May 1996
The choice for treating meningitis used to be easier — use a third-generation cephalosporin. Unusual causes of meningitis have complicated this therapeutic approach.
A few years ago, most cases of meningitis were due to Haemophilus influenzae type b (Hib) and most of the remainder were caused by pneumococci, which were sensitive to penicillin. The choice of therapy was simple — a third-generation cephalosporin. The major discussion was the use of steroids.
Then pneumococcal resistance to penicillin entered the equation. Many began recommending that initial therapy should include a third-generation cephalosporin and vancomycin because some pneumococci also became resistant to cephalosporins. The resistance to cephalosporins and to penicillin is mediated by alteration of penicillin binding proteins, which does not affect vancomycin.
In animal studies, however, steroids appeared to inhibit the penetration of vancomycin into the cerebrospinal fluid (CSF).
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The widespread use of Hib vaccines, however, has markedly decreased the total number of cases of meningitis. In reviewing our recent cases of meningitis, which have been much fewer than in the past, we find that the problems are different than in the pre-vaccine, pre-pneumococcal resistance days.
Our most recent cases have included Listeria in a 7-year-old child, group B streptococcus in children beyond the newborn period, meningococcus serogroup B, non-typeable Haemophilus cephalosporin-resistant pneumococcus, not to mention viral and tuberculous meningitis.
What have these changes taught us? First, the organism responsible for meningitis must be identified. Enteroviral meningitis is most common in the summer and early fall. In the past it was a disease that affected mainly school-aged boys. Now, it frequently affects young infants. In older children, enteroviruses usually cause meningitis and herpes simplex virus (HSV) usually causes encephalitis. The clinical distinction is less clear in newborns, but polymerase chain reaction (PCR) can be used to distinguish the two.
It is well to remember that the results during the development of these tests in research laboratories generally are more reliable than in commercial laboratories.
The diagnosis of tuberculous meningitis by PCR is not quite as far along. It probably is a good practice to place tuberculin skin tests on children admitted with a diagnosis of meningitis, remembering that children at greatest risk for this disease are from areas where use of BCG is routine. This may obfuscate the interpretation of skin test results.
It is not unusual, moreover, to have negative skin tests in children with tuberculous meningitis. In children suspected of having tuberculous meningitis, a chest film may be helpful.
Hospital laboratories have incorrectly identified the isolate from the CSF as a non-fermentive gram-negative rod that they believed was a contaminant in some cases of meningococcal meningitis. We must be sensitive to the fact that the hospital laboratories — which handle many specimens from adults and children from many sites — may not be as aware of the change in the etiology of meningitis. Thus reports of ''contaminants'' in CSF merit a call to the laboratory to re-examine the isolate.
All isolates should have antibiotic sensitivity studies. This is particularly true of pneumococcal isolates. It should be ascertained that the most accurate test be performed as soon as the isolate is identified or even suspected.
When an unusual isolate such as Listeria is obtained, the physician should call the laboratory to request the antibiotic sensitivities that may be useful in management based on clinical studies rather than having the laboratory provide its routine battery of tests.
Unusual isolates, e.g. Listeria and group B streptococcus beyond the newborn period, should arouse the suspicion of an underlying immunologic pattern. Our patient with the latter isolate turned out to be HIV positive.
Antimicrobial therapy and the use of steroids will continue to be debated. The latter has been found to be effective by some investigators in Hib infection. Others have failed to confirm these findings, but perhaps a larger sample might have been necessary to find the effect of steroids.
It has been argued that the mechanism of the effect of steroids, i.e., reduction in the production of mediators resulting in reduced inflammation, should make it effective in all cases of meningitis regardless of etiology. If steroids indeed reduce penetration of antimicrobials into the CSF, their anti-inflammatory effect may be vitiated.
Although the disease is less common, meningitis and its management will continue to be debated.
Philip A. Brunell, MD, is the Deputy Director of the Department of Pediatrics at Cedars-Sinai Medical Center in Los Angeles.
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