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54 Cards in this Set

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where are the flagella of spirochetes located?
they are endoflagella located in the periplasmic space
describe the membranous structures of the spirochetes.
it is gram neg like with a fairly thin peptidoglycan layer, inner and outer membranes, but no LPS except in Leptospira
what are the treponema species and the diseases that they cause?
T. pallidum - syphilis
T. pallidum endemicum - bejel
T. pallidum pertenue - yaws
T. carateum - pinta.
Note that there are other species that are normal flora in the mouth of ppl, so if there is an oral ulcer, it can have normal flora in it
describe the physiology and structure of T. pallidum
lacks LPS, cannot grow in cell free cultures and can only be grown in rabbit balls, very slow replication rate, can be seen by darkfield microscopy, very sensitive to drying and disinfectants, very sensitive to penicillin
how is syphilis aquired?
by direct mucosal contact with primary/secondary lesion and transmission only occurs in 1/3 such contacts
1. syphilis orgs can only penetrate intact mucosa.
2. syphilis can transmit transplacentally.
1. F. can penetrate broken skin as well.
2. T
what are the # of infections/year in the US? worldwide?
30-70,000. 12 mil
describe the clinical signs of primary syphilis.
incubates for 10 to 90 days, painless and hard chancre develops at site of initial penetration. note that lotsa ppl do not notice these bc they do not hurt, esp if it is in their ass. painless regional adenopathy is common, this heals in 4 to 6 wks
what toxins does T. pallidum have?
no known toxins, uses host hyaluronidase to "unglue" connective tissue and the orgs also become coated with fibronectin thus inhibiting them from being phagocytosed
describe secondary syphilis.
occurs in 50% of cases, flu like symptoms may precede rash, rash occurs 2-10 wks postinfection, can recur later, usually rash on palms and soles, lesions are infectious, few develop condylomata in warm moist areas, CNS involvement is occasional, 1/3 of pts may spontaneously clear infection at this stage
when can latent syphilis occur and is transmission possible at that time?
after secondary syphilis. transmission can occur to the fetus.
describe tertiary syphilis
can occur months or years after infection. not infectious - few orgs present, gummas - soft granulomatous masses with central necrosis can cause widespread tissue destruction (need treatment to heal). possible autoimmune or delayed type hypersensitivity reaction...? CNS involved (headache, fever, stiff neck, vomiting indicate meningitis; dementia and paralysis can occur; can be fatal or cause permanent disability)
what about syphilis allows it to become latent for so long?
it is a very slow replicator
describe congenital syph.
transplacental transmission can occur anytime, most fetuses die, survivors may develop symptoms of secondary/tertiary syph after birth including "snuffles" and severe rash. Those that survive may suffer tooth and bone malformation, blindness, deafness, CNS abnormalities, MR, saber shins, and saddle nose
what roles does immunity play in syph?
natural infection leads to long immunity, antibiotics will shorten immunity, both Ab's and CMI are important
describe the antigens present on T. pallidum as well as the Ab's produced during infection.
not many, outer membrane only has a few proteins, flagellar proteins not exposed til org dies, lipoproteins are prevalent, lotsa treponemal antibodies arise during infection as well as nontreponemal antibodies against host cardiolipin due to cell destruction
what are the ways to diagnose syphilis in the lab and what is the choice method?
detect treponemal antibodies in early infection, detect nontreponemal antibodies, detect spirochetes in primary/secondary lesions via darkfield microscopy
(only useful on genital lesions) or FLUORESCENT ANTIBODY TEST on genital, oral, or rectal specimens thus you won't misdiagnose other normal oral spirochete flora
what is the basis for using non treponemal antibodies to test for syph? what are these tests?
cardiolipin, lecithin and cholesterol might be in the treponema membrane and our bodies make auto antibodies against these compounds when our cells die. tests using the above antigems, VDRL, and RPR
when should the VDRL slide test be used for syph test?
when diagnosing neurosyph
describe the RPR test for syph.
rapid plasma reagin is easy to read, can use plasma, has good antigen stability
what are the advantages and disadvantages to using non treponemal serology tests for syph?
adv: fast, easy to perform, neg in 6+ months after treatment. Dis: prone to false positives
what are the advantages and disadvantages to serology tests that use treponema antigens itself?
Fluorescence Ab test is very specefic and sensitive and allows for early detection, but you need an entire bac, is expensive and not good for monitoring. Hemagglutination has simalar advantages and disadvantages with not quite as early detection rates. they are trying to make recombinant T. pallidum antigens to bring down costs
what can lead to false positives for syph in the serology tests and how can you resolve them?
nontreponemal tests can be false positive with acute febrile illness, pregnancy, recent immunization, and autoimmune disease with tissue destruction. Treponemal serology tests can use be false positive with elevated Ab's, autoimmune disease, and pregnancy. False positives can be resolved by western blot assay
how is syph treated?
penicillin is the choice, one IM dose is good for early infection, but need prolonged treatment for tertiary or latent. tetracycline or doxycycline are alternatives, not as good against the neurosyph, azithromycin is effective with some resistance
describe the Jarisch Herxheimer reaction.
reaction to products released as T. pallidum is killed by antibiotics causing fever, headache and malaise. not as bad as gram negs with LPS
what is prevention for syph? does it have a vaccine?
condoms. No
describe bezel syph.
AKA endemic syph, Africa, Asia, Australia, T pallidum endemicum. contaminated utensils, begins in mouth, then raised, eroding lesions on trunk and legs, inflammed leg bones common, gummas on nose and soft palate later, disability common, mainly children
describe Yaws/frambesia syph.
subspecies pertenue. tropical Africa, S. america, and SE asia; skin and bones hit, contact with lesions or eye gnats speads it, raspberry growths on skin with infectious exudate; sub Q growths later, deformity and disability
describe Pinta syph
T. carateum, Mexico, S. america, Philippines. contct with lesions will spread, skin only with initial raised papule that flattens and reddens area with changes in pigmentation, rare neuro and cardio complications, not as disabling as other groups and is treatable
describe the structure and phys of Borrelia.
large with irregular spirals, stains gram neg, microaerophilic, can be grown but is hard to grow, major variable protein on outer membrane
what is the chief way Borrelia evades the immune system?
highly antigenically variant, 10 or more variants expressed with a single infection
describe epidemiology of epidemic relapsing fever.
Borrelia disease caused by B. recurrentsis and carried by body lice, thus seen in overcrowding, war, natural disasters, and poverty, humans are only reservoir. parts of S. america, africa, and asia
describe epidemiology of endemic relapsing fever.
several Borrelia species, soft shelled ticks carry it, western US, rodents and associated ticks are primary reservoir
what are the clinical manifestations of relapsing fever?
1 wk incubation, bacteremia with high fever, headache, muscle pain, weakness, primary episode is 1 wk with abrupt end, less severe relapse in 1 wk, 1 to 2 relapses in epidemic, 3-4 in endemic, note most can clear it at this point, but if you catch it then treat it; may have splenomegaly/hepatomegaly, epidemic mortality is 40%, 5% for endemic, high in epidemic due to living conditions... death caused by cardiac failure, hepatic necrosis, cerebral hemorrhage
describe the pathogenicity of relapsing fever.
no toxins, spread to organs via blood, symptoms largely due to bac substances released by orgs in blood, antigenic shift crucial for persistent carriage of org, genes for membrane proteins on plasmids
what are the ways to do lab diagnosis of relapsing fever?
giemsa stain of blood smears during febrile period, culture is slow and not too useful, no serology not useful
what are the treatment and prevention for relapsing fever?
tetracycline or erythromycin. prevention: immunity is short lived, no vaccine, insecticides, rodent control, clothing barriers, improved hygeine
what bac causes lyme disease and what is the vector?
in US it is Borrelia burgdorferi, other species elsewhere. Vector is hard shelled tick
describe B. burgdorferi in terms of morphology and physiology.
large spirochete with loose, irregular spirals, gram neg, microaerophilic, limited antigenic variation
what is the epidemiology of lyme disease?
ixodes ticks AKA deer ticks, the tick nymphs feed on mice and humans and this is the way we get lyme disease usually. note need to be bitten for 24 hrs to get disease usually
T/F lyme disease pt usually knows they have been bitten by a tick.
false, the ticks, especially the nymphs, are tiny
what is the #1 arthropod borne disease in the US?
lyme disease
what are the clinical manifestations of lyme disease?
primary stage is erythema migrans (bull's eye rash) at site of bite, seen 3 to 30 days post bite, subsequent lesions may appear, bacteremia with usual symptoms that can last for a month result. Secondary stage: months to years after primary infection, skin becomes bluish with discoloration and swelling, nervous system shows facial palsy, meningitis, encephalopathy with memory, mood or sleep changes, joint problems also common (arthritis)
what is the pathogenesis of lyme disease?
no known toxins, virulent strains can resist macs/neutro killings, binds glycolipids on cell surface, lotsa plasmids with pathogenic genes, molecular mimicry may allow persistance, autoimmune symptoms may last after org has been cleared
how can lyme disease be diagnosed?
skin lesion is best tool, serology (false negs), PCR, culture takes a while...
treatments for lyme disease?
early: oral doxycycline or amoxicillin. later manifestations: 30 day regimine with doxycycline or amoxil for arthritis, IV ceftriaxone or cefotaxime for neuro issues, chronic arthritis does not always respond to Ab's
prevention for lyme disease?
used to be vaccine, but off market, mainly insect repellant stuff
describe the genetics, phys, and morph characteristics of Leptospira.
lotsa species and serovars, taxonomy is under debate, not sure which species are infective, 2 periplasmic flagella, obligat aerobe, slow grower, likes cooler temps, 2 circular chromosomes, has LPS
what is the epidemilogy and transmission of Leptospira?
worldwide, few cases in US, most in hawaii, reservoir is rodents (rats esp) and are shed in urine, can survive several weeks in water or moist soil. incidental hosts include dogs, farm animals, humans. Transmission via contaminated food or water, rec sports from environment like contaminated lakes, no person to person, epidemics occur usually after floods
describe the diseases caused by leptospira.
flu like illness usually with bacteremia, can have second phase which is similar with ab pain and conjunctivitis, severe case may have vascular collapse, pulmonary hemorrhage, renal and hepatic dysfunction; severity depends upon strain and host factors; immunity is serovar specefic; can get Weil's disease (aseptic meningitis), or pretibial or Fort Bragg fever (fever and rash over tibia)
what is the pathogenesis of leptospera?
not well understood, penetrate intact mucosa or skin cuts, spread to all tissues, may have hemolysins, bacs adhere to renal cells, cleared by humoral immunity
how is leptospira diagnosed?
easily confused with inluenza or viral meningitis, microscopy not reliable, culture needs special media and takes too long, PCR not widely available, serological tests are good for screening but have high false positive rate, microscopic agglutination tests uses live orgs and pt serum abilities... only reference labs can do it, with hepatitis, serum creatine phosphokinase will be raised unlike viral hep
what are the differentials for leptospira?
flu, encephalitis, hantavirus, viral hep, malaria, meningitis, mononucleosis
what are the treatment and prevention methods for leptospira?
most recover without treatment, but treatment recommended, penicillin, amoxil, or doxy/tetracycline, prophylaxis is doxy for ppl like emergency flood workers, control rats, vaccinate herds and pets