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Resistance to Treponema hyodysenteriae (serotypes 1, 2, 3, and 4) infection was evaluated in ligated colonic loops in pigs recovered from swine dysentery. Lesions were present in most loops from recovered swine inoculated with heterologous serotypes; however, lesions were not present in loops of recovered swine inoculated with homologous serotypes.
Discriminate analysis was used to evaluate the enzyme-linked immunosorbent assay (ELISA) for the detection of anti-Treponema hyodysenteriae antibodies in experimentally and naturally infected swine. In trial 1, 26 pigs were randomly divided into three groups (naturally infected, n = 8; experimentally infected, n = 11; and noninfected, n = 7), and samples were collected for 10 weeks. For trial 2, 31 pigs were randomly divided into two groups (naturally infected, n = 22; and noninfected, n = 7), and samples were collected for 20 weeks. Rectal swabs for T. hyodysenteriae isolation were collected daily, and fecal samples for isolation of Salmonella spp. were collected weekly. Serum samples for ELISA evaluation were collected biweekly (trial 1) or weekly (trial 2). Results of discriminate analysis indicated that the ELISA correctly identified 90% or more of the individually infected pigs at prior probabilities of infection ranging from 60 to 90%. The test correctly identified noninfected pigs at a lower rate (61 to 92% range). The mean ELISA titers of naturally infected pigs without clinical signs were not significantly different (P less than 0.05) from the titers of both groups of experimentally infected pigs. Mean ELISA titers of naturally infected pigs without clinical signs were significantly greater than the mean titers of naturally infected pigs with clinical signs. Naturally infected pigs with clinical signs had a mean ELISA titer that was significantly greater than that of noninfected pigs and significantly less than the mean titers of the experimentally infected pigs without clinical signs and the naturally infected pigs without clinical signs.
Mice of several inbred strains were studied for responses to Treponema pallidum (Nichols). Mice were injected with viable treponemes and observed daily for the presence of lesions or signs of illness. Although none of the mice developed detectable lesions, they did develop specific anti-T. pallidum antibodies that were observed as early as 21 days after inoculation with viable T. pallidum. The antibodies were detected by an enzyme-linked immunosorbent assay and by passive haemagglutination.
The study was performed to determine the association of seroprevalence of hepatitis C virus (HCV) and Treponema pallidum (T. pallidum) infection among HIV infected first time male blood donors (HIV group) in comparison with the HIV seronegative blood donors (control group) in the Northeast of Thailand (NET). Serum samples were collected from 10,321 first blood donation voluntary male donors. All samples were screened for anti-HIV and anti-HCV by particle agglutination test, and syphilis antibody by RPR. The anti-HIV positive sera were repeated by EIA and confirmed by western blot. The reactive anti-HCV samples were confirmed by EIA whereas reactive syphilis antibody samples were confirmed by TPPA. Fisher's exact test was used for statistical analysis. The prevalence of anti-HIV in first time male donors was 0.70 per cent (72/10,321). The age of HIV group and 10,018 male control group ranged from 17-50 years old. The prevalence of HIV among 21-40 years old age group was significantly higher than the 17-20 years old (p = 0.00003). The 17-20 years old HIV group showed significantly higher sero-prevalence of TPPA (p = 0.003). The 21-30 years old HIV group gave significantly higher sero-prevalence of anti-HCV (p = 0.0008) and TPPA (p = 0.045), but the seroprevalence of anti-HCV and TPPA among the 31-50 year old group were nonsignificantly different (p > 0.05). The concurrence of anti-HCV and TPPA in HIV groups was not found. This result indicated that HIV infection among NET voluntary male blood donors was significantly associated with T. pallidum infection in young adults and the HCV infection in mature adults.
We investigated by means of radiolabelled precursors the source and nature of the polyanionic macromolecules present in rabbit tissues during active syphilis infection. Previous studies indicated that Treponema pallidum itself does not synthesise glycosaminoglycans, at least in vitro. In replicate experiments on unilaterally infected rabbits, tissue from the orchitic testis incorporated two to three times more 35S-sulphate and 3H-glucosamine (on a wet weight basis) than tissue from the non-orchitic contralateral testis. Incorporation of 35S-sulphate was independent of the number of viable T pallidum organisms present in the infested tissue, which suggested that incorporation represented biosynthesis by the host and not the treponeme. Testes from syphilitic rabbits two days after treatment with high doses (100 mg/kg) of penicillin incorporated less 35S-sulphate than untreated infected testes, but more than normal uninfected rabbit testes. This suggests that active syphilitic infection was necessary for maximum biosynthesis of the macromolecule(s) by host tissue. Hydrodynamic profiles showed incorporation of radiolabelled precursors into two distinct fractions of different sizes, which may represent a proteoglycan and a sulphated glycoprotein. Alcian blue staining of syphilitic testes at or after peak orchitis showed focal deposition of newly synthesised polyanionic components during peak orchitis and a more generalised fibrosis in testes after peak orchitis.
Specific identifications by immunofluorescence of infecting organisms and lymphoid cells in lymphoid organs and testes of rabbits were compared with the light microscopic appearances of these cells and organs on days 10, 11, 13, and 20 after intratesticular inoculation with Treponema pallidum (Nichols strain). Large numbers of T. pallidum were observed in the interstitial tissues of the testes on days 10 and 11. These numbers had declined markedly by day 13, and by day 20 only rare organisms (estimated as fewer than one to three per cross section) were seen. Organisms were also easily identified in much smaller numbers in the lymph nodes and spleen on days 13 and 20. Disappearance of organisms from the testes were associated with infiltration of large numbers of T cells. Marked follicular and diffuse cortical hyperplasia of the lymph nodes as well as follicular and periarterial hyperplasia of the spleen were observed. Specific immunofluorescence revealed large numbers of T cells in the diffuse cortex of the lymph nodes and the periarteriolar zones of the spleen. There was also a periportal infiltration of T cells in the liver. It is concluded that rabbits infected intratesticularly with T. pallidum mount an intense immune response that effectively eliminates most of the infecting organisms. However, despite this response, surviving T. pallidum may be identified not only at the original site of infection, but also disseminated in lymphoid organs. Normal mechanisms for controlling immune responses apparently shut down the specific response at a time when infecting organisms have not been completely eradicated from the host's tissues.
Groups of 10 young male guinea pigs of inbred strains 2 and 13 and outbred strains Hartley A, Hartley B, and one deficient in the fourth component of complement (C4D) were infected intradermally with 80 X 10(6) Treponema pallidum (Nichols). The course of infection and production of antitreponemal antibody were examined. Strain C4D guinea pigs were the most susceptible to infection (100%); inbred strains 2 and 13 and outbred strain Hartley B showed 80-90% symptomatic infection; and the Hartley A strain was the least susceptible to infection (10%). Strain 13 animals responded with the highest antitreponemal antibody activity, and the Hartley A strain with the lowest. The results suggest that genetic factors or complement, or both, may influence the degree of susceptibility to infection with T pallidum in guinea pigs.
Guinea pigs of inbred strain 2 and of a strain deficient in complement component 4 (C4D) responded to intradermal infection with Treponema pallidum by production of antibodies to treponemal antigens, normal rabbit serum proteins, fibronectin, and creatine kinase and with formation of circulating immune complexes (IC). IC started to appear at low concentrations 1 mo after infection and increased between 3 and 5 mo post-infection. Antibodies to fibronectin appeared after the second month but were not detectable 30 days later. Antibody activity to creatine kinase was detectable at the fourth month and became significantly higher at 5 mo post-infection. Reinoculation with a dose similar to that used for primary infection caused a significant increase in all antibodies and IC. Dissociation products of IC formed after primary infection consisted predominantly of treponemal antibodies and antigens, whereas IC detected after reinfection consisted predominantly of antibodies and normal rabbit serum proteins. Antibodies to fibronectin and creatine kinase are considered autoantibodies, and the underlying mechanism responsible for their production in syphilis is discussed.
A serological survey to detect antibody titres against Treponema hyodysenteriae was conducted on pigs from 106 herds in Western Australia. Titres indicating a positive result in the tests were determined by examining 400 sera from 4 herds known to be free of swine dysentery, and sera from immunised or experimentally infected pigs. Samples of serum from 40 bacon-weight pigs from each of the 106 herds were then collected at 2 abattoirs. Each serum was tested in enzyme-linked immunosorbent assays (ELISA) against the lipopolysaccharide of T hyodysenteriae of serogroups A, B and E, respectively. To assist in evaluating the test, 19 herds were resampled and retested, and faecal samples from 17 herds were cultured for T hyodysenteriae. Thirty-five of the 106 herds (33%) had serological evidence of infection when only one batch of sera from each herd was tested. The ELISA to detect T hyodysenteriae infection in herds using 40 sera was estimated as having a sensitivity of 77.3% and a specificity of 81.8% based on the owners' opinion of their herds disease status. Prevalence of infection within herds ranged from 2.5% to 47.5%, with a mean of 18%.
The correlation between the level of cold autolymphocytotoxic activity in the sera of rabbits infected with T. pallidum, and the percentage of B and T cells in the peripheral blood of the same animals was determined. The percentage of cells was estimated by the E and EAC rosette techniques and by the immunofluorescence test on immunoglobulin-bearing (B) cells. It was found that the increase of the autolymphocytotoxic activity was connected with the proportional decrease of B lymphocytes and increase of T lymphocytes. Since the decrease of B cells was significant (p less than 0.05) it is suggested that the autolymphocytotoxic activity may be involved in killing of B lymphocytes also in vivo. The possible role of the complement-dependent autolymphocytotoxic serum activity in regulation of humoral response in syphilis is discussed.
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The therapeutic effects of subcutaneously administered sedecamycin on experimental Treponema hyodysenteriae infection in mice were evaluated. Sedecamycin was more active than tiamulin and lincomycin. The efficacy of sedecamycin upon subcutaneous administration was similar to that upon oral administration. Sedecamycin given subcutaneously provided similar degrees of protection in bile duct-ligated and intact mice. Pharmacokinetic studies utilizing a liquid chromatographic technique were carried out to determine the concentration of sedecamycin in the cecum, the site of T. hyodysenteriae infection in mice. Little sedecamycin was found; however, lankacidinol, a major metabolite of sedecamycin, was found in the cecal contents of intact mice after subcutaneous or oral administration of sedecamycin. Lankacidinol was also found in the cecal contents of bile duct-ligated mice, although the concentration found after subcutaneous administration of sedecamycin was much lower than that found after subcutaneous or oral administration to intact mice. These results indicate that sedecamycin is excreted directly into the intestinal tract as an active metabolite by a route other than the bile duct. It is suggested that this intestinal excretion plays an important role in the efficacy of subcutaneously administered sedecamycin against cecal infection of mice by T. hyodysenteriae.
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When 47 pigs were dosed orally with cultures of Treponema hyodysenteriae, 44 (94 per cent) developed swine dysentery. Of those which recovered and were rechallenged, nine of 21 (43 per cent) showed clinical signs, as did one of 10 (10 per cent) challenged on a third occasion. Clinical disease was associated with development of specific IgG, IgA and IgM antibodies in serum and the local production of IgA in gut mucosal tissues. The appearance of antibody was not directly related to protection but rather indicated either prolonged exposure (in the case of serum IgG) or recent exposure to T hyodysenteriae (for secretory IgA). Infection also resulted in the appearance of IgG and IgA memory cells in gut-associated lymphoid tissue. However, these studies indicated that humoral immunity alone is not responsible for the onset of a protective response to T hyodysenteriae in the colon.
Blood samples from 740 Egyptian Nationals working in the tourism industry at two sites in the South Sinai governorate were screened for markers of infection with hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), and Treponema pallidum. Study subjects included 467 individuals from a rural seashore tourist village and 273 persons at two hotels in a well-established resort town. Subjects' ages ranged from 15 to 70 years; 99.3% were male. The prevalence of serologic markers for currently asymptomatic or past HBV infection alone was 20.7% (n = 153), of markers for past or chronic HCV infection alone was 7.4% (n = 55), and of markers for both HBV and HCV was 6.9% (n = 51). Of the 204 individuals positive for anti-HBV core antibody, 12 (5.9%) were also positive for hepatitis B surface antigen. Two individuals (0.3%) had a serologic market suggestive of an active syphilitic infection. No subject was found to be HIV-seropositive. History of prior injections and number of injections were associated with infection with HCV. Primary residence in the Nile delta and valley areas where schistosomiasis is highly endemic, was also a statistically significant risk factor for HCV, but not HBV infection.
Resistance to cutaneous syphilitic reinfection in strain 2 and strain 13 guinea pigs developed gradually 3 to 7 months after primary infection and reached maximum levels at 6 to 7 months after the induction of primary cutaneous disease. Associated with this acquired resistance was the occurrence of Arthus reactions and anamnestic-type antibody responses. Passive transfer of immune serum containing high-titered treponemal antibody into normal strain 2 guinea pigs significantly delayed the appearance and markedly diminished the severity and duration of skin lesions that developed after these recipients were challenged with treponemes but did not prevent the dissemination of organisms to the draining lymph nodes. These findings provide direct evidence that syphilitic infection elicits the formation of serum factors that are, at least, partially protective against symptomatic disease.
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Five hundred and seventeen women attending the gynecology and obstetrics clinics of the Korle-Bu Teaching Hospital were examined for sexually transmitted infections (STIs). Vaginal swabs were examined for Trichomonas vaginalis, Candida albicans, and Gardnerella vaginalis infection. Endocervical swabs were examined for Neisseria gonorrhoea and Chlamydia trachomatis using a recently developed RNA detection kit. Strain typing was performed to identify serovars of C. trachomatis. Sera were analyzed for Treponema pallidum with a passive-particle agglutination assay kit. The prevalence of infection with N. gonorrhoea was 0.6%, C. trachomatis 3.0%, and T. pallidum 5.6%. Eight samples were PCR-positive for C. trachomatis. Five of these were serovar G, and the rest were serovar E. All cases of mixed infections occurred in pregnant women. In conclusion, a high transmissible risk of T. pallidum infection was observed among our study population and in particular among our pregnant women. The absence of association between the presenting symptoms, clinical findings, and specific pathogens has implications for the syndromic approach to STI case management. The low prevalence of C. trachomatis and N. gonorrhoea may be due to self medication and requires further research in primary health institutions in rural areas to compare rates.