DEPARTMENT OF PATHOLOGY
The Johns Hopkins Medical Institutions

Vol. 18, No. 17
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Monday, May 10, 1999
 

  1. Provided by Leslie Edwards Reger, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.


    2. 3 outbreaks reported from 5/2 - 5/7: 1 gastroenteritis outbreak in a nursing home, 1 foodborne gastroenteritis outbreak in a food-service facility, and 1 foodborne gastroenteritis outbreak lab confirmed as salmonella at a catered dinner
     

  2. The Johns Hopkins Hospital. Information provided by Stephanie Schreiner, M.D., Department of Pathology.
Clinical Presentation A six year-old white male with a history of Langerhans' cell histiocytosis and diabetes insipidus presented to an outside hospital complaining of sore throat, vomiting and headache. He was evaluated and sent home. Over the next 24 hours he became febrile, his nausea and vomiting worsened, and he developed a petechial rash over his shoulder, back, right groin and thigh. On the way to the hospital, he had a single episode of seizure activity. His labs on admission were remarkable for a WBC = 32,200 with 22% bands, acidosis, and a positive D-dimer. A LP was done and the resulting CSF showed the following: WBC=16,000 (88% PMN's), RBC=867, glucose < 2, and protein =48. A Gram stain was done on the CSF which showed moderate-heavy gram-negative diplococci. A latex antigen agglutination test confirmed the presence of Neisseria meningitidis.
Neisseria meningitidis

Background

The genus Neisseria contains two pathogenic species, N. meningitidis, the second leading cause of community-acquired meningitis in the U.S., and N. gonorrhoeae, the cause of gonorrhea. The majority of meningococci can currently be divided into 13 serogroups based on differences in their capsular polysaccharides. The most important serogroups are A, B, C, W-135, and Y. Groups A and C are often the cause of major epidemic disease in developing countries. Group B is the major cause of endemic, sporadic disease in developed countries. The peak incidence of serious infection is age 3 to 12 months, corresponding to the time between loss of maternal antibodies and appearance of naturally acquired antibodies. Transmission occurs through respiratory droplets and requires both close contact as well as susceptibility (i.e. lack of specific antibody). Other populations at risk include those in crowded environments (e.g. military camps, boarding schools), individuals with certain complement deficiencies, hepatic failure, SLE, multiple myeloma, and asplenia. Clinical Presentation Acute, purulent meningitis is the most frequent form of infection. Meningococcemia is heralded by the development of conjunctival and skin petechial hemorrhages. Approximately 10% of patients with meningococcemia develop purpura fulminans, a cutaneous hemorrhagic necrosis secondary to coagulopathy. Symptoms can progress to DIC and shock. If bilateral hemorrhagic destruction of the adrenal glands occurs, it is called Waterhouse-Friderichsensyndrome. Despite modern chemotherapy, mortality rates up to 30% are seen in patients who develop meningococcal meningitis with sepsis. A chronic meningococcemia can also occur associated with low-grade fever, arthritis and skin lesions that develop over days to weeks. Primary meningococcal conjunctivitis has also been recognized as a distinct entity. Less common are meningococcal pneumonia, infection of the male or female urogenital tract, anal canal, and peritonitis associated with chronic peritoneal dialysis. Diagnosis Direct Gram stained smears of CSF may show the typical "kidney bean"-shaped gram-negative diplococci, often located within the cytoplasm of neutrophils. Definitive diagnosis is by culture of CSF, blood or skin lesions. For rapid diagnosis, meningococcal polysaccharide antigen may be detected by latex agglutination or counterimmunoelectrophoresis from CSF, blood, or urine. False negative results are common with these latter methods, however, especially with serogroup B. Treatment Penicillin is the drug of choice since it can penetrate inflamed meninges. If the patient cannot tolerate penicillin, chloramphenicol is used. Family members of symptomatic patients are at 1000-fold increased risk versus the general population, so prophylactic chemotherapy with rifampin, ciprofloxacin, or ofloxacin is indicated. References
1. Koneman EW et al: Diagnostic Microbiology, fifth ed. Lippincott, Philadelphia, pp499-502, 1997.

2. Schwartz B, Moore PS, Broome CV: Global epidemiology of meningococcal disease. Clin Microbiol Rev 2 (suppl): S118-S124, 1989.

3. Sherris JC, ed: Medical Microbiology, an Introduction to Infectious Diseases. Elsevier, New York, pp343-348, 1990.

Gram stained CSF specimen showing intracellular
gram-negative "kidney-bean" shaped diplococci.

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