Bacterial Infections of Blood and Vasculature Flashcards
1
Q
What is a vector?
A
-transmits between individuals in the reservoir
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
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
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
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
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
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
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
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
10
Q
What is the prevention of Lymes
A
- avoidance
- inspection
- prophylaxis in some areas
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)
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
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
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
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
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
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
