To determine the epidemiology and clinical features of disease due to nontuberculous mycobacteria (NTM) in our institution, we reviewed the medical records of all patients from whom NTM isolates were recovered from 1988 to 1990 to extract selected clinical and laboratory data. On the basis of the likelihood of infection, patients were classified as having definite, probable, or unlikely NTM disease as defined by published guidelines. Of 80 patients who met the inclusion criteria, 17 had definite NTM disease, and 23 had probable NTM disease. No differences in age, sex, presence of underlying pulmonary or nonpulmonary disease, or chest radiographic abnormalities were noted between patients with and without NTM disease. More than 85% of all definite or probable cases were caused by Mycobacterium avium complex, Mycobacterium kansasii, and Mycobacterium fortuitum complex. The diagnosis of NTM disease was often delayed or missed, which resulted in unsatisfactory management of patients. There is a need to educate physicians about the diagnosis and management of NTM infections.

Objectives: To examine characteristics of pregnant women associated with cervical infection, and to evaluate the accuracy of symptom-based and risk assessment systems which have been developed for identifying cervical infection in antenatal women. Methods: Interviews were conducted and physical examinations performed on 291 consecutive antenatal clinic attenders in Nairobi, Kenya. Vaginal, cervical, urine and blood specimens were also obtained for analysis.Results: The following disease prevalences were observed: candidiasis 26-2%; trichomoniasis 19-9%; bacterial vaginosis 206%; any vaginal infection 53.8%; chlamydial cervicitis (CT) 8.8%; gonococcal cervicitis (GC) 2.4%; any cervical infection 10O8%. The only statistically significant association with GC and/or CT cervical infection was the presence of cervical friability (OR = 2-1, P = 0.05). There were trends towards associations with the presence of endocervical mucopus (OR = 2-6, P = 0.06), reporting a new sex partner in the past 3 months (OR = 2-2, P = 0 16) and reporting that a sex partner had an STD-related symptom (OR = 4.4, P = 0413).

We aimed to determine if the clinical and histological features of chancroid are altered by HIV infection. Male patients presenting to the Nairobi special treatment clinic with a clinical diagnosis of chancroid were eligible for the study. A detailed history, physical examination, swabs for Haemophilus ducreyi culture and blood for HIV serology, syphilis serology and CD4 counts were obtained from all patients. Punch biopsies from an ulcer were obtained from 10 patients and either fixed in 10% formalin or snap frozen in Optimum Cutting Temperature (OCT) medium compound at -70 degrees C. Patients were treated with erythromycin and followed for 3 weeks. Chi-square and Student's t-test were used to determine if the clinical and laboratory features of chancroid differed between HIV-seropositive and seronegative individuals. Cox regression survival analysis was used to determine if HIV infection altered cure rates of chancroid at 21 days. Immunohistochemical staining was performed using lymphocytic and macrophage markers and tissue sections were analysed by 2 pathologists in a blinded manner. Between February and November 1994, 109 HIV-seropositive and 211 HIV-seronegative individuals were enrolled in the study. HIV patients had ulcers of longer duration than HIV-seronegative patients (P=0.03). Although cure rates were similar at 3 weeks, HIV patients had lower cure rates at 1 week (23% v 54%, P=0.002). A dense interstitial and perivascular inflammatory infiltrate extending from the reticular to deep dermis was present in all biopsies. This consisted of equal amounts of CD4 and CD8 T-lymphocytes as well as macrophages. The histological and immunohistochemical picture was identical for HIV-positive and negative patients. HIV infection slows the healing rates of chancroid ulcers despite appropriate antibiotic therapy. This clinical difference cannot be attributed to an altered histopathological response to HIV infection. Additional studies are needed to elucidate the mechanisms responsible for this finding.

Focal and segmental, but not generalized, myoclonus have been described with human immunodeficiency virus (HIV) infection. We describe three patients with generalized myoclonus and acquired immunodeficiency syndrome (AIDS) dementia complex. In each, myoclonus persisted until death, invariably after a course of a few months. In two patients, myoclonus was elicited by sudden auditory stimuli and resembled a startle response. This form of myoclonus may be subcortical in origin. We suggest that the AIDS dementia complex be included among the causes of myoclonic dementia.

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