Relapsing Fever Flashcards by paul Leatham

Borrelia Recurrentis

Epidemic Relapsing fever

Louse Vector

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Borrelia Spp.

Endemic relapsing fever

Tick vector

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Relapsing Fever Characteristic

Antigenic variation
antigenic switching
- VIp
-Vsp

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How does borrelia reoccur?

Interplay w/ immune system
VMP1
VMP2

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Endemic Relapsing Fever

B hermsii carried by ornithodoros hermsii

B parkeri carried by ornithodors parkeri

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Ornithodoros Hermsii

is a vector and reservoir
Transvarial passage
can live 15 years without feeding 
Reservoir Host- Rodents
Multiple feedings, immediate disease transfer

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Relapsing Fever Epidemiology

Peak season is outdoor season

Ticks nocturnal

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Borrlia Recurrentis Epidemia

Reservoir Humans
Vector Human Body Louse
No transvarial

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Infection process B recurrentis

Louse feed on sick human
ingests bug,
Louse evades the fever, and goes to new host

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B recurrentis epidemiology

Does not occur in us

overcrowding

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Borrelia Etiology

Gram neg
Larger than burdogoferi
gram or giemsa stains
EXTRACELLULAR
cultures BSK

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3 stages of relapsing fever

Primary spirochetemia
Latent
Secondary spirochetemia

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Primary Sprichetemia

Acute Onset
Ends abruptly
High fever
hepatosplenomegaly
CRISIS after first episode

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Latent Phase

Afebrile- replication

NO ISOLATION FROM BLLOD BECAUSE IN ORGANS

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Secondary Spirochetemia

antigenic variation relaps

eache relapse = ↓ severity and ↓ duration

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Fatalities of relapsing fever

Rare in endemic

40% in epidemic

Immune response to relapsing fever

largely humoral
PMN phagocytosis
controlled when no longer evades system by switching
NO IMMUNITY TO REINFECTION

Diagnosis Relapsing Fever

Directly or Gram prep from blood
lumbar puncture if meningitis
Culture, mouse inoculation or BSK medium

Treatment and its complications

Doxycycline

Jarisch-Herxheimer response

Leptospirosis

acute zoonotic, NO VECTOR
HAWAII
Hosts: renal tubule
passed by urination
RODENTS

types of transmission of leptospirosis

Vertical and Horizontal

Patterns of transmission

Epidemic
Endemic
Sporadic

Leptospira interrogens

very thin tightly coiled

INTRACELLULAR PATHOGEN

Lepto ETIOLOGY

gram neg structure, microscop not DIAGNOSTIC
Darkfield microscope
EMJH medium for growth
Aerobic organisms SLOW GROWING

Lepto Characteristics

Sensitive to drying, disinfectants and acidic environments

Lepto Pathogenesis

1. crossss mucous membranes 2. enters bloodstream and tissue 3. OMP and Factor H binding Target organs Kidneys, Liver, Heart

Clinical Manifestations of Lepto

most infections subclinical Two anicteric stages 1. septicemic 2. Immune

Septicemic stage

``` last 4-7 days abrupt in onset flu symptom non specific isolated from blood fever recurs transitioning to second stage ```

Immune stage

immune response to microbe 0-30 days abs from blood microbe isolated from URINE

Specific organs of immune stage

1. aseptic meningitis, fever stiff neck, most important 2. Conjuctival suffusion 3. Renal symptoms

Icteric stage Weil syndrome

``` Most sever form MODS •Renal dysfunction •Hepatic necrosis •Pulmonary dysfunction •hemorrhagic diathesis ```

When to consider Leptospirosis

Fl u like disease w/ Aseptic meningitis or disproportionately myalgia

Diagnosis Lepto

1.Clinical finding consistent 2.Patient History • rats contaminated water other hosts 3. Culture Blood during septicemic stage Urine during immune stage 4. PCR amplification LEPTO CHECK MAT

Leptospirosis Treatment

Support | & Doxycycline