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  1. Neisseria Buga Rudolf HTC LECTURE SERIES
  2. Introduction •Family- Neisseriaceae. •Genus- Neisseria •Species- N.gonorrhoeae, N.meningitidis, N.pharyngis, N.lactamica, N.catarrhalis (Moraxella catarrhalis). •Two species of medical importance:N. gonorrhoeae and N. meningitidis. •Inhabit mucosal surfaces. •Gram negative diplococci with opposing surfaces flattened or with concavity.
  3. Neisseria gonorrhoeae Microscopy: •Gram negative diplococci. •Occurs in pairs with adjacent surfaces flattened or concave. •Intra/extracellular occurrence in polymorpho nuclear neutrophils (PMNs)
  4. Diagnosis…….. Direct: Gram stained smears. Culture: •Specimens: U/swabs, cervical swabs, eye/swab, ear/swabs, joint aspirate, etc. •Media: Choc, MTM, MNYC agar. •Incubation: 24-48 hrs, ambient air + 5- 10% CO2.
  5. Diagnosis…….. Identification: • Oxidase test +ve, Glucose +ve. • Immunofluoresnce or COA • Sero-grouping: A, B or C • DNA probe test (not as sensitive as culture). • Sensitivity test.
  6. Pathogenesis • Gonorrhoea is an STD, the sites are urethra (men) and cervix (women) • Transmission through sexual contact • GC adheres to columnar epithelial cells, penetrate and multiply on the basement membrane • Adherence is facilitated by pili and Opa proteins • GC LPS stimulates the production of tumour necrosis factor (TNF), which causes cell damage
  7. Pathogenesis….. • GC may disseminate via blood stream. • GC produces extracellular protease that cleaves a proline-threonine bond in Ig A. This causes loss of antibody activity. • Approximately 9-15% affected women with PID have polymicrobic infections.
  8. Virulence factors •LPS •Extracellular IgA protease •Pili/fimbriae • Opa proteins
  9. Host defenses •Gonorrhoea infection stimulates local immunity (secretory Igs may enhance association with PMNs) •Uncomplicated infection activates complement via classical pathway, while disseminated infections activate complement via alternate pathway
  10. Diseases caused • Gonorrhoea • Ophthalmia neonatorum • Conjunctivitis • Skin lesions • Tenosynovitis • Septic arthritis • Endocarditis • Meningitis (very rarely).
  11. Epidemiology •Sexually transmitted worldwide •Highest attack rate men and women occurs between 15 and 29 years of age •The number of sexual partners, sexual preference and population mobility contribute to incidence of gonorrhoea
  12. Antibiotics/Control •Antibiotics • 3rd Generation Cephalosporins •Fluoroquinolones •Doxycyline •Spectinomycin • Azithromycin
  13. Control • Treatment of sex partner • No effective vaccine • Abstinence • Use condoms