Chlamydia (C.) psittaci is an economically relevant pathogen in poultry and pet birds, where it causes psittacosis/ornithosis, and also a human pathogen causing atypical pneumonia after zoonotic transmission. Despite its well-documented prevalence, the agent has received less attention by researchers than other Chlamydia spp. in the last decades. In the present paper, we review recently published data on C. psittaci infection and attempt to single out characteristic features distinguishing it from related chlamydial agents. It is remarkable that C. psittaci is particularly efficient in disseminating in the host organism causing systemic disease, which occasionally can take a fulminant course. At the cellular level, the pathogen's broad host cell spectrum (from epithelial cells to macrophages), its rapid entry and fast replication, proficient use of intracellular transport routes to mitochondria and the Golgi apparatus, the pronounced physical association of chlamydial inclusions with energy-providing cell compartments, as well as the subversive regulation of host cell survival during productive and persistent states facilitate the characteristic efficient growth and successful host-to-host spread of C. psittaci. At the molecular level, the pathogen was shown to upregulate essential chlamydial genes when facing the host immune response. We hypothesize that this capacity, in concert with expression of specific effectors of the type III secretion system and efficient suppression of selected host defense signals, contributes to successful establishment of the infection in the host. Concerning the immunology of host–pathogen interactions, C. psittaci has been shown to distinguish itself by coping more efficiently than other chlamydiae with pro-inflammatory mediators during early host response, which can, to some extent, explain the effective evasion and adaptation strategies of this bacterium. We conclude that thorough analysis of the large number of whole-genome sequences already available will be essential to identify genetic markers of the species-specific features and trigger more in-depth studies in cellular and animal models to address such vital topics as treatment and vaccination.

Chlamydiae are evolutionarily well-separated bacteria that live exclusively within eukaryotic host cells. They include important human pathogens such as Chlamydia trachomatis as well as symbionts of protozoa. As these bacteria are experimentally challenging and genetically intractable, our knowledge about them is still limited. In this study, we obtained the genome sequences of Simkania negevensis Z, Waddlia chondrophila 2032/99, and Parachlamydia acanthamoebae UV-7. This enabled us to perform the first comprehensive comparative and phylogenomic analysis of representative members of four major families of the Chlamydiae, including the Chlamydiaceae. We identified a surprisingly large core gene set present in all genomes and a high number of diverse accessory genes in those Chlamydiae that do not primarily infect humans or animals, including a chemosensory system in P. acanthamoebae and a type IV secretion system. In S. negevensis, the type IV secretion system is encoded on a large conjugative plasmid (pSn, 132 kb). Phylogenetic analyses suggested that a plasmid similar to the S. negevensis plasmid was originally acquired by the last common ancestor of all four families and that it was subsequently reduced, integrated into the chromosome, or lost during diversification, ultimately giving rise to the extant virulence-associated plasmid of pathogenic chlamydiae. Other virulence factors, including a type III secretion system, are conserved among the Chlamydiae to variable degrees and together with differences in the composition of the cell wall reflect adaptation to different host cells including convergent evolution among the four chlamydial families. Phylogenomic analysis focusing on chlamydial proteins with homology to plant proteins provided evidence for the acquisition of 53 chlamydial genes by a plant progenitor, lending further support for the hypothesis of an early interaction between a chlamydial ancestor and the primary photosynthetic eukaryote.

Day-old chicks are very susceptible to infections withSalmonella entericasubspecies. The gut mucosa is the initial site of host invasion and provides the first line of defense against the bacteria. To study the potential of differentS. entericaserovars to invade the gut mucosa and trigger an immune response, day-old chicks were infected orally withSalmonella entericaserovar Enteritidis,S. entericaserovar Typhimurium,S. entericaserovar Hadar, orS. entericaserovar Infantis, respectively. The localization ofSalmonellaorganisms in gut mucosa and the number of immune cells in cecum were determined by immunohistochemistry in the period between 4 h and 9 days after infection. Using quantitative real-time reverse transcription (RT)-PCR, mRNA expression of various cytokines, chemokines, and inducible nitric oxide synthase (iNOS) was examined in cecum. As a result, allS. entericaserovars were able to infect epithelial cells and the lamina propria. Notably, serovar Enteritidis showed the highest invasiveness of lamina propria tissue, whereas serovars Typhimurium and Hadar displayed moderate invasiveness and serovar Infantis hardly any invasion capabilities. Only a limited number of bacteria of all serovars were found within intestinal macrophages. Elevated numbers of granulocytes, CD8⁺cells, and TCR1⁺cells and mRNA expression rates for interleukin 12 (IL-12), IL-18, tumor necrosis factor alpha factor, and iNOS in cecum correlated well with the invasiveness of serovars in the lamina propria. In contrast, changes in numbers of TCR2⁺and CD4⁺cells and IL-2 mRNA expression seemed to be more dependent on infection of epithelial cells. The data indicate that the capability ofSalmonellaserovars to enter the cecal mucosa and invade lower regions affects both the level and character of the immune response in tissue.

Bovine diseases due to Mycoplasma bovis can cause considerable economic losses in cattle production. While the pathogen is principally responsible for therapy-resistant mastitis on large dairy farms, on smaller farms the typical mycoplasma diseases are calf pneumonia and arthritis. Moreover, the pathogen is able to cause genital disorders. M. bovis infection can be controlled effectively only if appropriate measures are implemented at the earliest possible stage. Since immunoprophylaxis and antibiotic treatment are known to be ineffective, control measures must include the introduction of strict hygiene standards, the restriction of animal movement out of infected herds and the culling of clinically diseased animals and shedders of the mycoplasma (the latter only in the case of mastitis and genital disorders). In this review, symptoms of the various diseases caused by M. bovis are described and characteristics of the course of infection are outlined. To clarify the origin and spread of the infection, the authors describe the main properties and reservoirs of the pathogen and summarise experimental evidence on modes of transmission to susceptible organs. As effective diagnosis is a prerequisite for the introduction of early control measures, the advantages and disadvantages of currently used diagnostic methods are discussed in detail. It is a serious shortcoming if testing for mycoplasmas is not included in routine bacterial examination of clinical samples. As a consequence, some M. bovis infections will remain undetected and outbreaks cannot be controlled properly. Finally, practical recommendations are given for prevention and control, including the formation of mycoplasma-free herds.