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67 Cards in this Set
- Front
- Back
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Borrelia Burgdorferi (lyme disease) specs
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spirochete; flexible, motile bacterium; grown in Barbour, Stoenner, Kelly (BSK) medium; outer proteins OspA and OspB prominent antigens; transmitted via black-legged ticks (Ixodes scapularis and pacificus)
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reservior of Borrelia Burgdorferi
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rodents; white-tailed deer
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where do Borrelia Burgdorferi spirochetes live
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tick midgut whre 'activated' by blood meal, migrate to salivary glands where they innoculate host (takes 48-72 hours total)
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what causes erythema migrans with tick bite infected with Borrelia Burgdorferi
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cutaneous migration of spirochetes outward from bite
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treatment of Borrelia Burgdorferi infection
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doxycycline or amoxicillin (kids)
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disseminated infections of Borrelia Burgdorferi treated with
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IV cefriaxone for arthritis or meningitis
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endemic diseases in Africa that cause periodic fever
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malaria and trypanosomiasis
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Plasmodium falciparum (malaria) specs
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coccidian protozoal agents; 4 infective species (falciparum, ovale, vivax, and , malariae);
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Ring phase of Plasmodium falciparum
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early dvlp stage of asexual erythocytic parasite; ring-shape around central vacuole
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Trophozoite in Plasmodium falciparum
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losses ring shape and accumulates pigment
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trophozoite in vivax
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ameboid in shape and enlarged infected RBC contains numerous 'Scheffner dots'
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Schizont stage of Plasmodium falciparum
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late dvlp stage; division into merozoites and is characterized by multiple contiguous chromatin dots
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Gametocyte stage of Plasmodium falciparum
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sexual erythocytic stages; female macrogametocyte and male microgametocyte
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thick film
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RBCs lysed, and WBC, platelets, and parasites visible; doesn't differentiate malaria from babesia
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thin film
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morphologic features visible to differentiate malaria from babasia and definitive species ID possible
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what helps differentiate species of malaria on thin film
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1) number if intraerythocytic parasites 2) morphologic characteristics (crescent shaped gametocyte in falciparum) 3) degree of parasitemia (Heavy >10% = falciparum)
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how common are each of the malaria species
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vivax and falciparum = >95%; malariae ~4%; ovale extremely rare
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lifecycle of malaria
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Anopheles mosquito inoculates sporozoites into host; they infect liver and mature into schizonts, which transform into merozoites released from liver to invade RBCs; attach to Duffy on RBCs, feed on hemoglobin and other proteins and mature into trophozoites; nuclear division to form 16-32 parasite nuclei (schizonts), RBC ruptures, and schizonts pinch off to form new merozoites which infect new RBCs
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malaria energy usage
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derived solely from glucose and metabolize 70 times faster than RBCs-cause hypoglycemia and lactic acidosis
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why is falciparum infection more severe
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infect young, middle-aged, and old RBCs
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treatment of malaria depends on
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infecting species, geographic area where aquired, and severity of disease
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3 R's associated with management of malaria
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recrudescence (controllable # remain in blood stream due to inadequate immune response/antimalaria therapy, can reactivate on trauma or immunosuppression); relapse (dormant in liver-hypnozoites with vivax); resistance
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what kills intrahepatic organisms in malaria
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primaquine
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Riskettsia riskettsii (Rocky mountain spotted fever or RMSF) specs
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small, obligate intracellular bacteria-structurally similar to gram-neg rods; energy dependent; E and SE US; hard tick vector and dogs; 4-6 hours tick feeding required b4 activated and infectious
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where do Riskettsia riskettsii live and multiply
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within cells that line small to medium sized blood vessels; escape rapidly from phagosome and replicate in cytoplasm
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how do Riskettsia riskettsiis spread
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polarized actin polymerization of host cells
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what causes characteristic spotted (petechial) rash of Riskettsia riskettsii
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damage to vessels and leakage of blood into skin
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hypotension and hypoproteinemia in Riskettsia riskettsii
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loss of plasma into tissues and can lead to reduced perfusion of various organs and organ failure
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treatment of Riskettsia riskettsii
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Doxycycline for adults; Chloramphenicol for kids<8 and pregnant women
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Leptospira interrogens specs
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long, thin, motile spirochetes with characteristic hooked ends; viewed via darkfield microscopy; gram-neg cell wall; >200 serologic variants; blood cultures 7-10 days, only from urine thereafter
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Leptospira interrogens is aquired via
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indirect contact with urine of infected animals often through water exposure
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most important features of Leptospira interrogens pathogenesis
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hooked ends (adhesion factor), two periplasmic flagella that permit burrowing into tissues, and cellular toxicity
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phases of Leptospira interrogens infection
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multiply in blood causing bacteremia; secondary 'immune' phase involving immune-complex-mediated vasculitis (skin rash and vasculitis); systemic inflammatory response
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Weil syndrome
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severe hemorrhages and hypotension due to vascular collapse
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treatment of Leptospira interrogens
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mild-oral doxycycline; hospitilized-IV penicillin
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Pasteurella multocida specs
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short gram-neg rods; bipolar staining; fastidious-require chocholate agar for growth; oxidase pos and encapsulated; harbored in mouth of cats and dogs
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what in Pasteurella multocida triggers inflammation accompanied by purulent drainage
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capsule and endotoxin
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when do signs/symptoms of Pasteurella multocida appear
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within 2-12 hours after bite: pain, reddening, swelling
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treatment of Pasteurella multocida
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penicillin G
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widened mediastinum can be characteristic of
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histoplasmosis and inhalation anthrax
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Bacillus anthracis specs
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large, gram-pos, nonmotile, spore-forming rods found in chains; encapsulated, capsule of poly-D-glutamic acid; aerobic; colonies have ground-glass appearance and are nonhemolytic, nonpigmented, edge-irregular with commas projections
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risk for airborne infection with Bacillus anthracis is determined by
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virulence of the organism and balance btwn infectious aerosol production and removal, pulmonary ventilation rate, duration of exposure, and host susceptibility factors
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anthrax spored
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1.5-3 um; incubation 1-6 days; macrophages carry spored to nodes where Bacillus anthracis finds favorable milieu for growth and germination
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3 virulence factors of Bacillus anthracis
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antiphagocytic capsule and 2 toxins: 3 proteins (lethal factor, edema factor, and protective antigen) make up the 2 toxins
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edema toxin
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calmodulin-dependent adenylate cyclase
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lethal toxin
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specific endopeptidase that cleaves the kinase family of proteins and interferes with intracellular signaling; targets macrophages causing hemorrhagic necrosis in lymph nodes and release of Bacillus anthracis
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what occurs once Bacillus anthracis are released from lymph nodes
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gain acess to vascular circulation and multiply; nonspecific flu-like illness dvlps
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what causes an overwhelming mediastinal edema in Bacillus anthracis
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intracellular cAMP produced by edema factor (EF); chest x-ray shows widening of mediastinum with pleural effusions without infiltrates
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treatment of Bacillus anthracis
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ciprofloxacin or doxycycline IV
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Yersinia pestis specs
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nonmotile, nonspore-forming, gram-neg, bipolar, ovoid, 'safety-pin shaped' bacterium; grow well on standard media-gray-white to slightly yellow opaque with raised fried egg morphology; oxidase neg, ferment glucose, and reduce nitrates to nitrites
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reservoir of Yersinia pestis
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wild rodents, carnivores, and domestic cats and dogs; transmitted via flea bites
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3 clinical forms of Yersinia pestis (plague)
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1) bubonic (infection of lymph nodes) 2) septicemic (blood-stream infection-deadliest) 3) pneumonic
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virulence factors of Yersinia pestis in addition to antiphagocytic F1 glycoprotein
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protease (activates plasminogen and degrades serum complement); coagulase, and and exotoxin (adrenergic antagonist)
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what do DIC and cascular necrosis result from in Yersinia pestis
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systemic inflammatory response syndrome in septicemic plague
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treatment of Yersinia pestis
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streptomycin; gentamicin, tetracycline
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what should ppl exposed to Yersinia pestis be treated with
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chemoprophylaxis with tetracycline for 1 week
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Brucella melitensis specs
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4 species (abortus, melitensis, suis, and canis); poorly staining, small, gram-neg coccobacilli, seen mostly as single cells and appearing like 'fine-sand'; viable for >40 days in moist soil; facultative intracellular
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colonies of Brucella melitensis on blood agar
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small, convex, nonhemolytic, and translucent
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infective dose and incubation of Brucella melitensis
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<100 organisms; 5 days-6 months
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how do Brucella melitensis avoid phagocytic killing
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suppression of myeloperoxidase/H2O2-halide system and production of superoxide dismutase
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treatment of Brucella melitensis
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doxycycline and either streptomycin or rifampin for at least 6 weeks
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Franciesella tularensis specs
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poorly staining, very tiny Gram-neg, nonmotile coccobacillus, seen mostly as single cells; thin layer of polysaccharide capsule; difficult to culture
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reservoir of Franciesella tularensis
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wild animals (rabbits, hares, muskrats, deer) and some domestic animals
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infections of Franciesella tularensis are aquired via
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bite of infective ticks and direct contact with infected animal tissues through skin abrasions
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infective dose and incubation of Franciesella tularensis
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10-50 organisms; 3-5 days erythematous papule appears, ulcerating in 2-4 days
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ulcer formed from Franciesella tularensis
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erythematous, indurated, nonhealing and has 'punched out' appearance at 1-3 weeks
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treatment of Franciesella tularensis
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streptomycin given for 7-14 days; gentamicin or doxycycline alternatives
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