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Pneumococcus Pneumococcus Presentation Transcript

    • G+,lanceolate diplococcus
    • Formly classified as Diplococcus pneumoniae
    • Reclassified to streptococcus pneumoniae-genetic relation with strept.
    • Differs from strpt in-
    • 1.morphology
    • 2.bile solubility
    • 3.optachin sensitivity
    • 4.sp.polysach.capsule
    • First noticed –pasteur &Sternberg
    • Realtion betwn pneumococci &pneumonia –Frankel &Weichsalbaum
    • Morphology
    • Small-1 micron –slightly elongatd—one end broad ,other pointd,flame shaped /lanceolate shaped.
    • Occurs in pairs-with broad ends in apposition long axis of the coccus parellel to the line joining the two cocci in a pair.CAPSULATED-capsule enclosing each pair.
    • Capsules—bst seen in materials taken bst from exudates-may b lost onb repeatd cultivation NONMOTILE,NONSPORING
    • In culture typical morph—not apparent—cocci r more rounded tending to occur in short chains
    • Staind with Anilline dyes---G+
    • Capsule-clear halo –inidan ink
    • Cultural chr.
    • Grow only in enriched media.—aerobes+fac.anero.Temp-37C---PH 7.8—growth is improcved by 5-10%Co2
    • Blood agar-inc-18 hrscolonies-small,dome shaped,glistening,with an area of green discolouration(alpha hemolysis)
    • Resemble colonies of str. Viridans—
    • Furthr inc—colonies become flat—with raised edges and central umbonation---so concentric rings r seen on the surface whn viewd frm above—”Draughtsman/Carrom Coin appearance”
    • Sm strains that dvlp abundnt capsular material(3 &7)---form large mucoid colonies
    • Under anerobic condition---colonies in blood agar –sorrondd by zone of beta hemolysis due to—O2 labile hemolysin O
    • Liquid media(gluc broth)-growth occurs as uniform turbidity
    • Cocci readily undergoes autolysis in cultures due to activity of intracellular enzymes.,enhancd by bile salts,Na lauryl suphate,and other surface active antigens
    • Heat killd cultures do not undergo autolysis
    • Biochemical reactions
    • Fermnt---acid
    • Ferm.-testd in HISS’s serum water/srum agar slopes.inulin f-+(diff strp.)
    • -bile soluble—
    • 1ml culture+drops of 10% sodium deoxycholate=lysis overn8
    • Loopful of deoxycholate—lysis in few min
    • Bile/Bile salts--+ts---amidase---cleavs the bond between alanine &muramic acidin the peptidoglycan.---lysis of organism---soluble
    • Tst at nuetral PH using deoxycholate &youn culture
    • C-….O-
    • Resistance
    • Delicate—destroyd by 52C 15 min and antiseptics
    • Ic culture –destroyd on prolongd inc—accumulation of toxic peroxidase—strains maintaind in semisolid blood agar/by lyophilisation
    • Penicilline DOC
    • Resistance—intermediate(MIC 1micgm),high(2micgm)---due o mutation /gene transfer—by alteration penicillin binding proteinson surface—resistant to multiple strains—DRSP-Drug Resistant Streptococcus Pnuemoniae
    • sensitivity to Optochin—1/5lakh—diffr.from strp.
    • Antigenic properies
    • Most imp-Type specific capsular polsacharid/SSS/specific soluble substances-diffuse into cultural medium/infective exudates and tissues
    • Clas.of pneumococci-antigenic nature of capsular polysach.
    • From lobar pneumoniae—Types 1,2,3. and a heterogenus grp 4
    • Typing done by
    • 1.agglutinaion of cocci with type specific aniserum
    • 2.Precipitation of SSS with specific serum
    • 3.Capsule swelling reaction by Neufeld(quelling Reaction)—Suspn.pnuem+antiseum+loopful of methylene blue---in presence of homologous antiserum capsule becomes apparently swollen,sharply delineatd and refractile.can b done directly with spuum from a/c pneumoniae---antigencty varies in sp.—antegenic in humans-no resp in mice in large quantity(immunological paralysis)---small quatities---resp+
    • Othr antigens-nucleoprotein,somatic C cho antigen
    • In a/c pneumonia case’s sera—an abnl protein—”btea globulin”---tht ppts somatic C r found---but dissappears during convalescnce
    • B-globulin—C reactive protein-(CRP)-not an antbody—a/c phase substance produced in hepatocytes—production stimulated by bac.inf.inflm.,malignancy, tissue destrrction---disappear whn infl.reactions subside
    • CRP-index - response to t/t in Rheumatic fever
    • Variation
    • On repeatd subculture—S-R variation.
    • R-colonies-rough-noncaps-autoaggluable-avirulent—as spontaneous mutants and outgrow the S type-in tissues they r eliminated by phagocytsR form +DNA---Transformation—Griffith
    • Toxin &virulent factors
    • O2labile hemolysin+lecocidin---weak---no virulence
    • Virulence depends on capsule and production of a toxin calld “pneumolysin”
    • Capsular poly sach-not phagocytosd effectvly---but suscepatble to surface Phagocyosis—being engulfd against a firm surface.(fibrin clot/epithelium)
    • Enhanced virulence of Type3-abundance of capsulr mat.
    • Noncapsular –avirulent
    • antibody to capsular polys..provides protection against inf.
    • Pneumolysin-a membrane damaging toxin by pneumococci-has cytotoxic+ complement activating property.virulnt fctr-immunogenic—
    • Pneumococcal autolysins by releasin bacterial components in infectd tissues, may also contribut to virulence
    • Pathogenicity
    • Colonise in human nasopharynx—infection in middle ear-paranasal sinus-and respiratory tract by direct spreadalso meninges---pneumococcal bacteremia—distant infections as heart,peritonium joints.inf-mostly endogenous—also exo
    • ---commonst—otitis media & sinusitis
    • Most common bac causing pneumonia—both lobar and broncho..+a/c tracheobronchitis and empyema
    • Aspiaration from nasophryngl scrn---lower RT---nl evn during sleep—nl mucosl defence mech-entrapmnt,expulsion and cough reflex-+ciliary escalator effect prvnt establishmnt of infection
    • Whn compromised—viral inf.,anaesthesia,chilling/---penetrate bronchial mucosa—spread thru lung along peribranchial tissues and lymphatics—bacteremia is common during the early stages of lobar pneumonia—toxemia—due todiffusion of caps.polysach—into blood and tissues
    • Fall of temp by crisis &relief of symptoms coinside wth neutralisation os SSS by anticapsular antibodies
    • 50% fatality is due to pneumococcal bactermia
    • Bronchopneumonia –always secondary inf.—caused by any serotype of pneumococcus—due to primarly damaged epi+increasd bronchial secrn----termilnla evnt in agd and debilitatad ones
    • ---exacerbated by c/c bronchitis-also haemophilus influenzaeass. Wth this codition
    • Meningitis –most serius of pneumococcal inf.---secondry to pneumonia,otits media,..in all ages…with antibiotics—fatality rate 25%
    • Other suppurative lesions
    • Empyema,pericarditis otitis medis,sinusitis,conjunctivits,,,
    • Epidemiology
    • Respiratory tract of carriers.-source—Ds-only whn host’s resistance lowerd+viral inf./pulmon.congestion/stress/malnutrition/immunodefficincy/alcoholism
    • *splenectomy and sickle cell ds.---predispose to it
    • Lab dg
    • a/c phase of lobar pneumonia—Rusty sputum—pneumococci in large no. with hardly any othr kind of bacteria,G+inoc-Blood ag.over n8 -37C,5-10%Co2---laryngal swabs can b used
    • Scanty-intraperitoneal inoculation into mice --+--dies in 1-3 days
    • Isolation of pneumococci frm blood indicates bad prognosis
    • a/c otits media-pneum-fluid of inner ear..---meningitis---CSF—and culture---if negetive---do Demonstration of SSS in CSF by ppting with atisera
    • Capsular polysach—demon-blood,urine,CSF—by counter immuno electrophoresi---antibodies can b demonstratd by agglutination pptn,mouse protection test,bactericidal test eith whole blood
    • Prophylaxis
    • Polyvalent polysach vaccine for 23 most prevelnt serotypes -80-90% protection
    • T/t
    • Parenteral penicilline
    • Serious-amoxycillin
    • Third gen cephalosporin
    • Vancomycin-life threatning illness