Meningitis is an occasional cause of sudden unexpected death.54 Until the late 1980s, most of the victims were children between the ages of 3 months and 3 years, with the organism involved being Hemophilus influenza. Mass inoculation of children with Hemophilus vaccine has resulted in the virtual disappearance of such cases. At present, acute bacterial meningitis is a disease of adults. It is seen in association with infections of the ears and sinuses; alcoholism; splenec-tomy, pneumonia, and septicemia. The most common organisms now encountered are Streptococcus pneumoniae (40-60%); Neisseria meningitis (15-25%); Listeria monocytogene (10-15%) and Haemophilus influenzae (5-10%).54 In neonates, the coliform bacilli and group B streptococci predominant.

Most cases of meningitis develop secondary to septicemia. S. pneumoniae may develop secondary to pneumococcal pneumonia. This organism is also

Group Strep Meningitis Survivors
Figure 3.12 A 29-year-old female with pneumococcal meningitis. Purulent exudate in subarachnoid space.

the most common organism associated with head trauma in which the dura is disrupted. Hemophilus, pneumococcal, and meningococcal meningitis all may develop by direct extension from middle ear infections.

At autopsy, the brain is markedly swollen. The meninges appear cloudy on the ventral surface of the brain and, to a lesser degree, laterally due to purulent exudate (Figure 3.12). The exudate may be so slight as not to be seen grossly, or severe with copious quantities. In all cases of meningitis, the middle ears should be opened and examined to make sure that this is not the source of the meningitis.

Among bacteria that cause meningitis is Neisseria meningitidis.55 The posterior nasopharynx is the natural reservoir for this organism, with 2-15% of healthy individuals carrying the organism in non-epidemic times. Men-ingococcal is now second only to pneumococcus in causing meningitis and is more common than Hemophilus influenza in both children and adults. The fatality rate is approximately 3%. Infection may present as a pure purulent meningitis, meningococcemia (septicemia), or as both.

Meningococcemia may present as a mild febrile illness, a fulminant disease (Waterhouse-Friderichsen Syndrome) or a chronic illness. The patient may have chills, high fever, dizziness, nausea, headaches, or weakness. Petechiae appear on the body in 75% of cases. They may coalesce, forming purpura and intracutaneous lesions. In 10% of the cases, there is a rapidly progressive course with toxemia, shock, and collapse. The individual may die less than 10 h after onset of symptoms. Occasionally, a person who is walking around will suddenly collapse, die, and, at autopsy, be found to have meningococcemia. In such a case, one can only speculate that the symptoms were not severe enough to inconvenience the person. At autopsy, there will be cyanosis; a blotchy erythematous rash, petechiae and purpura of the skin, and conjunctivae and acute bilateral hemorrhagic adrenal necrosis, but no meningitis (Figure 3.13). Cultures of the blood and spinal fluid for meningococcus are generally negative after refrigeration of the body due to the fragile nature of the organisms and/or antemortem administration of antibiotics. In such cases, diagnosis can be made from blood by detection of specific meningococcal capsular polysaccharides using immunoelectrophoresis, latex agglutination or polymerase chain reaction.56 These, in the presence of the aforementioned autopsy findings, make the diagnosis of meningococcemia.

The same clinical and autopsy presentation that occurs in meningococ-cemia may occur from pneumococcal septicemia. The latter condition is commonly associated with absence of the spleen, either through surgery or congenital aberration. The pneumococcus organisms can usually be cultured from the blood even after refrigeration of the body.

Viral encephalitis is rarely seen in the medical examiner's office due to its protracted course, which leads to a clinical diagnosis. The brain will show severe edema with perivascular cellular infiltrates and infiltration of the meninges. The cells are predominantly lymphocytes and polymorphonuclear cells. Acellular plaques of necrosis may be seen throughout the brain.

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