Pachymeningitis –rare mostly due to extention of

pg­2 4.Meningococcal Meningitis  (acute bac. Meningitis) caused by N. meningitides A, B, C groups.: Gr. A & C –epidemics, gr B­sporadic It’s virulence is attributed to the polisaccharide capsule, wich resists phagocytosis & the lipo polysaccharide­ endotoxin complex which is responsible for it’s clinical toxicity, transmission by droplets or by direct contact.

I.P : 1 week. Humans are the only known reservoir, not stable in environmental optimal temp.­37oC, season is Spring. Pathogenesis­Spread by droplet infectionfrom naso pharyngeal colonization b/c of it’s humidity, & increased CO2 tension & specific receptor subst. Synthesized by naso pharynx to which they adherenaso pharyngeal cell invasionblood streem invasion transverses across bl. Brain barr. Enters CSF causes Meningitis Clinical Features­4 major clinical syndromes due to meningo cocci 1.Meningococcaemia –Associated w/ fever (spiking fever), headache, chills ,myalgia, arthralgia, malaise, tachycardia, tachypnoea,purpuric or petechial rash(skin manifestations occur early) Dg: i )bl. Culture ii)culture from scraping petechia, purpura. In 30%­50% of cases,there is meningococcaemia w/out meningitis.

2.Fulminent meningococcaemia(waterhouse­Friderichsen syndr.) Occurs in about 10% of pts.in whom there is high level of circulating toxins, Characterised by n extremely rappid downhill clinical cource, with extensive hemorrhage into the skin, petechia enlarged rapidly aswell, hypotention(can be due to adrenal hemorrhage Addisonian crisis hypotension) shock ,coma ,death­w/in a few hours from the onset of sympt. DIC may complicate the clinical picture further.Hemmor. into Adrenal gl. Mey or mey not occur., w/out treatment, 100% mortality.

3.Meningococcal Meningitis­Present w/ fever, nausea, vomiting, headache, photo phobia, altered consiousness, neck rigiditiy,etc.(same signs & sympt. As written b/4 under meningitis) 4.Chronic meningococcaemia.­Rare, intermittent fever,macculopapular rash, Arthralgia,splenomegally,bl.culture is positive during bacteraemic episodes.

Forms that can be identified clinically i)Local forms – 1. Nasopharyngitis, 2.carriers,3.pneumonias, ii)Generalised forms­1.meningococcaemia,2.Meningitis 1.Nasopharyngitis­clinicssore throat,subfebrile temp., light intoxication,running nose.Objectiveslocal lymphadenopathy 2.Pneumonea­clinicsunilateral lobular pneumonea w/high temp. & cough .

3.Mwningococcaemia & 4.Meningitis (3.& 4. clinics stated above & B/4) Complications­after Pneumonia­abscess & pleuritis: after meningitis­brain edema, micro abscesses in all the organs & brain .DIC, kidney damage w/ kidney failure or insufficiencytoxic shock Diagnosis­1)epidemiology­history of sinusitis, otitis,tonsillitis, TBc,lumbar puncture(c/I for Lumb. Punc.­ incr.i/c pressure, bleeding diathesis,cardiorespiratory compromise,infection­skin at the site) 2)clinics­symptoms & classical signs. 3)C.T.­to exclude SAH or i/cranial mass. 4. CSF , Bl.,petechial or joint aspirates examination.

5.Blood­routine tests(eg;Bl. Glucose) 6. 3 bac cultures from nasopharynx, from blood, from CSF & bacterioscopy(eg;CSF gram staining gr “­“ coci, meningococcus) 7.Urine analysis, LDH , ASSAT, ALLAT, CPK. 8. Detect the cause of infection­skull, sinus, spine X­ray.

Normal viral Bac. Tbc Malignant (1)colour Crystal clear Clear or turbid Turbid or Turbid or cloudy purulent viscous (2)amount 50­150ml (3)Pressure 60­150mm/H ↑ ↑ ↑ ↑ 2O (4)mononuclear 0­5/mm3 10­100/mm3 5­50/mm3 100­300/mm ­ C(lympho) 80%Lym.20%Ne 80%Neu. 3 u 20%Lym (5)PMN nil nil 200­3000/m 0­200/mm3 ↑