Chlamydiae have a worldwide distribution causing a wide range of diseases in human hosts, livestock, and companion animals as well as in wildlife and exotic species. Moreover, they can persist in their hosts as asymptomatic infections for extended periods of time. The introduction of molecular techniques has revolutionized the Chlamydia field by expanding the host range of known chlamydial species but also by discovering new species and even new families of bacteria in the broader order Chlamydiales. The wide range of hosts, diseases, and tissues affected by chlamydiae complicate the diagnosis such that standard diagnostic approaches for these bacteria are rare. Bacteria of the Chlamydiales order are small and their inclusions are difficult to detect by standard microscopy. With the exception of avian and ovine chlamydiosis, macroscopic and/or histologic changes might not be pathognomic or indicative for a chlamydial infection or even not present at all. Moreover, detection of chlamydial DNA in specimens in the absence of other methods or related pathological lesions questions the significance of such findings. The pathogenic potential of the majority of recently identified Chlamydia-related bacteria remains largely unknown and awaits investigation through experimental or natural infection models including histomorphological characterization of associated lesions. This review aims to summarize the historical background and the most important developments in the field of animal chlamydial research in the past 5 years with a special focus on pathology. It will summarize the current nomenclature, present critical thoughts about diagnostics, and give an update on chlamydial infections in domesticated animals such as livestock, companion animals and birds, as well as free-ranging and captive wild animals such as reptiles, fish, and marsupials.

Specified pathogen-free cats were naturally infected with FCoV or experimentally infected with FCoV type I. Seroconversion was determined and the course of infection was monitored by measuring the FCoV loads in faeces, whole blood, plasma and/or monocytes. Tissue samples collected at necropsy were examined for viral load and histopathological changes. Experimentally infected animals started shedding virus as soon as 2 days after infection. They generally displayed the highest viral loads in colon, ileum and mesenteric lymph nodes. Seroconversion occurred 3–4 weeks post infection. Naturally infected cats were positive for FCoV antibodies and monocyte-associated FCoV viraemia prior to death. At necropsy, most animals tested positive for viral shedding and FCoV RNA was found in spleen, mesenteric lymph nodes and bone marrow. Both experimentally and naturally infected cats remained clinically healthy. Pathological findings were restricted to generalized lymphatic hyperplasia. These findings demonstrate the presence of systemic FCoV infection with high viral loads in the absence of clinical and pathological signs.

To determine the role of Chlamydia trachomatis in miscarriage, we prospectively collected serum, cervicovaginal swab specimens, and placental samples from 386 women with and without miscarriage. Prevalence of immunoglobulin G against C. trachomatis was higher in the miscarriage group than in the control group (15.2% vs. 7.3%; p = 0.018). Association between C. trachomatis–positive serologic results and miscarriage remained significant after adjustment for age, origin, education, and number of sex partners (odds ratio 2.3, 95% confidence interval 1.1–4.9). C. trachomatis DNA was more frequently amplified from products of conception or placenta from women who had a miscarriage (4%) than from controls (0.7%; p = 0.026). Immunohistochemical analysis confirmed C. trachomatis in placenta from 5 of 7 patients with positive PCR results, whereas results of immunohistochemical analysis were negative in placenta samples from all 8 negative controls tested. Associations between miscarriage and serologic/molecular evidence of C. trachomatis infection support its role in miscarriage.