Peste-des-petits-ruminants virus (PPRV) causes a severe respiratory disease in small ruminants. The possible impact of different atypical host species in the spread and planed worldwide eradication of PPRV remains to be clarified. Recent transmission trials with the virulent PPRV lineage IV (LIV)-strain Kurdistan/2011 revealed that pigs and wild boar are possible sources of PPRV-infection. We therefore investigated the role of cattle, llamas, alpacas, and dromedary camels in transmission trials using the Kurdistan/2011 strain for intranasal infection and integrated a literature review for a proper evaluation of their host traits and role in PPRV-transmission. Cattle and camelids developed no clinical signs, no viremia, shed no or only low PPRV-RNA loads in swab samples and did not transmit any PPRV to the contact animals. The distribution of PPRV-RNA or antigen in lymphoid organs was similar in cattle and camelids although generally lower compared to suids and small ruminants. In the typical small ruminant hosts, the tissue tropism, pathogenesis and disease expression after PPRV-infection is associated with infection of immune and epithelial cells via SLAM and nectin-4 receptors, respectively. We therefore suggest a different pathogenesis in cattle and camelids and both as dead-end hosts for PPRV.
8 November 2017 in Transboundary and Emerging Diseases
BACKGROUND: The local recurrence rates of malignant skin tumors after micrographic controlled surgery using complete circumferential peripheral and deep margin assessment (CCPDMA) are reported to be low. However, in daily practice, tumor entities with a significantly higher recurrence rate are found. OBJECTIVE: The aim of the investigation was to identify these high-risk tumors to develop approaches for risk stratification. PATIENTS AND METHODS: We included different malignant tumors that were surgically treated and examined with CCPDMA using paraffin sections and H&E staining. Re-excisions were performed until the tumor was completely removed. RESULTS: Ninety-nine thousand three hundred seventy-two tumors were included in the study; the follow-up period was 4 years (median). Eight tumor entities were identified as high-risk entities, showing a significantly higher local recurrence rate of over 20%: desmoplastic squamous cell carcinoma, desmoplastic melanoma, Merkel cell carcinoma, microcystic adnexal carcinoma, pleomorphic sarcoma, liposarcoma as well as angiosarcoma, and extramammary Paget's disease. CONCLUSION: Complete circumferential peripheral and deep margin assessment allows complete control of the resection margins and enables skin-sparing resections with low recurrence rates for basal cell carcinomas, nondesmoplastic squamous cell carcinomas, lentiginous melanomas, and dermatofibrosarcoma protuberans. However, other tumors show significantly higher recurrence rates and therefore need to be classified as high-risk tumors.
Tick-borne encephalitis (TBE) is a severe neurologic disease in Europe and Asia. Disease expression ranges from asymptomatic to severe neurological clinical pictures, involving meningitis, encephalitis, meningoencephalitis and potentially fatal outcome. Humans mostly become infected with TBE virus (TBEV) by the bite of an infected tick. Gastrointestinal (GI) symptoms in humans are mainly attributed to the first viremic phase of TBEV infection with unspecific symptoms and/or resulting from severe neurological impairment of the central nervous system (CNS). We used the subcutaneous TBEV-infection of C57BL/6 mice as a model to analyze GI complications of TBE. We observed the acute distension and segmental dilation of the intestinal tract in 10 of 22 subcutaneously infected mice. Histological analysis revealed an intramural enteric ganglioneuritis in the myenteric and submucosal plexus of the small and large intestine. The numbers of infiltrating macrophages and CD3+ T lymphocytes correlated with the severity of ganglioneuritis, indicating an immune-mediated pathogenesis due to TBEV-infection of the enteric plexus. Our study demonstrates that the inflammation of enteric intramural ganglia presents to be a common feature in TBEV-infected mice. Accordingly, the results of this mouse model emphasize that GI disease manifestation and consequences for long-term sequelae should not be neglected for TBEV-infections in humans and require further investigation.