Gonorrhea and Chlamydia Flashcards
(31 cards)
N honorrhoeae bacteriology
-like n meningitidis:
-diplococci
-human restricted
-oxidase positive
-cleared from bloodstream by immune complement- complement deficiencies are predisposing for complications
-growth in vitro inhibited by trace metals and fatty acids- chocolate agar not blood agar
-gram negative LOS- just a few sugars instead of many (LPS)
unlike n meningitidis:
-not encapsulated
-hundreds of serotypes
-even more sensitive to dehydration, cold
-plasmid borne antibiotic resistance more common
-new and improved cephalosporin resistance
n gonorrhoear pathogenesis
- transmitted sexually or at birth
- neonate- purulent conjunctivitis
- male-usually symptomatic- anterior urethritis
- female- often asymptomatic, cervicitis
- genital tract infections most common, anorectal and pharyngeal also occur
- infection in children is reportable marker for sexual abuse
gonorrhea pathogenesis 2
- in US- 700 k new infections per year
- most common in african americans, rural southeast, inner cities, young unmarried, low education
- infection rates crashed in 1970s and have been creeping up more recently
virulence factors for gonorrhea
-IgA protease clears IgA from mucosal surfaces to facilitate colonization
-pili attach to columnar and transitional epithelium of mucosal surfaces, antiphagocytic
-opa-opacity associated proteins enhance cell adherence and entry
-porin A and B channels in outer membrane confer serum resistance, enhance cell entry
LOS- less immunogenic than LPS, but does induce local IF response (the drip, the clap)
gonorrhea pathogenesis 3
- most infections are vaginal or urethra
- antibodies, complement, neutrophils restrict to local site
- PID follows from mixing bacteria with refluxed menstrual blood or attachment to sperm
- can be some twitching mobility by pili
- dissemination can occur
- certain strains more likely to disseminate
- virulence factor is serum resistance, including protein porin A in cell wall (anti complement)
- more common in women
- asymptomatic infection, menses, pregnancy, and complement C6-C9 deficiency also predispose
diagnosis of gonorrhea on exam
- extremely contagious- single exposure contraction common
- symptoms develop quickly, within 10 days of infection
men: urethritis, dysuria, purulent discharge, sometimes unilateral epidiymitis
women: purulent vaginal discharge, cervicitis, PID, sterility, ectopic pregnancy
both: coinfection of pharynx, rectum, eye - all appear irritated/destroyed tissue with discharge
PID diagnosis
- lower abd pain
- vaginal discharge
- dysuria
- tenderness
- intermenstrual bleeding
- fitz-hugh-curtis syndrome- bacteria jump from fallopian tube to liver capsule- acute perihepatitis
- sonogram may show thick fallopian tubes or abscess
disseminated infection diagnosis
- DGI
- often lack urogenital symptoms
- arthritis, dermatitis syndrome with joint pain and skin pustules
- asymmetric tenosynovitis with pain in wrists and ankles
- moderate fever
- progression to septic asymmetric arthritis (knee common)
rare for gonorrhea
- gonococcal meningitis- admit, spinal tap
- endocarditis- echocardiogram, cardio consult
- more common in men
- aortic valve most common site
- subacute onset of fever, chills, sweats, malaise
- chest pain, cough
diagnosis in neonates
- bilateral conjunctivitis
- generally infected at birth, can happen postpartum of in utero
- eye pain, redness, discharge
- infection may also be pharyngeal, respiratory, rectal, or disseminated
- untreated, permanent blindness follows quickly
lab diagnosis G in males
- try first- urine and exudate testing
- obtain and centrifuge- morning void, swab exudate
- gram stain- PMN indicate urethritis, gram neg intracellular diplococci indicate gonorrhea
- nucleic acid amplification tests are available
- if negative- urethral swab
- gram stain again
- culture on thayer martin-chocolate agar with drugs to inhibit normal flora
- colonies tested for gram neg, oxidase pose, diplococci
- this is required if case has legal implications
- most sensitive and specific (urethral swab)
female Lab diagnosis for gonorrhea
- obtain endocervical smear (urethral sample if hysterectomy)
- wipe off exudate first
- culture on thayer martin
DGI lab diagnosis
- swab, gram stain, and culture al available mucosal surfaces and fluid draws
- samples from normally sterile sites may be cultured on non-selective chocolate agar (blood, joint fluid)
- immunofluorescence may give better results than gram stain on pustule samples
- *only meningococci ferment maltose
gonorrhea treatment
- begin promptly, in advance of lab work if necessary
- check local policy on antimicrobial resistance testing
- ceftriaxone, cefixime
- if allergic to penicillin, cephalosporin, but watch for resistance
- add azithromycin or doxy because chlamydia often co-infects
- aspirate septic joints
- if living in area with known Ab resistance, test cure 1 week after treatment, otherwise follow up in 3 months
- admit if pregnant, PID, DGI, endocarditis, meningitis, purulent joint infection
prevention of gonorrhea
- neonatal conjunctivitis-prophylatic application of erythromycin ointment or silver nitrate to eyes shortly after birth
- STD- condoms, prompt treatment of patient and all sexual contacts
- report incidence to local health authority, enlist them if patient resists informing sexual partners
- expedited partner treatment is warranted in some cases
chlamydia bacteriology
- doesn’t replicate by lysing or like a virus
- elementary bodies and reticulate bodies
- elementary bodies are tough and small, get into cell, turn into reticulate bodies to replicate, some turn back, the either lyse or reverse endocytosis to get back out
elementary bodies
- small- 0.3-0.4 microm
- infectious
- rigid outer membrane
- rugged
- bind to receptors on epithelium of lung or mucous membrane and initiate infection
reticulate bodies
- non infectious intracellular form
- metabolically active
- replicating
- synthesizes is own DNA, RNA, and proteins, but requires ATP from host
- fragile gram neg membrane
- inclusions- accumulate 100-500 progeny before release
immune response to chlamydia
- inflammatory cascade causes some of the symptoms-swelling, discharge
- IF response usually fails to clear infection or prevent reinfection
- no useful immune memory
urogenital chlamydia
- C trachomatis
- 18 serovars- A,B,Ba, C- blinding trachoma
- L1-L3- lymphogranuloma venereum
- D-K- genital tract infections
blinding trachoma
- infectious eye disease, leading cause of preventable blindness
- 84 million people suffer, 8 million visually impaired
- spread by secretions- direct and fomites
- untreated eyelids turn inward, causing eyelashes to scratch the cornea
- WHO aims to eradicate by 2020
lymphogranuloma venereum
- endemic in south and central america
- rare in US (obtain history of sex while traveling)
- a small, painless ulcer proceeds to swollen, painful lymph nodes
- symptoms are caused by bacterial replication in the mononuclear phagocytes of the local lymph nodes
- labwork and treatment are the same as for other genital chlamydia
- aspiration of buboes and fistulas may speed healing
genital chlamydia
- 4 million infections per year
- prevalence rates over 10% in sexually active adolescent females
- often asymptomatic, esp in male reservoirs
- most commonly local mucosal inflammation and discharge, urethritis or urethritis/vaginitis/cervicitis
- infection increases risk of acquiring HIV
- pregnant women infected can pass infection to infants during delivery
- leading cause of PID-chronic pain and ectopic pregnancy
risk factors for chlamydia
- non-barrier contraceptive use
- multiple sexual partners
- single marital status
- age <19
- socioeconomic disempowerment