Quite apart from acute and subacute bacterial endocarditis, which may give rise to cerebral embolism and characteristic inflammatory reactions in the brain (see further on), there are several systemic bacterial infections that are complicated by a special type of encephalitis or meningoencephalitis. Three common ones are Mycoplasma pneumoniae infections, L. monocytogenes meningoencephalitis, and Legionnaire disease. Probably Lyme borreliosis should be included in this category but it is more chronic and is described further on in this chapter with the spirochetal infections. The rickettsial encephalitides (particularly Q fever), which mimic bacterial meningoencephalitis, are also addressed later in the chapter. Catscratch disease is another rare cause of bacterial meningoencephalitis. Meningoencephalitis caused by brucellosis occurs very rarely in the United States. Whipple disease, discussed later, which appears to be a focal invasion of the brain by an unusual intracellular bacterium, is an oddity but also belongs in this category.
This organism, which causes 10 to 20 percent of community acquired pneumonias, is associated with a number of neurologic syndromes. Guillain-Barré polyneuritis, cranial neuritis, acute myositis, aseptic meningitis, transverse myelitis, global encephalitis, seizures, cerebellitis, acute disseminated (postinfectious) encephalomyelitis, and acute hemorrhagic leukoencephalitis (Hurst disease) have all been reported in association with mycoplasmal pneumonias or with serologic evidence of a recent infection (Westenfelder et al; Fisher et al; Rothstein and Kenny). We have observed several patients with striking cerebral, cerebellar, brainstem, or spinal cord syndromes incurred during or soon after a mycoplasmal pneumonia or tracheobronchitis. In addition to the cerebellitis, which is clinically similar to the illness that follows varicella, unusual encephalitic syndromes of choreoathetosis, seizures, delirium, hemiparesis, and acute brain swelling (Reye syndrome) have each been reported in a few cases. The incidence of these complications has been estimated as 1 in 1,000 mycoplasmal infections, but it may approach 5 percent when more careful surveillance is carried out during epidemics. A severe prodromal headache has occurred in most of the cases we have observed. At the time of onset of the neurologic symptoms, there may be scant signs of pneumonia, and in some patients, only an upper respiratory syndrome occurs.
The mechanism of cerebral damage that complicates mycoplasmal infections has not been established, but evidence suggests that the organism may be present in the CNS during the acute illness. To our knowledge, the organism has been cultured from the brain in only one fatal case, but PCR techniques have detected fragments of mycoplasmal DNA in the spinal fluid from several patients (Narita et al). In other instances, the nature of the neurologic complications and their temporal relationship to the mycoplasmal infection clearly suggest that secondary autoimmune factors are operative, that is, that these are instances of postinfectious encephalomyelitis (a type of acute disseminated encephalomyelitis as described in Chap. 35). This is almost certainly the mechanism of postmycoplasmal Guillain-Barrè syndrome. Most of the patients with the infectious variety have recovered with few or no sequelae, but rare fatalities are reported.
The CSF usually contains small numbers of lymphocytes and other mononuclear cells and increased protein content. The diagnosis can be established by culture of the organism from the respiratory tract (which is difficult), by rising serum titers of complement-fixing IgG and IgM antibodies, and by cold agglutinin antibodies in the blood and CSF, or by DNA detection techniques from the CSF.