LEPTOSPIRA INTERROGANS: Spirochete

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SPIROCHETEMIAS
LEPTOSPIRA INTERROGANS: Spirochete

Epidemiology / At Risk: Zoonotic.
Chronic animal carriers disseminate bugs in the urine.
Infection through breaks in skin or mucosa, or by ingestion.
Manifestations: Leptospirosis
Bacteremia: bugs circulate and produce disfunction in:
Liver: Jaundice, hemorrhage
Kidneys: Uremia
CNS: Aseptic meningitis (from immune complexes in CSF)
Organisms replicate in endothelial cells in the CSF.
Symptoms: fever, chills, myalgia, headache, vomiting.
Last about a week than rash follows.
Processing:
Specimen:
Blood especially in the first 7 days (during Spirochetemia)
Urine after first 7 days
CSF
Stain: Dark Microscopy: long, thin spirochetes. Two axial filaments per pole, with a hook or loop at end.
Culture: Takes 1-2 weeks.
Identification:
beta-Hemolytic
19 serogrops. 140 variations. A lot of cross-reactivity.
IgM titer therefore must be greater than 1:100.
Serology:
Screening (not specific due to cross-reactivity): Check for agglutination between formalin-killed bugs and patient serum.
Specific: Use live organisms and check for agglutination.
Virulence:
Cell-wall Lipids: ~25% of dry weight of cell. Accounts for endotoxin-like fever, chilld, headache.
Hemolysin: Heat-labile. Anti-phagocytic and responsible for beta-hemolysis.
Surface-Antigens: Induce host antibody and complement.
Host Immune Response:
IgM appears after 1 week and lasts for months.
IgG appears after 1 month and lasts for years.
Vaccine / Prevention:
Dog: Prevents chronic kidney infection and shedding of organisms in urine.
Sewer-Workers: At-risk population for the serovariety-specific vaccine for humans.
BORRELIA RECURRENTIS: Large spirochete, visible on light microscope

Name-Derivation: Recurrentis = relapsing-fever
Epidemiology / At Risk: Rodents and small animals are reservoires.
Head-Lice (Louse): Common vector. Prevention = get rid of head lice.
Transmitted by crushing lice when we scratch.
Tick: Another vector that carries B.Hermsii, similar to this bug. Bacterium is introduced upon biting by the tick.
Manifestations: Relapsing Fever. Bugs go straight to the blood.
Incubation time: 1 week
Spirochetemia:
Fever, chilld, headache, myalgia
Possible hepatosplenomegaly
Flu-like symptoms
Fever returns 1 to 2 weeks later, and cycle repeats 2 to 3 times.
Processing:
Specimen: Blood
Stain: Giemsa or Wright stain is most effective.
However it stains Gram-negative and is visible under light microscope
Darkfield: Shows cokscrew motility and 15-20 axial filaments per pole.
Culture: It can be cultured, but it is difficult. 7 - 14 days.
Identification: Culture
Microaerophilic
Virulence:
Antigenic Shift in vivo is responsible for the Relapsing Fever. Continuous antigenic shift of outer membrane proteins.
Host Immune Response: Antibody + Complement is protective.
Vaccine / Prevention: Prevention of lice in schools.
Treatment: Broad-spectrum
BORRELIA BURGDORFERI: Spirochete

Name-Derivation: Lyme = town in CT; Burgdorf = Researcher
Epidemiology / At Risk: Zoonotic
Vector = Deer Tick bin nymph (agressive) stage.
Host = Deer
Prevelant in Summer, outdoors.
Manifestations: Lyme Disease. Incubation of 3-30 days.
Early: Skin lesions; erythema chronicun migrans. Rash, necrotic in center, and grows. Then it clears. Most common manifestations.
Later: Appear to be immunological sequelae.
Neurological: Next most common manifestations in U.S.
Headache, encephalitis, Bell's Palsy.
Cardiac: Common manifestations in Europe.
AV-block, myocarditis
Rheumatoid: Non-erosive migratory arthritis (non-supparative)
Systemic spirochetemia symptoms can also be found: malaise, fatigue, fever, etc.
Processing:
Specimen: Blood
Stain: Giemsa or Wright stain.
Darkfield:
Motility Slower than B. Recurrentis
7-11 flagella at each pole -- not axial filaments.
Culture: Enriched Selected Kelly's Medium. Enriched with fatty acids, but it's still difficult to grow.
7 days
Identification:
Microaerophilic
Virulence:
Outer Membrane Proteins A & B: Polyclonal mitogenic antigens of B-Cells.
Antigenic shift seen in vivo.
Polyclonal B-Cell activation is probably responsible for the immunological sequelae.
Host Immune Response:
Lots of antibodies
Very few PMN's, because the bugs are so long that you cannot suck them up.
Bugs are presumably killed by antibody + complement.
Treatment: Penicillin

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