Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
141 Cards in this Set
- Front
- Back
|
What physical conditions cause UTIs?
|
stasis and reflux of urine
|
|
|
What are the 3 categories of UTIs?
|
1)community acquired vs. healthcare/hospital acquired (48 hr rule)
2)primary vs. recurrent UTIs 3)uncomplicated vs complicated |
|
|
What classifies recurrent UTIs?
|
3 or more episodes of symptomatic bacteriuria w/in a year
|
|
|
What constitutes a relapse of a UTI?
|
subsequent infection w/in 2 weeks of completing abx therapy
-same microbe b/c tx did not eliminate -indicative of structural abnormality or microbial invasion of tissues |
|
|
What constitutes a "reinfection" UTI?
|
-a new infection shortly (>2 wks) after resolution of the initial infection
-same or different pathogen -newly prescribed tx should interrupt cycle of colonization and infxn |
|
|
What classifies an uncomplicated UTI?
|
-structurally normal Urinary tract
-NO known compromises -ONLY associated with bacterial infxn -women>men -E.coli is the primary bacterium (UPEC-uropathogenic) |
|
|
What classifies a complicated UTI?
|
-result of some abnormality either anatomical or metabolic
-anatomical/structural include catheters, calculi, spinal cord injury, BPH, bladder/kidney dysfxn -metabolic abnormalities include diabetes, prego -impaired host responses such as AIDS or transplant recip. -unusual pathogens such as yeast -candida spp -M=F -all male UTIs are complicated! -can lead to prostatitis (but apparently are uncomplicated in men of age 15-50 yrs, no BPH and structural abnormalities with rare occurrence) -variety of bacterial pathogens |
|
|
What is the primary source of microbes for UTIs and what is the exception?
|
GI tract
-exception is Staph. saprophyticus can be transient flora of the skin as well as GI tract |
|
|
What are the organisms of uncomplicated UTIs in order from highest to lowest frequency?
|
1)E. coli
2)S. saprophyticus 3)proteus mirabilis, klebsiella pneumoniae, Group B strep |
|
|
Describe the occurrence of UTIs in the first few months of life by gender.
|
males>females
possibly due to congenital abnormality |
|
|
Describe the occurrence of UTIs in the elderly population by gender (>50 yrs old).
|
1:1 ratio of M:F
-males increase in frequency due to BPH |
|
|
What are the predisposing factors for UTIs in women?
|
1)anatomy-short female urethra
2)pregnancy-ureteric obstruction b/c fetal head is at pelvic brim blocks flow of urine, urinary stasis-hormonal effects on autonomic peristalsis 3)post menopausal-bladder or uterine prolapse, loss of estrogen leads to changes in vaginal flora 4)sexually active ppl-initial sex. activity "honeymoon cystitis", new sex. partner is new source of flora -some contraceptive methods such as spermicides (antibacterial kills lactobacilli), diaphragm 6)menses-loss of vaginal and uroepithelia + normal flora (inc. risk for E. coli and S. saprophyticus UTIs) |
|
|
What are the predisposing conditions for men to get UTIs?
|
1)anatomy-not circumcised, foreskin creates niche for gram neg. bacilli
2)sex. active ppl-female partner with UTI, anal intercourse 3)Urinary tract obstruction-BPH, stasis and reflux of urine |
|
|
What are predisposing factors for BOTH sexes in getting UTIs?
|
-underlying metabolic disorders (diabetes)
-iatrogenesis associated UTI (catheterization is most common cause nosocomial bacterial infxn) -completion of course of abx leads to disrupted normal flora -immune system disorders lead to inflammatory response defic. -chemokine receptor abnormalities (WBC) associated with pyelonephritis -congenital abnormality-like VUR (vesicoureteral reflux), similar response in prego women - |
|
|
Describe the use of adhesins in UTI pathogens.
|
-found in many UTI pathogens
-assist in colonizing vaginal epithelium and urinary mucous membranes -2 common fimbrial adhesions of E.coli are type 1 and P fimbriae |
|
|
What are the function of Type 1 fimbriae of E. coli?
|
-help to colonize LOWER urinary tract
-bind mannose residues on proteins of target cells |
|
|
What is the function of P fimbriae in E. coli that causes UTIs?
|
-pyelonephritis associated pili -UPPER urinary tract
-do not bind mannose and are therefore "mannose resistant" -do bind P blood group antigen/uroepithelial cells |
|
|
What are the uropathogenic virulence factors?
|
2 toxins and an enzyme
1)hemolysin-cytotoxic 2)endotoxin-LPS gram neg. bacteria 3)urease-raises pH of urine leads to possible formation of urinary stones -struvite crystals form in kidney and ureters -hydrolyzes urea to ammonia 4)capsular polysacchardies 5)motility |
|
|
What organisms are the urease producers?
|
P. aeruginosa
Proteus klebsiella ureaplasma urealyticum mycoplasma hominis |
|
|
What allows for biofilm formation in catheters and what organisms are commonly involved?
|
capsular polysaccharide virulence factor
-community of microbes such as Staph epi., E. faecalis, E. coli, proteus, P. aeruginosa -motility facilitates movement and swarming (coating of catheter) |
|
|
What is the capsular K antigen in uropathogenic bacteria?
|
protects from phagocytosis
-ONLY found in gram neg. enterobacteriacea |
|
|
Describe ascending UTIs.
|
the majority are this type
-most common pathogen is E.coli -caused by GI contamination for uncomplicated UTI -caused by iatrogenesis for complicated UTI |
|
|
Describe descending UTIs.
|
rare
-source is hematogenous and lymphatic -most common is S. aureus, M. tuberculosis and candida |
|
|
What is urethritis and what are sx?
|
-localized inflammation of urethra (NOT confirmatory sign of UTI)
-sx are dysuria, pyuria, hesitancy, increased frequency/urge to urinate, concurrent with cystitis in females and prostatitis in males -caused by STD and non STD organisms |
|
|
What is cystitis and what are the sx?
|
-localized infection/inflammation of the bladder
-sx are urethritis, bacteriuria (significant >10^3 CFU/mL), pyuria or odiferous urine, suprapubic tenderness |
|
|
How is cystitis differentiated from cystitis?
|
-more acute onset vs. urethritis
-more severe sx -hematuria |
|
|
Describe pyelonephritis.
|
upper UTI
-renal infxn., localized infection with systemic effects -pathogen can enter either descending or ascending -may ppt premature labor -sx include hallmark pain in flank, CVA tenderness, lower UTI sx (bacteriuria, dysuria, urgency, pyuria), spiking fever, systemic effects like N/V, HA, malaise |
|
|
Describe asx bacteriuria.
|
-UTI w/o specific sx
-presents a risk factor for upper UTI |
|
|
What is urethral syndrome?
|
-AKA frequency dysuria syndrome
-signs and sx of cystitis -NO urological abnormalities -STERILE urine cultures -occurs most often in white females aged 13-70 -there are theorized etiologies: Bacteroides fragilis, hormonal imbalances, inflammation of Skene's glands, rxn to certain foods, rxn to environmental chemicals |
|
|
Describe urine sampling techniques.
|
-midstream clean catch is most common
-others are catheter, suprapubic bladder aspiration -work up samples immed. or store at 4 C |
|
|
What are the standard definitions for diagnosis of UTIs based on bacterial counts?
|
-positive urine culture >10^5 CFU/mL
-pyuria-leukocyte count >10^5 WBC/mL -suggested definition is >10^2 CFU/mL + acute sx and pyuria -any CFU/mL with suprapubic aspiration or w/S. aureus |
|
|
What is the uricult test?
|
a dipstick method which can be used to quantify and tentatively ID bacteria in a suspected UTI
-normal flora may contaminate any lab sample (low CFU/mL may see S. epi, corynebact., lactobacillus, Viridans strep) |
|
|
What do urease producers do to the pH of urine?
|
increase it to near neutral
|
|
|
What does leukocyte esterase detect?
|
pyuria
-detects esterases released from degraded WBCs |
|
|
What does nitrate reductase detect?
|
-used to diagnose UTIs
-indirect test for bacteria -direct detection of nitrites -produced by E.coli, proteus, and klebsiella |
|
|
What is the Kirby Bauer test?
|
tests for abx susceptibility
-requires a PURE culture -uses the abx discs on agar plate |
|
|
Describe tx for an uncomplicated UTI.
|
-cystitis 3-7 days
-pyelo 5-7 days -abx for cystitis: nitrofurantoin, TMP/SMX, fosfomycin -main abx for pyelo is cipro |
|
|
What is methenamine hippurate used to tx?
|
AKA urex
-prophylaxis/suppressive tx for frequently recurring UTI -urinary antiseptic forms formaldehyde in acidic urine |
|
|
What is phenazopyridine hydrochloride?
|
-a urinary tract analgesic used for sx relief of dysuria, frequency, urgency
-dosage <2 days until abx take effect |
|
|
In whom do you tx asx bacteriuria?
|
1)prego women
2)preschool children due to possible renal scarring 3)pts with abnormal UT or scheduled for surg of UT |
|
|
In what location is HSV1 infection typically seen?
|
primarily above the belt infections
HSV2 is primarily below the belt -but either can cause dz at either site but distinction of viral type is important b/c genital HSV1 tends to be less severe and far less prone to recurrence |
|
|
What is "initial infection" with HSV?
|
-in pts with abs to one type of HSV who experience a first infxn with the opposite HSV type
|
|
|
What is "primary infection" with HSV?
|
in pts w/o HSV abs after first exposure to HSV1 or 2
|
|
|
Describe the sx of primary HSV 2 infxn.
|
-macules and papules that are followed by vesicles, pustules, and ulcers
-fever, malaise, inguinal adenopathy -severity of primary dz and complications are higher in women -lesions persist for about 3 wks |
|
|
Describe the sx of initial HSV2 infection.
|
-less severe than a primary infection and heals more quickly
-preexisting HSV1 abs do have a limiting effect on HSV2 dz severity -duration about 2 wks |
|
|
Describe HSV latency period.
|
-the viral genome remains in an episomal state in ganglial cells
-recrudescence will occur even in the presence of active humoral and cellular immunity -rule of thumb is the more extensive the initial outbreak, the more likely and frequent are recurrences -auto-inoculation of infection to new body sites is possible -unless superinfected, lesions will heal w/o scarring |
|
|
Are transplacental abs of the mother completely protective of exposed neonates?
|
NO!!
|
|
|
Describe the spread of HSV.
|
spread by contact with vesicular fluid, saliva, and secretions from infected to susceptible ppl
-most infxns are transmitted during asx shedding -for infxn, the virus must contact an abrasion or mucosal surface -HSV1 infxn is common and usually occurs early in life |
|
|
What is HSV2 infection associated with?
|
HIV1 acquisition
-lesions may facilitate HIV1 infection perhaps doubling the relative risk of HIV1 infxn |
|
|
What are the risk factors for HSV2 infxn?
|
sex-more common in females
marital status-more prevalent in divorced vs. married or single place of residence-more in cities strongest predictor is number of lifetime sex partners! |
|
|
What poses the major risk to the fetus for acquiring HSV infection?
|
-primary or initial HSV infection of the mother
-risk is much smaller with recurrent infxn (and is the most common form of HSV infxn during prego luckily) |
|
|
What are the routes of neonatal HSV infection?
|
1)in utero (rare)
2)intrapartum contact of fetus with infected maternal genital secretions (most this way) 3)postnatal acquisition (relatives and hospital personnel with orolabial HSV |
|
|
Describe the clinical manifestations neonatal HSV infection.
|
-typically symptomatic and sometimes lethal
-disseminated infxn has worst prognosis -intrauterine infxn. will see skin dz, eye dz, microcephaly or hydroceph. -encephalitis -skin, eye, and mouth infection |
|
|
How is diagnosis of HSV made?
|
direct samples of tissue helpful
-ballooning pathology -presence of enlarged and fused cells on a Tzanck smear -Cowdry type A inclusion bodies -PCR to detect CNS HSV infxns using specific primers that will reveal either HSV1 or 2 (does not distinguish active from latent) -culture preferred over PCR -ab tests in asx pts |
|
|
Describe the HPV virions.
|
they are tough, resist ether, acid, heat
-the largest and most complex of the Papova viruses -nonenveloped -DNA virus-circular dsDNA -est. latent infxns |
|
|
Describe HPV clinical manifestations.
|
-HPV gets to basal cell layer through breaks in the skin
-HPV early genes stimulate cell growth which allows for host cell (and virus) DNA replication -virus induced cell division increases # of prickle and basal cells which causes thickening (wart) -immune system resolves most infxns |
|
|
Describe HVP common warts (cutaneous).
|
HPV types 1-4
-common, flat -plantar warts are flat hyperkeratotic regions occurring on soles of feet |
|
|
Describe condylomata acuminata caused by HPV.
|
cauliflower like lesions on the genitalia, perineum, perianal regions
-primarily HPV 6/11 |
|
|
Describe cervical dysplasia caused by HPV.
|
types 16 and 18
precancerous lesions of the cervical epithelium |
|
|
Describe respiratory papillomatosis.
|
-juvenile form (<5 yrs old) by HPV types 6 and 11
-suggests that transmission from condylomata from mother occurs |
|
|
Describe HPV carcinogenesis.
|
-malignant transformation involves viral genes E6/E7 which interfere with host cell cycle regulation by interacting with p53 and Rb
-net effect is to trigger cell cycle progression -p53 degradation is accelerated by E6, E7 binds and inactivates RB -not entirely sufficient to cause cancerous transformation on their own -in cancerous cells, it has been shown that the viral genome has been integrated into host genome, in nonmalig. latent cells it is maintained as an episome (E2 expressed and prevents E6/E7 actions) |
|
|
What groups of people are prone to hand warts?
|
people working with meat, fish, and poultry
-HPV7 is the most frequent virus type observed in these lesions and is found oNLY in these lesions |
|
|
What is another STD associated with HPV infection?
|
-it is associated with HIV infxn
-HIV infxn increases risk of anogenital HPV infxns -immune suppression of transplant pts increase the risk of anogenital HPV infxns |
|
|
What are the most common viral venereal dz in the US?
|
HPV
-there are at least 100 recognized types of HPV -HPV 16 and 18 are most freq. assoc. with flat or subclinical warts and cancer |
|
|
How is HPV diagnosis made?
|
by eye or on clinical findings
-histology is the best means overall of confirmation but useless for detection of latent infxns -presence of an extensive cytoplasmic vacuolation in epithelial lesions is uniquely diagnostic for HPV infxn (koilocyte has distorted nucleus and large vacuoles) |
|
|
WHat are the top 3 biological threat agents?
|
anthrax
smallpox plague |
|
|
Describe anthrax.
|
-bacillus anthracis is causative agent
-spore forming rod shaped gram pos. -person to person transmission DOES NOT occur -incubation period following inhalation exposure is 1-60 days, but most cases occur w/in a week after exposure - |
|
|
Describe the clinical effects of anthrax.
|
-can present in 3 clinical forms: inhalation, GI, cutaneous
-pts with inhalation anthrax will have flu like sx, 2-4 days later pts will experience abrupt onset of resp. distress, high fever, and hemodynamic collapse, sx of resp. stridor and dyspnea caused by massive mediastinal lymphadenopathy, thoracic edema and pleural effusions -not a pneumonia, distinguishing feature of inhalation anthrax is a CXR showing widened mediastinum |
|
|
What is the mortality of anthrax?
|
w/o tx almost 100%
|
|
|
How is anthrax spread?
|
-primary contamination and methods of dissemination: may be delivered through aerosols, direct dermal inoc. w/spores, or contam. of food products
-secondary contamination and persistence of organism: spores can persist in the environment indefinitely -secondary aerosolization of spores from clothing or skin is unlikely |
|
|
How is anthrax decontamination and isolation carried out?
|
-in pts: exposed areas of skin should be washed with soap and water after potential contact with contaminated materials
-equipment, clothing, and other objects: a 0.5% hypochlorite solution effective |
|
|
What is the recommended tx for inhalation anthrax?
|
2 or more antimicrobial agents predicted to be effective are recommended due to the high mortality associated with inhalation anthrax
|
|
|
What is the prophylactic tx for anthrax exposure?
|
in asx pts confirmed or highly likely to have been exposed give cipro 500 mg BID X 60 days or doxy 100mg orally BID X 60 days
|
|
|
What are the routes of infection for smallpox?
|
inhalation or contact with skin lesions or secretions
-incubation period ranges from 7-17 days |
|
|
Describe the clinical manifestations of smallpox?
|
begins with generalized malaise, fever, rigors, HA, backache
-typical skin eruption characterized by progression over a period of 7-10 days -distribution of lesions is centrifugal and most prominent on face and extremities |
|
|
Is smallpox transmissible person to person?
|
yes, it is likely from airborne or droplet exposure or by contact with skin lesions or secretions
-most likely delivered by aerosolization |
|
|
Does the smallpox vaccine confer lifelong immunity?
|
no!!
|
|
|
What is the incubation period for the plague?
|
2-4 days
|
|
|
Describe the risk of secondary contaminatino and persistence of Y. pestis.
|
it is very sensitive to sunlight and heat and does not survive long outside of the host
-therefore, secondary contamination is not a concern |
|
|
Describe the outbreak control precautions for the plague.
|
-all pts with pneumonic plague should be isolated for the first 48 hrs after starting tx
-those who have been in contact with pneumonic plague should be given abx prophylaxis and placed under fever surveillance for 7 days |
|
|
What organism causes syphilis?
|
treponema pallidum
-a spirochete with a slow rotational motility, not visible by transmitted light with conventional stains -will grow in primary cell culture |
|
|
Describe the antigenicity of treponema pallidum.
|
-production of treponemal abs to somatic proteins
-production of nontreponemal abs to cardiolipin component of host mitochondrial membranes |
|
|
Describe the virulence of treponema pallidum.
|
-outer membrane proteins promote adherence to host cells
-hyaluronidase may facilitate perivascular infiltration -fibronectin coat in antiphagocytic -lesions are primarily the result of inflammatory response |
|
|
Describe the epidemiology of syphillis.
|
-exclusively a human pathogen
-horizontal and vertical transmission -usually acquired via direct sex. contact w/person who has prim. or secondary active lesion -can also get it via needle sharing, lesion near mouth, and transplacental transmission |
|
|
Describe the pathogenesis of primary syphilis.
|
-entry to subepithelial tissues through break in skin or passage btwn epithelial cells
-local mult. and dissemination to nearby LNs and other sites via blood -primary lesion develops and surface necrosis results in chancre formation which may be in an inapparent site (untx lesion heals in 3-8 wks with fibrosis) -the chancre is the principal lesion of primary syphilis (base is usually smooth and the border is raised firm) -a short latency lasts for 2-10 wks and then moves to secondary syphilis |
|
|
Describe the pathogenesis of secondary syphilis.
|
-development of superficial lesions of high infectivity (maculopapular rash)
-mucosal warty lesions develop in 1/3 of pts -immune complexes form in arteriolar walla |
|
|
Describe latent syphilis.
|
-absence of clinical signs and sx
-early latency (w/in 1 yr of infxn)-recrudescence of active secondary syph. -late latency (>1 yr after infxn)-relative immunity to relapse and reinfection, seropos. w/o dz in 2/3, tertiary syph. in 1/3 |
|
|
Describe tertiary syphilis.
|
-manifests in 5-20 yrs after infection
-meningovascular changes with focal neurologic changes and cortical degeneration=neurosyphilis -CV changes with aneurysm of ascending aorta=CV syphilis -granulomata in any tissue but esp in skin, bones, jts=late/benign syphilis |
|
|
Describe the manifestations of neurosyphilis.
|
-develops in 10% of untx cases
-late appearance in course of dz (5-35 yrs) -can be asx: positive CSF serology -meningovascular: meningitis, CNS damage due to vascular occlusion and infarction -parenchymatous: paralysis, tabes dorsalis |
|
|
Describe congenital syphilis.
|
-changes are seen after the fourth month of gestation, but infection probably occurred earlier
-earlier onset of sx after birth signals poor prognosis but most infants are born apparently healthy and develop signs and sx at 3 wks of age -maculopapular lesions, nasal obstruction w/mucoid discharge, osteitis of nasal bones, neurosyphilis, Hutchinson's triad: notched incisors, interstitial keratitis, 8th nerve deafness |
|
|
How is syphilis diagnosed?
|
-darkfield microscopy or direct immunofluorescence used to detect treponemes from prim. or secondary lesions
-most cases diagnosed serologically: nontreponemal tests (RPR) used for screening and treponemal tests (specific ab tests) are confirmatory for pos. screening tests |
|
|
What is the DOC for syphilis?
|
penicillin
-can also have Jarisch-Herxheimer rxn |
|
|
What are the virulence factors of Neisseria gonorrhoeae?
|
-antigenic variation of pili
-nonpiliated phase variants -porin protein and other proteins -IgA protease |
|
|
Describe the epidemiology of gonorrhea.
|
-adolescents have the highest rate
-major reservoir is the asx pt -genital, oral-genital, and rectal intercourse transmission -nonsexual transmission is extremely rare |
|
|
Describe the pathogenesis of gonorrhea.
|
-attachment to epithelia via pili and surface proteins is a critical step
-bacteria alter their surface properties as an adaptation to the host environment -nonimmunity due to antigenic variation of pili and surface proteins and retardation of phagocytic activity due to surface proteins -injury to cells via released lipooligosaccharide and PG -spread to other tissue via pilar attachment |
|
|
Describe the clinical features of gonorrhea in males.
|
-most common manifestation is acute anterior urethritis (inc. 1-14 days)
-predominant sx are urethral discharge or dysuria -frankly purulent discharge -spontaneous resolution over period of several wks -complications rare - |
|
|
What are the clinical sx of gonorrhea in females?
|
-increased vaginal discharge, dysuria, intermenstrual uterine bleeding and menorrhagia
-clinical assessment is confounded by the nonspecificity of signs/sx and high prevalence of coexisting cervical or vaginal infections -complications rare |
|
|
Describe the clinical features of gonorrhea in pregnancy.
|
manifestations are similar to those seen in nonprego women except: pharyngitis appears to be more prevalent and PID is less common
-complications include spontaneous abortion, PROM, premie delivery, ophthalmia neonatorum, pharyngeal infxns, urethritis, etc |
|
|
Describe the features of rectal gonorrhea.
|
-occurs in 35-50% of women with gonococcal cervicitis
-usually due to perineal contamination, usually asx -occurs in 25-40% of MSM due to direct inoculation through anal intercourse -sx range from minimal anal pruritis, painless mucopurulent discharge, or scant bleeding to overt proctitis w/severe pain, tenesmus, and constipation |
|
|
Describe the features of pharyngeal gonorrhea.
|
transmitted more readily by fellatio than by cunnilingus
-most are asx with spontaneous cure rate of 100% w/in 12 wks of infection -soreness and cervical adenitis may occur |
|
|
What are the complications of gonorrhea?
|
-acute salpingitis or PID
-long term sequelae include chronic pelvic pain, infertility and ectopic pregnancy secondary to scarring of tubes -Disseminated gonococcal infection (DGI)-any of the forms can lead to bacteremia, features include fever, migratory polyarthralgia, and petechial, or pustular rash -metastatic infxns such as endocarditis and meningitis may occur -Bartholin's gland abscess-apart from salpingitis is the most common complication of gonorrhea -epididymitis-present w/U/L testic. pain and swelling |
|
|
How is gonorrhea diagnosed?
|
-gram stain of exudate (good for males, but females it has a low sens/spec)
-cultivation-organism of fragile and requires careful collection technique and CO2 enriched atmosphere -noncultural techniques (DNA probe tests, nucleic acid amplification) |
|
|
What are some causes of nongonococcal urethritis?
|
-a "wastebasket" diagnosis
-caused by chlamydia, ureaplasma urealyticum, mycoplasma genitalium |
|
|
Describe the characteristics of Chlamydia trachomatis.
|
-obligate IC bacteria
-have gram-neg type outer membrane but w/o PG -metabolically deficient, rqre host derived ATP -have unique replicative cycle with hardy infectious form (elementary body) and fragile IC form (reticulate body) -development of glycogen inclusion bodies |
|
|
Describe the chlamydial elementary body.
|
highly infectious
small stable in extracell. environ. metabolically inactive cannot divide |
|
|
Decribe the chlamydial reticulate body.
|
noninfectious
large stable in IC environment metabolically active multiplies by binary fission |
|
|
What is the most prevalent STD in US?
|
chlamydia
|
|
|
What are the complications of untx chlamydial infxns in males?
|
urethritis
fever testicular pain and swelling inflammation of epididymis |
|
|
What are the complications of untreated chlamydial infections in females?
|
3-5 fold increased risk of HIV infxn
-cervicitis and salpingitis -ectopic prego -postpartum fever -neonatal conjunctivitis and pneumonia -PID |
|
|
Describe the pathogenesis of chlamydial infection.
|
-chronic inflammation may be due to certain toxin producing strains
-strains have a gene that encodes for a toxin that fxns like toxin B of C. difficile -protein scaffolding of the infected cells collapses causing mucosal cells to separate from each other |
|
|
How is chlamydial infection diagnosed?
|
-isolation in cell culture was the gold standard, detection of IC inclusions
-limitiations: technically difficult to obtain columnar epithelial cells, refrig. needed immed., long turnaround time -noncultural tests are available: ag detection, DNA amplification |
|
|
Why is control of Chlamydia so difficult?
|
-most cases are minimally sx or asx
-frequently unrecognized clinically, even with sx -very few screening programs -tx often inappropriate or inadequate |
|
|
What is lymphogranuloma venereum?
|
-occurs primarily in S. america and Africa
-due to other serotypes of C. trachomatis -inguinal adenopathy and eventual suppuration -abscesses, strictures, and fistulas with chronic infection -diagnosis via aspiration of node and isolation of agent |
|
|
Describe ureaplasma urealyticum and NGU.
|
-main reservoir is genital tract of sexually active persons
-colonization is present in >80% of ppl who have had 3+ sex partners -cause of chorioamnionitis and postpartum fever in women |
|
|
Describe the etiology of granuloma inguinale.
|
-due to klebsiella granulomatis, an encapsulated gram neg.
-occurs primary in developing countries -presence of chronic, persistent papules or ulcers on genitalia or groin -large ulcers become secondarily infected -presence of "pseudobubo" caused by induration of subcutaneous tissue in inguinal area |
|
|
How is diagnosis of granuloma inguinale made?
|
-impression smear of a biopsy specimen from the lesion
-stain with wright or giemsa stain -demonstration of clusters of encapsulated CB (Donovan bodies) in cytoplasm of mononuclear cells |
|
|
What are the characteristics of chancroid?
|
-more common in tropical countries
-females may be asx or have nondescript lesion -typical lesion is a tender papule on the genitalia that develops into a tender ulcer with sharp margins (soft chancre) -regional adenopathy and bubo development |
|
|
What causes chancroid?
|
H. ducreyi
|
|
|
Describe the soft chancre of chancroid?
|
-develops quickly
-vesicle or papule that quickly progresses to pustulation and ulceration -progressive enlargement w/autoinoculation and development of multiple ulcers -ulcer is painful and tender, bleeds easily, lacks induration |
|
|
How is diagnosis of chancroid made?
|
-requires ID of H. ducreyi from the genital ulcer or bubo material
-bubo material is frequently sterile -media requires growth supplements -PCR based method is commercially available |
|
|
Describe the etiology of trichomoniasis.
|
-due to trichomonas vaginalis, a flagellated protozoan
-exists only as a trophozoite -is an extracellular anaerobe -is transmitted by sex. intercourse -very common STD |
|
|
Describe the clinical features of trichomoniasis.
|
-in the male usually asx or with scanty, clear to mucopurulent discharge
-in the female, is usually symptomatic, profuse vaginal discharge, frothy and malodorous, associated with cell. atypism -creates an environment for bacterial vaginosis |
|
|
How is trichomoniasis diagnosed?
|
-a wet mount exam is most commonly used
-culture is more sensitive -monoclonal ab methods available -DNA probe test |
|
|
What are the epidemiologic features of bacterial vaginosis?
|
-hx of previous STDs
-hx of sex. activity -current use of intrauterine devices -hx of previous pregnancy or abortion -number of yrs of sex activity |
|
|
What are the criteria for bacterial vaginosis?
|
-pick any 3
-homogenous quality of secretions -presence of clue cells -release of fishy amine odor when 10% KOH is added -a vag. pH of >4.5 -presence of curved gram neg. or gram variable rods |
|
|
Describe purulent vaginitis.
|
-unclear etiology
-signs/sx are purulent discharge, lack of odor -diagnosis made by abundance of PMNs and desquamation |
|
|
What are some predisposing factors for yeast vaginitis?
|
-prego, esp. 3rd trimester
-onset of menses -suppression of T-cell fxn -presence of DM -usage of abx therapy -etc |
|
|
How is diagnosis of candidiasis made?
|
-a vaginal swab of the white exudate is used for gram stain and cultivation
-presence of pseudohyphae indicates a pathologic process -germ tube test -DNA probe test |
|
|
What is chorioamnionitis?
|
an acute inflammation of the fetal membranes during prego
|
|
|
Describe the etiology of chorioamnionitis.
|
-the source of the infection indicates the etiology
-vaginal source: gardnerella vaginalis, mycoplasma hominis, anaerobic bacteria -intestinal source: enterococci, E. coli, gram neg. bacilli |
|
|
What are the risk factors for chorioamnionitis?
|
-prolonged duration of labor or rupture of membranes
-multiple vaginal exams -young age -low socioeconomic class -multiparity -bacterial vaginosis |
|
|
Describe the pathogenesis of chorioamnionitis.
|
-majority of cases result from ascension of bacteria
-minority of cases result from hematogenous spread via the placenta |
|
|
What are the clinical manifestations and diagnosis criteria for chorioamnionitis?
|
fever, tachycardia, uterine tenderness
-diagnosis based primarily on the clinical signs -gram stain of amniotic fluid, leukocyte esterase activity, decreased glucose concentration are of added help |
|
|
Describe the pathogenesis of postoperative pelvic infxns.
|
-a biphasic response occurs in these infxns
-the peritonitis stage: an early onset phase with high rates of sepsis and death -gram neg. aerobes predominant -the abscess stage: a late onset phase, obligate anaerobes most common |
|
|
Describe the clinical manifestations of postoperative pelvic infections.
|
-pelvic cellulitis is the most common infxn associated with hysterectomy
-cuff cellulitis at the incisional margin is common -culture purulent material |
|
|
Describe the etiology of PID.
|
-usually due to N. gonorrhea or C. trachomatis
-can also be caused by various other aer. and anaer. bacteria |
|
|
Describe the epidemiology of PID.
|
-increased risk with STD (esp gonorrhea or chlamydia)
-prior episode of PID has occurred -sexually active adolescent -multiple sex partners -frequent douching |
|
|
What are the clinical manifestations of PID?
|
-lower abdominal pain
-abnormal vaginal discharge -painful intercourse -increased pain during menstruation -fever/chills -scarring |
|
|
How is diagnosis of PID made?
|
-clinical criteria are commonly used, but the method is often inaccurate
-evidence of inflammation-fever, leukocytosis, or elevated ESR -often requires further testing, sonography reveals an inflammatory adnexal mass -bacteria and WBCs in peritoneal fluid |
|
|
Describe the clinical manifestations of prostatitis.
|
-acute sx mimic those of lower UTIs
-edema of prostate can cause lower tract obstruction -presence of sudden onset chills/fever, generalized malaise and low back pain are common -chronic sx highly variable |
|
|
How is diagnosis of prostatitis made?
|
-for acute, gland is tender but palpation not recommended, pyuria present and urine culture reveals the pathogen usually E.coli
-chronic, accurate diagnosis requires pre and post massage specimens, pathogen usually a member of the enterobact. but STD pathogens possible -inflammatory cells characteristically present |
