Nonimmune hydrops fetalis (NIHF) is used to describe fetuses and newborns with generalized edema and cavity effusions. It is helpful to alert physicians about the presence of anemia, heart failure, and/or hypoproteinemia, but this diagnosis is frequently overlooked. We reviewed the autopsy files from 1990 to 2000, selected all cases with NIHF including clinical information (with maternal laboratory tests and ultrasound), and classified patients by etiology. Among 840 stillborn autopsies during the 11-year period, we found 51 with NIHF (6.07%). The clinical summary had mentioned hydrops in 14 patients and the etiology in another 7 by fetal ultrasonography, but without addressing the possibility of hydrops. In the remaining 30 cases neither hydrops nor an etiology was mentioned. Other pertinent diagnoses were maternal diabetes mellitus (4), congenital heart disease (3), and cystic hygroma (2). The following diagnoses were made in one instance each: cardiac tumor, twin transfusion syndrome, congenital adenomatoid malformation, syphilis, Turner syndrome, and cerebral arteriovenous malformation. Postmortem and placental examination confirmed the following etiologies: congenital infections (17); placental pathology significant enough to explain NIHF (10); cardiovascular diseases (8) (further classified as congenital heart disease [3], rhabdomyoma [1], and vascular malformations [4]); chromosomal abnormalities (6); uncontrolled maternal diabetes (4); intrathoracic lesions (2); prune-belly syndrome (2); and idiopathic NIHF (2). Only 3.9% of the cases studied had no identifiable etiology. The cause of hydrops was confirmed by autopsy in 47 fetuses (92%), which further supports the importance of performing an autopsy. Thirty-two cases (62.74%) had placental abnormalities helpful to the etiology (parvovirus, syphilis, Turner's syndrome, etc.). In 20 instances, the clinical summary had no mention of either hydrops or any of the diseases leading to it. The autopsy in conjunction with placental examination and fetal ultrasound represent the best combination to determine the etiology of NIHF among stillborn fetuses.

The in-vitro susceptibilities of 40 clinical isolates of Candida albicans to ketoconazole and fluconazole were determined and an attempt was made to correlate these data with the clinical responses of the patients from whom the strains were originally isolated to treatment with these agents. Of 40 patients with the acquired immunodeficiency syndrome (AIDS) with oropharyngeal and/or oesophageal candidosis, 21 received ketoconazole and 19 fluconazole. Susceptibility testing was performed by a microbroth dilution method with RPMI-2% glucose medium according to the recommendations of the National Committee for Clinical Laboratory Standards; growth inhibition was estimated spectrophotometrically and the MIC endpoint was defined in terms of the IC1/2. The MICs of 236 additional strains of C. albicans, which were also isolated from AIDS patients, were used to establish a susceptibility profile for this species. On the basis of the susceptibility test results and the clinical responses of the 40 patients, the following tentative breakpoints for ketoconazole and fluconazole are proposed: patients with infections caused by C. albicans strains with MICs of ketoconazole and fluconazole or < or = 0.001 and < or = 0.25 mg/L respectively would be expected to respond to treatment with these agents and isolates with MICs which meet these criteria are therefore classified as susceptible; patients with infections caused by strains with MICs of ketoconazole and fluconazole of > or = 0.06 and > or = 16.0 mg/L respectively would not be expected to respond to treatment with these agents and isolates with MICs which meet these criteria are therefore classified as resistant; the response of patients with infections caused by strains with MICs of ketoconazole and fluconazole of 0.003-0.03 and 0.5-8.0 mg/L respectively cannot be reliably predicted and isolates with MICs which fall within these ranges are therefore classified as being of indeterminate susceptibility. The present study demonstrates that the results of in-vitro susceptibility testing with RPMI-2% glucose broth correlate with the clinical response to therapy and can be used to facilitate optimal treatment in AIDS patients with oropharyngeal and/or oesophageal candidosis.

In order to determine the clinical significance of mixed oropharyngeal candidiasis (Candida albicans plus a non-albicans strain of Candida) in patients infected with HIV-1, a retrospective chart review was done in 12 HIV-1-infected patients with a clinical episode of oropharyngeal candidiasis, in whom a mixed culture of Candida albicans (found to be fluconazole-sensitive) plus a non-albicans species of Candida was obtained from their oral cavities. This group was compared with 26 HIV-positive patients (control group) with oropharyngeal candidiasis due to Candida albicans (found to be fluconazole-sensitive). Antifungal susceptibility testing was performed by a broth microdilution test with RPMI-2% glucose. A fungal strain was considered fluconazole-sensitive if its MIC was < 0.5 micrograms/ml. Both the study and control groups had similar clinical and demographic characteristics. All the patients were severely immunocompromised, with a mean CD4+ lymphocyte count of 63/mm3 (95% CI 41-84) and 80/mm3 (95% CI 25-135) in the study and control groups, respectively. In the study group, seven patients had Candida albicans and Candida krusei in their oral cavity, four had Candida albicans and Candida glabrata, and one had Candida albicans and Candida tropicalis. Antifungal therapy consisted of ketoconazole (5 patients in the study group, 14 in the control group) or fluconazole (7 patients in the study group, 12 in the control group); no statistically significant difference in clinical outcome was observed. Fungal strain persistence after therapy was frequently observed in both groups. It is concluded that non-albicans strains of Candida, less sensitive to azole drugs than their Candida albicans counterparts, are not clinically relevant in episodes of mixed oropharyngeal candidiasis in HIV-1-infected patients.

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