Mycobacterial Infections of the Head and Neck.

Mycobacteria are important causes of head and neck infections. Mycobacterial lymphadenitis may be caused by both Mycobacterium tuberculosis and a variety of nontuberculous myocbacteria. Changes in the epidemiology of tuberculosis have caused a shift of the peak age range of tuberculous lymphadenitis from childhood to ages 20 to 40 years. Short-course chemotherapy is highly effective. Mycobacterium avium has become the most common cause of nontuberculous lymphadenitis, but new mycobacterial species are increasingly recognized. Treatment consists primarily of complete surgical excision, although roles for antimycobacterial chemotherapy are being identified. Transient flares of mycobacterial lymphadenitis, which occur during initiation of antituberculous therapy and in HIV-infected patients after initiation of antiretroviral therapy, may respond to short courses of corticosteroids. Tuberculous otitis media has become uncommon. Otitis media due to nontuberculous mycobacterial infection is increasingly seen in patients with pre-existing ear disease and after surgical and otic interventions. Tuberculosis of the eye has also become uncommon but may occur via hematogenous dissemination or direct innoculation. Nontuberculous mycobacteria, most commonly Mycobacterium chelonae and Mycobacterium fortuitum, may cause keratitis, usually after some form of corneal trauma.

Tumor necrosis factor-alpha-stimulated polymorphonuclear leukocytes suppress migration and bactericidal activity of polymorphonuclear leukocytes in a paracrine manner.

OBJECTIVE: Polymorphonuclear leukocytes (PMN) and tumor necrosis factor-alpha (TNF-alpha) play prominent roles in acute respiratory distress syndrome, ischemia-reperfusion injury, trauma, and sepsis. Whereas direct effects of TNF-alpha on PMN function and viability are well documented, little data are available addressing the ability of PMN to communicate with each other in response to cytokine stimulation. Therefore, the aim of this study was to determine whether TNF-alpha can modulate PMN function by inducing PMN to secrete products upon stimulation, which would affect other PMN in vitro in a manner independent of cell contact. METHODS: PMN were purified daily from blood obtained from a pool of 22 healthy volunteers. Conditioned media (CM-TNF) was prepared by incubating PMN in Hanks' balanced salt solution plus TNF-alpha for 1-4 hrs. Freshly isolated PMN were resuspended in CM-TNF and analyzed for 1) phagocytosis of opsonized Escherichia coli, 2) oxidative metabolism as measured as an index of DCF-DA activation, and 3) migration to chemoattractants through Transwell inserts. RESULTS: CM-TNF decreased PMN phagocytotic activity by 8% to 15% and completely suppressed oxidative metabolism but did not modulate the expression of receptors associated with these functions. CM-TNF suppressed the migration of PMN to two biologically relevant agents, N-formyl-methionyl-leucyl-phenylalanine and leukotriene B4, by approximately 65%, but had no effect on PMN migration to interleukin-8. This suppression was observed for migration across plastic filters as well as extracellular matrix proteins. CONCLUSION: Our data demonstrate that PMN stimulated with TNF-alpha suppress the immunologic function and migration of other PMN independent of cell-cell contact and suggest that TNF-alpha may participate in a negative feedback loop by inducing a PMN-derived factor that counteracts its activity.

Paecilomyces lilacinus vaginitis in an immuno-competent patient.

Paecilomyces lilacinus, an environmental mold found in soil and vegetation, rarely causes human infection. We report the first case of P. lilacinus isolated from a vaginal culture in a patient with vaginitis.

Results of a cytomegalovirus (CMV)-specific CD8+/interferon- gamma+ cytokine flow cytometry assay correlate with clinical evidence of protective immunity in patients with AIDS with CMV retinitis.

To evaluate the potential clinical utility of a cytomegalovirus (CMV)-specific CD8+/interferon (IFN)- gamma+ cytokine flow cytometry (CFC) assay for patients with CMV retinitis (CMVR), stored peripheral blood mononuclear cell specimens were obtained from patients with active CMVR (i.e., having clinical evidence of absent CMV-protective immunity), as well as from highly active antiretroviral therapy-treated patients with CMVR who were able to discontinue anti-CMV therapy without subsequent progression of retinitis (i.e., having clinical evidence of restored CMV-protective immunity). Positive CD8+/IFN- gamma+ T lymphocyte responses to CMV phosphoprotein 65 or immediate early peptide-pool stimulation were present in specimens from only 3 of 10 patients with active CMVR but were present in at least 1 specimen from all 20 patients with immunorestored CMVR, with a mean of 2.4 specimens/patient tested, spanning up to 6 months of observation (P = .0001). Among the patients with immunorestored CMVR, positive responses were present in all longitudinal specimens from 15 of the 20 patients. These data suggest that further testing of the CMV-specific CD8+/IFN- gamma+ CFC assay, for clinical utility in predicting incident and progressive CMVR disease, is warranted.