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Meningitis

Meningitis is an inflammation of the protective membranes covering the brain and spinal cord. Bacterial meningitis is usually caused by bacteria entering the brain and spinal cord directly or through the blood. The most common symptoms are headache, fever, and neck stiffness. Complications can include seizures, brain damage, and hearing loss. Diagnosis involves examination of cerebrospinal fluid obtained through lumbar puncture. Treatment involves administration of broad-spectrum antibiotics until the specific bacterium is identified, then targeted antibiotics are given. Prompt treatment is important to reduce risk of serious complications or death from bacterial meningitis.

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Meningitis Presenter – Dr. Vaishali T Moderator – Dr. Shyamala R 1
Definition Meningitis is the inflammation of the leptomeninges ( pia and archanoid matter) surrounding the brain and spinal cord, with involvement of the subarachnoid space.
Types of meningitis Based on the onset Acute meningitis: • Progresses in few hours • Acute bacterial • Acute viral Chronic meningitis: • Progressively worsens over weeks (>4 weeks) • Bacterial, viral, fungal and parasitic.
Bacterial meningitis
Acute bacterial/pyogenic meningitis • Bacterial meningitis is an inflammation of the leptomeninges, usually causing by bacterial infection. • Bacterial meningitis may present acutely (symptoms evolving rapidly over 1-24 hours), sub acutely (symptoms evolving over 1-7days), or chronically (symptoms evolving over more than 1 week).
Epidemiology 6 • Annual incidence in the developed countries is approximately 5- 10 per 100000. • Approximately 90 per cent of cases occur in children during the first 5 years of life. • Cases under age 2 years account for almost 75% of all cases and incidence is the highest in early childhood at age 6-12 months than in any other period of life. • There are significant difference in the incidence of bacterial meningitis by season.
Etiological agents 7 • Acute: - Streptococcus pneumoniae (38%) - Neisseria meningitides (14%) - Hemophilus influenza (4%) - GNB’s ( E.coli, Klebsiella, Pseudomonas, Acinetobacter) - S. agalactiae - Listeria - Staphylococcus aureus (5%) • Chronic: - Mycobacterium tuberculosis
Etiology Dr.T.V.RaoMD 8 – Elderly and immunocompromised • Listeria Monocytogenes • Gram negative bacteria – Hospital-acquired infections • Klebsiella • Escherichia coli • Pseudomonas • Staphylococcus aureus
Etiology Dr.T.V.RaoMD 9 Children over 2 months  Haemophilus influenza type b  Neisseria meningitides  Streptococcus pneumoniae Children over 12 years  Neisseria meningitides  Streptococcus pneumoniae
Pathogenesis • Mode of transmission – droplets from respiratory secretions • Routes of infection: Hematogenous spread – most common, through choroid plexus Direct spread – otitis media, sinusitis, mastoiditis. Anatomical defect in CNS – surgery, trauma, congenital defects.
Predisposing factors 1. Age: neonates – highest prevalence d/t oImmature immune system oBirth canal oIncreased permeability to BBB 2. Vaccination: reduces meningitis (Hib) 3. Respiratory infections: alcoholism, diabetes, immunosuppression, splenectomy, etc. 4. CSF shunts: staphylococcus, pseudomonas, Acinetobacter. 5. Breach in BBB
Pathogenesis Dr.T.V.RaoMD 12 • Susceptibility of bacterial infection on CNS in the children – Immaturity of immune systems • Nonspecific immune – Insufficient barrier (Blood-brain barrier) – Insufficient complement activity – Insufficient chemo taxis of neutrophils – Insufficient function of monocyte-macrophage system – Blood levels of diminished interferon (INF) -γand interleukin -8 ( IL-8 )
Pathogenesis Dr.T.V.RaoMD 13 • Susceptibility of bacterial infection on CNS in the children – Specific immune • Immaturity of both the cellular and Humoral immune systems – Insufficient antibody-mediated protection – Diminished immunologic response – Bacterial virulence
Pathogenesis Dr.T.V.RaoMD 14  A offending bacterium from blood invades the leptomeninges.  Bacterial toxics and Inflammatory mediators are released. – Bacterial toxics • Lipopolysaccharide, LPS • Teichoic acid • Peptidoglycan – Inflammatory mediators • Tumor necrosis factor, TNF • Interleukin-1, IL-1 • Prostaglandin E2, PGE2
Pathogenesis 15 • Bacterial toxics and inflammatory mediators cause Suppurative inflammation. – Inflammatory infiltration – Vascular permeability alter – Tissue edema – Blood-brain barrier destroy – Thrombosis
Pathology 16 Diffuse bacterial infections involve the leptomeninges, arachnoid membrane and superficial cortical structures, and brain parenchyma is also inflamed. Ventriculitis (purulent material within the ventricles) – children. Subdural empyema may occur. Ventricle dilatation Hydrocephalus
Pathology 17 • Blood vessel walls may infiltrated by inflammatory cells. – Endothelial cell injury, Vessel stenosis, Secondary ischemia and infarction. Cerebral edema Meningeal irritation sign is found because the spinal nerve root is irritated. Cranial nerve may be damaged
Clinical manifestation 18 • Toxic symptom all over the body – Hyperpyrexia – Headache – Photophobia – Painful eye movement – Fatigued and weak – Malaise, myalgia, anorexia, – Vomiting, diarrhea and abdominal pain – Cutaneous rash – Petechiae, purpura
Dr.T.V.RaoMD 19
20 Clinical manifestation of CNS(Increased intracranial pressure) • Headache • Projectile vomiting • Hypertension • Bradycardia • Bulging fontanel • Cranial sutures diastasis • Coma • DE cerebrate rigidity • Cerebral hernia
21 Meningeal irritation sign • Neck stiffness • Positive Kernig’ s sign • Positive Brudzinski’ s sign
Kernig's sign. 22 • One of the physically demonstrable symptoms of meningitis is Kernig's sign. • Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
Brudzinski's sign • Another physically demonstrable symptoms of meningitis is Brudzinski's sign. • Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. 31
Clinical manifestation 24  Seizures occur in about 20%-30% of children with bacterial meningitis.  Seizures is often found in Haemophilus influenza and pneumococcal infection.  Transient or permanent paralysis of cranial nerves and limbs may be noted.  Deafness or disturbances in vestibular function are relatively common.  Involvement of the optic nerve, with blindness, is rare.  Paralysis of the 6thcranial nerve, usually transient, is noted frequently early in the course.  Skin rashes
Symptom and signs of the infant under the age of 3 months – Only irritability, restlessness, dullness, vomiting, poor feeding, cyanosis, dyspnea, jaundice, seizures, shock and coma may be noted. – Bulging fontanel may be found, but there is not meningeal irritation sign. 25
Complications Dr.T.V.RaoMD 26 • Subdural effusion – 10%-30% of children with bacterial meningitis. – Subdural effusions - age of 1 year - Haemophilus influenza and pneumococcal infection. – Clinical manifestations are enlargement in head circumference, bulging fontanel, cranial sutures diastasis and abnormal trans illumination of the skull. • Cerebellar hyponatremia – Syndrem of inappropriate secretion of antidiuretic hormone (SIADH)
Complication 27 • Ependymitis – Neonate or infant with meningitis – Gram-negative bacterial infection – Clinical manifestation • Persistent hyperpyrexia, • Bulging fontanel • Cerebrospinal fluid by ventricular puncture – WBC>50×109/L – Glucose<1.6mmol/L – Protein>0.4g/L
Complication 28 • Hydrocephalus – Increased intracranial pressure – Bulging fontanel – Augmentation of head circumference – Brain function disorder • Other complication – Deafness or blindness – Epilepsy – Paralysis – Mental retardation – Behavior disorder
Laboratory diagnosis Specimen collection: CSF – lumbar puncture in 3 sterile containers 1 - cell count 2 - biochemical analysis 3 bacteriological examination Blood – culture and sensitivity Urine – immunochromatographic test
Laboratory Findings Dr.T.V.RaoMD 30 • Peripheral hemogram –Total WBC count • 20×109/L ～ 40×109/L WBC • Decreased WBC count at severe infection –Leukocyte differential count • 80% ～ 90% Neutrophils
Cytological and biochemical parameters in CSF of normal individuals and in different types of meningitis Characteristics Normal individual Pyogenic meningitis Tuberculous meningitis Viral meningitis CSF pressure (mm of water) Normal (50–150) Highly elevated (>180) Moderately elevated Slightly elevated/normal TLC (per mm3 ) 0–5 100–10,000 10–500 25–500 Predominant cell type Lymphocytes Neutrophils Lymphocytes Lymphocytes Glucose (mg%) 40–70 < 40 mg/Dl 20-40 absent Total proteins 15-45 >45 100–500 mg/dL 20–80 mg/dL ( mg%) (moderately increased) (markedly increased) (mild increase)
• CSF microscopy ( gram stain): - Heaped smear - Centrifugation • Direct antigen detection: -From CSF: supernatant- latex agglutination test - S. pneumoniae, S.agalactiae, N.meningitidis, H.influenza or E.coli -From urine: ICT – C-polysaccharide antigen of S. pneumoniae. • Culture: chocolate agar, blood agar and MacConkey agar.
Culture and identification properties of common bacterial agents of pyogenic meningitis Streptococcus pneumoniae: • Culture: It produces α-hemolytic colonies on blood agar, described as draughtsman-shaped or carrom coin appearance • Biochemical identification: It shows bile soluble, ferments inulin and sensitive to optochin. Neisseria meningitidis: It produces non- hemolytic colonies on blood agar, which on smear shows gram-negative diplococci. • Biochemical identification: Meningococci are catalase and oxidase positive. They ferment glucose and maltose but not sucrose • Serogrouping: Slide agglutination serogrouping (SASG) test is done to identify the serogroups of meningococci isolates by using appropriate antisera. Haemophilus influenzae: • Culture: Blood agar with S. aureus streak line shows satellitism. • Biochemical identification: Disk test for X and V factor requirement shows growth surrounding combined XV disk.
Optochin sensitivity Quellung reaction S.Pneumoniae
N. meningitidis Colonies on blood agar Gram stain showing gram negative diplococci
Haemophilus influenzae Satellitism around S.aureus Colonies on chocolate agar Effect of growth factors
Streptococcus agalactiae: • Culture: It produces β-hemolytic colonies on blood agar, which on smear shows gram-positive cocci in short chain. • Biochemical identification: It shows CAMP test positive and resistance to bacitracin • Serogrouping with group specific antisera shows Lancefield group B. Gram-negative bacilli meningitis: • Escherichia coli and Klebsiella produce lactose-fermenting colonies on MacConkey agar; identified by ICUT tests • Non-fermenters: Pseudomonas is oxidase positive, whereas Acinetobacter is oxidase negative. They produce non-lactose fermenting colonies; identified by ICUT tests. Listeria monocytogenes: • Motility: It shows tumbling type of motility at 25°C but nonmotile at 37°C (called differential motility, which is due to temperature dependent flagella expression) • Culture: It grows on blood agar (β-hemolytic colonies), and chocolate agar. Note: Selective media such as PALCAM agar (containing mixture of
Small, β-hemolytic colonies of L. monocytogenes on Blood agar Umbrella-shaped zone of motile growth after 24 hrs in semisolid motility medium at 25°C. L.monocytogenes
Laboratory Findings Dr.T.V.RaoMD 39 • Other test of CSF • LDH • Lactic acid • CRP • TNF and Ig • Neuron specific enolase (NSE)
Antibiotic Therapy 40 • Selection of antibiotic – Not Certainly Bacterium • Community-acquired bacterial infection • Nosocomial infection acquired in a hospital • Broad-spectrum antibiotic coverage as noted below – Children under age 3 months » Cefotaxime and ampicillin » Ceftriaxone and ampicillin (children over age 1months) – Children over 3 months » Cefotaxime or Ceftriaxone or ampicillin and chloramphenicol
Antibiotic Therapy 41 • Certainly Bacterium – Once the pathogen has been identified and the antibiotic sensitivities determined, the most appropriate drugs should selected. • N meningitides : penicillin, - cephalosporin • S pneumoniae: penicillin, - cephalosporin, Vancomycin • H influenza: ampicillin, cephalosporin • S aureus: penicillin, nefcillin, Vancomycin • E coli: ampicillin, chloramphenicol, - cephalosporin
Antibiotic Therapy Dr.T.V.RaoMD 42 • Course of treatment – 7 days for meningococcal infection – 10 ～ 14 days for H influenza or S pneumoniae infection – More than 21 days for S aureus or E coli infection – 14 ～ 21 days for other organisms
General and Supportive Measures 43 Treatment of hyperpyrexia and seizures – Pyretolysis by physiotherapy and/or drug – Convulsive management • Diazepam • Phenobarbital Treatment of increased intracranial pressure – Dehydration therapy • 20%Mannitol 5ml/kg vi q6h • Lasix 1-2mg/kg iv Treatment of septic shock and DIC
Complication Measures • Subdural effusions – Subdural pricking • Ependymitis – Ventricular puncture — drainage • Pressure in ventricle be depressed. • Ventricular puncture may give ventricle an injection of antibiotic. • Hydrocephalus – Operative treatment • SIADH (Cerebral hyponatremia) – Restriction of fluid 44
Prognosis 45 • Appropriate antibiotic therapy reduces the mortality rate for bacterial meningitis in children, but mortality remain high. • Overall mortality in the developed countries ranges between 5% and 30%. • 50 percent of the survivors have some sequelae of the disease.
Chronic meningitis
Definition • It is characterized by persistence of signs and symptoms as well as the CSF abnormality for >4 weeks. Agents of chronic meningitis: Bacterial agents Common bacterial agents • Partially treated suppurative meningitis • Parameningeal infections (e.g. otitis media) • Mycobacterium tuberculosis • Borrelia burgdorferi (Lyme disease) • Treponema pallidum (secondary, tertiary syphilis) Rare bacterial agents: Nocardia, Actinomyces, Tropheryma whipplei, Leptospira, Brucella. Viral agents Some of the agents of acute viral meningitis may also present as chronic meningitis. Examples: Mumps, echoviruses, herpesviruses, HIV and lymphocytic choriomeningitis virus.
Parasitic agents • Toxoplasma gondii • Free-living amoebae • Trypanosoma brucei (African sleeping sickness) • Angiostrongylus cantonensis (Eosinophilic meningitis) • Gnathostoma spinigerum • Baylisascaris procyonis • Cysticercosis, schistosomiasis, echinococcal disease • Toxocara canis and Trichinella. Fungal agents • Cryptococcus neoformans • Candida albicans • Blastomyces dermatitidis • Histoplasma capsulatum • Coccidioides immitis • Aspergillus species • Sporothrix schenckii • Pseudallescheria boydii • Cladophialophora bantiana
TUBERCULOUS MENINGITS (TBM) • Most common form of CNS tuberculosis • If untreated, high frequency of Neurologic sequelae and Mortality • TBM complicates 0.3% of untreated TB infections in children. • Common between 6 months and 4 years of age • Clinical progression of TBM may be rapid or gradual Rupture of 1 or more Subependymal tubercle • Rapid progression more often in infants and young children • Occasionally, TBM occurs many years after the infection 2
DIAGNOSIS • TST – Nonreactive in up to 50% of cases • CXR - 20-50% of children have a normal findings • HIV serology • Lumbar CSF study • Polymerase chain reaction (PCR) • Cultures of other body fluids can help confirm the diagnosis • Other Radiographic studies 7
CSF Study Specimen: CSF – centrifuge - aliquots of the sediment transferred to appropriate culture media. Low-volume fluid samples can be added directly to broth and incubated. • CSF cells - leukocyte 10-500 cells/µl Lymphocytes predominates • CSF glucose - <40 mg/dl • CSF Protein - markedly high (400-5,000 mg/dl) • Early stage 1 Viral aseptic meningitis then progress severely • Success of CSF study related to its volume • 5-10 mL of lumbar CSF Acid-fast stain positive in up to 30% of cases culture is positive in 50-70% of cases 8
Direct microscopy by acid-fast staining: Ziehl-Neelsen (ZN) technique—long slender, beaded, less uniformly stained red color acid-fast bacilli Kinyoun’s cold acid-fast staining Fluorescent (auramine) staining Conventional culture media—take 6–8 weeks Lowenstein Jensen (LJ) medium—shows rough, tough and buff colored colonies in 6–8 weeks, Middlebrook media. Automated culture methods—take 3–4 weeks MGIT system: Detects growth as well as resistance to antitubercular drugs (ATDs) Automated identification—by MALDI-TOF MPT 64 antigen detection—by ICT Molecular methods PCR detecting IS6110 gene CBNAAT (GeneXpert) and Truenat—for identification and detection of resistance to rifampicin; has a turnaround time 2 hours Line probe assay (e.g. Genotype TB)—for identification and detection of resistance to 1st and 2nd line ATDs; has a turnaround time of 2–3 days
M.tuberculosis Auramine–rhodamine. Stain with yellow fluorescence of the very short, slightly curved bacilli. L-J media with rough buff colonies Middlebrook 7H10 agar with rough colonies.
Internationally accepted ATT for TBM/Tuberculoma • Intensive phase Four drugs (RHZE/S) are recommended for 2 months • Continuation phase Isoniazid and Rifampicin are recommended for 10 months • Corticosteroids (usually prednisone) HIV Negative All children with TB meningitis at 2 mg/kg daily for 4 weeks Then gradually tapered over 1– 2 weeks before stopping HIV Positive Advised in the absence of life threatening opportunistic infections 20
Viral meningitis
Aseptic Meningitis • It is the inflammation of subarachnoid space due to viral etiology. • It is the second most common type of meningitis, next to acute bacterial meningitis. • It is often less severe than bacterial meningitis and has a better prognosis. • Etiological Agents: -Enteroviruses (Coxsackie's and echovirus): most common. -Adenovirus -Arbovirus -LCM virus -Measles virus -Herpes Simplex Virus -Varicella 58
Viral Meningitis Dr.T.V.RaoMD 59 Reservoirs: -Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex, and Varicella -Natural reservoir for arbovirus birds, rodents etc. Modes of transmission: -Primarily person to person and arthopod vectors for arboviruses Incubation Period: -Variable. For enteroviruses 3-6 days, for arboviruses 2- 15 days Treatment: No specific treatment available. Most patients recover completely on their own.
Non Polio Enteroviruses Dr.T.V.RaoMD 60  Types:62 different types known:  -23 Coxsackie A viruses,  -6 Coxsackie B viruses,  -28 echoviruses, and 5 other  Non-polio enteroviruses - most common cause of viral meningitis.  Cases - sporadic or occur in clusters  Examples - Coxsackieviruses, echoviruses, parechoviruses and Enterovirus 71. Mode of trsnsmission: • Virus present in the respiratory secretions & stool of a patien • Direct contact with secretions from an infected person. • Parents, teachers, and child care center workers may also become infected by contamination of the hands with stool.
Enteroviruses : • Transmitted by feco-oral route. • Multiply in the intestine - do not cause any intestinal manifestations. • Associated with various systemic manifestations Coxsackieviruses • spread through an infected person’s nasal and throat secretions, fluid from blisters or scabs. • Inoculating into tissue culture - Cytopathic effect can be observed within 5-14 days. • PCR targeting specific genes (e.g. VP1) is highly useful as it is rapid, more sensitive and serotype-specific • Serology is performed to detect neutralizing antibodies.
Echoviruses • (enteric cytopathogenic human orphan viruses) infect humans by feco- oral route. • Associated with aseptic meningitis, encephalitis, rashes, common cold, and ocular disease. Arboviruses • sometime cause meningitis, especially in individuals – recently travelled to the areas where these viruses are endemic. • Transmitted by the bite of their arthropod vectors. West Nile virus Saint Louis encephalitis virus Tick-borne encephalitis California encephalitis virus
HIV meningitis Meningitis in HIV infection may occur following primary infection in 5–10% of cases and less commonly at later stages of illness. • Cranial nerve palsies - involving cranial nerves V, VII, or VIII, are more common in HIV meningitis than in other viral infections. MUMPS meningitis: • Meningitis in mumps - secondary to parotitis. • Mumps meningitis - more common in the late winter or early spring, especially in unvaccinated children with a male preponderance. LCM meningitis • Lymphocytic choriomeningitis (LCM) virus affects people with history of contact with rodent droppings or urine.
Laboratory criteria for diagnosis: Normal or slightly elevated protein level (20–80 mg/dL) • Normal glucose level • Normal or mildly elevated CSF pressure (100–350 mm H2O) • Cell count - 25–500/μL, in some viral meningitis (e.g. LCM virus and mumps) the cell counts of several thousands/μL may be seen. • Pleocytosis: Lymphocytes – predominant cell type, although neutrophils may predominate in the first 48 h of illness in some viral meningitis (e.g. West Nile virus) • Organisms are not seen on Gram staining of CSF. VIRAL CULTURE • Sensitivity of CSF cultures - generally poor. • In addition to CSF, specific viruses – isolated from throat swabs, stool, blood, and urine • Isolation of enteroviruses from stool – not diagnostic
• The CSF analysis showed higher values of lactate level in bacterial meningitis with comparison to viral meningitis 8.35 ± 3.18 mmol/L and 3.4 ± 5.62 mmol/L (p value) • The CSF glucose level was found to be lower in bacterial meningitis than in viral meningitis, 9.63 ± 0.57 mg/dl and 57.96 ± 14.11 mg/dl. • The CSF protein level was high in bacterial than viral meningitis patients, with mean 298.33 ± 88.32 and 95.05 ± 49.42 mg/dl. • The CSF protein and lactate values, as well as CSF glucose value, can rapidly differentiate between bacterial and viral meningitis when conventional Gram's staining and culture are negative.7
Cytological and biochemical parameters in CSF of normal individuals and in different types of meningitis Characteristics Normal individual Pyogenic meningitis Tuberculous meningitis Viral meningitis CSF pressure (mm of water) Normal (50–150) Highly elevated (>180) Moderately elevated Slightly elevated/normal TLC (per mm3 ) 0–5 100–10,000 10–500 25–500 Predominant cell type Lymphocytes Neutrophils Lymphocytes Lymphocytes Glucose (mg%) 40–70 < 40 mg/Dl 20-40 absent Total proteins 15-45 >45 100–500 mg/dL 20–80 mg/dL ( mg%) (moderately increased) (markedly increased) (mild increase)
Treatment Treatment of almost all cases of viral meningitis is primarily symptomatic: Analgesics, antipyretics, antiemetics and fluid and electrolyte replacement. Oral or intravenous acyclovir may be of benefit in patients with meningitis caused by HSV-1 or 2 and in cases of severe EBV or VZV infection. Patients with HIV meningitis should receive highly active antiretroviral therapy.
Parasitic infections of central nervous system Protozoan infections of CNS • Free-living amoebae infections of CNS* • Toxoplasma encephalitis* • Cerebral malaria (Plasmodium falciparum)* • African sleeping sickness (Trypanosoma brucei)* • Chagas’ disease (meningoencephalitis, Trypanosoma cruzi) • Cerebral amoebiasis (E. histolytica) Cestode infections of CNS • Neurocysticercosis (Taenia solium)* • Others: Taenia multiceps, Spirometra and Echinococcus Trematode infections of CNS • Schistosoma mansoni and S. japonicum infections • Cerebral paragonimiasis Nematode infections of CNS • Hyperstrongyloidiasis syndrome (Strongyloides) • Eosinophilic meningitis (Angiostrongylus cantonensis) • Others: Loa loa (meningoencephalitis), Trichinella spiralis, Toxocara, Baylisascaris procyonis and Gnathostoma infections
Fungal agents causing CNS infections Primary CNS pathogen: Cryptococcus neoformans Fungi which primarily cause infections of other body sites, rarely cause CNS infections • Agents of systemic mycoses: Blastomyces dermatitidis, Histoplasma capsulatum and Coccidioides immitis • Agents of subcutaneous mycoses: Sporothrix schenckii, Pseudallescheria boydii and Cladophialophora bantiana • Opportunistic fungal agents : Candida albicans, Aspergillus species and Mucor (rhinocereberal mucromycosis) • Others: Microsporidia
Cryptococcal meningitis Cryptococcal meningitis is caused by a capsulated yeast called Cryptococcus neoformans, which is capable of producing potentially fatal meningitis in HIV infected people. C.Neoformans C.Gattii
Pathogenesis and Virulence factors • Infection is acquired by inhalation of aerosolized forms of Cryptococcus. • Polysaccharide capsule—It is the principal virulence factor of the fungus. It is antiphagocytic and also inhibits the host’s local immune responses • Ability to make melanin by producing an enzyme called phenyl oxidase • Production of other enzymes such as phospholipase and urease. • CNS spread: The unique feature of Cryptococcus is its ability to cross blood-brain barrier which occurs by the yeast cells either they migrate directly across the endothelium or carried inside the macrophages as “Trojan horse”
Lab diagnosis • Specimens: CSF, blood or skin scrapings. • Direct Detection Methods 1. Negative staining: Modified India ink stain (added with 2% mercurochrome) and nigrosin stain - demonstrate the capsule - refractile delineated clear space surrounding the round budding yeast cells against black background. 2. Gram staining may show gram-positive round budding yeast cells. 3. Other stains include: Mucicarmine stain: It stains the carminophilic cell wall of C. neoformans Masson-Fontana stain: It demonstrates the production of melanin Alcian blue stain: To demonstrate the capsule. 4. Antigen detection: The capsular antigens can be detected from CSF or serum by latex agglutination test. It is a rapid and sensitive (95% sensitivity) and specific method.
Negative staining Mucoid colonies on SDA agar Dark pigmented colonies on Niger seed agar
Confirmation of Cryptococcus species is made by: • Niger seed agar and bird seed agar: They are used to demonstrate melanin production (brown colored colonies). • Growth at 37°C . • Urease test is positive • Assimilation of inositol and nitrate • Mouse pathogenicity test • Automated identification system such as MALDI-TOF
TREATMENT • Treatment depends upon the type of cryptococcosis. • Cryptococcosis without CNS involvement: Fluconazole is the drug of choice. • HIV-infected patients with CNS involvement: - The recommended regimen is induction phase for two weeks (amphotericin B ± flucytosine) - followed by oral fluconazole therapy till CD4 T cell count raises >200 /µL for 6 months.
References 1. Koneman EW, Allen SD, Janda WM, Schreckenberger PC, Winn WC. Diagnostic microbiology,6th edition, Philedelphia: Lippincott-Raven Publishers(2017), pg.1075- 145. 2. Scott Bailey, Forbes Betty A, et al. Diagnostic Microbilogy, 12th edition, St. louis, Missouri: Mosby Inc (2007). 3. Jawetz, Melnick, Adelberg’s. Medical Microbiology, 28th edition, McGraw-Hill Education eBooks (2019). 4. Mandell, Douglas, Bennett’s. INFECTIOUS DISEASE ESSENTIALS, Philadelphia:Elsevier Inc.(2017). 5. Janagond, Anand & Sastry, Apurba & Bhat, Sandhya & Rajshekar, Deepashree. (2018). Essentials of Medical Microbiology, 2nd Edition. 6. M. Knipe, David, M. Howley, Peter, et al. F I E L D S Virology, 6th edition, Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer business(2013). 7. Ahmed S, Rakib A, Nasrin F, Chowdhury RH, Azad AK, Hasan CM. Assessment of cerebrospinal fluid (CSF) to differentiate between bacterial meningitis and viral meningitis. Journal of Advances in Medical and Pharmaceutical Sciences. 2018 Sep 6;17(4):1-7.

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Meningitis

  • 1.
    Meningitis Presenter – Dr.Vaishali T Moderator – Dr. Shyamala R 1
  • 2.
    Definition Meningitis is theinflammation of the leptomeninges ( pia and archanoid matter) surrounding the brain and spinal cord, with involvement of the subarachnoid space.
  • 3.
    Types of meningitis Basedon the onset Acute meningitis: • Progresses in few hours • Acute bacterial • Acute viral Chronic meningitis: • Progressively worsens over weeks (>4 weeks) • Bacterial, viral, fungal and parasitic.
  • 4.
  • 5.
    Acute bacterial/pyogenic meningitis •Bacterial meningitis is an inflammation of the leptomeninges, usually causing by bacterial infection. • Bacterial meningitis may present acutely (symptoms evolving rapidly over 1-24 hours), sub acutely (symptoms evolving over 1-7days), or chronically (symptoms evolving over more than 1 week).
  • 6.
    Epidemiology 6 • Annual incidencein the developed countries is approximately 5- 10 per 100000. • Approximately 90 per cent of cases occur in children during the first 5 years of life. • Cases under age 2 years account for almost 75% of all cases and incidence is the highest in early childhood at age 6-12 months than in any other period of life. • There are significant difference in the incidence of bacterial meningitis by season.
  • 7.
    Etiological agents 7 • Acute: -Streptococcus pneumoniae (38%) - Neisseria meningitides (14%) - Hemophilus influenza (4%) - GNB’s ( E.coli, Klebsiella, Pseudomonas, Acinetobacter) - S. agalactiae - Listeria - Staphylococcus aureus (5%) • Chronic: - Mycobacterium tuberculosis
  • 8.
    Etiology Dr.T.V.RaoMD 8 – Elderlyand immunocompromised • Listeria Monocytogenes • Gram negative bacteria – Hospital-acquired infections • Klebsiella • Escherichia coli • Pseudomonas • Staphylococcus aureus
  • 9.
    Etiology Dr.T.V.RaoMD 9 Children over2 months  Haemophilus influenza type b  Neisseria meningitides  Streptococcus pneumoniae Children over 12 years  Neisseria meningitides  Streptococcus pneumoniae
  • 10.
    Pathogenesis • Mode oftransmission – droplets from respiratory secretions • Routes of infection: Hematogenous spread – most common, through choroid plexus Direct spread – otitis media, sinusitis, mastoiditis. Anatomical defect in CNS – surgery, trauma, congenital defects.
  • 11.
    Predisposing factors 1. Age:neonates – highest prevalence d/t oImmature immune system oBirth canal oIncreased permeability to BBB 2. Vaccination: reduces meningitis (Hib) 3. Respiratory infections: alcoholism, diabetes, immunosuppression, splenectomy, etc. 4. CSF shunts: staphylococcus, pseudomonas, Acinetobacter. 5. Breach in BBB
  • 12.
    Pathogenesis Dr.T.V.RaoMD 12 • Susceptibilityof bacterial infection on CNS in the children – Immaturity of immune systems • Nonspecific immune – Insufficient barrier (Blood-brain barrier) – Insufficient complement activity – Insufficient chemo taxis of neutrophils – Insufficient function of monocyte-macrophage system – Blood levels of diminished interferon (INF) -γand interleukin -8 ( IL-8 )
  • 13.
    Pathogenesis Dr.T.V.RaoMD 13 • Susceptibilityof bacterial infection on CNS in the children – Specific immune • Immaturity of both the cellular and Humoral immune systems – Insufficient antibody-mediated protection – Diminished immunologic response – Bacterial virulence
  • 14.
    Pathogenesis Dr.T.V.RaoMD 14  Aoffending bacterium from blood invades the leptomeninges.  Bacterial toxics and Inflammatory mediators are released. – Bacterial toxics • Lipopolysaccharide, LPS • Teichoic acid • Peptidoglycan – Inflammatory mediators • Tumor necrosis factor, TNF • Interleukin-1, IL-1 • Prostaglandin E2, PGE2
  • 15.
    Pathogenesis 15 • Bacterial toxicsand inflammatory mediators cause Suppurative inflammation. – Inflammatory infiltration – Vascular permeability alter – Tissue edema – Blood-brain barrier destroy – Thrombosis
  • 16.
    Pathology 16 Diffuse bacterial infectionsinvolve the leptomeninges, arachnoid membrane and superficial cortical structures, and brain parenchyma is also inflamed. Ventriculitis (purulent material within the ventricles) – children. Subdural empyema may occur. Ventricle dilatation Hydrocephalus
  • 17.
    Pathology 17 • Blood vesselwalls may infiltrated by inflammatory cells. – Endothelial cell injury, Vessel stenosis, Secondary ischemia and infarction. Cerebral edema Meningeal irritation sign is found because the spinal nerve root is irritated. Cranial nerve may be damaged
  • 18.
    Clinical manifestation 18 • Toxicsymptom all over the body – Hyperpyrexia – Headache – Photophobia – Painful eye movement – Fatigued and weak – Malaise, myalgia, anorexia, – Vomiting, diarrhea and abdominal pain – Cutaneous rash – Petechiae, purpura
  • 19.
  • 20.
    20 Clinical manifestation ofCNS(Increased intracranial pressure) • Headache • Projectile vomiting • Hypertension • Bradycardia • Bulging fontanel • Cranial sutures diastasis • Coma • DE cerebrate rigidity • Cerebral hernia
  • 21.
    21 Meningeal irritation sign •Neck stiffness • Positive Kernig’ s sign • Positive Brudzinski’ s sign
  • 22.
    Kernig's sign. 22 • Oneof the physically demonstrable symptoms of meningitis is Kernig's sign. • Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
  • 23.
    Brudzinski's sign • Another physically demonstrable symptomsof meningitis is Brudzinski's sign. • Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. 31
  • 24.
    Clinical manifestation 24  Seizuresoccur in about 20%-30% of children with bacterial meningitis.  Seizures is often found in Haemophilus influenza and pneumococcal infection.  Transient or permanent paralysis of cranial nerves and limbs may be noted.  Deafness or disturbances in vestibular function are relatively common.  Involvement of the optic nerve, with blindness, is rare.  Paralysis of the 6thcranial nerve, usually transient, is noted frequently early in the course.  Skin rashes
  • 25.
    Symptom and signsof the infant under the age of 3 months – Only irritability, restlessness, dullness, vomiting, poor feeding, cyanosis, dyspnea, jaundice, seizures, shock and coma may be noted. – Bulging fontanel may be found, but there is not meningeal irritation sign. 25
  • 26.
    Complications Dr.T.V.RaoMD 26 • Subduraleffusion – 10%-30% of children with bacterial meningitis. – Subdural effusions - age of 1 year - Haemophilus influenza and pneumococcal infection. – Clinical manifestations are enlargement in head circumference, bulging fontanel, cranial sutures diastasis and abnormal trans illumination of the skull. • Cerebellar hyponatremia – Syndrem of inappropriate secretion of antidiuretic hormone (SIADH)
  • 27.
    Complication 27 • Ependymitis – Neonateor infant with meningitis – Gram-negative bacterial infection – Clinical manifestation • Persistent hyperpyrexia, • Bulging fontanel • Cerebrospinal fluid by ventricular puncture – WBC>50×109/L – Glucose<1.6mmol/L – Protein>0.4g/L
  • 28.
    Complication 28 • Hydrocephalus – Increasedintracranial pressure – Bulging fontanel – Augmentation of head circumference – Brain function disorder • Other complication – Deafness or blindness – Epilepsy – Paralysis – Mental retardation – Behavior disorder
  • 29.
    Laboratory diagnosis Specimen collection: CSF– lumbar puncture in 3 sterile containers 1 - cell count 2 - biochemical analysis 3 bacteriological examination Blood – culture and sensitivity Urine – immunochromatographic test
  • 30.
    Laboratory Findings Dr.T.V.RaoMD 30 •Peripheral hemogram –Total WBC count • 20×109/L ～ 40×109/L WBC • Decreased WBC count at severe infection –Leukocyte differential count • 80% ～ 90% Neutrophils
  • 31.
    Cytological and biochemicalparameters in CSF of normal individuals and in different types of meningitis Characteristics Normal individual Pyogenic meningitis Tuberculous meningitis Viral meningitis CSF pressure (mm of water) Normal (50–150) Highly elevated (>180) Moderately elevated Slightly elevated/normal TLC (per mm3 ) 0–5 100–10,000 10–500 25–500 Predominant cell type Lymphocytes Neutrophils Lymphocytes Lymphocytes Glucose (mg%) 40–70 < 40 mg/Dl 20-40 absent Total proteins 15-45 >45 100–500 mg/dL 20–80 mg/dL ( mg%) (moderately increased) (markedly increased) (mild increase)
  • 32.
    • CSF microscopy( gram stain): - Heaped smear - Centrifugation • Direct antigen detection: -From CSF: supernatant- latex agglutination test - S. pneumoniae, S.agalactiae, N.meningitidis, H.influenza or E.coli -From urine: ICT – C-polysaccharide antigen of S. pneumoniae. • Culture: chocolate agar, blood agar and MacConkey agar.
  • 33.
    Culture and identificationproperties of common bacterial agents of pyogenic meningitis Streptococcus pneumoniae: • Culture: It produces α-hemolytic colonies on blood agar, described as draughtsman-shaped or carrom coin appearance • Biochemical identification: It shows bile soluble, ferments inulin and sensitive to optochin. Neisseria meningitidis: It produces non- hemolytic colonies on blood agar, which on smear shows gram-negative diplococci. • Biochemical identification: Meningococci are catalase and oxidase positive. They ferment glucose and maltose but not sucrose • Serogrouping: Slide agglutination serogrouping (SASG) test is done to identify the serogroups of meningococci isolates by using appropriate antisera. Haemophilus influenzae: • Culture: Blood agar with S. aureus streak line shows satellitism. • Biochemical identification: Disk test for X and V factor requirement shows growth surrounding combined XV disk.
  • 34.
    Optochin sensitivity Quellungreaction S.Pneumoniae
  • 35.
    N. meningitidis Colonies onblood agar Gram stain showing gram negative diplococci
  • 36.
    Haemophilus influenzae Satellitism around S.aureus Colonieson chocolate agar Effect of growth factors
  • 37.
    Streptococcus agalactiae: • Culture:It produces β-hemolytic colonies on blood agar, which on smear shows gram-positive cocci in short chain. • Biochemical identification: It shows CAMP test positive and resistance to bacitracin • Serogrouping with group specific antisera shows Lancefield group B. Gram-negative bacilli meningitis: • Escherichia coli and Klebsiella produce lactose-fermenting colonies on MacConkey agar; identified by ICUT tests • Non-fermenters: Pseudomonas is oxidase positive, whereas Acinetobacter is oxidase negative. They produce non-lactose fermenting colonies; identified by ICUT tests. Listeria monocytogenes: • Motility: It shows tumbling type of motility at 25°C but nonmotile at 37°C (called differential motility, which is due to temperature dependent flagella expression) • Culture: It grows on blood agar (β-hemolytic colonies), and chocolate agar. Note: Selective media such as PALCAM agar (containing mixture of
  • 38.
    Small, β-hemolytic coloniesof L. monocytogenes on Blood agar Umbrella-shaped zone of motile growth after 24 hrs in semisolid motility medium at 25°C. L.monocytogenes
  • 39.
    Laboratory Findings Dr.T.V.RaoMD 39 •Other test of CSF • LDH • Lactic acid • CRP • TNF and Ig • Neuron specific enolase (NSE)
  • 40.
    Antibiotic Therapy 40 • Selectionof antibiotic – Not Certainly Bacterium • Community-acquired bacterial infection • Nosocomial infection acquired in a hospital • Broad-spectrum antibiotic coverage as noted below – Children under age 3 months » Cefotaxime and ampicillin » Ceftriaxone and ampicillin (children over age 1months) – Children over 3 months » Cefotaxime or Ceftriaxone or ampicillin and chloramphenicol
  • 41.
    Antibiotic Therapy 41 • CertainlyBacterium – Once the pathogen has been identified and the antibiotic sensitivities determined, the most appropriate drugs should selected. • N meningitides : penicillin, - cephalosporin • S pneumoniae: penicillin, - cephalosporin, Vancomycin • H influenza: ampicillin, cephalosporin • S aureus: penicillin, nefcillin, Vancomycin • E coli: ampicillin, chloramphenicol, - cephalosporin
  • 42.
    Antibiotic Therapy Dr.T.V.RaoMD 42 •Course of treatment – 7 days for meningococcal infection – 10 ～ 14 days for H influenza or S pneumoniae infection – More than 21 days for S aureus or E coli infection – 14 ～ 21 days for other organisms
  • 43.
    General and SupportiveMeasures 43 Treatment of hyperpyrexia and seizures – Pyretolysis by physiotherapy and/or drug – Convulsive management • Diazepam • Phenobarbital Treatment of increased intracranial pressure – Dehydration therapy • 20%Mannitol 5ml/kg vi q6h • Lasix 1-2mg/kg iv Treatment of septic shock and DIC
  • 44.
    Complication Measures • Subduraleffusions – Subdural pricking • Ependymitis – Ventricular puncture — drainage • Pressure in ventricle be depressed. • Ventricular puncture may give ventricle an injection of antibiotic. • Hydrocephalus – Operative treatment • SIADH (Cerebral hyponatremia) – Restriction of fluid 44
  • 45.
    Prognosis 45 • Appropriate antibiotictherapy reduces the mortality rate for bacterial meningitis in children, but mortality remain high. • Overall mortality in the developed countries ranges between 5% and 30%. • 50 percent of the survivors have some sequelae of the disease.
  • 46.
  • 47.
    Definition • It ischaracterized by persistence of signs and symptoms as well as the CSF abnormality for >4 weeks. Agents of chronic meningitis: Bacterial agents Common bacterial agents • Partially treated suppurative meningitis • Parameningeal infections (e.g. otitis media) • Mycobacterium tuberculosis • Borrelia burgdorferi (Lyme disease) • Treponema pallidum (secondary, tertiary syphilis) Rare bacterial agents: Nocardia, Actinomyces, Tropheryma whipplei, Leptospira, Brucella. Viral agents Some of the agents of acute viral meningitis may also present as chronic meningitis. Examples: Mumps, echoviruses, herpesviruses, HIV and lymphocytic choriomeningitis virus.
  • 48.
    Parasitic agents • Toxoplasmagondii • Free-living amoebae • Trypanosoma brucei (African sleeping sickness) • Angiostrongylus cantonensis (Eosinophilic meningitis) • Gnathostoma spinigerum • Baylisascaris procyonis • Cysticercosis, schistosomiasis, echinococcal disease • Toxocara canis and Trichinella. Fungal agents • Cryptococcus neoformans • Candida albicans • Blastomyces dermatitidis • Histoplasma capsulatum • Coccidioides immitis • Aspergillus species • Sporothrix schenckii • Pseudallescheria boydii • Cladophialophora bantiana
  • 49.
    TUBERCULOUS MENINGITS (TBM) •Most common form of CNS tuberculosis • If untreated, high frequency of Neurologic sequelae and Mortality • TBM complicates 0.3% of untreated TB infections in children. • Common between 6 months and 4 years of age • Clinical progression of TBM may be rapid or gradual Rupture of 1 or more Subependymal tubercle • Rapid progression more often in infants and young children • Occasionally, TBM occurs many years after the infection 2
  • 50.
    DIAGNOSIS • TST –Nonreactive in up to 50% of cases • CXR - 20-50% of children have a normal findings • HIV serology • Lumbar CSF study • Polymerase chain reaction (PCR) • Cultures of other body fluids can help confirm the diagnosis • Other Radiographic studies 7
  • 51.
    CSF Study Specimen: CSF– centrifuge - aliquots of the sediment transferred to appropriate culture media. Low-volume fluid samples can be added directly to broth and incubated. • CSF cells - leukocyte 10-500 cells/µl Lymphocytes predominates • CSF glucose - <40 mg/dl • CSF Protein - markedly high (400-5,000 mg/dl) • Early stage 1 Viral aseptic meningitis then progress severely • Success of CSF study related to its volume • 5-10 mL of lumbar CSF Acid-fast stain positive in up to 30% of cases culture is positive in 50-70% of cases 8
  • 52.
    Direct microscopy byacid-fast staining: Ziehl-Neelsen (ZN) technique—long slender, beaded, less uniformly stained red color acid-fast bacilli Kinyoun’s cold acid-fast staining Fluorescent (auramine) staining Conventional culture media—take 6–8 weeks Lowenstein Jensen (LJ) medium—shows rough, tough and buff colored colonies in 6–8 weeks, Middlebrook media. Automated culture methods—take 3–4 weeks MGIT system: Detects growth as well as resistance to antitubercular drugs (ATDs) Automated identification—by MALDI-TOF MPT 64 antigen detection—by ICT Molecular methods PCR detecting IS6110 gene CBNAAT (GeneXpert) and Truenat—for identification and detection of resistance to rifampicin; has a turnaround time 2 hours Line probe assay (e.g. Genotype TB)—for identification and detection of resistance to 1st and 2nd line ATDs; has a turnaround time of 2–3 days
  • 53.
    M.tuberculosis Auramine–rhodamine. Stain with yellow fluorescenceof the very short, slightly curved bacilli. L-J media with rough buff colonies Middlebrook 7H10 agar with rough colonies.
  • 56.
    Internationally accepted ATTfor TBM/Tuberculoma • Intensive phase Four drugs (RHZE/S) are recommended for 2 months • Continuation phase Isoniazid and Rifampicin are recommended for 10 months • Corticosteroids (usually prednisone) HIV Negative All children with TB meningitis at 2 mg/kg daily for 4 weeks Then gradually tapered over 1– 2 weeks before stopping HIV Positive Advised in the absence of life threatening opportunistic infections 20
  • 57.
  • 58.
    Aseptic Meningitis • Itis the inflammation of subarachnoid space due to viral etiology. • It is the second most common type of meningitis, next to acute bacterial meningitis. • It is often less severe than bacterial meningitis and has a better prognosis. • Etiological Agents: -Enteroviruses (Coxsackie's and echovirus): most common. -Adenovirus -Arbovirus -LCM virus -Measles virus -Herpes Simplex Virus -Varicella 58
  • 59.
    Viral Meningitis Dr.T.V.RaoMD 59 Reservoirs: -Humansfor Enteroviruses, Adenovirus, Measles, Herpes Simplex, and Varicella -Natural reservoir for arbovirus birds, rodents etc. Modes of transmission: -Primarily person to person and arthopod vectors for arboviruses Incubation Period: -Variable. For enteroviruses 3-6 days, for arboviruses 2- 15 days Treatment: No specific treatment available. Most patients recover completely on their own.
  • 60.
    Non Polio Enteroviruses Dr.T.V.RaoMD60  Types:62 different types known:  -23 Coxsackie A viruses,  -6 Coxsackie B viruses,  -28 echoviruses, and 5 other  Non-polio enteroviruses - most common cause of viral meningitis.  Cases - sporadic or occur in clusters  Examples - Coxsackieviruses, echoviruses, parechoviruses and Enterovirus 71. Mode of trsnsmission: • Virus present in the respiratory secretions & stool of a patien • Direct contact with secretions from an infected person. • Parents, teachers, and child care center workers may also become infected by contamination of the hands with stool.
  • 61.
    Enteroviruses : • Transmittedby feco-oral route. • Multiply in the intestine - do not cause any intestinal manifestations. • Associated with various systemic manifestations Coxsackieviruses • spread through an infected person’s nasal and throat secretions, fluid from blisters or scabs. • Inoculating into tissue culture - Cytopathic effect can be observed within 5-14 days. • PCR targeting specific genes (e.g. VP1) is highly useful as it is rapid, more sensitive and serotype-specific • Serology is performed to detect neutralizing antibodies.
  • 62.
    Echoviruses • (enteric cytopathogenichuman orphan viruses) infect humans by feco- oral route. • Associated with aseptic meningitis, encephalitis, rashes, common cold, and ocular disease. Arboviruses • sometime cause meningitis, especially in individuals – recently travelled to the areas where these viruses are endemic. • Transmitted by the bite of their arthropod vectors. West Nile virus Saint Louis encephalitis virus Tick-borne encephalitis California encephalitis virus
  • 63.
    HIV meningitis Meningitis inHIV infection may occur following primary infection in 5–10% of cases and less commonly at later stages of illness. • Cranial nerve palsies - involving cranial nerves V, VII, or VIII, are more common in HIV meningitis than in other viral infections. MUMPS meningitis: • Meningitis in mumps - secondary to parotitis. • Mumps meningitis - more common in the late winter or early spring, especially in unvaccinated children with a male preponderance. LCM meningitis • Lymphocytic choriomeningitis (LCM) virus affects people with history of contact with rodent droppings or urine.
  • 64.
    Laboratory criteria fordiagnosis: Normal or slightly elevated protein level (20–80 mg/dL) • Normal glucose level • Normal or mildly elevated CSF pressure (100–350 mm H2O) • Cell count - 25–500/μL, in some viral meningitis (e.g. LCM virus and mumps) the cell counts of several thousands/μL may be seen. • Pleocytosis: Lymphocytes – predominant cell type, although neutrophils may predominate in the first 48 h of illness in some viral meningitis (e.g. West Nile virus) • Organisms are not seen on Gram staining of CSF. VIRAL CULTURE • Sensitivity of CSF cultures - generally poor. • In addition to CSF, specific viruses – isolated from throat swabs, stool, blood, and urine • Isolation of enteroviruses from stool – not diagnostic
  • 65.
    • The CSFanalysis showed higher values of lactate level in bacterial meningitis with comparison to viral meningitis 8.35 ± 3.18 mmol/L and 3.4 ± 5.62 mmol/L (p value) • The CSF glucose level was found to be lower in bacterial meningitis than in viral meningitis, 9.63 ± 0.57 mg/dl and 57.96 ± 14.11 mg/dl. • The CSF protein level was high in bacterial than viral meningitis patients, with mean 298.33 ± 88.32 and 95.05 ± 49.42 mg/dl. • The CSF protein and lactate values, as well as CSF glucose value, can rapidly differentiate between bacterial and viral meningitis when conventional Gram's staining and culture are negative.7
  • 66.
    Cytological and biochemicalparameters in CSF of normal individuals and in different types of meningitis Characteristics Normal individual Pyogenic meningitis Tuberculous meningitis Viral meningitis CSF pressure (mm of water) Normal (50–150) Highly elevated (>180) Moderately elevated Slightly elevated/normal TLC (per mm3 ) 0–5 100–10,000 10–500 25–500 Predominant cell type Lymphocytes Neutrophils Lymphocytes Lymphocytes Glucose (mg%) 40–70 < 40 mg/Dl 20-40 absent Total proteins 15-45 >45 100–500 mg/dL 20–80 mg/dL ( mg%) (moderately increased) (markedly increased) (mild increase)
  • 67.
    Treatment Treatment of almostall cases of viral meningitis is primarily symptomatic: Analgesics, antipyretics, antiemetics and fluid and electrolyte replacement. Oral or intravenous acyclovir may be of benefit in patients with meningitis caused by HSV-1 or 2 and in cases of severe EBV or VZV infection. Patients with HIV meningitis should receive highly active antiretroviral therapy.
  • 68.
    Parasitic infections ofcentral nervous system Protozoan infections of CNS • Free-living amoebae infections of CNS* • Toxoplasma encephalitis* • Cerebral malaria (Plasmodium falciparum)* • African sleeping sickness (Trypanosoma brucei)* • Chagas’ disease (meningoencephalitis, Trypanosoma cruzi) • Cerebral amoebiasis (E. histolytica) Cestode infections of CNS • Neurocysticercosis (Taenia solium)* • Others: Taenia multiceps, Spirometra and Echinococcus Trematode infections of CNS • Schistosoma mansoni and S. japonicum infections • Cerebral paragonimiasis Nematode infections of CNS • Hyperstrongyloidiasis syndrome (Strongyloides) • Eosinophilic meningitis (Angiostrongylus cantonensis) • Others: Loa loa (meningoencephalitis), Trichinella spiralis, Toxocara, Baylisascaris procyonis and Gnathostoma infections
  • 69.
    Fungal agents causingCNS infections Primary CNS pathogen: Cryptococcus neoformans Fungi which primarily cause infections of other body sites, rarely cause CNS infections • Agents of systemic mycoses: Blastomyces dermatitidis, Histoplasma capsulatum and Coccidioides immitis • Agents of subcutaneous mycoses: Sporothrix schenckii, Pseudallescheria boydii and Cladophialophora bantiana • Opportunistic fungal agents : Candida albicans, Aspergillus species and Mucor (rhinocereberal mucromycosis) • Others: Microsporidia
  • 70.
    Cryptococcal meningitis Cryptococcal meningitisis caused by a capsulated yeast called Cryptococcus neoformans, which is capable of producing potentially fatal meningitis in HIV infected people. C.Neoformans C.Gattii
  • 71.
    Pathogenesis and Virulencefactors • Infection is acquired by inhalation of aerosolized forms of Cryptococcus. • Polysaccharide capsule—It is the principal virulence factor of the fungus. It is antiphagocytic and also inhibits the host’s local immune responses • Ability to make melanin by producing an enzyme called phenyl oxidase • Production of other enzymes such as phospholipase and urease. • CNS spread: The unique feature of Cryptococcus is its ability to cross blood-brain barrier which occurs by the yeast cells either they migrate directly across the endothelium or carried inside the macrophages as “Trojan horse”
  • 72.
    Lab diagnosis • Specimens:CSF, blood or skin scrapings. • Direct Detection Methods 1. Negative staining: Modified India ink stain (added with 2% mercurochrome) and nigrosin stain - demonstrate the capsule - refractile delineated clear space surrounding the round budding yeast cells against black background. 2. Gram staining may show gram-positive round budding yeast cells. 3. Other stains include: Mucicarmine stain: It stains the carminophilic cell wall of C. neoformans Masson-Fontana stain: It demonstrates the production of melanin Alcian blue stain: To demonstrate the capsule. 4. Antigen detection: The capsular antigens can be detected from CSF or serum by latex agglutination test. It is a rapid and sensitive (95% sensitivity) and specific method.
  • 73.
    Negative staining Mucoidcolonies on SDA agar Dark pigmented colonies on Niger seed agar
  • 74.
    Confirmation of Cryptococcusspecies is made by: • Niger seed agar and bird seed agar: They are used to demonstrate melanin production (brown colored colonies). • Growth at 37°C . • Urease test is positive • Assimilation of inositol and nitrate • Mouse pathogenicity test • Automated identification system such as MALDI-TOF
  • 75.
    TREATMENT • Treatment dependsupon the type of cryptococcosis. • Cryptococcosis without CNS involvement: Fluconazole is the drug of choice. • HIV-infected patients with CNS involvement: - The recommended regimen is induction phase for two weeks (amphotericin B ± flucytosine) - followed by oral fluconazole therapy till CD4 T cell count raises >200 /µL for 6 months.
  • 76.
    References 1. Koneman EW,Allen SD, Janda WM, Schreckenberger PC, Winn WC. Diagnostic microbiology,6th edition, Philedelphia: Lippincott-Raven Publishers(2017), pg.1075- 145. 2. Scott Bailey, Forbes Betty A, et al. Diagnostic Microbilogy, 12th edition, St. louis, Missouri: Mosby Inc (2007). 3. Jawetz, Melnick, Adelberg’s. Medical Microbiology, 28th edition, McGraw-Hill Education eBooks (2019). 4. Mandell, Douglas, Bennett’s. INFECTIOUS DISEASE ESSENTIALS, Philadelphia:Elsevier Inc.(2017). 5. Janagond, Anand & Sastry, Apurba & Bhat, Sandhya & Rajshekar, Deepashree. (2018). Essentials of Medical Microbiology, 2nd Edition. 6. M. Knipe, David, M. Howley, Peter, et al. F I E L D S Virology, 6th edition, Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer business(2013). 7. Ahmed S, Rakib A, Nasrin F, Chowdhury RH, Azad AK, Hasan CM. Assessment of cerebrospinal fluid (CSF) to differentiate between bacterial meningitis and viral meningitis. Journal of Advances in Medical and Pharmaceutical Sciences. 2018 Sep 6;17(4):1-7.