Urethritis and Cervicitis Flashcards
1
Q
Neisseria gonorrhoeae Physiology and Structure
A
- Gram-neg. cocci
- Obligate human pathogen
*no natural animal reservoirs
*doesn’t survive long outside of host
*Fastidious: requires complex media for growth
- Outer membrane contains LOS (lipooligosaccharide)
*no repeating O antigen
- Don’t survive outside the human body long (cant get from a toilet seat)
2
Q
Neisseria gonorrhoeae Virulence Factors
A
All the surface structures on NG undergo extensive antigenic and phase variation
- Type IV pili
- Opacity Assoc. Proteins (Opa proteins)
- Lipooligosaccharide
- IgA protease
- Porin Protein (Por A and Por B)
- Iron binding proteins
3
Q
Type IV Pili
A
- Virulence factor of NG
- Required for infection, mediates binding to mucosal epithelial cells and tissues
- Mediates natural comopetence and biofilm formation
- Undergoes extensive intra-strain antigenic and phase variation
4
Q
Opacity Assoc. Proteins (Opa proteins)
A
- Virulence factor of NG
- Promotes attachment and invasion of human cells
- A single cell can have up to 12 opa genes
- Undergoes antigenic and phase variation; a single cell can express zero to several diff. Opa proteins
5
Q
Lipooligosaccharide (LOS)
A
- Virulence factor of NG
- Similar to LPS but lacks the long sugar O antigen
- Toxic to fallopian tube mucosa
- Sialylation of LOS prevents serum killing
- Subject to antigenic variaton
6
Q
IgA protease
A
- Virulence factor of NG
- Targets and cleaves IgA1
- Cleaves LAMP1 —> lysosome modification —> survival
7
Q
Porin Protein (Por A and Por B)
A
- Virulence factor of NG
- Abundant outer membrane protein
- Allows transport into cell, and contributes to survival
- PorBIA most commonly assoc. w/ DGI (serum resitance)
- Protein varies b/w strains
8
Q
Iron Binding Proteins
A
- Virulence factor of NG
- NG can scavenge iron from transferrin, lactoferrin, and haemoglobin
- Transferrin binding proteins (TbpA, TbpB): large surface proteins; transferrin receptor required for infection
9
Q
Neisseria gonorrhoeae Pathogenesis and Immune Response
A
- Attachment to mucosal cells followed by penetration and multiplication in cells and passage into sub-epithelial space
- Can survive in leukocytes, get into subepithelial space and produce a PMN rich exudate; its the immune response that is really damaging
- LOS and peptidoglycan induces TNF-alpha expression and sloughing of ciliated cells (i.e. inflammation)
- LOS inflammatory response or dissemination
- A protective immune response is not elicited, and there is no immune memory
10
Q
Clinical Syndromes of NG
A
- Urethritis (males)
- Cervicitis (females)
- Disseminated gonococcal infection
- Pharyngitis
- Purulent conjunctivitis (mild to aggressive)
- Proctitis (anorectal gonorrhea)
11
Q
Ng Urethritis
A
- Male NG clinical syndrome
- Uncomplicated mucosal infection
- 2-5 days incubation —> mucopurulent discharge and dysuria (discharge may be indistinguishable from NGU)
- Some infections may be asymptomatic
- Complications (rare): include epididymitis, disseminated gonococcal infection and reactive arthritis
12
Q
Ng Cervicitis
A
- Female NG clinical syndrome
- Commonly asymptomatic (up to 70%)
- Inflammation of the columnar epithelium and subepithelium of the endocervix
- When symptomatic: vaginal pruritis and/or mucopurulent discharge. Dysuria is atypical
- Abdominal pain and dyspareunia: suspect upper genital tract disease (eg. PID)
- Serious sequelae more common in women: includes salpingitis, PID, and DGI —> sterility, ectopic pregnancy, septic arthritis
13
Q
Disseminated Gonococcal Infection
A
- NG clinical syndrome
- Occurs in 0.5-3% of infected pts. (more common in women)
- Most that disseminate do not cause urethritis
- Most common cuase of septic arthritis in sexually active adults
- Pts deficient in complement components that form the MAC more susceptible
- Manifestations include:
*dermatitis-arthritis-tenosynovitis syndrome
*septic (purulent) arthritis (one joint)
*rarely, endocarditis, or meningitis
14
Q
Ng Pharyngitis
A
- NG clinical syndrome
- Usually acquired by oral sex exposure
- Majority asymptomatic
- Symptoms: sore throat, pharyngeal exudates, cervical lymphadenitis
- Thought to be site of acquisition of antibiotic resistance genes for Ng; we contain commensal neisseria in our throat and so the 2 can exchange genes
15
Q
Purulent conjunctivitis (mild to aggressive)
A
- In newborns: opthalmia neonatorum
- In adults and adolescents: autoinoculation from an anogenital source
- Non-sexual transmission reported in outbreak settings
16
Q
Ng Proctitis
A
- Ng clinical syndrome
- Anorectal gonorrhea
- Usually asymptomatic
- Males: typically in MSM, uncommon in heterosexual males; assoc. w/ a 3-fold increase in the risk of HIV infection
- Females: transmission to anal canal from vagina or anal intercourse
- Symptoms include: tenesmus, anorectal pain, bleeding and mucopurulent discharge
- Must be distinguished from other infectious causes of proctitis
37
Q
Lymphogranuloma venereum Stages
A
- 1st Stage (1-4wks post-infection): a painless ulcer develops at the site of infection that spontaneously heals. Pt may have fever headache, myalgia
- 2nd Stage (2-6wks later): local extension to inguinal or femoral lymph nodes (inflammation and swelling, Groove sign) —> inguinal buboes which gradually enlarge and may rupture
- Can spread further thru lymphatics to the rectum (proctitis) and/or progress to invasive infection, often w/ systemic symptoms
*abscesses can form in lymph nodes that suppurate and discharge thru the skin
- Late lymphogranuloma venereum: if left untreated can lead to other complications
