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153 Cards in this Set
- Front
- Back
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Bacillus anthracis
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• Anthrax
-can have inhalation or cutaneous types •Ab produced against antiphagocytic capsule but not protective •bioterrorism |
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Bacillus anthracis
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• Aerobic
• gram-pos rods • form spores • capsule w/ poly-D-glutamate (antiphagocytic) -capsule is encoded on plasmid pXO2 -Ab against capsule are not protective •Non-hemolytic on blood agar, but shows clear areas which are spores •overnight growth on blood agar shows medusa colonies (looks like snakes on head) |
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Bacillus anthracis
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• soil
• contact with infected animals or inhalation of spores from animal hair |
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Bacillus anthracis
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• anthrax toxin has 3 protein; have A/B subunits:
-edema factor (an adenylate cyclase, increase cAMP and cause outpouring of fluid = swelling) -lethal factor (kills cells by inhibiting cell division; protease to cleave phosphokinase for MAPK pathway) -both EF and LF are A-like and encoded on plasmid pXO1 -protective antigen (B-like) is in vaccine |
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Bacillus anthracis
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• Dx: gram stain plus aerobic culture (anthracis is non-motile)
• Tx: Penicillin G • Prevention: Vaccine for high-risk people like military |
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Bacillus cereus
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• Food poisoning/ gastroenteritis
• Diarrheal form: 8-24 hours later, heat labile enterotoxin • Emetic form: 1-5 hours later, heat-stable toxin; superantigen |
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Bacillus cereus
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•Aerobic
•gram pos rods (don’t take in dye really well though) •forms spores •Common in fried rice |
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Bacillus cereus
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• grains and rice
• spores survive boiling and germinate when rice is warmed/fried • no person-to-person transmission •Intoxication since early-onset rather than active infection |
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Bacillus cereus
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•Two enterotoxins: one like cholera(diarrheal) and one superantigen (emetic)
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Bacillus cereus
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•Dx: not done
•Tx: Symptomatic only • No vaccine •Self-limiting |
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Clostridium tetani
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• Tetanus
• Tetanus neonatorum (umbilical tetanus) -fatal for neonates of unimmunized mothers • without treatment, 85% mortality |
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Clostridium tetani
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• Anaerobic
• gram-pos rods • form spores • “tennis racket” due to terminal spore |
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Clostridium tetani
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• soil
• enters through traumatic breaks in skin • neonatorium caused by unsanitary treatment of umbilical cord • genetic info for tetanus toxin is encoded on plasmid |
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Clostridium tetani
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• exotoxin (tetanospasmin) blocks release of inhibitory neurotransmittors (GABA and glycine) from neurons (intra-axonally)
• excitatory neurons are unopposedmuscle spasm • lockjaw (trismus) and risus sardonicus (grimace) result • only one antigenic type of tetanus toxin |
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Clostridium tetani
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• Dx: clinical
• Tx: Hyperimmune human globulin to neutralize toxin + metronidazole or penicillin G + spasmolytic drugs (Valium a type of benzodiazeprine) • Prevention: Toxoid vaccine (toxin inhibited with formaldehyde), booster every 10 years (DPT) |
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Clostridium botulinum
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• Botulism
-takes 24-48 hours because ingest preformed toxin • Wound Botulism -localized infect at wound followed by systemic spread of toxin; stepping on rusty nail • Infant Botulism -localized infection w/ systemic spread; from honey |
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Clostridium botulinum
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• Anaerobic
• gram pos rods • forms spores • one of the most potent toxins known (1 mg of toxin can kill entire family) • spores are obligate anaerobes (survive in canned products) • infant is assoc. w/ eating of C. botulinum spores (honey) |
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Clostridium botulinum
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• soil
• failure to sterilize food during preservation allows spores to survive • genetic info encoded on bacteriophage and are obtained via lysogenic conversion |
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Clostridium botulinum
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• Botulinum toxin
-prevents release of ACh at cholinergic synapses causing flaccid paralysis -8 types (A,B,E common) • spores germinate in anaerobic environment and produce toxin • toxin is heat-labile |
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Clostridium botulinum
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• Dx: use antitoxin to detect toxin in pt’s stool, serum, or food
• Tx: antitoxin to A, B, E made in horses (serum sickness) • Prevention: proper food preservation |
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Clostridium perfringens
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• Gas gangrene (myonecrosis)
• food poisoning- enterotoxin acts as superantigen • gangrene: localized infection w/ systemic toxemia (shock and renal failure) |
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Clostridium perfringens
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• anaerobic
• gram pos (boxcar appearance) • form spores •use litmus milk test – organism can break down protein in milk and produce CO2 and H2 |
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Clostridium perfringens
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• soil and colon
• gangrene from contamination of wound w/ soil or feces • food poisoning from ingestion of contaminated food – self-limiting |
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Clostridium perfringens
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• alpha toxin- lecithinase (aka phospholipase C) that hydrolyzes lecithin (in cell membranes)cell lysis; punch holes in membrane (outer zone of hemolysis)
• theta toxin (hemolysin)- in double zone hemolysis, theta does inner complete zone • other toxins: hemolysin, DNase, hyluronidase, and collagenase; all contribute to tissue damage |
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Clostridium perfringens
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• Dx: Gram stain and anaerobic culture, lecithinase on egg yolk agar (Naegler test); if toxin produced you will see precipitate on side without specific antitoxin
• Tx: Penicillin G and debridement of the wound; symptomatic tx for food poisoning -hyperbaric O2 tx-inhibits alpha toxin • Prevention: debridement of wound, no vaccine |
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Clostridium difficile
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•Pseudomembranous colitis
• elaboration of toxin only after onset of active infection |
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Clostridium difficile
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• anaerobic
• gram pos rods with subterminal spores • form spores |
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Clostridium difficile
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• human colon
• fecal-oral transmission |
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Clostridium difficile
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• antibiotics suppress normal flora allowing C. difficile to produce exotoxin
• Toxin A: responsible for clinical disease, causes fluid production/damage to colon • Toxin B: cytopathic effect (CPE) -both inhibit GTPases, inhibiting signal transduction and depolymerization of actin apoptosis of enterocytes •glucosylate G protein called Rho GTPase -pseudomembranes are result of death of cells |
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Clostridium difficile
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• Dx: detect Toxin B in fecal sample via observed CPE, CPE can be prevented by adding antitoxin against Toxin B
• Tx: Metronidazone. Vancomycin, should not be used since it is broad spectrum that probably caused the disease in the first place; take patient off causative Ab • Prevention: no vaccine |
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Corynebacterium diphtheria
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• Diphtheria
-toxin production and spread following localized infection • Cutaneous diphtheria less life threatening • Diphtheroids- corynebacteria that do not cause diphtheria – non pathogenic |
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Corynebacterium diphtheria
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• club-shaped gram pos rods arranged in V or L shape
• aerobic • does not form spores •highly contagious |
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Corynebacterium diphtheria
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• human throat
• transmission via respiratory droplets • tox gene is carried by a lysogenic bacteriophage •Can have psuedomembrane, made of RBC and WBC |
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Corynebacterium diphtheria
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• Diphtheria toxin: synthesis is iron-regulated (in low iron, organism can produce toxin since toxin repressor inactivated)
-inhibits protein synthesis by adding ADP-ribose to EF2 (ADP-ribosylation abruptly stopping protein synthesis) -has A (active) and B (binds) fragments -host cell receptor: heparin-binding epidermal growth factor (HB-EGF) is in heart and nerve cells -pseudomembrane in throat caused by death of mucosal cells • Prevention: Toxid Vaccine (DTaP); diphtheria toxoid (exotoxin inactivated by formaldehyde) |
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Corynebacterium diphtheria
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• Dx: gram stain
-growth on Tellurite (Loffler’s medium) agar- reduces K tellurite, yielding black colonies, tellurite is reduced to the metal tellurium and precipitated -stained w/ Methylene Blue- Babes Ernst granules give a beaded appearance (composed of metachromatic volutin) -Elek test-identifies diphtheria exotoxin • Tx: antitoxin made in horses neutralizes toxin, Penicillin G kills it •Herd immunity important in non-vaccinated •vaccine at 2, 4, 6 mo; 10 yr booster |
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Listeria monocytogenes
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• Meningitis and sepsis in newborns/
immunocompromised adults/ pregnant mothers • Gastroenteritis |
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Listeria monocytogenes
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• small gram pos rods – show “tumbling motility”
• in V or L shaped formations • aerobic • do not form spores •Catalase (+) •facultative intracellular parasite (can survive in phagosome) •Can be confused w Group B strep, so use catalase test to distinguish •also confused with cornybacterium diphtheria – use motility test since diphtheria not mobile |
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Listeria monocytogenes
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• in GI and female genital tract; widespread in nature
• transmission across placenta or by contact during delivery – yields meningitis and sepsis • ingestion of unpasteurized milk |
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Listeria monocytogenes
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• listeriolysin (exotoxin) degrades cell membranes
• facultative intracellular pathogen – use cell-mediated immunity • uses internalins to direct endocytosis into the host cell in a phagosome; bind to our E cadherins • listeriolysin O disrupts the phagosomal membrane and releases organism into cytoplasm; activated by acidic pH • Actin-Based motility: uses host cell’s actin to transport itself into an adjacent host cell; actin froms “comet” tail, filapodia carry pathogen into next cell; “tumbling motility”; has actin receptors (can bind and use) |
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Listeria monocytogenes
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•Dx: gram stain, B-hemolytic, tumbling motility
•Tx: ampicillin /gentamycin or ampicillin/ trimethoprim-sulfamethoxazide •Prevention: pregnant women and immunocompromised should not ingest unpasteurized milk or raw vegetables; no vaccine |
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Escherichia coli
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• UTI
• sepsis • neonatal meningitis • ETEC- traveler’s diarrhea, watery non-bloody • EHEC-(O157:H7) enterohemorrhagic- from undercooked hamburger (causes hemorrhagic colitis), requires small # of bacteria, non-invasive • hemolytic-uremic syndrome (HUS) is complication of EHEC- have thrombocytopenia (big decrease in platelets leading to internal bleeding) and renal failure • EPEC-non-bloody diarrhea in infants/kid |
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Escherichia coli
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• facultative gram neg rods
• ferment lactose (pink colonies on MacConkey) • UTI more likely in women b/c of proximity of anus and to vagina and urethra, and short urethra • indwelling urinary catheters predispose to UTI, intravenous lines predispose to sepsis • MacConkey’s agar w/ sorbitol: E. coli (EHEC) does not ferment sorbitol (colorless colonies), while other E. coli strains do (pink) -MacConkey’s w/out sorbitol- lactose fermenters are pink •Unique characteristics: ferments lactose, decarboxylates lysine, produces indole from trp, uses acetate as only carbon source, motile •some not invasive, just produces toxin; does not produce fever; others are into-invasive and just like shigella •indole (+) since produces indole from tryptophan |
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Escherichia coli
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• human colon; colonizes vagina and urethraUTI
•acquired during birth in neonatal meningitis and by fecal-oral route in diarrhea UTI Related Stuff 2 pili types Type 1 – specific for mannose containing structures like in bladder epithelium (cause cystitis) ‘P’ pili – E coli for kidney infections – bind specific digalactose receptor of P blood group |
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Escherichia coli
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•ETEC enterotoxins:
-heat labile toxin (LT) stimulates adenylate cyclase (like cholera) -heat stable toxin (ST) activates guanylate cyclase (not able to reabsorb Na) • virulence factors: pili for attachment and antiphagocytic capsule • EHEC enterotoxin: -Verotoxin (Shiga-like) causes bloody diarrhea; inhibits protein synthesis by removing adenine from the 28S rRNA ribosome • Eosin-Methylene Blue (EMB)- differentiates btw lactose fermenters (green) and not •O Ag – for LPS in cell wall (>1500 types) •H Ag flagellar protein (>50 types) •K Ag for capsular protein (>90 types) |
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Escherichia coli
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• Dx: gram stain and culture; lactose fermenting colonies on EMB (green shade) or MacConkey’s
-TSI shows acid slant and acid butt with gas but no H2S • Tx: Amicillin or sulfonamides for UTI; third-gen cephalosporins for meningitis and sepsis; rehydration in traveler’s, antibiotic resistance due to B-lactamase •Prevention: for UTI limit urinary catheterization, for sepsis- switch IV lines, for traveler’s- only eat cooked food abroad -no vaccine •Peritonitis can be due to concurrent infection with both E. Coli and bacteroides fragilis (anaerobic); fragilis is one of the most Ab resistant anaerobes |
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Salmonella typhi
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• Typhoid fever
• chronic carrier state in gallbladder (same thing can happen with cholera)- form biofilms on gallstones; may have to remove gallbladder •isolated from blood, so systemic infection |
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Salmonella typhi
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• facultative gram neg rods
• do not ferment lactose – colorless on MacConkey • produce H2S (black colonies) •MOTILE • invasive (require more # than shigella), can cause bacteremia • ↓ stomach acid due to antacids predisposes to Salmonella • Phase Variation: -Salmonella can control which of the H antigenic types of flagella it produces •endotoxin – fever, shock, etc, lives on cell membrane of gram neg |
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Salmonella typhi
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• habitat: only human small intestine – multiply in Peyer’s patches
•Most frequent animal source is poultry or eggs • transmission by fecal-oral route • by 10-14 days pt has fever and headache (blood cultures pos), lasts 4-8 weeks |
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Salmonella typhi
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• infects cells of the reticuloendothelial system (liver and spleen)
• endotoxin causes fever •rose spots •Vi (capsule) antigen is virulence factor •Also have O Ag and H Ag for flagella • no exotoxins • enters cell by pathogen-directed endocytosis (ruffled membranes at entry site) by Type III secretion system (gene encoded on salmonella pathogenicity island)- promotes salmonella entry and prevents phagosome-lysosome fusion -pathogen is release out basal side to lamina propria -live in inactive macrophage |
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Salmonella typhi
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• Dx: gram stain and culture, TSI shows alkaline slant & acid butt
• Tx: ceftriaxone, resistance due to B-lactamase • Prevention: public health measures, chlorination of water, sewage disposal -2 vaccines for high risk and travelers: 1 w/ Vi polysaccharide capsule and 1 w/ live, attenuated S. typhi as immunogen |
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Salmonella enteritidis (aka Salmonella enterica)
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• Enterocolitis
• sepsis w/ metastatic abscesses •infection and not an intoxication; limited invasiveness •like typhi, can have chronic carrier state in gallbladder |
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Salmonella enteritidis (aka Salmonella enterica)
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• facultative intracellular gram neg rods
• do not ferment lactose • produce H2S • motile • >1500 serotypes • need >105 organisms (much more than Shigella): high infectious dose b/c it is inactivated in stomach •black colonies (H2S) on Salmonella-Shigella agar |
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Salmonella enteritidis (aka Salmonella enterica)
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• enteric tract of humans/animals
• transmission by fecal-oral route |
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Salmonella enteritidis (aka Salmonella enterica)
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• invades mucosa of intestine
• can enter blood causing sepsis • endotoxin in cell wall • no exotoxin •see virulence factors for typhi including O Ag and H Ag and secretion system |
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Salmonella enteritidis (aka Salmonella enterica)
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• Dx: gram stain and culture, TSI shows alkaline slant & acid butt
• Tx: antibiotics usually not recommended since usually self-limiting, ceftriaone for sepsis • Prevention: public health measures, don’t eat raw eggs or meat, no vaccine |
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Shigella dysenteria
Shigella sonnei |
• enterocolitis (dysentery = bloody diarrhea)
• no chronic carrier • Serogroups A, B, C, and D (of O Ag) are S. dysenteria, S. flexneri, S. boydii, and S. sonnei respectively •S. Dystenteria can go into the blood stream whereas the others don’t do so |
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Shigella dysenteria
Shigella sonnei |
• facultative gram neg rods
• non-lactose fermenting so colorless on MacConkey’s agar •TSI – alkaline slant, acid butt with no H2S or gas • nonmotile, and invasive • low infectious dose b/c resistant to stomach acid • expression of particular O antigens of LPS characterizes the species • dysentery-type stool, bloody diarrhea and pus (PMN - intestinal cell dies and becomes part of bloody diarrhea) •Frequently isolated from children younger than 5 yrs |
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Shigella dysenteria
Shigella sonnei |
•habitat: human colon only
• transmission by fecal-oral route • S. dysenteria causes most serious illness, while S. sonnei is predominant in U.S. •Shiga toxin: inhibits protein synthesis by inactivation of 60S ribosome; 2-componenet (A:B) exotoxin that acts intracellularly on villus cells; even without toxin, invasive bug can still cause disease |
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Shigella dysenteria
Shigella sonnei |
• invades mucosa of ileum and colon but doesn’t penetrate farther (sepsis is lower than salmonella)
• initially enter M cells due to outer membrane proteins celled invasion plasmid antigens • internalized bacteria escape vacuoles and use actin-based motility, once in lamina propria, shigella can invade basal surface of epithelial cells; induces cytokines and PMNs which separate tight junction and allow shigella to further invade |
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Shigella dysenteria
Shigella sonnei |
• Dx: gram stain and culture, no H2S
• Tx: fluid and electrolyte replacement in most cases (for severe cases: ciprofloxacin) • Prevention: public health measures such as proper sanitation, no vaccine •most often seen with individuals who had traveled abroad |
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Vibrio cholera
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• Cholera
Epidemic disease (El Tor in Peru) |
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Vibrio cholera
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• Comma-shaped gram neg rods
• ferment sucrose (yellow colonies on TCBS) • oxidase pos •MacConkey – colorless (does not ferment lactose) •TSI – acid slant, acid butt, no H2S or gas • TcpA: toxin co-regulated pili allow adherence (pili synthesis is regulated the same as toxin) gene that controls this also controls toxin production • GM1 ganglioside- cell surface receptor of toxin •motile and not invasive, colonizes on mucosal epithelium |
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Vibrio cholera
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• human colon
• transmission by fecal oral route by eating raw shellfish or by improper sanitation of water • genes for toxin are encoded by a temperate bacteriophage CTX (lysogenic conversion) |
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Vibrio cholera
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• massive watery diarrhea (rice water stool) caused by enterotoxin produced while bug lives in small intestine (choleragen) that activates adenylate cyclase by adding ADP-ribose to Gs
• ↑ cAMP causes loss of H20 • toxin: A (ADP-ribosylating activity) and B (binds ganglioside receptor on surface) • mucinase-enhances attachment to intestinal mucosa • 01 serotype – somatic cell antigen from the outer membrane lipopolysaccharide (2 biotypes: Classical and epidemic causing El Tor) associated with epidemics, non 01 not so much |
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Vibrio cholera
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• Dx: gram stain and culture; TCBS – yellow colonies
• Tx: fluid and electrolyte replacement (oral rehydration therapy); tetracycline not necessary but shortens duration • Prevention- public health measures -vaccine containing killed cells has limited effectiveness |
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Vibrio parahemolyticus
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• diarrhea
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Vibrio parahemolyticus
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• Comma-shaped gram neg rods that grows in warm sea water
• grows in 1% and 8% NaCl solution • doesnt ferment sucrose (green colonies on TCBS) |
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Vibrio parahemolyticus
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• marine organism
• transmitted by ingestion of raw or undercooked seafood (shellfish such as oysters) |
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Vibrio parahemolyticus
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• enterotoxin similar to choleragen is secreted and limited invasion sometimes occurs
• mild to severe diarrhea, nausea, vomiting, fever |
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Vibrio parahemolyticus
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• Dx: TCBS – green
• Tx: illness is self-limiting (lasts 3 days) • Prevention: proper refrigeration and cooking of seafood |
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Vibrio vulnificus
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• intense acute cellulitis
• life-threatening sepsis with hemorrhagic bullae •most invasive, most people though get severe gastroenteritis |
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Vibrio vulnificus
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• Comma-shaped gram neg rods that grows in warm sea water
•grows in 1% NaCl and NOT 8% TCBS – green colonies; 1% and NOT 8% NaCl |
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Vibrio vulnificus
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• acquired by trauma to skin (shellfish handlers) or ingestion of raw shellfish in immunocompromised or have liver disease
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Vibrio vulnificus
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• Thiosulfate-citrate-bile-salts-sucrose (TCBS) agar selects for Vibro spp b/c of its alkaline pH of 8.6 and differentiates btw V. cholerae that ferment sucrose (yellow) and V. parah/V. vulnificus that do not ferment sucrose (green)
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Vibrio vulnificus
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• Tx: doxycycline
•individuals with chronic liver disease have a worse time because viral infection weakens immune defenses against this systemic pathogen •wear gloves when handling sea water/sea animals |
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Campylobacter jejuni
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• enterocolitis
Smelly, green, and watery stool •can cause bacteremia especially in neonates |
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Campylobacter jejuni
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• Comma-shaped or S-shaped gram neg rods
• microaerophilic • grows well at 42°C •oxidase (+) •Motile •Localized tissue invasion •PMN in stool •Associated with Guillian Barre syndrome since Ab cross react with neuron |
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Campylobacter jejuni
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• habitat: human and animal feces (domestic animals like cattle, chicken, dog)
• transmission by fecal oral route |
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Campylobacter jejuni
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• invades mucosa of colon but does not penetrate (sepsis is rare)
• no enterotoxin • CAMPY blood agar- isolate Campylobacter spp. -Identify as C. jejuni if susceptible to nalidixic acid and resistant to cephalothin •Flagella helps bug jump from cell to cell |
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Campylobacter jejuni
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• Dx: gram stain plus culture on Skirrow’s agar, at 42°C in high Co2, low O2
• Tx: symptomatic • Prevention Public health measures, no vaccine |
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Helicobacter pylori
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• Gastritis
• Peptic ulcer • risk factor for gastric carcinoma • linked to MALT lymphomas |
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Helicobacter pylori
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• Curved gram neg rod
• urease pos from tissue biopsy • has not been isolated in stool, food, water, or animals; however probably person-to-person b/c clustering in families •urease test (+) •urea breath test (+) – radiolabeled urea ingested then cleaved by bug urease, radioactive CO2 evolved and exhaled |
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Helicobacter pylori
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• habitat: human stomach
• transmission by ingestion |
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Helicobacter pylori
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• synthesize urease, which produces ammonia that damages gastric mucosa
• ammonia neutralizes stomach acid allowing organism to live • pain in upper abdomen, no bacteremia |
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Helicobacter pylori
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• Dx: gram stain, culture, urease-pos, “urea breath” test-ingest radiolabeled urea
•See heliobacter Ag in stool and IgG in serum • Tx: Amoxicillin, metronidazole, and bismuth (pepto) • Prevention: none |
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Yersinia Enterocolitica
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•Mesenteric adentitis that resembles appendicitis
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Yersinia Enterocolitica
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•blood agar – tiny pin-point colonies
•gram negative oval rods •show motility in semi-solid agar – motile when cultured at 25 C but not at 37C •lactose negative, so colorless on MacConkey |
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Yersinia Enterocolitica
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•from animals such as dog, cat, cattle
•fecal-oral transmission |
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Yersinia Enterocolitica
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•toxin similar to heat stable toxin of ETEC
•does not have the same virulence factors as Y pestis (black plague) •colonizes the mesenteric lymph nodes so that it looks like appendicitis |
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Yersinia Enterocolitica
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•Dx: gram stain, culture, motility test
•Tx: with abcess treat with ciprofloxacin, trimethoprim-sulfamethoxazole •underlying disease can lead to bacteremia or abcesses in liver or spleen •also associated with autoimmune diseases such as reactive arthritis and Reiter’s syndrome |
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Bacteroides fragilis
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• sepsis
• peritonitis • abdominal abscess •B. corrodens – another human pathogen found in the oral cavity |
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Bacteroides fragilis
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• anaerobic, gram neg rods
• capsule is anti-phago •Commonly seen in peritonitis with E.Coli |
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Bacteroides fragilis
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• predominant anaerob in human colon
• transmission from colon to blood or peritoneum |
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Bacteroides fragilis
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• lipopolysaccharide in cell wall is chemically different form and less potent than typical endotoxin
• no exotoxin |
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Bacteroides fragilis
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• Dx: gram stain and culture
• Tx: metronidazole, clindmycin, and cefoxitin all effective, abscesses should be surgically drained, resistance to penicillin G (B-lactamase • Prevention: perioperative cefoxitin in bowel surgery no vaccine |
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Klebsiella pneumonia
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• Pneumonia (predisposed to by chronic pulmonary disease); currant jelly sputum
• UTI (predisposed to by catheter) • sepsis |
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Klebsiella pneumonia
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• lactose fermenting
• facultative gram neg rods w/ large polysaccharide capsule (impedes phagocytosis) •MacConkey agar shows pink colonies with a mucoid appearance •heavy growth on blood agar •indole (-) •not motile |
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Klebsiella pneumonia
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• human upper resp and enteric tracts
• transmitted by aspiration and inhalation of respiratory droplets •UTI by ascending spread of fecal flora •Important nosocomial infection – in hospital environment |
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Klebsiella pneumonia
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• endotoxin causes fever and shock assoc w/ sepsis
•Antiphagocytic capsule • no known exotoxin |
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Klebsiella pneumonia
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• Dx: gram stain and culture, characteristic mucoid colonies
• Tx: Need sensitivity test since resistant to a whole bunch of antibiotics Cephalosporins w/ aminoglycosides • Prevention: no vaccine or drug |
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Enterobacter cloacae
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• hospital acquired pneumonia, UTI, sepsis
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Enterobacter cloacae
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• gram neg rod
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Enterobacter cloacae
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• Highly antibiotic resistant
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Serratia marcescens
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• hospital acquired pneumonia
• UTI and sepsis |
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Serratia marcescens
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• enteric gram-neg rod
• red-pigmented colonies on nutrient agar; produgiosin; get more pigment when growth inhibited •MacConkey – pink, so lactose fermenting •blood agar - white |
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Serratia marcescens
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•Water contaminant but usually harmless; can be carried in from some hospital procedure
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Serratia marcescens
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•fever – from Il-1 and endotoxin
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Serratia marcescens
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• Highly antibiotic resistant
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Proteus species
(mirabilis) |
• UTI
• sepsis |
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Proteus species
(mirabilis) |
• facultative gram neg rods
• non lactose-fermenting • produce urease • antigens of OX strains of P. vulgaris cross-react w. many rickettsiae • highly motile •swarming motility especially seen on blood agar (appears as waves) •MacConkey/EMB – colorless •Produce H2S, indole (-) |
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Proteus species
(mirabilis) |
• habitat: human colon and environment
• transmission: to urinary tract by ascending spread of fecal flora |
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Proteus species
(mirabilis) |
• endotoxn causes fever and shock assoc w/ sepsis
• urease degrades urea to produce ammonia, pH •leads to “struvite” stones” •Main cause of renal infection stones |
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Proteus species
(mirabilis) |
•Dx: gram stain and culture- “swarming” effect over blood agar
• Tx: Trimeth-sulfa or ampicillin, but 3rd gen cephalosporin for serious infections • Prevention- no vaccine |
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Pseudomonas aeruginosa
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• wound infection
• UTI and sepsis • pneumonia • nosocomial infections in burn pts and people w/ CF • endocarditis in IV drug users **Most common cause of chronic pulmonary infection in patients with cystic fibrosis |
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Pseudomonas aeruginosa
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• aerobic gram-neg rods
• non-lactose fermenting • pyocyanin (blue-green colored pus) pigment produced •Pyoverdin – yellow green pigment that fluoresces and diffuses into agar • oxidase-pos; obligate aerobe •MacConkey – colorless colonies but see a yellow/green pigment •smells fruity •TSI – metallic sheen |
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Pseudomonas aeruginosa
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• environmental water sources (hospital)
• skin, upper respiratory tract and colon in 10% of people •Can find in the GI tract and soil/water •Pyocins encoded on plasmids – they are bacteriocins which can be typed for epidemiologic tracking; each type inhibits limited bacterial types |
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Pseudomonas aeruginosa
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• endotoxin causes fever and shock assoc w/ sepsis
• produces exotoxin A which acts like diptheria toxin (inactivates EF2) – tissue necrosis • pili mediate attachment, capsule prevents phagocytosis •produce siderophores, compete for bound iron •elastase and exotoxin A for tissue damage to increase [Fe] when it is scarce •when PO4 limited, secretes phospholipase C to degrade phospholipid membranes • type III secretion system •Nosocomial pathogen so prominent in hospital •Virulance factors contributing in CF patients: core polysacc of LPS to adhere to CFTR; glycocalyx slime with alginate to attach to epithelial cells and interfere with immune recognition |
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Pseudomonas aeruginosa
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• Dx: gram stain and culture
• Tx: antibiotics on the basis of sensitivities b/c resistance is common • Prevention: disinfection of water related equipment in hospital, no vaccine |
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Canida albicans
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• thrush (and oral esophagitis in AIDS), candidiasis, especially in hospitals
•In counting the (CFU)/mL, 10,000 is considered significant rather than the usual 100,000 •smells like bread yeast |
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Canida albicans
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•gram pos ovals (BIG) w/ budding
•Has pseudohyphae, which are not really true hyphae; pseudohyphae are elongated blastospores that look like sausage links •Appear s to be gram (+) •Also has budding yeast cells on culture •MacConkey – no growth •blood agar – white colonies with no hemolysis, but can visualize better with calcofluor staining |
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Canida albicans
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White pinpoint colonies w/ no hemolysis
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Canida albicans
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•yeast when part of normal flora, but hyphae when invades
•seen with immunocompromised and diabedes patients |
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Canida albicans
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Can use ketoconazole
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Staphylococcus saprophyticus
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UTI
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Staphylococcus saprophyticus
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No hemolysis
Catalase + Coagulase (-) Gram pos cocci in clusters White colonies on blood agar Novobiocin resistant |
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Staphylococcus saprophyticus
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•Some young females carry this as natural flora in mucosa of genital tract
•Almost always community acquired •produce hemaglutinin, extracellular slime •takes a very low dose to infect |
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Staphylococcus saprophyticus
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•Most common (behind e.coli) cause of community-acquired UTI in sexually active women
•Most women with infection have had sex in the past 24 h |
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Staphylococcus saprophyticus
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Tx: no vaccine; treat with a quinolone such as norfloxacin or trimethoprim-sulfamethoxazole
Dx: use clean catch method to catch urine mid-stream Px: pee after intercourse •No vaccine |
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Enterococcus faecalis
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• UTI and biliary tract infections
• endocarditis (rare; SBE) • assoc w/ bacteremia, bedsores, wounds, and intra-abdominal infections |
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Enterococcus faecalis
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• gram pos cocci chains
• catalase neg • grows in 6.5% NaCl and hydrolyzes esculin in the presence of bile • used to be classified as Group D, now distinct |
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Enterococcus faecalis
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• human colon, urethra and female genital tract
• can enter bloodstream during GI procedures |
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Enterococcus faecalis
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• No exotoxins or virulence factors identified
• part of the normal flora of GI tract •Have been shown to be resistant to penicillin and some are resistant to vancomycin (VRE); give linezolid |
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Enterococcus faecalis
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• Dx: gram stain, α, β, γ hemolytic (mostly alpha)
• Tx: need 2 antibiotics to kill: penicillin + aminoglycoside (gentimycin); (Ab synergism) • Prevention: penicillin + gentamicin to pts w/ damaged heart valves undergoing urinary tract procedures |
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Bordatella pertussis
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•Whooping Cough
•Spread during catarrhal stage where you don’t see the usual symptoms, but peak bacteria numbers produced •Followed by paroxysmal stage characterized by sudden intense (paroxysms) cough and the inspiratory whooping cough |
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Bordatella pertussis
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•Gram (-) coccobacillis (short rod that looks like it could be a coccus)
•Can see on Border Gengou media (high % of blood to inactivate inhibitors of agar; slow grower •Use nasopharyngeal swab, area where bug colonizes heavily – ciliated cells •Blood smear may show lymphocytosis; don’t usually see this (hallmark of pertussis) |
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Bordatella pertussis
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•Non-invasive and found in ciliated epithelium of the respiratory tract
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Bordatella pertussis
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•Filamentous hemagluttinin – pili protein attaches to cilial epithelial cells
•Tracheal cytotoxin works with endotoxin to produce NO to damage tissues •produce pertussis toxin, which does ADP glycosylation on Gi;, responsible for lymphocytosis since it is a potent Tcell mitogen •Adenylate cyclase exotoxin – internalized by PMNs and requires calmodulin (Ca dependent) •Toxic subunit (A) and 5 binding subunits (B) •Has two component regulatory system for the virulence gene (Bvg) in response to Mg and SO4 ion concentrations and temperature governed by sensor protein (BvgS) with kinase activity that catalyzes phosphorylation of response activator protein (BvgA) to activate transcription of virulence genes |
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Bordatella pertussis
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•Tx: erythromycin – toxins have already damaged the ciliated cells though
•Vaccine – DtaP – acellular vaccine with 5 Ag types, contains inactivated pertussis toxin, filamentous hemagglutinin, fimbriae, and pertactin |
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Legionella Pneumonia
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•Legionnaire’s disease (atypical pneumonia)
•facultative intracellular; cell-mediated immunityy •Can be confused with Mycoplasma pneumonia (walking pneumonia) |
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Legionella Pneumonia
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•Won’t grow on blood agar and MacConkeys
•Faint gram (-) stain – rod •Use charcoal yeast agar (BCYE) that is supplemented with high concentrations of iron salts and cysteine •Cold agglutination titer does not rise like it would with mycoplasma |
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Legionella Pneumonia
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•Can come from environmental water sources such as air conditioners, water cooling towers, and water taps in hospitals
•Predisposing factors – being treated with corticosteroids, older man who smokes and consumes a lot of alcohol, AIDS, cancer, renal transplant |
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Legionella Pneumonia
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•Endotoxin – lipopolysaccharide
•Type IV secretion system inhibits phagolysosomal fusion •produces Beta-lactamase •No exotoxin |
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Legionella Pneumonia
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Tx: azithromycin, erythromycin (w or w/o rifampin) or fluoroquinolones
•Prevention – reduce cigarettes and alcohol; eliminate aerosol from water source |
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Haemophilus influenzae
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•invasive; uses capsule
•Pneumonia (particular aspiration pneumonia); epiglottitis, laryngitis, tracheitis •Can also get meningitis, which was common in children 2 mo – 5y before vaccine •can get septic shock |
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Haemophilus influenzae
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•Gram (-) rod, coccobacillus; looks like Neisseria but look for filaments that are not seen with N.
•Grown on chocolate agar with growth on X (heme) and V (NAD) factors; mucoid growth •H. aegyptius – X and V for growth (acute purulent conjunctivitis); really similar to H. influenzae •H. ducreyi – X factor only (STD call chancroid) •H. aphrophilus – neither X or V (subacute endocarditis in patients with damaged valves) |
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Haemophilus influenzae
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•Spread as respiratory droplets by humans
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Haemophilus influenzae
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•Polysaccharide capsule (1 of 3 encapsulated pyogens – also pneumococcus and meningococcus); contains polyribitol phosphate-PRP and is anti-phagocytic
•Type b capsule is most invasive •Produces endotoxin •type b makes IgA protease and Beta lactamase •drug resistance from R plasmids – transferred via conjugation |
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Haemophilus influenzae
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Tx: ceftriaxone
•Vaccine: 1) purified capsular polysacc which are T cell-indep type 2 Ag, which doesn’t help young children who don’t have effective B-cell yet 2) Hib conjugate vaccine converts T-indep to T-dep response; TI-2 capsular PRP Ag coupled to toxin (commonly diphtheria) |
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Yersinia pestis
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•Bubonic plague (urban) or sylvanic plague (from wild animal)
•Facultative intracellular – in macrophages •Can spread to lungs and cause pneumonia (pneumonic plague) •can get disseminated intravascular coagulation |
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Yersinia pestis
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•Gram (-) rod
•blood agar – grows slowly into small pinpoint colonies •stained with Wayson’s reagent – see “safety pin” like features •coagulase (+) |
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Yersinia pestis
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•Can come from urban rats or wild animals
•Transferred to humans through infected flea or through humans via respiratory droplets if they have pneumonic plague •Buboes = enlarged lymph node; fever |
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Yersinia pestis
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•lipopolysaccharide
•iron-acquisition systems •Type III secretion system – Sec independent •endotoxin, exotoxin, V Ag, W Ag •Plasmids carry virulence genes: 1) Yad – adherence 2) Yops – cytotoxic activity against phagocytes 3) Fra – anti-phagocytic protein capsule called Fra1 (F1) 4) Pla – degrades fibrin clots, C3b, C5a inhibits opsonization and phagocyte migration |
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Yersinia pestis
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•Tx: streptomycin and tetracycline
•Vaccine – formalin killed, not fully protective, used in Vietnam war |
