Cerebral baylisascariosis in a rainbow lorikeet (Trichoglossus moluccanus) in a German Zoo.

BACKGROUND: The raccoon roundworm, Baylisascaris procyonis, can cause a meningoencephalitis as neural larva migrans which is known in avian species, including rainbow lorikeets in North America, but has not been described in Old World parrots in Germany yet. CASE PRESENTATION: A 2-month-old, male rainbow lorikeet from a zoo in Germany was submitted for necropsy. Prior to death the animal had progressive neurological signs like apathy and torticollis. In the cerebrum a focally extensive severe granulomatous to necrotizing encephalitis with an intralesional larval nematode was diagnosed. Based on the clinical and pathological findings, the larval morphology and the epidemiological background, the larva was identified as Baylisascaris procyonis. CONCLUSIONS: Cerebral baylisascariosis should be considered as a differential diagnosis in zoo and pet birds with neurological signs having contact to racoons or rather racoon faeces in Germany due to the high prevalence of Baylisascaris procyonis in the German raccoon population.

Science CommuniCa2+tion Developing Scientific Literacy on Calcium: The Involvement of CRAC Currents in Human Health and Disease.

All human life starts with a calcium (Ca2+) wave. This ion regulates a plethora of cellular functions ranging from fertilisation and birth to development and cell death. A sophisticated system is responsible for maintaining the essential, tight concentration of calcium within cells. Intricate components of this Ca2+ network are store-operated calcium channels in the cells' membrane. The best-characterised store-operated channel is the Ca2+ release-activated Ca2+ (CRAC) channel. Currents through CRAC channels are critically dependent on the correct function of two proteins: STIM1 and Orai1. A disruption of the precise mechanism of Ca2+ entry through CRAC channels can lead to defects and in turn to severe impacts on our health. Mutations in either STIM1 or Orai1 proteins can have consequences on our immune cells, the cardiac and nervous system, the hormonal balance, muscle function, and many more. There is solid evidence that altered Ca2+ signalling through CRAC channels is involved in the hallmarks of cancer development: uncontrolled cell growth, resistance to cell death, migration, invasion, and metastasis. In this work we highlight the importance of Ca2+ and its role in human health and disease with focus on CRAC channels.

First report of pulmonary cysticercosis caused by Taenia crassiceps in a Cape fur seal (Arctocephalus pusillus).

The cestode Taenia crassiceps parasitizes in the intestine of domestic and wild carnivores, especially in red foxes. Usually, the metacestode stage, also known as Cysticercus longicollis, is located in muscles, peritoneal and pleural cavity of wild rodents. In this case, larval stages were found in a female Cape fur seal, which lived in a German zoo since June 1998. In January 2019, the animal presented clinical signs in terms of inappetence and reduced mobility and, within a short time, it developed dyspnoea and died. Pathological and parasitological examinations were performed. In a large mass of the right thoracic wall and in nodular lung lesions, metacestodes with numerous protoscoleces were identified. Morphological and molecular analyses led to the diagnosis of a Taenia crassiceps infection. Probably, the urban fox population was the source of infection. Thus, regarding the zoonotic potential of this cestode, a regularly performed parasitological examination of pet dogs is recommended.

Disease Manifestation and Viral Sequences in a Bonobo More Than 30 Years after Papillomavirus Infection.

Pan paniscus Papillomavirus 1 (PpPV1) causes focal epithelial hyperplasia (FEH) in infected animals. Here, we analyzed the present disease manifestation and PpPV1 genomic sequence of an animal that was afflicted by an FEH epizootic outbreak in 1987 for which the sequence of the responsible PpPV1 was determined. The animal displayed FEH more than 30 years after the initial diagnosis, indicating persistence or recurrence of the disease, and evidence for active PpPV1 infection was obtained. Moreover, the sequences of the viral genomes present in the late 1980s and in 2018 differed at 23 nucleotide positions, resulting in 11 amino acid exchanges within coding regions. These findings suggest that PpPV1-induced FEH might not undergo complete and/or permanent remission in a subset of afflicted animals.