To our knowledge, this is the first US study to report a reemergence of gram-negative organisms as a cause of PHA-BSIs. This finding does not seem to be related to changes in specific gram-negative organisms or to antimicrobial resistance. If this trend continues, it will have important implications for the management of bloodstream infections.

We studied the ability of a new DNA probe-based assay system to correctly identify isolates of the thermophilic campylobacters Campylobacter jejuni, C. coli, and C. laridis grown in vitro. We examined 424 organisms, including 214 Campylobacter isolates and 210 other aerobic and anaerobic isolates. The probe assay, which uses a new homogeneous system in which ail reactions take place within a single tube, demonstrated 100% accuracy, producing neither false-positive nor false-negative results. The assay does not, however, distinguish among C. jejuni, C. coli, and C. laridis.

A commercial latex agglutination test [Meritec-Campy (jcl), Meridian Diagnostics, Cincinnati, Ohio] was evaluated for identification of Campylobacterjejuni, C. coli, C. laridis, and other Campylol2cter isolates. The test had 100% sensitivity in detecting C. jejuni and C. coli but low sensitivity with C. laridis isolates. C. upsaliensis strains reacted with the test. The test had 100% specificity for 101 non-Campylobacter organisms.

Niacin-positive Mycobacterium kansasii was isolated from three patients, two with respiratory infections and one with a perirectal abscess. The isolates were phenotypically similar to other strains of M. kansasii, differing only in their ability to produce niacin. This phenotype has been reported only twice in the literature, during the 1960s. Mycobacterium kansasii has been reported previously to cause both pulmonary and extrapulmonary infections (2, 14, 15). In addition to chronic pulmonary disease, M. kansasii may cause cervical lymphadenitis, dermatitis, osteomyelitis, and arthritis. Disseminated infection occurs most commonly in immunocompromised patients (10). The organism can be identified in the laboratory on the basis of pigment and biochemical studies: M. kansasii is usually photochromogenic (rare isolates may be nonpigmented or scotochromogenic), and niacin accumulation is thought to be uniformly negative for this species. However, we recently isolated niacin-producing isolates of M. kansasii from three of our patients with compromised immune function, one at the University of Pennsylvania and two at the University of Cincinnati (two patients had respiratory infections, and one patient had a perirectal abscess). Case 1 (University of Pennsylvania). A 34-year-old black man, known to be positive for human immunodeficiency virus (HIV) antibody since August 1988, presented in September 1989 with a cough productive of blood-streaked sputum, increasing shortness of breath, pleuritic chest pain, and low-grade fevers. Diffuse interstitial bilateral infiltrates were observed on the chest radiograph. Bronchial washings showed many acid-fast bacilli by fluorochrome and Kinyoun staining and Pneumocystis carinii on silver staining. He was treated with isoniazid (INH), rifampin, and ethambutol for mycobacterial infection and cotrimoxazole and methylprednisolone for pneumocystis infection, with clinical improvement. A follow-up chest radiograph showed cavitation of the left upper lung infiltrate, with resolving interstitial infiltrates. He improved clinically and was discharged after 3 weeks of treatment for P. cannii pneumonia with zidovudine, INH, rifampin, and ethambutol. The isolated Mycobacterium sp. was subsequently identified as niacin-positive M. kansasii. After 1 year of treatment for M. kansasii pneumonia, his left apical lung cavity resolved and his antituberculous therapy was discontinued. Case 2 (University of Cincinnati). A 37-year-old white man who had been HIV positive for several years developed a

The authors performed a prospective clinical evaluation of the Gonozyme (Abbott Laboratories, Chicago, IL) assay in a family planning clinic population. One thousand five hundred eighty-eight female patients were screened for gonococcal infection using culture and Gonozyme assay. One hundred nine patients were culture positive (6.9% disease prevalence). The sensitivity and specificity of the Gonozyme assay in this setting was 87.2% and 89.1%, respectively. The predictive value of a positive and negative test, given a disease prevalence of 6.9%, was 37.2% and 98.9%, respectively. The false-positive and false-negative rate was 10.9% and 12.8%, respectively. The authors prospectively followed patients with true-positive and false-positive Gonozyme results. The Gonozyme test showed a 83% correlation with test of cure cultures and, thus, should not be used for test cure analysis. False-positive Gonozyme tests could not be explained on the basis of cross-reacting bacteria or detection of vancomycin-sensitive gonococci. The authors' results suggest that the Gonozyme test should not be used in lieu of culture in a clinical setting with a similar population.