Bacteria Flashcards
(84 cards)
Staphylococcus aureus
Characteristics: gram (+) cocci in clusters, catalase (+), coagulase (+), beta-hemolytic, mannitol fermenting turns augar yellow (aureus=golden)
-commonly colonizes nares
Virulence factors: protein A (endotoxin) binds Fc-IgG inhibits complement activation and phagocytosis
Causes:
- Post viral URI infections - skin infectsion, organ absecesses, pneumonia
- endocarditis- usually tricuspid in IV drug users
- septic arthritis and osteomyelitis
- Toxin mediated disease
- Toxic shock syndrome (TSST-1)
- Scalded skin syndrome (exfoliative toxin)
- rapid-onset food poisoning (enterotoxins) - Heat stable, 2-6hr post ingestion -> nonbloody diarrhea and emesis
- MRSA infection - resistant to methicillin and nafcillin bc of altered penicillin-binding protein (PBP)
TSST is superantigen binds to MHCII and TCR -> Tcell activation –> Staphylococcal toxic shock syndrome (TSS) fever, vomiting, rash, desquamation, shock, end-organ failure *associated with prolonged tampon use and nasal packing
Treatment: vancomycin
Staphylococcus epidermidis
Characteristics: gram +, catalase +, coagulase -, Novobiocin sensitive
Normal flora of skin-> contaminates blood cultures, infects prosthetic devices (most common cause of endocarditis in artifical valves) and IV catheters by making biofilms
Treatment: vancomycin
Staphylococcus saprophyticus
Gram+, catalase+, coagulase -, Novobiocin resistant
2nd most common cause of uncomplicated UTI in young women (sexually active)
Streptococcus pneumoniae
gram+ lancet-shaped diplococci, catalase -, alpha hemolytic, polysaccharide capsule (required for virulence), optochin sensitive, bile soluble, IgA protease (important to invade mucosa)
Most common cause of:
- Meningitis
- Otitis media (in children)
- Pneumonia (#1 community acquired, usually lobar)
- sinusitis
Associated with “rusty sputum”, sepsis in sickle cell disease and splenectomy *spleen important in removing encapsulated organisms
Viridans group streptococci
gram + chains, alpha-hemolytic, NO capsule, bile resistant, optochin resistant
Normal flora of oropharynx -> causes dental caries (strep mutans) and subacture bacterial endocarditis at damaged heart valves (strep sanguinis) -> sangunis makes dextrans which bind to fibrin-plt aggregates on damaged heart valves
Strep pyogenes (group A strep)
Gram + chains, beta-hemolytic, bacitracin sensitive, encapsulated with hyaluronic acid, pyrrolidonyl arylamidase (PYR) +
Virulence factors: streptolysin O (beta-hemolytic, ASO), M protein (anti phagocytic)
Causes:
- Pyogenic - pharyngitis, cellulitis, impetigo (also caused by staph aureus), erysipelas (most common cause, superficial cellulitis w demarkated borders)
- Toxigenic
- scarlet fever
- scarlet rash w sandpaper-like texture (spares face!)
- strawberry tongue
- Toxic shock-like syndrome, necrotizing fasciitis
- scarlet fever
- Immunologic
- Rheumatic fever, usually follows pharyngitis
- Joints, polyarthritis
- <3 - carditis
- Nodules (subcutaneous) on elbows and knees
- Erythema marginatum
- Sydenham chorea
- post strep glomerulonephritis, usually follows impetigo or pharyngitis
- cola urine, facial edema
- Rheumatic fever, usually follows pharyngitis
Strep agalactiae (group B strep)
gram + cocci chains, polysaccharide capsule, beta-hemolytic, colonizes vagina
Causes: pneumonia, meningitis (#1 cause in neonates) and sepsis mainly in babies
Produces CAMP factor -> enlarges area of hemolysis of S. aureus; Hippurate test +
Screen pregnant women at 35-37 weeks gestation -> if (+) culture -> intrapartum penicillin prophylaxis
Group D strep, Enterococcus
Gram + cocci in chains, gamma hemolytic (no hemolysis), bile resistant and 6.5% NaCl resisitant, penicillin G resisitant (hardier than nonenterococcal group D)
Enterococci (E. faecalis (more common) and E.facium) are normal flora in colon
Cause: UTI, subacute endocarditis (following GI/GU procedures) and biliary tract infections
VRE are an important cause of nosocomial infection
Treatment: Linezolid, Tigecycline
Group D strep, Nonenterococcus
gram + cocci rods, catalase -, gamma hemolysis, bile resistant, 6.5% NaCl sensitive
Colonizes gut
(S. bovis biotype 1) S. gallolyticus can cause bactermeia and endocarditis, associated w colon cancer
Corynebacterium diphtheriae
gram + rod (club shaped), black colonies on cystiene-tellurite agar aka Loeffler’s medium
lab diagnosis: metachromtic (blue and red) granules and +Elek test for toxin
passed through respiratory droplets,
cuased by exotoxin encoded by Beta-prophage, inhibits protein synthesis via ADP-ribosylation of EF-2 (elongation factor) -> cell death
Clinical symptoms: psuedomembranous pharyngitis (grayish-white membrane) w LAD “bull neck”, myocarditis, and arrhythmias
Toxoid inactivated vaccine routine in US –> usually see in immigrants b/c not vaccinated
Clostridium tetani
gram + rod, spore-forming, obligate anaerobe
found in soil -> puncture wounds
Produces tetanospasmin exotoxin, tetanus toxin is protease cleaves SNARE proteins for NTs -> blocks release of GABA and glycine (inhibitory NTs) from Renshaw cells in spinal cord
Causes: spastic paralysis, trismus (lock jaw), risus sardonicus, opisthotonus (exaggerated arching of back)
Prevent with tetanus vaccine, treat with antitoxin +/- vaccine booster, diazepam for muscle spams
Clostridium botulinum
gram +, spore-forming, obligate anaerobic bacilli
Heat-labile toxin inhibits ACh release at neuromuscular jxn by cleaving SNARE proteins -> botulism: descending paralysis (see diplopia, ptosis 1st)
Adults: caused by ingestion of preformed toxin from cans of food
Babies: ingestion of spores in honey (floppy baby syndrome)
Treatment: antitoxin
Clostridium perfringens
gram + bacilli, spore-forming, obligate anaerobe
Usually large area wound exposed to dirt (eg motorcycle accident)
produces alpha toxin (lecithinase, a phospholipase) can cause myonecrosis (gas gangrene, crepitis) and hemolysis (double zone of hemolysis)
Treat with IV penicillin G
Clostridium difficile
gram + rod, spore-forming, obligate anaerobe
Most commonly secondary to antibitoic use (especially clindamycin or ampicilin)
Toxin A- enterotoxin, binds to brush border of gut -> inflammation -> watery diarrhea
Toxin B- cytotoxin, causes cytoskeletal disruption via actin depolyerization -> pseudomembranous colitis -> diarrhea
Diagnose by detecting toxin(s) in stool by PCR
Treatment: IV metronidazole or oral vancomycin; recurrent cases: fidaxomicin or fecal microbiota transplant
Bacillus anthracis
gram+, spore-forming rod in chains, obligate anaerobe, *polypeptide capsule contains D-glutamate*, edema factor (EF) via increased cAMP, lethal factor (LF) causes black eschar via protease cleaving MAP kinase
Cutaneous anthrax- ulcer w/ black eschar (painless, necrotic)
Pumonary anthrax “wool sorters disease” - inhalation of spores-> flu symptoms -> pulmonary hemorrhage, widened mediastinum (mediastinitis) and shock
Treatment: fluoroquinilone, doxycycline
Bacillus cerus
gram positive, aerobic, spore-forming
“reheated rice syndrome” warm rice -> germination of spores and enterotoxin cereulide formation
Nausea and vominting w/in 1-5hrs, watery diarrhea + GI pain w/in 8-18hrs
Listeria monocytogenes
Gram + rod, beta-hemolytic, catalase+, facultative intracellular microbe
Transmitted by unpasteurized dairy products, deli meats, consumption of certain cheeses; transplacental or vaginal transmission
“rocket tails” allow intracellular mvmnt and spread across membranes avoiding Abs
*ONLY gram+ organism to produce endotoxin
Caues:
pregnant women: amnionitis, septicemia, spontaneous abortion
infants: granulomatosis infantiseptica, neonatal meningitis
immunocompromised: meningitis
healthy individuals: mild gastroenteritis
Treatment: ampicillin in infants, immunocompromised and elederly aas empirical treatment of meningitis
Actinomyces (israelii)
Gram+ long branching filamentous rods, ANAEROBIC, Not acid fast staining
Normal oral flora
causes oral/facial abscesses that drain through sinus tracts -> forms yellow “sulfur granules”
Treatment: penicillin G
Nocardia
gram + branching filamentous rods, AEROBIC, urease +, catalase +, weakly acid fast staining
Found in soil (NO SPORES)
pulm infections in immunocompromised (pneumonia w cavitary lesions in lung)
and cutaneous infections after trauma in immunocompetent
patients with chronic granulometous disease have increase risk of infection with catalase+ organisms
Mycobacterium tuberculosis
gram + bacilli, acid-fast staining (mycolic acids), obligate aerobe, grows on Lewnstein-Jenses medium (inhibit growth of other organisms)
Virulence: cord factor (serpintine shape)- promotes TNFalpha to stimulate macrophages, sulfatides prevent phagolysosome fusion
Transmitted by respiratory droplets, proliferates in microphages
TB symptoms: fever, night sweats, weight loss, cough, hemoptysis
Primary TB: (nonimmune host, usually child)
- Ghon complex = caseating granulomatous lesion (usually in lower to mid lung) + hilar node LAD
- fibrosis healing-> immunity and type4 hypersensitivity -> PPD(+)
- progressive lung disease (HIV patients, malnutrition) -> death (rare)
- severe bacteremia -> miliary TB-> multi-organ failure -> death
- preallergic lymphatic or hematogenous dissemination -> dormant tubercle -> can reacivate (2o TB)
Secondary TB: (usually adult) reinfection, reactivation of TB in lungs can be caused by TNFalpha inhibitors (screen PPD before infliximab)
- Cough, night sweats, hemoptysis
- Fibrocaseous cavitary lesion usually upper lung lobes (higher O2)
- Extrapumonary TB -> CNS (parenchymal tuberculoma-brain cavitary lesion or meningitis), Pott disease (vertbral body)
PPD+ : current or past exposure, BCG vaccination gives false positive
PPD- : no infection or anergic (steriods, malnutrition, immunocomp) and in sarcoidosis
Treatment: Rifampin, Isoniazid, Pyrazinamide, Ethambutol “RIPE”
Prophylaxis: Rifamin and Isoniazid for 9mo.
Mycobacteria avium-intracellulare
acid-fast, gram+bacilli
causes disseminated non-TB disease in AIDS, usually multi-drug resisitant
Prophylaxis w azithromycin wihen CD4<50
Mycobacteria virulence factors
Cord factor inhibits macrophage maturation and induces release of TNF-alpha,
Sulfatides (surface glycolipids) inhibit phagolysosomal fusion
Mycobacterium scrofulaceum
cervical LAD in kids
Mycobacterium leprae
acid fast bacillus (mycolic acids), likes cool temps-> likes extremities, CANNOT be grown in-vitro
infects skin and superficial nerves - “glove and stocking” loss of sensation
Reservoir in US: armadillos
Leprosy (Hansen disease) forms:
-
Lepromatous form - bacteria NOT contained in Mphages
- lesions diffusely over skin, extensor surfaces
- lion-like faces- facial deformaty
- communicable transmission
- low-cell mediated immunity, humoral Th2 mediated response - lots of bacteria on biopsy
- Treatment: dapson and rifampin + clofazimine x2-5yrs
-
Tuberculoid form: bacteria contained in Mphages
- few hypoesthetic hairless skin plaque
- high cell-mediated immunity, Th1 mediated immune response
- Treatment: dapsone and rifampin 6mo
- Lepromin skin test + -> good cell mediated response -> Tuberculoid