Infections of soft tissue – Flashcards
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Unlock answers| General Properties of Rickettsia |
small, rod shaped bacteria related to gram negative organisms have diaminopimelic acid (DAP) in cell wall obligate intracellular parasites can persist in the body for a long time stains poorly with the gram stain better with Giemsa
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| how does rickettsia replicate |
| binary fission |
| Rickettsia rickettsii |
caused by rickettsia rickettssii most common rickettsial pathogen in US distribution- Rocky Mountain region, Eastern and SE United States endemic in TN |
| what is rickettsia rickettsii reservior |
| lower animals, rodents, birds |
| what is rickettsia rickettsii vector |
wood tick (Dermacentor andersonii) dog tick (Dermacentor variabilis) |
| how is borrelia burgdorferi transmitted |
by deer tick, Ixodes dammini hard ticks from mice to humans |
| how is rickettsia rickettsii transmitted |
| vertical transmission from adult tick to egg (transovarian transmission) |
| pathogenesis of rocky mountain fever |
rickettsia multiply in the skin at site of tick bite spread to blood and infect vascular endothelium in lung, spleen, brain, and skin after week onset of fever, severe headache, myalgia and other respiratory symptoms maculopapular rash appears a few days later often becoming petechial or purpuric splenomegaly and neurolgical involvement is frequent with later onset of clotting defects shock and death |
| rocky mountain spotted fever epidemiology |
individual camping, fishing, picnicking in wooded areas are highly susceptible children playing in weeds or brush in Nashville area are highly susceptible children are most commonly infected but their disease is milder |
| when is rocky mountain spotter fever most common |
| April through October |
| Rickettsia Rickettsii immunity |
cytokine-mediated intracellular killing clearance by cytotoxic CD8 lymphocytes antibody response to outer membrane proteins may also be important |
| how do you diagnosis r. rickettsii |
weil-felix test positive for proteus OX2 and OX19a microimmunoflourescence methods and demonstration of a four fold or greater rise in antibody titer (1:160 or greater) direct fluorescent antibody and PCR |
| how do you treat rocky mountain spotted fever |
tetracycline, doxycycline, flouroquinolones chloramphenicol, erythromycin no vaccine |
| what is leading vector borne disease in the US |
| borrelia burgdorferi (lyme disease) |
| general properties of genus borrelia |
weakly staining, gram negative stain well with Giemsa or Wright stain can be easily seen by light microscopy in smears of patients with relapsing fever from 7-20 periplasmic flagella are microaerophilic and have complex nutritional needs culture is generally unsuccessful
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| what are two important diseases Borrelia cause |
relapsing fever lyme disease |
| how do you diagnosis relapsing fever |
| microscopy |
| how do you diagnosis lyme disease |
| serology |
| what are the two forms of relapsing fever charcterized by |
recurrent episodes fever and septicemia seperated by afebrile periods this results from antigenic variation |
| what is the etiologic agent of louse borne relapsing fever |
| borrelia recurrentis |
| how is borrelia recurrentis transmitted |
| person to person by human body louse (Pediculus humanas) |
| endemic relapsing fever |
caused by as many as 15 species of borreliae spread by infected soft ticks (Ornithodoros) |
| what is borrelia burgdoferi reservoir |
| mice, deer, ticks |
| borrelia burgdorferi vectors |
Ixodes scapularis in the eastern and midwestern US Ixodes pacificus in the western US worldwide distribution |
| who is at risk for lyme disease |
| people exposed to ticks in areas of high endemicity |
| when do most US cases for lyme disease occur |
| late spring and early summer |
| borrelia burgdorferi epidemiology/transmission in year one |
adult ticks feed and mate on certain deer during late fall or winter and drop to the ground eggs deposited on bushes hatch into larvae in the spring in summer larvaue obtain blood meal from white-footed mouse (main reservoir) larvae into nymphs |
| borrelia burgdorferi epidemiology/transmission in year two |
during the following spring-summer, infected nymphs feed on vertebrate hosts including white footed mouse infected or non infected nymphs fall off host and mature into adult males or females and then parasitize available deer to start cycle all over again human host is usually infected by infected nymphs |
| early signs of lyme disease |
erythema migrans begins as small papule and then enlarges over the next few weeks headache, malaise, severe fatigue, fever, chills, myalgias, lymphadenopathy |
| three stages of lyme disease |
stage 1-localized (1-4 weeks) stage 2- disseminated (1-6 months) stage 3- latent, persistent infection (1-30 years) |
| stage one |
erythema migrans (bull's eye) disseminated blood (fever, headache, fever, malaise) |
| stage 2 |
localized: secondary annular lesions disseminated: meningitis, carditis musculoskeletal pain, eye |
| stage 3 |
localized: no manifestations acrodermatitis chronica atrophicans disseminated: arthritic, chronic progressive neurologic/cardiac disorders |
| how do you diagnosis b. burgdorferi |
can be cultured in NSK medium from early stage cutaneous tissues but rarely seen at later stages takes several weeks primarly diagnosised based on clinical presentation and known exposure |
| francisella tularensis |
small gram negative coccobacillus intracellular obligate aeorobe (macrophages) inhibits phagosome lysosome fusion requires cysteine for growth; can grow on BCYE (buffered charcoal yeast extract) |
| francisella tularensis virulence factors |
facultative intracellular pathogen LPS-appears to NOT be very toxic lipid capsule- anti-phagocytic factors taht inhibit phagosome-lysoome fusion and prevent acidification |
| where is francisella tularensis primarily observed |
Oklahoma, Missouri, and Arkansas, but distributed throughout North America |
| Francisella tularensis epidemiology |
| found in variety of wild animals, birds, blood-sucking arthropods, rabbits, ticks, hares, voles, muskrats, beavers |
| how is francisella tularensis acquired |
bite from infected "hard-shell" tick (Ixodes, Dermacentor) ingestion of contaminated meat or water, inhalation of infectious aerosol, skin abrasions, skinning of animals |
| how many types of francisella tularensis is there |
| two types |
| What are the two types of francisella tularenis |
A (most common) B |
| what are the forms of disease caused by francisella tularensis |
ulceroglandular oculoglandular glandular typhoidal pneumonic |
| ulceroglandular |
cutaneous ulcer/swollen lymph node most common following skin abrasion or tick/fly bite (2-5 days) |
| oculoglandular |
| direct inoculation by conjunctivitis; cervical and preauricular lymphadenopathy |
| glandular |
| usually vector borne exposure, enlarged regional lymph nodes with no skin involvement |
| typhodial |
ingestion or inhalation; baceteremic spread and seeding to lung, liver, spleen; fever, weight loss, pneumonia mimics typhoid fever, brucellosis, tuberculosis |
| pneumonic |
| results from inhalation of infectious aerosols |
| what type of agar does f. tularensis grows on |
| chocolate |
| is f. tularensis catalase postive or negative |
| negative |
| is f. tularensis oxidase positive or negative |
| negative |
| f. tularensis diagnosis/identification |
reactivity of bacteria with specific antiserum( agglutination of organism with antibodies against Francisella) microagglutination detects antibody titer in serum fluoresent Ab test can detect the organism in tissue specimen |
| f. tularensis immunity/prevention |
natural infection confers long lasting and protective immunity CMI plays a major role in resistance vaccine is given to high risk individuals |
| what antibiotics do you use to treat F. tularensis |
streptomycin-high level of toxicity gentamicin-alternative fluroquinolones (ciprofloxacin)- good bactericidal activity in vitro and mouse animal models |
| what is the etiologic agent of anthrax |
| bacillus anthracis |
| bacillus anthracis |
large, aerobic, non motile gram positive rods that produce lecithinase spore formers polypeptide capsule composed of D-glutamic acid interfers with phagocytosis (plasmid-encoded) |
| what are the toxin components of b. anthracis |
protective antigen EF LF (lethal factor) |
| what is the protective antigen function in b. anthracis |
| binds to host cell |
| what is the function of EF in b. anthracis |
| adenyl cyclase activity increase (increases cAMP) resulting in tissue edema |
| what is the function of lethal factor in b. anthracis |
| a protease that targets cell signaling proteins; cleaves MAP kinase leading to cell death |
| what are the three clinical forms of anthrax |
cutaneous (eshar) pulmonary (woolsorter's disease) ingestion |
| cutaneous anthrax |
characterized by lesions (malignant pustule) on hands, forearms or head that may contain a dark bluish black fluid erythematous papule develops 12-36 hours after entry of organism via breaks in skin which quickly progresses to the formation of a pustule and then a necrotic ulcer from which the infection may disseminate (eschar)
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| Pulmonary anthrax (Woolsorter's disease) |
aquired by inhalation of spores by handlers of raw wool, hides or horse hair spores germinate in the lungs or the tracheobronchial lymph nodes symptoms include non-specific malaise, mild fever, and non productive cough progressive respiratory distress and cyanosis will follow with massive edema of the neck and chest |
| ingestion anthrax |
infection of GI tract is common in animals but rare in humans infection in humans results in abdominal pain, nausea, vomiting, and bloody diarrhea |
| b. anthracis lab diagnosis |
gram stain, culture and immunofluorescent assays of fluid or pus from local lesions, blood and sputum can be cultured on normal blood agar serological tests can demonstrated the presence of agglutinating antibodies; antibodies to toxin antigen |
| b. anthracis treatment/immunity |
historically susceptible to penicillin- resistance genes to penicillin and doxycycline have been transferred to the organism now recommend ciprofloxacin early treatment is important |
| what is the b. anthracis made from |
| purified protective antigen is available for humans at high risk |
