thin spiral

visible w/ dark-field, silver impregnation, immunofluorescence

deficient in metabolic activity (glycolysis & TCA cycle); synthesizing essential AAs, lipids & NA

transmission: sexual contact w/ infected lesions; trans-placental

humans the only host

most cases: Sub-Saharan Africa, South America, South East Asia

not clear

rapidly penetrates intact mucosa-->enters lymphatics/blood => systemic infection w/in few hrs

3 stages of syphillis: 1*, 2*, 3*

pathogen: Treponema pallidum

progression: papule that erodes to painless ulcer w/ raised borders-->spontaneous healing ~2wks

mechanism: Tp replicates S/C @ site of entry => stim infiltration of CD4+/CD8+ T cells (into perivascular space) --> TH1 cytokine activates macrophages => kill most treponema in ulcerative lesion (leads to the spon healing)

*false sense of relief

mechanism: Tp --> lymphatics/bloodstream 

symptoms: whole body rash in 6-8 wks (maculopapular/pustular lesions) usually w/ diffuse lymphadenitis; sore throat, fever, wt loss, malaise, headache, acute meningitis, *enlargement of epitrochlear nodes

usually follows 2*, but possibly 1* syphilis

duration: 1-30yrs

mechanism: host is controlling treponemal replication & spread; Tp decr metabolism/generation time but NOT cleared

affected areas: any (arteritis, dementia, blindness); granulomatous lesions (gummas) likely in bones, skin & other tissues

disease presentation: depends on involved organ (neurosyphilis, cardiosyphilis, etc)

-trans-placental transmission rate ~100%

-perinatal death in >40% w/o tx

-organogenesis unaffected: no clinical signs @ birth

*fetus lacks inflammatory responses during first 4 mo of pregnancy

-2 types: 1. Early onset (disease manifests w/in first 2 yrs of life; similar to 2* w/o 1*; rhinitis, retarded wt gain, edematous appearance, severe anemia, widespread desquamating rash)

2. Late onset (usually non-contagious; Hutchinson's teeth, bone changes, saddle nose)

culture: hasn't happened yet in vitro

microscopy: exudates from 1* chancre under dark-field immediately; UV microscopy after stain w/ fluoresceinated anti-treponemal IgG

serology: specific antibody test (FTA-ABS & MHA-TP); non-specific serology tests (VDRL & RPR)

detection of Treponema pallidum using fluorescent antibody (fluorescent treponemal antibody absorption test FTA-ABS)

-pt serum absorbed w/ non-pathogenic treponemes before rxn w/ T. pallidum Ag

used in identification of Treponema pallidum

as non-treponemal antigen (eg cardiolipin)

VDRL=venereal disease research laboratory test

RPR=rapid plasma reagin test

*useful as screening (can give false+)

irregular spiral weakly gram- staining

twisting motility <= 7-20 periplasmic flagella

fastidious, long generation time

dx: history & serology

cause of 2 diseases: 1. relapsing fever 2. lyme disease

1. Louse borne epidemic relapsing fever (LBRF): caused by Borrelia recurrentis

2. tick born endemic relapsing fever (TBRF): caused by many species (Borrelia hermsil in N. America)

common to both forms:

-species --> antigenic shift => escape immune clearance

-progression: abrupt onset after ~1wk from exposure; shaking chills, myalgia, fever, 3-10 relapses; if extensive bact growth in speen/liver/kidney => serious illness

-single relapse=epidemic (louse borne)

-repeated relapses=endemic

identifying Borrelia recurrentis:

gram- spirochetes

seen w/ 70% of thick blood smears

serology ineffective (<= phase variation)

-bacterial pathogen: Borrelia burgdorferi

-epidemiology: human acquisition by tick bite; primary reservoir - white footed mouse

-most common insect-borne disease in US

-virulence factors: surface lipoproteins, FnBp, flagellar antigens, 2 HSPs (cross react w/ human protein)

-mechanism: replicate @ site --> extensive dissemination (can survive for yrs in joint fluid, CNS & skin of untx pt)

-3 distinct stages

primary lyme disease of Borrelia burgdorferi

after inoculation: spirochete multiplies locally in skin

1-4wks: slowly expanding circular erythematous lesion *erythema chronicum migrans (military target) -usually in axilla, behind knee, beltline (areas preferential to ticks)

represents dissemination of Borrelia burgdorferi

onset: days after onset of erythema migrans

symptoms: small annular lesion & flu-like illness; fever, myalgia, lymphadenopathy

-cardiovascular: Borrelia infiltrate myocardium (conduction defects)

-CNS: cranial nerve defect (Bell's palsy), peripheral neuritis

Borrelia burgdorferi

onset: mo-yrs after 1* disease

symptoms: musculoskeletal (migrating arthritis & arthalgia-Borrelia IgG rxn w/ host tissue proteins); encephalopathy (mood, sleep & congnitive disorders)

identification: high PMN count in joint fluid

gram- spirochete

rarely seen in skin biopsy (usually blood)

dx: clinical presentation & known exposure

serology: PCR, ELISA, western blot as confirmatory tests

-species: 1. Leptospira interrogans sensu lato (pathogenic) 2. Leptospira biflexa sensu lato (free-living)

-spiral w/ hooked end (like question mark)

-obligate aerobe, slow growth

-use darkfield or silver impregnation staining

-ingestion or exposure to contaminated food/water; rare human-->human transfer

-high risk: farmers, miners, sewage workers, water sports enthusiasts

pathogenesis not understood

enters through skin abrasions/mucous mem/mouth or throat/esophagus-->replicates w/in blood/tissues

*mainly infect kidneys & liver (other organs affected)

variable: mild anicteric disease --> fatality (Weil's disease:hemorrhage, severe jaundice, renal/liver failure)

incubation: 1-2wks

symptoms: many infected are asymptomatic

Weil's disease caused by Leptospira interrogans

-conjunctival hemorrhage (pathognomonic sign for leptospirosis)

icterus (jaundice): yellow epidermis & dark urine

very thin spirochetes w/ hook

serology: useful in detection in blood/CSF/urine