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23 Cards in this Set

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Clostridium perfringens
-multiplies extremely fast
-very large gram (-) rod, box-car shape
-double zone of hemolysis
-toxins: lecithinase (grow on egg yolk agar)
-disease: Clostridial Myonecrosis, Enterocolitis, Enteritis Necroticans
Clostridium perfringens (Clostridial Myonecrosis)
-pathogenesis: wound infection, surgical trauma, non-traumatic due to cancer, or uterine due to unsanitary abortions
-clinical manif: pain & heaviness, white shiny tense skin, systemic: low temp, ↑pulse
-diagnosis: gram stain, isolate & identify (double zone of hemolysis, lechithinase production test on egg yolk agar)
-treatment: surgical debridement, antibiotics, hyperbaric oxygen
Clostridium perfringens (Enterocolitis)
-epidemiology: C.perfringens type A (alpha toxin = lecithinase), food poisoning
-pathogenesis: ingest org  multiplication  sporulation  enterotoxin release
-clinical manif: food poisoning, diarrhea, abdominal pain, no vomiting, no fever
-no diagnosis/treatment, just food poisoning
Clostridium perfringens (Enteritis Necroticans)
-epidemiology: C.perfringens type C (alpha & beta toxins), New Guinea pig feasts,
-predisposing factors: low intestinal protease, sweet potato staple diet
-prevention: actively immunize (beta toxoid)
Clostridium botulinum
-epidemiology: intoxication, spores (very heat resistant), contaminated food (home canned food, preserved food, fish, Alaskan beached whales)
-toxin: neurotoxin (blocks ACh release  flaccid paralysis), 7 immunologically distinct toxins, bacteriophage mediated
-pathogenesis: food poisoning, wounds, infants (toxin in intestines  constipation, neck paralysis  floppy baby), inhalation
-immunity: no natural immunity, active immunity w/5 of the most common toxins
-clinical manif: nausea, vomiting, diarrhea (early), constipation (later), CNS
-diagnosis: symptoms, presence of toxin, isolation & identification
-treatment: horse antitoxin, antibiotics
-therapeutic uses: dystonias, strabismus, migraine headaches, botox
Clostridium tetani
-epidemiology: ubiquitous, in U.S. see it in elderly, rural south & drug addicts b/c not current on booster shots, worldwide see it more in infants b/c mothers not vaccinated so infant doesn’t have transplacental immunity & no normal flora
-pathogenesis: wound contamination, not invasive (unlike C.perfringens)
-toxins: tetanolysin, tetanospasmin (plasmid encoded neurotoxin – blocks release of GABA & glycine, inhibitory NT’s)
-clinical manif: generalized: risus (lock jaw), opisthotonous (whole body spasms), localized: twitching around wound area, neonatorum: infection of umbilical stump
-treatment: surgical debridement, passive immunization (human tetanus immune globin), active immunization (tetanus toxoid), antibiotics (Metronidazole)
Clostridium difficile
-epidemiology: antibiotic-associated intestinal disease, very common in hospitals
-pathogenesis: if come in contact w/spores when on antibiotics  multiplies in intestinal tract  makes toxins
-toxins: Enterotoxin (toxin A), Cytotoxin (toxin B)
-clinical manif: diarrhea w/o colitis, non-specific colitis, pseudomembranous colitis
-diagnosis: sigmoidoscopy, isolation & identification, toxin demonstration
-treatment: discontinue antimicrobial agent, switch to another antibiotic
Treponema pallidum
(card 1 of 2)
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-causes Syphilis via (1) sexual contact (doesn’t survive well outside host), (2) congenital (crosses placenta or contact while passing through birth canal, White Pneumonia), (3) blood transfusions, (4) direct innoculation (contact w/secondary lesions in mouth by dentists)
-virulence: hyaluronidase (spreading factor, destroys CT), fibronectin coating (prevent phagocytosis), outer membrane proteins, multiplies extremely quickly
-clinical manif: “the great imitator” b/c mimics symptoms of many diseases, host response causes the symptoms not the org itself
Treponema pertenue
(Yaws)
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-transmission: contact w/skin lesions, children come into contact w/open lesion  infected  spreads to skin & bones  cripples bones
Treponema carateum
(Pinta)
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-transmission: contact w/skin lesions, children
-causes secondary skin lesions, skin depigmentation, disfiguring
Treponema syphilis var. endemic syphilis
(Bejel)
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-transmission : oral mucosal lesions (kissing, sharing utensils), children
-causes primary mouth lesion, secondary skin & oral lesions, late granulomatous lesions on skin, nasopharynx, & bones
Borrelia
(Relapsing Fever)
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-only one that can grow in vitro is Leptospira
-louse-borne: B.recurrentis, more severe
-tick-borne: B.hermsii, B.turicatae, B.parkerii
-pathogenesis: incubation  febrile illness  afebrile period  febrile again  afebrile, org changes antigenicity b/w relapses, each relapse becomes less severe & eventually host response eliminates the organism
-diagnosis: Borrelia in blood in febrile stage
-treatment: Tetracycline, Erythromycin, Jarisch-Herxheimer Reaction (very high fever)
Borrelia
(Lyme Disease)
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-only one that can grow in vitro is Leptospira
-epidemiology: tick-borne, white-footed mouse, white-tailed deer, B.burgdoferi, B.garinii, B.afzelii
-clinical manif: primary stage (erythema chronicum migrans = bull’s-eye lesion), secondary stage (skin rash, arthritis, CNS & heart), tertiary stage (severe arthritis)
-diagnosis: immunofluorescence antibody
-treatment: antibiotics
Leptospira interrogans
-spiral-shaped, non-sporulating, motile, can’t classify as gram (-) or (+) b/c don’t stain well
-staining: biological stains (Borrelia), silver, darkfield microscopy, fluorescent microscopy
-only one that can grow in vitro is Leptospira
-epidemiology: animal reservoir, survives well in environment, org concentrated in bladder
-pathogenesis: penetration  subclinical leptospirosis  aniteric leptospirosis (first stage: flu-like symptoms, afebrile period, second stage: Fort Bragg Fever, Swine Herd’s Disease, conjunctivitis)  icteric leptospirosis (Weil’s Syndrome, infectious jaundice, first stage, afebrile period, second stage: kidney & liver disease)  immunity (serotype specific)
-diagnosis: darkfield examination (of blood, CSF, urine), isolation, serologic tests
-treatment: antibiotics, vaccinate livestock
Legionella pneumophila
-gram (-) rods, stain w/silver, single flagella
-clinical manif: Pontiac Fever (abrupt onset fever, chills, headache, myalgia) which can progress to Legionnaires Disease (severe pneumonia, more common in pts over 50),
-transmission: air conditioning units, summer
-virulence: cytotoxin stops oxidative burst inside macrophage so it can survive inside, also makes beta-lactamase
-high-risk pts: smokers, COPD, alcohol, immunosuppressed, dialysis, renal transplants
-diagnosis: fluorescent antibody, culture
-treatment: Erythromycin
Bartonella bacilliformis
-gram (-) rods, aerobic, fastidious (humid, ↑CO2, long incubation), animal reservoirs
-clinical manif: Bartonellosis (acute febrile disease), starts as Oroya fever (acute fever & anemia), followed by Verruga (chronic small skin eruptions of reddish-purple nodules)
-transmission: bite of infected sand fly
-endemic: Peru, Ecuador, Columbia
-pathogenesis: bite  org in blood  enters RBCs  anemia (oroya fever)  verruga
Bartonella quintana
-gram (-) rods, aerobic, fastidious (humid, ↑CO2, long incubation), animal reservoirs
-clinical manif: “Five Day Fever” (WWI), severe headache, extreme weakness, tibial pain, subacute bacterial endocarditis (SBE)
-transmission: person-to-person via human lice
-causes bacillary angiomatosis (vascular proliverative disease) when it infects bones, skin, & subcutaneous tissue (AIDS patents)
-treatment: Gentamycin
Bartonella henselae
-gram (-) rods, aerobic, fastidious (humid, ↑CO2, long incubation), animal reservoirs
Bartonella henselae
-causes bacillary angiomatosis but it infects lymph nodes, skin, or liver & spleen (peliosis hepatis) unlike B.quintana, also causes SBE and cat-scratch disease (usually benign in children, chronic regional adenophaty)
-treatment: Gentamycin
Mycoplasma pneumoniae
-bacteria w/o cell walls, capable of self-reproduction, requires sterols for growth, pleomorphic, stains poorly (b/c no cell wall)
-causes Primary atypical pneumonia (PAP)
-clinical manif: fever, nonproductive cough, headache, no response to penicillin (b/c no cell wall), has cold agglutinins (antibodies that agglutinate RBCs in at 4oC)
-epidemiology: children & young adults, illness is more severe w/inc age so think that part of illness due to delayed type hypersensitivity reaction from host response
-replication: polar P1 adherence structure replicates and moves to other end of cell  cell divides into 2  identical sister cells
-colony morphology: microscopic size, fried egg appearance (high pop density in center = egg yolk), can produce satellite colonies
-treatment: kanamycin, tetracyclines (resistant to penicillin & sulfonamides), easily killed by soap & H2O or by saline
Mycoplasma hominus
-bacteria w/o cell walls, capable of self-reproduction, requires sterols for growth, pleomorphic, stains poorly (b/c no cell wall)
-causes postpartum fever, pelvic inflammatory disease, pyelonephritis
Mycoplasma genitalium
-bacteria w/o cell walls, capable of self-reproduction, requires sterols for growth, pleomorphic, stains poorly (b/c no cell wall)
-causes nongonococcal urethritis (NGU)
Ureaplasma urealyticum
-bacteria w/o cell walls, capable of self-reproduction, requires sterols for growth, pleomorphic, stains poorly (b/c no cell wall)
-requires urea for growth, produces urease, breaks down urea for energy
-causes nongonococcal urethritis (NGU)
Treponema pallidum
(card 2 of 2)
-diagnosis: symptoms, microscopy, serologic tests, can’t gram stain, can culture in vitro
-serologic tests: start w/non-Treponemal test (Rapid Plasma Reagin, if infant w/IgM against treponeme  infected b/c IgM doesn’t cross placenta), can have false positives so verify with Treponemal tests (fluorescent antibody, hemeagglutination, ELISA)
-treatment: penicillin, Jarisch-Herxheimer Rxn (pt being treated gets really high fever due to RBC lysis  releases LPS endotoxin)