Chlamydia psittaci

About: Chlamydia psittaci is a research topic. Over the lifetime, 1484 publications have been published within this topic receiving 38058 citations.

Emended description of the order Chlamydiales, proposal of Parachlamydiaceae fam. nov. and Simkaniaceae fam. nov., each containing one monotypic genus, revised taxonomy of the family Chlamydiaceae, including a new genus and five new species, and standards for the identification of organisms.

Abstract: The current taxonomic classification of Chlamydia is based on limited phenotypic, morphologic and genetic criteria This classification does not take into account recent analysis of the ribosomal operon or recently identified obligately intracellular organisms that have a chlamydia-like developmental cycle of replication Neither does it provide a systematic rationale for identifying new strains In this study, phylogenetic analyses of the 16S and 23S rRNA genes are presented with corroborating genetic and phenotypic information to show that the order Chlamydiales contains at least four distinct groups at the family level and that within the Chlamydiaceae are two distinct lineages which branch into nine separate clusters In this report a reclassification of the order Chlamydiales and its current taxa is proposed This proposal retains currently known strains with > 90% 16S rRNA identity in the family Chlamydiaceae and separates other chlamydia-like organisms that have 80--90% 16S rRNA relatedness to the Chlamydiaceae into new families Chlamydiae that were previously described as ‘Candidatus Parachlamydia acanthamoebae’ Amann, Springer, Schonhuber, Ludwig, Schmid, Muller and Michel 1997, become members of Parachlamydiaceae fam nov, Parachlamydia acanthamoebae gen nov, sp nov ‘Simkania’ strain Z becomes the founding member of Simkaniaceae fam nov, Simkania negevensis gen nov, sp nov The fourth group, which includes strain WSU 86--1044, was left unnamed The Chlamydiaceae, which currently has only the genus Chlamydia, is divided into two genera, Chlamydia and Chlamydophila gen nov Two new species, Chlamydia muridarum sp nov and Chlamydia suis sp nov, join Chlamydia trachomatis in the emended genus Chlamydia Chlamydophila gen nov assimilates the current species, Chlamydia pecorum, Chlamydia pneumoniae and Chlamydia psittaci, to form Chlamydophila pecorum comb nov, Chlamydophila pneumoniae comb nov and Chlamydophila psittaci comb nov Three new Chlamydophila species are derived from Chlamydia psittaci: Chlamydophila abortus gen nov, sp nov, Chlamydophila caviae gen nov, sp nov and Chlamydophila felis gen nov, sp nov Emended descriptions for the order Chlamydiales and for the family Chlamydiaceae are provided These families, genera and species are readily distinguished by analysis of signature sequences in the 165 and 235 ribosomal genes

A new Chlamydia psittaci strain, TWAR, isolated in acute respiratory tract infections.

Abstract: During a 2 1/2-year period, we studied 386 University of Washington students with acute respiratory disease, to determine whether a Chlamydia psittaci strain, here designated TWAR, is an important respiratory pathogen. Serologic evidence of recent TWAR infection was found in 13 students, and the organism was isolated from 8 of these. TWAR infection occurred in 12 percent of the students who had pneumonia (9 of 76), 5 percent of those with bronchitis (3 of 63), and 1 percent of those with pharyngitis (1 of 150). The TWAR infections occurred throughout the study period. Pharyngitis, often accompanied by laryngitis, was a common first symptom. Clinically, the infections resembled those with Myco-plasma pneumoniae; therefore, the patients were given courses of erythromycin used for the treatment of M. pneumoniae infections. This therapy proved to be inadequate. The limited data available suggest that the TWAR strain is a "human" C. psittaci that is spread from human to human, without a bird or animal host.

Secretion of proinflammatory cytokines by epithelial cells in response to Chlamydia infection suggests a central role for epithelial cells in chlamydial pathogenesis.

Abstract: Chlamydia species infect epithelial cells at mucosal surfaces, and are major causes of sexually transmitted diseases. Infection is characterized by inflammation which is exacerbated upon reinfection, ultimately leading to tissue damage and scarring. Although central for the development of disease manifestations, little is known about the mechanisms that initiate and sustain the inflammatory response to Chlamydia. Infection of cervical and colonic epithelial cells with Chlamydia trachomatis and Chlamydia psittaci is shown in the present studies to upregulate mRNA expression and secretion of the proinflammatory cytokines IL-8, GRO alpha, GM-CSF, and IL-6. In contrast to the rapid, but transient, cytokine induction following infection with other invasive bacteria, the epithelial cytokine response to Chlamydia was delayed until 20-24 h after infection, persisted throughout the chlamydial growth cycle (2-4 d), and required bacterial protein synthesis. Moreover, epithelial cell lines and primary endocervical epithelial cells released IL-1alpha after Chlamydia infection, and increased secretion of the proinflammatory cytokines could be inhibited by anti-IL-1alpha. This suggests that IL-1alpha, released following lysis of infected epithelial cells, may amplify the inflammatory response by stimulating additional cytokine production by noninfected neighboring cells. These findings suggest a novel pathophysiologic concept wherein the acute host response to Chlamydia at mucosal surfaces is primarily initiated and sustained by epithelial cells, the first and major targets of chlamydial infection.

Evidence for an Association Between Chlamydia psittaci and Ocular Adnexal Lymphomas

Abstract: Background: Ocular adnexal lymphomas may be antigen-driven disorders; however, the source of the putative antigen or antigens is still unknown. Hence, we assessed whether Chlamydiae infection is associated with the development of ocular adnexal lymphomas. Methods: The presence of Chlamydia psittaci, trachomatis, and pneumoniae DNA was investigated by polymerase chain reaction in 40 ocular adnexal lymphoma samples, 20 nonneoplastic orbital biopsies, 26 reactive lymphadenopathy samples, and peripheral blood mononuclear cells (PBMCs) from 21 lymphoma patients and 38 healthy individuals. Seven patients with chlamydia-positive PBMCs were treated with the antibiotic doxycycline, and objective response was assessed in four patients with measurable lymphoma lesions. Differences in Chlamydiae DNA detection between the case patients and the control subjects were analyzed using the Fisher exact test. All statistical tests were two-sided. Results: Thirty-two of the 40 (80%) ocular adnexal lymphoma samples carried C. psittaci DNA, whereas all lymphoma samples were negative for C. trachomatis and C. pneumoniae. In contrast, none of the 20 nonneoplastic orbital biopsies (0% versus 80%; P<.001) and only three of 26 (12%) reactive lymphadenopathy samples (12% versus 80%; P<.001) carried the C. psittaci DNA. Nine of 21 (43%) patients with chlamydia-positive lymphomas carried C. psittaci DNA in their PBMCs, whereas none (0%) of the healthy PBMC donors carried C. psittaci DNA in their PBMCs (43% versus 0%; P<.001). One month after doxy-cycline treatment, chlamydial DNA was no longer detectable in the PBMCs of all seven treated patients, and objective response was observed in two of the four evaluable patients. Conclusion: Patients with ocular adnexal lymphoma had a high prevalence of C. psittaci infection in both tumor tissue and PBMCs. Persistent C. psittaci infection may contribute to the development of these lymphomas, as was also supported by the clinical responses observed in this study with C. psittaci-eradicating antibiotic therapy.

Induction of tryptophan catabolism is the mechanism for gamma-interferon-mediated inhibition of intracellular Chlamydia psittaci replication in T24 cells.

Abstract: Human uroepithelial (T24) cells were incubated for 24 h in the presence of various concentrations of human recombinant gamma interferon (Hu-rIFN-gamma) and then infected with the 6BC strain of Chlamydia psittaci. This resulted in a reduction of intracellular chlamydial inclusion development in proportion to the concentration of Hu-rIFN-gamma present when Giemsa-stained cells were examined by light microscopy 24 h after infection. When tryptophan was added to Hu-rIFN-gamma-treated cells just after infection, reversal of the Hu-rIFN-gamma-mediated inhibition occurred in proportion to the concentration of tryptophan added. Addition of either isoleucine or lysine did not result in reversal of the antichlamydial state. Transport of L-[3H]tryptophan into acid-soluble intracellular pools was found to be greatly enhanced in Hu-rIFN-gamma-treated T24 cells compared with the rates measured for untreated cells. Transport of [3H]leucine was not increased in treated cells. Cells treated with Hu-rIFN-gamma also degraded L-[3H]tryptophan to catabolites that cochromatographed with N-formylkynurenine and kynurenine as measured by high-performance liquid chromatography. We conclude that Hu-rIFN-gamma-mediated inhibition of intracellular C. psittaci replication in T24 cells occurs by depletion of the essential amino acid tryptophan, most likely via the induction of indoleamine-2,3-dioxygenase, the initial enzyme of tryptophan catabolism.