A simple technique for mass cultivation of Campylobacter fetus.
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Studies using 86 media for maximum growth of Campylobacter fetus for antigen production showed that a diphasic medium (solid base with liquid overlay) was most suitable. The solid base was double strength cystine heart agar. The liquid overlay was thioglycollate medium of Brewer (135-C) without agar. This medium yielded maximum growth of C. fetus in six days with good motility, less clumping and less filament formation than all other media tried. (+info)
Roles of the surface layer proteins of Campylobacter fetus subsp. fetus in ovine abortion.
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The role of the surface (S)-layer proteins of Campylobacter fetus subsp. fetus has been investigated using an ovine model of abortion. Wild-type strain 23D induced abortion in up to 90% of pregnant ewes challenged subcutaneously. Isolates recovered from both dams and fetuses expressed S-layer proteins with variable molecular masses. The spontaneous S-layer-negative variant, strain 23B, neither colonized nor caused abortions in pregnant ewes. A series of isogenic sapA and recA mutants, derived from 23D, also were investigated in this model. A mutant (501 [sapA recA(+)]) caused abortion in one of five challenged animals and was recovered from the placenta of a second animal. Another mutant (502 [sapA recA]) with no S-layer protein expression caused no colonization or abortions in challenged animals but caused abortion when administered intraplacentally. Mutants 600(2) and 600(4), both recA, had fixed expression of 97- and 127-kDa S-layer proteins, respectively. Two of the six animals challenged with mutant 600(4) were colonized, but there were no abortions. As expected, all five strains recovered expressed a 127-kDa S-layer protein. In contrast, mutant 600(2) was recovered from the placentas of all five challenged animals and caused abortion in two. Unexpectedly, one of the 16 isolates expressed a 127-kDa rather than a 97-kDa S-layer protein. Thus, these studies indicate that S-layer proteins appear essential for colonization and/or translocation to the placenta but are not required to mediate fetal injury and that S-layer variation may occur in a recA strain. (+info)
Chronic atrophic gastritis in SCID mice experimentally infected with Campylobacter fetus.
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Campylobacter fetus is a cause of enteritis and invasive extraintestinal disease in humans. In order to develop an animal model of C. fetus infection, outbred ICR SCID mice were orally challenged with a clinical isolate of C. fetus. The stomachs of SCID mice were heavily colonized with C. fetus, and colonization was associated with the development of chronic atrophic gastritis. This lesion was characterized by an inflammatory infiltrate of granulocytes and macrophages that over time resulted in a loss of specialized parietal and chief cells in the corpus and the appearance of a metaplastic mucous epithelium. This lesion bears similarity to that encountered during experimental murine infection with Helicobacter pylori or Helicobacter felis. Despite colonization of the cecum and colon tissues by C. fetus in SCID mice, no lesions were noted in these tissues. A follow-up study confirmed these findings for SCID mice and also demonstrated that C. fetus could also infect the gastric mucosa of wild-type, outbred ICR mice. However, in ICR mice, the anatomic extent of colonization was more limited and the severity of inflammation and epithelial alterations was significantly less than that observed in infected SCID mice. The stomach may represent an unrecognized environmental niche for Campylobacter species. (+info)
Campylobacter fetus sap inversion occurs in the absence of RecA function.
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Phase variation of Campylobacter fetus surface layer proteins (SLPs) occurs by inversion of a 6.2-kb DNA segment containing the unique sap promoter, permitting expression of a single SLP-encoding gene. Previous work has shown that the C. fetus sap inversion system is RecA dependent. When we challenged a pregnant ewe with a recA mutant of wild-type C. fetus (strain 97-211) that expressed the 97-kDa SLP, 15 of the 16 ovine-passaged isolates expressed the 97-kDa protein. However, one strain (97-209) expressed a 127-kDa SLP, suggesting that chromosomal rearrangement may have occurred to enable SLP switching. Lack of RecA function in strains 97-211 and 97-209 was confirmed by their sensitivity to the DNA-damaging agent methyl methanesulfonate. Southern hybridization and PCR of these strains indicated that the aphA insertion into recA was stably present. However, Southern hybridizations demonstrated that in strain 97-209 inversion had occurred in the sap locus. PCR data confirmed inversion of the 6.2-kb DNA element and indicated that in these recA mutants the sap inversion frequency is reduced by 2 to 3 log(10) units compared to that in the wild type. Thus, although the major sap inversion pathway in C. fetus is RecA dependent, alternative lower-frequency, RecA-independent inversion mechanisms exist. (+info)
Recurring febrile illness in a slaughterhouse worker.
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A slaughterhouse worker presented with fever and a pleuropericardial effusion. Conventional microbiology failed to identify the responsible organism. However, DNA sequencing definitively identified Campylobacter fetus ssp fetus, which is rare in immunocompetent individuals. Prolonged treatment was required to eradicate the infection. (+info)
Bovine veneral vibriosis: cure of genital infection in females by systemic immunization.
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Cure of female cattle with venereal vibriosis by systemic immunization with killed Campylobacter fetus cells in incomplete Freund adjuvant was investigated. Heifers infected in the cervicovaginal area with a cloned population of C. fetus venerealis were vaccinated subcutaneously 14 and 24 days thereafter with the infecting strain in incomplete Freund adjuvant. Six of eight vaccinated heifers were free of infection 25 to 48 days postinfection. One of the cured animals had an intercurrent infection which precluded interpretation of a vaccine effect. All controls remained infected 48 to 51 days postinfection, when the experiment was terminated. In vaccinated animals, agglutination titers against whole cells of the infecting strain reached peaks varying from 1,280 to 20,480 in serum and from 20 to 5,120 in cervicovaginal mucus (CVM) within days 24 to 32 postinfection. No consistent relationship was noted between levels of whole cell antibodies in serum and those in CVM. Evidence for the occurrence of antigenic variation in the organism after vaccination was sought by comparing the agglutinability of the infecting strain and CVM isolates in serum and CVM extracts. Serum samples of most cured heifers agglutinated whole cells prepared from isolates of the respective heifers to the same extent as cells of the infecting strain. In the corresponding comparisons, those from noncured animals agglutinated isolates to lower titers. CVM extracts from one cured animals agglutinated isolates derived from the same or closely spaced CVM samples to titers comparable with those obtained with the infecting strain. In the remaining animals, CVM extracts which agglutinated the infecting strain produced lower or undetectable reactions with corresponding isolates. It is proposed that the elimination of infection is dependent upon opposing responses of host and parasite, of which the degree of antigenic alteration in the infecting strain and the rate of mobilization and the concentration of specific antibodies in the genital secretions are key factors. (+info)
Thermophilic multidrug-resistant Campylobacter fetus infection with hypersplenism and histiocytic phagocytosis in a patient with acquired immunodeficiency syndrome.
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We present a case report of a patient who had acquired immunodeficiency syndrome (AIDS) and Campylobacter fetus infection with a number of unusual clinical and microbiological features. The patient had prominent gastrointestinal symptoms, splenic infarction, splenomegaly with hypersplenism, and hemophagocytic histiocytosis in the spleen and lymph nodes; the organism displayed growth on Campy-selective blood agar, thermotolerance, and resistance to quinolones, piperacillin/tazobactam, ceftazidime, and erythromycin. (+info)
Evidence that the Campylobacter fetus sap locus is an ancient genomic constituent with origins before mammals and reptiles diverged.
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Campylobacter fetus bacteria, isolated from both mammals and reptiles, may be either subsp. fetus or subsp. venerealis and either serotype A or serotype B. Surface layer proteins, expressed and secreted by genes in the sap locus, play an important role in C. fetus virulence. To assess whether the sap locus represents a pathogenicity island and to gain further insights into C. fetus evolution, we examined several C. fetus genes in 18 isolates. All of the isolates had 5 to 9 sapA or sapB homologs. One strain (85-387) possessed both sapA and sapB homologs, suggesting a recombinational event in the sap locus between sapA and sapB strains. When we amplified and analyzed nucleotide sequences from portions of housekeeping gene recA (501 bp) and sapD (450 bp), a part of the 6-kb sap invertible element, the phylogenies of the genes were highly parallel. Among the 15 isolates from mammals, serotype A and serotype B strains generally had consistent positions. The fact that the serotype A C. fetus subsp. fetus and subsp. venerealis strains were on the same branch suggests that their differentiation occurred after the type A-type B split. Isolates from mammals and reptiles formed two distinct tight phylogenetic clusters that were well separated. Sequence analysis of 16S rRNA showed that the reptile strains form a distinct phylotype between mammalian C. fetus and Campylobacter hyointestinalis. The phylogenies and sequence results showing that sapD and recA have similar G + C contents and substitution rates suggest that the sap locus is not a pathogenicity island but rather is an ancient constituent of the C. fetus genome, integral to its biology. (+info)