Bacterial Infections of Blood and Vasculature Flashcards

1
Q

What is a vector?

A

-transmits between individuals in the reservoir

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2
Q

What is a reservoirs?

A

-whatever life forms the pathogen is adapted to infect; the poor of hosts in which the pathogen is maintained

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3
Q

B. burgdorferi Bacteriology

A
  • motile spirochete
  • flat-wave shape, not spiral
  • stainable with giemsa, silver stain, IF, visible by standard microscopy
  • tick-borne (I. scapularis in East, I. pacificus in West), most common one in US, much more common on East Coast
  • highest risk in summer, when nymphs are feeding: many of them, smaller, people outside
  • small mammal reservoirs (white footed mouse, wood rat) preferred by nymphs, large mammal hosts (deer) preferred by adults
  • incidence in US is increasing due to expansion of deer herds; 20,000-30,000/yr; rate in Europe is similar
  • almost always requires 24h attachment to transmit
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4
Q

B. burgdorferi Pathogenesis

A
  • disease begins w/ injection of B. Burgorferi into host by tick.
  • asymptomatic clearance possible
  • over the next 6 months, organism spreads. Erythema migrans rash (75%), antispirochete/autoantibodies raised. Very persistent skin infection established
  • months to 1 yr after infection, immune and/or neurological issues arise. Lyme arthritis predisposed by HLA-DR4 and HLA-D2 genotypes and certain strains
  • post lyme- 80% of untreated/undertreated report some neurological sequelae
  • reinfections occur
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5
Q

B Burgdorferi Exam Stage 1

A
  • patient usually does not recall tick bite- get history of outdoor activity, not season and geographic location
  • erythema migrans expanding rashes at or near bite site, bulls-eye appearance in a minority
  • rash around tick = hypersensitivity, not Lyme
  • Flu-like symptoms, fatigue, muscle aches, regional lymphadenopathy, low fever
  • coinfection with erlichia or babesioa: high fever
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6
Q

B Burgdorferi Exam Stage 2

A
  • musculoskeletal and/or neurologic symptom
  • intermittent arthritis, episodes about a week and recur, knee most common
  • contracted in europe- blueish borrelial lymphocytoma on earlobe or nipple; also Acrodermatitis Chronica Atrophicans (ACA), a progressive fibrosing skin process on extremities
  • lyme neuroborreliosis with cranial neuropathy, meningitis, or rarely encephalopathy- MRI or CT
  • rarely cardiac involvement: arrhythmia or transient block
  • rarely ophthalmic symptoms
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7
Q

B Burgdorferi Exam Stage 3

A
  • chronic lyme disease
  • arthritis
  • subacute encephalopathy
  • chronic progressive encephalomyelitis
  • late axonal neuropathies
  • fibromyalgia
  • patient may recall earlier episodes of Bell palsy, aseptic meningitis
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8
Q

What are the labs for B. burgdorferi

A
  • serology, ELISA, IFA can confirm exposure but not current infection, also takes 6-8 weeks
  • patients who received the Lyme vaccine seropositive, seropositivity reamintains long term, seronegativity is reliable
  • equivocal-positive titers can be confirmed by Western Blot
  • biopsy of borrelial lymphocytoma or acrodermatitis might be useful
  • organism may be cultured from tick
  • Neuro symptoms= anti-Lyme IgM, IgG
  • PCR testine
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9
Q

What is the treatment for Lyme disease-

A
  • treat patient who present with erythema migrans
  • attempt empiric treatment of seropositive patients with symptoms unless pregnant
  • early lyme improves rapidly with antibiotics
  • amoxillin or doxycycline
  • no evidence of benefit from longer antibiotic courses
  • don’t add steroids for arthritis
  • Jarisch-Herxheimer reaction
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10
Q

What is the prevention of Lymes

A
  • avoidance
  • inspection
  • prophylaxis in some areas
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11
Q

What is the bacteriology of Louse-borne Relapsing Fever

A
  • pathogen: B. recurrentis
  • vector: Pediculus corporis- Louse
  • reservoir: humans
  • endemic to Africa, also seen in overcrowded homeless shelters
  • transmission: louse crushing/ inoculation by scratching (scratch and crush transmission- attachment, feeding, defecating, scratching, inoculation)
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12
Q

What is the bacteriology of tickborn bacteriology?

A
  • pathogens: B hermsii, B turicatae, B parkeri, B duttonii, others
  • vectors: soft-bodies ticks Ornithodoros spp
  • reservoirs: many mammals and reptires
  • transmission: bite of infected tick- usualy noctural, unnoticed
  • endemic to Western US, southern British Columbia, Mexico, Central and South America, Asia, Africa, Mediterranean region
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13
Q

What is the relapsing fever pathogenesis?

A
  • spirochetes across vasculature, disseminate to spleen, bone marrow, liver, lungs, kidneys, CNS
  • a strong IL10 response and neutralizing antibodies clear sepsis -> fever
  • spriochetes vary their surface antigens in response to immune selection, when a new pool predominates, disease resumes
  • fevered episodes repeat, lower fever and increasingly long breaks between as immune response improves
  • louse borne- average of one relapse, mortality 4% treated, 40% un-
  • tick borne- average 3 relapses, mortality <2% treated, 4-10% un-
  • tickborne causes complications of pregnancy: abortion, premature birth, neonatal death
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14
Q

How does relapsing fever show up on exam?

A
  • two or more episodes of 3-5 days of high fever with low blood pressure, then a well week between
  • also chills, arthralgias, nausea/vomiting, abdominal pain, mental status changes, nonproductive cough, diarrhea, dizziness, neck pain, photophobia, rash, and dysuria
  • in louse-borne, also jaundice, petechiae, hemoptysis, epistaxis, and CNS involvement
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15
Q

how does relapsing fever look on lab?

A
  • perpheral blood smear: spirochetes visible by microscopy with Wright or Giemsa stain if blood taken during febrile period
  • can also visualize bacteria with IF, darkfield, wet mounts, silver-stained biopsies
  • CSF: mononuclear pleocytosis
  • organism can be cultured from blood in special liquid medium, takes 2-6 weeks
  • PCR assay available
  • ELISA is available, better one in pipeline
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16
Q

What is the relapsing fever treatment?

A
  • tetracycline, doxycycline, erythromycin, penicillin G used in adults
  • erythromucin in children and pregnant/nursing women
  • IV penicillin or ceftriaxone for meningitis
  • louse-borne takes one dose, tick-borne treat for 7-10 days
  • Jarisch-Herxheimer reaction
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17
Q

How do you prevent relapsing fever?

A
  • prophylaxis with doxycycline may be recommended after exposure
  • tick-borne- avoid rodents, use protective clothing, DEET
  • Louse-borne- delousing- social policy, hygiene, 1% lindane, DDT powder, Lysol
18
Q

What are the Rickettsial Pathogens?

A
  • Rickettsia- The spotted fever group and typhus
  • Coxiella burnetti- previously called Rickettsia diaporica and burnetii, causes Q fever
  • Ehrlichia- human monocytic ehrlichiosis
  • Anaplasma
19
Q

How are Rickettsial Pathogens and Borrelia alike/unlick?

A

Like: Arthropod vectors, mammalian reservoirs, tetracycline sensitivity
Unlike Borrelia: small cocci-to short rods, intracellular replication

20
Q

What is the bacteriology of Rickettsia

A
  • very short rods
  • hard to stain Gram neg
  • all except Q fever are vectored by arthropods
  • easily enter bloodstream -> bacteremia
  • obligate intracellular parasites- must grow in tissue culture
  • Dermacentor veriabilis (dog tick) vector of Rocky Mountain Spotty Fever, Dermacentor andersoni in the Rocky Mountain region and Canada
  • mouse reservoir
  • for most Rickettsia, Q fever, Ehrlichia and Anaplasma, humans are accidental hosts (Exception Typhus)
21
Q

What is Rocky Mountain Spotted Fever Pathogenesis

A
  • rickettsia are obligate intracellular parasites: reproduce by binary dission only within host cells
  • RMSF invades and muliples in vascular endothelium
  • virulence factors:
  • OmpA and B adhesion
  • Type 4 secretion system: entry
  • phospholipase A2: escape from endosome
  • ActA: actin-based cell-cell spread
  • rash caused by damaged blood vessels
22
Q

How does Rocky Mountain Spotted Fever present?

A
  • the rickettsial disease most dangerous to previously-healthy patients
  • begins nonspecific: headache, fever, myalgia
  • vasculitis -> Rash, begins on extremities, spreads to trunk
  • rash is very common but not unviersal
  • may progress to delerium, coma, DIC, edema, circulatory collapse (18% untreated mortality)
  • actually most common on East coast (dog tick)
23
Q

What makes poor prognosis for Rocky Mountain Spotted Fever?

A
  • age >40 years

- antibiotic treatment delayed/absent

24
Q

What is the treatment for spotted fevers?

A
  • doxycycline works so well that failure suggests misdiagnosis, but unsafe in pregnancy
  • APP allows it for children
  • chloramphenicol for pregnant or allergic patients
  • prevention: protective clothing, insect repellent
25
Q

What is Mediterrean Spotted Fever?

A
  • transmitted by dog tick, common in Europe, Africa, Central Asia
  • rather than the body rash of RMSF, MSF begins with eschar at the site of the tick bite
  • other symtpoms are similar but less severe
  • severe cases can arise if predisposed: older age, alcholism, or GP6D
26
Q

What is epidemic typhus

A
  • unlike all other Rickettsia, humans are normal host and reservoir
  • vectored by body louse, sometimes head or public lice
  • organism comes from previous humans blood (rickettsemia), multiplies in louse alimentary tract
  • same kind of crush and scratch
  • louse eventually dies of infection (obstruction)
  • bacteria multiple in vascular endothelium (Same OmpA&B surface adherence as RMSF) -> vasculitis
27
Q

What are the symptoms of Epidemic typhus?

A
  • abrupt onset fever, chills
  • generalized lymphadenopathy
  • abrupt-onset unremitting headache
  • macular, maculopapular, or petechial rash occurs on days 4-7
  • may begin on the axilla and trunk and spread peripherally (RMSF rash begins on extremities and spreads centrally)
  • CNS symtpoms (meningoencephalitis) may include dullness, delerium, coma
  • less common: nonproductive cough, deafness
  • untreated course ~2 weeks, mortality from vascular collaspe or pneumonia (20-60% untreated)
  • several months may pass before complete recovery
28
Q

What is the typhus patient history?

A
  • louse bite
  • natural disaster or war
  • medical and military personnel
  • overcrowding
  • lack of personal hygiene
  • season: cold weather -> epidemic typhus, warm weather -> murine and scrub typhus
29
Q

What is Brill-Zinsser Disease

A
  • 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
30
Q

What is murine typhus?

A
  • flea-borne endemic typhus
  • milder than epidemic
  • accidental transmission to humans of cat/rat typhus
  • southern and southwest US
31
Q

What is scrub typhus?

A
  • humans are accidental host to the Leptotrombidium akamushi (chigger) vector and O. tsutsugamushi bacterium
  • milder than epidemic
  • 60% Eschar forms at bite site
  • regional lymph node and pulmonart involvement (cough) more common
32
Q

How do you diagnose typhus (all types)

A
  • begin antibiotics before final confirmation

- confirm with immunofluorescence assay or enzyme immunoassay or PCR

33
Q

How do you treat typhus

A
  • doxyclycline 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)
34
Q

How do you prevent typhus?

A
  • epidemic: hygiene and delousing militrary vaccine

- murine and scrub- protective clothing, insect repellent

35
Q

What is human monocytic ehrlichiosis?

A
  • caused by Ehrlichia chaffeensis

- human granulocytic ehrlichiosis also called human granulocytic anaplasmosis, is caused by Anaplasma phagocytophilium

36
Q

What is the bacteriology of E. chaffeensis?

A
  • tiny gram (-)
  • obligate intracellular
  • resemble rickettsia
  • replicate in cytoplasm of white cells
  • form clusters called morulae
  • reservoirs- white footed mouse, dog, white tailed deer
37
Q

What are the symptoms of Human monocytic ehrlichiosis symtoms?

A
  • infection often asymptomatic; most cases resolve without diagnosis
  • symptoms may appear a week after bite: severe headache, myalgias, fever, shaking chills, GI symptoms
  • elderly or immunocompromised patients are at increased risk for severe ehrlichiosis; may develop meningitis or DIC
  • co-infections of two tick borne pathogens transmitted by the same vector do happen (rule out babesiosis and Lyme disease)
38
Q

Diagnosis and Treatment of Human monocytic ehrlichiosis?

A
  • patient history: travel to endemic areas, hiking
  • CBC (neutropenia, lymphocytopenia, thrombocytopenia)
  • serum transaminases (often up in tickborne)
  • morulae
  • confirm by PCR or immunostaining
  • begin antibiotic without delay: doxycycline
  • chloramphenicol is not effective, fluoroquinolones may be
39
Q

What is Human granulocytic ehrlichiosis/anaplasmosis

A
  • identified in 1990 in a wisconsin patient who died with a severe febrile illness 2 weeks after a tick bite
  • clusters of small bacterial were noted within neutrophils
  • 13 cases with similar intraneutrophilic inclusions in the same region in 2 years
40
Q

What is the bacteriology of anaplasma?

A
  • small gram (-)
  • obligate intracellular
  • reside in early endosome of white blood cells
  • grow into morulae
  • ehrlichia, anaphasma, and C. pneumoniae only organisms known to grow within neutrophils
41
Q

How is human granulocytic anaplasmosis diagnosed

A
  • presentation: fever, headache, myalgia, malaise, absence of skin rash
  • patient history: travel to endemic areas, hiking
  • CBC (neutropenia, lymphocytopenia, or thrombocytopenia)
  • serum transasminases
  • morulae
  • confirm by PCR or immunostraing
  • rule out babesiosis and Lyme Disease
  • 5-7% of cases require intensive care
42
Q

How is human granulocytic anaplasmosis treated?

A
  • begins antibiotics without delay: doxycycline

- chloramphenicol is not effective, fluroquinolones may be