In the latest Case Record of the Massachusetts General Hospital, a 39-year-old man was admitted to the hospital, 10 days after receiving prednisone for severe contact dermatitis, because of headache, nausea, and photophobia. Examination of the cerebrospinal fluid revealed white cells and gram-positive cocci. Diagnostic tests were performed. The most common cause of bacterial meningitis in the United States is Streptococcus pneumoniae, a gram-positive coccus that is responsible for 58% of all cases.
• What is the classic presentation of and CSF findings associated with a diagnosis of acute bacterial meningitis?
Abrupt onset of fever and neck stiffness are classic symptoms of acute bacterial meningitis that are found on initial physical examination in 95% and 88% of cases, respectively. CSF analysis typical for bacterial meningitis includes an elevated white-cell count with neutrophil predominance, hypoglycorrhachia (a low CSF glucose level), and an elevated total protein level. A white-cell count of more than 2000 per cubic millimeter or the presence of more than 1180 neutrophils per cubic millimeter in the CSF is nearly 100% specific for the diagnosis of bacterial meningitis, as is the finding of bacteria on Gram’s staining of the CSF.
• What are the symptoms of chronic strongyloidiasis?
The intestinal nematode Strongyloides stercoralis is endemic in tropical and subtropical areas, such as the Dominican Republic, and can survive for decades in a single host because it can complete its life cycle inside the human body without passing into the environment. Patients with chronic strongyloidiasis often have fluctuating eosinophilia, intermittent abdominal pain, and recurrent rashes, the two most common of which are urticaria around the waist and buttocks and larva currens, a rapidly migrating serpiginous dermatitis. These symptoms develop as filariform larvae, the infectious form of Strong. stercoralis, initiate the autoinfection cycle by penetrating the perianal skin or the intestinal wall.
Morning Report Questions
Q: What is the strongyloides hyperinfection syndrome?
A: The strongyloides hyperinfection syndrome can develop in patients with chronic strongyloidiasis when host immune function is impaired. The stongyloides autoinfection cycle accelerates, which leads to more egg-laying adult nematodes in the intestine and a subsequent vast increase in the number of migrating larvae. The administration of glucocorticoids and, increasingly, the use of tumor-necrosis-factor inhibitors are major risk factors for the strongyloides hyperinfection syndrome (also called severe complicated strongyloidiasis); even short courses of these medications can cause overwhelming infection and death. Eosinophilia is usually absent during hyperinfection. In the most fulminant form of the strongyloides hyperinfection syndrome, called disseminated strongyloidiasis, filariform larvae can migrate to the liver, brain, kidneys, meninges, and skin. Furthermore, migrating filariform larvae can carry enteric bacteria into the bloodstream and also cause breaks in the intestinal mucosa that may provide a portal of exit for intestinal bacteria. As a consequence, bacterial sepsis, pneumonia, and meningitis are common complications of the strongyloides hyperinfection syndrome. Bacterial meningitis that occurs concurrently with the strongyloides hyperinfection syndrome is often caused by enteric gram-negative organisms.
Q: How is the strongyloides hyperinfection syndrome diagnosed?
A: The diagnosis of the strongyloides hyperinfection syndrome can be made by examining the stool for filariform or rhabditiform larvae. This approach is not sensitive for the diagnosis of chronic strongyloidiasis, but during hyperinfection, a large number of larvae are present in the intestine, which improves the diagnostic yield of a stool sample.