Neisseria

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Neisseria

  1. 1. INFECTIOUS DISEASE OF PATHOLOGY (Bacterial Diseases) Niesseria Dr. Naila Awal
  2. 2. Classification Neisseria Pathogenic • N. gonorrhea • N. meningitidis Non- Pathogenic N. flava N. subflava N. pharyngitidis
  3. 3. Virulent factor 1) Pili- attach with host cell & anti phagocytic. 2)LPS- causes endotoxic shock 3)Ig A protease- Degrade Ig A coating --> invade mucus. 4) Capsule- Adhesion & antiphagocytic.
  4. 4. Pathogenesis of Neisseria gonorrhoeae • • • • • Agent- Neisseria gonorrhoeae Host- Human Reservoir- Patient suffering from gonorrhea Source of infection- Urethral/ Endocervical discharge Mode of transmission- a) Sexual contact b) Vertical transmission-Mother to fetus through the birth canal (Opthalmia neonatorum) Incubation period- 2-10 days
  5. 5. Primary infection begins at the columnar epithelium of urethra & peri urethral gland. Also in endocervix, rectal mucosa & conjunctiva. After contact, bacteria attach to epithelial cell by pili Then pass between the epithelial cell & goes to submucosa & multiply Immune response, manifested by inflammatory exudates which is at 1st serous & later on purulent together with infiltration of huge number of neutrophil & pus cell. From primary site they spread upward to involve the other sides of the body & causes lesion
  6. 6. Primary lesion • Male- Acute anterior urethritis Proctitis Pharyngitis • Female- Acute anterior urethritis Endocervicitis Note- They do not cause vaginitis, B/cA) vagina contain stratified squamous epithelium which prevents attachment of N. gonorrhea. B) Vaginal pH- acidic (Lactobacillus) • Children- Vulvo vaginitis • New born- Opthalmia neonatorum.
  7. 7. Secondary lesion 1)Via direct spreadMale Prostatitis Epididymitis Female Oophoritis Salphingitis Endometritis Tubo- ovarian abscess Bartholinitis Pelvic peritonitis
  8. 8. 2)Via lymphaticsCystitis Pyelonephritis Pyelitis 3) Via hematogenous route• • • • Ulcerative endocarditis Septic arthritis Tenosynovitis Iritis
  9. 9. Pathogenesis of N meningitidis • Mode of transmission- By airborne droplet N meningitidis Enter into nasopharynx & attach to epithelial cell of nasopharynx. Invade mucous membrane Colonize Enters to the blood stream CNS Through pili, they attach to the meninges--> Meningitis
  10. 10. Complication Male     Chronic prostatitis Vesiculitis Urethral stricture Sterility –Due to fibrosis caused by bilateral epididymitis Female Sterility Abortion-due to Endometritis PID Ectopic pregnancy( Due to fibrosis of FT)
  11. 11. Lab diagnosis SampleAcute infection• Male-Urethral discharge • Female-Endocervical discharge Chronic case• Male-Prostatic discharge by prostatic massage. • Female-Endocervical discharge Note- Not High vaginal swab b/c vaginal wall usualy not infected by N. gonorrhoeae b/c it is lined by stratified squamous epithelium .
  12. 12. 3) In case of proctitis- Rectal swab 4) In case of arthritis- Joint fluid 5) In case of opthalmia neonatorum –conjunctival discharge. Lab procedure1) Gram staining- Gram negative Intracellular & extracellular diplococci plenty of pus cell & neutrophil.
  13. 13. 2)CultureNon- specificChocolate agar- Heat lysed sheep blood+ Agar Specific culture mediaA) Modified New York City media (MNYCM) Heat lysed sheep blood+ Agar+ Antibiotic (Lincomycin, Colistin, Nystatin, Trimethoprim) B) Thayer Martin Media (TMM) Heat lysed sheep blood+ Agar+ Antibiotic (Vancomycin, Colistin, Nystatin, Trimethoprim)
  14. 14. • NoteWhich 1 is better, MNYCM/TMM? MNYCM b/c1) Contain Lincomycin 2)10% of Niesseria are sensitive to Vancomycin. ( Vancomycin kill Niesseria) So we will miss 10% case if we use TMM. But all gonococci are resistant to Lincomycin.
  15. 15. Incubate at 37C for 18-24 hrs in microaerophilic environment by candle jar. • Observation- 0.5-1 mm, circular, convex, graiysh white translucent colony. 4) Gram staining- Gram negative diplococci 5) Biochemical test• Oxidase test- Positive test • Rapid carbohydrate utilization test (RCUT)• N. Gonorrhoeae ferment glucose but not maltose. • N. meningitidis ferment both. 6) Detection of Ag/Ab- Can be detected in serum but it is useless as N. Gonorrhoeae undergoes rapid antigenic mutation.
  16. 16. Pathology of gonorrhoea in female genital tract Acute Suppurative salphingitis- Tubal mucosa --> congested Infiltration of neutrophil, plasma cell & lymphocytes. Salphingo-oophoritisTubal lumen is filled with exudates--> leak out of fimbriated end--> Spill over to ovary. Tubo-ovarian abscess- Collection of pus within tube & ovary. Pyosalphinx-Collection of pus within tube. Chronic follicular salphingitis- The tubal epithelium is denuded--> adhere to 1 another -->fuse to form gland like space / pouch
  17. 17. Pathology of gonorrhea in male genital tract Extension of infection• Posterior urethra-->prostate-->Seminal vesicle->Epididymis • Epididymis--> Frank abscess-->Extensive destruction of the organ. In neglected cases, the infection may spread to testis & produce suppurative orchitis.

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