• Spriochaetaceae
  • Treponema
  • Borrelia
• Leptospiraceae
  • Leptospira

• Treponema pallidium pallidium- venereal syphilis
• Treponema pallidum pertenue- yaws
• Treponema pallidum endermicum- endemic symphilis (bejel)
• Teponema carateum- pinta

• regular helices
• ends pointed and lack of hoock shape appearance of commensal human spirochetes
• organism exhibit rapid rotation about axis (corkscrew motility)

• epidemiology- endemic in rural areas
• organisms morphologically, and antigenically indistiguishable but cause distinct clinical diseases
• like symphilis, disease char. by:
  • self limited primary and secondary phase, latent disease free period, destructive tertiary phase

• occurs in warm, humid areas (Africa, SE asia, South America)
• infection usually acquired in childhood

• transmission through skin contact
• blood stream invasion, following initial infection leads to involvment of bone, lymph nodes, and distant skin sites

• primary lesions on extremities
  • papules that enlarge w/ superficial erosions and then heal spontaneously
• months later, a generalized eruption of similar lesions occur with multiple remisions and exacerbations
  • assoc. w/osteitis of fingers, long bones, paranasal maxillae
• cutaneous plaques, nodules, gummatous lesions, ulcers occur in later phase with hyperkeratosis of palms, soles

• endemic in arid inland regions (S Mexico, central America, Columbia)
• transmit via skin contact
• organisms multiply locally and spread via blood and lymphatics

• initially, small pruritc, erythematous papules on face, neck, extremities, or chest and may persist for years
• months later, scaly papules appear, which may develop into brown, gray, blu lesions
• late phase- depigmentation lesions on wrists, elbows, ankles

• occur in africa, west asia
• transmit via skin contact, eating and  drinking utensils

• primary lesions- oral mucosal lesions
• secondary disease involve mucous patches, periostitis, adenopathy
• lat phase- gummatous lesions

• serological test
• dark field microscopy of fluid from lesion
• treat w penicillin

• highly motile, helical organisms
• outermembrane enclose periplasmic flagella and protoplasmic cylinider
• lack microtubles, which along with unsheathed flagella distinguish from Treponemes
• all are arthropod born, differ in vector, host species they infect and diseases they cause

• louse borne relapsing fever is cause by B. recurrentis, transmitted person to person via human body louse
• disease results from crushing lice, releasing organisms that penetrate skin
• endemic in E Africa, S America, catostrophic event areas

• caused by many species of Borrelia
• transmitted via soft ticks
• worldide distributions
• rodents are reservois, infection when saliva or excrement is released by the tick while feeding

• borreliae prsent in blood during febrile episodes, disappear when fever resolves, and return during subsequent fever
• during afebrile period, they are sequestered by inernal organs and reemerge Ag diff.
• cyclincal process of Ag variation and subsequent specific Ab production allows for relapsing nature

• bothy types: fever, headache, myalgia, athralgia, photophobia, cough, truncal rash
• on exam: conjunctival suffusion, petechiae, abdomnial tenderness, hepatosplenommegally
• neurological findings
• myocarditis, CNS hemorrhage, liver failure most common caues of death
• intensity of symptoms decrease with relapse
  
  Louse borne usually has single relapse

• demonstrations of borreliae in peripheral blood
• dark field microscopy
• Giemsa, Wright stain thin or thick disease

• tetracyclin for louse born (alt: erythromyc.) in single dose
• 5-10 day course due to rates ofrelapse

• Ixodes scapularis in NE, larvae and nymphs feed on rodents
• white footed mice
• adults who feed on larger mamanls
• Ixodes pacificus in west
• Ixodes ricinus in Europe

• mainly in NE
• affects all age groups
• onset usually May-November (esp. June-July)

• after intro to host, organism spread via lymph/blood to any site
• initial immune response appears suppresed
• specific IgM peak at 3-6 wks
• specific IgG reposne gradually dev. over months

• stage 1: localized erythema migraines
• stage 2- follows by days or weeks where infection disseminate
• stage 3- persistent infection months to years after initial infection, can follow long latent period

• erythema chronicum migrans
  • occurs at tick bite site
  • can occur 3-30 days after bite
  • usually red outer borders w/central clearing
  • other presentation include indurated, vesicular or necrotic centers
  • assoc. w/
    • fatige
    • adenopathy
    • meningeal signs
    • hepatitis
    • splenomegally

• usually follows ECM after several days
• 50% of untreated cases
• usually mult., smaller, can appear and fade
• can be associated with
  • malar rash
  • conjunctivitis
  • urticaria
• ECM and secondary lesions usually fade in 3-4 weeks (range 1 day-14 mnths)

• very common
• can occur 2 wks-2 yrs
• range from joint pain to intermittent arthritis to chronic erosive synovitis
• early disease: migratory pain in joings, tendonitis, bursae can be affected
• frank arthritis with marked swelling
• primarly affects large joints, attacks last from few weeks to months, separated by periods of complete remission
• small percentatge develop chronic arthritis (one year or more of continuous joint inflam.)
• histologically suggests delayed hypersensitivity

• symtpoms of meningeal irritation concomitant with ECM
• not associated with CSF pleocytosis or neurological deficits

• several weeks to months after disease onset
• includes:
  • meningitis
  • encephalitis
  • chorea
  • cranial neuritis (CN VII- Bell's)
  • motoor/sensory radiculitis
  • myelitis
• usual pattern- fluctuation meningitis with superimposed cranial N. palsy or peripheral neuropathy
• w/meningits CSF reveal lympocytic pleocytosis (many WBC's), elevated protein, normal glucose
• can develop chronic symptoms
  • subacute encephalopathy affecting memory, mood, sleep, language, peripheral sensory symptoms

• RARE
• within several weeks
• usually AV block (1st degree, complete)
• may present with EKG chanes, myopericarditis, LV dysfunc.
• usual brief duration- 3 days-6 weeks

• clinical picture, exposure in endemic area
• culture- ECM skin lesions
• serologic testing- ELISA followed by Western blot when positive
• serodiagnosis insensitive in early disease: 30-40% of patients with ECM seropositive with acute phase serology, 60-70% by convalescent sera 2-4 weeks later
• after 4-6 wks, 90% have elevated IgG
• after antibiotic treatme, titers fall slowly, BUT those with later manifestations remain seropositive for years
• ELISA for C65 Ab- highly sensitive and specific
• PCR testing for serum, CSF, synovial fluid

• treat with oral antibiotics unless neurological (except Bell's) or cardiac
• oral: doxycyclin 100 mg BID
  • for kids Amoxacillin 500 mg TID 14 days
  • loner treatment with arthritis or Bells (3-4 weeks)
• IV regimen- Ceftriaxon 2 g QD for 3 weeks
• can have Jarish Herxheimer reaction
  • symptoms could become worse after first night of treatment

• flexible, helical rods
• right handed helxi formation
• motile with 2 periplasmic flagella
• ends are bent or hooked

• zoonosis with worldwide distrb.
• transmit via indirect contact with infected animals via water or soil contaminated with infected urine
• occupational and recreational exposure common in summer, fall
• wild animals are reservoir for infecting domestic animals
• organisms establish symbiotic relationship with animal host, persistin in renal tubules

• after penitratin skin, organism enters blood stream and disseminates
• jaundice is due to hepatocellular dysfunc.
• renal failure occurs as result of tubular damage which can be immune mediated
• meningits
• organism can live in aqueous humor causing chronic uveitis

• subclinicial disease is common in persons exposed to infected animals
• 90% of those who become ill get milder anicteric form, the rest get severe disease with jaundice (Weil's disease)
• disease is biphasic
  • initial flu like phase where leptospira can be isolated from most tissues
  • immune phase char. by presence of Ab when meningitis, uveitis, rash occur

• abrupt fever, headache, severe muscle pain for 4-7 days
• second stage may not occur, but can present with severe headache and clinical meningitis, severe myalgias, abdominal pain, conjunctival hemorrhage, splenomegally, rash, pulm. infiltrates

• char. with jaundace along with impaired renal failure and hepatic dysfunction
• also shock , hemorrage, changes in consciousness

• isolation from body fluids or tissue require special lab techniques
• types of culture depend on stage of disease
• serologic test
  • ELISA (4x rise in Ab titer)

• penicillin or ampicillin IV in severely ill patients
• oral doxycycline or amoxicillin, ampicillin in those who tolerate oral meds

tick borne

louse borne