Microbiology Exam 6

Which of the following is not considered a defense of the GI system? A. commensal microbes B. IgA C. ciliated epithelia D. GALT E. peristalsis

C. ciliated epithelia

Gastritis & Gastric Ulcers

CAUSE: -Helicobacter: ***Curved rods ***First detected by J. Robin Warren in 1979 in stomach biopsies from ulcer patients J. Robin Warren and partner Barry J. Marshal first isolated the microbe in culture: -Proved that the microbe would cause gastric ulcers by swallowing a large inoculum and subsequently developed gastritis S&S: -Gastritis: ***Sharp, burning pain emanating from the abdomen -Gastric ulcers: ***Lesions in the mucosa of the stomach or in the uppermost portion of the small intestine ***Also called peptic ulcers -Severe ulcers can be accompanied by bloody stools, vomiting, or both. -Symptoms are often worse at night, after eating, or under conditions of psychological stress. PATHOGENESIS & VIRULENCE: -Once the bacterium passes into the gastrointestinal tract: ***Bores through the outermost mucus layer that lines the stomach epithelium ***Attaches to specific binding sites on the cells and entrenches itself -Before the bacterium was discovered, spicy food, high-sugar diets, and psychological stress were considered to be the causes of gastritis: ***These factors merely aggravate the underlying infection. TRANSMISSION & EPIDEMIOLOGY: -Mode of transmission remains a mystery -Studies have revealed that the pathogen is present in a large portion of the population. -H. pylori is probably transmitted from person to person by the oral-oral or fecal-oral route. -Seems to be acquired early in life and carried asymptomatically until its activities begin to damage the digestive mucosa. -Other animals are susceptible to H. pylori and develop gastric ulcers. PREVENTION & TREATMENT: -The only preventative approaches currently are those that diminish some of the aggravating factors. -Over-the counter remedies offer symptom relief: ***Most of them neutralize stomach acid. -Best treatment is a course of antibiotics augmented by acid suppressors: ***Clarithromycin or metronidazole are the antibiotics most often prescribed.

Which organism is the primary biota of the female vagina? A.Staphylococcus B.Lactobacillus C.Pseudomonas D.Streptococcus E.Candida

B. lactobacillus

Life Cycle of Chlamydia

1. The infectious stage of Chlamydia is the elementary body (EB), which is taken into a phagocyte and ends up in its phagosome. 2. in the phagosome, each elementary body develops into a reticulate body (RB) 3. RBs multiply by binary fision 4. Mature RBs become reorganized into EBs 5. Completed EBs are released from the host cell

Group B Streptococcus "Colonization" - Neonatal Disease

10 - 40% of women in the U.S. are colonized asymptomatically by beta-hemolytic Streptococcusin the Lancefield group B. Nonpregnant women experience no ill effects from this colonization. Colonization of pregnant women can result in preterm delivery: -Half of infants become colonized with the bacterium during passage through the birth canal or by ascension of the bacteria through ruptured membranes. -Colonization is considered a reproductive tract disease. A small percentage of infants experience life-threatening bloodstream infections, meningitis, or pneumonia: -If they recover from these acute conditions, they may have permanent disabilities such as developmental disabilities, hearing loss, or impaired vision. -In some cases, the mothers also experience disease, such as amniotic infection or subsequent stillbirths. In 2002, the CDC recommended that all women be screened for group B Streptococcusat 35-37 weeks of pregnancy -Recommendations modified to recommend earlier screening now that colonization has been associated with preterm birth. -Women positive for the bacterium should be treated with penicillin or ampicillin, unless the bacterium is found to be resistant, in which case erythromycin may be used.

Other E. coli

5 categories of E. coli can cause diarrhea diseases: 1. enterotoxigenic E. coli (ETEC) 2. enteroinvasive E. coli (EIEC) 3. enteropathogenic E. coli (EPEC) 4. diffusely adherent E. coli (DAEC) 5. enteroaggregative E. coli (EAEC) In clinical practice, most physicians are interested in differentiating STEC from the others.

Salmonella

A decade ago, 1 out of 3 chickens was contaminated with salmonella: -today the rate is about 10% -other poultry such as ducks and turkeys are affected -eggs are infected because the bacteria may enter the egg when the shell is being formed In 2007, peanut butter was found to be the source of a Salmonella outbreak in the US. Salmonella is a large genus of bacteria, but only S. enteritica is of interest. Salmonella is a large genus of bacteria with a complicated nomenclature. Salmonella enterica subspecies enterica is further divided into serogroups: salmonella enterica subspecies enterica serovar Typhi. Characteristics of Salmonella: -motile -ferment glucose with acid and sometimes gas -most produce hydrogen sulfide but not urease -grow readily on most laboratory media -survive outside the host in inhospitable environments -resistant to bile and dyes S&S: -causes a variety of illnesses in the GI tract and beyond (until recently, the most severe manifestation was typhoid fever) (salmonellosis: aka enteric fever or gastroenteritis is milder and has been more common since the mid-1900s) -typhoid fever is caused by Typhi variant -gastroenteritis is caused by Typhimurium, enteritidis, heidelberg, newport, javiana -normal intestional biota in cattle, poulty, rodents, reptiles -severe forms of salmonellosis can include elevated body temperatures and septicemia -milder forms of salmonellosis: ***vomiting ***diarrhea ***mucosal irriation ***blood can appear in stool ***in healthy adults, symptoms subside within 2-5 days ***death is infrequent except in debilitated patients PATHOGENESIS & VIRULENCE: -ability of salmonella to cause disease is dependent on its ability to adhere effectively to gut mucosa -endotoxin is also an important virulence factor TRANSMISSION & EPIDEMIOLOGY: -ID50: measurement of how many organisms must be ingested to cause disease ***salmonella has a high ID50, meaning that a lot of organisms must be ingested in order for disease to result -animal products such as meat and milk can be readily contaminated with salmonella during slaughter -most cases are traceable to a common food source such as milk or eggs PREVENTION & TREATMENT: -only prevention is avoiding contact with the bacterium -uncomplicated cases of salmonellosis are treated with fluid and electrolyte replacement -if the patient is immunocompromised or if the disease is severe, trimethoprimsulfamethoxazole is recommended

Entamoeba

Amoebas are widely distributed in aqueous habitats and are frequent parasites of animals: -Only a few have the necessary virulence factors to invade tissues and cause serious pathology. Entamoeba histolytica: -One of the most significant pathogenic amoebas -Simple life cycle alternates between a large trophozoite and a smaller, nonmotile cyst. Trophozoite: -Motile by means of pseudopods -Lacks most of the organelles of other eukaryotes -Has a large single nucleus that contains a prominent nucleolus called a karyosome Cyst: -Encased in a thin yet tough wall -Contains four nuclei and four cigar-shaped chromotoidal bodies, which are dense clusters of ribosomes. S&S: Intestinal amoebiasis: -Initial targets are the cecum, appendix, colon, and rectum. -Amoeba secretes enzymes that dissolve tissues, actively penetrating deeper layers of the mucosa, and leaving ulcerations. -This phase is marked by dysentery, abdominal pain, fever, diarrhea, and weight loss. -Life-threatening manifestations include hemorrhage, perforation, appendicitis, and tumor-like growths called amoebomas. -Lesions in the mucosa have a characteristic flask-like shape. Extraintestinal infection: -Occurs when amoebas invade the viscera of the peritoneal cavity -Most common site of invasion is the liver. -Abscesses containing necrotic tissue and trophozoites develop and cause amoebic hepatitis. -Pulmonary amoebiasis is more rare. -Other infrequent targets: spleen, adrenals, kidney, and brain -Severe forms result in a 10% fatality rate. TRANSMISSION & EPIDEMIOLOGY: -Harbored by chronic carriers whose intestines favor the encystment stage of the life cycle: ***Cyst formation cannot occur in active dysentery because the feces are so rapidly flushed from the body. ***After recuperation, cysts are spread in the feces. -Infection is usually acquired by ingesting food or drink contaminated with cysts released by an asymptomatic carrier: ***The amoeba is thought to be carried by one-tenth of the world's population. ***It kills up to 100,000 people a year. -Occurrence is highest in tropical regions: ***Africa, Asia, and Latin America ***"Night soil" (human excrement) or untreated sewage is used to fertilize crops ***Sanitation of water is substandard. -Prevalence is lower in the U.S.: ***Estimated that 10 million people could harbor the agent PREVENTION: -Prevention relies on purification of water: -Regular chlorination of water supplies does not kill cysts. -More rigorous methods such as boiling or iodine are required. TREATMENT: -Iodoqunol: acts in the feces -Metronidazole or chloroquine: work in the tissues -Dehydroemetine used to control symptoms, but will not cure the disease -Drugs given to relieve diarrhea and cramps -Oral or IV therapy used to replace electrolytes and fluid

Molluscum Contagiosum

An unclassified virus in the Poxviridae family can cause molluscum contagiosum: -Can take the form of skin lesions -Can be transmitted sexually The wartlike growths that result from this infection can be found on the mucous membranes or the skin of the genital area: -Few problems are associated with these growths beyond the warts themselves -In severely immunocompromised people, the disease can be more serious. Virus can also be transmitted through fomites such as clothing or towels, and autoinoculation.

Staphylococcus aureus Exotoxin

Associated with eating foods such as custards, sauces, cream pastries, processed meats, chicken salad, or ham: -Food has been contaminated by handling and left unrefrigerated for a few hours. -Foods containing salt as a preservative are not exempt due to the high salt tolerance of S. aureus. -Toxins produced by multiplying bacteria do not noticeably alter the food's taste or smell. -Exotoxin is heat stable; inactivation requires 100°C for at least 30 minutes. -Heating the food may not prevent disease. Ingested toxin acts on the gastrointestinal epithelium: -Stimulates nerves causing symptoms of cramping, nausea, vomiting, and diarrhea Recovery is rapid, usually within 24 hours. Disease is not transmissible from person to person. A single source will contaminate several people, leading to a mini-outbreak. Condition is always self-limiting. Antibiotics are definitely not warranted.

Which of the following types of organisms are not considered normal biota of the GI system? A. bacteria B. archaea C. fungi D. protozoa E. none of the above

B. archaea

Bacillus cereus Exotoxin

Bacillus cereus: -Sporulating gram-positive bacterium naturally present in the soil -Common resident on vegetables and other products in close contact with the soil Produces two exotoxins: -One causes a diarrheal-like disease -The other causes an emetic, or vomiting disease Emetic form: -Linked to fried rice that has been cooked and kept warm for long periods of time -Conditions are ideal for the expression of the low-molecular-weight, heat-stable exotoxin. Diarrheal form: -Usually associated with cooked meats or vegetables held at a warm temperature for long periods of time -These conditions favor the production of a high-molecular weight, heat-labile exotoxin -Watery, profuse diarrhea that lasts for about 24 hours PREVENTION: -Proper handling of food

Prostatitis Table (615)

CAUSE: GI tract biota TRANSMISSION: endogenous transfer from GI tract, otherwise unknown VIRULENCE: various CULTURE/DIAGNOSIS: digital rectal exam to examine prostate; culture of urine or semen PREVENTION: none TREATMENT: abx, muscle relaxers, alpha blockers DISTINCT FEATURE: pain in genital area and/or back, difficulty urinating EPIDEMIOLOGY: US 50% of men experience during lifetime

Vaginitis & Vaginosis (page 614)

CAUSE: cadida albicans TRANSMISSION: opportunism VIRULENCE: NA CULTURE/DIAGNOSIS: wet prep or gram stain PREVENTION: NA TREATMENT: topical or oral azalea drugs, some OTC drugs DISTINCT FEATURE: white curdlike discharge EPIDEMIOLOGY: US 20% of all vaginitis; 75% of women report at least one case during lifetime CAUSE: mixed infection, usually including gardnerella TRANSMISSION: opportunism or STI VIRULENCE: NA CULTURE/DIAGNOSIS: visual exam of vagina, or clue cells seen in Pap smear or other smear PREVENTION: NA TREATMENT: metronidazole or clindamycin DISTINCT FEATURE: discharge may have fishy smell EPIDEMIOLOGY: US estimated 7.4 million/year; internationally prevalence rates vary from 20-50% CAUSE: trichomonas vaginalis TRANSMISSION: direct contact (STI) VIRULENCE: NA CULTURE/DIAGNOSIS: protozoa seen on Pap smear or gram stain PREVENTION: barrier use during intercourse TREATMENT: metronidazole, tinidazole DISTINCT FEATURE: discharge may be greenish EPIDEMIOLOGY: US 3-8 million people infected, is one of CDC's neglected parasitic infections

Chronic Diarrhea Table (page 579)

CAUSE: enteroaggregative E. coli (EAEC) TRANMISSION: vehicle (food, water), fecal-oral VIRULENCE: ? CULTURE/DIAGNOSIS: difficult to distinguish from other E. coli PREVENTION: ? TREATMENT: none or ciprofloxacin FEVER?: no BLOOD IN STOOL?: sometimes, mucus also DISTINCTIVE FEATURE: chronic in the malnourished EPIDEMIOLOGY: developing countries 87% of chronic diarrhea in children >2 years old CAUSE: cyclospora cayetanensis TRANMISSION: fecal-oral vehicle VIRULENCE: invasiveness CULTURE/DIAGNOSIS: stool examination, PCR PREVENTION: washing, cooking food, personal hygiene TREATMENT: TMP-SMZ FEVER?: usually BLOOD IN STOOL?: no DISTINCTIVE FEATURE: NA EPIDEMIOLOGY: US 16,000/year, internationally endemic in 27 countries, mostly tropical CAUSE: giardia lamblia TRANMISSION: vehicle, fecal-oral, direct and indirect contact VIRULENCE: attachment to intestines alters mucosa CULTURE/DIAGNOSIS: stool examination, ELISA PREVENTION: water hygiene, personal hygiene TREATMENT: tinidazole, nitazoxanide FEVER?: not usually BLOOD IN STOOL?: no, mucus present (greasy & malodorous) DISTINCTIVE FEATURE: frequently occurs in backpackers, campers EPIDEMIOLOGY: US 1.2 million/year, internationally prevalence rates from 2-5% in industrialized world, 40-50 million/year CAUSE: entamoeba histolytica TRANMISSION: vehicle, fecal-oral VIRULENCE: lytic enzymes, induction of apoptosis, invasive CULTURE/DIAGNOSIS: stool examination, ELISA, serologya PREVENTION: water hygiene, personal hygiene TREATMENT: metronidazole, chloroquine FEVER?: yes BLOOD IN STOOL?: yes DISTINCTIVE FEATURE: NA EPIDEMIOLOGY: internationally 40,000-100,000 deaths annually

Intestinal Distress Table (page 591)

CAUSE: enterobius vermicularis (pinworm) TRANMISSION: cycle A: vehicle (food, water), fomites, self-inoculation VIRULENCE: NA CULTURE/DIAGNOSIS: adhesive tape + microscopy PREVENTION: hygiene TREATMENT: mebendazole, piperazine DISTINCTIVE FEATURE: common in US EPIDEMIOLOGY: US prevalence in children 0.2-20%, higher in the south CAUSE: trichuris trichiura TRANMISSION: Cycle A: vehicle (soil), fecal-oral VIRULENCE: burrowing and invasiveness CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: hygiene, sanitation TREATMENT: mebendazole DISTINCTIVE FEATURE: humans sole host EPIDEMIOLOGY: US prevalence approx 0.1%; internationally prevalence high as 80% in SE Asia, Africa, Caribbean, Central America, South America CAUSE: diphyllobothrium latum (fish tapeworm) TRANMISSION: Cycle C: vehicle (seafood) VIRULENCE: vitamin B12, usage CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: cook meat TREATMENT: praziquantel DISTINCTIVE FEATURE: large tapeworm, anemia EPIDEMIOLOGY: estimated 20 million infections worldwide CAUSE: hymenolepis nana and H. diminuta TRANMISSION: Cycle C: vehicle (ingesting insects), fecal-oral VIRULENCE: NA CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: hygienic environment TREATMENT: praziquantel DISTINCTIVE FEATURE: most common tapeworm infection EPIDEMIOLOGY: US prevalence approx 0.4%; internationally single most prevalent tapeworm infection

Urinary Tract Infections Table (page 606)

CAUSE: escherichia coli TRANMISSION: opportunism- transfer from GI tract (community acquired) or environment or GI tract (via catheter) VIRULENCE: adhesins, motility CULTLURE/DIAGNOSIS: usually culture-based; antimicrobial susceptibilities always checked PREVENTION: hygiene practice, in case of CA-UTIs, limit catheter usage TREATMENT: based on susceptibility testing EPIDEMIOLOGY: causes 90% of community UTIs and 50-70% of CA-UTIs CAUSE: staphylococcus saprophyticus TRANSMISSION: opportunism- transfer from GI tract (community acquired) or environment or GI tract (via catheter) VIRULENCE: NA CULTURE/DIAGNOSIS: usually culture-based; antimicrobial susceptibilities always checked PREVENTION: hygiene practice, in case of CA-UTIs, limit catheter usage TREATMENT: based on susceptibility testing EPIDEMIOLOGY: causes small percentage of community UTIs and even lower percentage of CA-UTIs CAUSE: enterococcus TRANSMISSION: opportunism- transfer from GI tract (community acquired) or environment or GI tract (via catheter) VIRULENCE: NA CULTURE/DIAGNOSIS: usually culture-based; antimicrobial susceptibilities always checked PREVENTION: hygiene practice, in case of CA-UTIs, limit catheter usage TREATMENT: based on susceptibility testing; vancomycin-resistant enterococcus is in Serious Threat category of CDC EPIDEMIOLOGY: frequent cause of CA-UTIs

Group B Streptococcus Colonization Table (624)

CAUSE: group b streptococcus TRANSMISSION: vertical VIRULENCE: NA CULTURE/DIAGNOSIS: culture of mother's genital tract PREVENTION: treat mother with penicillin/ampicillin; watch for clindamycin resistant strains as they are in Concerning Threat of CDC Abx Resistant Report TREATMENT: same as prevention EPIDEMIOLOGY: US vaginal carriage rates 15-45%; neonatal sepsis due to this occurs in 1.8-3.2 per 1,000 live births; internationally vaginal carriage rates 12-27%

Gastritis & Gastric Ulcers Table (page 584)

CAUSE: helicobacter pylori TRANMISSION: NA VIRULENCE: adhesins, urease CULTURE/DIAGNOSIS: endoscopy, urea breath test, stool antigen test PREVENTION: none TREATMENT: amoxicillin followed by clarithromycin + tinidazole EPIDEMIOLOGY: US infection (not disease) rates at 35% of adults; internationally 50%

Hepatitis Table (587)

CAUSE: hepatitis A or E virus TRANMISSION: fecal-oral, vehicle VIRULENCE: NA CULTURE/DIAGNOSIS: IgM serology PREVENTION: hepatitis A vaccine or combined: HAV/HBV vaccine TREATMENT: HAV: hepatitis A vaccine or immune globulin; HEV: immune globulin INCUBATION PERIOD: 2-7 weeks EPIDEMIOLOGY: Hep A US: 20,000/year and 40% of adults show evidence of prior infection; internationally 1.4 million/year, Hep E internationally 20 million/year, 60% in East and SE Asia CAUSE: Hep B virus TRANMISSION: parenteral (blood contact), direct contact (especially sexual), vertical VIRULENCE: latency CULTURE/DIAGNOSIS: serology (ELISA, radioimmunoassay) PREVENTION: HBV recombinant vaccine TREATMENT: interferon, tenofovir, or entecavir INCUBATION PERIOD: 1-6 months EPIDEMIOLOGY: US prevalence rate 1.5/100,000 to 1.4 million have chronic infection; internationally 240 million CAUSE: Hep C virus TRANMISSION: parenteral (blood contact), vertical VIRULENCE: core protein suppresses immune function CULTURE/DIAGNOSIS: serology PREVENTION: NA TREATMENT: pegylated interferon, with or without ribavirin INCUBATION PERIOD: 2-8 weeks EPIDEMIOLOGY: US 17,000 new cases per year, 2.7 million with chronic HCV; internationally 150 million chronically infected

Leptospirosis Table (page 607)

CAUSE: leptospira interrogans TRANSMISSION: vehicle (contaminated soil or water) VIRULENCE: adhesins, invasion proteins CULTURE/DIAGNOSIS: slide agglutination test of patient's blood for antibodies PREVENTION: avoid contaminated vehicles TREATMENT: doxycycline, penicillin G, ceftriaxone EPIDEMIOLOGY: US 100-200/year, half in Hawaii; internationally 80% of people in tropical areas are seropositive

Mumps (page 582)

CAUSE: mumps virus (genus paramyxovirus) TRANMISSION: droplet contact VIRULENCE: spike-induced syncytium formation CULTURE/DIAGNOSIS: clinical, fluorescent Ag tests, ELISA for Ab PREVENTION: MMR live attenuated vaccine TREATMENT: supportive EPIDEMIOLOGY: US fluctuates between a few hundred/year and a few thousand; internationally are epidemic peaks every 2-5 years

Periodontitis Table (page 581)

CAUSE: polymicrobial community including some or all of: tannerella forsythia, aggregatibacter actinomycetemcomitans, porphyromonas gingivalis, others TRANMISSION: NA VIRULENCE: induction of inflammation, enzymatic destruction of tissues CULTURE/DIAGNOSIS: NA PREVENTION: oral hygiene TREATMENT: removal of plaque and calculus, gum reconstruction, possibly anti-inflammatory treatments EPIDEMIOLOGY: US: smokers 11%, nonsmokers 2%; internationally 10-15% of adults

Acute Diarrhea Table (page 572)

CAUSE: salmonella (bacteria) TRANMISSION: vehicle (food, beverage), fecal oral VIRULENCE: adhesins, endotoxin CULTURE/DIAGNOSIS: stool culture, not usually necessary PREVENTION: food hygiene and personal hygiene TREATMENT: rehydration, no antibiotic for uncomplicated disease FEVER?: usually BLOOD IN STOOL?: sometimes DISTINCTIVE FEATURE: often associated with chickens, reptiles EPIDEMIOLOGY: US 20% of all cases require hospitalizations; death rate of 0.6% CAUSE: shigella (bacteria) TRANMISSION: fecal-oral, direct contact VIRULENCE: endotoxin, enterotoxin, shiga toxins in some strains CULTURE/DIAGNOSIS: stool culture, antigen testing for shiga toxin PREVENTION: food hygiene, personal hygiene TREATMENT: ciprofloxacin in severe cases, retardation, in serious threat - CDC antibiotic resistance report FEVER?: often BLOOD IN STOOL?: often DISTINCTIVE FEATURE: very low ID50 EPIDEMIOLOGY: US esteemed 450,000 cases per year; internationally 165 million CAUSE: shiga-toxin producing E. coli (STEC) (bacteria) TRANMISSION: vehicle (food, beverage), fecal-oral VIRULENCE: shiga toxins, proteins for attachment, secretion, effacement CULTURE/DIAGNOSIS: stool culture, antigen testing for shiga toxin PREVENTION: avoid live E. coli (cook meat and clean vegetables) TREATMENT: abx contraindicated, supportive measures FEVER?: often BLOOD IN STOOL?: usually DISTINCTIVE FEATURE: hemolytic uremic syndrome EPIDEMIOLOGY: internationally causes HUS in 10% of patients; 25% of HUS patients suffer neurological complications; 50% have chronic renal sequelae CAUSE: other E. coli (non shiga-toxin producing) (bacteria) TRANMISSION: vehicle, fecal-oral VIRULENCE: various: proteins for attachment, secretion, effacement, heat-labile and/or heat-stable exotoxins, invasive CULTURE/DIAGNOSIS: stool culture not usually necessary in absence of blood, fever PREVENTION: food and personal hygiene TREATMENT: rehydration, antimotility agent FEVER?: sometimes BLOOD IN STOOL?: sometimes DISTINCTIVE FEATURE: EIEC, ETEC, EPEC CAUSE: campylobacter (bacteria) TRANMISSION: vehicle (food, water), fecal-oral VIRULENCE: adhesins, exotoxin, induction of autoimmunity CULTURE/DIAGNOSIS: stool culture, not usually necessary, dark-field microscopy PREVENTION: food and personal hygiene TREATMENT: rehydration, azithromycin in severe cases (abx resistance rising), in serious threat - CDC abx resistance report FEVER?: usually BLOOD IN STOOL?: no DISTINCTIVE FEATURE: Guillain-barre syndrome EPIDEMIOLOGY: US: 2.4 million cases per year, internationally: 400 million CAUSE: yersinia (bacteria) TRANMISSION: vehicle (food, water), fecal-oral, indirect contact VIRULENCE: intracellular growth CULTURE/DIAGNOSIS: cold enrichment stool culture PREVENTION: food and personal hygiene TREATMENT: none in most cases, doxycycline, gentamicin, or TMP-SMZ for bacteremia FEVER?: usually BLOOD IN STOOL?: occasionally DISTINCTIVE FEATURE: severe abdominal pain EPIDEMIOLOGY: uncommon, more likely in children than adults and in winter than in other seasons CAUSE: clostridium difficile (bacteria) TRANMISSION: endogenous (normal biota) VIRULENCE: enterotoxins A & B CULTURE/DIAGNOSIS: stool culture, PCR, ELISA demonstration of toxins in stool PREVENTION: NA TREATMENT: withdrawal of abx, in severe cases metronidazole or fidaxomicin (dificid) FEVER?: sometimes BLOOD IN STOOL?: not usually, mucus prominent DISTINCTIVE FEATURE: abc-associated diarrhea EPIDEMIOLOGY: US 3 million cases per year CAUSE: vibrio cholerae (bacteria) TRANMISSION: vehicle (water and some foods), fecal-oral VIRULENCE: cholera toxin (CT) CULTURE/DIAGNOSIS: clinical diagnosis, microscopic techniques, serological detection of antitoxin PREVENTION: water hygiene TREATMENT: rehydration, in severe cases doxycycline FEVER?: no BLOOD IN STOOL?: no DISTINCTIVE FEATURE: rice-water stools EPIDEMIOLOGY: global estimate: 100,000-130,000 deaths annually CAUSE: cryptosporidium (nonbacterial) TRANMISSION: vehicle (water, food), fecal-oral VIRULENCE: intracellular growth CULTURE/DIAGNOSIS: fluorescence microscopy PREVENTION: water treatment, proper food handling TREATMENT: none, nitazoxanide used sometimes FEVER?: often BLOOD IN STOOL?: not usually DISTINCTIVE FEATURE: resistant to chlorine disinfection EPIDEMIOLOGY: US 748,000 cases per year, 30% seropositive CAUSE: rotavirus TRANMISSION: fecal-oral, vehicle, fomites VIRULENCE: NA CULTURE/DIAGNOSIS: usually not performed PREVENTION: oral live virus vaccine TREATMENT: rehydration FEVER?: often BLOOD IN STOOL?: no DISTINCTIVE FEATURE: severe in babies EPIDEMIOLOGY: US 2-3 million cases per year; internationally 125 million cases of infantile diarrhea annually CAUSE: norovirus TRANMISSION: fecal-oral, vehicle, VIRULENCE: NA CULTURE/DIAGNOSIS: rapid antigen test PREVENTION: hygiene TREATMENT: rehydration FEVER?: sometimes BLOOD IN STOOL?: no DISTINCTIVE FEATURE: NA EPIDEMIOLOGY: US most common cause of diarrhea in <18 year olds

Schistosomiasis Table (page 593)

CAUSE: schistosoma mansoni, S. japonicum TRANMISSION: cycle D: vehicle (contaminated water) VIRULENCE: antigenic "cloaking" CULTURE/DIAGNOSIS: identification of eggs in feces, scarring of intestines detected by endoscopy PREVENTION: avoid contaminated vehicles TREATMENT: praziquantel DISTINCTIVE FEATURE: penetrates skin, lodges in blood vessels of intestine, damages liver EPIDEMIOLOGY: internationally 230 million new infections/year by these and the urinary schistosome

Food Poisoning Table (page 575)

CAUSE: staphylococcus aureus exotoxin TRANMISSION: vehicle (food) VIRULENCE: heat-stable exotoxin CULTURE/DIAGNOSIS: usually based on epidemiological evidence PREVENTION: proper food handling TREATMENT: supportive FEVER?: not usually BLOOD IN STOOL?: no DISTINCTIVE FEATURE: suspect in foods with high salt or sugar content EPIDEMIOLOGY: US estimated 240,000 cases per year CAUSE: bacillus cereus TRANMISSION: vehicle (food) VIRULENCE: heat-stable toxin, heat-labile toxin CULTURE/DIAGNOSIS: microscopic analysis of food or stool PREVENTION: proper food handling TREATMENT: supportive FEVER?: not usually BLOOD IN STOOL?: no DISTINCTIVE FEATURE: 2 forms: emetic & diarrheal EPIDEMIOLOGY: US 63,000/year CAUSE: clostridium perfringens TRANMISSION: vehicle (food) VIRULENCE: heat-labile toxin CULTURE/DIAGNOSIS: detection of toxin in stool PREVENTION: proper food handling TREATMENT: supportive FEVER?: not usually BLOOD IN STOOL?: no DISTINCTIVE FEATURE: acute abdominal pain EPIDEMIOLOGY: US 966,000/year

Cysticercosis Table (page 592)

CAUSE: taenia solium (pork tapeworm) TRANMISSION: Cycle C: vehicle (pork), fecal-oral VIRULENCE: NA CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: cook meat, avoid pig feces TREATMENT: praziquantel DISTINCTIVE FEATURE: ingesting larvae embedded in pork leads to intestinal tapeworms; ingesting eggs (fecal-oral route) causes cysticercosis, larval cysts embedded in tissue of new host EPIDEMIOLOGY: US considered neglected parasitic infection, common cause of seizures; internationally very common in Latin America and Asia

Intestinal Distress Plus Migratory Symptoms Table (page 592)

CAUSE: toxocara species TRANMISSION: Cycle A: dog or cat feces VIRULENCE: NA CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: hygiene TREATMENT: albendazole DISTINCTIVE FEATURE: can cause migration symptoms or blindness EPIDEMIOLOGY: nearly 100% of newborn puppies in US infected; 14% of people in US have been infected CAUSE: ascaris lumbricoides (intestinal roundworm) TRANMISSION: Cycle A: vehicle (soil, fecal-oral), fomites, self-inoculation VIRULENCE: induction of hypersensitivity, adult worm migration, abdominal obstruction CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: hygiene TREATMENT: albendazole DISTINCTIVE FEATURE: most cases mild, unnoticed EPIDEMIOLOGY: internationally up to 25% prevalence, 80,000-100,000 deaths per year CAUSE: necator americanus and ancylostoma duodenale (hookworms) TRANMISSION: Cycle B: vehicle (soil), fomite VIRULENCE: induction of hypersensitivity, adult worm migration, abdominal obstruction CULTURE/DIAGNOSIS: blood count, serology, egg or worm detection PREVENTION: sanitation TREATMENT: albendazole DISTINCTIVE FEATURE: penetrates skin, serious intestinal symptoms EPIDEMIOLOGY: US widespread in SE until early 1900s; internationally 800 million infected

Shigella

CHARACTERISTICS: - gram-negative rods -non-motile -non spore forming -does not produce urease or hydrogen sulfide -primarily human parasites, but can infect apes -all produce similar disease that varies in intensity -all resemble some types of pathogenic e. coli S&S: -frequent, watery stools -fever -intense abdominal pain -nausea, vomiting are common -dysentery: diarrhea containing blood (in Shigella: stools often contain obvious blood and even more often found to have occult blood) -mucus from GI tract is also present in stools PATHOGENESIS & VIRULENCE: -shigella invades the villus cells of the large intestine rather than the small intestine -does not perforate the intestine or invade the blood -enters the intestinal mucosa by means of special cells in Peyer's patches (once in the mucosa, Shigella initiates an inflammatory response that causes extensive tissue destruction) -Enterotoxin: toxin that affects GI tract, damages mucosa and villi, and causes fever -Shiga Toxin: seems to be resonsible for more serious damage to the intestine and systemic effects TRANSMISSION & EPIDEMIOLOGY: -oral route -direct person-to-person contact (small infectious dose: 10-200 bacteria) -disease mostly associated with lax sanitation, malnutrition, and crowding -spread epidemically in day care centers, prisons, mental institutions, nursing homes, military camps -shigella can establish a chronic carrier condition in some people that can last several months PREVENTION & TREATMENT: -only prevention is good hygiene and avoiding contact with infected persons -some experts in the US say that bloody diarrhea should not be treated with antibiotics, which is generally accepted for E. coli 0157:H7 infections ***some physicians recommend prompt treatment of shigellosis with trimethoprim-sulfamethoxazole

Candida albicans

CHARACTERISTICS: -Dimorphic fungus -Normal biota in 50-100% of humans -Live in low numbers on mucosal surfaces of the mouth, gastrointestinal tract, vagina, etc. VULVOVAGINAL CANDIDIASIS: -Yeast is easily detectable in a wet prep or a Gram stain of material obtained during a pelvic exam.-Presence of pseudohyphae in the smear is a clear indication of the yeast growing rapidly and causing infection. In otherwise healthy people, the fungus is not invasive and limits itself to a surface infection. Candida infections of the bloodstream do occur and have high mortality rates: -Do not normally stem from vaginal infections -Seen most frequently in hospitalized patients -AIDS patients are at risk of developing systemic Candida infections. TRANSMISSION: -Vaginal infections are nearly always opportunistic: ***Disruptions in normal biota or even minor changes in the mucosal epithelium in the vagina can lead to overgrowth of the fungus. ***Mechanical disruptions: trauma to the vagina ***Chemical disruptions: broad-spectrum antibiotics diminish vaginal bacterial population ***Diabetics and pregnant women are also predisposed to vaginal yeast overgrowths. ***Some women are prone to infections during menstruation. -Possible to transmit yeast through sexual contact, especially if a woman is experiencing an overgrowth: ***Recipient's immune system may subdue the yeast so that it acts as normal biota to them. But the yeast may be passed back to the original partner during further sexual contact after treatment. -Women with HIV experience frequently recurring infections. -A small percentage of women with no underlying immune disease may experience chronic or recurrent vaginal infections with Candida. PREVENTION & TREATMENT: -No vaccine is available for Candida. -Topical and oral azole drugs are used to treat vaginal candidiasis, many of them available over the counter. -If infections recur frequently or fail to resolve, it is important to see a physician for evaluation

Human Papillomavirus Infection

Causative agents of genital warts -An individual can be infected with these viruses without having any warts, while still risking serious consequences. S&S: -Warts: ***Outgrowths of tissue on the genitals ***In females: occur on the vulva and in and around the vagina ***In males: can occur in or on the penis and the scrotum ***In both sexes, warts can appear on the anus and the skin around the groin. -Appearance of warts: ***Tiny, flat, inconspicuous bumps ***Condyloma acuminata: extensively branching, cauliflower-like masses ***Can be unsightly and obstructive, but don't generally lead to more serious symptoms -Certain types of viruses can infect the cervix: ***This infection may be "silent" or lead to abnormal cell changes in the cervix. Some of these cell changes can lead to malignancies of the cervix. -The vast majority of cervical cancers are caused by HPV: ***Approximately 4,000 women die each year in the U.S. from cervical cancer. -Males can also get cancer from infection from these viruses: ***The penis and the anus are the sites most often affected. ***Much less common than cervical cancer -Mouth and throat cancers have been more recently associated with HPV infection and are thought to be a consequence of oral sex. CAUSE: -Human papillomaviruses: ***Nonenveloped DNA viruses belonging to the Papovaviridae family ***Over 100 different types of HPV ***Some types are specific for mucous membranes. ***Others invade the skin. ***Plantar warts: occur on the soles of the feet ***Common or "seed warts" and flat warts are also caused by HPV. -HPVs that infect the genital tract: ***Some are more likely to cause the appearance of warts. ***Others have a preference for growing on the cervix and can lead to cancerous changes. ***Five types are associated with cervical cancer: HPV-16, -18, -31, -33, and -35. ***Other types put you at higher risk for vulvar or penile cancer. PATHOGENESIS & VIRULENCE: -Scientists are working hard to determine how viruses cause warts and how some cause cancer. -Major virulence factor is their ability to activate oncogenes, which code for proteins that interfere with normal cell function, resulting in uncontrolled growth. TRANSMISSION & EPIDEMIOLOGY: -Young women have the highest rate of HPV infections: ***25 - 46% of women under the age of 25 are infected with genital HPV ***Estimated that 14% of female college students become infected each year ***15% of people between 15 and 49 are HPV-positive ***It is difficult to determine if genital herpes or HPV is more common, but it is probably safe to assume that any unprotected sex carries a good chance of encountering HSV or HPV. -Mode of transmission is direct contact: ***Autoinoculation is also possible. ***Virus can be spread to other parts of the body by touching warts. ***Indirect transmission occurs, but it is more common for nongenital warts caused by HPV. CULTURE & DIAGNOSIS: -PCR-based screening tests can be used to test samples from a pelvic exam for the presence of dangerous HPV types: ***These tests are now recommended for women over the age of 30. PREVENTION: -Prevention of infection with the viruses: ***Prevented the same way all other sexually transmitted diseases are prevented; avoiding direct, unprotected contact. -Gardasil vaccine approved in 2006: ***Prevents infection by four types of HPV ***Recommended for girls as young as age 9 ***Being vaccinated does not encourage girls to become sexually active. ***Instead, causes them to realize the dangers of sex, according to a study conducted in 2009 among 553 teenage girls in Britain. PREVENTION: -Prevention of cervical cancer: ***Even with the vaccine, cancer can still result from HPV types not included in the vaccine. ***Cervical cancer is slow in developing. ***Regular screening of the cervix can detect abnormal changes early. -Pap smear: ***Standardized screen for cervical cell changes ***Precancerous changes show up very early. ***Development process can be stopped by removal of the affected tissue. -Women should have their first Pap smear by age 21 or within 3 years of their first sexual activity, whichever comes first: ***New Pap smear technologies have been developed. ***Depending on which one is used, it is now possible that screening be performed every 2-3 years. ***Base screening practices on the sound advice of your physician. TREATMENT: -Infection with HPV is incurable. -Genital warts can be removed through a variety of methods, some of which can be used at home: ***Virus causing the warts will remain with you. ***Possible for the virus to resolve itself, but this is very unpredictable.

Vibrio cholerae

Cholera has been a devastating disease for centuries: -Has shaped a good deal of human history in Asia and Latin America where it has been endemic Outbreaks of cholera occur: -After natural disasters -War -Large refugee movements, especially in underdeveloped parts of the world CAUSE: -Vibrios are rods with a single polar flagellum. -Belong to the family Vibrionaceae -Freshly isolated specimens of Vibrio choleraereveal quick, darting cells that slightly resemble a comma. -Vibrio shares many cultural and physiological characteristics with members of the Enterobacteriaceae family: ***Fermentive and grow on ordinary or selective media containing bile at 37°C. ***Possess unique O and H antigens ***Two major biotypes: classic and El Tor S&S: -Incubation period of a few hours to a few days -Abrupt symptoms of vomiting followed by copious, watery feces called secretory diarrhea: ***Contains flecks of mucus and is described as "rice water stool" -Fluid losses of 1 liter per hour have been reported: ***In severe cases, an untreated patient can lose up to 50% of body weight in the course of the disease. -Secondary circulatory consequences: ***Hypotension ***Tachycardia ***Cyanosis ***Collapse from shock within 18 - 24 hours -If cholera is left untreated, death can occur in less than 48 hours. Untreated, the mortality rate is between 55 - 70%. PATHOGENESIS & VIRULENCE: -High infectious dose: 10^8cells -Vibrios penetrate the mucus barrier at the junction of the duodenum and jejunum using their flagella: ***Adhere to microvilli of epithelia and multiply ***Never enter host cells or invade mucosa -Virulence of V. cholerae due entirely to the cholera toxin (CT): ***Disrupts the normal physiology of intestinal cells ***Cells shed large amounts of electrolytes into the intestine, accompanied by profuse water loss. TRANSMISSION & EPIDEMIOLOGY: -Pattern of cholera transmission and the onset of epidemics are greatly influenced by the season of the year and the climate: ***Cold, acidic, dry climates inhibit the migration and survival of Vibrio. ***Warm, monsoon, alkaline, and saline climates favor the migration of Vibrio. -Bacteria survive in water sources for long periods of time: ***Outbreaks have been traced to giant cargo ships that pick up ballast water in one port and empty it elsewhere in the world. -Cholera ranks among the top seven causes of morbidity and mortality: ***Affects several million people in endemic regions in Asia and Africa -In nonendemic areas such as the U.S., the microbe is spread by water and food contaminated by asymptomatic carriers: ***Relatively uncommon PREVENTION & TREATMENT: -Effective prevention is contingent on proper sewage treatment and water purification. -Vaccines are available for travelers and people living in endemic regions: ***One vaccine contains killed Vibrio and only protects for 6 months or less. ***An oral vaccine containing live, attenuated bacteria was developed, but only confers short-term immunity. ***Not routinely used in the U.S. -Key to cholera therapy is prompt replacement of water and electrolytes: ***Loss accounts for severe morbidity and mortality ***Until the 1970s, rehydration was accomplished through an IV drip, which required travel to a hospital or clinic. ***Most children received no treatment and 3 million died every year. ***Then scientists tested a simple sugar-salt solution that patients could drink -Oral rehydration therapy (ORT): ***Incredibly simple and astonishingly effective ***Developed by the WHO ***Consists of a mixture of sodium chloride, sodium bicarbonate, potassium chloride, and glucose dissolved in water ***When administered early at 100 - 400 ml/hour, the solution can restore patients in 4 hours. ***Infants and children, who once would have died, now survive so often that the mortality rate for treated cases of cholera is near zero. -Advantages of ORT: ***Does not require medical facilities, high-technology equipment, or complex medication protocols ***Eliminates the need for clean needles -Oral antibiotics such as trimethoprim-sulfamethoxazole can terminate the diarrhea in 48 hours: ***Diminish the period of vibrio excretion

Campylobacter

Considered to be most common bacterial cause of diarrhea in US (2.4 million cases credited to it per year) S&S: -frequent, watery stools -fever -vomiting -headaches -severe abdominal pain -symptoms may last longer than 2 weeks (symptoms may subside and then recur over a period of weeks) CAUSE: -campylobacter jejuni (other campylobacter species exist) -characteristics: ***slender, curved, or spiral gram-negative bacteria ***propelled by polar flagella at one or both poles ***often appears in S-shaped or gull-winged pairs ***microaerophilic inhabitants of the intestinal tract, genitourinary tract and oral cavity PATHOGENESIS & VIRULENCE: -transmission via ingestion of contaminated beverages and food (water, milk, meat and chicken) -once ingested, C. jejuni cells reach the mucosa at the last segment of the intestine near its junction with the colon (adhere, burrow through the mucus, and multiply; symptoms commence after an incubation period of 1-7 days) -heat-labile enterotoxin stimulates secretory diarrhea similar to cholera -guillain-barre syndrome (GBS): ***leading cause of acute paralysis since the eradication of polio ***seems to be an autoimmune reaction brought on by infection with viruses and bacteria, vaccination and surgery ***campylobacter infection is the single most common precipitating event ***20-40% of GBS cases are preceded by an infection with campylobacter ***reasons for this are not clear -Resolution of infection: ***Simple, nonspecific rehydration and electrolyte balance therapy ***in severely affected patients, erythromycin treatment may be necessary. ***Antibiotic resistance is increasing in these bacteria. ***No vaccine exists. ***Prevention depends on rigid sanitary control of water and milk supplies and care in food preparation.

Cyclospora

Cyclospora cayetanensis is an emerging protozoan pathogen: -First occurrence in 1979 -Hundreds of outbreaks have been reported in the U.S. and Canada. Fecal-oral transmission: -Most cases associated with consumption of fresh produce and water contaminated with feces Disease occurs worldwide and is not spread from person to person. Outbreaks traced to imported raspberries, salad made with fresh greens, and drinking water.

Chronic Diarrhea

Diarrhea lasting longer than 14 days: -Can have infectious causes or can reflect noninfectious conditions Irritable bowel syndrome and ulcerative colitis: -Neither caused by a microorganism -Increasing evidence that a chronically disrupted intestinal biota can contribute to these conditions People suffering from AIDS suffer from chronic diarrhea: -Cryptosporidium -Mycobacterium avium -HIV status should be considered if a patient presents with chronic diarrhea.

Acute Diarrhea

Diarrhea: -3 or more loose stools in 24 hour period -on average: US citizens experience 1.2-1.9 cases of diarrhea per person per year -children experience double the rate of adults -in tropical countries, children may experience more than 10 episodes of diarrhea per year -more than 3 million children a year die from a diarrheal disease -often accompanied by fever, abdominal pain, cramping, nausea, vomiting, dehyrdation -in US, acute diarrhea is transmitted by contaminated food -it is necessary for consumer to be aware and to practice good food handling -most diarrhea episodes are self-limiting and do not require treatment -others, such as E. coli 0157:H7 have devastating effects -in most diarrheal illnesses, antimicrobial treatment is contraindicated, but with some, such as shigellosis, quick treatment with antibiotics is necessary -for public health reasons, it is important to know which agents are causing the diarrhea; but in most cases, identification of the agent is not performed Some species of bacteria are subdivided into serotypes or subtypes. Gram-negative enteric bacteria are named and designated according to the following antigens: -H: flagellar antigen -K: capsular antigen -O: cell wall antigen Many species of gram-negative enterics exhibit a variety of subspecies, variants or serotypes, based on slight variations in the chemical structure of HKO antigens.

Tooth & Gum Infections

Difficult to pinpoint when the "normal biota biofilm" described for the oral environment becomes a "pathogenic biofilm": -If left undisturbed, the biofilm structure eventually contains anaerobic bacteria that can damage the periodontium. -Also, the introduction of carbohydrates to the oral cavity can result in the breakdown of dentition due to the production of acid.

Discharge Diseases with Major Manifestation in the GU Tract:

Discharge diseases: -Infectious agent causes an increase in fluid discharge in the male and female reproductive tract. -Causative agents are transferred to new hosts when the fluids in which they live contact the mucosal surfaces of the receiving partner. Trichomoniasis Gonorrhea Chlamydia

Intestinal Distress Accompanied by Migratory Symptoms:

Diverse group of helminths: -Enter the body as larvae or eggs -Mature to the worm stage in the intestine -Migrate to the circulatory or lymphatic system -Travel to the heart and lungs -Migrate up to the respiratory tree and are swallowed -Mature worms return to the intestinal tract where they take up residence. All conditions produce: -Symptoms in the digestive tract -Inflammatory reactions along their migratory routes -Eosinophilia -Pneumonia during their lung stage Cysticercosis: -Taenia solium is a tapeworm: ***Adult worms are usually around 5 meters long. ***Have a scolex with hooklets and suckers to attach to the intestine. -Transmission is through cycle C: ***Humans are infected by eating animal flesh that contains worm eggs or even the worms themselves. -The pig tapeworm is distributed worldwide: ***Concentrated in areas where humans live in close proximity with pigs or eat undercooked pork -In pigs, the eggs hatch in the small intestine: ***Released larvae migrate throughout the organs. ***Encyst in the muscles ***Cysticeri: young tapeworms that are the infective stage for humans -When humans ingest live cysticerus in pork, the coat is digested and the organism is flushed into the intestine: ***Attaches firmly by the scolex and develops into an adult tapeworm. -When humans ingest the tapeworm eggs, another form of T. solium infection occurs. -One of the five neglected parasitic infections (NPIs) in the U.S. -Estimated that tens of thousands of Latinos living in the US are affected: ***Not recognized, because U.S. physicians may not know to look for it Neurocysticercosis: ***Larvae encyst in the brain. ***Estimated that it is responsible for 10% of seizures in the ER in some US cities.

Shiga-Toxin-Producing E. coli

Dozens of different strains of E. coli exist, most of which cause no disease at all. E. coli 0157:H7 and its close relatives are the most virulent of them all: -generally referred to as shiga-toxin-producing E. coli (STEC) S&S: -mild gastroenteritis -fever -bloody diarrhea -10% of patients develop hemolytic uremic syndrome (HUS) ***severe hemolytic anemia that can cause kidney damage and failure -neurological symptoms such as blindness, seizure, stroke -in 2011, a new HUS-causing E. coli strain caused a large and deadly outbreak in Germany (E. coli 0104:H4 which was identified as an STEC strain) -a total of six additional STEC strains have been identified (USDA started testing ground beef for all these strains in 2012) PATHOGENESIS & VIRULENCE: -much of its virulence due to shiga toxins: ***identical to shiga toxin secreted by virulent Shigella species ***shiga toxin genes present on prophage genes donated by bacteriophage in E. coli ***also present on the chromosome of Shigella, suggesting E. coli acquired the gene through phage-mediated transfer ***interrupts protein synthesis on target cells and responsible especially for systemic effects of the infection -ability to efface enterocytes in the large intestine, resulting in bloody diarrhea TRANSMISSION & EPIDEMIOLOGY: -most common mode of transmission for EHEC is ingestion of contaminated or undercooked beef -products eaten raw such as lettuce, vegetables, apples used in unpasteurized cider are particularly problematic -can also be spread by the fecal-oral route, especially among young children in group situations (even touching surfaces contaminated with cattle feces can trasmit the disease) (as few as 10 cells can initiate disease) CULTURE & DIAGNOSIS: -infection with this type of E. coli should be confirmed with stool culture or with ELISA or PCR PREVENTION & TREATMENT: -best prevention: never eat raw or rare hamburger and to wash raw vegetables well: (shiga toxin is heat-labile and E. coli is killed by heat) -antibiotics are contraindicated for this infection as they increase pathology -supportive therapy, including plasma transfusions to dilute the toxin in blood, is the only option

Which organism is not a common cause of UTIs? A. escherichia coli B. staphylococcus saprophytic C. pseudomonas aeruginosa D. proteus mirabilis E. all of the choices cause UTIs

E. all of the choices cause UTIs?

Enteroaggregative E. coli

EAEC is particularly associated with chronic disease, especially in children. First recognized in 1987: -Difficult to diagnose in the clinical lab Secretes neither heat-stable nor heat-labile exotoxins Distinguished by its ability to adhere to human cells in aggregates rather than as single cells Stimulates secretion of large amounts of mucus in the gut: -May be part of its role in causing chronic diarrhea

GI Tract and Its Defenses

GI tract can be thought of as a long tube, extending from mouth to anus. AKA digestive tract or enteric tract 8 Main Organs: 1. mouth 2. pharynx 3. esophagus 4. stomach 5. small intestine 6. large intestine 7. rectum 8. anus 4 Accessory Organs: 1. salivary glands 2. liver 3. gallbladder 4. pancreas 5. add digestive fluids and enzymes to assist in digesting and processing the food we take in GI tract has heavy load of microorganisms and it encounters millions of new ones every day. Defenses: -all intestinal surfaces are coated with layer of mucus -secretory IgA can be found on most surfaces -muscular walls of GI tract keep food and microorganisms moving through the action of peristalsis -saliva contains lysozyme and lactoferrin -stomach fluid is antimicrobial due to its high acidity -bile is also antimicrobial Gut-Associated Lymphoid Tissue (GALT): -tonsils and adenoids in the oral cavity and pharynx -small areas of lymphoid tissue in the esophagus -Peyer's patches in the small intestine -appendix -all packets of lymphoid tissue consisting of T and B cells as well as cells of nonspecific immunity -produce IgA, but perform a variety of other functions Commensal Organisms: -provide the protection of microbial antagonism -avoid immune destruction by cloaking themselves with host sugars found in the intestinal walls

Genital Discharge Diseases (page 612)

GONORRHEA CAUSE: neisseria gonorrhoeae TRANSMISSION: direct contant (STI), also vertical VIRULENCE: fibril adhesins, antigenic variation, IgA protease, membrane blebs/endotoxin CULTURE/DIAGNOSIS: gram stain in males, rapid tests (PCR, ELISA) for females, culture on Thayer-Martin agar PREVENTION: avoid contact, condoms TREATMENT: coinfection with gonorrhea and c. trachomatis should be assumed; treat with doxycycline or azithromycin. Be on alert for multi drug resistant n. gonorrheae, which is in Urgent Threat category of CDC Abx Resistant Report DISTINCT FEATURE: rare complications including arthritis, meningitis, endocarditis EFFECT ON FETUS: eye infections, blindness EPIDEMIOLOGY: US rates decreased 16% between 2006-2010; internationally 26 million CHLAMYDIA CAUSE: chlamydia trachomatis TRANSMISSION: direct contact (STI), vertical VIRULENCE: intracellular growth resulting in avoiding immune system and cytokine release, unusual cell wall preventing phagolysosome fusion CULTURE/DIAGNOSIS: PCR or ELISA, can be follow by cell culture PREVENTION: avoid contact, condom TREATMENT: coinfection with gonorrhea and c. trachomatis should be assumed; treat with doxycycline or azithromycin. Be on alert for multi drug resistant n. gonorrheae, which is in Urgent Threat category of CDC Abx Resistant Report DISTINCT FEATURE: more commonly asymptomatic than gonorrhea EFFECT ON FETUS: eye infections, PNA EPIDEMIOLOGY: US 2.8 million new infections/year; internationally eye infection (trachoma) has 90% prevalence rate in developing world

Giardia

Giardia lamblia: -Pathogenic flagellated protozoan first discovered by Antonie van Leeuwenhoek in his own feces -Considered a harmless or weak intestinal pathogen for 200 years -Only has been recognized as a cause of diarrhea since the 1950s -Most common flagellate isolated in clinical specimens Appearance of Giardia lamblia: -Unique symmetrical heart shape -Organelles positioned in such a way that it resembles a face -Four pairs of flagella emerge from a ventral surface -Ventral surface is concave and acts like a suction cup -Giardia cysts are small, compact, and contain four nuclei S&S: -Diarrhea of long duration -Abdominal pain -Flatulence -Stools have a greasy, malodorous quality to them -Fever is usually not present TRANSMISSION & EPIDEMIOLOGY: -Protozoan has been isolated from the intestines of beavers, cattle, coyotes, cats, and human carriers -Both trophozoites and cysts escape in the stool, but cysts play a greater role in transmission: ***Giardia cysts can survive for 2 months in the environment. ***Cysts are usually ingested with food or swallowed after close contact with infected people or contaminated objects. ***Infectious dose is 10 - 100 cysts. PREVENTION & TREATMENT: -Vaccine against Giardia can be given to animals, including dogs: ***No human vaccine is available -Avoiding drinking from freshwater sources is the major preventative measure. -Treatment with tinidazole or metronidazole

Yersinia Species

Gram-negative bacteria: -Includes the species Yersinia pestis, cause of the plague Two species that cause GI tract disease: -Y. enterocolitica -Y. pseudotuberculosis Notable for the high degree of abdominal pain they cause: -Accompanied by fever -Often mistaken for appendicitis

Clostridium perfringens Exotoxin

Gram-positive sporulating bacterium: -Also the cause of gas gangrene Endospores contaminate many types of foods: -Meat and fish are most frequently indicated. -Vegetables and beans that have not been cooked thoroughly enough to destroy endospores -When foods are cooled, endospores germinate and cells multiply, especially when food is not refrigerated. If the food is eaten without adequate reheating: -Live C. perfringens cells enter the intestine and release exotoxin -Toxin acts on epithelial cells and initiates acute abdominal pain, diarrhea, and nausea in 8 - 16 hours. -Recovery is rapid, and deaths are extremely rare. C. perfringens also causes an enterocolitis infection similar to that caused by C. difficile: -Diarrhea acquired from contaminated food and transmissible by inanimate objects

Clostridium difficile:

Gram-positive, endospore-forming rod: -Normal biota of the intestine Causes pseudomembranous colitis: -Antibiotic-associated colitis -Precipitated by therapy with broad-spectrum antibiotics such as ampicillin, clindamycin, or cephalosporins. Major cause of diarrhea in hospitals The use of gastric acid inhibitors for the treatment of heartburn can predispose people to this infection. Able to superinfect the large intestine when drugs have disrupted the normal biota. Enterotoxins: toxins A and B -Cause areas of necrosis in the wall of the intestine S&S: -Diarrhea commencing in late antibiotic therapy or even after therapy has stopped: ***Severe cases exhibit abdominal cramps, fever, and leukocytosis. ***Colon is inflamed and gradually sloughs off loose, membranelike patches called pseudomembranes. ***If the condition is not stopped, perforation of the cecum and death can result. PREVENTION & TREATMENT: -Over 15,000 people in the U.S. die each year from C. difficile infections. -Uncomplicated cases respond to withdrawal of antibiotics and replacement therapy for lost fluids and electrolytes. -More severe infections are treated antibiotics for several weeks until the intestinal biota returns to normal: ***Vancomycin ***Fidaxomicin (Dificid): approved in 2011 -Treatment techniques on the horizon ***Fecal transplants provide the GI tract with a new healthy microbiome.

Wart Disease Table (623)

HPV CAUSE: human papilloma virus TRANSMISSION: direct contact (STI), also auto inoculation, indirect contact VIRULENCE: oncogenes (in the case of malignant types of HPV) CULTURE/DIAGNOSIS: PCR tests for certain HPV types, clinical diagnosis PREVENTION: vaccines available, avoid direct contact, prevent cancer by screening cervix TREATMENT: warts or precancerous tissue can be removed, virus not treatable DISTINCT FEATURE: infection may or may not result in warts; infection may result in malignancy EFFECT ON FETUS: may cause laryngeal warts EPIDEMIOLOGY: US estimated 6 million new infections/year, 12,000 new cases of HPV-associated cervical cancer MOLLUSCUM CONTAGIOSUM CAUSE: poxvirus, sometimes called the molluscum contagious virus (MCV) TRANSMISSION: direct contact (STI), also indirect and autoinoculation VIRULENCE: NA CULTURE/DIAGNOSIS: clinical diagnosis, also histology, PCR PREVENTION: avoid direct contact TREATMENT: warts can be removed, virus not treatable DISTINCT FEATURE: wartlike growth are only known consequence of infection EFFECT ON FETUS: NA EPIDEMIOLOGY: US affects 2-10% of children annually

GI Tract Diseases Caused by Helminths

Helminths that parasitize humans are amazingly diverse: -Barely visible roundworms (0.3 mm) -Huge tapeworms (25 m) Three categories: -Nematodes (roundworms) -Trematodes (flukes) -Cestodes (tapeworms) Helminthic diseases are usually accompanied by an additional set of symptoms that arise from the host response to the helminth. Eosinophilia: -Increase in granular leukocytes called eosinophils -Have a specialized capacity to destroy helminths -Hallmark of helminthic infection Helminthic infections acquired through: -Fecal-oral route -Penetration of the skin Most organisms spend part of their lives in the intestinal tract: -While in the intestine, helminths run the gamut of intestinal symptoms, -Some produce symptoms outside of the intestines. CLINICAL CONSIDERATIONS: -Wide variety of helminthic diseases that affect humans and animals -Two classic types of infections will be discussed in detail: ***Enterobius vermicularis ***Taenia solium -Disease tables will be provided for several more helminthic diseases. PATHOGENESIS & VIRULENCE: -Helminths do not have sophisticated virulence factors. -Numerous adaptations to survive in their hosts: ***Specialized mouthparts for attaching to tissues and feeding ***Enzymes with which they liquefy and penetrate tissues ***Cuticle or covering to protect them from host defenses -Organ systems are reduced to the essentials: ***Getting food and processing it ***Moving ***Reproducing -The damage they cause in the host is often the result of the host's response to the presence of the invader. -Definitive host: the host in which the adult worm is found: ***Humans become the accidental definitive hosts for helminths whose normal definitive host is a cow, pig, or fish -Intermediate host: ***Larval stages of helminths ***Humans can serve as intermediate hosts as well DIAGNOSIS: Diagnosis of almost all helminthic infections follows a similar series of steps: -A differential blood count showing eosinophilia -Serological tests indicating sensitivity to helminthic antigens -History of travel to or immigration from the tropics, even if it occurred years ago; some flukes and nematodes persist for decades Definitive evidence: -Discovery of eggs, larvae, or adults worms in stools or other tissues -Worms are sufficiently distinct in morphology that positive identification can be based on any stage, including eggs. -Not all diseases result in eggs or larval stages that can be readily found in the stool. PREVENTION & TREATMENT: -There are no vaccines for the helminthic infections described here. -Preventative measures are aimed at minimizing human contact with the parasite and interrupting its life cycle. -Several antihelminthic medications exist: ***Cellular physiology of eukaryotic parasites resembles that of humans. ***Drugs toxic to helminths can be toxic to us. -Some antihelminthic drugs suppress a metabolic process more important to the worm than the human. -Other antihelminthic drugs inhibit the worm's movement and prevent it from maintaining its position in a certain organ. -Some helminths have developed resistance to drugs used to treat them. -In some cases, surgery may be necessary to remove worms or larvae. Helminthic Infections: intestinal distress as the primary symptom: -both tapeworms and roundworms can infect the intestinal tract and cause primary symptoms there -nematode: enterobius vermicularis -tapeworm: taenia solium

HEPATITIS B & D VIRUSES:

Hepatitis B virus (HBV): -Enveloped DNA virus in the family Hepadnaviridae -Intact viruses are called Dane particles. -Surface (S) antigen is an antigen of clinical and immunologic significance. -Genome is partly double-stranded and partly single-stranded. Hepatitis D virus: -Enveloped RNA Virus -Subvirus satellite of HBV: ***Can propagate only in the presence of HB S&S: -Direct damage to liver cells: ***Fever, chills, malaise, anorexia, abdominal discomfort, diarrhea, and nausea ***Rashes may appear and arthritis may occur. -HBV infection can be serious, even life-threatening: ***A small number of patients develop glomerulonephritis and arterial inflammation. -Complete liver regeneration and restored function occur in most patients: ***A small number of patients develop chronic liver disease in the form of cirrhosis or necrosis. ***In some cases, chronic HBV infection can lead to liver cancer. -Patients who become infected as children have significantly higher risks of long-term infection and disease: ***90% of neonates infected at birth develop chronic infection. ***30% of children infected between ages 1 and 5 also develop chronic infection. ***Only 6% of persons infected after age 5 develop chronic infection. ***This finding is one of the justifications of routine vaccination of children. -Patients infected with both HBV and HDV experience more severe disease and are more likely to progress to permanent liver damage. PATHOGENESIS & VIRULENCE: -Hepatitis B virus enters the body through a break in the skin, mucous membrane, or by injection into the bloodstream. -Eventually reaches liver cells (hepatocytes) where it multiplies and releases viruses into the blood: ***Incubation period 4 - 24 weeks (7 weeks average) -The majority of those infected exhibit few overt symptoms and eventually develop an immunity to HBV. TRANSMISSION & EPIDEMIOLOGY: -Multiplies exclusively in the liver and continuously seeds the blood with viruses: ***Electron microscopy studies have shown up to 107virions per milliliter of infected blood. ***Even a minute amount of blood can transmit infection. -HBV has been detected in semen and vaginal secretions, and can be transmitted by these fluids. -Vertical transmission is possible: ***Predisposes the child to development of the carrier state and increased risk of liver cancer ***Also known as serum hepatitis -One of the major infectious concerns for healthcare workers: ***Needlesticks can easily transmit the virus. ***Healthcare workers are required to have the full HBV vaccination series. -HBV remains infective for days in dried blood, or months when stored in serum at room temperature, and for decades when frozen. -Not inactivated after 4 hours of exposure to 60°C -Disinfectants containing chlorine, iodine, and glutaraldehyde show potent anti-hepatitis B activity. CULTURE & DIAGNOSIS: -Serological tests can detect either virus antigen or antibodies: ***Radioimmunoassay and ELISA testing permit early detection of the surface antigen of HBV early in infection. -Antibody tests are most valuable in patients who are negative for the antigen. PREVENTION & TREATMENT: -Primary prevention for HBV is vaccination: ***Most widely used vaccines are recombinant, containing pure surface antigen cloned in yeast cells. -Vaccination is a must for medical and dental workers and students, patients receiving multiple transfusions, immunodeficient patients, and cancer patients. -Vaccine now strongly recommended for newborns as part of a routine immunization schedule. -A combined HAV/HBV vaccination may be appropriate for some people. -Passive immunization with hepatitis B immune globulin (HBIG): ***Gives significant immediate protection to people who have been exposed to the virus through needle puncture, broken blood containers, or skin or mucosal contact with blood. ***Also recommended for neonates born to infected mothers -Mild cases of HBV are managed with symptomatic treatment and supportive care. -Chronic infection can be controlled with: ***Recombinant human interferon ***Tenofovir or entevir ***Each of these can help stop virus multiplication in many but not all patients. -None of the drugs are considered curative.

Normal Biota of GU Tract:

In both genders, the outer region of the urethra harbors some normal biota: -Kidneys, ureters, bladder, and upper urethra are presumably kept sterile by urine flow and regular bladder emptying. Principal known residents of the urethra: -Nonhemolytic streptococci -Staphylococci -Corynebacteria -Lactobacilli Female urethra is short (3.5 cm long) and in close proximity to the anus: -Can act as a pipeline for bacteria from the GI tract to the bladder, resulting in urinary tract infections Flora of the penis: -Colonized by aerobic Pseudomonasand Staphylococcus species -In an uncircumcised penis, the area under the foreskin is colonized by anaerobic gram-negatives Normal Biota of the Male Genital Tract: -Because the urethra is the terminal organ of the genital tract, it is comprised of the same residents mentioned previously. -After sexual activity begins, microbes associated with STIs can sometimes become long-term residents. Normal Biota of the Female Genital Tract: -Only the vagina harbors a normal population of microbes. -Before puberty and after menopause, the pH is close to neutral and the vagina harbors the same biota as the urethra. -After the onset of puberty, estrogen leads to glycogen release in the vagina, resulting in an acidic pH. -Lactobacillus species thrive in the acidic environment and contribute to it by converting sugars to acid. -The predominance of Lactobacillus, combined with the acidic environment, discourages the growth of many microorganisms. -Candida albicans is also present at low levels

Prostatitis

Inflammation of the prostate gland Acute prostatitis: -Virtually always caused by a bacterial infection. -Bacteria are usually normal biota from the intestinal tract or may have caused a previous urinary tract infection. Chronic prostatitis: -Also often caused by bacteria -Often unresponsive to antibiotics, can be caused by mixed biofilms of bacteria in the prostate -Some forms have no microbial cause. -Though infectious disease specialists feel that one or more bacteria are involved, but cannot be cultured using current techniques S&S: -Pain in the groin and lower back -Frequent urge to urinate -Difficulty urinating -Blood in the urine -Painful ejaculation TREATMENT: -broad spectrum antibiotics

Hepatitis:

Inflammatory disease marked by necrosis of hepatocytes and a mononuclear response that swells and disrupts the liver architecture: -Jaundice: yellow tinge in the skin and eyes caused by bilirubin accumulation in the blood and tissues Can be caused by a variety of different viruses: -Cytomegalovirus -Epstein-Barr virus -Hepatitis viruses A - E Noninfectious conditions that cause hepatitis: -Autoimmune diseases -Drug abuse -Alcohol abuse

Syphilis

Marked by clinical stages designated as: -Primary syphilis -Secondary syphilis -Tertiary syphilis Also has latent periods of varying duration during which it is quiescent Spirochete appears in the lesions and blood cultures during the primary and secondary stages, and is transmissible at these times: -Also transmissible during the early latency period between secondary and tertiary syphilis -Largely nontransmissible during the "late latent" and tertiary stages PRIMARY SYPHILIS: -Early indication of syphilis is the appearance of a hard chancre at the site of entry of the pathogen: ***These ulcers tend to be painless and may escape notice, especially on internal surfaces. ***Chancre heals spontaneously without scarring in 3-6 weeks. ***At this point the spirochete has escaped into circulation and is entering a period of tremendous activity. SECONDARY SYPHILIS: -Appears about 3 weeks to 6 months after the chancre heals: ***Many systems of the body have been invaded. ***Symptoms are more profuse and intense. -Initial symptoms are: ***Fever ***Headache ***Sore throat ***Lymphadenopathy ***Peculiar red or brown rash that breaks out on all skin surfaces ***Lesions contain viable spirochetes. ***Major complications linger for months and years. LATENT & TERTIARY SYPHILIS: -30% of infections enter a highly varied latent period that can last 20 years or longer: ***Antibodies to the bacterium are readily detected, but the bacterium is not. ***This final stage of syphilis is relatively rare today because of widespread use of antibiotics. ***By the time a patient reaches this stage, numerous pathologic complications occur in susceptible tissues and organs. -Cardiovascular syphilis: ***Results from damage to the small arteries in the aortic cell wall ***As the fibers in the wall weaken, the aorta is subject to distention and fatal rupture. ***Aortic valves can also be damaged, resulting in insufficiency and heart failure. -Gummas: ***Painful, swollen, syphilitic tumors ***Develop in tissues in the liver, skin, bone, and cartilage ***Usually benign and only occasionally lead to death, but can impair function -Neurosyphilis: ***Can involve any part of the nervous system ***Shows particular affinity for the blood vessels in the brain, cranial nerves, and dorsal roots of the spinal cord ***Diverse results include severe headaches, atrophy of the optic nerve, blindness, and dementia ***Argyll-Robertson pupil: a condition caused by adhesions along the inner edge of the iris that affix the pupil's position into a small irregular circle Congenital syphilis: -The syphilis bacterium can pass from a pregnant woman's circulation into the placenta and be carried throughout the fetal tissues: -Infection leading to congenital syphilis can occur at any of the three trimesters. -Inhibits fetal growth and disrupts critical periods of development -Can result in mild defects to spontaneous miscarriage or stillbirth -Early congenital syphilis: ***Encompasses the period from birth to 2 years of age and is detected 3-8 weeks after birth ***Profuse nasal discharge ***Skin eruptions ***Bone deformation ***Nervous system abnormalities Late congenital syphilis: ***Unusual assortment of problems in the bones, eyes, inner ear, and joints ***Causes formation of Hutchinson's teeth SYPHILIS CAUSE: -Treponema pallidum: ***Spirochete: thin, regularly coiled cell ***Gram-negative cell wall ***Strict parasite with complex growth requirements that necessitate cultivating it in living host cells PATHOGENESIS & VIRULENCE: -Binds to the epithelium of mucus membranes by its hooked tip -Moves into circulation and the body is transformed into a large receptacle for incubating the pathogen -Produces no toxins and does not kill cells directly -Although phagocytes act against it and antitreponemal antibodies are formed, immune responses are unable to contain it. TRANSMISSION & EPIDEMIOLOGY: -Humans are the sole natural hosts and source of T. pallidum: ***Bacterium is extremely fastidious and cannot survive for long outside the host. ***Rapidly destroyed by heat, drying, disinfectants, soap, high oxygen tension, and pH changes ***Survives for a few minutes to hours when protected by body secretions ***Survives for about 36 hours in blood. ***Risk of infection from an infected sexual partner is 12-30% per encounter. -Common and devastating disease for centuries: ***"Departments of Syphiology" in major medical centers in the U.S. existed for many years ***Enormous effect on social life ***Effect diminished quickly when antibiotics were discovered -Rates have been increasing in the U.S. since 2003. -Continues to be a serious problem worldwide, especially in Africa and Asia:•Persons with syphilis often suffer coinfections with other STIs, especially HIV. CULTURE & DIAGNOSIS: -Can be detected in patients most rapidly by using dark-field microscopy of a suspected lesion: ***A single negative test is not enough to exclude syphilis, and follow-up tests are recommended. -Blood tests based on antibody detection are used for diagnosis: ***Specifically reacts with treponemal antigens ***FTA-ABS: fluorescent treponemal antibody absorption test PREVENTION: -The core of an effective prevention program depends on detection and treatment of the sexual contacts of syphilitic patients: ***Public health departments are charged with the task of questioning patients and tracing their contacts. -All individuals identified as being at risk, even if they do not show signs of infection, should be given immediate prophylactic penicillin in a single long-acting dose. -Barrier protection, such as condoms, provide excellent protection during the primary phase -No vaccine currently exists. TREATMENT: -Historical treatment: ***A dose of mercury or a "mercurial rub"applied to external lesions ***In 1906, Paul Ehrlich discovered that a derivative of arsenic called salvarsan could be effective. ***The use of such toxic compounds shows what lengths people would go to rid themselves of this dreaded disease. -Penicillin replaced all other treatments: ***Penicillin G retains its status as a wonder drug in the treatment of all stages and forms of syphilis.

Rotavirus

Member of the Reovirus group: -Unusual dsRNA genome with an inner and outer capsid -Shape resembles a spoked wheel. Primary cause of morbidity and mortality resulting from diarrhea: -Accounts for 50% of all cases -1 million cases in the U.S. per year, with 70,000 hospitalizations Peak occurrences are seasonal: -Southwest: fall -Northeast: spring TRANSMISSION: -Fecal -oral route -Contaminated food, water, fomites -Most prevalent in the world with poor sanitation -U.S.: relatively common, course is mild S&S: -Effects vary with age, nutritional state, general health, and living conditions of the patient -Babies from 6 - 24 months lacking maternal antibodies have the greatest risk of fatal disease. -Watery diarrhea -Fever -Vomiting -Dehydration -Shock -Damage to the intestinal mucosa that chronically compromises nutrition -Long-term or repeated infections can retard growth -In adults, the infection is mild and self-limiting. TREATMENT: -Children are treated with oral replacement fluid and electrolytes. -Oral live virus vaccine has been available since 2006. Hospital visits have declined by nearly 90% since then.

Normal Biota of GI Tract

Normal Biota of Oral Cavity: -populated by more than 600 known species of microorganisms -bacteria: streptococcus, neisseria, veillonella, staphylococcus, fusobacterium, lactobacillus, corynebacterium, actinomyces, treponema -fungi: cadida albicans -protozoa: trichomonas tenax, entamoeba gingivalis -bacteria live on the teeth as well as the soft structures of the mouth Numerous species live in large accretions known as dental plaque, a type of biofilm: -bacteria held in the biofilm by specific recognition molecules -alpha-hemolytic streptococci are the first colonizers of the tooth surface after it has been cleaned -pellicle: mucinous glycoprotein covering on the tooth to which streptococci attach -other species attach specifically to proteins or sugars on the surface of streptococci Pharynx: ontains a variety of microorganisms described in Chapter 19. Stomach: -previously thought to be sterile due to its very low pH -researches in 2008 found molecular signatures of 128 different species of microorganisms in the stomach -some may be "just passing through," while others may be permanent residents (bacillus, clostridium, staphylococcus, streptococcus are premanent residents) Large Intestine: -has always been known to be a haven for billions of microbes: 10 to the 11 degree per gram of contents -bacteria: bacteroides, fusobacterium, bifidobacterium, clostridium, streptococcus, peptostretpococcus, lactobacillus, escherichia, enterobacter -fungi: candida -several protozoans and archea have been found -normal biota in the gut provide protective function Other functions of normal biota: -help with digestion -provide nutrients that we can't provide ourselves -e.coli synthesizes vitamin K -prescence of normal biota important for proper functioning of epithelial cell structure -plays an important role in "teaching" the immune system to react to microbial antigens -mix of microbiota in the gut can influence the host's chances for obesity or autoimmune diseases Accessory organs and all internal organs are free of microorganisms.

Reproductive Diseases Caused by Microorganisms:

Not all reproductive tract diseases are sexually transmitted, though many are: -Vaginitis/vaginosis may or may not be sexually transmitted. -Prostatitis is probably not sexually transmitted. Sexually transmitted infections (STIs) now are more common in the U.S. than any other industrialized country: -Discharge diseases are responsible for unprecedented numbers of infertility cases. -Herpes and human papilloma virus (HPV) infections are incurable.

Periodontal Disease / Periodontitis

Periodontal disease is so common that 97 - 100% of the population has some manifestation by age 45. Most kinds of periodontal diseases are due to bacterial colonization and varying degrees of inflammation that occur in response to gingival damage. GINGIVITIS: -initial stage of periodontal disease -S&S: ***swelling ***loss of normal contour ***patches of redness ***increased bleeding of gums ***pockets or spaces develop between the tooth and gum PERIODONTITIS: -occurs if gingivitis persists -Increases the size of the pockets in the gum -Can cause bone resorption severe enough to loosen the tooth in its socket -If the condition progresses, the tooth can be lost CAUSE: -Periodontal disease is mediated by communities of microorganisms rather than a single organism: ***Polymicrobial biofilms containing the right combination of bacteria begin the periodontal destruction process. -Common predisposing factor: when the plaque becomes mineralized: ***Produces a calculus above and below the gingival margin that can induce varying degrees of periodontal damage ***Presence of a calculus leads to a series of inflammatory events that allow the bacteria to cause disease TREATMENT: -Removal of calculus and plaque: ***Maintenance of good oral hygiene -Surgery to reduce the depth of periodontal pockets may be required. -Antibiotic therapy, either systemic or in periodontal packings, may be utilized.

Food Poisoning

Refers to symptoms in the gut that are caused by a preformed toxin of some sort: -Staphylococcus aureus -Bacillus cereus -Nonmicrobial sources such as fish, shellfish, or mushrooms Food poisoning should be suspected when: -A patient presents with severe nausea and frequent vomiting accompanied by diarrhea -Reports that companions with whom he or she shared a meal have the same symptoms -Onset within the last 1 - 6 hours INTOXICATION: -Symptoms are violent. -Incubation time is short.

Mumps

S&S: -Incubation period of 2-3 weeks -Fever, nasal discharge, muscle pain, and malaise -May be followed by inflammation of the parotid salivary glands, producing the gopherlike swelling of the cheeks -Parotitis: Swelling of the parotid salivary gland -Viral multiplication in the salivary glands is followed by invasion of other organs. -Despite invasion of multiple organs, prognosis of most infections is complete, uncomplicated recovery with permanent immunity. COMPLICATIONS: -In 20-30% of young adult males, mumps infection localizes in the epididymis and testes, usually on one side only: ***Orchitis and epididymitis can be painful ***No permanent damage usually occurs TRANSMISSION & EPIDEMIOLOGY: -Humans are exclusive natural hosts. -Communicated primarily through salivary and respiratory secretions -Most cases occur in children under the age of 15, and most are subclinical. -Incidence spiked in the U.S. in 2006 and 2010. PREVENTION & TREATMENT: -Symptomatic treatment to relieve fever, dehydration, and pain -Vaccine recommendations: ***MMR at 12 and 15 months ***Booster at 4 - 6 years ***Healthcare workers and college students who haven't had both doses are advised to do so.

Cryptosporidium

S&S: -Mimic other types of gastroenteritis: ***Headache, sweating, vomiting, severe abdominal cramps, and diarrhea ***AIDS patients may experience chronic persistent cryptosporidial diarrhea CAUSE: -Cryptosporidium is an intestinal protozoan of the apicomplexan type: ***Infects a variety of mammals, birds, and reptiles ***Once considered an intestinal ailment exclusive to calves, pigs, chickens, and other poultry, it is clearly a zoonosis as well. -Life cycle: ***Oocysts accidentally ingested by humans with water or food contaminated by feces from infected animals ***Oocyst "excysts" once it reaches the intestine and releases sporozoites that attach to the epithelium of the small intestine. ***Organism penetrates the intestinal cells and lives intracellularly in them. ***Undergoes asexual and asexual reproduction of cells that produces more oocysts, which are released into the gut ***Oocysts are excreted in the feces and in a short time become infective again. ***Oocysts are highly infectious and resistant to treatment with chlorine and other disinfectants. TRANSMISSION & EPIDEMIOLOGY: -Half of the outbreaks of diarrhea associated with swimming pools are caused by Cryptosporidium: ***Chlorination is not entirely successful in eradicating the cysts. ***Filtration is often used by water treatment plants, but this method can fail as well. CULTURE & DIAGNOSIS: -Agent can be detected in fecal samples or in biopsies using ELISA or acid-fast staining: ***Stool cultures should be performed to rule out other bacterial causes of infection. PREVENTION & TREATMENT: -Treatment is not usually required for otherwise healthy patients. -Antidiarrheal drugs may be used. -No curative antimicrobial agent for Cryptosporidium exists. Physicians will try paromomycin, an aminoglycoside effective against protozoa.

Genital Herpes

S&S: -Multiple presentations: ***After initial infection, a person may notice no symptoms ***Could also cause the appearance of a single or multiple vesicles on the genitalia, perineum, thigh, and buttocks ***Vesicles are small and filled with clear fluid. ***Intensely painful to the touch -Appearance of lesions may be accompanied by: ***Malaise ***Anorexia ***Fever ***Bilateral swelling and tenderness in the groin -Initial infection can either be completely asymptomatic or serious enough to require hospitalization. -After initial recovery from infection: ***May have recurrent episodes of lesions ***Generally less severe than the original symptoms, but the whole gamut of possible severity is seen as well ***Some people never have recurrent lesions. ***Some people have nearly constant outbreaks with little recovery time between them. ***Average recurrences is four to five a year. -Most patients remain asymptomatic or experience recurrent "surface" infections indefinitely. -Every year, one or two persons per million with chronic herpes infections develop encephalitis: ***Virus disseminates along nerve pathways to the brain or spinal cord. ***Effects on the nervous system begin with a headache and stiff neck that can progress to mental disturbances and coma. ***Fatality rate is 70% in untreated cases, but acyclovir is effective. HERPES IN NEWBORNS: -In the neonate and fetus, HSV infections can be destructive and fatal. -Most cases occur when infants are contaminated by the mother's reproductive tract immediately before or during birth: ***Have also been traced to hand transmission from the mother's lesions to the baby -In infants whose disease is confined to the mouth, skin, or eyes, mortality rate is 30%: ***Disease infecting the central nervous system has a 50 - 80% mortality rate. -Pregnant women with a history of recurrent infections must be monitored for any signs of viral shedding, especially in the last 4 weeks of pregnancy: ***If no evidence of recurrence is seen, vaginal birth is indicated. ***Any evidence of an outbreak at the time of delivery necessitates a caesarean section. CAUSE: -Both HSV-1 and HSV-2 can cause genital herpes if the virus contacts the genital epithelium: ***HSV-1 is thought of as the virus that infects the oral mucosa, resulting in "cold sores" or "fever blisters." ***HSV-2 is thought of as the genital virus. ***In reality, either virus can infect either region, depending on the type of contact. PATHOGENESIS & VIRULENCE: -Herpesviruses have the tendency to become latent: ***Molecular basis of latency is not entirely clear. ***During latency, some type of signal causes most of the HSV genome not to be transcribed. ***This allows the virus to be maintained within cells of the nervous system between episodes. ***Recent research has shown that microRNAs are responsible for latency in HSV-1. ***Suggested that in some peripheral cells, viral multiplication occurs at a constant, slow rate -Reactivation can be triggered by a variety of stimuli: ***Stress ***UV radiation ***Injury ***Menstruation ***Another microbial infection -At this point, the virus begins manufacturing large numbers of virions on the surface of the body, usually at the same site as other lesions. TRANSMISSION & EPIDEMIOLOGY: -Herpes simplex infection occurs globally in all seasons and among all age groups. -Viruses are relatively sensitive to the environment. -Transmission is primarily through direct exposure to secretions containing the virus: ***People with active lesions are the most significant source of infection. ***Genital herpes can be spread even when no lesions are present. -Herpes is more common than Chlamydia and gonorrhea, but is not a reportable disease: ***Estimated that 20% of American adults have genital herpes ***Number of infected people in the U.S. is estimated to be 42 million. ***Two-thirds of people who are infected don't even know it, either because they have rare symptoms that they fail to recognize or because they have no symptoms at all. CULTURE & DIAGNOSIS: -HSV-1 and HSV-2 can sometimes be diagnosed based on the characteristic lesions alone -PCR tests are available to test for these viruses directly from lesions. -Alternatively, antibody to either virus can be detected from blood samples: ***Detecting antibody does not necessarily indicate whether the infection is oral or genital or whether the infection is new or preexisting. -Herpes-infected mucosal cells display notable characteristics on a Pap smear. -Laboratory culture and specific tests are essential for diagnosing severe or complicated herpes infections. PREVENTION: -No vaccine is currently available for HSV, but more than one is being tested in clinical trials: ***Vaccines may be available very soon. -Avoiding contact with infected body surfaces is the only way to avoid HSV: ***Condoms provide good protection when they actually cover the site where the lesion is, but lesions can occur outside the area covered by a condom. -Mothers with cold sores should be careful in handling their newborns: ***They should never kiss their newborn on the mouth. TREATMENT: -Several agents are available for treatment: ***Results in reduced viral shedding and decrease in the frequency of lesion occurrence. -Acyclovir (Zorivax) and valacyclovir (Valtrex) are very effective: ***Topical formulations can be applied directly to lesions. ***Pills are available as well. -Sometimes medicines are prescribed on an ongoing basis to decrease the frequency of recurrences: ***Sometimes given at the beginning of a recurrence to shorten it

Gonorrhea

S&S: Male -Urethritis -Painful urination -Yellowish discharge -Relatively large number of cases are asymptomatic -In most cases, infection is limited to the distal urogenital tract. -Can occasionally spread from the urethra to the prostate gland and the epididymis -Scar tissue formed in the spermatic ducts during the healing of an invasive infection can render a man infertile. Female -Likely that both the urinary and genital tracts will be infected during sexual intercourse -Mucopurulent (containing mucus and pus) or bloody vaginal discharge occurs in about half the cases. -Painful urination if the urethra is affected. -Major complications occur when the infection ascends the vagina and cervix to higher reproductive structures such as the uterus and fallopian tubes. -Salpingitis: inflammation of the fallopian tubes -Pelvic inflammatory disease (PID): salpingitis that includes inflammation of other parts of the upper reproductive tract -Not unusual for the microbe that causes PID to become involved in mixed infections with anaerobic bacteria -Buildup of scar tissue from PID can block fallopian tubes, causing sterility or ectopic pregnancies. Serious consequences of gonorrhea can occur outside of the reproductive tract: -In a small number of cases, the gonococcus enters the bloodstream and is disseminated to the joints and skin. -Involvement of the wrist and ankle can lead to chronic arthritis and painful, sporadic, papular rash on the limbs. -Rare complications of gonococcal bacteremia are meningitis and endocarditis. Children born to gonococcus carriers are in danger of being infected: -Physicians screen pregnant mothers for its presence. -Gonococcal eye infections are very serious and result in keratitis, ophthalmia neonatorum, and blindness. -Antibiotic eye drops or ointments are applied at birth as a universal precaution. -Finding gonorrhea in children other than neonates is strong evidence for sexual abuse by adults. CAUSE: Neisseria gonorrhoeae: -Gram-negative diplococcus -Appears as kidney-bean-shaped bacteria with their flat sides touching -Figure 21.6: ***gram stain of urethral pus from a male patent with gonorrhea (1000x) PATHOGENESIS & VIRULENCE: -Successful attachment is key to the organism's ability to cause disease: ***Gonococci use specific chemical groups on the tips of fimbriae to anchor themselves to mucosal epithelial cells. ***Once the bacterium attaches, it invades the cells and multiplies on the basement membrane. -Fimbriae play a role in slowing down effective immunity: ***Phase variation: bacteria can turn genes coding for fimbrial proteins on or off depending on the bacterium's situation. -Fimbrial genes can rearrange themselves to put out fimbriae of different configurations: ***This antigenic variation confuses the body's immune system. ***Antibodies that previously recognized fimbrial proteins may not recognize them once they are rearranged. -IgA protease:•Cleaves IgA molecules stationed on mucosal surfaces -"Blebs" of outer membrane containing endotoxin are shed, causing localized damage. TRANSMISSION & EPIDEMIOLOGY: -Except for neonatal infections, the gonococcus is spread through some form of sexual contact. -Gonorrhea is strictly a human infection: ***Occurs worldwide ***Ranks among the most common sexually transmitted diseases ***35,000 cases are reported in the U.S. every year. -Important to consider the reservoir of asymptomatic males and females when discussing transmission of the infection: ***10% of infected males and 50% of infected females are asymptomatic. ***Disease is often spread unknowingly. CULTURE & DIAGNOSIS: -Males: gram stain of urethral discharge is diagnostic -Females: ***ELISA or PCR tests ***Culture on Thayer-Martin agar -N. gonorrhoeae grows best in an atmosphere containing increased CO2: ***Best to inoculate it onto media directly from the patient rather than using a transport tube -Identification: ***Catalase test ***Enzymes for fermenting various carbohydrates ***Oxidase test -Gonorrhea is a reportable disease. PREVENTION: -No vaccine is yet available for gonorrhea: ***Using condoms is an effective way to avoid this and other discharge diseases. TREATMENT: -Gonococcal Isolate Surveillance Project (GISP) run by the CDC: ***Monitors the occurrence of antibiotic resistance in N. gonorrhoeae ***Highly resistant strains have not been observed in the U.S. -CDC recommendations for the treatment of gonorrhea worldwide: Ceftriaxone + azithromycin or doxycycline -Bacterium is highest threat level on the CDC's list of antibiotic resistant organisms.

Vaginitis & Vaginosis:

S&S: Vaginitis: -Inflammation of the vagina -Characterized by some degree of vaginal itching, depending on the etiologic agent -Symptoms may include burning and discharge, which may take different forms as well Vaginosis: -Similar to vaginitis, but does not include significant inflammation CAUSE: -Can be caused by a variety of bacteria and even protozoa -Candida albicans: ***Most common cause of vaginitis ***Known as a yeast infection ***Most women experience this condition one or multiple times during their lives.

Genital Ulcer Diseases Table (620)

SYPHILIS CAUSE: treponema pallidum TRANSMISSION: direct contact and vertical VIRULENCE: lipoproteins CULTURE/DIAGNOSIS: direct tests (immunofluorescence, dark-field microscopy), blood test for treponemal and nontreponemal antibodies, PCR PREVENTION: Abx treatment of all possible contacts avoid contact TREATMENT: penicillin G DISTINCT FEATURE: three stages of disease plus latent period, possibly fatal EFFECT ON FETUS: congenital syphilis EPIDEMIOLOGY: US estimated 90,000 new cases/year; internationally 12 million new infections/year CHANCROID CAUSE: haemophilus ducreyi TRANSMISSION: direct contact (vertical transmission not documented) VIRULENCE: hemolysin (exotoxin) CULTURE/DIAGNOSIS: culture from lesion PREVENTION: avoid contact TREATMENT: ceftriaxone or azithromycin DISTINCT FEATURE: no systemic effects EFFECT ON FETUS: none EPIDEMIOLOGY: US no more than 200/year; internationally 7 million/year HERPES CAUSE: herpes simplex 1 & 2 TRANSMISSION: direct contact, vertical VIRULENCE: latency CULTURE/DIAGNOSIS: clinical presentation, PCR, antibody tests, growth of virus in cell culture PREVENTION: avoid contact antivirals can reduce recurrences TREATMENT: acyclovir, derivatives DISTINCT FEATURE: ranges from asymptomatic to frequent recurrences EFFECT ON FETUS: blindness, disseminated herpes infection EPIDEMIOLOGY: US 20% prevalence in adults; internationally estimated 536 million infected in 15-49 age group

Hospitalizations

Salmonella, nontyphoidal: 19,000 Norovirus: 15,000 Campylobacter species: 8,000 Toxoplasma gondii: 5,000 E. coli (STEC) 0157: 2,500

Norovirus

Second most common cause of hospitalizations from food-borne diseases in the U.S. TRANSMISSION: -Fecal-oral via contaminated food and water S&S: -Profuse, watery diarrhea of 3 - 5 days' duration -Vomiting and fever may accompany the disease. TREATMENT: -Rehydration

Hepatitis A & E Viruses:

Single-stranded, nonenveloped RNA viruses Both transmitted through the fecal-oral route Both cause relatively minor, self-limited hepatitis HEV infects pregnant women, causing a 15-25% fatality rate. S&S: -Subclinical or accompanied by vague, flulike symptoms -Overt cases: ***Jaundice ***Swollen liver -Viruses are not oncogenic. -In most cases, everyone besides pregnant women, experience uncomplicated recovery results. TRANSMISSION & EPIDEMIOLOGY: -Associated with deficient personal hygiene and lack of public health measures -In countries with inadequate sewage control, outbreaks are associated with fecally contaminated water and food. -Most infections result from: ***Unhygienic food handling ***Eating shellfish ***Sexual transmission ***Travel to other countries -Hepatitis A can occasionally be spread by blood or blood products. However, this is the exception rather than the rule. -In developing countries, children are the most common victims because exposure occurs early in life. -In North America and Europe, more cases appear in adults. -The virus is not carried chronically: ***Principal reservoirs are asymptomatic, short-term carriers (often children) or people with clinical disease. PREVENTION & TREATMENT: -Prevention of hepatitis A is based primarily on immunization: ***Inactivated viral vaccine (Havrix) has been in use since the 1990s. ***Administration after exposure can prevent symptoms. -Short-term protection can be conferred by passive immune globulin: ***Useful for people who have come into contact with HAV-infected people ***Also used when people have eaten at a restaurant that was the source of a recent outbreak.

Trichomonas vaginalis

Small, pear-shaped protozoa with four anterior flagella and an undulating membrane: -Has no cyst form, and does not survive long out of the host Causes asymptomatic infections in approximately 50% of females and males: -Considered asymptomatic infectious agents rather than normal biota -Some people experience long-term negative effects. S&S: Males seldom have symptoms. Females have a white to green frothy discharge. Chronic infection can make a person more susceptible to other infections, including HIV: -May also lead to infertility Women who have become infected during pregnancy are predisposed to premature labor and low-birth-weight infants. Easily transmitted through sexual contact since it is common biota in many people. Does not appear to undergo opportunistic shifts within hosts: -Does not become symptomatic under certain conditions -Causes symptoms when transmitted to a noncarrier

Hepatitis C

Sometimes called the "silent epidemic" 4 million Americans are infected with the virus. It takes many years to produce noticeable symptoms. Incidences fell between 1992 and 2003, but no further decreases have been seen since then. Liver failure from hepatitis C is one of the most common reasons for liver transplants in the U.S. RNA virus in the family Flaviviridae Diagnosed with a blood test for antibodies to the virus S&S: -People have widely varying experiences with this infection: ***Shares many characteristics with HBV ***More likely to become chronic ***Of those infected, 75 - 80% will remain infected indefinitely. -Possible to have severe infections without permanent liver damage -More common to have chronic liver disease even without overt symptoms -Cancer may result from chronic HCV infection .-Worldwide, HBV infection is the most common cause of liver cancer. In the U.S., liver cancer is more likely caused by HCV TRANSMISSION & EPIDEMIOLOGY: -Virus is acquired in ways similar to HBV -More commonly transmitted through blood contact: ***Blood transfusions ***Injecting drug users -Vertical transfer is also possible. -Frequently transmitted through blood transfusions before a blood test was available: ***Hemophiliacs who were treated with clotting factor before 1985 were infected with HCV at a high rate. ***Once blood began to be tested for HIV and screened for "non-A, non-B"hepatitis, the risk of contracting HCV was reduced. PREVENTION & TREATMENT: -Currently no vaccine for hepatitis C -Current treatment regimen: ***Ribavirin ***Pegylated interferon ***Treatments are not curative, but prevent or lessen damage to the liver ***Two new protease inhibitors were approved in 2011 to treat HCV.

Enterobius vermicularis:

Sometimes called the pinworm or the seatworm: -Most common worm disease of children in temperate zones. Transmission is of the cycle A type: -Freshly deposited eggs have a sticky coating that causes them to lodge beneath the fingernails and onto fomites. -Upon drying, eggs become airborne and settle in house dust. -Eggs are ingested from contaminated food or drink, or self inoculation. -Eggs hatch in the small intestine and release larvae that migrate to the large intestine. -There the larvae mature into adult worms and mate. Hallmark symptom: pronounced anal itching when the mature female emerges from the anus and lays its eggs. Infection is not fatal, and most cases asymptomatic. An afflicted child may experience disrupted sleep, nausea, abdominal discomfort, and diarrhea. Simple rapid test can be performed by pressing a piece of adhesive tape against the anal skin and then applying it to a slide for microscopic examination. When one member of the family is diagnosed, the entire family should be treated.

Schistosomiasis: Liver Disease

Suspected when liver swelling or malfunction is accompanied by eosinophilia Has afflicted humans for thousands of years Caused by the blood flukes Schistosoma masoni orS. japonicum: -Species are morphologically and geographically distinct -Share similar life cycles, transmission methods, and general disease manifestations One of the few infectious agents that can invade intact skin Schistosoma haematobium causes disease in the bladder. S&S: -Most severe consequences: ***Hepatomegaly ***Liver disease ***Splenomegaly -Occasionally eggs are carried into the central nervous system and heart: ***Create a severe granulomatous response -Adult flukes can live for many years: ***Cause a chronic affliction by eluding the immune defenses CAUSE: -Schistosomes are trematodes or flukes: ***More cylindrical than flat ***Often called blood flukes ***Humans are the definitive hosts. ***Snails are the intermediate host. PATHOGENESIS & VIRULENCE: -Once inside the host: ***Coats itself with proteins from the host's bloodstream, "cloaking" itself from the host defense system ***Coat reduces surface antigenicity ***Allows it to remain in the host indefinitely TRANSMISSION & EPIDEMIOLOGY: -Life cycle D, and very complex: ***Life cycle begins when humans release eggs into irrigated fields or ponds, either by deliberate fertilization with excreta or defecating or urinating in water. -Endemic to 74 countries located in Africa, South America, the Middle East, and the Far East -Schistosomiasis is the second most prominent parasitic disease after malaria: ***Probably affects 200 million people worldwide

Urinary Tract Infections

The flushing action of urine helps to keep infections to a minimum in the urinary tract. Urine itself is a good growth medium for many microorganisms. Cystitis: infection of the urinary bladder that occurs when urine flow is reduced or bacteria are accidentally introduced into the bladder Pyelonephritis: infection of the kidneys Urethritis: infection limited to the urethra S&S: -Cystitis is a disease of sudden onset: ***Pain ***Frequent urges to urinate, even when the bladder is empty ***Dysuria: burning pain accompanying urination ***Urine can be cloudy due the presence of bacteria and white blood cells ***Hematuria: presence of blood in the urine causes it to have an orange color ***Low-grade fever and nausea -Signs and symptoms of pyelonephritis: ***Back pain ***High fever -A serious infection that can result in permanent damage to the kidneys if improperly or inadequately treated -Acute uncomplicated UTI: only the bladder is involved in infection CAUSE: -We must distinguish between UTIs that are acquired in health care facilities and those acquired outside the health care setting: ***Catheter-associated UTIs (CA-UTIs) -95% of UTIs are caused by normal biota of the gastrointestinal tract: ***Escherichia coli is responsible for 80% of these. ***Staphylococcus saprophyticus and Enterococcus are common culprits. TRANSMISSION & EPIDEMIOLOGY: -Community-acquired UTIs: ***Not transmitted from one person to another but from the GI tract to the urinary system. ***More common in women than men because of the nearness of the urethral opening to the anus. -Many women experience "recurrent urinary tract infections": ***Some E. coli can invade the deeper tissue of the urinary tract and avoid being killed by antibiotics. ***They emerge later to cause symptoms again. -Catheter-associated UTIs: ***Most commonly caused by E. coli, S. saprophyticus, Enterococcus, and Klebsiella ***The National Healthcare safety network is now recommending minimizing the use of urinary catheters to limit the incidence of these infections. TREATMENT: -Sulfa drugs such as trimethoprim-sulfamethoxazole are used for UTIs of various etiologies. -Non-antibiotic drug phenazopyridine (Pyridium) is administered simultaneously: ***Relieves the uncomfortable symptoms of burning and urgency ***Should only be administered for two days ***Azo dye that turns the urine dark red or dark orange -A large percentage of E. coli strains are resistant to penicillin: ***E. coli ST131 is highly virulent and resistant to multiple antibiotics

Dental Caries (Tooth Decay):

The most common infectious disease of human beings: -Involves the dissolution of solid tooth surface due to the metabolic action of bacteria Symptoms not noticeable, but range from: -Minor disruption in the outer enamel surface of the tooth -Complete destruction of enamel -Destruction of deeper layers Deeper lesions can result in infection to the soft tissue inside the tooth called the pulp: -Infection leads to pain known as a "toothache." CAUSE: -Streptococcus mutans: ***Oral, alpha-hemolytic streptococcus -Likely a mixed-species consortium consisting of other Streptococcus species and some lactobacilli -Early childhood caries may be caused by a newly discovered species, Scardovia wiggsiae -In the absence of dietary carbohydrates, bacteria do not cause decay PATHOGENESIS & VIRULENCE: -In the presence of sucrose, S. mutans and other streptococci produce sticky polymers of glucose called fructans and glucans: ***These adhesives help bind them to the smooth enamel surfaces and contribute to the sticky bulk of the plaque biofilm. -If plaque is not removed from sites that readily trap food, it can result in a carious lesion: ***Streptococci and other bacteria produce acid as they ferment carbohydrates. -If acid is immediately flushed and the plaque is diluted in the mouth, it has little effect. -In denser regions of plaque, acid can accumulate in direct contact with enamel: ***pH lowers to below 5 and calcium phosphate in the enamel can be dissolved -The initial lesion can remain localized in the enamel and repaired with inert materials (fillings). -If the deterioration reaches the level of the dentin, tooth destruction speeds up, and the tooth can be destroyed. TRANSMISSION & EPIDEMIOLOGY: -Bacteria that cause dental caries are transmitted to babies and children by their close contacts: ***Mother or closest caregiver ***Evidence for transfer of oral bacteria between children at daycare centers CULTURE & DIAGNOSIS: -Dental professionals diagnose caries based on the tooth condition: ***Culture of the lesion is not routinely performed. PREVENTION & TREATMENT: -The best way to prevent dental caries is through dietary restriction of sucrose and refined carbohydrates: ***Regular brushing and flossing to remove plaque are also important. ***Trace amounts of fluoride added to drinking water can incorporate into tooth structure and strengthen enamel. ***Fluoride also encourages the remineralization of teeth that have begun the demineralization process. ***Fluoride is also added to toothpastes and mouth rinses. -Treatment of a carious lesion: ***Removal of the affected part of the tooth, or whole tooth in advanced caries ***Restoration of the tooth structure with an artificial material

Chlamydia

The most common reportable infectious disease in the US: -More than 1 million cases reported annually -Actual infection rate may be 5-7 times that number -Prevalence among sexually active young women ages 14-19: 6.8% -At least 2-3 times as common as gonorrhea -Vast majority of cases are asymptomatic S&S: Males: -Causes inflammation of the urethra -Symptoms mimic gonorrhea: discharge and painful urination -Untreated infections may lead to epididymitis.- Females: -Cervicitis -Discharge -Salpingitis -PID is a frequent sequela of female chlamydial infection: ***A woman is even more likely to experience PID as a result of a Chlamydiainfection than gonorrhea. ***75% of Chlamydia infections are asymptomatic, which puts women at risk for developing PID because they don't seek treatment for the initial infection. ***PID itself may be acute and painful, or asymptomatic, allowing damage to the upper reproductive tract to continue unchecked. Certain strains of C. trachomatis can invade lymphatic tissues, resulting in lymphogranuloma venereum: ***Condition accompanied by headache, fever, and muscle aches ***Lymph nodes near the lesion begin to fill with granuloma cells and become inflamed and tender. ***"Nodes" cause long-term lymphatic obstruction that lead to chronic, deforming edema of genitalia or anus. ***Disease endemic in South America, Asia, and Africa, but can occur in other parts of the world. Babies born to mothers with Chlamydiainfections can develop eye infections and pneumonia if they become infected during passage through the birth canal: ***Conjunctivitis caused by contact with maternal Chlamydia is the most prevalent form of conjunctivitis in the U.S., causing 100,000 cases per year. ***Antibiotic drops or ointment applied to newborn's eyes are chosen to eliminate both Chlamydia and N. gonorrhoeae. PATHOGENESIS & VIRULENCE: -Chlamydia is able to grow intracellularly and avoid the host's immune response: ***Unique cell wall prevents the phagosome from fusing with the lysosome inside phagocytes. ***Presence of bacteria inside cells causes the release of cytokines that provoke intense inflammation. ***The defensive inflammatory response leads to most of the actual tissue damage in Chlamydiainfections. ***Repair of inflammation leads to scarring, which can severely damage the fallopian tube. TRANSMISSION & EPIDEMIOLOGY: -The reservoir of pathogenic strains of C. trachomatis is the human body: ***Microbe shows surprisingly broad distribution among the population. ***Adolescent women are more likely than older women to harbor the bacterium because it prefers to infect cells prevalent in the adolescent cervix. ***Transmitted vertically and through sexual contact ***50% of untreated babies born to infected mothers will acquire chlamydial conjunctivitis or pneumonia. CULTURE & DIAGNOSIS: -Usually detected through rapid techniques such as PCR or ELISA: ***Direct fluorescent antibody detection is also used. ***Serology is not always reliable. ***Antibody to Chlamydia is very common in adults and often indicates past, not present infection. ***A urine test is available, which has definite advantages for widespread screening, but is slightly less accurate for females than males. PREVENTION: Avoiding contact with infected tissues and secretions through abstinence or barrier protection (condoms) is the only means of prevention. TREATMENT: Treatment for this infection relies on awareness: ***CDC recommends annual screening of young women for the presence of the bacterium. ***Screening of older women with some risk factor (such as a new partner) should also be recommended. -Doxycycline or azithromycin -Coinfection with gonorrhea should be assumed and treated similarly. -Recommendation for patients to be rechecked for Chlamydia infection 3-4 months after treatment. -Treatment of all sexual partners of the patient is recommended to prevent reinfection. -Repeated infections with Chlamydia increase the likelihood of PID and other serious sequelae.

The Genitourinary Tract and Its Defenses:

The structures in the genitourinary tract are really two distinct organ systems: -Urinary tract: removes substances from the blood, regulating certain body processes, and forming urine and transporting it out of the body -Genital system: also known as the reproductive system, functions mainly in reproduction The urinary tract: -Kidneys: remove metabolic wastes from the blood, acting as a sophisticated filtering system -Ureters: tubular organs extending from each kidney to the bladder -Bladder: collapsible organ that stores urine and empties it into the urethra -Urethra: conduit of urine to the exterior of the body In males, the urethra is the terminal organ of the reproductive tract. In females, the urethra is separate from the vagina. Defenses of the urinary tract: -Flushing action of urine flowing out of the system -Urine flow also encourages desquamationof epithelial cells lining the urinary tract, shedding microbes with the cells. Normal biota are the most common microbial threat to the urinary tract: -Cells of the lining of the urinary tract have different chemicals on their surface than those lining the GI tract. -Bacteria that are adapted to adhere to the chemical structures in the GI tract cannot attach to the urinary epithelium. Defenses in the urine: -Acidic pH -Lysozyme: enzyme that breaks down peptidoglycan -Lactoferrin: iron-binding protein that inhibits bacterial growth -Secretory IgA: specific for previously encountered microorganisms Male reproductive tract: -Produces, maintains, and transports sperm cells -Source of male sex hormones Male reproductive anatomy: -Testes: produce sperm cells and hormones -Epididymides: coiled tubes leading out of the testes -Vas deferens: combines with the seminal vesicle and terminates in the ejaculatory duct -Contents of the ejaculatory duct empty into the urethra during ejaculation -Prostate gland: walnut-shaped structure at the base of the urethra that contributes to the released semen -Scrotum: contains the testes -Penis: cylindrical organ that houses the urethra Innate defenses of the male reproductive system: -flushing action of the urine, which helps move microorganisms out of the system. Female reproductive anatomy: -Uterus -Fallopian tubes (uterine tubes) -Ovaries -Vagina -Cervix: lower one-third of the uterus that connects to the vagina, serves as the opening to the uterus, and a common site of infection Innate defenses of the female reproductive tract: -Vagina is lined with mucus membranes and the protective covering of secreted mucus -Mucus is a major nonspecific defense during childhood and menopause. -Secretory IgA antibodies specific for any previously encountered infections Major defense provided by changes in pH of the vagina: -Estrogen stimulates release of glycogen secretion by vaginal mucosa. -Bacteria ferment glycogen into acid, lowering the pH of the vagina to about 4.5. -Before puberty, little estrogen is produced, and the vagina has a pH of about 7. -Change in pH beginning in adolescence results in vastly different biota in the vagina. -Biota of women in their childbearing years prevents the establishment of microbes that might harm the developing fetus.

Genital Ulcer Diseases

Three common infectious conditions can result in lesions on the genitals: -Syphilis -Chancroid -Genital herpes Infection with an ulcer disease increases the chances of infection with HIV because of open lesions.

Other Helminths Responsible for Intestinal Distress:

Trichuris trichiura: -Whipworm -Type A lifestyle-Highest incidence in area of the tropics and subtropics with poor sanitation -Symptoms: ***Localized hemorrhage of the bowel caused by worms burrowing and piercing the intestinal mucosa ***Dysentery ***Loss of muscle tone ***Rectal prolapse: can prove fatal in children Diphyllobothrium latum: -Intermediate host in fish -Life cycle C -Common in the Great Lakes, Alaska, and Canada -Mammals, including humans, act as definitive host -Develops in the intestine and can cause long-term symptoms -Transmitted in raw food such as sushi and sashimi made from salmon Hymenolepis species -Small tapeworms ***Most common human tapeworm infections in the world. -Life cycle type C -Hymenolepis nana: ***Dwarf tapeworm: 15 - 40 mm -Hymenolepis diminuta: ***Rat tapeworm ***20 - 60 cm in length

Chancroid

Ulcerative disease: -Begins as a soft papule or bump at the point of contact -Develops into a "soft chancre," which is very painful in men, but may go unnoticed in women -Inguinal lymph nodes can become swollen and tender. CAUSE: -Haemophilus ducreyi -Pleomorphic gram-negative rod -Hemolysin important in the pathogenesis of chancroid -Common in the tropics and subtropics, but is becoming more common in the U.S. TRANSMISSION & EPIDEMIOLOGY: -Transmitted exclusively through direct contact, especially sexually: ***Associated with prostitutes and poor hygiene ***Uncircumcised men seem to be more commonly infected than circumcised men. ***People may be asymptomatic carriers.

Gardnerella Species

Vaginosis: -Common condition in women in their childbearing years -Doesn't appear to induce inflammation in the vagina -Also known as bacterial vaginosis (BV) -A vaginal discharge with a very fishy odor is the result of metabolic by-products of anaerobic metabolism by the bacteria causing the infection. -Likely a result of a shift from a predominance of "good" bacteria (lactobacilli) in the vagina to a predominance of "bad" bacteria -Probably a mixed infection leads to this condition -Mobiluncus found in high numbers PATHOGENESIS & VIRULENCE: -Mechanism of damage is not well understood. -Can lead to PID, infertility, and ectopic pregnancies -Babies born to mothers with vaginosis have low birth weights. TRANSMISSION & EPIDEMIOLOGY: -Not considered to be sexually transmitted, although women who have never had sex rarely develop this condition: ***Very common in sexually active women - may be associated with sex, but not transmitted by it ***Could occur if the act of penetration in the absence of semen (or saliva) causes changes in the vaginal epithelium or biota ***We do not know what exactly causes increased numbers of Gardnerella. ***Low pH typical of the vagina is higher in vaginosis. CULTURE & DIAGNOSIS: -Simple stain of vaginal secretions is used to examine sloughed vaginal epithelial cells: ***In vaginosis, some cells appear to be nearly covered with adherent bacteria. ***Normally, vaginal epithelial cells are sparsely covered with bacteria. ***These cells are called clue cells and are a helpful diagnostic indicator. ***Can also be found in Pap smears PREVENTION & TREATMENT: -Women who find the condition uncomfortable or who are planning on becoming pregnant should be treated. -Women who use intrauterine devices (IUDs) for contraception should also be treated. ***IUDs can provide a passageway for the bacteria to gain access to the upper reproductive tract. -Usual treatment is oral or topical metronidazole or clindamycin

Leptospirosis:

Zoonosis associated with wild and domesticated animals: -Shed into the environment through animal urine Can affect: -Kidneys -Liver -Brain -Eyes S&S: -Leptospiremic phase: ***Pathogen appears in the blood and cerebrospinal fluid ***Sudden high fever ***Chills ***Headache ***Muscle aches ***Conjunctivitis ***Vomiting -Immune phase: ***Blood infection is cleared by natural defenses ***Milder fever; headache due to leptospiral meningitis ***Weil's syndrome: kidney invasion, hepatic disease, jaundice, anemia, neurological disturbances ***Long-term disability and death can result from damage to kidneys and liver, but they occur primarily with the most virulent strains and in elderly persons. CAUSE: -Typical spirochete bacteria with tight, regular, individual coils with a bend or hook at one or both ends. -Leptospira interrogans: ***Species that causes leptospirosis in humans and animals ***Nearly 200 serotypes, resulting in extreme variations in disease manifestation TRANSMISSION & EPIDEMIOLOGY: -Transmission occurs entirely through contact of skin abrasions or mucous membranes with animal urine or some environmental source containing urine. -In 1998, dozens of athletes competing in the swimming phase of a triathlon in Illinois contracted leptospirosis from the water. TREATMENT: -Early treatment with amoxicillin or doxycycline rapidly reduces symptoms and shortens the course of the disease: ***Delayed therapy is less effective. ***Other spirochete diseases, such as syphilis, exhibit this same pattern of being susceptible to antibiotics early in infection but less so later on.