Influence of human immunodeficiency virus infection on pelvic inflammatory disease.

OBJECTIVE: To examine the influence of human immunodeficiency virus (HIV) infection on clinical and microbiologic characteristics of pelvic inflammatory disease (PID). METHODS: Forty-four HIV-infected women and 163 HIV noninfected women diagnosed with PID by standard case definition were evaluated by using clinical severity scores, transabdominal sonograms, and endometrial biopsies. After testing for bacterial infections, patients were prescribed antibiotics as recommended by the Centers for Disease Control and Prevention (CDC). RESULTS: Symptoms of PID and analgesic use before enrollment did not differ by HIV serostatus. More HIV-infected women had received antibiotics before enrollment (40.9% versus 27.2%, P =.08), a factor associated with milder signs regardless of serostatus. More HIV-infected women had sonographically diagnosed adnexal masses at enrollment (45.8% versus 27.1%, P =.08), a difference that yielded higher median severity scores (17.5 of 42 points versus 15 of 42 points, P =.07). However, those differences were not significant at the P <.05 level. Mycoplasma (50% versus 22%, P <.05) and streptococcus species (34% versus 17%, P <.05) were isolated more commonly from biopsies of HIV-infected women. Within 30 days after enrollment, HIV-infected women generally responded as well to therapy as HIV-noninfected women did, regardless of initial CD4 T-lymphocyte percentage. CONCLUSION: Among women with acute PID, HIV infection was associated with more sonographically diagnosed adnexal masses. Clinical response to CDC-recommended antibiotics did not differ appreciably by serostatus. Mycoplasmas and streptococci were isolated more commonly from HIV-infected women, but those organisms also might be associated with PID in immunocompetent women.

Macrophage-like effector of spontaneous cytotoxicity from the shark.

The effector of spontaneous cytotoxicity from shark peripheral blood has been shown to be a macrophage-like cell. Effector cells are isolated by centrifugation over Lymphocyte Separation Medium, adherence to glass, Percoll density gradient centrifugation and adherence to fibronectin sequentially. Effector cells are adherent to glass, sediment to densities of 1.048-1.052 g/ml and are adherent to fibronectin. The isolated effectors represent less than 1% of the peripheral blood leukocytes, and exhibit potent cytotoxic capability, both spontaneous and in the presence of phytohemagglutinin. In addition, the activity of these cells is resistant to 3000 rads gamma irradiation. Although nurse sharks have natural antibody to trinitrophenol, spontaneously cytotoxic cells are incapable of killing trinitrophenol modified targets indicating that natural antibody is not required for reactivity, and that natural antibody and spontaneous effectors do not have the same repertoire. However, cold target inhibition studies showed that these effector cells can recognize four of five human lymphomyeloid targets. It is concluded that the spontaneous, extracellular killing by the macrophage-like effector most closely resembles that of activated mammalian tumoricidal macrophages with the exception that they do not appear to require in vitro activation.