Vectored Bacterial Infections Flashcards
reservoir
whatever life forms the pathogen is adapted to infect. the pool of hosts in which the pathogen is maintained
vector
transmits between individuals in the reservoir
borrelia burgdorferi (lyme disease) bacteriology
motile spirochete. flat-wave, not spiral. stainable with giemsa, silver stain, immuno fluorescence, and visible by standard microscopy. tick-borne on most common in US. small mammal reservoirs for nymphs, large mammals for adults. requires 24h attachment to transmit
b. burgdorferi pathogenesis
begins with injection by tick. asymptomatic clearance posible. 6 months, organism spread. get rash, anti-spirochete/autoantibodies raised. persistent skin infection established. after 1 yr, immune/neuro things happen. HLA-DR4 and HLA-DR2 lead to lyme arthritis. 90% of untreated/undertreated cases report some neuro sequelae. reinfections occur
b. burgdorferi exam stage 1
get history of outdoor activity. stage 1: erythema migrans expanding rashes at or near bite. bulls eye only in minority. rash around a still attached tick is hypersensitivity. flu-like constitutional symptoms. coinfection with erlichia or babesioa lead to high fever
b. burgdorferi exam stage 2
musculoskeletal and/or neuro symptoms. intermittent arthritis, episodes last about a week and recur. if in europe, may get blue rash on ear or nipple. also get ACA, fibrosing skin process on extremities. neuroborreliosis with cranial neuropathy, memingitis, or rarely encephalopathy may need MRI. rarely cardiac involvement: arrhythmia or transient block. rarely opthalmic symptoms
b. burgdorferi exam stage 3
chronic lyme disease. arthritis, subacute encephalopathy, chronic progressive encephalomyelitis, late axonal neuropathies, fibromyalgia, patient may recall earlier episodes of bell palsy, aseptic meningitis
b. burgdorferi diagnosis: Lab
serology, ELISA, and IFA can confirm exposure, but not until 6-8 weeks later. patients who got briefly available lyme vaccine will be seropositive. seropositivity remains long term, and is not useful for testing the cure. positive titers can be confirmed by western blot. seronegativity is pretty reliable. elevated synovial and spinal fluid cell counds may suggest current activity. organisms may be culturable from the tick. examine CSF if neuro symptoms. PCR can be used
what factor most complicates the development of a lyme vaccine
immunological: antibodies raised against lyme disease are not protective!
b. burgdorferi treatment
treat patients who present with erythema migrans. attempt empiric treatment of patients who are seropositive with symptoms unless pregnant. amoxicillin or doxycycline, or ceftriaxone, cefuroxime, axetil. 10-30 days. dont add steroids. Jarisch herxheimer reaction expected
relapsing fever bacteriology
louse-borne. From B. recurrentis, the vector is pediculus corporis. reservoir is humans. transmitted by louse curshing/inoculation by scratching. tick-borne are B.hermsii, turicatae, parkeri, duttonii, and others. reservoirs are many mammals and reptiles. usually transmitted by bite of infected tick.
relapsing fever pathogenesis
spirochetes access vasculature, disseminate to spleen, bone marrow, liver, lungs, kidney, and CNS. IL10 response and neutralizing antibodies clear sepsis, leading to fever. spirochestes vary surface antigens, and eventually come back. fever repeats. louse borne have average of 1 relapse, tick have 3 relapses average. tick-borne can mess with pregnancy
relapsing fever diagnosis: Exam
two or more episodes of 3-5 days of high fever, then a well week in between. in louse borne, also see jaundice, petechiae, hemoptysis, epistaxis, and CNS involvement.
relapsing fever diagnosis: Lab
peripheral blood smear: spirochetes visible by microscopy, with wright or giemsa stain if blood taken during febrile period. can also visualize with IF, dark field, wet mounts, silver stained biopsies. CSF: mononuclear pleocytosis. can be cultured in special liquid medium. PCR and ELISA available
relapsing fever treatment
tetracycline, doxycycline, erythromycin, penicillin G used in adults. erythromycin in kids and pregnant bitches. IV penicillin or ceftriaxone for meningitis. louse-borne takes one dose, tick-borne treat for 7-10 days. will see jarisch herxheimer rxn
rickettsial pathogens similarities/differences to borrelia
similar: arthropod vectors, mammalian reservoirs, tetracycline sensitivity. unlike: small cocci to short rods, intracellular replication
rickettsia bacteriology
very short rods. hard to stain. all (except Q fever) are vectored by arthropods. easily enter bloodstream and progress to bacteremia. obligate intracellular paracites. binary fission inside cells.
most rickettsia infect humans ______
by accident!
rocky mountain spotted fever pathogenesis
reproduce by binary fission only within host cells. invades and multiplies in vascular endothelium. virulence factors include OmpA and B (adhesion), type 4 secretion system (entry), phospholipase A2 (escape from endosome), ActA (actin-based cell-cell spread). rash happens when leakage from blood vessels occurs
rocky mountain spotted fever diagnosis/presentation
begins headache, fever, myalgia. vasculitis: rash begins on extremities and spreads to trunk. May progress to delerium, coma, DIC, edema, circulatory collapse. most common on east coast. lab diagnosis by immunochemical methods
treatment for rocky mountain spotted fever
doxycycline works so well that failed treatment suggests misdiagnosis. Chloramphenicol for prego people.`
mediterranean spotted fever
shows with eschars (red sores with black spots in middle). transmitted by dog tick, common in europe, africa, central asia. begins with eschar at site of bite. severe cases can arise in old, alcoholics, G6PD deficient. same treatments as RMSF
epidemic typhus
humans are normal host and reservoir. vectored by body louse, sometimes head or pubic lice. organisms come from previous human’s blood, multiplies in louse alimentary tract. bacteria multiply in vascular endothelium leading to vasculitis
epidemic typhus symptoms
abrupt onset of fever and chills. generalized lymphadenopathy. abrupt onset unremitting headache. macular, macropapular, or petechial rash on day 4-7. begins on trunk and spreads out, opposite of RMSF. CNS symptoms are dullness, delerium, coma. uncommon: deafness/nonproductive cough. untreated course 2 weeks, mortality from vascular collapse or pneumonia.
typhus patient history
louse bite, natural disaster or war, medical and military personnel, overcrowding, lack of personal hygiene. cold weather = epidemic typgus, warm weather = murine and scrub typhus
brill-zinsser disease
recrudescent typhus. mechanisms of latency and reactivation are unknown. less severe than initial course. risk factors include malnutrition and improper or incomplete antibiotic therapy. may be seen in US among geriatric patients who had typhus during WWII.
murine typhus
milder than epidemic typhus. accidental transmission to humans of cat/rat typhus. southern and southwest US
scrub typhus
humans are accidental hosts to leptotrombidium akamushi vector and O. tsutsugamushi bacterium. milder than epidemic. 60% eschar forms at bite site. regional lymph node and pulmonary involvement common (cough)
diagnosis of typhus
begin antibiotics before final confirmation. confirm with immunofluorescence assay or enzyme immunoassay or PCR.
treatment of typhus
doxycycline or chloramphenicol. for recrudescent disease, a second course of antibiotic therapy is usually curative. azithromycin and rifampicin have been shown to be effective in small trials conducted in areas with known doxycycline resistance (thailand).
E. chaffeensis bacteriology
tiny gram negative. obligate intracellular. reselmbles rickettsia. replicates in cytoplasm of white blood cells. forms clusters called morulae.
human monocytic ehrlichiosis symptoms
often asymptomatic. symptoms may appear a week after bite: severe headache, myalgias, fever, shaking chills, GI symptoms. elderly or immunocomproised are at risk for severe ehrlichiosis, may develop meningitis or disseminated intravascular coagulation. co-infection of two tick-borne pathogens transmitted by the same vector do happen.
human monocytic ehrlichiosis diagnosis
travel to endemic area, hiking. do a CBC (will see neutropenia, lymphocytopenia, or thrombocytopenia.) serum transaminases. morulae. confirm by PCR or immunostaining
human monocytic ehrlichiosis treatment
doxycycline immediately! fluoroquinolones may be effective, chloramphenicol is not!
human granulocytic ehrlichiosis and human granulocytic anaplasmosis
identified in wisconsin. clusters of small bacteria in neutrophils.
anaplasma bacteriology
small, gram neg. obligate intracellular. reside in early endosome of white blood cells. grow into morulae. ehrlichia, anaplasma, and C. pneumoniae only organisms known to grow within neutrophils. ehrlichia, anaplasma, and C. pneumoniae only organisms that grow in neutrophils
human granulocytic anaplasmosis diagnosis
present with fever, headache, myalgia, malaise, absence of skin rash. CBC shows penia of neutro, lympho, and thrombo. Serum transaminases. morulae. confirm by PCR or immunostain. rule out babesiosis and lyme.
human granulocytic anaplasmosis treatment
doxycycline. chloramphenicol is not effective, fluoroquinolones may be.
