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We retrospectively evaluated the CT studies of 9 children who presented with intracranial tuberculosis during 1981-1987, and compared their radiographic appearance with the clinical outcome. The most common radiographic findings were: 1) ventriculomegaly (7/9) ,2) tuberculoma formation (6/9), and 3) infarction (4/9). Of 7 patients with ventriculomegaly, 3 required a ventricular shunt and 2 had spontaneous resolution of ventricular dilatation. Four children with ventriculomegaly were moderately or severely retarded, one had cognitive dysfunction, and one was neurologically normal. Four of six children with tuberculoma also had infarction and/or ventriculomegaly; of these four children, three were moderately or severely retarded. Two patients with tuberculoma as the only intracranial abnormality had complete resolution of the granuloma with normal neurologic outcome following antituberculous therapy. The four children with large vessel infarction also had ventriculomegaly; three had poor clinical outcome. The presence of tuberculoma alone is not necessarily predictive of poor neurologic outcome; age less than 20 months, infarct, and/or ventriculomegaly are usually associated with sequelae.

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Objectives:To characterize risk factors associated with pneumococcal disease and asymptomatic colonization during an outbreak of multidrug-resistantStreptococcus pneumoniae(MDRSP) among AIDS patients in a long-term–care facility (LTCF), evaluate the efficacy of antimicrobial prophylaxis in eliminating MDRSP colonization, and describe the emergence of fluoroquinolone resistance in the MDRSP outbreak strain.Design:Epidemiologic investigation based on chart review and characterization of SP strains by antimicrobial susceptibility testing and PFGE and prospective MDRSP surveillance.Setting:An 80-bed AIDS-care unit in an LTCF.Participants:Staff and residents on the unit.Results:From April 1995 through January 1996, 7 cases of MDRSP occurred. A nasopharyngeal (NP) swab survey of all residents (n = 65) and staff (n = 70) detected asymptomatic colonization among 6 residents (9%), but no staff. Isolates were sensitive only to rifampin, ofloxacin, and vancomycin. A 7-day course of rifampin and ofloxacin was given to eliminate colonization among residents: NP swab surveys at 1, 4, and 10 weeks after prophylaxis identified 1 or more colonized residents at each follow-up with isolates showing resistance to one or both treatment drugs. Between 1996 and 1999, an additional 6 patients were diagnosed with fluoroquinolone-resistant (FQ-R) MDRSP infection, with PFGE results demonstrating that the outbreak strain had persisted 3 years after the initial outbreak was recognized.Conclusions:Chemoprophylaxis likely contributed to the development of a FQ-R outbreak strain that continued to be transmitted in the facility through 1999. Long-term control of future MDRSP outbreaks should rely primarily on vaccination and strict infection control measures.

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The fourth component of complement (C4) is encoded by two separate but linked loci (C4A and C4B), each of which produces functionally active C4. Although C4A and C4B share certain antigenic and functional characteristics that identify them as C4, they differ with respect to other structural and functional properties. For example, C4B possesses four times the functional hemolytic activity of C4A. This suggests that homozygous deficiency of C4B might be associated with an increased susceptibility to infection. Forty-six children with bacterial meningitis were examined. Of these, 5 (10.9%) were homozygous deficient for C4B versus 7 (3.1%) of 223 controls (P = 0.038). There was no relation between the prevalence of heterozygous C4B deficiency and meningitis or between the prevalence of either homozygous or heterozygous C4A deficiency and meningitis. These results suggest that homozygous C4B deficiency is a relatively common immunodeficiency disorder that is clinically significant and predisposes children to bacterial meningitis.

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Bioterrorism is an emerging public health and infection control threat. Potential biological agents include smallpox, anthrax, plague, tularemia, botulinum toxin, brucellosis, Q fever, viral encephalitis, hemorrhagic fever, and staphylococcal enterotoxin B. An understanding of the epidemiology, clinical manifestations, and management of the more likely candidate agents is critical to limiting morbidity and mortality from a biological event. Effective response requires an increased index of suspicion for unusual diseases or syndromes, with prompt reporting to health authorities to facilitate recognition of an outbreak and subsequent intervention. Hospital epidemiology programs will play a crucial role in this effort.