Emergency department-based surveillance for syphilis during an outbreak in Philadelphia.

STUDY OBJECTIVE: To identify missed opportunities for syphilis treatment during an outbreak. DESIGN: Prospective prevalence survey. SETTING: Urban hospital emergency department. PARTICIPANTS: Nine hundred sixty-one persons aged 15 to 44 years seeking medical attention in the ED who were not suspected of having any sexually transmitted disease (STD) at the time of their visit. INTERVENTION: Serologic testing for syphilis and public health follow-up as needed. MEASUREMENTS AND MAIN RESULTS: Twenty-one non-STD patients (2%) had untreated early syphilis, and 22 (2%) had positive serology but were lost to follow-up. Among 271 STD patients seen in the ED during the same period, 15 cases (6%) were detected. We estimate that 80 or more additional untreated early syphilis cases would have been identified had all 15- to 44-year-old patients entering the ED been tested. The cost of screening was $251 per case detected. CONCLUSION: Patients not suspected of having any STD account for most early syphilis cases among all ED patients. Screening and on-site treatment for syphilis should be offered to all young adults seeking medical attention in the ED during syphilis outbreaks.

Cellular changes and antitumor responses in the plasmacytoma-bearing mouse following cyclophosphamide treatment.

Mice bearing the immunosuppressive plasmacytoma TEPC-183 exhibit a marked splenic hyperplasia. We have characterized these tumor-reactive splenocytes on the basis of cell surface marker expression, nonspecific esterase activity, and morphology. Although splenocyte numbers increased progressively throughout tumor growth, B- and T-lymphocytes, as defined by surface immunoglobulin and Thy-1 antigen expression, respectively, did not increase significantly. Fourteen days after tumor implantation, T-lymphocytes decreased from 70 million to 50 million per spleen. However, cells expressing Mac-1 antigen or nonspecific esterase activity increased from 10 to 65 million. This constituted a 6-fold increase in splenic macrophages. Further studies utilizing the expression of PC.2 antigen in conjunction with morphological examination indicated that metastatic TEPC-183 cells comprise approximately 5% of the tumor-host splenocyte population 14 days after implantation. Ablation of plasmacytoma by cyclophosphamide inhibited the tumor-associated splenocytosis and led to an increase in splenic T-cells (from 70 to 120 million). In addition, macrophage numbers returned to normal. This study also assessed the ability of splenocytes from animals with either actively growing tumors or those from cyclophosphamide-treated tumor-bearing mice to mediate an antitumor response. Splenocytes, when assessed 1 wk following tumor ablation by cyclophosphamide, demonstrated antitumor activity in Winn neutralization assays. This activity was not detectable in splenocytes from animals with progressively growing tumors. Additional studies revealed that the cell population involved in the antitumor effect was glass nonadherent, nylon-wool nonadherent, and expressed Thy-1 antigen. These observations were consistent with the expansion of the splenic T-lymphocyte population following cyclophosphamide treatment. However, the immune response directed against primary TEPC-183 tumor cells was not inhibitory to metastatic tumor cells.

Effects of pesticides on the reticuloendothelial system.

The information available concerning the effects of compounds utilized as pesticides on functions of the reticuloendothelial system is quite limited. Review of selected examples of such studies in this and other reports (3) reveals considerable diversity in terms of species of experimental animal, purity and dose of pesticide, length of exposure, and class of pesticide employed. Observations include depression, enhancement, or no significant effect on the selected reticuloendothelial system function studies. With the present available information it is difficult to formulate general conclusions or to predict whether or not any individual pesticide will consistently and significantly alter any specific function of the reticuloendothelial system. At the present time, it is not known if pesticides within a single chemical class act in a similar manner in regard to their ability to influence reticuloendothelial system function. In addition, the relationship, if any, between the toxic, mutagenic teratogenic, or carcinogenic potential of any pesticide and its ability to alter the reticuloendothelial system is also unknown. More extensive systematic studies in experimental animal models would appear to be required before protocols to effectively evaluate the potential of pesticides to influence reticuloendothelial system function in man can be developed.

Humoral immunity in mice following oral administration of selected pesticides.

Five pesticides (carbaryl, DDT, parathion, chlordimeform, and ametryne) were tested for their effects on the immunocompetence of Balb/c mice. All five of the test pesticides were observed to induce statistically significant suppression of the humoral immune response if administered orally, at near lethal doses, during an ongoing immune response. Ametryne and chlordimeform were also observed to have a suppressive effect on humoral immune competence if orally administered in a sufficiently large quantity, 1 LD50, at the time of, or prior to, immunization. Administration of 0.1 LD50 parathion per day, over an extended period of time, resulted in a statistically significant suppression of the humoral immune response.

Friend virus-induced immunodepression: effect of neuraminidase treatment on Thy-1.2 antigen expression and cytotoxic potential of splenocytes from virus-infected mice.

Infection of susceptible strains of mice with Friend leukemia virus (FLV) results in a profound depression of cell-mediated immunity as assessed by lymphocyte-mediated cytotoxicity. This depression occurs early in the disease, before the onset of splenomegaly, and is associated with a decline in the susceptibility of splenocytes from FLV-infected mice to lysis by anti-Thy-1. 2 serum and complement. Treatment of splenocytes from FLV-infected mice with neuraminidase restores, in large part, their susceptibility to anti-Thy-1.2 serum as well as their cytolytic capacity. These studies suggest that one early immunosuppressive consequence of infection with FLV involves alteration of the effector T-lymphocyte cell surface.

Macrophage-induced reversal of immunosuppression by leukemia viruses.

Suppression of the humoral immune response by several murine leukemia viruses has been well documented. However, the mechanism of suppressed immunoresponsiveness is not well characterized. Macrophages have been reported to be intimately involved in host-tumor relationships, and were therefore examined for their role in reversing suppression in two leukemia virus-induced tumor models. In vivo studies with the Friend leukemia virus (FL virus) were unsuccessful in demonstrating any role for stimulated peritoneal exudate (PE) cells, rich in macrophages, in restoration of antibody function in leukemic mice. However, in vitro studies with FL virus demonstrated that proteose-peptone stimulated PE cells from normal syngeneic mice in restricted numbers (1-3 x 10(5)), when added to 5 x 10(6) FL virus infected spleen cells, could partially restore immunity. Furthermore, using the Rowson-Parr virus (RP virus) model system it was shown that PE cells from RP virus-infected mice, as well as normal PE cells, were capable of restoring immunocompetence. Neither splenic adherent cells nor lymphoid cells from other tissues, when added to RP virus-infected spleen cells, were able to induce recovery of the immune response. In addition, treatment with antitheta serum plus complement had no effect on the ability of PE cells to restore immunity, implying that macrophages were solely responsible for reversal of immunosuppression. An alteration of antigen "processing" or "focusing" may be an important mechanism by which recovery of immune competence is achieved.

Failure of peritoneal exudate macrophages to reverse immunologic impairment by Friend leukemia virus.

Transfer experiments with peritoneal exudate macrophages from normal donor mice were performed to determine if a defect of normal macrophage function or activity was a major or contributing factor to the immunosuppression characterizing leukemia virus infection of mice. Challenge immunization of Friend leukemia virus-infected mice with sheep erythrocytes resulted in markedly depressed hemolytic antibody responses, as compared to responses of normal noninfected mice. When PE cell suspensions rich in macrophages were transferred from normal donor mice to leukemia virus infected recipients there was no affect on the FLV-induced impairment of the immune response. Similar transfer of PE cells to normal uninfected mice generally resulted in a moderate depression of the expected immune response. In no case did the PE cells enhance the immune responses in normal or virus-infected mice.

Intracellular localization of the migration inhibitory factor (MIF) in a long-term human lymphoid cell line.

Subcellular fractions of the human lymphoid cell line PGLC-33H were obtained by N2 cavitation and differential centrifugation. The purity of the fractions was assessed by the use of the following marker enzymes: beta-glucuronidase for the lysosomal-intermediate fraction; a nonspecific esterase for the microsomal fraction; and LDH for the supernatant fraction. These subcellular fractions were studied for MIF activity utilizing human lymphoid cells from established lines as target cells. MIF activity was most consistently found in the microsomal fraction. Also, MIF activity was closely associated with the relative specific activity of exterase. No such correlation with MIF activity could be demonstrated for beta-glucuronidase or LDH.

Immunosuppression by leukemia viruses. Effect of Friend leukemia virus on humoral immune competence of leukemia-resistant C57BL/6 mice.

Infection of genetically resistant C57BL/6 mice with Friend leukemia virus resulted in a marked but transient immunodepression of the humoral immune response to sheep erythrocytes. The primary immune response to sheep erythrocytes was depressed in mice infected 1 or 3 days before challenge immunization, but no suppression was observed when the interval was greater. The suppression coincided with the time of transient viremia in the mice. The secondary immune response to sheep erythrocytes was inhibited when virus was injected within a few days before booster immunization. Induction of immunologic "memory" to sheep erythrocytes was also blocked in C57BL/6 mice given virus before priming with the SRBC. The immunosuppressive activity appeared due to a marked but transient effect of the virus on antibody precursor cells, as ascertained by cell transfer experiments. These observations are pertinent to the general question to the cellular site of action of immunosuppressive tumor viruses and the relationship between immunosuppression and the neoplastic properties of the RNA viruses.