Meningococcal meningitis should be suspected when the evolution is extremely rapid (delirium and stupor may supervene in a matter of hours), when the onset is attended by a petechial or purpuric rash or by large ecchymoses and lividity of the skin of the lower parts of the body, when there is circulatory shock, and especially during local outbreaks of meningitis. Because a petechial rash accompanies approximately 50 percent of meningococcal infections, its presence dictates immediate institution of antibiotic therapy, even though a similar rash may be observed with certain viral (echovirus serotype 9 and some other enteroviruses), rickettsia, as well as S. aureus infections, and, rarely, with other bacterial meningitides.
Pneumococcal meningitis is often preceded by an infection in the lungs, ears, sinuses, or heart valves. In addition, a pneumococcal etiology should be suspected in alcoholics, in splenectomized patients, in the very elderly, and in those with recurrent bacterial meningitis, dermal sinus tracts, sickle cell anemia (“autosplenectomized”), and basilar skull fracture. On the other hand, H. influenzae meningitis usually follows upper respiratory and ear infections in the uninocualted child.
Other specific bacterial etiologies are suggested by particular clinical settings. Meningitis in the presence furunculosis or following a neurosurgical procedure directs attention to the possibility of a coagulase-positive staphylococcal infection. Ventricular shunts or drains inserted for the relief of hydrocephalus are particularly prone to infection with coagulase-negative staphylococci and Proprionobacerium acnes and diphteroids. HIV infection, myeloproliferative or lymphoproliferative disorders, defects in cranial bones (tumor, osteomyelitis), rheumatologic diseases, metastatic cancer, and therapy with immunosuppressive agents are clinical conditions that favor invasion by such pathogens as Enterobacteriaceae, L. monocytogenes, A. calcoaceticus, Pseudomonas, and occasionally by parasites. In acute myelogenous leukemia patients, we have seen several instances of fatal Bacillus cereus meningitis (see Vodopivec et al).
Focal cerebral signs in the early stages of the disease, although seldom prominent, are most frequent in pneumococcal and H. influenzae meningitides as outlined by Adams and colleagues (1948). Some of the transitory focal cerebral signs may represent postictal phenomena (Todd paralysis); others may be related to an intense focal meningitis, for example, purulent material collected in one sylvian fissure. Seizures are encountered most often with H. influenzae meningitis. Although seizures are most common in infants and children, it is difficult to judge the significance, because young children may convulse with fever of any cause. Persistent focal cerebral lesions or intractable seizures usually develop in the second week of the meningeal infection and are caused by an infectious vasculitis, as described earlier, usually with occlusion of surface cerebral veins and consequent infarction of cerebral tissue. Cranial nerve abnormalities are particularly frequent with pneumococcal meningitis, the result of invasion of the nerve by purulent exudate and possibly ischemic damage as the nerve traverses the subarachnoid space. Of course, bilateral abducens weakness can be due to increased intracranial pressure as a result of any form of meningitis.