Zoonotic Infections Flashcards
Pathogenesis of Rickettsia rickettsii
Injected into skin by dog and wood ticks in late spring and summer. Proliferates in skin, disseminates via bloodstream (transmitted via adult tick). Survives in host cell cytoplasm; spreads cell-to–cell, producing plaques of necrotic cells. Causes hemorrhage in skin, intestine, pancreas, liver, skeletal muscle, and kidneys.
Signs and Symptoms of R. Rickettsii
Incubation period is 2-14 days: Acute onset of nonspecific symptoms: fever, headache, malaise, myalgias, and nausea. Abdominal pain may mimic cholecystitis or appendicitis. Macular, petechial rash begins on ankles and wrists spreads to trunk 5 days after symptoms begin. Death w/in 8-15 days if treatment is not initiated w/in 5 days
Dx of R. Rickettsii
Presumptive dx must be made based on epidemiology and clinical manifestations, Culture not recommended. Skin biopsy w/ immunofluorescence staining has high specificity. (Not recommended if abx have been given)
Tx for R. Rickettsii
Doxycycline, Chloramphenicol for pregnant women
B. burgdorferi
Most common insect-borne disease in US, a microaerophilic spirochete
Pathogenesis of B. burdorferi
Expressed lipoproteins on surface help organism survive in hosts. Produces fibronectin-binding protein, flagellar antigen, and two heat-shock proteins that ccross-react w/ human proteins. Transmitted by nymph of the Ixodes tick. Moves from deer to white-footed mouse to humans (common in summer, in nymph stage of development). Begins in skin, and then disseminates. Induces cell-mediated and humoral immunity. Can survive for years in joint fluid, CNS, and skin of untreated humans
Signs and symptoms of B. burdorferi
(Primary, secondary, late and tertiary lyme disease)
primary disease:erythema migrans: (“target lesion”-Macular expanding erythematous lesion, central clearing). (Painless, can cause itching); Dissemination assoc. w/ small annular lesions and flu-like illness (secondary; early disseminated). In cardiovascular involvement, spirochetes infiltrate myocardium, causing conduction defects. Musculoskeletal complaints are most common: (late).Migrating arthritis and arthralgias. Acrodermatitis chronica atrophicans, chronic skin infection, contains spirochetes (tertiary)
Dx of B. burdorferi
Dx made by combination of epidemiology, clinical manifestations, and serology
Tx of B. burdorferi
Tx early disease w/ amoxicillin or doxycycline; Tx disseminated disease characterized by mild carditis (first-degree heart block) or 7th nerve palsy w/ doxycycline. Prophylactic antibiotics are recommended if small tick has been attached for >24 hours or if engorged tick is found
Etiology and transmission of Y. Pestis
Spread by rodent fleas; Ingested by PMNs and monocytes, able to replicate in monocytes. Produces acute inflammation and tissue necrosis. Spreads to regional lymph nodes, forming fluctuant buboes. Readily enters bloodstream.
Signs and symptoms of Y. Pestis
Fever, chills, weakness, and headache; and Bubo formation (very painful). W/in 2 -4 days, septic shock leads to peripheral gangrene and death
Dx of Y. Pestis
Gram stain of sputum or lymph node aspirate; cx usually require 48 hrs.
Tx of Y. Pestis
Streptomycin, gentamicin, or doxycycline
F. tularensisis
gram-negative coccobacilli usually spread cutaneously from infected rabbits, muskrats, beaver, squirrels, and birds (also tick bites!) Aerosolized form can be manufactured. Cell wall has high fatty-acid content; produces a LPS endotoxin that is considerably less potent than that produced by E. coli. An intracellular pathogen, induces acute inflamm and granuloma formation. LOW inoculum (10-50 organisms) can cause disease (very dangerous)
Signs and symptoms of Tularemia
Abrupt onset: fever, h/a, malaise, myalgias, abd pain, & diarrhea. Ulceroglandular form presents as a painful ulcer with raised borders and associated regional lymphadenopathy. Bronchopneumonia expected in bioterrorist attack (aerosol): similar to plague except cough is dry, hacking; hemoptysis is rare
Tx of Tularemia
Gentamicin
B. anthracis
aerobic gram-positive rod, nonhemolytic on blood agar plates. Under poor nutrient conditions, B. anthracis forms spores: Spores resist heat, high salinity, alkaline pH, and many disinfectants.
Signs and symptoms of B. antracis
Aerosolized form, spores enter lung, ingested by macrophages, and transported to mediastinum
c. Spores germinate in mediastinum, and bacteria produce three exotoxins:
i. Protective antigen binds host cell receptors, and allows entry of lethal factor and edema factor
ii. Lethal factor and edema factor paralyze immune system and cause cell edema and death
d. Natural transmission of disease occurs through infected animal products—for example, wool, goat hair, animal hides
e. Spores can be aerosolized as bioterror weapon. “Weaponized” anthrax transmitted by mail in 2001. Postal workers & other mail handlers at high risk
Inhalation Anthrax
FIRST phase p/w viral-like syndrome. No pharyngitis or rhinitis, but chest heaviness described. Tx can abort second lethal phase. SECOND phase follows after brief asymptomatic period, can include:
Sudden onset of severe respiratory distress, fever, tachycardia, and tachypnea. Thoracentesis reveals hemorrhagic fluid positive for B. anthracis on Gram stain and culture
TERMINAL stage, blood cx positive for anthrax bacilli. Death follows w/in 24h and can occur “in mid-sentence”
Cutanrous Anthrax
Usually single lesion develops on exposed area of body, an arm being most common. Develops 1-7 days after inoculation; begins as papule. Progresses 3-4 days to vesicle filled w/ organisms; margin edematous. Lesion then ruptures and forms black eschar. Not painful, but often itches. Spontaneously heals over several weeks, leaving scar
Tx of anthrax
Give IV ciprofloxacin, levofloxacin, or doxycycline. Combination therapy is recommended for seriously ill patient: add rifampin, vancomycin, imipenem, clindamycin, or clarithromycin to basic regimen.
