Zoonotics Flashcards
Lyme: agent, what spreads it,
borrelia burdoferi (spirochete). transmitted by deer tick.
clinical manifestation of Lyme disease
7-10 days after tick bite, see erythema migrans (target rash). may be as late as 30 days post bite.
then, if undetected, you may see multiple erythema migrans lesions or may get flu symptoms (fever, arthralgia, headache, meningitis). May see cranial nerve deficits, esp. Bell’s Palsy. may see cardiac condition problems and heart block. monitor carefully- but these shouldn’t persist and don’t require long-term pacemakers.
late disease involves arthralgias and arthritis and CNS invasion with COGNITIVE DIFFICULTIES, fatigue, and mood issues.
Diagnosis of Lyme disease
erythema migrans in kids and adults in endemic areas. Perform an EKG and an LP if pt has neuro deficits other than Bell’s Palsy.
In later disease, do antibody testing if you have a strong clinical suspicion of Lyme. Must to IgM and IgG Elisa plus a western blot. in positive cases you will see 2/3 positive IgM and 4/7 positive IgG bands. antibodies may persist for a long time and don’t indicate treatment failure.
Treatment of Lyme: prophylaxis
singe dose of doxy for adults and kids >8 if it can be started within 72 hrs and the tick was attached at least 36 hrs and the local borrelia burgoferi pop is infected at a rate of at least 20%.
treatment of lyme with erythema migrans
doxycyclin 14 days if no neuro or heart problems are found
treatment of Lyme with cardiac complications or radiculopathy/meningitis or late disease
also start ceftriaxone with pts hospitalized for cardiac problems. give IV ceftriaxone on late stage Lyme for 2-4 wks and to adults with neuro disease like meinigitis or radiculopathy for about 14 days.
2 forms of ehrlichia
- Human monocytic ehrilichia. transmitted by lone star tick and infects monocytes and macrophases.
- human granulocytic anaplasmosis (HGA) by deer tick
pathogenesis of ehrlichia
HME infects monocytes and macrophoages and prevents fusion with lysozomes. see morulae
HGA infects neutrophils. both invade the bone marrow and block leukocytes, RBCs, and platelets. incubation is about 7 days and begins with a flu-like prodrome. Both cause thrombocytopenia
HME: what does it cause
resp probs, renal probs, and meningoencephalitis. thrombocytopenia and increased transaminases.
HGA: what does it cause
infects neutrophils. may have resp. problems, rhabdomylolysis, leukopenia, and left shift. thrombocytopenia and increased transaminases. won’t cause meningoencephalitis.
Dx of HME and HGA
look for morulae, serology, PCR
Tx of HME and HGA
doxycycline, even in kids and preg women.
Rocky mountain spotted fever: organism that causes it, vector, location
most common in North Carolina
caused by Rickettsia rickettsia
obligate intracellular gram negative coccobaccilli
gain entry through phagocytosis and may survive in phagocytic vessels or in the cytoplasm (unlike ehrlichia). spread by dogtick vector.
rocky mountain spotted fever pathophysiology
enter through dogtick bite after tick has fed to engorgement. then disseminates throughout the bloodstream. often invades the vascular endothelium. causes vasculitis of the lungs, heart, and CNS. may see hemorrhagic areas.
Rocky Mountain Spotted Fever: results of the pathophysiology (vasculitis)
thrombocytopenia from platelet consumption
increased vascular permeability and fluid leakage leading to edema and shock
renal failure in severe cases
Clincal presentation of Rocky Mountain Spotted Fever
2-14 days post bite from dogtick.
flu, then rash within 5 days: macular, then petechial. sen first on extremities, even palms and soels.
treatment for Rocky Mountain Spotted Feve
doxycycline, even if this is a child or preg lady
Q fever: source and disease
mostly from farm animals; some from cats and dogs
enters through the lungs. bacteria eaten by alveolar macrophages, gows in the phagolysosome, then spreads to the liver, where it makes a granuloma. Also can spread to heart valves in people with damaged heart valves. 3 wk incubation. usually causes mild initial symptoms but can occassionally cause ARDS, liver problems, and fetal demise.
Dx and Tx for Q fever
Dx by culture in BL3 facility
Tx with doxy. maybe fluoroquinilones, esp. as a combo for endocarditis.
Rabies
enters and spreads up nerves in a retrograde fashion. incubation depends on innoculum and wound site. p
rabies presentations
shooting pain in the limb. then, one of three forms:
- encephalitic with fever, hydrophobia, aerophobia, laryngeal spasms, hyperactivity, coma, and death.
- paralytic form: flaccid paralysis, death
- atypical form (usually from bats): neuropathic pain, choreiform movements, brainstem signs, coma, death
Dx and tx of rabies
Dx: specimen and antibody testing, neck biopsy, negri bodies seen post-mortem
Tx: none. must prophalax before it gets to CNS. Give shots on days 0,3,7, and 14. and give RIG around the site of the wound on day 0.
Leptospirosis: what is it, vecto, disease
spirochete from dog, rodent, amphibian pee
gets in through cuts on skin or pulmonary invasion. goes to lymphatics and bloodstream.
5-14 day incubation
usually mild and self-limiting.
biphasic disease:
1. fevers, photophobia, myalgies, nausea, vomiting, conjunctivitis. resolution.
2. may be followed by photophobia, stiff neck, lymphadenopathy, hepatosplenomegaly.
What do we see in severe leptospirosis disease? Treatment?
Weil’s disease: hemorrhage, jaundice, and renal failure. treat with penicillin
