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PubMed2000

A possible association between Chlamydiae psittacci infection and temporal arteritis.

Some arguments are in favor of the role of Chlamydia in the pathogenesis of atherosclerosis and some vasculitis. Illustrating this possible relation, we report the case of a patient developing consecutively a Chlamydia psittacci infection and a temporal arteritis. A 73-year-old woman, with no significant medical history, was hospitalized for constitutional symptoms. Three weeks before, she had described fever and sore throat of two days' duration. Since that time, she had remained exhausted and developed a mild intermittent claudication of the jaws. Clinical examination was poor. A biological inflammatory syndrome was noticed. Chest X-ray revealed bilateral interstitial opacities. The titer of anti-C. psittaci antibodies was significant (positive 1g G at 1/2048). Soon after initiation of doxycycline, a temporal arteritis biopsy was performed, due to the persistence of clinical symptoms and high inflammatory syndrome, conclusive for the diagnosis of temporal arteritis. Corticotherapy was added to antibiotic therapy, resulting in the decrease of inflammatory syndrome and an improvement in the general status of the patient. X-ray opacities decreased in three weeks. Serological control after three months showed a decrease of the titer of anti-C. psittacci antibodies to 1/256, confirming the initial diagnosis of Chlamydia pneumopathy. Our observation could provide one more argument for the role of bacteria-like Chlamydia in the pathogenesis of vascular diseases. Prospective seroepidemiological and molecular biology studies could allow us to clarify the association between Chlamydia infections and inflammatory vasculitis-like temporal arteritis.

Adrenal Cortex Hormones↗
PubMed2001

Detection of Chlamydia pneumoniae antigenin PBMNCs of healthy blood donors.

BACKGROUND: Because it has been increasingly recognized that Chlamydia pneumoniae may be linked to some chronic inflammatory diseases, including atherosclerosis, detection of this pathogen in blood from patients may be valuable in the diagnosis of such diseases. However, the prevalence of chlamydia in the blood of healthy donors has not yet been extensively studied. STUDY DESIGN AND METHODS: The presence of C. pneumoniae in PBMNCs obtained from healthy persons who donated blood for blood transfusion was assessed by a PCR that was specific for the C. pneumoniae 16S rRNA gene and by the use of staining with FITC-conjugated chlamydia MoAb. RESULTS: Twenty-one (8.9%) of 237 blood samples tested showed the presence of C. pneumoniae DNA and antigen in the PBMNCs. There was no significant difference in the presence of chlamydia in blood according to sex or to age between 20 and 59 years of age. However, a possible seasonal variation in the presence of chlamydia in blood from healthy donors was suggested by the results obtained. CONCLUSION: A significant percentage of healthy donors carry C. pneumoniae, which may be a risk factor for some chronic diseases.

Adolescent↗
PubMed2003

Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in healthy control subjects and patients with diabetes mellitus, acute coronary syndrome, stroke, and arterial hypertension.

Infection with Chlamydia pneumoniae has been suggested to play a role in the development and maintenance of atherosclerosis based on differences in the prevalence of antibodies against Chlamydia pneumoniae in patients with and without atherosclerotic lesions. We evaluated the prevalence of Chlamydia pneumoniae DNA in the white cells of the peripheral blood in 194 patients with diabetes mellitus, 50 patients with acute coronary syndrome, 102 hypertensive patients, 193 patients having suffered a stroke and in 368 healthy subjects with a nested polymerase chain reaction (nPCR). Overall the prevalence of Chlamydia pneumoniae DNA in peripheral blood cells was: diabetes mellitus (11.9%), stroke (10.4%), hypertension (6.9%), acute coronary syndrome (4.0%) and healthy subjects (7.9%). The prevalence of Chlamydia pneumoniae DNA in the patients was not significantly different from prevalence in the healthy subjects. However, a significant association was found between high levels of triglycerides and presence of C. pneumoniae DNA (OR = 3.27, p < 0.04). The prevalence of C. pneumoniae DNA was not associated with age, gender, smoking, BMI, HDL, CRP, plasma creatinine and symptoms or signs of ischaemic heart disease. The association between high levels of triglycerides and C. pneumoniae DNA suggests that infection by C. pneumoniae affects lipid metabolism.

Adolescent↗
PubMed1997

A study to evaluate Chlamydia screening in colposcopy clinics.

A preliminary study of 329 colposcopy patients was conducted to investigate the prevalence of endocervical chlamydial infection using the VIDAS Chlamydia Enzyme Immune Assay (EIA) and Chlamydia Immune Fluorescent Antigen (IFA) collection kits. The overall antigen positive rates of five of the 329 (1.5%) in the study group compared exactly with the four out of the 260 (1.5%) in the gynaecological outpatient controls. Women in the age group 16-20 years had the highest Chlamydia detection rates (7%) followed by those aged 21-30 years (2.3%). Four of the 119 (3.4%) single women in the study group were Chlamydia antigen positive compared with one of the 210 (0.5%) married women (P < 0.005). Among the controls, three of the 65 (4.6%) single and one of the 195 (0.5%) married women were positive. In both the study and control populations, Chlamydia antigen was more prevalent among younger women and non-contraceptive users. Routine screening in colposcopy patients may not be cost effective, but a policy of selective screening in young single women aged 20 years or less should be considered. Larger sample studies using the more specific and sensitive DNA amplification techniques would have probably yielded higher detection rates and are recommended.

Journal Article↗
PubMed2003

In silico inference of inclusion membrane protein family in obligate intracellular parasites chlamydiae.

Chlamydiae are obligate intracellular pathogens that proliferate only inside a vacuole, called an inclusion. Chlamydial Inc proteins are known to be a major component of the inclusion membrane, but little is known about the gene number and function. The Inc proteins share very low sequence similarity but a similar hydropathy profile among them. Using the hydropathy profile, we computationally searched the open reading frames (ORFs) having a similar profile and predicted 90 and 36 ORFs (Inc-like ORFs) as candidates for Inc proteins in Chlamydia pneumoniae J138 and Chlamydia trachomatis serovar D, respectively. On the other hand, only a few Inc-like ORFs were found in organisms other than chlamydiae, suggesting that the Inc-like ORFs are specific to chlamydiae. Comparative genome analysis also revealed that the Inc-like ORFs have multiplied and diverged as paralogues and orthologues in the chlamydial genomes, and that some Inc-like ORFs lacked the N-terminal portion or encoded the split form. The data suggest that these gene products constitute a large protein family and may play an important role in chlamydial infection, growth and survival in the host cell.

Chlamydiaceae↗
PubMed1983

Resistance of wild birds to infection by Chlamydia psittaci of mammalian origin.

Numerous species of birds are natural hosts of C. psittaci and have been implicated as sources of certain strains that cause disease in other vertebrate species, notably those producing psittacosis or ornithosis in humans [1]. Although direct evidence of their involvement in the transmission of chlamydiae to other mammals, especially domesticated ruminants, has not been reported, a careful examination of this possibility is justified [1]. When inoculated parenterally, polyarthritis-producing chlamydiae of ovine origin affected leg joints of turkeys, and abortion-producing chlamydiae of ovine origin was infectious for pigeons and fatal for sparrows [2]. However, several species of small wild birds (three of which were used in the experiments reported here), when inoculated perorally with C. psittaci of turkey origin, seroconverted (36%) and shed the organism (79%) [3]. Therefore, the present study was undertaken to determine whether strains of C. psittaci from domesticated ruminants would infect, multiply in, or be shed by these wild birds. The results indicate that these species of birds are not natural hosts or biologic vectors of these strains. However, considering the heterogeneity of Chlamydia species, certain birds may harbor strains that are associated with naturally occurring infections in some animals. The results also are additional evidence of the more restricted host range of mammalian Chlamydia species as compared to that of avian isolates.

Animals↗
PubMed2004

High prevalence of Chlamydia pneumoniae infection in cyclosporin A-induced post-transplant gingival overgrowth tissue and evidence for the possibility of persistent infection despite short-term treatment with azithromycin.

BACKGROUND: Cyclosporin A (CsA) induces gingival overgrowth (GO) in up to a quarter of CsA-treated renal transplant recipients. A short-term therapy with azithromycin effectively reduces GO, indicating a possible involvement of microorganisms in the pathogenesis of CsA-induced GO. We aimed to determine if there could be any relationship between infection with Chlamydia pneumoniae and GO pathogenesis. In addition, we determined the long-term persistence rate of C. pneumoniae infection in residual GO tissue when azithromycin treatment failed to eliminate GO. METHODS: Chlamydia pneumoniae IgG and IgM antibody titres were measured by microimmunofluorescence technique in sera of kidney recipients with (n = 11) and without (n = 89) GO. GOs were rated and gingivectomies were performed before treatment with 500 mg of azithromycin for 3 days and at months 6 and 12 post-treatment when C. pneumoniae titres were re-evaluated. Nested polymerase chain reaction was performed to identify C. pneumoniae-specific DNA in GO tissues. Results of C. pneumoniae antibody titres from patients with GO were compared with pair-matched controls without GO. RESULTS: Chlamydia pneumoniae IgM titres were elevated in five of 11 patients with GO and in none without GO, whereas the difference of C. pneumoniae IgG titres between patients with GO and pair-matched controls did not reach significance (P<0.57). Chlamydia pneumoniae-specific DNA was found in 10 of 11 GO tissue samples pre-treatment. Azithromycin therapy effectively reduced GO and C. pneumoniae IgM titres. In residual GO, C. pneumoniae-specific DNA remained detectable after 1 year in all GO tissue samples despite azithromycin treatment. The C.pneumoniae IgM titres correlated with GO scores. CONCLUSION: Chlamydia pneumoniae infection is highly prevalent in CsA-induced GO. The infection can persist over a long period in residual GO despite short-term azithromycin therapy. The results indicate that CsA immunosuppression enhances C. pneumoniae infection rates in non-cardiovascular tissue.

Adult↗
PubMed1996

[A family outbreak of Chlamydia psittaci infection].

A family outbreak (3 cases) of Chlamydia psittaci infection was reported. The first case, a 56-year-old man was admitted with fever and general fatigue. Chest X-ray film revealed a consolidation in the right lower lung. One month before admission he had purchased 2 parakeets (chick) and one parakeet died. On learning of his history of contact with the chick, psittacosis was suspected. After administration of fixation (CF) antibody titer against chlamydia rose to 1:128 and IgA titer against Chlamydia psittaci by microimmunofluorescence antibody technique (MAF) rose to 1:128 in 21 days after admission. The second case, the wife of the first, a 53-year-old woman had a fever and a cough about two weeks before the admission of the first case. At the time of her husband was admitted, she attended the outpatient department. The chest CT X-ray film showed a ground glass appearance in both lower lung fields. The third case, the daughter of the first, didn't have any signs. Chest X-ray film was normal. But IgM titer against Chlamydia psittaci by MAF rose to 1:16 and IgA titer against Chlamydia psittaci by MAF rose to 1:128. This case was considered as inapparent infection.

Adult↗
PubMed1977

Toxicity of low and moderate multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).

When mouse fibroblasts (L cells) were infected in suspension or in monolayer with 10 to 100 50% infectious doses (ID(50)) of Chlamydia psittaci (6BC) per host cell, they showed signs of damage 24 to 48 h later. Host-cell injuries were termed multiplication dependent when both the ingestion and subsequent reproduction of C. psittaci were required; when only ingestion but not replication was needed, the injuries were considered to be multiplication independent. The time that the injury was first apparent, as well as its final magnitude, was proportional to the multiplicity of infection. When L cells ingested infectious or ultraviolet-inactivated C. psittaci, damage was manifested by failure to exclude trypan blue, by leakage of lactic dehydrogenase, by inhibition of reproduction as measured by ability to form colonies, by inhibition of protein and deoxyribonucleic acid synthesis, and eventually by cell disintegration. Infectious, but not ultraviolet-killed, chlamydiae stimulated host-cell glycolysis. Heat-killed chlamydiae were without measurable toxicity. The time of appearance of host-cell injury was always earlier, and its terminal magnitude always greater, with infectious inocula than with ultraviolet-inactivated ones. The multiplication-independent toxicity of ultraviolet-killed C. psittaci disappeared with inocula of less than 10 ID(50) per L cell, but an inoculum of only a single ID(50) of infectious chlamydiae per host cell injured most of the cells it infected, as evidenced by increased trypan blue staining and decreased efficiency of colony formation. The toxicity of multiplicities of infection between 10 and 100 ID(50) of infectious C. psittaci per host cell was the sum of both multiplication-dependent and -independent components. The effects of chloramphenicol and isoleucine deficiency on the ability of C. psittaci to injure L cells suggested that some synthesis of protein by both parasite and host may be essential for expression of multiplication-independent chlamydial toxicity. The failure of infectious chlamydiae to stimulate host-cell glycolysis in the presence of cycloheximide suggested that this multiplication-dependent consequence of chlamydial infection was also dependent on protein synthesis by the host.

Bacterial Proteins↗
PubMed1978

Growth of Chlamydia psittaci in macrophages.

Survival and growth of L-cell-cultivated Chlamydia psittaci occurred in mouse macrophages in vitro. Two major factors governing the intracellular fate of chlamydiae in macrophages are: (i) the multiplicity of infection (MOI), i.e., the elementary body (EB)-to-macrophage ratio, and (ii) the state of the EB. At a low MOI (1:1) survival and growth of live, untreated chlamydiae were optimal. The chlamydiae were internalized in macrophages within 30 to 40 min. EB proceeded to differentiate into reticulate bodies, which underwent multiplication and further matured into infectious EB in the professional phagocytic cells. In contrast, at a high MOI (100:1), survival of untreated chlamydiae was greatly reduced as a result of immediate damage to the macrophages. eb that were pretreated with heat (56 degrees C for 10 to 30 min) or coated with homologous antibody were rapidly destroyed in macrophage phagolysosomes. Fusion of ferritin-labeled lysosomes with heat-treated or opsonized EB-laden phagosomes occurred in 2 to 4 h, resulting in transfer of the ferritin marker into phagolysosomes.

Animals↗
PubMed1978

Interaction of Chlamydia psittaci with mouse peritoneal macrophages.

L-cell-grown Chlamydia psittaci elementary bodies (EB) were rapidly phagocytized by mouse peritoneal macrophages in vitro. However, the intracellular fate of chlamydiae in macrophages appeared to be dependent on the multiplicity of infection (MOI), i.e., the EB-to-macrophage ratio, and the treatment of the EB. At an MOI of 1:1 or less, survival is maximal, and growth and multiplication of live, untreated chlamydiae did occur. In contrast, at a high MOI (100:1), survival of chlamydiae is reduced, as confirmed by release of 3H-labeled nucleic acid into the supernatant. At the high MOI, macrophage damage occurred that resulted in significant release of the lactic dehydrogenase, beginning 2 h postinfection. This immediated macrophage cytotoxicity as abolished by pretreatment of EB with heat (5 min at 56 degrees C) and was reduced about 50% by coating EB with homologous antibody. Pretreatment of the chlamydia with heat or opsonizing antibody provides increased uptake of EB by macrophages but may contribute to increased destruction of these obligate intracellular pathogens in professional phagocytic cells.

Animals↗
PubMed1981

Inhibition of phagolysosome fusion is localized to Chlamydia psittaci-laden vacuoles.

Intracellular survival of Chlamydia psittaci is in part dependent on the ability of the organism to thwart phagolysosome formation. Circumvention of phagolysosome fusion could be either localized to chlamydia-laden vacuoles or generalized to all phagosomes in the host cell. To determine which of these modes is in operation the ability of chlamydia elementary and reticulate bodies to protect Saccharomyces cerevisiae from degradation in macrophage phagolysosomes was examined via acridine orange and Giemsa staining. No statistically significant difference was evident between the amount of fusion observed in coinfected macrophages and those infected with yeast cells alone. This was ot dependent on some unique interaction between the chlamydia and the yeast cells since viable count studies to determine the protection of a second organism, Escherichia coli, also failed to show significantly different amounts of inactivation of the bacteria by macrophages in the presence of C. psittaci. Therefore, the inhibition of phagolysosome fusion is localized to chlamydia-laden phagosomes.

Animals↗
PubMed1998

Characterization of a neutralizing monoclonal antibody directed at the lipopolysaccharide of Chlamydia pneumoniae.

Identification of protective epitopes is one of the first steps in the development of a subunit vaccine. One approach to accomplishing this is to identify structures or epitopes by using monoclonal antibodies (MAb) that can attenuate infectivity in vitro and in vivo. To date attempts to use this approach with Chlamydia pneumoniae have failed. This report is the first description of a MAb directed to the lipopolysaccharide (LPS) of Chlamydia that neutralizes both in vitro and in vivo the infectivity of C. pneumoniae. MAb CP-33, an immunoglobulin G2b (IgG2b), was identified from a fusion using splenocytes from mice immunized with C. pneumoniae TW-183. By Western blot analysis, MAb CP-33 exhibited genus-specific reactivity in that it recognized the LPSs of C. pneumoniae, Chlamydia trachomatis, and Chlamydia psittaci. MAb CP-33 did not react with 15 genera of gram-negative and gram-positive bacteria and Candida albicans. By using isolated LPS of Re mutants of Escherichia coli, Salmonella enterica serovar Minnesota, and recombinants expressing the 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo) transferase gene kdtA of C. trachomatis, MAb CP-33 was shown to require for binding the presence of the genus-specific trisaccharide epitope alphaKdo(2-->8)alphaKdo(2-->4)alphaKdo. By employing synthetic oligosaccharides and neoglycoconjugates in an enzyme immunoassay (EIA) and EIA inhibition, it was further shown that MAb CP-33 differed from the extensively investigated prototype chlamydial LPS MAb S25-23. Most likely, MAb CP-33 recognizes a conformational epitope in which the alphaKdo(2-->8)alphaKdo(2-->4)alphaKdo trisaccharide is an essential structural component. When tested in an in vitro neutralization assay, MAb CP-33 gave a 50% neutralization titer of 8 ng/ml against C. pneumoniae TW-183. However, this MAb did not neutralize other C. pneumoniae strains, C. trachomatis, or C. psittaci. C. pneumoniae TW-183 was treated with either MAb CP-33 or a control IgG and then used to inoculate mice by the respiratory route. Five days after inoculation, there was a difference between the mice inoculated with the control IgG-treated inoculum and those inoculated with the MAb CP-33-treated organisms as to the number of mice infected as well as the number of inclusion-forming units recovered from lung cultures (P < 0.05). In summary, a Chlamydia-specific LPS MAb was able to neutralize in vitro the infectivity of C. pneumoniae TW-183.

Animals↗
PubMed2005

Effect of clarithromycin treatment on Chlamydia pneumoniae in vascular tissue of patients with coronary artery disease: a randomized, double-blind, placebo-controlled trial.

Several small clinical trials have indicated that antibiotic treatment of Chlamydia pneumoniae infection is associated with a better outcome in patients with coronary artery disease (CAD). It has not been demonstrated whether antibiotic treatment eradicates C. pneumoniae from vascular tissue. The aim of the present study was to assess the effect of clarithromycin on the presence of C. pneumoniae in the vascular tissue of patients with CAD. Patients who had CAD and who were waiting for coronary artery bypass graft surgery were enrolled in a randomized, double-blind, placebo-controlled trial. Patients were treated with clarithromycin at 500 mg or placebo once daily from the day of inclusion in the study until surgery. Several vascular tissue specimens were obtained during surgery. The presence of C. pneumoniae in vascular tissue specimens was examined by immunohistochemical staining (IHC) and two PCR assays. Chlamydia immunoglobulin G (IgG) titers were determined by an enzyme-linked immunosorbent assay at the time of inclusion in the study and 8 weeks after surgery. A total of 76 patients were included, and 180 vascular tissue specimens were obtained (80 specimens from the group treated with clarithromycin and 100 specimens from the group treated with placebo). Thirty-five patients received clarithromycin (mean duration, 27 days; standard deviation [SD], 12.2 days), and 41 patients received placebo (mean duration, 27 days; SD, 13.9 days). IHC detected the C. pneumoniae major outer membrane protein antigen in 73.8% of the specimens from the group treated with clarithromycin and 77.0% of the specimens from the group treated with placebo (P was not significant). Chlamydia lipopolysaccharide antigen was found in only one specimen from the group that received placebo. C. pneumoniae DNA was not detected in any specimen. Baseline Chlamydia-specific IgG titers were equally distributed in both groups and were not significantly different after treatment. There was no indication of an active C. pneumoniae infection in vascular tissue. Chlamydia-specific IgG titers remained unchanged throughout the study in both the antibiotic- and the placebo-treated patients.

Aged↗
PubMed1976

Autoradiography of [3H]thymidine-labeled Chlamydia psittaci 6BC in mononuclear phagocytes.

Incorporation of tritiated [3H]thymidine by Chlamydia psittaci 6BC was achieved by growing the parasites in chick embryo yolk sac explants which were exposed to exogenous labeled thymidine. These labeled, purified chlamydiae were next observed by autoradiography within mouse peritoneal macrophages. The number of silver grains remained constant in the cytoplasm of macrophages throughout the developmental cycle of the parasite. The proliferation of labeled chlamydiae in macrophages was confirmed by Giemsa staining and immunofluorescence. Chlamydiae have never been successfully labeled with thymidine in earlier studies when assayed in cultured mammalian fibroblasts. It is suggested that a critical factor in the successful incorporation thymidine in chlamydiae may be the host-parasite system used.

Animals↗
PubMed2003

Chlamydia species as a cause of community-acquired pneumonia in Canada.

Chlamydia pneumoniae has been implicated as a cause of community-acquired pneumonia (CAP) in several studies. However, there has been no comprehensive study of the role of Chlamydia species (C. pneumoniae, C. psittaci (avian and feline strains) and C. pecorum) as a cause of CAP. The aim of the present study was to determine the role of C. pneumoniae, C. psittaci and C. pecorum as causes of CAP. A prospective cohort observational study of CAP was conducted at 15 teaching centres in eight Canadian provinces between January 1996-October 1997. Acute (n=539) and convalescent (n=272) serum samples were obtained for determination of antibody titres to C. pneumoniae, C. psittaci, C. pecorum, C. trachomatis, Mycoplasma pneumoniae, Legionella pneumophila serogroups I-VI, Streptococcus pneumoniae and various respiratory viruses. Twelve of 539 (2.2%) patients had acute C. pneumoniae pneumonia and an additional 32 (5.9%) had possible acute infection. C. pneumoniae was the sole pathogen in 16 of 42 (38.1%) of these patients. The most common copathogens were S. pneumoniae, respiratory syncytial virus and influenza virus type A. C. pneumoniae pneumonia patients were older and more likely to show congestive heart failure compared to bacteraemic S. pneumoniae patients. The latter had a lower mean diastolic blood pressure, a higher white blood cell count and a lower arterial carbon dioxide tension. Two patients had antibody titres suggestive of recent infection with the feline strain of C. psittaci. Although numerically Chlamydia pneumoniae is an important cause of community-acquired pneumonia, no distinctive clinical features associated with this pathogen were detected in the present study. Feline Chlamydia psittaci may cause a few cases of community-acquired pneumonia. Avian Chlamydia psittaci should be considered only if there is a compatible epidemiological history.

Adolescent↗
PubMed2006

The association of metabolic syndrome and Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes simplex virus type 1: the Persian Gulf Healthy Heart Study.

BACKGROUND: The metabolic syndrome together with insulin resistance and their consequences are basic factors in pathogenesis of atherosclerosis. Chronic infections with herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), and Chlamydia pneumoniae are associated with the development of atherosclerosis and coronary heart disease. The infectious aspects of metabolic syndrome have not been investigated. METHODS: In a cross-sectional, population-based study, we used National Cholesterol Education Program (NCEP)-Adult Treatment Panel (ATP)-III criteria in 1791 subjects, aged 25 years and over, selected by cluster random sampling in three Iranian ports in the northern Persian Gulf. Sera were analyzed for IgG antibodies to Chlamydia pneumoniae, HSV-1, Helicobacter pylori (H. pylori) and CMV using ELISA. RESULTS: In multiple logistic regression analysis, of the infectious agents, CMV [OR = 1.81 (1.05-3.10); p = 0.03], H. pylori [OR = 1.50 (1.12-2.00); p = 0.007] and Chlamydia pneumoniae [OR = 1.69 (1.27-2.25); p < 0.0001] showed a significant association with the metabolic syndrome in men and HSV-1 [OR = 1.95 (1.22-3.11); p = 0.005], H. pylori [OR = 1.45 (1.09-1.94); 0.01] and Chlamydia pneumoniae [OR = 1.65 (1.23-2.21); p = 0.001] in women. CONCLUSION: The metabolic syndrome, which occurs very frequently in the general population, has a significant association with prior infection with Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus and herpes simplex virus type 1. Hypothesis about participation of infection in pathogenesis of metabolic syndrome should be investigated.

Adult↗
PubMed1988

Common surface epitope of Bartonella bacilliformis and Chlamydia psittaci.

A serosurvey revealed intense cross-reactivity between Bartonella bacilliformis and Chlamydia psittaci. One of the cross-reacting Bartonella antigens was identified as lipopolysaccharide which reacted with Bartonella as well as with Chlamydia serum antibodies. A monoclonal Bartonella antibody bound to Bartonella lipopolysaccharide as well as to the surfaces of Bartonella bacilliformis and Chlamydia psittaci. It was thus demonstrated that Chlamydia psittaci carries a surface epitope identical to an epitope of Bartonella lipopolysaccharide. The lipopolysaccharide was preliminarily characterized by polyacrylamide gel electrophoresis and by a lectin-binding assay. The lipopolysaccharides of Bartonella bacilliformis and Chlamydia psittaci are not identical.

Antibodies, Bacterial↗