Intestinal parasites and lungworms in stray, shelter and privately owned cats of Switzerland.

Endoparasitic infections represent relevant causes of respiratory and gastrointestinal diseases in cats. The aim of the study was to investigate the occurrence of endoparasites in Swiss cats in order to evaluate the risk of onset of parasitic diseases and potential correlated zoonoses. Therefore 664 faecal samples from privately owned (n = 299), shelter (n = 197) and stray (n = 168) cats were investigated by sedimentation-flotation and 468 samples additionally by the Baermann technique. Overall, 77.4% (n = 130), 21.8% (n = 43) and 11.7% (n = 35) of stray, shelter and privately owned cats, respectively, were positive, with significant differences between the groups. Among infected cats, 58.7% (n = 122) harboured a single, 30.8% (n = 64) two and 10.6% (n = 22) more than two parasite species. Toxocara cati, with an infection rate of 18.5% (n = 123), was the most frequently detected parasite. The rates for other intestinal parasites were: Taenia sp. 11.1% (n = 74), Isospora sp. 8.1% (n = 54), Capillaria sp. 4.7% (n = 31), hookworms 1.1% (n = 7), Giardia duodenalis 0.8% (n = 5), Dipylidium caninum 0.6% (n = 4), Toxoplasma gondii 0.6% (n = 4), Hammondia hammondi 0.5% (n = 3), Sarcocystis sp. 0.2% (n = 1) and Diphyllobothrium latum 0.2% (n = 1). First-stage larvae of the lungworm Aelurostrongylus abstrusus were found in 2.3% (n = 15) of all samples. The morphological identification of Taenia sp., T. gondii, H. hammondi and A. abstrusus was confirmed by molecular techniques. Overall, cats younger than one year and intact animals were more frequently infected with parasites than older and neutered animals. The observed infection rates were comparable to those from other European studies, except for Taenia sp. showing a significantly higher occurrence. This implicates that there is a persistent risk of environmental contamination with parasitic stages especially by stray cats, and a risk of infection for cat owners with potential zoonotic pathogens, emphasizing the need for appropriate parasite control measures.

The role of the NADPH oxidase NOX2 in prion pathogenesis.

Prion infections cause neurodegeneration, which often goes along with oxidative stress. However, the cellular source of reactive oxygen species (ROS) and their pathogenetic significance are unclear. Here we analyzed the contribution of NOX2, a prominent NADPH oxidase, to prion diseases. We found that NOX2 is markedly upregulated in microglia within affected brain regions of patients with Creutzfeldt-Jakob disease (CJD). Similarly, NOX2 expression was upregulated in prion-inoculated mouse brains and in murine cerebellar organotypic cultured slices (COCS). We then removed microglia from COCS using a ganciclovir-dependent lineage ablation strategy. NOX2 became undetectable in ganciclovir-treated COCS, confirming its microglial origin. Upon challenge with prions, NOX2-deficient mice showed delayed onset of motor deficits and a modest, but significant prolongation of survival. Dihydroethidium assays demonstrated a conspicuous ROS burst at the terminal stage of disease in wild-type mice, but not in NOX2-ablated mice. Interestingly, the improved motor performance in NOX2 deficient mice was already measurable at earlier stages of the disease, between 13 and 16 weeks post-inoculation. We conclude that NOX2 is a major source of ROS in prion diseases and can affect prion pathogenesis.