What Is Viral Meningitis;Etiology,Pathogenesis,Treatment

. The term  viral meningitis is used to describe a syndrome characteristic of acute viral infections of the central nervous system manifested by signs of meningeal irritation, cerebrospinal fluid pleocytosis (predominantly lymphocytic), and a short uncomplicated course. The syndrome can be induced by a variety of different viruses.

 

Etiology of viral meningitis

At present a specific cause can be established in approximately two thirds of the cases of presumed viral origin. The relative fre­quency and importance of the many agents that have been implicated vary in different parts of the world. In the United States and in temperate climates generally, the enteroviruses and mumps virus are the most common causes. More than 60 enteroviruses have been identified; not all have yet been associated with meningitis, but in view of the frequent additions from among previously known and newly recognized members of this family of agents, the list can be expected to grow.

Herpes simplex and lymphocytic chorio­meningitis viruses are less frequently responsible for viral meningitis; rarely, the syndrome may be seen as a complication of adenovirus infections, infectious mononucleosis, viral hepatitis, and herpes zoster. Aseptic meningitis associated with the arthropod-borne group of viruses follows the geographic distribution of these agents, which is dependent upon specific arthropod vectors.

Epidemiology.

In temperate climates, aseptic meningitis resulting from enteroviruses occurs most characteristically in small or large outbreaks during the summer and autumn, whereas in tropi­cal and semitropical areas there is no striking seasonal incidence. Children are more frequently affected than adults, but in some epidemics as many as 50 per cent of cases occur in persons over 15 years of age. The agents are often widely dis­seminated in the population, giving rise chiefly to inapparent infections or minor febrile ill­nesses. Spread is primarily by contact with an infected person, and the healthy transient carrier is as infectious as the frank case. Dissemination is greatest in areas of poor sanitation with a high density of young preschool children, who are the most frequent carriers.

Although one virus tends to be dominant and to account for the bulk of illness at any given time and place, it is not unusual during epidemic or endemic periods to find several agents circulating at the same time, causing similar illnesses, including meningitis. Mumps meningitis follows the epidemiologic pattern of mumps infections generally, with a peak seasonal incidence in winter and spring. On rare occasions, it appears in epidemic form, without accompanying parotitis.

Lymphocytic choriomeningitis is an uncommon disease, oc­curring in the late autumn and winter. The infection is endemic in the common house mouse, Mus ‘musculus, and is probably spread to man through dust or food contaminated by mouse excreta. Wild rodents are also the probable source of infections with encephalomyocarditis virus, which may rarely be associated with typical aseptic meningitis. Herpes simplex meningitis occurs sporadically, either as a primary herpetic infection spread by contact, or in some instances as a result of reactivation of a latent infection. It has no seasonal distribution.

Aseptic meningitis owing to infection with one of the arthropod-borne viruses (arboviruses) oc­curs usually during an epidemic in which most of the cases have the more characteristic encephalitic picture. However, St. Louis and western equine in the United States and Murray Valley encepha­litis virus in Australia often may induce a milder disease with aseptic meningitis as a common form.

Pathogenesis.

Like the epidemiology, the pathogenesis of the syndrome varies with the nature of the infecting agent. The general pattern for enteroviruses is thought to be similar, the sequence being primary multiplication in the ali­mentary tract, spread to regional lymph nodes, a viremic phase, and eventually invasion of the central nervous system. There is evidence that in enteroviral infections in humans, as well as in experimentally infected primates, viremia pre­cedes the onset of illness by several days and hashas usually disappeared by the time neurologic signs appear.

Mumps, lymphocytic choriomeningitis, herpes, and the arthropod-borne viruses probably reach the central nervous system mainly via the bloodstream. There is experimental evidence that herpes virus is also capable of traveling by neural spread. In the central nervous system, the lesion of aseptic meningitis is apparently limited to an inflammatory response in the menin­ges, although in nonparalytic poliovirus ejections in monkeys scattered anterior horn cell involve­ment also occurs.

Clinical Manifestation of  Viral Meningitis

Whatever the spe­cific viral cause, the symptoms and signs are simi­lar and not readily distinguishable from the pat­tern of aseptic meningitis from other causes. The onset is commonly abrupt. The most constant features are severe headache, fever, and stiff neck; other symptoms that may occur are sore throat, nausea and vomiting, listlessness, drowsi­ness, vertigo, pain in the back and neck, photo­phobia, paresthesias, myalgias, abdominal pain, and chills or chilly sensations.

With certain Coxsackie and echovirus infections a striking skin eruption may appear. In general, the severity of symptoms increases with, the age of the patient. Although sudden onset is characteristic, in some patients there is a prodromal nonspecific “minor illness” followed by several days of well-being before the reappearance of fever and the develop­ment of signs of central nervous system involve­ment. This occurs most commonly with poliovirus infections in young children, but may be asso­ciated with other enteroviruses and with lympho­cytic choriomeningitis.

On physical examination there are few findings. The temperature is elevated ‘100 to 104° F.), but the patient does not appear as ill as one with bacterial meningitis. Neck and back stiffness are the only neurologic signs in the typical case; Kemig and Brudzinski signs are sometimes posi­tive. Nuchal rigidity may be minimal and ap­parent only in the last degrees of neck flexion. The deep tendon reflexes are normal or hyperactive. Transient weakness (rarely frank paralysis) has been noted with the Coxsackie B group, Coxsackie A7, and echoviruses 6 and 9. Rash is en­countered chiefly in young children.

It has been a prominent feature in certain epidemics in which aseptic meningitis has also occurred, including outbreaks associated with echoviruses 4, 6, 9, and 16, and Coxsackie A9 and 16; rash has also been observed occasionally with many other enterovirus types. The eruption usually appears with the fever and lasts four to five days, in severe cases eight or nine days. Characteristically it is maculo- papular, discrete, erythematous and nonpruritic. The lesions may be confined to the face and neck, or may spread over the chest and extremities and sometimes involve the palms and soles.

Simulation of Brain Abscess or Bacterial Meningitis.

Confusion with meningococcal and other bacterial meningitis may also arise .in echo-9 or other enterovirus infections with petech­ial rash. The milder clinical course, the lower cerebrospinal fluid cell count and normal glucose, and the peripheral blood picture usually indicate a viral infection. If reasonable doubt exists, how­ever, the case should be treated as one of purulent meningitis until this has been excluded by appropriate cultures. Inadequately treated bac­terial meningitis and mechanical irritation of the meninges owing to brain abscess (or other intra­cranial lesions) may also produce an aseptic meningitis syndrome.

The possibility of a silent brain abscess is suggested by a history of recent pneumonia, chronic pulmonary infection, congeni­tal heart disease, bacterial endocarditis, otitis media, or infection of the paranasal sinuses. Tuberculous meningitis in its early stages is another remote possibility. Aseptic meningitis owing to neurosyphilis may present as an acute ill­ness, although the course is more typically subacute, with papilledema, cranial nerve pal­sies, and little or no fever.

Other Forms of Aseptic Meningitis. Among other causes of aseptic meningitis, the presence of severe sore throat, generalized lymph node enlargement, mild icterus, and a transient rash are compatible with infectious mononucleosis. Leptospirosis is to be considered seriously in areas where the infection is common and when there is a history of exposure to dogs, cattle, swine, or rats, which excrete the agent in their urine. Mycoplasma pneumoniae infections may be com­plicated by aseptic meningitis or meningoen­cephalitis, with cerebrospinal fluid findings as in viral meningitis. The presence of respiratory symptoms and central nervous system signs suggests the possibility of infection with this agent; a significant titer of cold agglutinins in the serum supports the diagnosis.

Treatment of viral meningitis.

There is no specific therapy for the syndrome of aseptic meningitis. Bed rest, adequate fluid intake, and symptomatic treatment are indicated ..as in any acute febrile illness.

Prognosis.

Aseptic meningitis caused by viruses is a self-limited disease, complete re­covery occurring in three to five days in mild cases, and in seven to fourteen days in the more severe ones

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