Neisseria

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Neisseria

  1. 1. NEISSERIA G-
  2. 3. <ul><li>G-,aerobic,NONSPORING,NONMOTILE,O+ </li></ul><ul><li>Cocci typically arrangd in pairs/diploccci </li></ul><ul><li>Imp memb—N.meningitidis,gonorrhoeae,lactamica-(commensal) </li></ul>
  3. 4. Neisseria Meningitidis <ul><li>Meningococcus-Diplococcus intracellularis meningitidis </li></ul><ul><li>Weichselbaum—describd and isolatd first </li></ul><ul><li>Cause meningococcal meningitis/cerebrospinal fever </li></ul>
  4. 5. <ul><li>Morphology </li></ul><ul><li>G-,oval/spherical cocci,0.6-0.8 micron size,typically arrangd in pairs,with the adjescnt sides flattend </li></ul><ul><li>Long axis of the coccus is at rt angles to a line joinig the two cocci in a pair </li></ul><ul><li>older cultures—autolysis </li></ul><ul><li>In smear frm lesions cocci r more regular—generally intracellular—NONMOTILE,most fresh r capsulated </li></ul>
  5. 6. <ul><li>Cultural characters </li></ul><ul><li>Donot grow on ordinary media—only in blood ,serum/ascitic fluid---which provide growth by neutralising certain inhibiting substances in the cultural media…rather than providing additional nutritional needs </li></ul><ul><li>Strict aerobes---35C,no growth below 30C,PH-7.4-7.6, </li></ul><ul><li>Growth facilitd by 5-10% Co2 & hogh humidity </li></ul><ul><li>On solid media---inc 24hrssmall-translucnt—round ,convex,bluish grey—smooth glistening surface,with entirs edges </li></ul>
  6. 7. <ul><li>Colonies –lenticular shape,btyrous in consistansy,easily emulsifiable </li></ul><ul><li>Weak hemolysis occurs in blood agar </li></ul><ul><li>S&R type r foundGrowth is poor in liquid media—produce granular turbidity with no suface growth </li></ul><ul><li>Media of culture—Blood ag,choclate ag,Muller-Hinton starch Casein hydrolysate agar </li></ul><ul><li>Modified Thayer Martin—withvancomycin,colistin,nystatin)-ia a usefl selctv med </li></ul>
  7. 8. <ul><li>Biochemical reactions </li></ul><ul><li>C+O+,1% soln of oxidase reagent(TMPDH)---colonies turn deep purple </li></ul><ul><li>Subcultures should be made fast—dies on prolongd exposure to reagnt </li></ul><ul><li>Also Kovac’s method—rubbing growth ---filtr papr with oxidase reagnt </li></ul><ul><li>Indole & H2s not produced—nitrates not reduced </li></ul><ul><li>Glu &mal—utilised,not sucrose/lactose----producing acid but no gas </li></ul><ul><li>Acid formn is weak---being oxidativebest testd on peptones serum agar slopeswith sugar and indicator </li></ul>
  8. 9. Antigens <ul><li>Capsular polysaccharides –A,B,C </li></ul><ul><li>Endotoxin -LPS </li></ul>
  9. 10. <ul><li>Antigenic pro.and classification </li></ul><ul><li>Meningococci-capsulated unlike other neisseriae </li></ul><ul><li>Based on capsular polysach. Antigens—13 serogroups (A,B,C-imp) </li></ul><ul><li>A-epidemics---B-epidemics &outbreaks—29E,W135,Y—frequently cause meningitis. </li></ul><ul><li>Sergroups furthr classified into serotypes and subtypes basd on outer membrane proteins & polysacharids </li></ul>
  10. 11. <ul><li>Resistance </li></ul><ul><li>Meningococci-delicate-highly suscetable to heat dessication,alterations in PH and disinfectants </li></ul><ul><li>They wr resistant to penicillin,but now resistant strains hav emergd </li></ul><ul><li>Pathogenicity </li></ul><ul><li>Main ds.---Cerebrospinal meningitis&Meningococcal septicemia </li></ul><ul><li>Meningococci –strict human pathogens inhibiting nasopharynx </li></ul><ul><li>Infections usually asymptomatic </li></ul><ul><li>--sometimes-local inflammation arises with rhinitis and pharyngitis—Dissemination occurs only in small proportions </li></ul>
  11. 12. <ul><li>Method od spread—directly naso—thru perineural sheath of olfactory nerve---cribrifirm plate—subarachnoid space </li></ul><ul><li>Or thru blood stram </li></ul><ul><li>Site of entry may be conjucntiva also-Meningococcal purulence conjunctivitis occurs </li></ul><ul><li>On CNS –a suppurative lesion of meninges is setup.—involving the surface of spinal cord+base and cortex of the brain—cocci r found invariably in spinal fluid-free and within the wbc </li></ul><ul><li>Untreatd –fatal 80%,survivers-blindness/deafnss </li></ul><ul><li>Som can dvlp chroonic/reccrnt meningitis </li></ul>
  12. 13. <ul><li>Meningococcimia presents with—A/c fever with chills, malaise and prostration </li></ul><ul><li>Typiacal petechial; rash occurs eary,meningococci may b isolatd from the lesions- </li></ul><ul><li>Metastaic involvmnt of joints, ears ,eyes, lungs and adrenals may occur </li></ul><ul><li>About 10% dvlp pneumonia </li></ul><ul><li>A few dvlp—WaterHouse Frederichsen Syndrome-/Fulminent meningococcimia—fatal condition—shock,DIC,multisystem failure---rarly chonic meningoccemia is seen </li></ul><ul><li>Meningococcal ds.is favourd by deff. Of terminal complemnt components(C5-C9) </li></ul>
  13. 14. <ul><li>Pathogenic agent—endotoxin-LPS –releasd by autolysis. </li></ul><ul><li>Vascular endothelium is particularly sensitive to endotoxin </li></ul><ul><li>All major inflammtory cascades,cytokines,NO,are triggrd and upregulated </li></ul><ul><li>In fulminent cases adrenal haemorrhage and profound shock r presnt. </li></ul>
  14. 15. <ul><li>Epidemiology </li></ul><ul><li>Only reservoir-human nasopharynx </li></ul><ul><li>Transmission-airborne droplets,formites </li></ul><ul><li>During inter epidemic period-carriesr rate is 5-10% </li></ul><ul><li>Common betwn 3-5yrs of age </li></ul><ul><li>Meningitis bet of Africa—Ethiopia to Senegal </li></ul>
  15. 16. <ul><li>Lab dig. </li></ul><ul><li>Primary agents causing purulnt bacterial meningitis— </li></ul><ul><li>Meningococci </li></ul><ul><li>Pneumococci </li></ul><ul><li>Haemophilus influenzae.b </li></ul><ul><li>B streptococci </li></ul><ul><li>Staphylococci </li></ul><ul><li>Ecoli </li></ul><ul><li>Listeria monocytogenes </li></ul>
  16. 17. <ul><li>Meningococcal meningitis-cocci presnt in large no. in CSF,and in early stages-in blood as well </li></ul><ul><li>Demontration in nasopharynx-detects carriers </li></ul><ul><li>Ex. Of CSF-fluid under pressure,pus cell.CSF collectd-three portions---centrifuged-one-gram stains—Meningococci is seen inside poymorphs+extra-(presumtiv dig-start antobiotic treatmnt)--- </li></ul>
  17. 18. <ul><li>Supernatent will contain meningococcl antigens—dem by Latex aggl/counter immunoelectrophoresis..---using meningococcal antisera </li></ul><ul><li>2 nd portion-inoc blood ag/choc ag.---31C,5-10% Co2—colonies appear aftr 18-24hrs—identified by moph&biochem. </li></ul><ul><li>Morphologically similar—N.flavescens,N.flave,Acinetobacter—may also cause purulent meningitis </li></ul><ul><li>3 rd portion-incubatd overn8 as it is/aftr adding equal vol of glu broth—and then subcultured on choc.ag.—sm times succed whr direct plating fails </li></ul>
  18. 19. <ul><li>2.blood culture- </li></ul><ul><li>3.Nasopharyngeal swab-sampling shud be done without contamination with saliva </li></ul><ul><li>4.Petechial lesions </li></ul><ul><li>5.Autopsy </li></ul><ul><li>6.Retrospective evidence-by detection of antibodies </li></ul><ul><li>7.Molecular dig. </li></ul><ul><li>Treatmnt </li></ul><ul><li>Intravenous penicillin G </li></ul><ul><li>Chloramphenicol,latr cephalosporins—for initiation of treatment before the cause if meningitis in known </li></ul>
  19. 20. <ul><li>Prophylaxis </li></ul><ul><li>Penicillin is unable to eradicate carrier state </li></ul><ul><li>Rifampicin/ciprofloxacin-recommended for chemoprophylaxis </li></ul><ul><li>Monovalent and polyvalent vaccines containing capsular polysacharides of groups—A,C,W135 and Y are available </li></ul><ul><li>Induce good immunity in adults and older children-little value below 3yrs </li></ul><ul><li>Immunity is grp specific </li></ul><ul><li>No grp B vaccine available present </li></ul>
  20. 21. Nesseria Gonorrhoeae <ul><li>Cause vaneral ds.-gonorrhea </li></ul><ul><li>Neisser- first describd in gonorrheal pus </li></ul><ul><li>Bumm-cultured-proved pathogenecity by inoculating into human volunteers </li></ul><ul><li>Gonococci resemble meningococci very close in many properties </li></ul>
  21. 22. <ul><li>Morphology </li></ul><ul><li>From urethral discharge-diplococcus,adjesnt sides concave,kidney shaped.—found more inside polymorphs—som cells cotain as many as 100 cocci </li></ul><ul><li>Gonococci posses pili on their surface—adhesion to mucosal surface+virulence inhibiting phagocytosis—agglutinate human red cells—haemagglutination is not inhibitd by mannose </li></ul>
  22. 23. <ul><li>Cultural characters </li></ul><ul><li>More difficult to grow thn meningo—aerobic—grow anerobically also—PH-7.2-7.6,temp-35-36C—essential to provide 5-10% Co2. </li></ul><ul><li>Grow well on Choc ag & Muller Hinton agar </li></ul><ul><li>Proper selsctive medium—Thayer-Martin medium(vancomycin,colistin and nystatin)—which inhibits most contaminents including nonpathogenic neisseria </li></ul><ul><li>Colonies-round-translucent-convex/slightly umbonate,with a finely granular surface and lobate margins.-soft & easily emulsifiable </li></ul><ul><li>Four types of colonies identified—T1-T4 </li></ul>
  23. 24. <ul><li>T1 & T2/(P+ & P++)-small brown colonies-pilated,autoagglutinable,virulent-a/c cases form this.—on serial subclture they change to T3/T4 </li></ul><ul><li>T3&T4/(P-)-larger-granular-nonpigmented colonies-nonpilated-forms smooth suspensions-avirulent </li></ul><ul><li>Biochemical reactions-Gonococci diff from meningococci except in the effect on maltose—Gonococci acidify only glucose and not maltose </li></ul>
  24. 25. Antigens of gonococci <ul><li>Pili </li></ul><ul><li>Trilaminar outer membrane </li></ul><ul><li>Protein 1 </li></ul><ul><li>Protein 2 (OPA) </li></ul><ul><li>Protein 3 </li></ul><ul><li>LPS </li></ul><ul><li>IG A1 protease </li></ul>
  25. 26. <ul><li>Antigenic properties-antigenically heterogenous-capable of changing their surface structures invitro –also invivo to avoid host defence— </li></ul><ul><li>Surface structures include—Pili &Trilaminar outer membrane </li></ul><ul><li>Pili-with repeatd peptide subunits(pilins)—includes constant & variable regions—undergoes antigenic &phase variations </li></ul>
  26. 27. <ul><li>Trilaminar outer membrane of Gonococci—with many diff.proteins </li></ul><ul><li>Protein 1-antigenic diversity shown-used for typing----Protein 1 of a single strain is antigenically constantbut variation in diff strains-(1A &1B)-on strain contains either of this –not both.—using monoclonal antibodies to protein 1 epitopes-gonococci can b classified into several serovars—A1-24—B1-32 </li></ul><ul><li>Protein 1&3 –ligand btwn coccus and host cells forms transmembrane channels/porins –exchange of molecules across the outer membrane </li></ul>
  27. 28. <ul><li>3.Protein 2 is related to the opacity of the gonococcal colonies----Opacity Associated Outer Membrane Prtein(OPA)---strains with OPA forms opaque colonies –others transparent-a strain may express 0 & 3 varieties of OPA protein at a time----OPA-responsible for attachment to host cells—clumping of cocci </li></ul><ul><li>4.Outer membrane lipopolysacharides(endotoxin)-resp-for toxicity in gonococcal infections </li></ul><ul><li>5.Both gonococci and meningococci elaborate IgA1 protease-that splits and inactivates IgA </li></ul>
  28. 29. <ul><li>Resistance-delicate organism-killd by heat, dryingf and antiseptics—it is a strict parastites and dies 1-2hrs in exudates outside the body </li></ul><ul><li>In cultures the cocci dies in 3-4 days.—but survives in slant cultures at 35C,if kept under sterile paraffin oil </li></ul><ul><li>Culture may be kept for year if frozen quickly and left at -70C </li></ul>
  29. 30. <ul><li>Pthogenecity-gonorrhea(flow of seed)-was first employed by Galen— </li></ul><ul><li>Aquinted by sexual cotact—steps </li></ul><ul><li>Adhesion to urethra/mucosal surface.(pili)-rapid &firm-so miucturtion after exposure wont protect. </li></ul><ul><li>Penetrates thru intercellular spaces---reach sub epithelial connective tissue-by the third day after infection-(inc.p-2-8 days) </li></ul><ul><li>Infection spreads thru the urethra to prostate ,seminal vescicles and epididymis </li></ul><ul><li>Ds starts with a/c urethritis with a mucopurulent discharge containing gonococci in large no. </li></ul><ul><li>C/c urethritis may lead to stricture formation </li></ul>
  30. 31. <ul><li>Infection may spread to periurethral tissues—causing abcesses and multiple discharging sinuses(Watercan perineum) </li></ul><ul><li>In women-initial inf—urethra &cervix-Vaginal mucosa is not usually affectd in adults(stratified sq.epi+acid PH) </li></ul><ul><li>Vulvovaginitis occurs in prepubertal girls </li></ul><ul><li>Infection may extend to bertholins glands-endometrium-fallopian tubes---pelvic inflammatory ds. And salpingitis may lead to sterility—rarly peritonitis may devlp with perihepatic inflammation(Fitz-Hugh-Curtis syndrome) </li></ul>
  31. 32. <ul><li>Proctitis occur in both sexes—it may dvlp by direct contiguous spread in women but in men it is usually the result of anal sex </li></ul><ul><li>Conjunctivitis may occur –usually due to auto inoculation by patient’s fingers </li></ul><ul><li>Blood invasion may occur from the primary sites—lead to metastatic lesions---arthritis-ulcerative endocarditis and very rarely meningitis </li></ul><ul><li>Occasional case of pyemia have been reorded </li></ul>
  32. 33. <ul><li>Gonococcal ophthalmia—nonvaneral---in newborn occurs due to direct infection via passage thru birth canal </li></ul><ul><li>Gonococcal bacteremia-leads to skin lesions –esp. haemorrhagic papules and pustules on hand,forarms,feet,legs---and to tenosynovitis and suppurative arthritis—usually of knees ,ankles and wrist </li></ul><ul><li>Gonococci contains several plasmids—transmissible codes for beta lactamase. </li></ul>
  33. 34. <ul><li>Epidemiology—source—carrier/patient </li></ul><ul><li>Mode of infection-vaneral </li></ul><ul><li>Only nonveneral-ophthalmia neonetaorum </li></ul><ul><li>-cotrolled by instilling-1% Silver Nitrate soln into all newborn babies—CREDE’S METHOD. </li></ul><ul><li>Higher incidence in persons belonging to blood group B </li></ul>
  34. 35. <ul><li>Lab dig </li></ul><ul><li>a/c-urethral discharge-gonococci in large no. </li></ul><ul><li>Meatus is cleand—gauze soakd in saline—discharge collectd with platinum loop(for culture)/directly on slide for smears </li></ul><ul><li>In women urethral discharge+cervical swab shud b collectd-using speculum-High vaginal; swabs r not satisfactory </li></ul><ul><li>C/C-no urethral discharge---morning drop of secretion examined-or some exudate obtained after prostatic massage- </li></ul><ul><li>If no discharge—centrifuge urine to dem. </li></ul>
  35. 36. <ul><li>Dem. Of intracellular G-ve diplococci-in stained smears presumptive evidence of gonorrhea in men. </li></ul><ul><li>Unreliable in women—as som of the normal genital flora hav an essentially similar morphology </li></ul><ul><li>Fluorscent antibody technques can be used </li></ul><ul><li>For culture—inoculated on prewarmed plates-immediately on collection-----if this is not possible collect with charcoal impregnated swabs- and sent in STUART’s transport medium </li></ul>
  36. 37. <ul><li>In a/c—cultures can b obtained readily on Choclate agars-/Mueller-Hinton Agr.-incubated at 35-36C-under 5-10% Co2— </li></ul><ul><li>In c/c-whr mixed infection is usual-and in examination of lesions such as proctitis---better to use selective medium –THAYER-MARTIN----growth is identified by biochemical and morphology </li></ul><ul><li>If not possible to obtain culture—as in metastatic lesions—Serological test-Complement Fixation test—becomes +ve only aftr some weeks of infection and remains +ve for years aftr cure---it is also +ve aftr meningococcal inf. </li></ul>
  37. 38. <ul><li>It is necessery to use polyvalent antigen—due to its antigen hetero. </li></ul><ul><li>Serological test not suitable for routine use </li></ul><ul><li>Othr serological tests attemptd—precipitation,passive agglutination,immunofluorescece,RIA—using whole cell lysate,pilus protein,lipopolysacharride antigens </li></ul>
  38. 39. <ul><li>Treatment </li></ul><ul><li>PPNG-Penicillinase Producing ones present </li></ul><ul><li>For uncoplicated gonorrhea— </li></ul><ul><li>Ceftriaxone 125mg IM/ciprofloxacin 500mg /oflaxacin 400mg </li></ul><ul><li>Doxycycline 100mg twice daily—7 days/Erythromycin 1g single oral dose </li></ul><ul><li>Works well against gonococci and coexisting chlamydial infection </li></ul>
  39. 40. <ul><li>Prophylaxis </li></ul><ul><li>No vaccination </li></ul><ul><li>Awareness </li></ul>
  40. 41. Non gonococcal urethritis/nonspecific urithritis <ul><li>c/c urethritis whr gonococci cannot b demonstratd </li></ul><ul><li>If conjunctivitis +arthritis in addition—REITER’S syndrome </li></ul><ul><li>Som –due to gonococci-in L forms –hence undetectable </li></ul>
  41. 42. <ul><li>Others </li></ul><ul><li>Chlam trachomatis </li></ul><ul><li>Ureaplasma urealyticum </li></ul><ul><li>Mycoplasma hominis </li></ul><ul><li>Herpis virus </li></ul><ul><li>Cytomegalovirus </li></ul><ul><li>Gardeneralla vaginalis </li></ul><ul><li>Acinetobacter lwoffi </li></ul><ul><li>Acinetobacter calcoaceticus </li></ul><ul><li>Fungi(Candida albicans) </li></ul><ul><li>Protozoa(Trichomonas Vaginalis) </li></ul><ul><li>Mechanical and chemical irritation </li></ul>
  42. 43. Commensal neisseriae <ul><li>In nl respiratory tract </li></ul><ul><li>N.flavescenes,N.catarrhalis-may cause meningitis </li></ul><ul><li>N.lactamica-avirulent—closely relatd to meningococci---diff. Being +ve on ONPG test for beta-galactosidase---presence in young children—antibodies protective against meningococcal inf. </li></ul><ul><li>N.catarrhalis-/Moraxella c/Branhamella c.-opportunistic pathogen—cause-laryngitis,bronchopneumonia,meningitis,sinusitis&middle ear disease. </li></ul>

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