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PubMed1984

Experimental Treponema hyodysenteriae infection of mice.

Factors such as strain, fasting period, sex and age of the animals, and challenge dose were examined for their effects on the development of infection with Treponema hyodysenteriae in mice. Among mice tested, Ta:CF#1 mice were the most susceptible to the infection. Ta:CF#1 mice developed gross cecal lesions by a single oral dose ranging 10(2)-10(7) colony-forming units of T. hyodysenteriae without preinoculation fast. Oral challenge with 10(7) colony-forming units of the treponeme resulted in the development of gross lesions in all the mice at day 10. The number of T. hyodysenteriae in the feces and cecum of the mice reached the highest level at day 7 and 10, respectively; the levels lasted until day 21, the termination of the experiment. Macroscopic, microscopic and scanning electron microscopic findings of the lesions were similar to those of swine dysentery. These studies indicate that the Ta:CF#1 mice may be used as an excellent in vivo model system for swine dysentery.

Animals↗
PubMed1981

Sequential changes in susceptibility to Treponema pallidum of rabbits previously infected with Treponema paraluis-cuniculi.

Rabbits immunised with virulent Treponema paraluis-cuniculi were challenged intradermally with graded doses of Treponema pallidum at three, five, seven, 12, and 30 months to ascertain the level of protection to T pallidum at various intervals after immunisation.Rabbits challenged at three months after immunisation showed no protection against T pallidum and developed syphilitic lesions significantly faster than the control rabbits, which suggests that the former rabbits were immunosuppressed. Some protection was evident at five and seven months after immunisation, as fewer inoculation sites developed syphilitic lesions with challenges of 10(3), 10(2), and 10 T pallidum and lesions developed significantly slower with 10(6) challenge. Two rabbits showed significant protection at 12 months after immunisation but a third, presumably still immunosuppressed, developed lesions significantly faster than the control rabbits after challenge. At 30 months after immunisation one rabbit was completely protected and developed no lesions after challenge; the other rabbit showed only partial protection against challenge with 10(4), 10(3), and 10(2) but complete protection against challenge with 10 T pallidum.T paraluis-cuniculi appeared to induce a state of immunosuppression by three months after infection; in one rabbit this may have been 12 months. In most immunised rabbits, however, limited cross-protection to low challenge doses of T pallidum developed by five months and was also detectable at seven and 12 months. Only one rabbit was completely resistant to challenge with 10(4)T pallidum after 30 months and another was only partly immune. Thus, T paraluis-cuniculi infection does not produce a rapid pronounced cross-immunity to T pallidum in rabbits, which may thus limit its usefulness as a vaccine against syphilis.

Animals↗
PubMed1990

Effect of Treponema hyodysenteriae infection on mucosal mast cells and T cells in the murine cecum.

The pathogenic mechanisms responsible for the development of lesions in swine and mice after infection with Treponema hyodysenteriae have not been fully characterized. The release of inflammatory mediators from mast cells has been postulated to play a role in lesion development during swine dysentery. Therefore, C3H/HeN mice were infected with T. hyodysenteriae, and mucosal mast cell (MMC) numbers were examined in cecal sections. An initial increase in MMC numbers from 13 to 22 per 50 crypt villus units was observed, but at 20 days postinfection the numbers significantly decreased (P less than 0.05) to 5 MMC per 50 crypt villus units. Immunohistochemical analysis performed on cecal sections failed to show a significant change in lamina proprial T-lymphocyte subsets. Numbers of T. hyodysenteriae CFU recovered from the cecum were stable throughout the experimental time period. Mast cell-deficient W/Wv mice and their mast cell-sufficient littermates were also infected to determine whether MMCs were necessary for the occurrence of T. hyodysenteriae-induced lesions. W/Wv mice were as susceptible to infection as their normal littermates and developed similar macroscopic and microscopic lesions. These results indicate that changes in MMC numbers can be detected after an infection with T. hyodysenteriae; however, on the basis of observations of infected W/Wv mice, mast cells are not required for lesion development in the murine model.

Animals↗
PubMed1986

Enhanced primary resistance to Treponema pallidum infection and increased susceptibility to toxoplasmosis in T-cell-depleted guinea pigs.

Strain 2 guinea pigs made T-cell deficient by thymectomy and irradiation and protected with syngeneic bone-marrow cells (TXB guinea pigs) have a surprisingly high level of resistance to cutaneous syphilis and to the dissemination of treponemes to the draining lymph node. Compared with normal euthymic controls infected with Treponema pallidum Nichols, syphilitic TXB guinea pigs developed fewer and less severe skin lesions and their lymph nodes contained lower numbers of treponemes. Associated with this evidence for enhanced innate resistance was the ability of the TXB host to produce, during each test interval of a primary infection, more antitreponemal antibodies than that of their euthymic counterparts. Similar levels of partial protection against cutaneous and disseminated syphilitic infection and elevated antibody levels occurred in challenged normal guinea pigs passively immunized with lymphocytes from T. pallidum-infected TXB donors. In contrast, the capacity of the TXB host to be protected against a lethal infection with the unrelated intracellular protozoan parasite Toxoplasma gondii was greatly impaired unless it received an intravenous infusion of normal syngeneic thymocytes. These seemingly paradoxical results are explained primarily in terms of a residual T-helper-cell population in the TXB guinea pig which is large and competent enough to generate antisyphilis, but not anti-Toxoplasma, immunity.

Animals↗
PubMed2002

The immune response to infection with Treponema pallidum, the stealth pathogen.

Cutaneous immunobiology and spirochetal molecular biology have allowed investigators to propose a conceptual framework for the development of both the innate and adaptive immune response to Treponema pallidum infection. While some clinical manifestations can be attributed to humoral responses, most can be attributed to a combination of local innate and adaptive cellular immunity.

Antibody Formation↗
PubMed2004

[Syphilis. Clinical aspects of Treponema pallidum infection].

Syphilis is a sexually transmitted infection by Treponema pallidum. Without antibiotic treatment syphilis lasts for several decades and may develop up to 4 different clinical stages. Usually, the disease begins with a distinct painless and indurated ulcer at the contact site: the primary chancre. An indolent regional lymph node swelling is usually associated with the syphilitic chancre. After spontaneous healing of the primary lesion and several weeks of latency, the clinical symptoms of secondary syphilis occur. Treponema pallidum bacteremia leads to common symptoms like fever and malaise, but also to a generalized lymphadenopathy, and a broad variety of lesions of the skin and mucosal membranes. Non-pruritic transient exanthems often involving palms and soles, condylomata lata, and a specific angina with mucous patches of the oral cavity are prominent signs. After several relapses, which are characterized by a decreasing intensity of clinical symptoms, secondary syphilis then resolves spontaneously. A second period of latency follows, lasting 3-12 years. Then the outcome of untreated syphilis becomes apparent: spontaneous healing by elimination/inactivation of the spirochetes (75%) or transition to tertiary syphilis (25%). Two kinds of granulomatous skin reactions are typical for tertiary syphilis: superficial nodular syphilids and gummas. The bones, as well as the cardiovascular and central nervous system, may also be involved. Finally, metasyphilis with severe and sometimes lethal neurological symptoms (tabes dorsalis, progressive paralysis) occurs 10 to 30 years after primary infection. Except for irreversible tissue destruction which occurs prior to therapy, all stages of syphilis can be cured completely.

AIDS-Related Opportunistic Infections↗
PubMed1990

Role of Bacteroides uniformis in susceptibility of Ta:CF# 1 mice to infection by Treponema hyodysenteriae.

Among the various strains and colonies of mice tested specific-pathogen-free (SPF) Ta:CF#1 mice exhibited the highest susceptibility to Treponema hyodysenteriae infection. Staphylococcus epidermidis 1047, Streptococcus faecalis 2039, Lactobacillus murinus 3010, Escherichia coli 1049, and Bacteroides thetaiotaomicron 3008 were administered to the Ta:CF#1 mice. B. uniformis IK, which appeared to colonize in the breeding facility under SPF conditions, was isolated from the cecal content of a Ta:CF#1 mouse and identified in the mouse flora. Germfree mice were infected with these six bacteria and challenged with T. hyodysenteriae DJ70P3 to elucidate the causal relationship between these bacteria and the sensitivity of mice to T. hyodysenteriae infection. No cecal lesions were observed in gnotobiotic mice either monoassociated with T. hyodysenteriae DJ70P3 or B. uniformis IK or inoculated with T. hyodysenteriae DJ70P3 combined with the 5 a.m. strains. Gross cecal lesions appeared only in mice inoculated with T. hyodysenteriae DJ70P3 combined with B. uniformis IK. A new SPF mouse colony (CF#1/b Ta) established from gnotobiotic mice by inoculation with B. uniformis IK and the 5 laboratory stock cultures was as susceptible to T. hyodysenteriae as the original Ta:CF#1 mice. This suggests that B. uniformis IK plays an important role in the high susceptibility of Ta:CF#1 mice to T.hyodysenteriae.

Animals↗
PubMed1976

Cellular and humoral immune response to guinea pig infected with Treponema pallidum.

Guinea pigs infected intradermally with Treponema pallidum Nichols strain were examined for the presence of lesions and for cellular and humoral response. Of the 26 guinea pigs (77%) demonstrated darkfield positive lesions between 6 and 20 days after infection. Animals divided into six groups of 4-5 in each were sacrificed between 2 and 24 weeks. The peritoneal exudate cells, obtained 4 days after injection of oil, were examined by the direct and the cells from lymphoid organs by the indirect capillary leukocyte migration method in the presence of 10 and 30 mug/ml of Reiter antigen. The peritoneal exudate cells responded with enhancement of leukocyte migration, reaching significant values between 6 and 24 weeks after injection. The cells from the lymphoid organs showed enhancement of leukocyte migration until the 4th week of infection. Treponemal antibodies, found in all animals, started to appear at the 4th week reaching a maximum titer at the 12th week after infection. The appearance of the antibodies correlated well (p less than 0.05) with the appearance of the enhancement of leukocyte migration. Wassermann antibodies were not detected throughout the 24 weeks of infection. The unique immune responses are discussed in view of the available data concerning natural acquired and experimental syphilis.

Animals↗
PubMed1980

Susceptibility of rabbits venereally infected with Treponema paraluis-cuniculi to superinfections with Treponema pallidum.

Three female rabbits, venereally infected with Treponema paraluis-cuniculi between five and eight months previously, had treponeme-containing genital lesions and positive results to serological tests for syphilis. These rabbits and four normal female rabbits were challenged with Treponema pallidum intradermally on the shaved back with triplicate doses of 10(4), 10(3), 10(2), and 10 treponemes (all at different sites). Significantly fewer syphilitic lesions developed in the rabbits previously infected with T paraluis-cuniculi (4/36) compared with the control rabbits (37/48), and the mean size of the lesions (diameter of induration) was significantly less (4 mm compared with 10 mm). It appears that previous venereal infection of female rabbits with T paraluis-cuniculi induced a level of cross-immunity against infection with T pallidum. Protection was however not complete.

Animals↗
PubMed2005

Upregulation of intercellular adhesion molecule 1 and proinflammatory cytokines by the major surface proteins of Treponema maltophilum and Treponema lecithinolyticum, the phylogenetic group IV oral spirochetes associated with periodontitis and endodontic infections.

Treponema maltophilum and Treponema lecithinolyticum belong to the group IV oral spirochetes and are associated with endodontic infections, as well as periodontitis. Recently, the genes encoding the major surface proteins (Msps) of these bacteria (MspA and MspTL, respectively) were cloned and sequenced. The amino acid sequences of these proteins showed significant similarity. In this study we analyzed the functional role of these homologous proteins in human monocytic THP-1 cells and primary cultured periodontal ligament (PDL) cells using recombinant proteins. The complete genes encoding MspA and MspTL without the signal sequence were cloned into Escherichia coli by using the expression vector pQE-30. Fusion proteins tagged with N-terminal hexahistidine (recombinant MspA [rMspA] and rMspTL) were obtained, and any possible contamination of the recombinant proteins with E. coli endotoxin was removed by using polymyxin B-agarose. Flow cytometry showed that rMspA and rMspTL upregulated the expression of intercellular adhesion molecule 1 (ICAM-1) in both THP-1 and PDL cells. Expression of proinflammatory cytokines, such as interleukin-6 (IL-6) and IL-8, was also induced significantly in both cell types by the Msps, as determined by reverse transcription-PCR and an enzyme-linked immunosorbent assay, whereas IL-1beta synthesis could be detected only in the THP-1 cells. The upregulation of ICAM-1, IL-6, and IL-8 was completely inhibited by pretreating the cells with an NF-kappaB activation inhibitor, l-1-tosylamido-2-phenylethyl chloromethyl ketone. This suggests involvement of NF-kappaB activation. The increased ICAM-1 and IL-8 expression in the THP-1 cells obtained with rMsps was not inhibited in the presence of the IL-1 receptor antagonist (IL-1ra), a natural inhibitor of IL-1. Our results show that the Msps of the group IV oral spirochetes may play an important role in amplifying the local immune response by continuous inflammatory cell recruitment and retention at an infection site by stimulation of expression of ICAM-1 and proinflammatory cytokines.

Cell Line↗
PubMed1986

Secondary lesions in rabbits experimentally infected with Treponema pallidum.

Thirty rabbits infected with 10(3) of either Nichols or Melbourne 1 strains of Treponema pallidum were observed for the development of secondary lesions, which appeared outside areas inoculated with viable treponemes. More rabbits infected with Melbourne 1 strain (eight of 15 rabbits) than were infected with the Nichols reference strain (three of 15 rabbits) developed secondary lesions. The mean (SD) incubation periods of secondary lesions were 52 (8) days for rabbits infected with Melbourne 1 and 56 (4) days for rabbits infected with Nichols strain. These mean incubation periods did not correlate with appreciably increased concentrations of immune complexes or glycosaminoglycans in the serum of infected rabbits.

Animals↗
PubMed1986

Autoantibodies to creatine kinase in rabbits infected with Treponema pallidum.

Sera from rabbits infected intratesticularly with Treponema pallidum (Nichols) for 30 days were examined for autoantibody reactivity against muscle and testis extracts by Western immunoblotting. Syphilitic sera (30 day) reacted with an autoantigen of 43,000 daltons in muscle extracts. The antigen was shown to be creatine kinase (CK). Studies with the use of an anti-CK ELISA showed that the autoantibody to CK first appeared 3 wk after infection, declined by 7 wk infection, and was absent in rabbits "mock"-infected with heat-killed T. pallidum. CK activity was not detected in sonicated or intact, washed T. pallidum, suggesting that the antibody was not produced in response to treponemal CK.

Animals↗
PubMed2005

Treponema denticola infection is not a cause of false positive Treponema pallidum serology.

It has long been assumed that parodontal disease can be a cause of false positive results in syphilis serology, but so far there are no definitive data supporting this hypothesis. In this study we tested 250 serum samples obtained from blood donors. All of them were negative when routinely screened for antibodies against Treponema pallidum. Then, all these samples were tested by immunoenzymatic (ELISA) and Western Blot (WB) assays to investigate reactivities against T. denticola. Thirteen samples showed a strong positivity when tested by both methods. When tested by WB against T. pallidum no sample met the positivity criteria. Nevertheless, bands with molecolar weights of about 30-35 KDa (endoflagellar core antigens) were recognized. All the 13 subjects serologically T. denticola positive underwent oral clinical and radiological observation: all showed a very poor parodontal status (CPSS > 103). Eleven crevicular fluid samples out of the total of 13 patients were T. denticola positive by Real Time PCR carried out using a LightCycler system. In this study we demonstrated that the presence of T. denticola in the crevicular fluid samples obtained from patients with a severe periodontal status and/or a positive serology against T. denticola is not a cause of false positive results in syphilis serology.

Antibodies, Bacterial↗
PubMed1977

Host response to treponema pallidum infection. II. Rabbit leukocyte migration inhibition in the presence of homologous organ extracts.

Peripheral leukocytes of 67 rabbits infected intratesticularly with Treponema pallidum, Nichols' strain for various lengths of time were examined by the migration inhibition test for their response to extracts of normal rabbit heart, skin, brain and T. pallidum antigen. A control group of 14 animals injected intratesticularly with extract of normal rabbit tests was similarly examined for the leukocyte response to the same antigens except the brain extract. The percentage of infected animals responding to T. pallidum antigen with significant migration inhibition varied from 13 to 31. Transitional cellular response to heart and skin but not brain was observed (12-28%). Leukocytes of all but 2 control rabbits responded to the organ extracts within the limit of 2 SD. The response of the infected animals to the homologous organ extracts may suggest that during infection, lymphocytes are activated by the host tissue antigens.

Animals↗
PubMed1978

Host response to Treponema pallidum infection. III. Demonstration of autoantibodies to heart in sera from infected rabbits.

Sera from rabbits infected intratesticularly with Treponema pallidum but not from animals injected intratesticularly with other bacteria or with extract of normal rabbit testes demonstrated autoantibody to heart tissue. The antibody was organ-specific with cross-reactivity to skeletal muscle but was not species-specific. It could not be absorbed by T. pallidum, T. reiteri, Veneral Disease Research Laboratory reagent or rabbit mitochondrial preparation. The antibody had a transitional pattern of appearance; it could be demonstrated between 30 and 60 days after infection but it decreased or disappeared thereafter. In many instances, it could be shown between 2 and 3 years after infection. The finding of the heart-reacting antibody strongly suggests an autoimmune phenomenon associated with T. pallidum infection.

Absorption↗
PubMed1988

Experimental syphilitic orchitis. Relationship between Treponema pallidum infection and testis synthesis of proteoglycans.

The relationship between Treponema pallidum infection and the synthesis of proteoglycans by organ cultures of rabbit testes was investigated. Two proteoglycan fractions, large (CL-6B Kav 0.05) and small (Kav 0.25), that were not synthesized at detectable levels by cultures from rabbits infected with T. pallidum for 0 or 5 days, were produced by cultures from 10-, 15- and 20-day infected rabbits. The small proteoglycan appeared to be synthesized first because greater amounts of this fraction were detected in extracts of cultures from 10-day infected animals. The large proteoglycan fraction may have been induced directly by T. pallidum because increased synthesis correlated with maximal treponemal numbers, 15 days after infection. In contrast, the induction of the smaller proteoglycan did not appear to be directly related to numbers of elutable organisms. The proteoglycans synthesized between 10 and 20 days after infection were analyzed for glycosaminoglycan (GAG) size and composition. The size of GAGs beta-eliminated from the proteoglycans generally increased over the 10-20-day infection period. Whereas the composition of the small proteoglycan fraction was largely unchanged during the 10-20-day period (45% chondroitin sulphate (CS), 55% dermatan sulphate (DS)), the amount of DS in the high molecular weight proteoglycan fraction decreased from 50-20% during this period (CS 50-80%). Autoradiography studies revealed that increased proteoglycan synthesis in T. pallidum-infected testes was localized to cells lining the seminiferous tubules and to fibroblasts infiltrating peritubular spaces.

Animals↗