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21 Cards in this Set
- Front
- Back
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describe Trichomonas vaginalis
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a. etiology
protozoan, motile (jerky/twitchy), pear-shaped anaerobic, reproduces by mitotic division exists only as vegetative cell (no cyst forms) b. epidemiology Sexual transmission (non-barrier methods of contraception) c. clinical features incubation period is 5-28 days infection in women ranges from asymptomatic carrier state to severe acute inflammatory disease |
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describe vulvovaginal candidiasis
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a. etiology
most are Candida albicans-DIMORPHIC fungus existing as yeast when present as normal flora and pseudohyphae when invading tissue aerobic, grow at 20-40°C, pH 3-8 b. epidemiology predisposing factors to growth of yeast in vagina: i. glycosuria ii. diabetes mellitus iii. obesity iv. pregnancy-increased vaginal carriage rate, susceptibility to infection, and lower cure rates v. recent use of antibiotics (ampicillin, cephalosporins, and tetracyclines), steroids, immunosuppressants, or oral contraceptives factors that contribute to candidal vaginitis: 1. tight, poorly ventilated clothing 2. nylon underclothing 3. chemical contact 4. local allergy or hypersensitivity reactions |
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describe bacterial vaginosis
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result of massive overgrowth of mixed flora:
i. Gardnerella vaginalis (100X increase) ii. peptostreptococci (10X increase) iii. Bacteroides species (1000X increase) iv. Mobiluncus species v. genital mycoplasmas minimal inflammation; disorder represents disturbance of vaginal microbial ecosystem rather than true infection of tissues anaerobes produce amines (responsible “fishy” odor and elevated pH) |
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describe toxic shock syndrome
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a. etiology
Vaginal colonization w/ S. aureus and production of toxic shock syndrome toxin-1 (TSST-1) Changes in microflora and biochemical environment of vagina during menses may predispose to overgrowth of staphylococci b. clinical manifestations young woman b/t 15-25 years of age using tampons during menstrual periods 1. Fever 2. Hypotension 3. Multiple organ system dysfunction (renal and hepatic insufficiency, pancreatitis, cardiac dysfunction, ARDS, and hematologic abnormalities) 4. diffuse (“sunburnlike”) erythematous rash 5. desquamation-on palms of hands and soles of feet (during or after recovery) 6. prodrome of diarrhea, vomiting and myalgias c. Diagnosis vaginal and cervical culturing of S. aureus |
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describe the etiology and epidemiology of Streptococcus agalactiae (Group B Strep)
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a. etiology
Lancefield Group B carbohydrate antigen contained in cell wall; further divided into serologic types based on 7 capsular polysaccharide antigens Gram-positive coccus in pairs or chains weakly beta-hemolytic (narrow zone of hemolysis agglutination w/ anti-B serum (latex bead agglutination test) b. epidemiology source of neonatal infections is the colonized female GU or lower GI tract Infants of mothers who have protective antibodies are protected by maternal Ab |
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describe the clinical syndromes associated with S. agalactiae (GBS)
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i. Early-Onset Neonatal Disease (w/in 7 days of birth)
acquired in utero in last stages of pregnancy, or by infected vaginal secretions during birth process; manifests as bacteremia, pneumonia, or meningitis; case-fatality rate 5-10%; neurologic sequelae (blindness) is common Risk factors are maternal genital tract colonization and bacteriuria, preterm labor and delivery, premature rupture of membranes, and fever during delivery ii. late onse neonatal disease (1 week-3 months after birth) Infection acquired by exposure to mother or infected infants in nursery; commonly bacteremia w/ meningitis; case-fatality rate is low, but neurologic sequelae of meningitis are common iii. Infections in Pregnant Women Intra- and post-partum UTIs; post-partum infection of uterus or surgical incision site iv. Infections in Men and Non-Pregnant Women older patients w/ debilitating underlying conditions (diabetes); outnumber neonatal infections, but incidence is much higher in neonates |
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describe streptococcus pyogenes (Group A Strep)
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i. puerperal fever/sepsis
following childbirth or abortion, uterine lining is wounded and presents ready avenue for infection; source of infection may be patient’s own bacterial flora or acquired from carrier present at the delivery ii. streptococcal toxic shock syndrome pyogenic inflammation; blood cultures are positive; mortality rate of is 30% site of soft tissue infection is not in female genital tract in the majority of cases |
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describe clostridium sordellii
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causes pneumonia, endocarditis, septic arthritis, peritonitis, myonecrosis, and sepsis (rarely)
infects female genital tract to cause a form of toxic shock syndrome; occurs following live birth or abortion can cause uterine gas gangrene associated w/ septic abortion prominent component of microbial flora in vaginal secretions toxigenic, and one of its toxins is named Lethal Toxin (case-fatality rate is 100%) |
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describe TORCH syndrome
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TORCH=Toxoplasma, Other, Rubella, Cytomegalovirus, Herpesvirus (acquired at birth)
Other-includes Treponema pallidum (syphilis), hepatitis B virus, coxsackie virus, Epstein-Barr-virus, varicella zoster virus, and human parvovirus B19 these infections can cross the placenta and infect developing fetus in utero frequently infect developing nervous system-->causes neurological abnormalities that manifest as birth defects-low birth weight, fever, rash (petechiae), hepatosplenomegaly, and jaundice primary infection much more likely to cause infection of fetus than are secondary infections, because pre-existing immunity confers protection TORCH test/panel-serological test for IgM against each TORCH agent; performed on maternal serum during pregnancy or newborn serum after birth |
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describe parvovirus B19 (human erythrovirus B19)
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replicates in hematopoietic cells in bone marrow and causes “fifth disease” (erythema infectiosum), a mild self-limited rash occuring in children (characterized by “slapped cheek” appearance)
sometimes infects non-immune adults, resulting in rash or arthralgia (self-limited) Pregnant women in contact w/ small children are at risk; can cross placenta and infect fetus in 1/3 of cases (usually w/out serious consequences); in some instances fetal infection results in miscarriage or fetal hydrops (whole-body edema) secondary to anemia caused by inhibition of hematopoiesis Infection is detected serologically by presence of IgM against viral antigens and by PCR testing for viral DNA Fetal anemia is diagnosed by cordocentesis; fetal hydrops is detected by prenatal ultrasound risk of hydrops fetalis is greatest when infection occurs b/t 9-20 weeks gestation; risk of miscarriage is greatest b/t 9-16 weeks |
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describe Haemophilus ducreyi
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a. etiology
short Gram-negative rods b. epidemiology causes Chancroid; associated w/ poor socioeconomic and hygienic conditions; women are often asymptomatic carriers c. Clinical Manifestations incubation period is 2-5 days Lesions are confined to genitalia and perianal areas; lesion begins as tender vesicle or papule, then ruptures, leaving small ulcer w/ erythematous base; painful and tender to palpation but soft and not indurated Regional (inguinal) lymphadenopathy is characteristic of chancroid; adenopathy is unilateral and painful but may be bilateral; unilocular suppuration (bubo) commonly follows d. Diagnosis commonly made on clinical grounds alone; confirmation of diagnosis is smear and culture of lesion or bubo aspirate; gram stains often give false-negative results |
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describe Calymmatobacterium granulomatis
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a. etiology
short, gram-negative rod; shows bipolar staining Capsulation is related to developmental cycle; extracellular bacilli are capsulated; intracellular bacilli are unencapsulated in cytoplasmic vacuoles; capsule re-forms as bacilli mature, and are released when the host cell ruptures b. epidemiology common in tropical or subtropical environments; repeated exposure necessary for development of most clinical cases; non-sexual transmission can occur c. Clinical Manifestation: causes Granuloma inguinale (Donovanosis), a chronic indolent ulcerogranulomatous disease of skin and mucous membranes; incubation period is 8-80 days genitalia is involved; ulcers are irregular in outline, covered w/ abundant granulation tissue, beefy red and nontender Diagnosis stained crushed preparation of clean granulation tissue from the lesion is spread on a slide; impression is air dried and stained Donovan bodies are individual cells of Calymmatobacterium granulomatis, seen as clusters of blue or black staining organisms w/ "safety pin" appearance in vacuoles in cytoplasm of large mononuclear cells |
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describe the etiology, epidemiology, and diagnosis of Neisseria gonorrhoea
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a. etiology
small Gram-negative cocci which grow in pairs (diplococci) w/ adjacent sides flattened produces cytochrome c (basis for oxidase test) rapidly oxidize tetramethyl-paraphenylene diamine; turns colonies pink, then purple produce acid from glucose (but not other sugars) Optimal growth is 35-37°C in presence of CO2; obligate aerobes Ultrastructure and Immunochemistry: pili-outermost surface structure; hairlike proteins composed of repeating protein subunits (pilin); Pili enhance virulence by mediating attachment of organism to human epithelial cells and by impeding phagocytosis; antibodies to pili block gonococcal attachment to epithelial cells and promote phagocytosis by PMNs Protein I-predominant protein in gonococcal outer membrane; act as porins, forming transmembrane channels that permit exchange of hydrophilic molecules across outer membrane; also initiates endocytosis of gonococcus Protein II-responsible for attachment to human epithelial cells and PMNs, and for intergonococcal adhesion Gonococcal outer membrane contains endotoxin similar to most Gram-negative bacteria, but lacks long O-antigen polysaccharide chains; called lipo-oligosaccharide (LOS); LOS possesses endotoxin activity that contributes to local cytotoxicity and inflammation, fever, and systemic toxicity b. Epidemiology risk factors for spread of gonorrhoea include low socioeconomic level and promiscuity c. diagnosis If Gram-negative diplococci are found in Gram stain of a direct smear, assume gonococcal infection (not high sensitivity); specimens from sites of infection submitted for polymerase chain reaction (PCR)/nucleic acid amplification test (NAAT) or microbiological culture; culturing for gonococci is sensitive and accurate; plates must be incubated for 1-2 days to allow growth to occur |
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describe the clinical manifestations of N. gonorrhoea
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a. Urogenital Gonorrhea
Urethral infection in men produces purulent urethral discharge and dysuria; often asymptomatic for long periods most common site of infection in women is the cervix; signs and symptoms of primary gonococcal infection in women are less specific than in men (majority are asymptomatic); symptoms include vaginal discharge, dysuria, urinary frequency, menstrual abnormalities, and lower abdominal pain b. Anorectal Gonorrhea: occurs in individuals who are receptive partner in anal sex; can be acquired by neonate during birthing the process; usually asymptomatic c. Pharyngeal Gonorrhea: acquired by orogenital sex; usually asymptomatic, organism is spontaneously eliminated from oropharynx in several weeks; can cause sore throat and local lymphadenitis d. Gonococcal Pelvic Inflammatory Disease: caused by spread of N. gonorrhoeae upward from cervix; results in endometritis, salpingitis, and peritonitis; most common in women from lower socioeconomic settings e. Gonorrhea in Pregnancy: Ascending gonococcal infection can cause PID that affect fetus (septic abortion and chorioamnionitis); increased risk of premature rupture of membranes and premature delivery f. Gonococcal Infection in Children: Infected mothers can transmit gonococci to newborn in utero, during passage through birth canal, or in postpartum period; Gonococcal ophthalmia neonatorum causes blindness and conjunctivitis in neonates Neonates may also develop systemic illness (septicemia or arthritis) g. Disseminated Gonococcal Infections (DGI): occurs predominantly in women; patients have asymptomatic local infection for several weeks prior to dissemination; in women, onset occurs at 1st menstruation following local infection Dissemination may occur from pharyngeal, rectal, or genital sites of infection; onset characterized by fever, polyarthralgia, and skin lesions on the extremities (spares face and trunk) |
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describe Chlamydia trachomatis etiology and epidemiology
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a. etiology
On basis of outer membrane antigenic differences, divided into 15 different serotypes (A-L and subtypes) obligate intracellular parasites, but classified as Gram-negative bacteria life cycle: i. elementary body (EB)-infectious particle capable of entering uninfected cells; metabolically inert and survives extracellularly ii. reticulate body (RB)-metabolically active and found only intracellularly; divides by binary fission and produces inclusions that can be identified iii. pathogenesis-EB attaches to susceptible host cell; enters cell by endocytosis, remaining in cytoplasmic vacuole; EB converts to RB; and replicates 8-24 hours, then forms new EBs; new EBs are released by rupture of infected cells and cycle starts again (process takes 2-3 days) b. epidemiology: exclusively genital tract pathogen transmitted by sexual contact; predictors of infection include age, socioeconomic status, number of sexual partners, and method of contraception |
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describe the clinical manifestations of C. trachomatis
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1. men
a. Nongonococcal Urethritis (NGU) : incubation period is 2-35 days; presents w/ dysuria, frequency and discharge Presence of >4 PMN per oil immersion field of Gram-stained smear of endourethral contents in absence of gonococci is diagnostic for NGU b. Epididymitis: majority of cases in men <35; major complication of chlamydial urethritis in men c. Proctitis: both men and women d. Prostatitis e. Reiter’s Syndrome: following bouts of NGU 2. women: a. Endocervicitis b. Urethritis c. Endometritis: d. Acute Salpingitis (Pelvic Inflammatory Disease; PID) 3. Lymphogranuloma Venereum (LGV): caused by serotypes L1, L2, and L3; most commonly occurs in tropical areas Primary infection occurs in endocervical canal, rectal mucosa or on external genitalia; most prominent clinical feature is enlarged, painful inguinal lymph nodes (buboes), usually unilateral; nodes can be present above and below inguinal ligament (Groove or Shelf Sign) Lymph nodes are very tender and form buboes that break down to form chronic draining sinuses; w/out treatment, inguinal nodes fibrose, causing lymphatic obstruction and lymphedema of the external genitalia |
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describe the etiology and epidemiology of Treponema pallidum
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thin, tightly wound spirochete
visualized by dark-field microscopy or staining w/ silver salts motile (corkscrew rotation) can't be cultivated in vitro; rabbits used for maintaining virulent organisms readily killed by variety of physical and chemical agents, including refrigeration >48 hours, heat, desiccation, and soap b. epidemiology: transmitted by sexual intercourse; can be acquired by passage through placenta (congenital syphilis) highest rate of infection occurs b/t 20-24 |
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describe primary, secondary, and latent syphilis
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a. Primary Syphilis:
characterized by the development of a lesion (chancre) that begins at site of inoculation as a painless papule; appears after 21 days incubation period; lesion quickly erodes and becomes indurated; regional lymphadenopathy w/ enlarged, firm, nonsuppurative, painless lymph nodes (satellite buboes) accompany primary lesions Spirochetes are found in the chancre; chancre usually heals w/out treatment in a few weeks, leaving a thin scar b. Secondary Syphilis: manifests 2-8 weeks after appearance of a chancre Maculopapular and/or pustular lesions and occur on the trunk and proximal extremities; lesions persist from few days-8 weeks; can become widely distributed to involve entire body, especially on palms and soles (diagnostic); when hair follicles are involved, temporary patchy alopecia or thinning and loss of eyebrows and beard may develop In warm, moist areas papules coalesce and erode to produce painless, highly infectious plaques (condylomata lata) Infectious lesions (mucous patches) may also develop on mucous membranes; mucous patches are silvery gray superficial erosion surrounded by a red periphery Malaise, anorexia, headache, sore throat, arthralgias, low-grade fever and weight loss and generalized painless lymphadenopathy are other common manifestations of secondary syphilis c. Latent Syphilis: no clinical signs or symptoms of the disease, but patient is positive for treponemal antibody test (FTA-abs, TPHA-TP, TPI) Latent syphilis begins w/ passing of secondary syphilis and persists until manifestations of late syphilis develop i. early latency-period of time (first year) during which a relapse of secondary syphilis may occur ii. Late latent syphilis-noninfectious except in the case of pregnant women who may transmit the disease to their fetus |
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describe late (tertiary) syphilis and its manisfestations
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destructive stage of syphilis; noninfectious and occurs only if early syphilis is untreated
Manisfests in different organs: 1) Late Benign Syphilis (Gumma): granulomatous lesion most commonly found in skeletal system, skin, and mucocutaneous tissues; can appear as superficial nodules or deep granulomatous lesions that break down to form punched-out ulcers 2) Cardiovascular Syphilis: develops in 10% of late untreated syphilis >10 years after initial infection; men are more frequently affected than women The basic lesion is aortitis; elastic tissue is destroyed and replaced by fibrous tissue; complications of aortitis are aortic regurgitation, aneurysm, and obstruction of coronary ostia 3) Neurosyphilis: seen more frequently in white than black patients and men Asymptomatic neurosyphilis no clinical manifestations of neurosyphilis but have CSF abnormalities; positive CSF-FTA or CSF-FTA-abs suggests neurosyphilis Meningovascular syphilis-includes meningitis and CNS damage resulting from cerebrovascular occlusion, infarction, and encephalomalacia; CSF is abnormal and serologic tests are reactive Parenchymatous-includes syphilitic paresis and tabes dorsalis; CSF is abnormal and serologic tests reactive |
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describe congenital (prenatal) syphilus
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a component of TORCH Syndrome; infection of fetus in utero most common in primary or secondary syphilis; treatment of mother in 1st 4 months of pregnancy assures fetus won't be affected
In untreated prenatal syphilis, 25% of fetuses die before birth, 25-30% die shortly after birth, 40% of survivors develop late symptomatic syphilis Usually no abnormal physical findings at birth; in perinatal period the most striking lesions affect mucocutaneous tissues and bones; earliest sign of congenital syphilis is rhinitis (snuffles) followed by diffuse maculopapular desquamative rash; vesicular rash and bullas may develop (teeming w/ spirochetes) Osteitis of the nasal bones can lead to saddle-nose deformity; other characteristics include centrally notched, widely spread peg-shaped upper central incisors (Hutchinson's teeth), bilateral knee effusions (Clutton's joints), and interstitial keratitis |
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describe how to diagnose syphilis
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a. Dark-field Examination:
material from chancres, condylomas, and mucous patches show a large number of spirochetes b. Serologic Tests: i. Nontreponemal Reaginic Tests: Venereal Disease Research Laboratory (VDRL) slide test tests serum for its ability to flocculate a suspension of cardiolipin antigen; most often used to follow a patient's response to therapy ii. Specific Treponemal Tests: fluorescent treponemal antibody-absorption test (FTA-abs or FTA-ABS) is a standard indirect immunofluorescent antibody test that uses T. pallidum cells as the antigen; patient's serum is absorbed w/ nonpathogenic treponemal antigen (sorbent) to remove "natural" cross-reacting Ab T. pallidum hemagglutination assay (TPHA-TP) and micro-hemagglutination assay-TP (MHA-TP) also measure specific treponemal antibody, but are less sensitive in early disease Treponema pallidum immobilization (TPI) test determines ability of specific antibody plus complement to kill T. pallidum cells as visualized under dark-field microscope 3) False-Positive Reactions: A false-positive nontreponemal reaginic test can be recognized, and syphilis excluded, by obtaining negative result in a specific treponemal antibody test (FTA-ABS) In summary, the reaginic antibody tests (VDRL) are used for screening large numbers of sera, the specific treponemal tests (FTA-ABS) for confirming the diagnosis and the quantitative nontreponemal antibody tests (RPR, VDRL) for assessing the adequacy of therapy |
