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53 Cards in this Set
- Front
- Back
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most common cause of UTI
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E. coli
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E coli specs
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enterobacteriaceae family; gram-neg rods singly or in pairs; facultatively anaerobic; all ferment glucose; ferments lactose; oxidase neg; nonmotile or motile by peritrichous flagella; fast growing gray large colonies on blood agar
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antigens of e. coli (may have 2 or 3)
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somatic O antigen (LPS carrying), H antigen (flagellum), K antigen (polysaccharide capsule)
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pyuria
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presence of 10 or more WBCs per HPF of unspun, voided midstream urine
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leukocyte esterase
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surrogate marker for WBC presence using urine dipstick test
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significant bacteriuria is based on
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cultures of clean-voided midstream urine specimen with >10^5 CFUs per mL urine
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fimbriae of e. coli that infect urinary tract
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P-fimbriae (share epitopes with P blood group antigens), type-1 fimbriae; instrumental in colonizing tract and stimulate local inflammatory responses
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virulence factors that contribute to kidney pathology from ascending bladder infections
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LPS endotoxin, urease production (proteus, hemolysin, aerobactin
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white cell casts in urine, bladder infection likely represents
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pyelonephritis
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antibiotics used in UTIs
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B-lactam, trimethoprim-sulfamethoxazole, or a flouroquinolone
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Treponema pallidum specs (syphilis)
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spirochetes, thin-walled, flexible, spiral rods, invisible by light microscopy; dual membrane system, corkscrew motility (endoflagella)
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treponemal membrane lipids
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cardiolipin; induce nonspecific antibodies that cross-react with beef heart cardiolipin; basis of RPR and VDRL tests
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how is Treponema pallidum transmitted
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obligate human pathogen; intimate contact with infectious lesions or transplacentally
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pathogenesis of Treponema pallidum
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penetrate intact mucous membranes or microscopic dermal abrasions; generates indurated painless ulcer; enter lymphatics and blood
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how does Treponema pallidum evade immune system
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maintain outer membrane rich in lipid
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secondary syphilis
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lesions may appear as maculopapular rash on skin or mucous membranes or may involve lymph nodes; rash on palms and soles; usually appear 6-8 weeks after healing of chancre (primary syphilis)
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treatment of Treponema pallidum
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long-acting penicillin G; doxycycline alternative
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HSV type 2 specs
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herpesvirus family; large virions with icosahedral nucleocapsid, linear dsDNA, lipoprotein envelope; mulitnucleated giant cells on Tzanck smear
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prevalence of HSV2 in US
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20% among adults
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male sites of infection of HSV2
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glans penis or prepuce; anus and rectum if anal sex
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women sites of infection of HSV2
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cervix and vulva
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what are primary lesionf of HSV2 due to
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cytopathic effect of virus on mucocutaneous epithelium
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treatment of HSV2
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acyclovir in first-episode genital herpes and in recurrences-no effect on latency
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HPV specs
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nonenveloped virus of icosohedral symmetry; 72 capsomeres that surround genome with circular dsDNA; >100 types; humans only known reservoir
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HPV 6 and 11
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cause genital warts-proliferation and thickening of the basal layer; genome exists as circular, episomal DNA separate from host nucleus
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risk factors for HPV infection leading to carcinomas of cervix
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sexual activity before 15, multiple partners, exposure to STD, mother or sister with cervical cancer, smoking, immunosuppression, HIV/AIDS, and chronic corticosteroid use
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What do HPVs infect
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squamous epithelial cells of basal layer of skin or mucous membrane
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where do HPV virions replicate
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nucleus-infected cells exhibit a high degree of nuclear atypia
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mild Pap abnormalities due to HPV
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koilocytosis-intracellular changes with perinuclear clearing and shrunken nucleus
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treatment of HPV
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remove symptomatic warts
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HPV 16 and 18
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cause carcinoma of cervix; genome integrated into host cell DNA; E6 and 7 inactiveate host tumor suppressors p53 and RB
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Neisseria gonorrhoeae specs
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gram-neg diplococci; peptidoglycan backbone; pili, cell-wall lipo-oligosaccharide (LOS) and outer membrane proteins (OMP); fastidious; oxidase positive; glucose fermentation
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what is diagnostic of gonorrhea
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multiple pairs of bean-shaped, gram-neg diplococci within a neutrophil in a gram smear of urethral discharge
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risk factors for gonorrhea
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multiple sex partners, early age begin sex, low socioeconomic status; complement deficiencies
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how does N gonorrhea infect
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coloizes mucosal epithelium by binding columnar epithelial cells mediated by pili and OMPs
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why don't host antibodies protect against pili and OMPs with gonococcal infection
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phase variation-genetic mechanisms control presence or absence of these components
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IgA protease of gonococcus
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extracellular enzyme that hydrolyzes IgA mucosal antibodies and inhibits opsonization needed for phagocytic killing
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what other components help gonococci avoid immune destruction
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OMPs protect against phagocytosis and protein I interferes with neutrophil degranulation
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what do gonococci initiate in subepithelial matrix
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intense inflammaotry rxn with PMNs
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treatment of gonorrhea
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third gen cephalosporins or quinolones; single injection of ceftriaxone recommended; should be simultaneously treated for chlamydia due to high coinfection rate
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C trachomatis specs
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obligate intracellular bacteria; energy dependent (can't produce ATP); grow in monolayers of cell cultures; D and K most common STD serotypes
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how does Chlamydia infect
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minute abrasions on mucosal surface as metabolically inert elementary bodies-target receptors on columnar epithelial cells
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what occurs once EB taken into cells
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remain within host-derived vacuole called cytoplasmic inclusion where they differentiate into larger, metabolically active reticulate bodies (RB)
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Reticulate bodies
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multiply and divide by binary fission; after 8-12 rounds of multiplication they reorganize into Ebs and cease multiplication; at 30-84 hours postinfection, may EB particles released and initiate another round of infection
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when do primary lesions of chlamydial disease occur
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when columnar epithelial cell destruction during acute disease process causes release of proinflammatory cytokines-chemotaxic for neutrophils and mononuclear cells
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treatment of chlamydia
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doxycycline; cefoxitin for organisms from lower bowel and anaerobes in PID
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fishy odor upon application of 10% potassium hydroxide to vaginal swab sample indicates
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trichomoniasis or bacterial vaginosis
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discharge differences in common vaginal infections
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candida whitish, Trichomonas yellow and frothy, and bacterial vaginosis faoul smelling
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Trichomonas vaginalis specs
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motile, pear-shaped, protozoan organism; pus cells interspersed with nucleated flagellated trichomonads (slightly larger than PMNs); identified by ameboid mobility; binary fission; do NOT have cyst form
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where does Trichomonas vaginalis favor
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female lower genital tract and male urethra and prostate
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where is Trichomonas vaginalis found in women
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vagina, cervix, urethra, bladder, Bartholin and Skene glands; incubation of 4-28 days before vaginitis may occur
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where is Trichomonas vaginalis found in men
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anterior urethra, external genetalia, prostate, epididymis, and semen; most asymptomatic
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treatment of Trichomonas vaginalis
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metronidazole and tinidazole
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