Pterygodermatites nycticebi infections in golden lion tamarins (Leontopithecus rosalia rosalia) and aye-ayes (Daubentonia madagascariensis) from a German zoo.

In a golden lion tamarin (Leontopithecus rosalia rosalia) colony kept indoors in a German zoo, two animals presented a sudden onset of reduced general condition, lethargy, and diarrhea. At animal capture for clinical examination, adult nematode stages were observed after stress-induced defecation. Despite treatment, two golden lion tamarins died in the following 2 days. At necropsy, spirurid stages were found in the lungs and intestine. Additionally, adult Pterygodermatites spp. were identified in histopathological samples of intestine and pancreas, confirming the previous diagnosis. Upon diagnosis, all animals were treated with ivermectin (0.2 mg/kg; SC). Thereafter, the general condition of the golden lion tamarins improved, whereby some of them excreted spirurid nematodes over 3 days. Four weeks after treatment, 20 fecal samples from the colony were examined and proved negative for parasitic stages. Given that common German cockroaches (Blattella germanica) are suitable intermediate hosts of Pterygodermatites nycticebi, 30 specimens were collected from seven different locations around the golden lion tamarins housing. Third-stage larvae of Pterygodermatites spp. were recovered from those cockroaches. Regular anthelmintic treatments, coprological screenings, and controls for intermediate hosts were recommended. More than 2 years later, P. nycticebi infection was diagnosed again histopathologically in an aye-aye (Daubentonia madagascariensis) which suddenly died. Coprological analysis confirmed the presence of spirurid eggs. Due to prosimian primates' cockroach-eating habits and given that total cockroach eradication proved impossible, continuous cockroach control strategies and regular treatments of primates are currently performed to prevent further P. nycticebi infections.

Split spinal cord malformations in 4 Holstein Friesian calves.

BACKGROUND: The split spinal cord malformation (SSCM) is an uncommon congenital malformation of the vertebral canal in which parts of the spinal cord are longitudinally duplicated. In SSCM Type I, each spinal cord has its own dura tube. In the SSCM Type II, both parts of the spinal cord are surrounded by a common dura tube. CASES PRESENTATION: During the clinical examination one calf showed ambulatory paresis and 3 calves non-ambulatory paraparesis. Calf 4 additionally had a congenital tremor. The examination of calf 4 using magnetic resonance imaging (MRI) showed a median hydrosyringomyelia at the level of the 4th lumbar vertebra. The caudal part of this liquid-filled cavity was split longitudinally through a thin septum. From there, the spinal cord structures duplicated with an incomplete division, so that the transverse section of the spinal cord appeared peanut-shaped and in each half a central canal could be observed. The pathological-anatomical examination after euthanasia showed a duplication of the spinal cord in the area of the lumbar vertebral column in all calves. The histopathological examination revealed two central lumbar vertebral column channels. The two spinal cord duplicates were each surrounded by two separate meninges in calf 2 (SSCM type I); in the other calves (1, 3, 4, and) the two central canals and the spinal cord were covered by a common meninx (SSCM type II). A pedigree analysis of calves 2, 3 and 4 showed a degree of relationship suggestive of a hereditary component. This supports the hypothesis of a possible recessive inheritance due to common ancestors, leading to partial genetic homozygosity. CONCLUSIONS: The clinical appearance of SSCM can vary widely. In calves with congenital paralysis SSCM should always be considered as a differential diagnosis. A reliable diagnosis intra vitam is possible only with laborious imaging procedures such as MRI. Further studies on the heritability of this malformation are necessary to confirm a genetic cause of this disease.

Influenza A virus infection instructs hematopoiesis to megakaryocyte-lineage output.

Respiratory tract infections are among the deadliest communicable diseases worldwide. Severe cases of viral lung infections are often associated with a cytokine storm and alternating platelet numbers. We report that hematopoietic stem and progenitor cells (HSPCs) sense a non-systemic influenza A virus (IAV) infection via inflammatory cytokines. Irrespective of antiviral treatment or vaccination, at a certain threshold of IAV titer in the lung, CD41-positive hematopoietic stem cells (HSCs) enter the cell cycle while endothelial protein C receptor-positive CD41-negative HSCs remain quiescent. Active CD41-positive HSCs represent the source of megakaryocytes, while their multi-lineage reconstitution potential is reduced. This emergency megakaryopoiesis is thrombopoietin independent and attenuated in IAV-infected interleukin-1 receptor-deficient mice. Newly produced platelets during IAV infection are immature and hyper-reactive. After viral clearance, HSC quiescence is re-established. Our study reveals that non-systemic viral respiratory infection has an acute impact on HSCs via inflammatory cytokines to counteract IAV-induced thrombocytopenia.

Specific elimination of CD133+ tumor cells with targeted oncolytic measles virus.

Tumor-initiating cells (TIC) are critical yet evasive targets for the development of more effective antitumoral strategies. The cell surface marker CD133 is frequently used to identify TICs of various tumor entities, including hepatocellular cancer and glioblastoma. Here, we describe oncolytic measles viruses (MV) retargeted to CD133. The viruses, termed MV-141.7 and MV-AC133, infected and selectively lysed CD133(+) tumor cells. Both viruses exerted strong antitumoral effects on human hepatocellular carcinoma growing subcutaneously or multifocally in the peritoneal cavity of nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. Notably, the CD133-targeted viruses were more effective in prolonging survival than the parental MV-NSe, which is currently assessed as oncolytic agent in clinical trials. Interestingly, target receptor overexpression or increased spreading kinetics through tumor cells were excluded as being causative for the enhanced oncolytic activity of CD133-targeted viruses. MV-141.7 was also effective in mouse models of orthotopic glioma tumor spheres and primary colon cancer. Our results indicate that CD133-targeted measles viruses selectively eliminate CD133(+) cells from tumor tissue, offering a key tool for research in tumor biology and cancer therapy.