232 infection
Virus treatment/ antiviral drugs
Anyviral drugs alter the virus dna so it can replicate- it doesn't kill the virus. (acyclovir- stops reclipation of herpies virus, Tamiflu- works on flu) Immunoglobulins- concentrated antibodies inflused and it kills the virus Interferons - stimulate immune system
Pathogens: a disease-producing microbes (bacteria and virus most common). so how can a pathogen cause a disease?
Must be able to bind to specific receptors on the human cell in order to cause disease. Can cause disease by: Direct destruction of host cell Interference with metabolic function of host cell Exposing the host cell to toxins produced by pathogen.
Virus effect on host cells. cervical cancer
HPV can lay latent- messes with DNA and cervial cells, the virus causes them to not form normaly and that can cause cancer. Most of the time the body will clear them and most of the time you don't know you have that infection
why does a fever happen?
Hypothalamus raises temperature raises temperature in response to pryogens (chemical mediators) - when there is no infection then there is no more release of pryogens the fever stops
definition of infection
Infection is the invasion and multiplication of microorganisms in body tissues, which may be unapparent or the result of local cellular injury caused by competitive metabolism, toxins, intracellular replication, or antigen-antibody response.
innate Immune Mechanisms
Innate Immunity - inflammatory response Neutrophils /Mast cells/complement proteins in tissue where microbe enters. They encounter microbe and Release chemical mediators (histamine, prostaglandin) Trigger more cells to come and macrophages Macrophages release cytokines which go to liver and Triggers complement system (then more- cascade) Natural Killer Cells detect viruses (intracellular activity)
what is an interferon and what does it do?
Interferons are a type of cytokine, signaling proteins released by host cells in response to the presence of pathogens. Interferons activate immune cells such as macrophages and NKCs, and interfere with viral replication by protecting cells from from virus infections.
Chain of Infection
Reservoir refers to the source (holding tank) of infection Person, animal or environment with microorganism Person who is asymptomatic Portal of exit: means whereby the agent leaves the reservoir Mode of transmission: method whereby the agent reaches a new susceptible host Can be via air, water, direct contact, food Portal of entry: access to new host Susceptible host: susceptibility will depend on: Health status, chronic disease Immunity Age Nutrition Genetic susceptibility Severe physical and emotional stress infectious agent
What aspects of bacterial activity would be effective targets for pharmacologic treatment?
The membrane or capsule The nuceli- can't replicate without nuceli The flegella or mobility
Protozoa
Unicellular, motile, lack a cell wall, occur in a number of shapes, May live independently, some live on dead organic matter, and others are parasites. Transmitted through contaminated water, food or through a vector (mosquito). Diseases caused by protozoan infection include trichomoniasis, malaria, giardiasis, and amebic dysentery.
antimicrobial protective mechanisms
eyes: washing and antimicrobial activity of tears lymph nodes: phagocytosis by macrophages , and attach by natural killer cells skin- physical barrier respiratory tract- phagocytosis by alveoli macrophages. entrapment by mucus. transport to throat by capillary motion. blood-phagocytosis by macrophages granulocytes. digestion by lyzozymes. attack by complement proteins bone marrow -phagocytosis by macrophages and granulocytes and attack by natural killer cells liver- phagocytosis by kupffer cells (macrophages) spleen-phagocytosis by macrophages and attack ny natural killer cells digestive tract - destruction by gastric acid, bile and enzymes. completion for nutrients by billions of normal bacteria. urogential tract - flushing and acidity of urine.
Tinea: Pathophysiology Clinical Manifestations treatment
A group of fungal infections Transmitted via direct contact Fungal infections of skin, hair & nails also referred to as dermatophyte Dermatophyte attaches to and produces thickening of keratinized cells Infections often remain localized clinical maefestations: Variable depending upon location Tinea Corporis- "ring worm" Tinea Versicolor-hypopigmentation Tinea Capitis-hair loss/breakage Tinea Pedis-maceration between and around toes Tinea Cruris- "jock itch" erythema, itching Tinea Unguium-nail thickening, discoloration Treatment Prevention Antifungal drugs
infection vs. disease
A state of cellular, tissue destruction resulting from invasion of microorganisms (pathogen) An infection results when a pathogen invades and begins growing in the host. Disease results when tissue is harmed and function is impaired as a result. An infection results when a pathogen invades and begins growing within a host. Disease results only if and when, as a consequence of the invasion and growth of a pathogen, tissue function is impaired. Our bodies have defense mechanisms to prevent infection and, should those mechanisms fail, disease can result after infection occurs.
Viral Hepatitis
Acute or chronic inflammation of the liver caused by infection with one or more hepatitis viruses Transmitted via fecal-oral route or direct contact with blood/body fluids of infected person Results in varying levels of hepatic necrosis Hep A you get it from food and you can get over it but it damages the lievr - you can get rid of it All the other ones you cant get rid of. Clinical Manifestations-Prodrome- fatigue, anorexia, low-grade fever Icterus-jaundice, hepatomegaly, clay stools, dark urine Recovery-improvement with residual hepatomegaly or chronic state.
Bacterial pathogenicity
Affected by bacterial structural properties & endotoxin/exotoxin release. is the process by which bacteria infect and cause disease in a host. Not all bacteria are pathogens and have the ability for pathogenesis (also known as virulence).
What is the difference between endotoxin and exotoxin?
An endotoxin is a lipopolysaccharide that is contained in the cell wall of gram-negative bacteria and is released during lysis or destruction of the bacteria or possibly during bacterial growth or antibiotic treatment. An exotoxin is a protein released during bacterial growth that elicits the production of antibodies called antitoxins. Many vaccines target exotoxins.
How do bacteria develop antibiotic resistance?
Antibiotic resistance is usually a result of genetic mutations that can be transmitted directly to neighboring microorganisms by plasmid exchange or incorporation of free DNA. Lack of compliance in completing the therapeutic regimen with antibiotics allows the selective resurgence of microorganisms that are more relatively resistant to the antibiotic. Overuse of antibiotics can lead to the destruction of the normal microbiome, allowing the selective overgrowth of antibiotic-resistant strains or pathogens that had previously been controlled. There also is concern that overuse of antibiotics to promote growth in cattle results in ingestion of antibiotic-containing meat.
Immune responses to bacterial invasion:
B lymphocytes are activated, resulting in the production of antibodies. T lymphocytes are activated, resulting in phagocytosis. Complement system is activated to enhance overall response. Bacteria release endotoxins or exotoxins, which damage the cells of the host and initiate an inflammatory response.
how do Antifungal drugs work? and what are some examples?
Bind to fungal cell membrane, increasing permeability, and reducing viability of fungal cells. Antifungals don't kill human cell membranes Cell memebrane is different Enzymes not in human cells examples: Amphottericin B (PO and IV) Flyuconazole (PO) Nystatin (topical)
Chlamydiae
Chlamydiae: obligate intracellular parasites but reproduce through binary fission (use host metabolism). Cause STIs, PID (pelvic inflammatory disease) Treated with Azithromycin
Chronic Hepatitis & Cirrhosis
Chronic hepatitis is represented by impaired liver function for more than 6 months. The liver is infiltrated with macrophages and lymphocytes. Patients with chronic hepatitis also carry an increased risk of developing hepatocellular carcinoma related to persistent cell injury. Cirrhosis is an end-stage liver disease marked by interference of blood flow to the liver and wide-spread hepatocyte damage. Interference of blood flow to the liver (1) exacerbates hypoxia of the hepatocytes and results in further cell death; (2) causes blood and bile to back up into the liver resulting in further injury and inflammation; and (3) obstructs blood flow from portal circulation. Liver failure and death may result.
Complement system:
Complement system: a large number of distinct plasma proteins that react with one another to opsonize (make more attractive) pathogens and induce a series of inflammatory responses that help to fight infection. There are three ways in which the complement system protects against infection: First, it generates large numbers of activated complement proteins that bind covalently to pathogens, opsonizing them for engulfment by phagocytes bearing receptors for complement. Covalent means the molecules share electrons rather than donate them so the bond is tight because they are sharing Second, the small fragments of some complement proteins act as chemoattractants to recruit more phagocytes to the site of complement activation, and also to activate these phagocytes. Third, the terminal complement components damage certain bacteria by creating pores in the bacterial membrane. The pores allow extracellular contents to flood the cell bacteria cell and destroy its contents.
Common Diagnostic Tests
Complete blood count (with WBC differential): Leukocyetes- bacterial infection Basophils and ensophils- parasitic Monocytes- chronic infection Bands -infection Serological tests (detect specific antibodies or viruses) eg monospot Antigen identification Antibody titer Culture and sensitivity-Finger out whats growing and what kills it. C-reactive protein (CRP) (complement activation) Erythrocyte sedimentation rate (ESR) -Elevated CRP and ESR means - sign of inflammation Radiographic studies PET and indium scans- check for infection, check the bones, they put die in and the infected area will light up
Antibiotic Therapy Empiric therapy: Definitive therapy: Prophylactic therapy:
Empiric therapy: treatment of an infection before specific culture information has been reported or obtained Definitive therapy: antibiotic therapy tailored to treat organism identified with cultures- you have done culture and sensitivity ( see what it is and what the bacteria is sensitive to) Prophylactic therapy: treatment with antibiotics to prevent an infection, as in intra-abdominal surgery or after trauma
explain endotoxins, exotoxins and enzymes
Endotoxins Gram-negative bacteria contain endotoxin, a complex of lipopolysaccharide molecules that form the cell wall and are released during lysis. Cause a massive inflammatory response and clotting - this causes sepsis Exotoxins (imp for vaccine dev b/c trigger antibody prod of antitoxins) Potent substances, often bacterial-derived proteins, released into the surrounding tissues that cause local or systemic injury to the host Referred to according to tissue involved (neurotoxic, hepatotoxic) Enzymes Produced by some bacteria and similar effect to exotoxins (hemolysin = hemolytic streptococcus
5 phases of infection
Exposure Incubation: exposure to onset signs and symptoms Prodrome: feeling "under the weather" Icterus: Acute clinical illness & full manifestations-peak of illness Convalescence: waning manifestations to full recovery
fungi
Fungi: large organisms that have a membrane bound nucleus, cytoplasm, organelles (Eukaryotic) Unicellular - yeast Multicellular - molds Common resident microbes Only a few are pathogenic Yeast reproduces by budding, pseudohyphae and produce spores. Mold reproduce hyphae, clusters = mycelium Infections with fungi referred to as mycoses or mycotic infection. Fungus: opportunistic pathogen
when does infection occurs?
Infection occurs when microorganisms have penetrated the three lines of defense. 1. physical barriers and external defences 2. innate immunity ((inflammation, fever, phagocytes, complement, interferon) 3. adaptive immunity (( you make antibodies to get rid of the infection and usually takes 7-10 days)
Risk Factors: Populations at Greatest Risk
Infections potentially affect all individuals, regardless of age, gender, race, and socioeconomic status. Populations at greatest risk are the: Very young- novle immune system, haven't been exposed so they don't have antibodies Ekderly- bodies weak and can indure the illness Poor Uninsured Residents of geographic areas where an infection is prevalent
Bacterial Meningitis what is it? clinical manifestations treatment
Inflammation of the meninges of the brain and spinal cord Respiratory droplet transmission; mechanism for entry into CNS unknown Bacteria proliferate in CNS, exudate damages and obstructs CNS structures leading to reduced oxygen to the brain Inflammatory and immune responses are waged. clinical manifestations: Rapid and severe onset Severe headache Photophobia Nuchal rigidity Altered level of consciousness Vomiting Seizures treatment: Prevention Antimicrobial drugs Symptom care Treatment of close contacts
What are the three mechanisms pathogens use to block the immune system?
Pathogens can block the immune response by antigenic drift, antigenic shift, and gene switching. Antigenic drift occurs when key surface antigens on the virus are mutated, producing a new strain of the virus. Antigenic shift occurs when surface antigen genes undergo recombination to create new strains of the virus. Gene switching is a mechanism used by parasites and occurs when the parasite can switch surface molecules on or off at frequent intervals. As a result, the immune system cannot generate an effective immune response to the antigens.
Rickettsiae & Mycoplasmas
Rickettsiae: obligate intracellular microbe (aka intracellular parasite) but also gram-negative bacteria that can produce energy (usually rod shaped). Transmitted by insect vectors (ticks, fleas, lice). Typhus fever and Rocky Mountain spotted fever (target endothelial cells of blood vessels and capillaries) Mycoplasma lack a cell wall, survive on the cell surface but do not enter the host cell. Atypical pneumonia, genitourinary infections characteristics of virus and bacteria, tetracycline treatment can help this
how does endotoxisn cause septic shock?
Septic shock- such a great release of endotoxins that causes the body to shut down because it is overwhelming the blood vessels dilate which causes edema and therefore you would lose a lot of fluid which causes blood to get thicket and blodd pressure drops which causes the vessles to collaps because you don't get enough oxygen. - causes circulatory collaps
shapes of bacteria
Shapes: may be cocci (spheres), bacilli (rods), and spirochetes (spirals)
Action of Antiprotozoal agents
Similar characteristics to antifungal agents Protozoans are eukaryotic cells. Many pathogenic protozoa have several stages in their life cycles. Require treatment with different agents at different stages of the cycles
how to know the difference between the flu and a cold
Stffy nose and sore throat and sneezing is normally with a cold and not the flu You get this for an influenza (colds don't have these three symptoms) Chills Fever Body aches
UTI clinical manifestations and treatment
The inflammatory response leads to edematous, hyperemic tissue and symptoms: Dysuria Urgency Frequency Hematuria Cloudy (purulent exudate) urine- mucosal lining coming out treatment: Antimicrobial drugs Symptomatic care Education
Viral Hepatitis: Treatment
Treatment of acute viral hepatitis, as with other viral infections, is symptomatic. Fluids, rest, and analgesics are recommended, particularly during the icteric phase of illness. Avoidance of strenuous physical activity or contact sports is often recommended because of liver enlargement. Because bile helps with fat emulsification and absorption and because bile production may be impaired during liver disease, a low-fat diet is recommended. Anti-viral drugs (chronic)
How do antigenic changes in viral pathogens promote disease?
Viruses can elude the immune response by undergoing antigenic variation. This variation includes changing appearance by altering surface antigens. For example, new strains of influenza emerge as a result of mutations in surface antigens. This results in a new form of a disease or process.
Pathogenicity:
ability of an organism to cause disease Characteristics that promote the production of disease: Virulence- potency of the pathogen to make you sick. Expressed in a ration ex. 7/10 if it 7 out of 10 people exposed get sick Infectivity- ability of the microb to get in and replicate Toxigenicity- ability to causeing toxins Antigenicity- ability to causes an immune response Antigenic variability- mechanism by which an infectious agent such as a protozoan, bacterium or virus alters its surface proteins in order to evade a host immune response. Pathogenic defense mechanisms- ways that pathogens avoid getting caught ex. cloaking mechanisms Co-infection- more tan one infection happening at the same time Super-infection- infection occurring after or on top of an earlier infection, especially following treatment with broad-spectrum antibiotics.
Why are virusses hard to kill
it can lay dormant ex. HIV or shingles) it is in your host cells Virus attaches to host cell and viral genetic material enters the cell, takes control of cell nucleus. Uses host's cell to synthesize viral proteins and nucleic acids New viruses are assembled in cytoplasm of cell and released virions by lysis of host cell or sometimes budding from host cell membrane but usually lysis May result in host-cell DNA mutation leading to altered differentiation & proliferation
Bacteremia
occurs when microorganisms gain access to the blood and circulate throughout the body. i.e. the presence of bacteria in the blood Bacteriema leads to Septicemia: pathogens multiply in the blood and cause illness.too much bacteremia and the body cant fight it off
Re-assortment:
the process by which the Influenza viruses escapes host defenses by changing genetic composition during replication in the human host cell. Results in viral offspring with altered antigenic properties which result in ongoing host susceptibility to the influenza virus It constantly mutates so that is why its hard for the body to fight it off
