This is a presentation on acute bacterial meningitis. The learning objectives of the presentation are to know the common pathogens causing acute meningitis, to understand the pathophysiology process of meningitis and the mechanisms by which complications of meningitis occur, to identify characteristic profiles of cerebral spinal fluid, or CSF, in meningitis, and to identify meningitis as a medical emergency and understand its management. Meningitis is an infection within the subarachnoid space causing a central nervous system inflammatory reaction, and is often characterized by decreased consciousness, seizures, and raised intracranial pressure, as often caused by bacteria or viruses. Other pathogens like mycobacterium tuberculosis and fungi usually cause subacute meningitis. Meningitis refers to involvement of meninges alone. Membrane tissue is also directly [INAUDIBLE]. It is referred to as meningoencephalitis. Bacterial meningitis is the most common form of superlative central nervous system infection, with an annual incidence of more than cases per 100,000 persons.

The epidemiology of bacterial meningitis has changed in recent years due to a dramatic decline of meningitis, caused by haemophilus influenza, and neisseria meningitidis. This is a result in widespread use of vaccinations for these organisms. Streptococcus pneumoniae is the most common organism causing acute bacterial meningitis. This is followed by neisseria meningitidis, group B strepococci, and listeria monocytogenes. Streptococcus pneumoniae accounts for more than 50% of reported acute bacterial meningitis in adults. Risk factors for this form of meningitis are pneumococcal pneumonia, sinusitis, or otitis media, alcoholism, diabetes, and spinectomy. Mortality remains high at about 20%, despite appropriate antibiotic therapy. Neisseria meningitidis accounts for about 25% of meningitis in adults and about 60% in children.

Presence of [INAUDIBLE] and particular lesions is an important diagnostic clue. The infection is initiated by nasopharyngcal colonization. Individuals with complement deficiencies are highly susceptible to many [INAUDIBLE] infections. The disease can be fulminant, leading to death within hours of symptom onset. Enteric gram negative bacilli are increasingly an common cause of meningitis, especially in those who have debilitating chronic diseases, like diabetes, cirrhosis, or alcoholism, and endulged with chronic urinary tract infections. It can also complicate neurosurgical procedures, such as craniotomies. Group B strepococci, or streptococci agalactiae, perversely responsible for many cases of neonatal meningitis, is not an increasingly common cause in individuals over 50 years of age. Listeria monocytogenes is more common in elderly patients in immunal compromised individuals. Hemophilus influenzae meningitis is declining due to vaccination.

Staphylococcus meningitis is associated if neurosurgical procedures and cerebral spinal fluid shunts. Staphylococcus pneumoniae and neisseria meningitidis initially colonized colonize the nasal pharynx. They don’t invade the bloodstream by escaping the immune attack, due to its polysaccharide capsule. They infect the choroid plexus of ventricles via bloodstream, and gain access to the cerebral spinal fluid, or CSF. Bacteria can multiply rapidly within a CSF, because of absence on effective host immune defenses. Many of the neurological manifestations and complications of bacterial meningitis result from the immune response to the invading pathogen, rather than direct bacteria induced tissue injury. Neurologic injury can progress, even after the CSF has been sterilized by antibiotic therapy. The bacterial invasion and an inflammation response within a subarachnoid space give rise to multiple pathologic processes. Cerebral edema occurs due to cytotoxic and vasogenic processes. Interstiial edema also occurs. Subarachnoid exudates have [INAUDIBLE] CSF circulation, leading to hydrocephalus. Edema and hydrocephalus cause raised intracranial pressure and cerebral herniation. Vasculitis of the intracranial vessels affects both arteries and veins, causing infarction, thrombophebitis, and cerebral venous sinus thrombosis.

Cerebral auto regulation is also impaired, and in late stages, results in decreased blood flow, inducing ischemia, and seizures. Acute bacterial meningitis classically presents with the triad of fever, headache, and neck stiffness. Nausea, vomiting, and photophobia are also common symptoms. A decreased level of consciousness is often present, and can vary from lethagy to coma. Seizures can occur during any phase of meningitis. Signs of raised intracranial pressure, or ICP, include decreased level of consciousness, papilledema, and six nerve palcies as a false localizing sign.

[INAUDIBLE] and [INAUDIBLE] occurs in extreme raised ICP, and presents with bradycardial hypertension, and irregular respiration. Death may occur due to cerebral herniation. A petechial rash or septic shock will suggest a possibility of meningialcocci as the underlying pathogen. Neck stiffness is the pathognomonic sign of meningeal irritation. It is present when neck receives passive flexion. Kernig’s and Brudzinski’s signs are classic signs of meningeal irritation. Clinic sign is [INAUDIBLE] with patient in supine position. [INAUDIBLE] is a flex over the abdomen with knee flexed. Attempts to passively extend a knee elicits pain where meningeal irritation is present. Brudzinski’s sign is elicited with patient in supine position, and is positive when passive flexion of the neck results in spontaneous flexion of the hips and knees. Investigations include routine tests, like full blood count, ESR, CRP, urea, and electrolytes, liver function tests, and a chest x-ray. Blood cultures should preferably be sent prior to commencing antibiotics. But at the same time, antibiotic initiation should not be delayed for blood cultures. Neuroimaging, either CT brain with contrast or MRI brain with contrast, is indicated to exclude focal infections processes like abcess, or subdural empyema.

Diffused meningeal enhancement may be seen, but it’s not specific for meningitis. A lumbar puncture should be done if there’s still significant raised intracranial pressure. CSF studies are the definitive diagnostic tests for meningitis. The CSF profile in meningitis is discussed later. Viral and bacterial meningitis can mimic each other clinically. CSF findings, neuroimaging, and EEG often help to distinguish them. Subdural empyema and epidural abscess should be considered as differentials, especially when focal neurological deficits are present. Non-infectious conditions like subarachnoid hemorrhage, aseptic meningitis due to drugs, carcinomatous and lymphomatous meningitis, auto-immune conditions can mimic bacterial meningitis. Subacute meningitis, due to tuberculosis or fungi, are differential diagnoses, and CSF studies are required to diagnose these. In acute bacterial meningitis, the CSF pressure is usually increased. The CSF shows predominantly raised neutral fields, which can range from about 100 to 60,000 per microlitre of CSF. CSF protein content is increased, and CSF glucose is typically less than 40% of blood glucose level. Please refer to the table for CSF profiles in other forms of meningitis. The choice of antibiotic cover depends on a patient’s age and other associated features.

Brain imaging and lumbar puncture should not delay the first dose of antibiotic. Immunocompetent adults should be treated with cefotaxime, ceftriaxone, and vancomycin. Ampicillin should be [INAUDIBLE] in older adults, and in patients with alcoholism, or with other debilitating illnesses. Hospital acquired or post traumatic meningitis, and meningitis in neutropenic patients, should be treated with ampicillin, plus ceftazidime, plus vancomycin. Corticosteroids have been shown to reduce morbidity in streptococcal pneumoniae, and to tubercular meningitis. Empirical intravenous dexamethasone, 10 mg, six hourly for four days, with first dose given with the first antibiotic dose is a reasonable approach.

Raised ICP is a medical emergency and should be treated with urgency. Seizures should be managed accordingly. Mortality following acute bacterial meningitis depends on the underlying pathogen. Neurological sequelae occur in up to 25% of survivors, and include decreased intellectual function, memory impairment, seizures, hearing loss, and dizziness, and gait disturbances. In summary, acute bacterial meningitis is a medical emergency. Streptococcal pneumoniae and naiseria meningitidis are the most common bacterial cause of meningitis. CSF examination and neuroimaging are helpful in diagnosis, and in excluding other differential diagnosis. Antibiotics should be started as soon as possible, and initial treatment is empirically based on the patient’s profile, and thus, lightly underlying pathogen. We hope you have a better understanding of bacterial meningitis. Thank you..