of uninfected bystander cells,[10] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8+ cytotoxic lymphocytes that recognize infected cells.[11] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections, leading to the development of AIDS. Many HIV-positive people are unaware that they are infected with the virus.[103] For example, in 2001 less than 1% of the sexually active urban population in Africa had been tested, and this proportion is even lower in rural populations.[103] Furthermore, in 2001 only 0.5% of pregnant women attending urban health facilities were counselled, tested or receive their test results.[103] Again, this proportion is even lower in rural health facilities.[103] Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.[104] HIV-1 testing is initially done using an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a non-reactive result from the initial ELISA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate.[105] If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., a polymerase chain reaction (PCR), western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA or PCR or reactive by western blot are considered HIV-positive and indicative of HIV infection. Specimens that are repeatedly ELISA-reactive occasionally provide an indeterminate western blot result, which may be either an incomplete antibody response to HIV in an infected person or nonspecific reactions in an uninfected person.

Leishmania donovani

-is a species of intracellular parasites belonging to the genus Leishmania, a group of haemoflagellate kinetoplastids that cause the disease leishmaniasis. It is a human blood parasite responsible for visceral leishmaniasis or kala-azar, the most severe form of leishmaniasis. It infects the mononuclear phagocyte system including spleen, liver and bone marrow. Infection is transmitted by species of sandfly belonging to the genus Phlebotomus in Old World and Lutzomyia in New World. Therefore, the parasite is prevalent throughout tropical and temperate regions including Africa (mostly in Sudan), China, India, Nepal, southern Europe, Russia and South America.[1][2][3] It is responsible for thousands of deaths every year and has spread to 88 countries, with 350 million people at constant risk of infection and 0.5 million new cases in a year -The parasite requires two different hosts for a complete life cycle, humans as the definitive host and sandflies as the intermediate host. In some parts of the world other mammals, especially canines, act as reservoir hosts. In human cell they exist as small, spherical and unflagellated amastigote form; while they are elongated with flagellum as promastigote form in sandflies. Unlike other parasitic protists they are unable to directly penetrate the host cell, and are dependent upon phagocytosis -a unicellular eukaryote having a well-defined nucleus and other cell organelles including a kinetoplast and a flagellum -is the causative agent of visceral leishmaniasis, traditionally known as kala-azar ("black fever", particularly in India), because of its characteristic symptoms. The disease is highly lethal if not treated properly. The incubation period generally ranges from 3 to 6 months, and in some cases may be over a year. In Indian leishmaniasis, incubation can be as short as 10 days. The target cells are those of mononuclear phagocyte system. The two main tissues of infection are spleen and liver.[37] Clinical symptoms include pyrexia (recurring high fever which may be continuous or remittent), enlargement of spleen and liver, and heavy skin pigmentation which darkens the physical appearance (the reason for naming "black fever"). To a lesser extent mucosa of the small intestine and lymph nodes are also invaded by the parasite. Morphological symptoms are noticeable particularly on facial and abdominal regions. Skin becomes coarse and hard. In African infections, warty eruptions are common. In a fully developed stage, the patient shows emaciation and anaemia. Where medical facilities are poor, mortality can be as high as 75-95% within 2 years of epidemics. The disease is often accompanied by complications with dysentery, tuberculosis, septicaemia and even HIV infection -The conventional treatment method is an intravenous injection with antimony compounds, such as pentostam.[citation needed] Unfortunately, these chemotherapeutics are so poisonous that about 15% of the patients die from the treaments.

Rhizobium spp.

-gram-negative, motile, non-sporulating rods -nitrogen-fixing bacteria that from nodules on host plants -responsible for the worlds largest portion of fixed atmospheric nitrogen -have a symbiotic relationship with legume plants, which can't live without these bacteria's essential nitrogen-fixing processes -In nodules, the rhizobia bacteriods use carbon and energy from the plant in the form of dicarboxylic acids -the bacteriods act like plant organelles to cycle amino acids back to the plant fro asparagine synthesis -can be found in the roots, or rhizosphere of other types of plants where they cause the formation of nodules

Bacillus anthracis

Anthrax is a serious infectious disease caused by gram-positive, rod-shaped bacteria known as Bacillus anthracis. Although it is rare, people can get sick with anthrax if they come in contact with infected animals or contaminated animal products. Bacillus anthracis is the etiologic agent of anthrax—a common disease of livestock and, occasionally, of humans—and the only obligate pathogen within the genus Bacillus.[1] B. anthracis is a Gram-positive, endospore-forming, rod-shaped bacterium, with a width of 1.0-1.2 µm and a length of 3-5 µm.[1] It can be grown in an ordinary nutrient medium under aerobic or anaerobic conditions. The symptoms in anthrax depend on the type of infection and can take anywhere from 1 day to more than 2 months to appear. All types of anthrax have the potential, if untreated, to spread throughout the body and cause severe illness and even death.[21] Four forms of human anthrax disease are recognized based on their portal of entry. Cutaneous, the most common form (95%), causes a localized, inflammatory, black, necrotic lesion (eschar). Inhalation, a rare but highly fatal form, is characterized by flu like symptoms, chest discomfort, diaphoresis, and body aches.[21] Gastrointestinal, a rare but also fatal (causes death to 25%) type, results from ingestion of spores. Symptoms include: fever and chills, swelling of neck, painful swallowing, hoarseness, nausea and vomiting (especially bloody vomiting), diarrhea, flushing and red eyes, and swelling of abdomen.[21] Injection, symptoms are similar to those of cutaneous anthrax, but injection anthrax can spread throughout the body faster and can be harder to recognize and treat compared to cutaneous anthrax. A number of anthrax vaccines have been developed for preventive use in livestock and humans. Anthrax vaccine adsorbed (AVA) may protect against cutaneous and inhalation anthrax. However, this vaccine is only used for at-risk adults before exposure to anthrax and has not been approved for use after exposure.[22] Infections with B. anthracis can be treated with β-lactam antibiotics such as penicillin, and others which are active against Gram-positive bacteria.[23] Penicillin-resistant B. anthracis can be treated with fluoroquinolones such as ciprofloxacin or tetracycline antibiotics such as doxycycline.

Gardnerella vaginalis

Gardnerella is a genus of Gram-variable-staining facultative anaerobic bacteria of which Gardnerella vaginalis is the only species. The organisms are small (1.0-1.5 µm in diameter) nonspore-forming, nonmotile coccobacilli. Once classified as Haemophilus vaginalis and afterwards as Corynebacterium vaginalis, G. vaginalis grows as small, circular, convex, gray colonies on chocolate agar; it also grows on HBT agar. A selective medium for G. vaginalis is colistin-oxolinic acid blood agar. G. vaginalis is a facultatively anaerobic Gram-variable rod that is involved, together with many other bacteria, mostly anaerobic, in bacterial vaginosis in some women as a result of a disruption in the normal vaginal microflora. The resident facultative anaerobic Lactobacillus population in the vagina is responsible for the acidic environment. Once the anaerobes have supplanted the normal vaginal bacteria, prescription antibiotics with anaerobic coverage may have to be given to re-establish the equilibrium of the ecosystem and allow the balance to be restored. G. vaginalis is not considered the cause of the bacterial vaginosis, but a signal organism of the altered microbial ecology associated with overgrowth of many bacterial species.[3] While typically isolated in genital cultures, it may also be detected in other samples from blood, urine, and the pharynx. Although G. vaginalis is a major species present in bacterial vaginosis, it can also be isolated from women without any signs or symptoms of infection. It has a Gram-positive cell wall,[4] but, because the cell wall is so thin, it can appear either Gram-positive or Gram-negative under the microscope. It is associated microscopically with clue cells, which are epithelial cells covered in bacteria. G. vaginalis produces a pore-forming toxin, vaginolysin, which affects only human cells. G. vaginalis is associated with bacterial vaginosis,[14] which may be asymptomatic,[15] or may have symptoms including vaginal discharge, vaginal irritation, and a "fish-like" odor. In the amine whiff test, 10% KOH is added to the discharge; a positive result is indicated if a fishy smell is produced. This and other tests can be used to distinguish between vaginal symptoms related to G. vaginalis and those caused by other organisms, such as Trichomonas and Candida albicans, which are similar and may require different treatment. Trichomonas vaginalis and G. vaginalis have similar clinical presentations and can cause a frothy gray or yellow-green vaginal discharge, pruritus, and produce a positive "whiff-test". The two can be distinguished using a wet-mount slide, where a swab of the vaginal epithelium is diluted and then placed onto a slide for observation under a microscope. Gardnerella reveals a classic "clue cell" under the microscope, showing bacteria adhering to the surface of squamous epithelial cells.

Shigella dysenteriae

Shigella dysenteriae Scientific classification Kingdom: Bacteria Phylum: Proteobacteria Class: Gammaproteobacteria Order: Enterobacteriales Family: Enterobacteriaceae Genus: Shigella Species: S. dysenteriae Binomial name Shigella dysenteriae (Shiga 1897) Castellani & Chalmers 1919 This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (February 2010) (Learn how and when to remove this template message) Shigella dysenteriae is a species of the rod-shaped bacterial genus Shigella.[1][page needed] Shigella species can cause shigellosis (bacillary dysentery). Shigellae are Gram-negative, nonspore-forming, facultatively anaerobic, nonmotile bacteria.[2] S. dysenteriae, spread by contaminated water and food, causes the most severe dysentery because of its potent and deadly Shiga toxin, but other species may also be dysentery agents.[3] Contamination is often caused by bacteria on unwashed hands during food preparation, or soiled hands reaching the mouth. The most commonly observed signs associated with Shigella dysentery include colitis, malnutrition, rectal prolapse, tenesmus, reactive arthritis, and central nervous system problems. Further, S. dysenteriae is associated with the development of hemolytic-uremic syndrome, which includes anemia, thrombocytopenia, and renal failure. Shigellosis is a diarrheal disease caused by a group of bacteria called Shigella. Shigella causes about 500,000 cases of diarrhea in the United States annually 1. There are four different species of Shigella:

Salmonella enterica

Salmonella enterica (formerly Salmonella choleraesuis) is a rod-shaped, flagellate, facultative anaerobic, gram-negative bacterium and a species of the genus Salmonella.[1] A number of its serovars are serious human pathogens. Most cases of salmonellosis are caused by food infected with S. enterica, which often infects cattle and poultry, though other animals such as domestic cats[2][citation needed] and hamsters[3] have also been shown to be sources of infection in humans. Investigations of vacuum cleaner bags have shown that households can act as a reservoir of the bacterium; this is more likely if the household has contact with an infection source (i.e., members working with cattle or in a veterinary clinic). Raw chicken eggs and goose eggs can harbor S. enterica, initially in the egg whites, although most eggs are not infected. As the egg ages at room temperature, the yolk membrane begins to break down and S. enterica can spread into the yolk. Refrigeration and freezing do not kill all the bacteria, but substantially slow or halt their growth. Pasteurizing and food irradiation are used to kill Salmonella for commercially produced foodstuffs containing raw eggs such as ice cream. Foods prepared in the home from raw eggs such as mayonnaise, cakes, and cookies can spread salmonella if not properly cooked before consumption. Secreted proteins are of major importance for the pathogenesis of infectious diseases caused by Salmonella enterica. A remarkable large number of fimbrial and non-fimbrial adhesins are present in Salmonella, and mediate biofilm formation and contact to host cells. Secreted proteins are also involved in host cell invasion and intracellular proliferation, two hallmarks of Salmonella pathogenesis.[5]

Escherichia coli

-Gram-negative bacterium -short rod/random -often part of the normal human microbiome -disease is dependent on strain and can be mild (intestinal cramping, or UTI), moderate (diarrhea) or severe (bloody diarrhea, HUS and renal failure)

Clostridium difficile

-is found in nature in water, air, human and animal feces, on most surfaces (especially in hospitals) and most prevalently in soil. -is a gram-positive spore-forming anaerobe. -Overgrowth of the bacteria in the intestines of human and animal hosts leads to buildup of its toxins and their deleterious effects. It can be transferred from person to person through the fecal-oral route. -Patient symptoms with C. difficile intestinal infections include diarrhea, inflammation, fever and abdominal pain.

Corynebacterium diphtheriae

- a Gram-positive, aerobic, nonmotile, toxin-producing, rod-shaped bacteria -is typically found in soil, but also has pathogenic members such as streptomyces and mycobacteria. -is best known for causing the disease Diphtheria in human beings, which results from production of Diphtheria toxin in conjunction with infection by a bacteriophage which provides it with the toxin-producing gene. Because historically it has been a very deadly disease, especially for children where mortality rates before vaccines and antitoxin amounted to nearly 80%, it has been heavily studied. Oddly enough, mice and other rodents are naturally immune to the Diphtheria toxin so it has been difficult to study Diphtheria in the lab. -is only found in the mouth, throat, nose, skin, bodily secretions, and wounds of infected persons. Animals do not easily contract Diphtheria from human beings, and naturally have immunity. -primarily causes the disease diphtheria in human beings, and is prevalent in Eastern European countries, Latin America, the Caribbean, and undeveloped countries. Widespread vaccinations have nearly eradicated the disease in the United States. Diphtheria is very contagious and is spread through direct contact and aerosolized expulsions. -"Balto" -when a person is infected with this microbe, they develop a thick covering at the back of the throat; the toxic effects are due to a virus

Schizosaccharomyces pombe

- a fungus -a unicellular eukaryote that is rod shaped - is usually found in sugar-containing fermentations of alcohol from the subtropical regions -Researchers have identified fifty genes of S. pombe associated with human diseases including cystic fibrosis, hereditary deafness, and diabetes - a rod-shaped fission yeast -is a chemoorganotroph, so it uses organic compounds as a source of energy and does not require light to grow. -can grow under both aerobic and anaerobic conditions -is found in alcoholic beverages -Kombucha

Listeria monocytogenes

- are a Gram-positive rod-shaped bacterium that form single short chains, and can be resistant to the effects of freezing, drying, and heat surprisingly well for a non spore forming bacterium. -Listeria are mainly found in the soil, though Listeria monocytogenes, a pathogen, may specifically be found in raw foods, such as unpasteurized fluid milk, raw vegetables, raw and cooked poultry. -It has the ability to grow at low temperatures; thus, allowing it to grow in refrigerated foods. -Listeria monocytogenes was thought to be exclusively associated as infections in animals, but recently, this pathogenic species has also been isolated, in its dormant form, in the intestinal tract of small percentage of the human population. -Because Listeria monocytogenes is an agent of listeriosis, a serious disease where the overt form has a severe mortality greater than 25 percent, sequencing of the bacterium's genome is of significant importance. -do not form spores or branch and are motile via peritrichous flagella at room temperature (20º-25º), but surprisingly cannot synthesize flagella at body temperature (37º) - has been found widely distributed throughout the environment, especially in the soil and fecal matter. Studies have shown that infected animals may contribute to Listeria monocytogenes 's dispersal into the environment through animal fecal matter and feedstuff -as an intracellular pathogen, has been associated with severe food borne infections in humans and animals, though rarely through raw animal-derived food products. -Listeria monocytogenes have also been shown to survive in different habitats with extreme conditions including high salt concentrations, high pH, and high temperature. -Listeria monocytogenes can also form biofilms, which enables them as a community to attach to solid surfaces where they proliferate and become extremely difficult to remove. -are pathogenic to both animals and humans to some degree; however, the bacterium has been reported to be carried in the intestinal tract of a small percentage of the human population without apparent symptoms -causes the disease listeriosis in humans, with common manifestations in septicemia, meningitis, encephalitis, corneal ulcer, pneumonia, and cervical infections in pregnant women, which may have resulted in spontaneous abortion or stillbirth. -Patient symptoms include influenza- like symptoms, and gastrointestinal symptoms of vomiting and diarrhea

Legionella pneumophila

- are fastidious gram-negative bacteria that reside in aquatic environments all over the globe. In their natural environment, the Legionellaceae are intracellular parasites of free-living protozoa. These organisms may also inhabit man-made water distribution systems -is a gram-negative, non-encapsulated, aerobic bacillus with a single, polar flagellum. -culprit behind hospital-acquired Legionnaires' disease -prefer to grow and localize in hot, moist environments where there is a supply of nutrition from the sediment -can only be acquired from an environmental source; therefore, infection never occurs between humans or humans and animals. Another interesting thing is, unlike other pathogens that cause bacterial pneumonia, L. pneumophila do not inhabit the upper respiratory tract. Once inhaled, they are small enough to avoid the defenses of the upper airway. -Legionnaires' disease, which is characterized by fever, myalgia, cough, pneumonia, or Pontiac fever, a milder illness without pneumonia. The symptoms of Legionnaire's disease range from a mild cough and low fever to rapidly progressive pneumonia, coma, and death. Early symptoms include slight fever, headache, aching joints and muscles, lack of energy or tiredness, and loss of appetite. Later symptoms include high fever, cough, difficulty breathing/shortness of breath, chills, chest pain, common gastrointestinal symptoms including vomiting, diarrhea, nausea, and abdominal pain. The symptoms of Pontiac fever include flu-like symptoms such as fever, headache, tiredness, loss of appetite, muscle and joint pain, chills, nausea, and a dry cough. Patients usually reach full recovery within two to five days without medical attention and no deaths have been reported.

Human papillomavirus (HPV)

-HPV is a group of more than 150 related viruses. Each HPV virus in this large group is given a number which is called its HPV type. HPV is named for the warts (papillomas) some HPV types can cause. Some other HPV types can lead to cancer. Men and women can get cancer of mouth/ throat, and anus/rectum caused by HPV infections. Men can also get penile HPV cancer. In women, HPV infection can also cause cervical, vaginal, and vulvar HPV cancers. But there are vaccines that can prevent infection with the types of HPV that most commonly cause cancer. HPV is transmitted through intimate skin-to-skin contact. You can get HPV by having vaginal, anal, or oral sex with someone who has the virus. It is most commonly spread during vaginal or anal sex. HPV is so common that nearly all men and women get it at some point in their lives. HPV can be passed even when an infected person has no signs or symptoms. You can develop symptoms years after being infected, making it hard to know when you first became infected. In most cases, HPV goes away on its own and does not cause any health problems. But when HPV does not go away, it can cause health problems like genital warts and cancer.

Thermus aquaticus

- gram negative bacterium -appears as either a rod or short filaments, and the rod-shaped cells will tend to form either a rosette or a linear pattern. When exposed to sunlight, Thermus can exhibit a yellow, pink, or red color due to pigments within the bacteria. Along with the coloration, Thermus aquaticus can either have flagella or be immotile. - has proven to be quite a useful organism in the field of Biotechnology, as its enzyme Taq polymerase is harvested for use in polymerase chain reactions (PCR) -These properties of Taq polymerase- it's heat resistance, accuracy, and potency- make PCR, and technologies that utilize PCR, such as DNA fingerprinting, enzyme production, and medical diagnoses possible. -needs organic compounds from the surrounding environment in order to grow and sustain life -Thermus aquaticus was first found in several of the Yellowstone National Park hot springs. It can survive at temperatures of 55-100 degrees Celsius in weakly acidic to alkaline (pH 5-9) waters. It was also discovered in marine thermal springs, low saline solfataric springs and thermally polluted waters. The ideal conditions for this organism to grow are around 70 to 75 degrees Celsius at a pH of 7.5 to 8 [4]. There are also some other environmental factors to consider, such as: the oxygen and nitrate concentration and the effects of light and salinity. Since these organisms exist at high temperatures, there is only a small amount of dissolved oxygen in the water.

Giardia lamblia

- is a flagellated, microaerophilic microorganism, first discovered by Van Leeuwenhoek in 1681, who found it in his own diarrheal stool. The G. lamblia trophozoite, vegetative, motile form of G. lamblia is pear-shaped and have unique morphology such as two identical nuclei, a ventral disc for adhesion to the host intestine, and flagella -one of the major cause of waterborne diseases worldwide (CDC, 2004), and infection results in giardiasis (characterized by malabsorption and severe diarrhea). Giardia-induced intestinal infection is particularly severe in developing world, where giardiasis occurrence relates heavily to water source contamination. In the united states, G. lamblia has been found in both drinking and recreational water. Due to the high prevalence of giardiasis, G. lamblia is of significant interest in the clinical research community. -is known to infect human, mammals, reptiles, and birds, cows, sheep and pigs, depending on the strain -The G. lamblia life cycle consists of two stages: the cyst and trophozoites -Giardiasis is the clinical manifestation of G. lamblia infection. It is characterized by severe diarrhea, malnutrition weight loss, and slight intestinal epithelial injury. The complete pathogenesis is no well known, but several theories exist

Bordatella pertussis

- small, Gram-negative, coccoid bacterium -an encapsulated, immotile aerobe that does not make spores -produces a number of virulence factors, including pertussis toxin, adenylate cyclase toxin, filamentous hemagglutinin, and hemolysin -cannot survive in the environment; it must reside in a host either in small groups or singly -is a strict human pathogen that is the causative agent of pertussis (whooping cough) -its natural habitat is in the human respiratory mucosa -Whooping Cough, or pertussis, is a respiratory infection in which a "whooping" sound is produced when the sufferer breathes -kills an estimated 300,000 children annually, most of which occur in developing countries -humans are its only host -transmitted from person to person through droplets of respiratory secretions that are either coughed or sneezed into the air by an infected person -without its host's respiratory mucus, the pathogen cannot be sustained in the environment -symptoms of pertussis are similar to a common cold: runny nose, sneezing, mild cough, and low-grade fever -Pertussis is a sever, highly contagious respiratory disease

Adenovirus

-Adenoviruses are common causes of respiratory illness, but most infections are not severe. They can cause cold-like symptoms, sore throat, bronchitis, pneumonia, diarrhea, and pink eye (conjunctivitis). You can get an adenovirus infection at any age, but infants and people with weakened immune systems are more likely than others to develop severe illness from adenoviruses... -Adenoviruses usually spread from infected people to others through close personal contact such as touching or shaking hands the air by coughing and sneezing touching objects or surfaces with adenoviruses on them then touching your mouth, nose, or eyes

Ascaris lumbricoides

-Ascaris lumbricoides is the "large roundworm" of humans, growing to a length of up to 35 cm (14 in).[1] It is one of several species of Ascaris. An ascarid nematode of the phylum Nematoda, it is the most common parasitic worm in humans. This organism is responsible for the disease ascariasis, a type of helminthiasis and one of the group of neglected tropical diseases. An estimated one-sixth of the human population is infected by A. lumbricoides or another roundworm.[2] Ascariasis is prevalent worldwide, especially in tropical and subtropical countries. -An estimated 1 billion people are infected with A. lumbricoides worldwide.[7] While infection occurs throughout most of the world, A. lumbricoides infection is most common in sub-Saharan Africa, the Americas, China, and east Asia.[8] Ascaris lumbricoides eggs are extremely resistant to strong chemicals, desiccation, and low temperatures. The eggs can remain viable in the soil for several months or even years.[6] Eggs of A. lumbricoides have been identified in archeological coprolites in the Americas, Europe, Africa, the Middle East, and New Zealand, the oldest ones being more than 24,000 years old. -Infections with these parasites are more common where sanitation is poor,[10] and raw human feces are used as fertilizer. -Often, no symptoms are seen with an A. lumbricoides infection. However, in the case of a particularly bad infection, symptoms may include bloody sputum, cough, fever, abdominal discomfort, intestinal ulcer, and passing worms.[11][12] Ascariasis is also the most common cause of Löffler's syndrome worldwide. Accompanying symptoms include pulmonary infiltration, eosinophilia, and radiographic opacities.[13] Significant increases in fertility are observed in infected women -Preventing any fecal-borne disease requires educated hygienic habits/culture and effective fecal treatment systems.

Clonorchis sinensis

-Clonorchis sinensis, the Chinese liver fluke, is a human liver fluke belonging to the class Trematoda, phylum Platyhelminthes. This parasite lives in the liver of humans, and is found mainly in the common bile duct and gall bladder, feeding on bile. These animals, which are believed to be the third most prevalent worm parasite in the world, are endemic to Japan, China, Taiwan, and Southeast Asia, currently infecting an estimated 30,000,000 humans.[1] 85% of cases are found in China. The infection called clonorchiasis generally appears as jaundice, indigestion, biliary inflammation, bile duct obstruction, even liver cirrhosis, cholangiocarcinoma (CCA), and hepatic carcinoma.[2] -It is the most prevalent human trematode in Asia, and is still transmitted in Korea, China, Vietnam and also Russia, with 200 million people at constant risk. Recent studies have proved that it is definite cancer-causing agent in the liver (carcinoma) and bile duct (CCA). -An adult C. sinensis is a flattened (dorso-ventrally flat) and leaf-shaped fluke

Cytomegalovirus (CMV)

-Humans and monkeys serve as natural hosts. There are currently eight species in this genus including the type species, human cytomegalovirus (HCMV, human herpesvirus 5, HHV-5), which is the species that infects humans. Diseases associated with HHV-5 include glandular fever, and pneumonia. In the medical literature, most mentions of CMV without further specification refer implicitly to human CMV. Human CMV is the most studied of all cytomegaloviruses. -The genus of cytomegalovirus is in the group, dsDNA, in the order, Herpesvirales, in the family, Herpesviridae, and the subfamily, Betaherpesvirinae -enveloped -All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals

Ebola virus

-RNA virus -long, thin filaments -named after the Ebola River -virus causes Ebola hemorrhagic fever, which is serious and usually fatal for those who contract it -damages the endothelial cells that make-up the lining of blood vessels and creates difficulty in coagulation of blood and hypovolemic shock (dramatic decrease in blood pressure) -depending on the type of virus, Ebola can have up to a 90% mortality rate for those infected -transmitted through bodily fluids and/or direct contact with infected individuals -due to extensive bleeding, most patients will die of hypovolemic shock and/or systematic organ failure

Rabies virus

-Rabies (derived from Latin word Rabere, meaning 'Rage') is a viral disease caused by Lyssavirus rabies virus - It is a neurotropic virus, capable of invasive infection of the central nervous system. The disease is extremely lethal to those unfortunate enough to show symptoms of the infection. The primary transmission of the virus to humans occurs through dog bites and scratches. The numbers vary widely form country to country, however, it is estimated that 55,000 people die per year from the rabies virus in Asia and Africa . The disease can be dramatic in its appearance as seen among many animals. The disease is known to cause hyperactivity, sporadic behavior, and aggressiveness to things around them. Infected animals and humans eventually succumb to paralysis of muscles -animals going "mad" -Rhabdoviruses are negative stand RNA virues, having only a single strand of RNA genome -Infection to humans usually occurs through a bite or scratch from an infected animal. Saliva from infected animals, as well as humans, can cause rabies when in contact with mucous tissues or recent skin wounds. Inhalation of aerosols containing virus particles as well as transplant of viral infected tissues have also been documented as possible forms of transmission. Many animals have the potential to carry the virus, but the most common source is dogs. Bats are a common source in the Americas. Other animals known to carry the disease include foxes, raccoons, skunks, jackals, and mongooses. Human to human infection through bite or scratch is hypothetically possible, but has never been confirmed. -During the incubation/Prodormal periods of the disease, symptoms may include itching and burning sensation at the wound or bite, fever, headache, and gastrointestinal problems. As the disease progresses into the neurological phase, about half of all cases begin to show hydrophobia and pains associated with drinking water. Other possible symptoms include hallucinations and seizures from neuron degradation in the central nervous system. The virus can lead to many various symptoms not all are required for a clinical diagnosis, but all eventually lead to respiratory failure. Some cases have been documented only showing symptoms of paralysis leading to coma and eventually respiratory failure. The symptoms of rabies can be vivid and graphic in their appearance, but none can completely confirm the diseases presence in a host. -Rabies is an extremely lethal disease with a almost absolute 100% death rate in all hosts in the late stages of the disease. there are only a hand full of documented human cases in which a person has the late stages of the disease and survives. The only way to treat the disease is before late stages of the virus can develop in the brain by using classical vaccination and antibodies treatments. -get the vaccine

Rhizopus spp.

-Rhizopus is a genus of common saprophytic fungi on plants and specialized parasites on animals. They are found on a wide variety of organic substrates, including "mature fruits and vegetables",[2] jellies, syrups, leather, bread, peanuts, and tobacco. They are multicellular. Some Rhizopus species are opportunistic agents of human zygomycosis (fungal infection) and can be fatal. Rhizopus infections may also be a complication of diabetic ketoacidosis.[3] This widespread genus includes at least eight species. -Rhizopus species grow as filamentous, branching hyphae that generally lack cross-walls (i.e., they are coenocytic). They reproduce by forming asexual and sexual spores. In asexual reproduction, sporangiospores are produced inside a spherical structure, the sporangium. Sporangia are supported by a large apophysate columella atop a long stalk, the sporangiophore. Sporangiophores arise among distinctive, root-like rhizoids. In sexual reproduction, a dark zygospore is produced at the point where two compatible mycelia fuse. Upon germination, a zygospore produces colonies that are genetically different from either parent.

Enterobius vermicularis

-The pinworm (species Enterobius vermicularis), also known as threadworm (in the United Kingdom and Australasia) or seatworm, is a parasitic worm. It is a nematode (roundworm) and a common intestinal parasite or helminth, especially in humans.[5] The medical condition associated with pinworm infestation is known as pinworm infection (enterobiasis)[6] (a type of helminthiasis) or less precisely as oxyuriasis in reference to the family Oxyuridae.[7] Other than human, Enterobius vermicularis were reported from bonnet macaque.[8] Other species seen in primates include Enterobius buckleyi in Orangutan [9] and Enterobius anthropopitheci in chimpanzee. Enterobius vermicularis is common in human children and transmitted via the faecal-oral route. Humans are the only natural host of Enterobius vermicularis.[10] Enterobius gregorii, another human species is morphologically indistinguishable from Enterobius vermicularis except the spicule size.[11] Throughout this article, the word "pinworm" refers to Enterobius. In British usage, however, pinworm refers to Strongyloides, while Enterobius is called threadworm. -The pinworm has a worldwide distribution,[22] and is the most common helminth (i.e., parasitic worm) infection in the United States, western Europe, and Oceania.[19][24] In the United States, a study by the Center of Disease Control reported an overall incidence rate of 11.4% among children.[19] Pinworms are particularly common in children, with prevalence rates in this age group having been reported as high as 61% in India, 50% in England, 39% in Thailand, 37% in Sweden, and 29% in Denmark.[19] Finger sucking has been shown to increase both incidence and relapse rates,[19] and nail biting has been similarly associated.[25] Because it spreads from host to host through contamination, pinworms are common among people living in close contact, and tends to occur in all people within a household.[22] The prevalence of pinworms is not associated with gender,[22] nor with any particular social class, race, or culture.[19] Pinworms are an exception to the tenet that intestinal parasites are uncommon in affluent communities.[19] A fossilized nematode egg was detected in 240 million-year-old fossil dung,[26] showing that parasitic pinworms already infested pre-mammalian cynodonts. The earliest known instance of the pinworms associated with humans is evidenced by pinworm eggs found in human coprolites carbon dated to 7837 BC found in western Utah.

Dengue virus

-a mosquito-borne flavivirus, is the causative agent of dengue fever, currently one of the most significant emerging disease challenges to global public health. -Although dengue is an old disease, recent decades have seen an unprecedented increase in the geographic range, incidence, and severity of infection. -The virus infects 100 million people annually and is endemic in many tropical and sub-tropical regions in the world -The four serotypes of dengue virus are single-stranded positive-sense RNA viruses -Dengue is a disease caused by the mosquito-borne dengue viruses. -In the last century, dengue has escalated in geographic distribution and disease severity to become now the most common arboviral infection of humans in the subtropical and subtropical regions of the world. -Dengue is currently endemic in more than one hundred countries around the world. It causes approximately 50-100 million infections annually, including 250,000-500,000 cases of dengue hemorrhagic fever/dengue shock syndrome. According to the World Health Organization (WHO), two fifths of the world population is at risk of dengue virus infection. It has been suggested that globalization and climate change have had a significant impact on the emergence of DENV in new areas -there are no available vaccines or antivirals against DENV

Treponema pallidum

-a Gram-negative bacteria which is spiral in shape. It is an obligate internal parasite which causes syphilis, a chronic human disease. Syphilis is a sexually transmitted disease but transmission can also occur between mother and child in utero; this is called congenital syphilis -it requires a mammalian host for survival. In the absence of mammalian cells, T. pallidum will be killed by the absence of nutrients, exposure to oxygen and heat. -T. pallidum is the causative agent of syphilis, a chronic infectious human disease transmitted between individuals via sexual intercourse or from mother to child in utero. T. pallidum's virulence factor is still unknown. -early treatment with penicillin can cure syphilis -Untreated syphilis progresses in a series of distinct stages (primary, secondary, latent, and tertiary.) "Infection is initiated when T. pallidum penetrates dermal microabrasions or intact mucous membranes" resulting in primary syphilis. Primary syphilis usually presents itself as a single chancre at the site of infection. Secondary syphilis occurs approximately 3 months after infection and presents itself with a variety of symptoms, most notably lesions of the skin and mucous membranes. These include a rash commonly on the palms of the hands, soles of the feet, face, and scalp. The breakdown of mucous membranes appears as patches on lips, inside the mouth, vulva, and vagina. Infected individuals may also experience fever, loss of appetite and weight loss during this stage. After several months, secondary symptoms will disappear; this is called the latent phase. Even though the infected individual is no longer showing symptoms, testing confirms that T. pallidum is still present. Transmission at this stage via sexual contact is rare. If untreated, latent phase may progress to tertiary phase. Tertiary syphilis doesn't manifest until years after initial infection (if it does at all) and can affect many different areas of the body. Tertiary syphilis can cause destructive lesions on skin and bones which are usually benign. The more deadly manifestations of late syphilis affect the cardiovascular system (especially the aorta) and the central nervous system causing infected individuals to experience insomnia and changes in personality.

Borrelia burgdorferi

-a Gram-negative, helical shaped spirochete bacteria that is well known as the causative agent of Lyme disease -is transmitted to humans by ticks is maintained in a natural cycle of infection by ticks. -The ticks acquire and transmit the bacteria by feeding on a variety of small mammals and birds that act as a reservoir host for the Borrelia. -B. burgdorferi is transmitted specifically by ticks of the genus Ixodes, which include a variety of different species found in different geographical locations. -icks use many small mammals to harbor the bacteria, and humans only become inadvertently infected when bitten. It is believed that the bacteria use a variety of mechanisms to evade the host immune response. -The first sign of infection is the erythema migrans, a circular rash at the site of the tick bite that appears after a few days delay. From there, infected humans may develop similar rashes on other sites of the body as well as symptoms such as fatigue, fever, headache, and muscle and joint aches. If the infection spreads throughout the body it has reached Stage II of the infection, which is marked by symptoms such as facial palsy, meningitis, extreme joint pain and heart palpitations. If it is left untreated for a few months the infection will reach Stage III and patients may develop arthritis as well as severe joint pain and swelling.

Propionibacterium acnes

-a commensal, non-sporulating bacilliform (rod-shaped), gram-positive bacterium found in a variety of locations on the human body including the skin, mouth, urinary tract and areas of the large intestine. P. acnes is most commonly associated with its implicated role as the predominant cause of the common inflammatory skin condition Acne vulgaris. -has been associated with a wealth of human pathologies including pulmonary angitis, endocarditis, sarcoidosis, corneal ulcers, hyperostosis, cholesterol gallstones, allergic alveolitis and synovitis, pustulosis and most commonly acne vulgaris.

Histoplasma capsulatum

-a fungal pathogen that can result in a wide range of clinical presentations, from asymptomatic through fatal infection. It usually causes lung disease called Histoplamosis or Darling's disease -a biologically interesting inhabitant of soil and mammalian hosts, a clinically significant cause of respiratory and systemic infection, and an excellent fungal model of dimorphic cell development and facultative intracellular pathogenesis. [4] H. capsulatum is unique in its dimorphism. Dimorphism allows H. capsulatum to infect mammals by going through three significant development stages depends on the temperature shift from 25 °C to 37 °C. [1, 12] In the moist soil that is rich in bird or bat guano at temperature about 25 °C, H. capsulatum exists in a filamentous mycelia form. [4] However, when humans inhale H. capsulatum into their respiratory tracks, in order to replicate its DNA in the host at 37C, the pathogen has to be able to convert its tissue from one form to another. In this case, H. Capsulatum changed from fungi to yeast when it's growing in the human bodies. [5, 16] H. capsulatum is thought to cause approximately 500,000 respiratory infections a year in the central river valleys in the Midwestern and south central United States -reproduces when it is in the mold form of the fungus and is heterothallic. - is widely distributed throughout the sutropial and tropical zones of the world. It is the etiologic agent of the most common respiratory fungal infection affecting humans, especially those who have weak immune systems such as AIDS patients. In n America, H. capsulatum is particularly associated with the Mississippi and Ohio River valleys. [2, 4, 5] Throughout the development of H. capsulatum, three distinct stages depending on the temperature shift between 25°C to 37°C have been identified.

Neisseria gonorrhoeae

-a gram-negative coccus, or bacteria whose overall shape is spherical. It is usually seen in pairs with adjacent sides flattened. -The organism is usually found interacellulary in polymorphonuclear leukocytes, or a specific category of white blood cells with varying shapes of nuclei, of the gonorrhea pustular exudates with humans as its only natural host. -a human pathogen -This organism is relatively fragile and is susceptible to temperature changes, drying, UV light, and some other environmental conditions. -Neisseria gonorrhoeae is the cause of the sexually transmitted disease gonorrhea. It natural environment is in the human body and it only known for its pathogenic characteristic. -Neisseria gonorrhoeae infections are acquired by sexual contact and usually affect the mucous membranes of the urethra in males and the endocervix and urethra in females. -is only found after sexual contact with an infected person (or in the case of infections in the newbord, direct contact). -Although it does not produce any exotoxins, Neisseria gonorrhoeae has a wide range of virulence determinants. -In males there is an approximate 2-3 day incubation period after which a purulent discharge from the urethra and dysuria develops. Around 95% of infected males are symptomatic. Rare complications include prostatitis, epididymitis, and periurethral abcesses. -In women, Neisseria gonorrhoeae primarily infects the cervix in women. The symptoms of gonorrhea are often mild and most women who are infected do not have symptoms. Even when a woman has symptoms, they can be so non-specific and can be mistaken for a bladder or vaginal infection. Symptoms include vaginal discharge, dysuria, and abdominal pain. Around 10%-20% of infected women develop these complications. In 1%-3% of infected women and a lower percentage of infected men the bacterium disseminates via the blood causing bacteremia and arthritis.

Yersinia pestis

-a rod shaped, gram-negative bacteria that can also have a spherical shape. -It is also covered by a slime envelope that is heat labile. -When the bacteria is in a host, it is nonmotile (incapable of self-propelled movement), but when isolated it is motile. -uses aerobic respiration and anaerobic fermentation to produce and consume hydrogen gas for energy. -Yersinia pestis interacts mainly with rodents such as rats and fleas. Through these carriers, Yersinia pestis is able to invade human cells and create diseases. -Y. pestis causes diseases through the bite of an infected rat or flea, but can also be transmitted by air. Fleas can become infected by taking the blood of other infected animals. -grows in the midgut and eventually blocks the proventriculus, starving the flea for blood. The insects attempt to feed more often but end up giving back infected blood into the wound of the bite. -Symptons include: Sudden onset of high fever, Emergence of a smooth, painful swelling of the lymph gland(s), called a buboe. The most common area is the groin, but swollen glands may also occur in the armpits or neck. Pain may occur in the area before the swelling. Chills General discomfort or ill feeling (malaise) Muscular pain Severe headache Seizures

Toxoplasma gondii

-a single-celled eukaryotic protozoan parasite. The name Toxoplasma is derived from the shape of the organism, which is crescent-like (toxon is Greek for "arc"). T. gondii holds notoriety as the pathogen that causes the disease toxoplasmosis in humans. Infants (especially via vertical transmission) and immuno-compromised hosts (including cats) are readily infected with the pathogen and show accelerated and concentrated symptoms, but it is interesting to observe that the pathogen is generally docile and useless in healthy individuals with a competent immune system[7,8]. Nearly 1/3rd of the world human population has Toxoplasma infection, though this is the latent form of the disease and is non-fatal[19]. The microbe preferentially encysts itself within the tissues of the brain and the central nervous system of the host, causing encephalopathy, loss of normal cognitive brain function, impaired judgment, peripheral neuropathy, slowed reflexes, pathological lesions and other disorders classically associated with the invasion of brain tissue -mainly spreads via contaminated cat feces, consumption of undercooked meat, tainted water and vertical transmission -causes the disease toxoplasmosis, and is an important human pathogen that is present in up to 1/3rd of the world's human population [19]. The microbe is usually not a threat to hosts with a competent immune system, and thus a great majority of the microbe is latent within those infected, but nearly 30% of AIDS patients have toxoplasmosis, and is almost always fatal unless continually treated with antibiotics for the rest of their life [15]. It can also be spread via vertical transmission (mother-to-child prenatal transmissions via placenta), and unfortunately, medicines administered to the mother do not assist in protecting or aiding the fetus while still inside the womb.

Mycobacterium tuberculosis

-acid-fast bacteria -pathogen that lives in the host -causes tuberculosis, an infectious disease -pulmonary, extrapulmonary, and miliary TB -loss of appetite, night sweats, coughing, and fatigue -pulmonary TB is easily spread by coughing or sneezing -weakened immune systems, medical conditions, and working in hospitals increases chances of getting the infection -bacteria can travel from the lungs by blood to other parts of the body -skin test, chest x-ray, blood test, sputum sample, and culture test -treated with a combination of several antibiotics for 6-12 months -scientists are discovering more antibiotic resistant strains -BCG vaccine

Bartonella henselae

-aerobic, slow growing, gram-negative, rod shaped, slightly curved bacteria -does not have flagella but there has been evidence of twitching motility -is very sensitive to pH changes -under the microscope, the colonies are cauliflower-like -is found primarily in cats and humans -Cat Scratch Disease - bitten or scratched by a cat -the vectors can be either the cat or the cat flea that transmits it to the cat -when cats are infected, they show no symptoms, thus making it difficult for researchers to identify the disease -is known to be the agent of bacillary angiomatosis, peliosis hepatitis, septicemia, endocarditis, recurring fever, and neurological disorders -the latter symptoms are fatal when misdiagnosed and improperly treated -headaches, anorexia, weight loss, vomiting, and occasionally, a sore throat

Entamoeba histolytica

-an anaerobic parasitic protozoan that infects the digestive tract of predominantly humans and other primates. It is a parasite that infects an estimated 50 million people around the world and is a significant cause of morbidity and mortality in developing countries. Analysis of the genome allows new insight into the workings and genome evolution of a human pathogen. -Transmission of the parasite occurs when a person ingests food/water that has been contaminated with infected feces. The infection E. histolytica is called Amebiasis (or Amoebiasis). Cysts of the parasite are the viable form outside the host. They can survive weeks in water, soils and on foods under moist conditions. Once inside the host, cysts divide into four trophozoites in the small intestines. E. histolytica strains have been isolated from foreigners outside the U.S., homosexual men, patients with HIV and cynomolgus monkeys. -Cysts are viable in water, soils and on foods. They are formed by trophozoites and excreted in feces. There they survive for weeks in moist conditions. -The infection of E. histolytica causes the disease, Amebiasis (or Amoebiasis). E. histolytica infects the digestive tracts of predominantly humans and other primates. E. histolytica can infect dogs and cats, but these animals do not contribute significantly to transmission since they usually do not produce cysts. Cysts do not invade tissue and are shed with the host's feces. The thick protective walls allow the cysts to remain viable for several weeks in the external environment and the internal acid content of the stomach.

Nitrosomonas spp.

-genus of ammonia-oxidizing proteobacteria -gram-negative -important players in wastewater treatment plants, where they get rid of excess ammonia by converting it to nitrite -are rod-shaped chemolithoautothrophs with an aerobic metabolism -while they do not grow by photosynethsis, their unusual metabolic behavior involoves burning ammonia with oxygen -cells grow either in pairs or short chains -play an important role in providing nitrogen to plants and limiting carbon dioxide fixation -found widely distributed in soil or water, where there are large amounts of ammonia, such as lakes or streams into which treated and untreated sewage is pumped -does whatever it can to avoid light, and so may appear ass clumps of slime in order to protect itself -often found on the walls of stone bulidings or on the surface of monuments, where its production of nitric acid from the air may cause erosion of the stone beneath -while in some respects the bacterias' effect on ammonia is positive, agriculturally it can pose a problem -Nitrification, the cycle in which the bacteria acts as the initiator by oxidizing ammonia to nitrite, can leave the nitrate in the soil more susceptible to leaching and therefore less available to plants

Chlamydia trachomatis

-an obligate, aerobic, intracellular parasite of eukaryotic cells. It is a Gram-negative bacteria and has a coccoid or rod shape -require growing cells in order to remain viable since it cannot synthesize its own ATP. Without a host organism, C. trachomatis cannot survive on its own -is the leading cause of sexually transmitted disease worldwide--in the United States, alone, over 4 million cases are diagnosed each year. It is also the leading cause of preventable blindness (caused by a chlamydia infection called trachoma) in the world. C. trachomatis is also one of the major causes of pelvic inflammatory disease (PID) and infertility in women. -Chlamydia trachomatis is a pathogenic bacteria. It cannot survive outside of a eukaryotic host. In fact, humans are the only known natural host for C. trachomatis. The bacterium is transmitted by sexual contact with an infected individual. -Usually, C. trachomatis is asymptomatic in its hosts, but can cause discharge from the penis, pain and burning during urination, infection or inflammation in the ducts of testicles, and tenderness or pain in the testicles -Chlamydia is transmitted through infected secretions only. It infects mainly mucosal membranes, such as the cervix, rectum, urethra, throat, and conjunctiva. -It is primarily spread via sexual contact and manifests as the sexually transmitted disease. The bacterium is not easily spread among women, so the STD is mainly transmitted by heterosexual or male homosexual contact. However, infected secretions from the genitals to the hands and eventually to the eyes can cause trachoma

Penicillium spp.

-are filamentous fungi -have branched conidiospores -are round and unicellular -are osmotolerant, meaning that although they grow better with high water levels, they are able to tolerate low water potential. -are heterotrophic. The pathogenic species feed off of the fruit they destroy. -produces asexually, and are unable to sporulate when submerged. -are versatile and opportunistic -are post-harvest pathogens -are one of the most common causes of fungal spoilage in fruits and vegetables. -These species like cooler temperatures, which explains why they are usually found on foods left too long in the refrigerator. Many species produce mycotoxins -bleu cheese -most famous for the drug penicillin (an antibiotic)

Bacteroides spp.

-commonly found in the human intestine where they have a symbiotic host-bacterial relationship with humans -They assist in breaking down food and producing valuable nutrients and energy that the body needs. However, when Bacteriodes are introduced to parts of the body other than the gastrointestinal area, they can cause or exacerbate abscesses and other infections. -are gram-negative, non-spore forming, anaerobic, and rod-shaped bacteria -bacteroides are the most predominant bacteria found in the bacterial flora found in the human colon -process complex molecules into simpler compounds -When Bacteroides escape the gut, they are responsible for many types of infections and abscesses that can occur all over the body including the central nervous system, the head, the neck, the chest, the abdomen, the pelvis, the skin, and the soft tissues. -Along with diarrhea and abscesses, Bacteroides have been known to be involved in cases of meningitis and shunt infections, especially in children. Any tissue not normally colonized with Bacteroides has a possibility of infection when introduced to mucous or other materials containing Bacteroides. Diagnosis and treatment are complicated due to the slow growth of Bacteroides, the increasing resistance to antibiotics, and the polymicrobial nature of an infection with Bacteriodes (most infections deemed Bacteriodes infections can actually involve between 5 and 10 organisms).

Epstein Barr virus (EBV or HHV4)

-double stranded DNA virus (making it more stable and less likely for mutations than RNA viruses) -most common virus among the human population -more than 95% of the human population contain EBV antibodies, meaning that they have come into contact with the virus at some point in life and it is lying latent -many people are asymptomatic when infected, but under certain stresses diseases, such as infectious mononucleosis (IM), can arise -main virus responsible for Burkitt's Lymphoma, Hodgkin's Lymphoma and nasopharyngeal carcinoma (EBV is not the sole cause of these cancers, but it does play an important role in their development) -requires a host to replicate and survive -EBV is transmitted through salivary contact -"kissing disease" -transmission through blood and air are very rare -extremely infectious; the frequency of EBV transmission is between 95-100% -mostly contracted in adolescence -almost impossible to avoid the virus -main virulence factor of EBV is its ability to remain latent for years -symptoms: swollen lymph nodes, sore throat, headaches, chills, and fever; more severe include spleen tenderness and rashes

Herpes simplex virus (HSV1/2 or HHV1/2)

-dsDNA virus -HSV-1 (produces most cold sores) -HSV-2 (produces most genital herpes) -both types are ubiquitous and contagious -they can be spread when an infected person is producing and shedding the virus -about 67% of the world population under the age of 50 have HSV-1 -Symptoms of herpes simplex virus infection include watery blisters in the skin or mucous membranes of the mouth, lips, nose or genitals.[1] Lesions heal with a scab characteristic of herpetic disease. Sometimes, the viruses cause very mild or atypical symptoms during outbreaks. -It is therefore possible to acquire the virus even if no active HSV blisters or sores are present. -HSV-1 and -2 are transmitted by contact with an infected person who has reactivations of the virus. -Both viruses may also be transmitted vertically during childbirth. -Herpes simplex viruses can affect areas of skin exposed to contact with an infected person (although shaking hands with an infected person does not transmit this disease). An example of this is herpetic whitlow which is a herpes infection on the fingers. This was a common affliction of dental surgeons prior to the routine use of gloves when conducting treatment on patients. -Herpes viruses establish lifelong infections, and the virus cannot yet be eradicated from the body. Treatment usually involves general-purpose antiviral drugs that interfere with viral replication, reduce the physical severity of outbreak-associated lesions, and lower the chance of transmission to others. -

Merkel cell polyomavirus

-dsDNA virus -human tumor virus -it is suspected to be the cause of about 80% of a rare skin cancer called Merkel cell carcinoma -relatively recent discovery so no vaccines yet -avoiding excessive sun exposure and using appropriate sun lotion can help prevent the virus from mutating and causing cancerous tumors -blood tests have shown that the majority of adults have already been exposed to the virus and continue to carry it as an asymptomatic infection -Merkel cell carcinoma, an aggressive neuroendocrine skin cancer linked to lymphoid malignancies such as chronic lymphocytic leukemia -it can also be found in healthy tissues of people without Merkel cell carcinoma -can also be found in respiratory secretions, suggesting a possible respiratory transmittance -viruses found in Merkel cell carcinoma tumors are nontransmissible because the virus is integrated into the host DNA and cannot replicate independently -MCV mainly infects the elderly (over 50) or immunosuppressed individuals, such as AIDS patients

Pseudomonas aeruginosa

-gram-negative -coccobacillus -unipolar motility -colonies are large, pearl color, and have a sweet corn tortilla odor -aerobic and is widely known as a common opportunistic human pathogen. -It is also known as a hydrocarbon-using microorganism (or "HUM bug") because it is capable of growing in things like diesel and jet fuel and causes microbial corrosion. - thrives in warm, moist environments -is very well-known amongst the medical community because of it's remarkable ability to cause disease. It is commonly found in patients with compromised immune systems. -It causes pneumonia in those who are immuocompromised and is resistant to many antibiotics and grows rapidly, which makes recovering from pneumonia with a P. aeruginosa origin difficult. It is a dangerous yet common respiratory infection in cystic fibrosis patients. Most children with CF will be colonized with P. aeruginosa and it will never be completely removed from their bodies. It causes thick secretions and extreme coughing fits when in the lungs. VAP infections (ventilator-acquired pneumonia) are also commonly from and invasion of P. aeruginosa. -In CAUTIs; P. aeruginosa is also one of the common bacterial infections resulting from a patient having a foley catheter. Urinary tract infections s/p catheters and cross-contamination are often P. aeruginosa. -In Gastrointestinal infections; P. aeruginosa is often the bacteria in NEC (necrotizing entercolitis) which is often seen in premature infants. NEC requires surgeons to remove the dead portion of the intestine and leaves babies with temporary ostomies while their bowels are healing. NEC is fatal if untreated. -Treatment of P. aeruginosa infections depend on which specific strain the patient is infected with. But often times Zosyn, cefepime, ceftazadime, ciprofloxacin, and tobramycin can be used.

Leptospira spp.

-gram-negative bacteria -are long and helical in shape and have hooked ends; the hooked ends occur as the result of the two periplasmic flagella located at either pole of the cell -are obligate aerobes -results in leptospirosis -leptospirosis: a zoonotic disease, predominant in the subtropical and tropical regions of the world -most cases of the disease in humans originate from a reservoir host, most commonly rodents, and are transmitted through water or contaminate soil -symptoms in humans can range from mild symptoms such as a fever or a headache, to fatal problems causing death (these can be renal failure, jaundice, and pulmonary hemorrhage and are typically termed Weil's disease; vomiting and dogs

Francisella tularensis

-gram-negative bacteria -small and rod-shaped -nonmotile, aerobic, and non-spore forming -in nature, it can survive up to weeks at low temperatures in water, soil, and animal carcasses -is a highly contagious bacteria that causes tularemia, or "rabbit fever" (it is called this because rabbits are vectors for the disease) that is contagious to humans -the bacteria was used in development of biological weapons in WWII and post wars, and is considered a very dangerous biological terror threat today -is listed as a "category A select agent" by the US govt due to its high virulence and ease of spread, and if the disease is left untreated, the mortality rate can be as high as 30 to 60% of the cases -have pili on their surface -affects its environment by infecting small animals such as rabbits and rodents with the disease tularemia -the animals can acquire the disease through contact with fleas, flies, or contaminated soil, water, and vegetation -can infect humans through contact with infected animals or vectors such as fleas and mosquitoes -the disease can also be spread by human handling of animal or flesh infected with the disease -It can also be spread to humans by being in their water or food supply (It can survive for along time in animal carcasses). However, the disease is not known to spread through human-human contact -While more uncommon, it is also possible for airborne infection of tularemia to occur in nature. -The bacteria infects humans through skin, mucous membranes, lungs, and the gastrointestinal tract. -The major target organs are lymph nodes, lungs, liver, and kidneys. -People infected with tularemia through inhalation also develop hemorrhagic inflammation of the airways early in the disease, and it might develop into bronchopneumonia. -No proven vaccine has been created for tularemia, and the general treatment for the disease is antibiotics.

Helicobacter pylori

-gram-negative bacterium -has a helical or spiral shape and has 6-8 flagella at on end -found in very acidic environments, at a pH of 2.0 or less -the bacterium has been cultured in microaerobic (low oxygen conditions) but it adapts to high oxygen at high culture densities -is commonly found inside the lining of the stomach and the duodenum -are slow growing organisms that can cause peptic ulcers and gastritis that can lead to gastric cancer and gastric MALT (mucosa-associated lymphoid tissue) lymphoma -very common in humans and animals; half of the population is infected -in order to survive, the organism uses urea to produce ammonia and bicarbonate to neutralize the acid in the stomach

Klebsiella pneumoniae

-gram-negative bacterium -is facultative anaerobic -rod-shaped -Klebsiella is the pathogen that causes pneumonia -is commonly found in the gastrointestinal tract and hands of hospital personnel; also can be found in the nasopharynx -infections are typically nosocomial infections, which means they are contracted in a hospital or healthcare setting -the reason for its pathogenicity is the thick capsule layer surrounding the bacterium -its habitat is not limited to humans but is ubiquitous to the ecological environment; this includes surface water, sewage, and soil -resistant infection -is pathogenic and responsible for a large number of infections every year -causes a range of diseases that depends on which part of the body it infects: pneumonia, bloodstream infections, wound infections, surgical site infections, meningitis, and urinary tract infections (UTI) -"superbug" pneumonia symptoms: fever and chills, flu-like symptoms, cogh, which many produce mucus that is yellow, green, or bloody, and breathing issues

Rickettsia rickettsii

-gram-negative bacterium -small, rod-shaped -known to cause Rocky Mountain spotted fever (RMSF) -RMSF (a disease) can be transmitted to humans either from a tick bite with an incubation period of 1 week, or by contamination of a cut on the skin or a wound with ticks feces -Dr. Ricketts first isolated this microbe in Montana, 1906 -needs host cells to be able to grow -require arthropods as vectors; therefore, ticks are the vectors -are aerobic -are obligate, intracellular bacteria -symptoms include fever, headache, and muscle aches; a rash may be present, frequently with blackened or crusted skin at the site of a tick bite; spotted fever responds well to prompt treatment with antibiotics

Vibrio fischeri

-gram-negative; bioluminescent bacterium -rod-shaped and motile -natural inhabitants of seawater but can be found in fresh water -frequently found in symbiotic relationships with marine animals like the bobtail squid -bioluminescence is controlled by a small set of genes known as the lux operon -luminescent bacteria are found in free-living, symbiotic, saprophytic or parasitic relationships -is capable of causing human disease; there are two main groups: Vibrio cholerae infection and noncholera Vibrio infections -Vibrio infections are often characterized as a foodborne disease due to consumption of contaminated seafood, exposure of wounds to contaminated seawater, or injury caused by shark and/or alligator bites -Infections associated with noncholera Vibrio species are gastroenteritis, wound infection and septicemia, which is blood poisoning -Patient symptoms associated with gastroenteritis include diarrhea, abdominal cramps, nausea, vomiting, headaches, bloody stools, etc. -Symptoms associated with noncholera wound infection include swelling, pain, erythema, bullae, and necrosis -Symptoms associated with septicemia include fever, hypothermia, hypotension, acute respiratory distress syndrome, and multiple organ dysfunction

Cyanobacterium spp.

-gram-positive bacteria -lack flagella, making it difficult for them to move under their own power -harness energy through the process of photosynthesis -originally got their name from their bluish-green color -they produce gaseous oxygen as a product of their photosynthetic process -found in inland and coastal environments -have the ability to explosively reproduce given the proper environmental conditions -caused the near-extinction of oxygen-intolerant organisms -produce a variety of toxins like neurotoxins, cytotoxins, endotoxins, or hepatotoxins; they produce these toxins to kill off other local species, giving themselves more room for growth -create algal blooms; these blooms are not only harmful for many aquatic species, but also for humans who ingest contaminated fish and shellfish or swim in or are exposed to contaminated water -are an environmental cause of degenerative neurological diseases such as Amyotrophic Lateral Sclerosis (ALS), Parkinson's disease, and Alzheimer's disease

Clostridium tetani

-gram-positive bacterium -bacillus/rod-shaped; commonly appears to be shaped like a drumstick or tennis racket when stained (this strange appearance is due to the sporulation that occurs inside the cell -is an obligate anaerobe and must rely on fermentation -causes tetanus (a disease) -spores of the bacterium enter the body through open wounds and germinate through dead cells, spreading toxins -move around by the use of rotary flagella -found in many different environments, but most commonly in soil, dust, or sediment; warm, damp areas -also found in human and animal intestinal tracts, where they become pathogenic -is heat sensitive and cannot survive in the presence of oxygen -tetanus can only be prevented by immunization -tetanus causes unwanted muscle contractions and spasms, and in bad cases, individuals can experience severe seizures -without treatment, death is highly possible

Staphylococcus aureus

-gram-positive bacterium -spherical, immobile and form grape-like clusters; divide in 2 planes; colonies are yellow and grow large on a rich medium; they are facultative anaerobes (they grow by aerobic respiration or fermentation) -antibiotic resistant -most common hospital acquired pathogen -normal inhabitant of the skin and mucous membranes in the nose of a healthy human -is infectious to both animal and humans -may only survive on dry skin -can spread through contaminated surfaces, air and people -most common cause of "staph" infections -mild skin infections (impetigo), invasive diseases (wound infections), and toxix mediated diseases (food poisoning and TSS)

Clostridium botulinum

-gram-positive bacterium -typically rod-shaped and arranged as singles, pairs, or chains -most commonly found in soil, but also in food products, and grow most efficiently in low-oxygen conditions -survive by forming spores, remaining in a dormant state until environmental conditions arise that allow them to grow; these spores are very resistant to adverse environmental effects, aking them amenable to most environments and very hard to kill; these spores will grow under favorable conditions (anaerobiosis and substrate-rich environments) and will begin to produce their toxins as they rapidly propagate -discovered and isolated by Emile van Ermengem in 1896 -produces a toxin known as botulin, one of the most powerful toxins that leads to the paralytic illness known as botulism -botulism: paralysis, asphyxiation, impaired vision and muscular weakness -although antitoxins do exist, by the time the symptoms show, the toxin is irreversibly bound

Deinococcus radiodurans

-has radiation resistant properties -It has been known to withstand radiation levels of up to 1,000 times that which would kill a normal human, living up to its latin name, "strange little berry that withstands radiation." -a gram-positive bacteria that usually forms in spherical pairs or tetrads. -has been found in a wide variety of environments which therefore make its "natural" habitat difficult to define. It is often cultured in the lab from the feces of animals, such as elephants. However, many scientists have found it peacefully existing in the soil of various settings, including the rocky granite of Anartica's dry valleys. These numerous soil dwellings have led many to classify D. radiodurans as a soil bacteria. There is no current findings that suggest that D. radiodurans significantly interacts with other organisms in nature -scientists are interested in using the bacteria to clean up waste sites containing hazardous materials.

Yellow fever virus

-human-pathogenic virus -a Group IV positive-sense single stranded RNA virus, due to its direct mRNA-like functions in a host cell -arthropod vectors are the main source fro the spread of the virus (e.g. mosquitoes) -causes yellow fever -infected individuals are characterized by general flu-like symptoms that in 15% of cases develop into the more toxic phase -humans are a dead-end host for the virus and fail to allow it to complete its life cycle -jaundice, blood in urine or feces, and liver dysfunction -get vaccinated

Haemophilus influenzae

-is bacterial infection in the blood stream -in general, the bacteria lives in the upper respiratory tract which can be transmitted by close contact with patients. This bacterial infection can also be air born transmitted through sneezing. -small, gram-negative bacteria; lacks flagella and pili, which means it lacks mobility -When inflected with haemophilus influenzae different children will show different symptoms, the symptoms also depends which part of the human body has been infected. -H. influenzae type b causes meningitis, which is an inflection in the membrane around the brain and epiglottitis which is infection around the throat and trachea. Haemophilus influenzae is a non-motile Gram-negative rod-shaped bacterium. H. influenzae can cause serious invasive disease especially in young children. Invasive disease is usually caused by encapsulated strains of the organism.

Streptococcus agalactiae (GBS)

-is a diplococcal (a pair of cocci, circular, pair) gram-positive, non acid-fast bacterium (~2.0µm) that does not form spores, is not motile, and is catalase-free (catalase is an enzyme that catalyzes the reduction of hydrogen peroxide). It occurs in pairs or short chains and has group B Lancefield antigen present. -originally discovered as a cause of bovine mastitis, is part of the normal bacterial flora colonizing the gastrointestinal(GI) tract and genitourinary tract of a significant proportion of the human population. However, it occasionally becomes an infectious pathogen colonizing the uterus, blood, brain, and meninges. -This pathogen is one of the leading causes of invasive infections in non-pregnant immunocompromised individuals and also causes bacteremia, septicaemia, meningitis, and pneumonia. Colonization of the rectum and vagina of pregnant women with GBS is correlated with GBS sepsis in newborn infants with early onset disease -can be isolated in infected sites of human or in secretions from infected mammary gland of female cattle and related ungulates. In some samples these bacteria are numerous and easily found in stained films; in other cases they may be so scarce that they can be located only with great difficulty. Also, most stains can be used to stain GBS to locate them, since the GBS is gram-positive and readily stained - responsible for 2-3 cases per 1000 live birth and to lives of human, especially elderly persons and those with weakened immune systems. This microorganism is considered one of the major causes of economic losses to dairy producers without a control program. Because of its significance as an threat to both human and related ungulates, such as cow, its genome was sequenced and is still being studied to gain more insight into the virulence factor and to develop treatments and preventive prophylactic antibodies. - is host-associated facultative anaerobe, that is capable of using oxygen or not using oxygen depending on surrounding environment to generate ATP, aerobic respiration or fermentation, respectively. -colonizes in the body of some animals, including cow, sheep, and humans without causing any harm -The habitat of this microorganism is largely confined to the intestine and vagina in human and the mammary gland of cows and sheep. This microorganism also colonizes in the genital and/or intestinal tract of about 10-30% of pregnant women

Measles virus

-is a single-stranded, negative-sense, enveloped (non-segmented) RNA virus of the genus Morbillivirus within the family Paramyxoviridae. -Humans are the natural hosts of the virus; no animal reservoirs are known to exist. -The measles virus is the cause of measles, an infection of the respiratory system. Symptoms include fever, cough, runny nose, red eyes and a generalized, maculopapular, erythematous rash. The virus is highly contagious and is spread by coughing and sneezing via close personal contact or direct contact with secretions. -The measles virus evolved from the formerly widespread rinderpest virus, which infects cattle

Necator americanus

-is a species of hookworm (a type of helminth) commonly known as the New World hookworm. Like other hookworms, it is a member of the phylum Nematoda. It is a parasitic nematode that lives in the small intestine of hosts such as humans, dogs, and cats. Necatoriasis—a type of helminthiasis—is the term for the condition of being host to an infestation of a species of Necator. Since N. americanus and Ancylostoma duodenale (also known as Old World hookworm) are the two species of hookworms that most commonly infest humans, they are usually dealt with under the collective heading of "hookworm infection". They differ most obviously in geographical distribution, structure of mouthparts, and relative size. -In the United States, 95% of human hookworm cases are caused by N. americanus, primarily in young school children in economically deprived rural areas. Juveniles cannot survive freezing temperatures, therefore the highest prevalence occurs in areas with warmer temperatures and greater rainfall. The greatest incidence of infections occurs in Asia and sub-Saharan Africa, especially in poverty-stricken areas with poor sanitation.[6] A. duodenale infections occur at a lesser rate and are seen primarily in Europe and the Mediterranean. -The most common treatment for N. americanus are benzimidazoles, specifically albendazole and mebendazole. -The most effective prevention technique is to not walk barefoot in areas where hookworm is common and where there may be contamination of the soil. Locations for outdoor activities should be considered if there will be skin-to-soil contact. -Infection and transmission of others can be prevented by not defecating outdoors or using human feces fertilizer.

Ancylostema duodenale

-is a species of the roundworm genus Ancylostoma. It is a parasitic nematode worm and commonly known as the Old World hookworm. It lives in the small intestine of hosts such as humans, cats and dogs, where it is able to mate and mature. Ancylostoma duodenale and Necator americanus are the two human hookworms that are normally discussed together as the cause of hookworm infection. They are dioecious.[1] Ancylostoma duodenale is abundant throughout the world, including in the following areas: southern Europe, north Africa, India, China, southeast Asia, some areas in the United States, the Caribbean, and South America. -Ancylostoma duodenale is prevalent in southern Europe, northern Africa, India, China, and southeast Asia, small areas of United States, the Caribbean islands, and South America. This hookworm is well known in mines because of the consistency in temperature and humidity that provide an ideal habitat for egg and juvenile development. It is estimated 1 billion people are infected with hookworms. Transmission of Ancylostoma duodenale is by contact of skin with soil contaminated with larvae. The way Ancylostoma duodenale enters the human body was understood in the 1880s, after an epidemic of ancylostomiasis among miners working in the hot and humid Gotthard Tunnel (Switzerland). -A light infection causes abdominal pain, loss of appetite and geophagy. Heavy infection causes severe protein deficiency or iron deficiency anemia. Protein deficiency may lead to dry skin, edema and potbelly, while iron deficiency anemia might result in mental dullness and heart failure. Women who are pregnant and infected should be aware that this parasite is able to infect the fetus and can cause complications such as low birth weight, maternal anemia, and infant mortality.[5] The eggs of Ancylostoma duodenale and Necator americanus cannot be distinguished. Larvae cannot be found in stool specimen unless they are left at ambient temperature for a day or more. Education, improved sanitation and controlled disposal of human feces are important. Wearing shoes in endemic areas can reduce the prevalence of infection as well. Ancylostoma duodenale can be treated with albendazole, mebendazole and benzimidazoles. Pyrantel pamoate is an alternative. In severe cases of anemia, blood transfusion may be necessary.

Saccaromyces cerevisiae

-is a species of yeast. It has been instrumental to winemaking, baking, and brewing since ancient times. It is believed to have been originally isolated from the skin of grapes (one can see the yeast as a component of the thin white film on the skins of some dark-colored fruits such as plums; it exists among the waxes of the cuticle). It is one of the most intensively studied eukaryotic model organisms in molecular and cell biology, much like Escherichia coli as the model bacterium. It is the microorganism behind the most common type of fermentation. S. cerevisiae cells are round to ovoid, 5-10 μm in diameter. It reproduces by a division process known as budding.[2] Many proteins important in human biology were first discovered by studying their homologs in yeast; these proteins include cell cycle proteins, signaling proteins, and protein-processing enzymes. S. cerevisiae is currently the only yeast cell known to have Berkeley bodies present, which are involved in particular secretory pathways. Antibodies against S. cerevisiae are found in 60-70% of patients with Crohn's disease and 10-15% of patients with ulcerative colitis (and 8% of healthy controls). -"Brewer's Yeast" -In nature, yeast cells are found primarily on ripe fruits such as grapes (before maturation, grapes are almost free of yeasts).[9] Since S. cerevisiae is not airborne, it requires a vector to move. -all strains can grow aerobically

Mycobacterium leprae

-is responsible for leprosy or Hansen's disease -is an intracellular bacterium, infecting nerve, skin and mucosal cells. In laboratory environments, Mycobacterium leprae is cultured on the feet of mice or on nine banded armadillos due to the inability to culture in vitro. -acid fast bacterium -Mycobacteria, as genus, are typically found in the soil, water and in the air. The majority of Mycobacteria are non-pathogenic and non-parasitic. M. leprae is suspected to be found in the soil, but due to the fact that it can not be plated it is hard to conclude that this is the case -M. leprae is responsible for the disease leprosy (1). In 2006, there were 219,826 cases of leprosy reported. It primarily affects the peripheral nerves and skin (9). It is also known to affect the central nervous system, mucus lining of the mouth, throat and lungs. Patients often experience numbness, skin lesions, joint pain and weakness. Lesions of the skin can leave individuals physically maimed and socially shunned. The innate immune response to the infection is inflammation. The inflammation in the neural cell causes neuropathy and serious nerve damage. Nerve damage doesn't occur until an immune response happens. The nerve damage quickly progresses to numbness, paralysis and deformity

Trypanosoma cruzi

-parasite -a kinetoplast eukaryotic cell that is associated with causing the often fatal Chagas Disease, which spreads through insects -Chagas Disease, which is mainly found in South America, is characterized by organ failure, usually in the digestive tract and heart -needs calcium to survive -is most often spread through the reduviid insect, which bites the host and then leaves excrement with the pathogen near the open wound. It is most prevalent in the rural and poorer areas of Latin America -causes Chagas Disease by invading mammalian cells. They show no specificity and can invade many different cell types. T. Cruzi spreads among mammals through hematophagous triatomines insect. It is known to cause chronic symptoms of various digestive problems and by causing the more serious problem of weakening the heart muscle. -this microbe may be transmitted by a vector called a "kissing bug"

Neisseria meningitidis

-parasitic, aerobic, Gram-negative, non-endospore forming, nonmotile, coccal bacterium -responsible for causing meningitis, inflammation of the meninges layer covering the brain -has catalase and oxidase activity -colonies appear smooth, moist, and glistening -resides primarily in humans on the surface of mucosal membranes such as those found in the respiratory tract -progression through meningitis almost always follows after entering the blood stream -in terms of metabolism, it requires mineral slats, lactate, some amino acids such as cysteine, and glutamic acid as a carbon source -iron reduction is a necessary part of its metabolism -humans are its primary reservoir from which heme iron, along with other nutrients in the blood, satisfies its requirement for growth -often transferred from person to person in aerosol form as from a sneeze

Clostriduim perfringens

-rod shaped, nonmotile, anaerobic, gram-positive bacterium -is an inhabitant of human normal intestinal flora -is responsible for many gastrointestinal illnesses with severity ranging from mild enterotoxaemia to fatal gas gangrene -caused the death of many injured soldiers during WWI -primary targets are humans and animals -also found in sewage and soil

Proteus vulgaris

-rod-shaped, nitrate-reducing, hydrogen sulfide- producing, gram-negative bacterium -inhabits the intestinal tracts of humans and animals -It can be found in soil, water, and fecal matter. -It is grouped with the Enterobacteriaceae and is an opportunistic pathogen of humans. -It is known to cause wound infections and other species of its genera are known to cause urinary tract infections.

Serratia marcescens

-short, rod-shaped, motile, gram-negative, facultative anaerobe bacterium, classified as an opportunistic pathogen -produces red pigmentation called "prodigiosin" -"Operation Sea Spray" -typically grows on bread and communion wafers stored in moist places; has led scientists to suggest Serratia contamination as a possible explanation for transubstantiation miracles (the conversion of bread to the body and blood of Christ) -is ubiquitous; is commonly found in soil, water, plants and animals -is widely present in non-potable water in underdeveloped countries due to poor chlorination -is a pathogenic microorganism, it is only so with immunocomprimised individuals such as those found in hospitals where many of the documented infections take place -the mode of transmission of this microorganism is by either direct contact, or by catheters, droplets, saline irrigation solutions, and other solutions that are believed to be sterile -causes nosocomial infections -is resistant to many antibiotics traditionally used to treat bacterial infections, such as penicillin and ampicillin -many diseases are associated with the bacterium including: sepsis, bacteremia, meningitis and cerebral abscesses, urinary tract infections, osteomyelitis, ocular infections, and endocarditis -due to the wide range of diseases that it causes, there is not one determining symptom or source of origin

Hantavirus

-ssRNA negative-strand virus -causes a range of clinical manifestations collectively known as haemorrhagic fever with renal syndrome (HFRS) -lives in rodents such as rats and mice without causing any symptoms -urine, feces or saliva from the rodents can transmit the viruses to humans -the five different kinds of hantaviruses discovered so far are found in different geographical regions and in different kinds of rodents -it is the causative agent of two serious diseases: hantaan virus causes HFRS while Sin Nombre, another hantavirus, causes severe cases of Hantavirus Pulmonary Syndrome (HPS)

Chikungunya virus

Chikungunya (pronunciation: chik-en-gun-ye) virus is transmitted to people by mosquitoes. The most common symptoms of chikungunya virus infection are fever and joint pain. Other symptoms may include headache, muscle pain, joint swelling, or rash. Outbreaks have occurred in countries in Africa, Asia, Europe, and the Indian and Pacific Oceans. In late 2013, chikungunya virus was found for the first time in the Americas on islands in the Caribbean. There is a risk that the virus will be imported to new areas by infected travelers. There is no vaccine to prevent or medicine to treat chikungunya virus infection. Travelers can protect themselves by preventing mosquito bites. When traveling to countries with chikungunya virus, use insect repellent, wear long sleeves and pants, and stay in places with air conditioning or that use window and door screens. No vaccine exists to prevent chikungunya virus infection or disease. The most effective way to avoid chikungunya virus infection is to prevent mosquito bites. The mosquitoes that spread the chikungunya virus bite during the day and at night. Chikungunya virus is transmitted to people through mosquito bites. Mosquitoes become infected when they feed on a person already infected with the virus. Infected mosquitoes can then spread the virus to other people through bites. Chikungunya virus is most often spread to people by Aedes aegypti and Aedes albopictus mosquitoes. These are the same mosquitoes that transmit dengue virus. They bite during the day and at night. Chikungunya virus is transmitted rarely from mother to newborn around the time of birth. To date, no infants have been found to be infected with chikungunya virus through breastfeeding. Because of the benefits of breastfeeding, mothers are encouraged to breastfeed even in areas where chikungunya virus is circulating. Most people infected with chikungunya virus will develop some symptoms. Symptoms usually begin 3-7 days after being bitten by an infected mosquito. The most common symptoms are fever and joint pain. Other symptoms may include headache, muscle pain, joint swelling, or rash. Chikungunya disease does not often result in death, but the symptoms can be severe and disabling. Most patients feel better within a week. In some people, the joint pain may persist for months. People at risk for more severe disease include newborns infected around the time of birth, older adults (≥65 years), and people with medical conditions such as high blood pressure, diabetes, or heart disease. Once a person has been infected, he or she is likely to be protected from future infections.

Streptomyces spp.

-usually inhabit soil and are important decomposers. They also produce more than half of the world's antibiotics, and are consequently invaluable in the medical field. -They are able to metabolize many different compounds including sugars, alcohols, amino acids, and aromatic compounds by producing extracellular hydrolytic enzymes. Their metabolic diversity is due to their extremely large genome which has hundreds of transcription factors that control gene expression, allowing them to respond to specific needs. -In addition to echoing fungi in their cellular structure, streptomycetes also resemble fungi in their elaborate life cycle. During the vegetative growth stage of streptomycete development, DNA replication takes place without cellular division, creating the previously mentioned filamentous structure. Streptomycetes reproduce and disperse through the formation of spores, called conidia, which follows the period of vegetative growth. The spores are produced in aerial filaments called sporophores, which rise above the colony. Because the complex life cycle of streptomycetes resembles that of multicellular eukaryotes, it enables researchers to study the development of these more complex systems using a simpler system. -are found worldwide in soil, and are largely responsible, through the secretion of chemicals called geosmens, for the earthy smell of soil. streptomycetes consequently play an important role in the degradation of organic matter, most commonly noted in compost piles. Several species of Streptomyces are involved in a symbiotic relationship with species of ants in the genus Attini. Attine ants cultivate fungus in, what are termed fungal gardens. They perform all the motions of human farmers, weeding, and nurturing their gardens. The small bacterium in the streptomyces genus inhabits the cuticles of the ants, and aids in weeding their fungal gardens. Streptomycetes produce toxins that keep the main weed in ant fungal gardens, another fungi, Escovopsis, at bay. -Because streptomycetes inhabit soil, they are mainly phytopathogens, known for attacking root vegetables, such as potatoes, beets, radishes, rutabaga, turnips, carrots, and parsnip. Most commonly found on potatoes, Streptomyces scabies creates a condition known as "common scab," which manifests itself as sores on the external surface of the potato. The scabs do not harm the meat on the the inside of the potato but create an extremely unpleasant appearance that devalues the potato. -Streptomycetes are most widely known for their ability to synthesize antibiotics. Over 50 different antibiotics have ben isolated from streptomycetes, providing most of the world's antibiotics.

Vibrio cholerae

Cholera, caused by the bacteria Vibrio cholerae, is rare in the United States and other industrialized nations. However, globally, cholera cases have increased steadily since 2005 and the disease still occurs in many places including Africa, Southeast Asia, and Haiti. CDC responds to cholera outbreaks across the world using its Global Water, Sanitation and Hygiene (WASH) expertise. Cholera can be life-threatening but it is easily prevented and treated. Travelers, public health and medical professionals and outbreak responders should be aware of areas with high rates of cholera, know how the disease spreads, and what to do to prevent it. Most persons infected with the cholera bacterium have mild diarrhea or no symptoms at all. Only a small proportion, about 5-10%, of persons infected with Vibrio cholerae O1 may have illness requiring treatment at a health center. Cholera patients should be evaluated and treated quickly. With proper treatment, even severely ill patients can be saved. Prevention of cholera is dependent on access to safe water, adequate sanitation, and basic hygiene needs. The following materials cover the basics of cholera and other diarrheal disease prevention. Vibrio cholerae is a Gram-negative, comma-shaped bacterium. The bacterium's natural habitat is brackish or saltwater. Some strains of V. cholerae cause the disease cholera. V. cholerae is a facultative anaerobe[1] and has a flagellum at one cell pole as well as pili. V. cholerae can undergo respiratory and fermentative metabolism. When ingested, V. cholerae can cause diarrhea and vomiting in a host within several hours to 2-3 days of ingestion. V. cholerae was first isolated as the cause of cholera by Italian anatomist Filippo Pacini in 1854,[2] but his discovery was not widely known until Robert Koch, working independently 30 years later, publicized the knowledge and the means of fighting the disease V. cholerae is Gram-negative and comma-shaped. Initial isolates are slightly curved, whereas they can appear as straight rods upon laboratory culturing. The bacterium has a flagellum at one cell pole as well as pili. V. cholerae is a facultative anaerobe, and can undergo respiratory and fermentative metabolism.

Taenia saginata

Taenia saginata (synonym Taeniarhynchus saginatus), commonly known as the beef tapeworm, is a zoonotic tapeworm belonging to the order Cyclophyllidea and genus Taenia. It is an intestinal parasite in humans causing taeniasis (a type of helminthiasis) and cysticercosis in cattle. Cattle are the intermediate hosts, where larval development occurs, while humans are definitive hosts harbouring the adult worms. It is found globally and most prevalently where cattle are raised and beef is consumed. It is relatively common in Africa, Europe, Southeast Asia, South Asia, and Latin America.[1] Humans are generally infected as a result of eating raw or undercooked beef which contains the infective larvae, called cysticerci. As hermaphrodites, each body segment called proglottid has complete sets of both male and female reproductive systems. Thus, reproduction is by self-fertilisation. From humans, embryonated eggs, called oncospheres, are released with faeces and are transmitted to cattle through contaminated fodder. Oncospheres develop inside muscle, liver, and lungs of cattle into infective cysticerci.[2] T. saginata has a strong resemblance to the other human tapeworms, such as Taenia asiatica and Taenia solium, in structure and biology, except for few details. It is typically larger and longer, with more proglottids, more testes, and higher branching of the uteri. It also lacks an armed scolex unlike other Taenia. Like the other tapeworms, it causes taeniasis inside the human intestine, but does not cause cysticercosis. Its infection is relatively harmless and clinically asymptomatic. Cattle acquire the embryonated eggs, the oncospheres, when they eat contaminated food. Humans contract infective cysticerci by eating raw or undercooked meat. The disease is relatively common in Africa, some parts of Eastern Europe, the Philippines, and Latin America.[2] This parasite is found anywhere where beef is eaten, even in countries such as the United States, with strict federal sanitation policies. In the US, the incidence of infection is low, but 25% of cattle sold are still infected.[5] The total global infection is estimated to be between 40 and 60 million.[1] It is most prevalent in Sub-Saharan Africa and the Middle East T. saginata infection is usually asymptomatic, but heavy infection often results in weight loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, chronic indigestion, and loss of appetite. Intestinal obstruction in humans can be alleviated by surgery. The tapeworm can also expel antigens that can cause an allergic reaction in the individual.[7] It is also a rare cause of ileus, pancreatitis, cholecystitis, and cholangitis.

Trichomonas vaginalis

Trichomonas vaginalis is an anaerobic, flagellated protozoan parasite and the causative agent of trichomoniasis. It is the most common pathogenic protozoan infection of humans in industrialized countries.[1] Infection rates between men and women are similar with women being symptomatic, while infections in men are usually asymptomatic. Transmission usually occurs via direct, skin-to-skin contact with an infected individual, most often through vaginal intercourse. The WHO has estimated that 160 million cases of infection are acquired annually worldwide.[2] The estimates for North America alone are between 5 and 8 million new infections each year, with an estimated rate of asymptomatic cases as high as 50%.[3] Usually treatment consists of metronidazole and tinidazole. Trichomonas vaginalis, a parasitic protozoan, is the etiologic agent of trichomoniasis, and is a sexually transmitted infection.[2][5] More than 160 million people worldwide are annually infected by this protozoan. Pap smear, showing infestation by Trichomonas vaginalis. Papanicolaou stain, 400x Trichomoniasis, a sexually transmitted infection of the urogenital tract, is a common cause of vaginitis in women, while men with this infection can display symptoms of urethritis. 'Frothy', greenish vaginal discharge with a 'musty' malodorous smell is characteristic Some of the complications of T. vaginalis in women include: preterm delivery, low birth weight, and increased mortality as well as predisposing to HIV infection, AIDS, and cervical cancer.[10] T. vaginalis has also been reported in the urinary tract, fallopian tubes, and pelvis and can cause pneumonia, bronchitis, and oral lesions. Condoms are effective at reducing, but not wholly preventing, transmission.[11] Trichomonas vaginalis infection in males has been found to cause asymptomatic urethritis and prostatitis.[12] It has been proposed that it may increase the risk of prostate cancer; however, evidence is insufficient to support this association as of 2014. Infection is treated and cured with metronidazole[18] or tinidazole. The CDC recommends a one time dose of 2 grams of either metronidazole or tinidazole as the first-line treatment; the alternate treatment recommended is 500 milligrams of metronidazole, twice daily, for seven days if there is failure of the single-dose regimen.[19] Medication should be prescribed to any sexual partner(s) as well because they may be asymptomatic carriers.

Varicella zoster virus (VZV or HHV3)

Varicella-zoster virus (VZV) causes chickenpox and herpes zoster (shingles). Chickenpox follows initial exposure to the virus and is typically a relatively mild, self-limited childhood illness with a characteristic exanthem, but can become disseminated in immunocompromised children. Reactivation of the dormant virus results in the characteristic painful dermatomal rash of herpes zoster, which is often followed by pain in the distribution of the rash (postherpetic neuralgia). Signs and symptoms Pain and paresthesia are typically the first symptoms of VZV infection. Until the characteristic vesicular rash erupts, diagnosis may be difficult. A prodromal period during which symptoms may vary is common. Pain occurs in 41% of patients, itching in 27%, and paresthesias in 12%. During the acute illness, patients may experience the following: Pain (90%) Helplessness and depression (20%) Flulike symptoms (12%) Herpes zoster (shingles) The most common presentation is the shingles vesicular rash, which most commonly affects a thoracic dermatome After a prodromal illness of pain and paresthesias, erythematous macules and papules develop and progress to vesicles within 24 hours The vesicles eventually crust and resolve Pain and sensory loss are the usual symptoms Motor weakness also occurs and is frequently missed on examination Cases of actual monoplegia due to VZV brachial plexus neuritis have been reported Background Varicella-zoster virus (VZV) is the cause of chickenpox and herpes zoster (also called shingles). Chickenpox follows initial exposure to the virus and is typically a relatively mild, self-limited childhood illness with a characteristic exanthem. Approximately 1 per 4000 children develops VZV encephalitis, an acute neurologic disorder with potentially severe complications. In addition, immunocompromised children (eg, those receiving chemotherapy for leukemia or those with advanced HIV infection) can develop disseminated VZV infection, a potentially fatal complication. After primary infection, VZV remains dormant in sensory nerve roots for life. Upon reactivation, the virus migrates down the sensory nerve to the skin, causing the characteristic painful dermatomal rash. After resolution, many individuals continue to experience pain in the distribution of the rash (postherpetic neuralgia). In addition, reactivation of VZV infection can cause a spectrum of atypical presentations, ranging from self-limited radicular pain without rash to spinal cord disease with weakness.