Meningitis

Overview, Types of meningitis - bacterial, viral, fungal, parasitic and non infectious, pathology, clinical presentation, investigations and treatment

1. MRS. M. PRADEEPA MPT (NEURO) VICE PRINCIPAL PPG COLLEGE OF PHYSIOTHERAPY COIMBATORE, TAMILNADU, INDIA

2. INTRODUCTION Meningitis is a devastating disease and remains a major public health challenge. Meningitis can be caused by many different pathogens including viruses and fungi but the highest global burden is seen with bacterial meningitis. Together with sepsis, meningitis is estimated to cause more deaths in children under 5 years of age than malaria. Survivors can suffer severe sequelae with considerable social and economic costs

3. Meninges

4. Definition It is defined as an acute inflammation of the protective layer - the meninges covering brain and the spinal cord. The arachnoid and pia mater become inflamed and opaque along with the first two layers of the cortex and the spinal cord. Many complications can result from this inflammation such as the increased risk of infarctions leading to blockage of cerebral spinal fluid flow, thromboses in the cortical veins and additional clinical symptoms

5. Types of Meningitis based on duration 1. Acute It is a life-threatening inflammation often caused by a bacterial or viral infection which develop over the course of a few hours to days 2. Subacute Develops over days to a few weeks – mainly bacterial 3. Chronic Persists for at least 1 month without spontaneous resolution. The most common etiologies of chronic meningitis fall into 3 broad categories: fungal and tuberculous infectious, autoimmune, and neoplastic

6. Types based on etiology Bacterial Viral Fungal Parasitic Non - infectious More severe form, less common than viral Most common (85%) and less severe Rare type Less common type Less common Streptococcus pneumoniae , Neisseria meningitidis , Haemophilus influenza, Listeria monocytogenes and Staphylococcus aureus Coxsackievirus , Echoviruses, West Nile virus, Influenza, mumps, HIV, Measles and herpes viruses Cryptococcus , Blastomyces , Histoplasma ,  Coccidioides Angiostrongylus cantonensis , Baylisascaris procyonis , Gnathostoma spinigerum Lupus, a head injury, brain surgery, cancer and certain medications

7. Risk factors Age- children younger than 5 years Use of immunosuppressive drugs Chronic malnutrition AIDS CSF Shunt Chronic alcoholism Diabetes Pneumonia

8. Pyogenic Meningitis Other wise called as acute bacterial meningitis, a life-threatening CNS infectious disease with elevated mortality and disability rates. Acute bacterial meningitis is rapidly developing inflammation of the meninges that cover the brain and spinal cord and of the fluid-filled space between the meninges (subarachnoid space) when it is caused by bacteria. Infection causing meningitis arises in the nasopharynx

9. Prevalance Bacterial meningitis appears more frequently in populations that are in close living quarter Although the prevalence of meningitis has decreased, it is believed that many cases go unreported.  The incidence of meningitis is 2 of 6 per 10,000 adults per year in developed countries and is up to ten times higher in less-developed countries.

10. Can develop in infants and children, particularly in geographic areas where children are not vaccinated. As people age, acute bacterial meningitis becomes more common If meningitis develops within the first 48 hours after birth, it is usually acquired from the mother. It may be transmitted from mother to newborn as the newborn passes through the birth canal. In these cases, meningitis is often part of a serious bloodstream infection ( sepsis )

11. Etiology In neonates: Gram – ve bacilli, e.g. E. coli, Klebsiella . Haemophilus influenzae . In children: Haemophilus influenzae . Pneumococcus (Strep. pneumoniae ). Meningococcus . ( Neisseria meningitidis ). In adults: Pneumococcus . Meningococcus . Other bacteria: Listeria monocytogenes , Streptococcus pyogenes and Staphylococcus aureus are occasionally responsible. Infections of mixed aetiology (two or more bacteria) may occur following head injury, mastoiditis or iatrogenically after lumbar puncture.

12. Route of entry Spread through the bloodstream from an infection in another part of the body (the most common route) Spread from another infection in the head, such as sinusitis or an ear infection (often caused by Streptococcus pneumoniae ) After a wound penetrates the skull or meninges (often caused by Staphylococcus aureus ) Surgery is done of the brain or spinal cord (often caused by gram-negative bacteria) When a drain (shunt), placed in the brain to relieve increased pressure in the skull, becomes infected When bacteria enter through a birth defect in the skull or spine (such as  spina bifida )

13. Pathology Causative organism enters into CSF through blood brain barrier A purulent exudate most evident in the basal cisterns extends throughout the subarachnoid space. The underlying brain becomes congested, oedematous and ischaemic . The integrity of the pia mater normally protects against brain abscess formation

14. The cytokines, interleukin, tumour necrosis factor, and prostaglandin E2 are released as part of an acute inflammatory response. They increase vascular permeability, cause a loss of cerebrovascular autoregulation and exacerbate neuronal injury. The inflammatory exudate may also affect vascular structures crossing the subarachnoid space producing an arteritis or venous thrombophlebitis with resultant infarction. Similarly, cranial nerves may suffer direct damage. Hydrocephalus can result from CSF obstruction.

15. Clinical presentation The classical clinical triad is fever, headache and neck stiffness. Prodromal features (variable) A respiratory infection otitis media or pneumonia associated with muscle pain. Meningitic symptoms Severe frontal/occipital headache Stiff neck Photophobia

16. Systemic signs: High fever, Transient purpuric or petechial skin rash in meningococcal meningitis. Meningitic signs: Brudzinki’s sign - is caused by passive neck flexion producing flexion of the hips or knees.  Kernig’s sign presents, as restrictive passive extension of the knee while the hip is flexed. [

17. Associated neurological signs Impaired conscious level Focal or generalised seizures are frequent. Cranial nerve signs occur in 15% of patients. Sensorineural deafness (not due to concurrent otitis media but to direct cochlear involvement) – 20% Focal neurological signs – hemiparesis, dysphasia, hemianopia , papilloedema – occur in 10%.

18. Non-neurological complications Shock ← Meningitis → Arthritis ↓ Septic complications Inappropriate secretion of ADH Acute bacterial endocarditis Coagulation disorders: Thrombocytopenia – disseminated intravascular coagulation

19. Features specific to causative bacteria Haemophilus meningitis Meningococcal meningitis Pneumococcal meningitis Generally occurs in small children. Preceding upper respiratory tract infection. Onset abrupt with a brief prodrome . Organism is carried in the nasopharynx . Septicaemia can occur with arthralgia ; purpuric skin rash. When overwhelming, confluent haemorrhages appear in the skin due to disseminated intravascular coagulation. Predominantly an adult disorder. Often associated with debilitation, e.g. alcoholism. May result from pneumonia, middle ear, sinus infection or follow splenectomy . Onset may be explosive, progressing to death within a few hours. Outcome Generally good Less than 5% mortality. Gradual onset – good prognosis. Sudden onset with septicaemia – poor outcome. Overall mortality – 10%. Mortality – 20%. Poor prognostic signs – coma, seizures, increased protein in CSF.

20. Investigation CT/MRI Typically shows thin and linear  leptomeningeal enhancement CSF examination Moderate increase in pressure < 300 mm CSF, Gram stain of spun-down sediment Serological/immunological tests The latex particle agglutination (LA) test, for the detection of bacteria antigen in CSF Blood cultures Organism isolated in 80% of cases of Haemophilus meningitis. Pneumococcus and meningococcus in less than 50% of patients.

21. Check serum electrolytes. important in view of the frequency of inappropriate antidiuretic hormone secretion. Detect the source of infection. Chest X-ray – pneumonia Skull X-ray – fracture Sinus X-ray – sinusitis Petrous views – mastoiditis

22. Management Initial therapy Neonates (above 1 month) – ampicillin , + aminoglycoside and cephalosporin Children (under 5 years) – vancomycin + 3rd generation cephalosporin Adults – vancomycin + 3rd generation cephalosporin Immunocompromised patient – vancomycin + ampicillin + cephalosporin

23. Steroids A four-day regimen of dexamethasone , starting before or with the first dose of antibiotics, is now recommended in children with haemophilus and adults with bacterial meningitis likely to be pneumococcal.

24. Prevention Haemophilus vaccine ( HiB vaccine) in children. The pneumococcal conjugate vaccine is now a routine childhood immunization and is very effective at preventing pneumococcal meningitis. Household members and others in close contact with people who have meningococcal meningitis should receive preventive antibiotics

25. VIRAL MENINGITS Meningitis is the commonest type of viral infection of the central nervous system. The term aseptic meningitis includes viral meningitis as well as other forms of meningitis where routine culture reveals no other organisms.

26. ETIOLOGY Common causal viruses Enteroviruses Mumps virus Herpes simplex (subtype 2) Epstein- barr virus ( ebv ) Rare causal viruses Lymphocytic choriomeningitis Human immunodeficiency virus West nile virus

27. Enterovirus infection - affects children/young adults and occurs seasonally in late summer. Spread is by the faecal/oral route. Mumps – affects children/young adults. Winter/spring incidence. Herpes simplex (type 2) – accounts for 5% of viral meningitis. Develops in 25% of patients with primary genital infection (suspect in sexually active adults). Can cause a recurrent meningitis ( Mollaret’s meningitis). Lymphocytic choriomeningitis – affects any age and is a consequence of airborne spread from rodent droppings. Human Immunodeficiency Virus (HIV) – suspect in high risk groups. HIV antibodies are often absent and develop 1–3 months later during convalescence.

28. Transmission of Viral Meningitis Spread through the bloodstream from an infection in another part of the body (the most common way) Contact with contaminated stool, which may occur when infected people do not wash their hands after a bowel movement or when they swim in a public swimming pool (for enteroviruses ) Sexual intercourse or other genital contact with an infected person (for HSV-2 and HIV) A bite of an insect, such as a mosquito (for West Nile virus, St. Louis virus, Zika virus, or Chikungunya virus) Spread through the air by inhaling the virus (for varicella -zoster virus) Contact with dust or food contaminated by the urine or stool of infected mice or pet hamsters (for lymphocytic choriomeningitis virus) Use of infected needles to inject drugs (for HIV)

29. CLINICAL PRESENTATION PRODROMAL PHASE Fever Malaise Sore throat MENINGEAL PHASE Headache Photophobia Drowiseness RECOVERY PHASE 7- 14 days

30. Signs Mild meningism Neck stiffness Kernig’s sign + ve No focal signs Skin rashes, parotitis , diarrohea , myalgia may or may not present

31. Complications Febrile seizures Inappropriate ADH secretion.

32. Investigations The CSF cell count is elevated (lymphocytes or monocytes ) with a normal glucose and protein. PCR detection of viral DNA/RNA in CSF though diagnostic Virus may be cultured from throat swabs or stool. Serological tests on serum in acute and convalescent phases are especially valuable in detecting mumps and herpes simplex (type 2).

33. Differential diagnosis Tuberculous or fungal meningitis Leptospirosis Sarcoidosis Carcinomatous meningitis Partially treated bacterial meningitis Parameningeal chronic infection which evokes a meningeal response, e.g. mastoiditis .

34. Treatment Treatment for viral meningitis is mostly supportive. Rest, hydration, antipyretics, and pain or anti-inflammatory medications may be given as needed Prognosis is excellent

35. THANK YOU