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107 Cards in this Set
- Front
- Back
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Corynebacterium diphtheriae
Gram & Shape Virulence Diagnosis |
G+ pleiomorphic rod
diphtheria toxin (AB subunit) throat culture on tellurite agar |
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Corynebacterium diphtheriae
Transmission Disease |
Aerosol transmission
• Attach to mucosal surface of URT; not systematic • Detects iron level to tell if it’s inside organism before acting (DtxR regulator) |
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Corynebacterium diphtheriae
Mortality |
• Mechanical destruction of airway & suffocation
• Effects of systemic toxinemia (myocarditis or paralysis |
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Vibrio cholera
Lab characteristics |
Gram -
curved rods oxidase positive grows on MacConkey agar facultative anaerobe |
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Vibrio cholera
virulence |
flagella, mucinase
adhesins cholera toxin (AB subunit) |
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Vibrio cholerae
pathogenesis |
bacteria multiply in large intestine
AB subunit toxin encoded by lysogenic phage enters intestinal epithelial cells by type II secretion (binds GM1 gangliosides) increase cAMP levels --> rice stools |
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Vibrio cholerae
reservoir |
contaminated water, shellfish
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Clostridium tetani
Lab characteristics |
Gram + rods
Anaerobic spore-forming |
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Clostridium tetani
virulence transmission pathogenesis |
tetanus toxin (AB subunit)
spore injection into deep traumatic wound • Blocks release of inhibitory neurotransmitters & leads to spastic paralysis • Toxin spread systemically up nerve to CNS or bloodstream |
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Clostridium tetani
mortality |
respiratory muscle paralysis
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Clostridium botulinum
Lab characteristics |
Gram + rods
anaerobic spore-forming |
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Clostridium botulinum
virulence pathogenesis |
botox AB subunit neurotoxin
Toxin enters cell; bacteria itself doesn’t not cause disease Botox blocks release of ACh at NMJ --> flaccid paralysis |
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clostridium botulinum
symptoms mortality |
• Double / blurred vision
• Drooping eyes • Slurred speech • Widespread muscle weakness mortality: respiratory muscle paralysis |
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clostridium botulinum
reservoir transmission |
normal human flora
food, mother-fetus, wound |
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Staph aureus
Lab characteristics |
• Gram +
• Cluster of cocci • Extracellular pathogen • Catalase + (distinguished from strep) • Coagulase + (distinguished from other staph) • Facultative anaerobe High salt media (MSA); form yellow colonies |
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Staph aureus
virulence - toxins |
Toxins:
• Pore-forming / dermonecrotic: α-hemolysin, β-toxin, δ-toxin • Exfoliating: serine proteases, ETA (heat stable), ETB • Superantigens, enterotoxins |
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Staph aureus
virulence - surface antigens |
• Sugar capsule: adherence to foreign objects
• Peptidoglycan • Teichoic acid |
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Staph aureus
virulence - enzymes |
Enzymes:
• Staphylokinase: dissolves clots • Hyaluronidase: dissolves CT • Penicillinase: dissolves antibiotics • DNAase, protease, lipase |
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Staph aureus
evasion of immune system |
• Leukocidins & hemolysins: kill phagocytes
• Protein A: prevents opsonization and blocks Ab • Catalase: resist respiratory burst |
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Staph aureus
localized disease pathogenesis |
Boils, carbuncles, impetigo, pneumonia
• Attach to surface proteins • Produce toxins tissue damage |
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Staph aureus
3 toxigenic diseases |
• Scalded skin syndrome
• Toxic shock syndrome: fever, rash, hypotension • Food poisoning: enterotoxin, no organism necessary |
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Staph aureus
3 toxigenic diseases |
• Scalded skin syndrome
• Toxic shock syndrome: fever, rash, hypotension • Food poisoning: enterotoxin, no organism necessary |
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Staph aureus
reservoir transmission |
normal human flora
wound aerosol food poisoning |
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Staph aureus
control of production |
• Cell-density dependent control; wait until lots before attacking
• Agr D --> sensed by Agr C --> transduced into Arg A --> activate RNA III • RNA III regulates several virulence factors • Repressed: enterotoxin A, nucleases, hyaluronidase • Activated: all other toxins, adhesins, and enzymes |
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Staph aureus
treatment |
• Vancomycin!
• Penicillin-resistant |
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Strept pyogenes
lab characteristics |
• Gram +
• Cocci in pairs/chains • Facultative anaerobe • Catalase – • Group A: β-hemoltyic, pyogenic, bacitracin-sensitive |
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Strept pyogenes
virulence - surface antigens |
Surface antigens:
• Hyaluronic acid capsule (mucoid) • M protein class I and II — rheumatic fever (class I) • Lipoteichoic acid • Proteins F and G • M-like proteins |
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Strept pyogenes
virulence - toxins |
• Streptolysin O: O2-labile (anaerobic)
• Streptolysin S: serum-dependent |
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Strept pyogenes
virulence - enzymes |
• Streptokinase
• Hyaluronidase • C5a peptidase • DNAses |
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Strept pyogenes
Direct infection diseases pathogenesis |
• Pharyngitis, Tonsillitis
• Skin infections: impetigo, necrotizing fasciitis Lipoteicholic acid binds fibronectin M and F proteins bind closer for invasion Phagocytosis & opsonization are avoided |
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Strept pyogenes
toxin-mediated diseases |
• Erythrogenic toxin scarlet fever
• TSS-like symptoms |
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Strept pyogenes
Delayed immunologic reaction ds |
• Rheumatic fever (M protein I)
• Glomerulonephritis |
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Strept pyogenes
reservoir transmission |
transient normal flora
aerosol, contact |
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Strept pyogenes
treatment |
penicillin
erythromycin |
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Strept pneumoniae
Lab characteristics |
• Gram + rod
• Pyogenic • Catalase – • Facultative anaerobe • α-hemolytic, bacitracin-resistant, optichin-sensitive |
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Strept pneumoniae
virulence |
• Pneumolysin encoded on lysogenic phage
• Sugar capsule • Cell wall: peptidoglycan, teicholic acid • Neuraminidase • Secretory IgA protease • H2O2 |
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Strept pneumoniae
diseases |
• Pneumonia
• Sinusitis • Otitis media • Meningitis • Bacteremia |
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Strept pneumoniae
reservoir transmission |
human URT
aerosol |
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Strept pneumoniae
treatment |
• Penicilin
• Erythromycin • Vancomycin • Vaccine: Pneumovax, Prevnar |
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Legionella pneumophila
Lab characteristics |
Legionella pneumophila
• Gram – (doesn’t stain well) • Pleimorphic rod • Aerobic • Fastidious (needs cystine, iron, and low pH) • Catalase + |
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Legionella pneumophila
virulence |
Legionella pneumophila
• Pili • Outer membrane (MOMP): enhances phagocyte uptake • DOT: defect in organelle trafficking proteins; helps growth inside macrophage • ICM: intracellular multiplication proteins; Type IV secretion for export of proteins • Tissue-degradating enzymes |
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Legionella pneumophila
Infection & immunity |
• Uptake by coiling phagocytosis
• Multiply inside macrophage • Bacterial proteases lead to lung damage • Only cell-mediated immunity can help (not humoral) • Activated macrophages kill by limiting iron |
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Legionella pneumophila
Legionnaire's disease |
• Any progressive, atypical pneumonia should be suspicious
• Pneumonia symptoms but also intersitial infiltrates, shock, multi-organ failure |
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Legionella pneumophila
Pontiac fever |
• Non-progressive, self-limiting
• Fever, chills, dry cough no pneumonia-like symptoms |
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Legionella pneumophila
reservoir transmission |
fresh water, air conditioning
• Inhalation (going deep into lungs) • No person-person transmission |
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Legionella pneumophila
treatment |
erythromycin (macrophage-penetrating antibiotic)
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Mycobacterium tuberculosis
Lab characteristics |
• Acid fast
• Facultative intracellular pathogen • Aerobic • Needs rich medium: Lowenstein Jensen |
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Mycobacterium tuberculosis
virulence factors |
• Cord factor: inhibit PMN migration
• Wax D: stimulates CMI • Tuberculin / PPD: type IV hypersensitivity |
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Mycobacterium tuberculosis
immune response |
CMI – CD4 T cells recruit macrophages to site
- CTLs release bacteria from Macrophage hosts (allow ingestion and killing) Humoral Abs develop, but not provide sig protection - bacteria inside of cells not accessible to Ab - mycobacteria serum resistant Tuberculin hypersensitivity - if large doses of Ag present, --> tissue destrxn, necrosis - causes most tissue damage characteristic of TB |
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Mycobacterium tuberculosis
Primary TB |
• Primary TB: bacteria reach alveoli, phagocytized by macrophages, inhibit oxidative burst, survive/multiply spread to lymph nodes bloodstream to other organs
• Circulating bacteria can be cleared but lymph still has some |
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Mycobacterium tuberculosis
Miliary TB |
• Nonspecific inflammatory response: granulotomas form tubercles cord factor inhibit PMNs form granulomas
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Mycobacterium tuberculosis
Reactivation TB |
• Reactivation of secondary TB: from healed primary lesion; classic case of TB; blood in sputum, wt loss, fever, night sweats
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Mycobacterium tuberculosis
Treatment |
• Immunoprophylaxis: give some protection (vaccine)
• First line: isoniazid (INH), pyrazinamide, ethambutol, streptomycin, rifampin • Second line: para-aminosalicylic acid, cycloserine, ethionamide, kanamycin, fluoroquinolones |
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Treponema pallidum
Appearance |
Gram negative like
flagella spirochete |
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Treponema pallidum
virulence |
NO known toxins
Adhesins Hyaluonidase Fibronectin-binding proteins: Ab to Ag-FN complex AtIm |
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Treponema pallidum
diseases |
• Primary Syphilis: painless, crusty pustule; clears after several weeks
• Secondary Syphilis: lesions throughout body, palms/feet • Tertiary Syphilis: immune complexes form tissue damage • Neurosyphilis: can infect CSF and CNS • Congenital Syphilis: cross placental barrier |
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Treponema pallidum
reservoir transmission |
human mucosa
mucosal contact |
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Treponema pallidum
treatment |
Penicillin
(only primary and secondary) |
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Borrelia burgdorferi
Lab characteristics |
• Gram – like, but no LPS, Krebs, or ETC
• Spirochete • Flagella • Linear genome • Iron abstinent |
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Borrelia burgdorferi
virulence |
• OspA: sticks to midgut of tick
• OspC: targets bacteria to salivary glands • OspE: inhibits complement • Expression of surface protein is temp-regulated (to detect human vs tick) |
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Borrelia burgdorferi
Diseases (stages) |
• Stage 1: skin infection from tick bite; red spot “bulls-eye rash”
• Stage 2: systemic infection; arthritis if joints infected • Stage 3: chronic, autoimmunity, inflammation; aspetic meningitis • Lyme Disease |
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Borrelia burgdorferi
reservoir transmission |
Animals (rodents, ticks, deer) (saliva)
tick bites |
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BOrrelia burgdorferi
treatment |
Suspected ds (tickbite) – ABS prophylaxis, watch for lesion
Dx’d ds – doxycycline, amoxicillin, cefuroxime Most effective early; must take 3-4 weeks Difficult to det. cure b/c still Ab+ |
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Chlamydia trachomatis
Lab characteristics |
• Gram – like, but no peptidoglycan or LPS
• Obligate intracellular pathogen; can’t synthesise amino acids |
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Chlamydia trachomatis
virulence factors |
• IncA-G: involved in EB—RB transition, RB survival and replication
• Endotoxin |
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Chlamydia trachomatis
pathogenesis |
• 1: Tarp protein injected by Type III secretion; forms a receptor for the bacteria
• 2: EBs enter by endocytosis, pinocytosis, or phagocytosis (not zipper or trigger) • 3: EBs turn into RBs and multiply; can fuse vacule with other vessicles for nutrients • 4: IncA-G prevent lysosomal fusion • 5: RBs change back to EBs before exiitng • Symptoms caused by inflammatory response |
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Chlamydia trachomatis
diseases |
trachoma: follicular eye ds --> blindness
chlamdyia --> discharge (PNA, conjunctivitis in infants) LGV - lymphogranuloma venereum genital lesions, inflammation in LNs, can spread systemically |
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Chlamydia trachomatis
treatment |
Antibiotics: doxycycline (gets inside cell!); azithromycin
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Neisseria gonnorhoeae
Lab characteristics |
• Gram – diplococci
• Pyogenic • Oxidase + • Catalse + • Fastidious (needs chocolate agar, Thayer-Martin agar) • Ferments glucose only (distinguishes from neisseria meningitidis) • Facultative intracellular pathogen |
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Neisseria gonnorhoeae
virulence factors |
• Type IV Pili: primary adhesion; extensive phase and antigenic variation
• PI: Porin; adhesion and invasion; resists phagolysosomal fusion and oxidative burst • PII: Opa; adhesion and invasion; extensive phase and antigenic variation • PIII: Rmp; blocks antibodies • Iron-binding proteins • Lipooligosaccharide (LOS): endotoxin; lacks the O-antigen of LPS • IgA1 proteases • Peptidoglycan: cytotoxic |
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Neisseria gonnorhoeae
pathogenesis |
• 1: Direct contact leads to attachment
• 2: LOS and peptidoglycan damage surrounding epithelium; inflammatory response • 3: Multiply and spread across mucosal surface or through to submucosa; into blood |
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Neisseria gonnorhoeae
diseases |
• Gonorrhea (STD): urethritis in men, vaginitis / cervicitis in women
• Pharyngitis • Conjunctivitis • Dissemininated infection to rest of body, often joints • Facilitates HIV transmission |
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Neisseria gonnorhoeae
toxin |
endotoxin (LOS)
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Neisseria gonnorhoeae
reservoir transmission |
human mucosa
contact |
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Neisseria gonnorhoeae
treatment |
antibiotics
(antibiotic resistance - beta-lacatamase) |
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Neisseria meningitidis
Lab characteristics |
• Gram – diplococci
• Pyogenic • Oxidase + • Catalse + • Fastidious (needs chocolate agar, Thayer-Martin agar) • Ferments glucose and maltose (distinguishes from neisseria gonorrhoeae) • Facultative intracellular pathogen |
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Neisseria meningitidis
virulence factors |
• Type IV Pili: primary adhesion; extensive phase and antigenic variation
• PI: Porin; adhesion and invasion; resists phagolysosomal fusion and oxidative burst • PII: Opa; adhesion and invasion; extensive phase and antigenic variation • PIII: Rmp; blocks antibodies • Iron-binding proteins • Lipooligosaccharide (LOS): endotoxin; lacks the O-antigen of LPS • IgA1 proteases • Peptidoglycan: cytotoxic • CAPSULE: anti-phagocytic, phase variable |
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Neisseria meningitidis
symptoms of endotoxin LOS |
fever, petechial skin rash, thrombocytopenia, disseminated intravascular coagulation (DIC), endotoxic shock
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Neisseria meningitidis
pathogenesis of meningococcemia |
• 1: Direct contact leads to attachment in nasopharynx
• 2: LOS and peptidoglycan damage surrounding epithelium; inflammatory response • 3: Multiply and spread into systemic blood, leading to meningococcemia |
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Neisseria meningitidis
pathogenesis of meningitis |
• 1: Direct contact leads to attachment in nasopharynx
• 2: LOS and peptidoglycan damage surrounding epithelium; inflammatory response • 3: cross blood-brain barrier to meninges, leading to meningitis |
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Neisseria meningitidis
reservoir transmission |
human URT
aerosol |
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Neisseria meningitidis
treatment |
• No antibiotic resistance! (unlike neisseria gonorrhoeae)
• Penicillin • Chloramphenicol • Prophylactic: rifampin, sulfonamide • Vaccine: capsular polysaccharide subunit vaccine |
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Shigella dysenteriae
lab characteristics |
• Gram – rod
• Facultatively anaerobic • Ferments glucose but NOT lactose • Oxidase – • Does NOT produce H2S • Strict pathogen |
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Shigella dysenteriae
virulence factors |
• Ipa: adherence, invasion, and escape from endocytic vesicle; secreted by Type III
• IscA, IscB: contact hemolysin (IscB), intracellular spread on actin tails • Shigatoxin: enterotoxin, neurotoxin, cytotoxin • LPS: inflammatory response |
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Shigella dysenteriae
pathogenesis |
• 1: Ingested; only needs small amount
• 2: Attaches to M cells; uptake via trigger mechanism and membrane ruffling • 3: Pass through M cells to lamina propria; inflammatory response • 4: Trigger uptake into epithelial cells from basal side • 5: Escape phagosome to cytoplasm; multiply there, spread laterally on actin tails • Causes dysentery (diarrhea w/ blood & mucus) |
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Shigella dysenteriae
shigatoxin |
Shigatoxin: AB subunit toxin,
inhibits protein synthesis neurocytotoxin |
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Shigella dysenteriae
Reservoir transmission |
human intestinal tract
contaminated food, water ingestion |
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Shigella dysenteriae
treatment |
antibiotics
rehydration |
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Salmonella (typhi)
Lab characteristics |
• Gram – rod
• Facultatively anaerobic • Ferments glucose but NOT lactose • Oxidase – • Produces H2S |
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Salmonella (typhi)
virulence factors |
• LPS: multiple antigenic types
• Flagella: multiple antigenic types • Invasins: invA-H • Vi antigen: capsular polysaccharide • Survive in macrophage (Type III secretion) • Acidic stomach turns on multiple virulence genes |
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Salmonella (typhi)
pathogenesis |
• 1: Ingested: only needs small amount
• 2: Attaches through M cells in large intestine; triggers its own endocytosis • 3: Pass through M cells to submucosal layer to be ingested by macrophages • 4: Multiply inside macrophages, carried to lymphatics then bloodstream and gallbladder |
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Salmonella typhi
disease |
• Diarrhea: not watery like cholera or bloody like shigella
• Food poisoning • Typhoid fever: flushed appearance, anorexia, chills, convulsions, delirium • Reinfection: was stored in gallbladder, leads to server ulceration |
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Salmonella typhi
endotoxin |
LPS endotoxin
responsible for most of typhoid fever symptoms |
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Salmonella (typhi)
reservoir transmission |
humans
contaminated food, water ingested |
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Salmonella (typhi)
treatment |
antibiotics that get inside macrophages:
Fluoroquinolones including ciprofloxacin, levofloxacin or ofloxacin; chloramphenicol |
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Èscherichia coli
Lab characteristics |
• Gram – rods
• Facultatively anaerobic • Oxidase – • Ferments glucose and lactose |
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ETEC: enterotoxigenic E. coli
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• Heat-labile toxin LT
• Heat-stable toxin ST Toxin-mediated: cause cholera-like diarrhea |
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EIEC: enteroinvasive E. coli
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• No shiga toxins
• Ipas: invasion proteins (like shigella) • Plasmid encoded Diarrhea; similar to shigella but not bloody usually |
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EPEC: Enteropathogenic E. coli
virulence factors |
• Type IV class pili attaches first
• Type III secretion happens next • LEE locus: pathogenicity island encoding for Type III secretion system • Tir: protein injected by Type III; creates receptor for intimin • Intimin: binds to tir to bring bacteria close |
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EPEC
disease |
• Colonize small intestine
• Fever, nausea, vomiting • Diarrhea (especially in infants) |
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EHEC: enterohemmorhagic E. coli
virulence factors |
• Effectively = EPEC + shiga toxin (AB subunit toxin)
• Acid-resistant, low infection dose • Sorbitol – • LEE locus: pathogenicity island encoding for Type III secretion system • Encodes cryptic prophage |
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EHEC
disease |
• Colonize large intestine
• From undercooked or contaminated meat • Don’t treat with antibiotics! Will retaliate more strongly! Use hydration! • Hemorrhagic colitis: very bloody, watery diarrhea |
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UPEC
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• Type I pili: mannose-sensitive, stick inside urinary tract
• Pap pili: helps to urinary tract • Hemolysin: creates pores to lyse cells • CNF-1: cytotoxic necrotizing factor; affects blatter cells disease: UTI |
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SEC: Septic E. coli
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• Capsule: antiphagocytic, poorly immunogenic
• Adhesins: Type I pili, same as UPEC; S-fimbriae used to bind within brain • Invasins: Ibe (invasion of brain endothelium) Disease: Neonatal sepsis and meningitis |
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Extracellular pathogens
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Staphyloccocus aureus & Streptococcus pyogenes
Bordetella pertussis Corynebacterium diphtheriae Clostridium botulinum & Clostridium tetani Vibrio cholerae Enterotoxigenic E. coli (ETEC) |
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Do you gram stain a purulent throat swab?
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No
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Endotoxic shock is NOT caused by what type of bacteria?
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Gram positive
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