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Unlock answers3 categories of Exotoxins |
1. Cytotoxin 2. A-B toxins 3.Superantigens
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Cytolytic Toxins |
enzymatically attack cell contituents. lead to cell death/lysis. Act on animal cytoplasmic membrane aka- Hemolysins- lyse red blood cells in lab, create zone of clearing |
A-B Toxins |
2 covalently bound subunits -B component binds to cell surface receptor -Allows A to be transferred across membrane B binds host cell receptor A cleaved and enters cell Shuts down protein synthesis
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Diphtheria Toxin |
An A-B TOXIN: produced by strains of C. Diphtheriae that are lysogenized with phage beta which carries the toxin encoding gene |
Botulinum Toxin |
An A-B Toxin: clostridium botulinum-- normal soil organism, doesn't grow in body and improperly in preserved foods. MOST POTENT TOXIN KNOWN. Is encoded by lysogenic bacteriophages. It binds to presynaptic motor neurons and prevents muscle contraction by blocking release of Acetylcholine. |
Tetanus Toxin |
An A-B Toxin: Clostridium tetani-- sil born organism, normal soil organism grows in deep puncture wounds, anaerobic enviornments, transported through motor neurons back to spinal cord, binds to ganglioside lipids on inhibitory motor neurons, prevents release of inhibitory signal, muscle stays contracted gram + anaerobic spore-forming rod toxoid vaccine effective at preventing disease |
Cholera Toxin |
An A-B Toxin: Vibrio Cholerae. B-subunit binds to epithelial lining of small intestine, A-subunit activates adenylate cylase-cAMP produced from ATP 1. Normal movement, Na from lumen to blood, no net Cl movement 2.Colonization and toxin production, activation of epithelial adenly cylclase cholera toxin 3.Na movement blocked, net Cl movement to lumen 4.Massive water movement to the lumen |
Superantigens |
stimulate large numbers of immune response cells: excessive inflammatory reaction. Superantigens are proteins that elicit a very strong immune response. Large number of T cells activated. Extensive cytokine production, sometimes fetal |
Endotoxins |
Gram -, LPS is called the endotoxin. causes host cells to release endogenous pyrogens--cause fever, decrease in lymphocyte, leukocyte, and platelet number, cause hemorrhagic shock and tissue necrosis. Lipid A portion toxic, polysaccharide portion makes it water soluable and immunogenic, both nec. to cause toxic effects in vivo. Very small amts of LPS will cause rxn in pple |
Streptococcus Pyogenes |
causes strep throat, can cause ear stuff, swollen mammary glands and impetigo, scarlet fever (cause by strain containing a lysogenic phage that codes for pyrogenic toxins) Other strep syndrome: Nectrotizing Faciitis, Rheumatic Fever, Glomerulonephritis |
Diphtheria |
caused by Cornybacterium diphtheriae disease: resp. tract, form pseudomembranes of mucous that interfere with breathing and can lead to suffocation. Pathology: mediated by secreted exotoxin which interferes with protein synthesis |
Corynebacterium Diphtheriae |
causes Diphtheria gram + rod or club shape lysogenized by bacteriophage b, which encodes the toxin cells lodge in throat, produce toxin that leads to pseudomemrane formation |
Bordetella Pertusis |
causes whooping cough gram - bacillus adheres to cells of resp. tract produces exotoxin which induces cAMP production |
TB |
caused by Mycobacterium tuberculosis spread easy, acquired by inhalation leading cause of death from an infectious agent 90 percent of those infected mount effective CD4+ T cell mediated response in the lung containing the bacteria in a granulomatous tubercle TB GRANULA FORMATION- chronic activation of CD4 T cells---accumulation of macrophages, formation of a granuloma, tissue necrosis, tubercles seens as rings of marcophages with caseous in middle |
Mycobacterium Leprae |
causes leprosy, cannot be grown in culture so experimented on armadillos. Transm. by direct contact and resp. routes, incubation time weeks to decades, grows within macrophages less serious: tuberculoid most serious: lepromatous |
Neisseria Meningitidis |
gram - transmitted to host through air, attaches to cells in nose cause upper resp. tract. infection can lead to bacterial meningitis--inflammation of meninges (lining around brain and spinal cord) |
Measles |
highly cont. virus resp. transmission, with viral replication in nasopharynx and lymph nodes |
Mumps |
highly cont. viral illness, spread by droplets of saliva or mucous from the mouth, nose, or throat of an infected person swelling of salivatory glands, inflammation of testes, ovaries, breasts, deafness LIVE ATTENUATED VIRUS introduced in 1967 |
Rubella |
virus caused by rubella virus spread by airborne droplets derived from upper resp. tract of an active case, fever and rash, major complication is congential rubella syndrome (moms have it and affects uterus) live attenuated vaccine introduced in 1969 |
Influenza Virus |
enveloped single stranded RNA virus orthomyxoviridae family negative sense segmented genome codes for 11 proteins Subtype of type A: -Hemagglutinin (H) -Neuraminidae (N) |
Antigenic drift |
mutations in the virus lead to slightly altered forms of virus |
Antigenic Shift |
major change in the virus (new H or N). Most people have no protection against this virus. Different strains of the influenza are typically named for their HA and NA genes |
Staphylococcus |
gram + cocci resistent to drying disperse in dust and surfaces common pathogens of humans esp wounds contact with asymptomatic carrier causes variety of disease SUPPURATIVE infection---produce PUS Coaulase- causes fibrin to accumulate around bacterial cells making it difficult for immune system to get to them many strains are antibiotic resistant |
H Pylori |
gram - pathogen associated with gastritis, ulcers, and gastric cancer colonizes the non-acid secreting mucous of stomach and upper gi 80 percent of ulcer patients have this bacterial infection |
Ebola and Marburg Viruses |
Viruses infect immune cells (macrophages and dendritic cells), produce inflammatory response, cause blood clotting, massive hemmorage and death |
Rickettsial Diseases |
Rickettsia- small bacteria, intracellular parasites in vertebate assoc. with blood sucking arthropods-fleas, lice, tiks closely related to mitochondria 3 groups: typhus hroup, spotted fever group, ehrlichiosis group |
Typhus Group-- Rickettia Prowazekii |
typhus- human to human by common louse infection occurs when puncture from louse bite contaminated with louse feces fever, headache, weakness, rash, damage to CNS, lungs, kidney, heart. mortality rate of 6-30 percent |
Lyme Disease |
Borrelia Burgdorferi---spirochete spread by bite of deer tick headache, backache, fever, chills 75 percent of cases develop erythema migrans at site of tick bite bulls eye rash
untreated can progress to chromic stage arthritis, neuro involvement diagnosis difficult |
West Nile Virus |
member of flavivirus group -symmetrical, enveloped icosahedral capsid -positive, ssRNA genome spread by mossy, primarily disease of birds |
Plague |
caused by Yersinia Pestis gram - aerobic rod rodents fleas lymph nodes--causes swollen areas called buboes--bubonic plague capsule prevents phagocytosis eventually enter bloodstream causing septicemia multiple hemorrages under skin---black splotches===black death in 3-5 days Pneumonic plague occurs when cells are inhaled directly into lungs--2 days then dead, highly contagious Septicemic plaque when bacteria rapidly spread through bloodstream, death occurs quickly rare disease |
Rabies |
caused by rabies virus, member of Rhabdovirus family Negative-sense ssRNA virus infects CNS, present in saliva of infected animal enters body by bite wound proliferates in brain death by respiratory paralysis
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Hantavirus |
member of bunyaviridae family enveloped negative-sense ssRNA virus fever and pulmonary capillary leakage reduced exposure by elimanating rodents |
How has H pylori adapted for life in the GI tract? |
Survives in stomach Attaches to human gastric epithelium (extracellular) Produces Urease: breaks down urea to ammonia, protecting bacteria from highly acidic enviornment (adaptation to life in GI tract) |
What are the 3 main virulence factors in H pylori? |
VacA--> vacuolating cytotoxin causes vacuoles and pore formation-->apoptosis Cag---> cytotoxin associated gene, codes for protein that is secreted into host cell, messes with host proteins Bab/Sab--->? |
Clinical tests for H pylori |
Endoscopic methods: histology, rapid urease test, culture Non-invasive methods: stool test, urea breath test, serology Urease breath test: radioactive isotope found in exhaled breath if broken down by urease, indicates H pylori in stomach |
How does H pylori cause ulcers? |
Due to direct cell damage, mucous degradation, increased gastrin/decreased somatostatin, inflammatory cytokines |
how does H pylori cause cancer? |
H pylori infection makes stomach cancer 2-10 times more likely Stomach cancer occurs as a result of inflammation, cell death, p27 decrease -reactive oxygen species, cytokines, DNA damage Hpylori-->apoptosis--->compensatory cell proliferation--->cancer p27 is tumor suppressor (acts by inhibiting cell cyle progression), h pylori decreases p27, cell cycle less regulated--> cancer |
How do host factors influence whether H pylori cause disease?
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Host factors determine pathology (cancer vs ulcers, or no symptoms) -every immune system responds diff. to infect. -certain genes predispose host toward certain symptoms -different strains of h pylori can cause different pathology |
What does H pylori cause? |
mostly asymptomatic, can cause superficila gastritis, atrophic gastritis (carcinoma), peptic ulcers, and lymphoma H pylori is a class I carcinogen, directly implicated in 70 percent of stomach cancer cases |
What are the 3 classes of parasitic worms? |
1. Nematodes: Roundworms 2. Cestodes: Tapeworms 3. Trematodes: Flukes both 2 and 3 are flatworms |
Taenia Solium |
The pork tapeworm (cestode) adult worms aquired from eating undercooked pork containing cysticeri (larvael form), adult attaches to intestinal mucosa using scolex (four suckers and hooks) worm may grow 6 meters and contain many proglottids hundreds of thousands of eggs released from proglottids and excreted in feces where they contaminate enviornment and may be ingested by pig and pple adult worms cause few symptoms, but serious disease results from ingestion of eggs larval form called cysticeri get deposited in brain, muscle, form little holes |
Schistomas mansoni--trematode/fluke |
causes schistosomiasis-->liver and bladder disease aquired by contact with contaminated water snail is intermediate host, cercaria form penetrates skin (while host is in water), migrates throughout body prefered route: intestine to feces washback route: like to elave through feces but sometimes get washed back to liver, causes pathology liver inflammation and worms clogging liver blood vessels cause gigantic swollen vessels; granulomas form around eggs |
Clincal features of Nematode infections |
intestinal nematodes: anemia, malnutrition, enteritis, colitis, intestinal obstruction intestinal/tissue: inflammation muscle, intestine, tissue migration may damage heart, muscle, cns, eye tissue: lymphedema, disfigurement, loss of mobility, blindness, skin disease |
Hookworms: Ancylostoma Duodenale and Necator americanus (nematodes) |
larvae infect human, grows into adult, lay eggs, eggs leave through feces, grow into larvae in enviornment, can infect next person adult hookworms attach to small int. villi, suck up blood cells and tissue cause anemia, intestinal malabsorption, growth delay, cognitive deficits migrating dog and cat larvae cannot grow into adults in humans, instead they migrate around skin causing "creeping eruption" known as lara migrans |
2 categories of foodborne illness |
Food poisoning: caused by eating foods with preformed toxins Food infection: caused by eating food with pathogen |
Coliforms |
indicators of fecal contamination of water live in intestinal tract presence of coliforms indicates fecal contamination of water and suggests water is unsafe for human consumption |
cryptosporidiosis |
protozoan cryptosporidium parvum small, coccidia invade and grow intracellularly in mucosal epithelium of stomach and intestine produces thickwalled oocysts--resistant to chlorine. water must be filtered consumption of fecally contaminated water. responsible for largest waterborne outbreak in us |
Legionellosis--legionnaires' disease |
caused by Legionella Pneumophila found in large number of cooling towers and evaporative condensers of large air conditioning systems found in hot water tanks and spas resistant to heating and chlorination infection occurs by breathing airborne droplets intracellular parasite--invades and grows in alveolar marcophages and monocytes can be asymptomatic or cause mild cough |
Typhoid Fever |
Salmonella typhi humans are only hosts infection via ingestion of contaminated food or water contaminated with feces from asymptomatic carrier bacteria in blood phagocytized, not killed by marcophages
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Amebiasis |
Entamoeba hystolytica contaminated water anaerobic amoeba-lack mitrocondria produces cysts
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Staphylococcal Food Poisoning |
S. Aureus common cause food poisoning. produces several heat stable toxins causes nausua, vomiting, diarrhea with 1-6 hours of ingestion foods kept at rm temp toxin is heat stable- reheating foods does not inactivate it can be serve clears up within 48 hrs antibiotics don't help--caused be preformed toxin |
Clostridial Food Poisoning |
Clostridium perfringens and clostridium botulinum both gram + spore formers canning and cooking won't destroy the spores under anaerobic conditions the spores will germinate Clostridium perfringens: found in soil and gi tract, sewage most common cause of food poisoning in us found in cooekd and uncooked animal meatonce ingested, organism sporulates in intestine and triggers enterotoxin production which alters permeability of intestinal epithelium begins 7-15 hours after eating, resolves within 24 hrs Clostridium botulinum: severe, often fatal, consuming botulinum toxin, inhabits soil or water, spores may contaiminate raw foods before harvest or slaughter causes flaccid paralysis, destroyed by high heat rare
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Salmonellosis |
food infection caused by salmonella inhabits animal gi tract ALL SALMONELLA SPECIES ARE PATHOGENIC TO HUMANS 8-48 hr after infection if enters blood, causes typhoid fever
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Pathogenic E. Coli |
200 known pathogenic e coli strains--can cause fatal diarrheal disease and UTI
EHEC: causes hemorrhagic diahea and kidney failure
E Coli 0157:H7 causes 60,000 infections and 50 deaths per year
Irradiation of ground beef was approved specifically to prevent infection by this strain
Pathogenic e coli form pedestals
pedestal formation assoc. with attaching and effacing (AE) lesions in epithelial cells |
What are the three points for the perfect pathogen? |
1. Quick deaths, outbreaks self contained 2. Efficient killing, limits its effectiveness 3. Sign that humans are not the natural host |
Pathlogical route of Schistosomiasis 3 types |
S mansoni, S japonicum: Those cause liver pathology
Hematobium--bladder. UTI kind of thing |