Toxoplasma (T.) gondii is an obligate intracellular parasite with felids, including domestic cats, as definitive hosts. In immunocompetent individuals, T. gondii infection is usually asymptomatic. However, under immunosuppression, it may have severe pathological impacts, which often result from the reactivation of a chronic infection. In this case study, a 21-month-old female domestic shorthair cat—diagnosed with primary immune-mediated hemolytic anemia three months prior and treated with cyclosporine and prednisolone—presented with acute tachypnea, dyspnea, diarrhea, and anorexia. Thoracic radiography suggested severe pneumonia. Testing for Mycoplasma spp., Anaplasma spp., Ehrlichia spp., and lungworm infection was negative. Serology for T. gondii revealed seroconversion of IgG, but not of IgM, indicating previous exposure to T. gondii. The cat remained stable but tachypneic for three days, followed by an acute onset of dyspnea and clinical deterioration, after which euthanasia was elected. Numerous protozoa were present in a postmortem transtracheal bronchoalveolar lavage and fine-needle aspiration of the lung. Microsatellite typing classified the extracted DNA as T. gondii type II variant TgM-A. This case demonstrates that T. gondii reactivation, leading to fulminant pneumonia, can be a sequela of immunosuppressive treatment in cats and should, therefore, be considered as a differential diagnosis in immunosuppressed cats with acute-onset respiratory signs. Rapid diagnosis may prevent fatal consequences.

With exception of the Northeast, the raccoon roundworm (Baylisascaris procyonis) is widespread in Germany. This zoonotic parasite can cause neurological disease in paratenic and aberrant hosts, like humans. As the name indicates, raccoons are the definitive host of B. procyonis. However, and despite the successful expansion of the raccoon population, parasite and host ranges do not always overlap. B. procyonis has been largely absent from the northeastern part of the country, notwithstanding the stable presence of raccoons in this area. In this study, faecal and intestinal samples were opportunistically collected from 166 free-ranging raccoons from 9 federal states in Germany. In 68 animals (41.0 %), B. procyonis was identified either through PCR or morphological identification of adult worms. The positive raccoons originated from 6 federal states, including for the first time animals from the northern state of Mecklenburg-Western Pomerania. The results of this study highlight the dissemination of the parasite in the north of the country, while maintaining its presence in the rest of Germany.

Chicken coccidiosis causes annual losses exceeding GBP 10 billion globally. The most pathogenic species for domestic fowls including Eimeria tenella, E. acervulina, and E. maxima, can lead to gastrointestinal issues ranging from mild to fatal. In this study, stages of E. tenella and freshly isolated chicken heterophils were co-cultured for 180 min. These interactions were analyzed using live 3D holotomographic and confocal microscopy. We observed that E. tenella stages were entrapped by heterophils and heterophil extracellular traps (HETs). Notably, different HET phenotypes, specifically sprHETs and aggHETs, were induced regardless of the stage. Furthermore, the quantification of extracellular DNA release from co-cultures of heterophils and sporozoites (ratio 1:1) for 180 min demonstrated a significantly higher release (p = 0.04) compared to negative controls. In conclusion, research on the chicken innate immune system, particularly fowl-derived HETs, remains limited. More detailed investigations are needed, such as exploring the time-dependent triggering of HETs, to establish a standard incubation time for this pathogen defense mechanism. This will enhance our understanding of its role in parasite survival or death during HET confrontation.

Streptococcus equi subsp. zooepidemicus (SEZ) causes diseases in various animals and humans. In pigs, it is an emerging pathogen that causes septicemia and other severe pathologies. SEZ expresses the M-like protein SzM, which recruits host proteins such as fibrinogen to the bacterial surface. The objective of this study was to investigate the survival mechanism of a zoonotic SEZ strain in porcine blood. The zoonotic SEZ C33 strain proliferated in porcine blood of 10-week-old piglets in vitro despite comparably high levels of IgM binding to the bacterial surface. Comparison with the isogenic szm deletion mutant showed that SzM_C33 expression is crucial for porcine blood survival. Flow cytometry analysis revealed that SEZ C33 was associated with porcine blood granulocytes, exhibiting a prominent generation of reactive oxygen species. Cytochalasin D treatment significantly inhibited this association. Furthermore, we found viable intracellular SEZ C33 in a penicillin/streptomycin protection assay in porcine blood and purified porcine granulocytes, in agreement with the microscopic detection of streptococci in neutrophils. Experimental infection with SEZ C33 confirmed the virulence of this strain in pigs, including one case of fibrino-suppurative meningoencephalitis and tarsitis. In conclusion, SEZ C33, originally isolated from a diseased human, demonstrated SzM-mediated intracellular survival in porcine blood granulocytes in vitro and is most likely involved in the pathogenesis of diseases such as meningitis and arthritis in vivo .