Pachymeningitis –rare mostly due to extention of

pg­1 Report on Etiology, Epidiology, pathogenesis, the treatment principles of the meningococcal infections.

Pachymeningitis –rare mostly due to extention of inflammation from the bones of the skull. Eg­ from chronic suppurative otitis media or compound fracture of the skull) (1) Etiology 1)Bacteria­ E.coli,B,Hemolitic Strep.(gr.B),Listeria monocytogenicmostly in neonates H.influenza, N,meningitidis, strep. Pneumoneae, M.tuberculosiskids <14yrs N.meningitides,Strep. Pneumoneaeadults Strep. Pneumoneae, Listeria monocytogens,M.tuberculosis,gr”­ “organisms elderly & immunocompromised 2)Virus­1.enterovirus group­coxsackie, echo, polio 2.mumps 3.Herpes simplex, H.zoster, V. zoster, EBV 4. HIV 5. Arbo V. (tick borne encephalitis) 3)Fungi 1.Cryptococcus 2. candida 4)Spirochaets­Leptospyra, treponema, Borellia5)Malignant cells 6)Blood, following subarachnoidal hemorrhage7)systemic dis. –LED 8)Drugs 9) Protozoa­malaria(cerebral or P. falsiparum) Toxoplasmosis 10) Poisoning(Pb, Hg) 5,6,7,8,10non infectious causes ( 2)Mode of transmission

1. Blood stream­due to septicemia or metastasis from infection in heart, lung, resp.tract 2. Direct spread – from septic foci in skull­sinusitis, otitis media: From septic foci in spine –osteitis,potts dis.: From trauma­ Lumbar puncture, penetrating wound.

(3)Meningitis (a)Pathology Bacterial­Pia, arachnoid is conjested w/ polymorphonuclear LeucocytesPus formation organised to form adhesionsleading to cranial N. lesions, hydrocephalus, cerebral edema(inTbc, brain is covered in a viscous, grey­green exudates, numerous tubercles found on the meninges) Viral­ there is predominantly Lymphocytic, inflammatory reaction in the CSF w/out the formation of puss or adhesions. There is no cerebral edema, hydrocephalus(unless viral encephalitis develops.) (b)clinical features – Intense malaise, fever, rigors, severe headaches, photophobia, vomiting, patient is irritable, often preffers to lie still, petechial rash, decr. Appetite Signs – Stiff neck, positive Kernig’s sign appears w/in a few hours, upper Brudzinski­when flexing neckflexion of leg, lower Brudzinsli­when flexing 1 legflexion of other leg, nistagmus In uncomplicated meningitis, consiousness is not impared, although pt. May be delirious w/ high fever, papillo edema may occur, drowsyness maybe (c)complications –1. CNS  hydrocephalus, deafness , cranial N. lesions 2. Heart pericarditis, endocarditis 3. Jointsarthritis (meningismus­state of irritation in Meninges­clinics are the same, but CSF is normal­eg:in severe intoxication) (d) Specific varieties of Meningitis – 1. Viral Meningitis­almost always benign,self limiting condition, lasting 4­10days. Consists of fever,headache(frontal & retro orbital) Meningeal irritation present , but sever meningeal irritation,.

Evidence­such as Kernig’s, Brudzinzski’s are absent, but neck stiffness positive.fever maybe with myalgia, malaise, anorexia,nausea, vomiting,mild degree of lethargy or drowsiness can be present. Photophobia, pain on moving eyes.

2.Tuberculous meningitis TBc causes chroninc meningitis w/ headache, lassitude , anorexia, & vomiting meningitic signs may appear only after some weeks., drowsiness, focal signs & seizures may occur.

3.Malignant Meningitis Malignant cells sometimes causes a subacute or chroninc meningitis process.

Meningitis, cranial N. palsy , para paresis & root lesions are seen often in complex pattern. CSFincreased.

Cells, incr. Prot. & often low glucose Treatmentintrathecal cytotoxic agents . Prognosis is poor.

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 ↑

(6)Prot (7) Glucose

0.2­0.4g/l

0.4­0.8g/l

50­80mg/dl( >1/2 of bl.

Glucose) (2.5­4.2mmol /l)

50­80mg/dl(>1/2 of bl. Glucose) (2.5­4.2)can be ↓­ mumps, fungal

m3 0.5­2g/l

0.5­3g/l

↓ (<1/2 of bl. ↓ (< 1/3 of Gluc.) bl. Glucose) (<2mmol/l) (<2mmol/l)

↑ (<3)

pg­3 Treatment: 1.bed rest . 2. isolation. 3. symptomatic­vit, antipyretics,analgesics, for convulsions­Diazepams,rehydration, disintoxication,diuretics. 4. etiological­I)Benzyl penicillin 2.4 mil U /i/v / 6h. ii) Cefotaxime (3rd gen) 2­4g/i/v can be used too(b/c of resistance) iii)if allergic to penicillin Cloramphenicol 75­100mg/Kg/day . iv) Steroids­for children w/ meningococcal meningitis (Dexamethazone) v) TBc – Rifampicine, Isoniazide, Pyrazinamide is the combination. vi) Local/nasopharyngitis­Amoxicillin, Doxaciclin (5­6 days) 5.Prevention­Polyvalent vaccines against recurrent pneumococcal meningitis & for some strains of meningococci. Rifampicine prophylaxis is given to contacts & family members.

DD of Meningitis­ According to etiological agents, which can lead to meningitis are D/D Main D/d in Latvia is tick borne encephalitis in which there are 3 stages ­ i ) fever(3­7 days)apyrexia(20) days  ii)Meningo encephalitisiii)Paralytic stage in meningo encephalitis stage there are meningial as well as encephalitis signs. Mental characteristics are encephalitis clinics­nervousness, tremor, halusinations, aggressiveness, memoty loss, to differentiate between Meningitis & encephalitis, can use clinics, if only encephalitisCSF normal findings & in later stages in encephalitisMRI, C.T. abnormalities positive. & if only Meningitisno MRI , C.T. abnormalities.

If Leptospirosis, MeningitisEncephalitis, if not treated.

Local infections­causing neck stiffness eg; cervical lymph nodes,tetanus (CSF normal in both these conditions) Concept about Aseptic Meningitis­ febrile, meningeal inflammation, characterized by CSF mono nuclear pleocytosis,normal glucose, mild elevation of prot. & an absence of Bac. On examination & culture. Can be due to i) infectivevirus(echo, coccackie.HSV, VZV,HIV,Measles)partly treated bact. Meningitis, fungi,atypical TB, syphilis, Lyme dis, Leptospyrosis, Lysteria, after SAH, after infections (Measles, small pox, Rubella, Varicella) ii)Non infectiveMeningeal infiltration of malignant cells(Leukemia, Lymphoma), chemical meningitis(intrathecal drugs, contrast,LP, contaminants), drugs(NSAID like Ibuprofen,Trimethoprim), Sarcoidosis,SLE, Parameningeal Disease­eg;sinusitis(chronic) or otitis, brain tumor.

Report on Etiology, Epidiology, pathogenesis, the treatment principles of the meningococcal infections.

Report prepared by 1. Dr. Sajid Mahmood, MD (EU), Accident & Emergency Department, NHS Royal infirmary Liverpool United Kingdom.

2. Dr. Adnan Akram, MD (EU), Department of Infectious Diseases. University Hospital Riga Latvia.

3. Dr. Aftab Ahmed, MD (EU), Infection Control Department, Kaunas Medical University Clinic. Lithuania.

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