Bohumil Sak

Cryptosporidium muris is a gastric species primarily infecting rodents, whereas natural infections in cats are rarely documented and biologically poorly characterized. Oocysts of C. muris were detected in a cat and monitored for 120 days. Molecular characterization was performed on the small subunit rRNA, actin, 70-kDa heat shock protein , Cryptosporidium oocyst wall protein and thrombospondin-related adhesive protein of Cryptosporidium -1 loci. Oocyst morphology was evaluated microscopically. Infectivity and shedding dynamics were assessed in BALB/c mice and compared with C. muris RN66 and C. proliferans . Oocyst integrity during storage at 4°C was monitored for 60 days at 15-day intervals using flow cytometry and viability assays. The infected cat shed oocysts for 97 days, with a maximum intensity of 371 200 oocysts per gram (OPG), yet remained clinically asymptomatic. Developmental stages were confirmed histologically in gastric biopsy specimens. Haematological and biochemical parameters remained within reference ranges, and no concurrent parasitic, bacterial or viral infections were detected; only seropositivity to Toxoplasma gondii was recorded. All analysed loci showed 100% identity with C. muris RN66. Oocyst morphology did not differ from reference isolates. However, oocysts originating from the cat exhibited markedly reduced environmental stability, with a 90% decline in integrity within 60 days. Experimental infection of mice confirmed infectivity, but total oocyst output (32 300 OPG/days) was several orders of magnitude lower than that of C. muris RN66. Although genetically identical to rodent isolates, the feline-derived C. muris displayed altered biological properties, including reduced oocyst stability and transmission fitness. Cats may serve as susceptible but epidemiologically inefficient hosts.

Taenia crassiceps (Zeder, 1800), a zoonotic cestode with a wide geographical distribution, utilises canids as definitive hosts and small rodents as intermediate hosts. However, accidental infections in non-human primates, particularly in captive lemurs, have been increasingly documented. In this case report, we describe the first documented case of cysticercosis caused by the larval stage of T. crassiceps (metacestode; also known as Cysticercus longicollis Rudolphi, 1819) in a captive western grey bamboo lemur (Hapalemur occidentalis Rumpler). The affected female lemur showed progressive abdominal distension over a period of two months, which initially indicated pregnancy. At necropsy, multiple thin-walled metacestodes were discovered throughout the abdominal and thoracic cavities, including a large polycystic mass involving the liver and peritoneum. Histopathological analysis revealed larval cestodes with armed (hook-bearing) scoleces embedded in vascularised stromal tissue, accompanied by marked eosinophilic and macrophage infiltration and focal necrosis, particularly in the lungs. Morphological and molecular identification based on COI gene sequencing confirmed the presence of T. crassiceps. Despite extensive parasitological investigations, no definitive host excreting T. crassiceps eggs was found in the zoological facility where the lemur was kept. These results emphasise the possibility of indirect environmental transmission and highlight the susceptibility of lemurs as atypical intermediate hosts. This case confirms previous reports of lethal cysticercosis in lemurs, which is often characterised by rapid systemic spread of metacestodes. Our findings also emphasise the need for increased awareness and preventive measures to reduce the risk of parasite infections in vulnerable captive primates.

The number of mountain gorillas (Gorilla beringei beringei) has grown steadily in recent decades thanks to intensive conservation efforts. But as they live in restricted areas, they experience changes in population dynamics and pathogen epidemiology. These changes have been demonstrated by the emergence of gastrointestinal problems linked to strongylid infections in the Virunga population, highlighting the need to study changes in other parasite infections. We assessed the patterns of Cryptosporidium, Giardia and microsporidia infections in mountain gorillas across the Virunga Massif. We examined 152 faecal samples from 16 gorilla groups collected in 2018 using PCR and qPCR on three genetic markers and detected Cryptosporidium muris (< 1%), Enterocytozoon bieneusi (genotypes-D 14%, CHN-F1 < 1%) and Giardia intestinalis (13%). No significant spatial or sex/age differences were observed in microsporidia and Giardia infections. However, a temporal comparison with previous data suggests changes in the protist communities over time. We conclude that these protists were not impacted by the changes in mountain gorilla population dynamics and did not contribute to the increasing occurrence of severe gastrointestinal problems in Virunga gorillas. These results aid our epidemiological understanding of parasite communities in mountain gorillas, an asset for their ongoing conservation management in the face of newly emerging health challenges.

We detected 24 Encephalitozoon cuniculi positive Ixodes ricinus ticks of 284 collected in the Czech Republic. Since the route of transmission of microsporidia is not fully understood, the presence of microsporidia in ticks raises the question of whether they may be involved in the transmission of these pathogens.

We retrospectively analyzed of 211 frozen cerebrospinal fluid samples from immunocompetent persons in the Czech Republic and detected 6 Encephalitozoon cuniculi-positive samples. Microsporidiosis is generally underestimated and patients are not usually tested for microsporidia, but latent infection in immunodeficient and immunocompetent patients can cause serious complications if not detected and treated.