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24 Cards in this Set
- Front
- Back
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general characteristics of B. pertussis
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gram negative coccobacili,stricly aerobic, non-motile and oxidize amino acids, grow in a special chocolate agar
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where does B. pertusis live
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mucous membranes of the upper respiratory tract and colinize in ciliated mucosal cells
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hallmark of B. pertusis infection
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increased percentage of lymphocytes
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epidimiology of B. pertusis
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high infectous spread by airborne droplet nuclei to those in close contact, newborns are highly susceptible with a high infant mortality rate
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B. pertusis vriulence factor
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Adhesins - Fha has an Arg-Gly-Asp domain taht binds to integrins on ciliated respiratory cells and receptors on macrophages. Also pertacin (P69) and PT
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B. pertusis virulence factor
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toxin - pertusis toxin is the major virulence factor. it is a classic A-B exotixin encded by a single operon. S1 subunit is internalized and ADP-ribosylated a G protein. this host's ability to inactivate adenylate cyclase is inhibitied. cCAMP rises, resulting incrased respiratory secretions and mucus production
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pathogenesis B. pertusis
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strict human pathogen, coordiante transcriptional regulation of 20 unlinked genes requried for pathogenesis
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initial stage of B. pertusis
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catarrhal - resemble common cold, runny nose, malaise, fever, sneezing, anorexia. (most infectious stage)
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2nd stage of B. pertusis
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convulsive coughing. paroxymsmal - whooping is heard after coughing often followed by vomitting. major airway restriction
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final stage B. pertusis
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convalescent - gradual decrease in coughing and other symptoms is observed
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diagnosis of B. pertusis
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confirmed by isolation from nasopharyngeal syntehtic-fiber swab or apirate that is directly plated ontl special chocloate agar medium. PCR amplification is used
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treatment of B. pertusis
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antimicrobial therapy with erythromycin in catarrhal. if in paroxysmal no real treatment
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prevention of B. pertusis
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active immunization with DpaT vaccine
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immunity of B. pertusis
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infants do not seem to acquire passive immunity from mothers, vaccination is not life long
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where does L. pneumonphila live in the body
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lower respiratory track
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general characteristics L. pneumonpila
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gram-negative aerobic coccobacili in tissue, but pleomorphic on media, inhibit phaglysomal fusion and acidfication
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incidene of L. pneumonphila
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significant percentage of the population has acquired immunity, suggesting asymptomatic infection is common
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reservoir of L. pneumonphila
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natural aquatic bodies, polluted water, and moist soil. can also infect and multiply in amoebae and ciliated protozoa isolated from hot water tanks
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pathogeneiss of L. pneumonphila
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develops when inhale infectious aerosols, phagocytosis by alveolar macrophages and moncytes are inhibited by bacteria
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severe disease from L. pneumonphila
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severe pneumonia - hallmark is an intra-alveolar exudate of both polymorphonuclear leukocytes (PMNs) and macrophages,
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milder disease from L. pneumonphila
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Pontiac fever - normal chest x-ray, pathology of this diease is caused by hypersensitivty reaction to organism
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laboratory diagnosis of L. pneumonphila
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gram-negative, aerobic, non-spre forming, plemorphic bacilli in infected tissue or secretions. long filamentous forms, grows optimal growth 35 degrees.
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method of detection L. pneumonphila
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Direct flurorescence antibody (DFA) test is the most sensitive method of microscopic detection
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treatment of L. pneumonphila
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severe diseas is treated with azithromycin or levelfloxacin. less severe is erythromycin or tetracyclin. Pontiac fever is self-limiting
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