Get Clinical Tree app for offline access
Meningitis is an inflammation of the meninges (dura mater, arachnoid, and pia mater). It can be acute, with symptoms occurring in hours to days, or chronic, with an onset and duration of weeks to months. Meningitis usually results from a viral or, less commonly, bacterial infection. Viral meningitis is usually mild and often clears on its own in 10 days or less. Bacterial meningitis requires prompt treatment with I.V. antibiotics.
Noninfectious causes of meningitis include medications (such as nonsteroidal anti-inflammatory drugs and antibiotics) and carcinomatosis. Viruses cause most cases of aseptic meningitis. (See Lymphocytic choriomeningitis.)
Other infectious agents include bacterial, fungal, mycobacterial, and parasitic agents. Neisseria meningitidis is implicated in most epidemics. Transmission takes place through inhalation of infected droplets from a carrier, with the virus often localizing in the nasopharynx. After incubating about 3 to 4 days, the microorganisms spread through the bloodstream to the joints, skin, adrenal glands, lungs, and central nervous system. Resulting tissue damage may be due to the effects of bacterial endotoxins. In fulminating meningococcemia and meningococcal bacteremia, hemorrhage, thrombosis, and necrosis occur.
Complications of meningitis include visual impairment, optic neuritis, cranial nerve palsies, personality changes, paresis or paralysis, vasculitis, endocarditis or pericarditis, and respiratory failure. Other complications include disseminated intravascular coagulation, septic arthritis, pericarditis, endophthalmitis, neurologic deterioration, and death.
Two-thirds of patients infected with meningitis present with fever, headache, neck stiffness, photophobia, nausea, vomiting, and signs of cerebral dysfunction (lethargy, confusion, coma).
Atypical presentation may occur in elderly individuals (especially those with diabetes or renal or liver disease), those with neutropenia, and immunocompromised patients (transplant recipients and those with human immunodeficiency virus [HIV] and acquired immunodeficiency syndrome).
Signs of increased intracranial pressure include headache, vomiting and, rarely, papilledema. Signs of meningeal irritation include nuchal rigidity, positive Brudzinski’s and Kernig’s signs, exaggerated and symmetrical deep tendon reflexes, and opisthotonos. (See Two signs of meningitis, page 196.)
Other manifestations are irritability, sinus arrhythmias, and photophobia, diplopia, and other visual problems. The patient may also develop delirium, deep stupor, and coma.
Systemic findings can provide clues to the etiology of the organism. A morbilliform rash with pharyngitis and adenopathy may indicate a viral etiology (Epstein-Barr virus [EBV], cytomegalovirus [CMV], adenovirus, HIV). Macules and petechiae that rapidly evolve into purpura may indicate meningococcemia. Varicella-zoster virus often produces vesicular lesions in a dermatomal distribution, whereas genital vesicles suggest herpes simplex virus type 2. Streptococcus pneumoniae and Haemophilus influenzae may cause sinusitis or otitis. Rhinorrhea or otorrhea indicates a cerebrospinal fluid (CSF) leak, possibly from a basilar skull fracture, most commonly caused by S. pneumoniae. Systemic disease may produce hepatosplenomegaly and lymphadenopathy, possibly indicating a viral (EBV, CMV, HIV) or fungal (histoplasmosis) origin. A heart murmur occurs in infective endocarditis, and mumps meningitis can produce parotitis.
Lymphocytic choriomeningitis (LCM) is a mild, biphasic, febrile illness lasting about 2 weeks. Infection occurs through inhalation of the LCM virus or arenavirus from infectious aerosolized particles of the host (rodents such as mice or hamsters) or its excreta (urine, feces, or saliva) 1 to 3 weeks before the onset of symptoms. It can also result from contact with food that has been contaminated with the virus or by contamination of mucous membranes, skin lesions, or cuts with infected body fluids. Handlers of infected animals or their excreta are at risk for this disease. Most cases occur in the northeast and eastern seaboard areas of the United States. LCM is more common during fall and winter.