Relapsing Fever Flashcards
Borrelia Recurrentis
Epidemic Relapsing fever
Louse Vector
Borrelia Spp.
Endemic relapsing fever
Tick vector
Relapsing Fever Characteristic
Antigenic variation
antigenic switching
- VIp
-Vsp
How does borrelia reoccur?
Interplay w/ immune system
VMP1
VMP2
Endemic Relapsing Fever
B hermsii carried by ornithodoros hermsii
B parkeri carried by ornithodors parkeri
Ornithodoros Hermsii
is a vector and reservoir Transvarial passage can live 15 years without feeding Reservoir Host- Rodents Multiple feedings, immediate disease transfer
Relapsing Fever Epidemiology
Peak season is outdoor season
Ticks nocturnal
Borrlia Recurrentis Epidemia
Reservoir Humans
Vector Human Body Louse
No transvarial
Infection process B recurrentis
Louse feed on sick human
ingests bug,
Louse evades the fever, and goes to new host
B recurrentis epidemiology
Does not occur in us
overcrowding
Borrelia Etiology
Gram neg Larger than burdogoferi gram or giemsa stains EXTRACELLULAR cultures BSK
3 stages of relapsing fever
Primary spirochetemia
Latent
Secondary spirochetemia
Primary Sprichetemia
Acute Onset Ends abruptly High fever hepatosplenomegaly CRISIS after first episode
Latent Phase
Afebrile- replication
NO ISOLATION FROM BLLOD BECAUSE IN ORGANS
Secondary Spirochetemia
antigenic variation relaps
eache relapse = ↓ severity and ↓ duration
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
- crossss mucous membranes
- enters bloodstream and tissue
- 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
- aseptic meningitis, fever stiff neck, most important
- Conjuctival suffusion
- 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
