Compartment 1 acidosis associated with hemorrhagic diathesis causing mortalities among racing camels in Oman.

Camels are adapted to digestion of dry rough forages for their nutrition, and sudden change to highly digestible feed during the racing season causes digestive disorders. The current study investigated the cause of death among racing dromedary camels within 3-7 days following a sudden onset of fever ≈ 41 °C, colic with tarry feces, and enlarged superficial lymph nodes. Marked leukopenia, low RBC count and thrombocytopenia, deranged liver and renal function tests, and prolonged coagulation profiles were reported. Compartment 1 fluid revealed a pH of 4.3-5.2 with absence or few ciliated protozoa and Gram-positive microbial flora. Widespread petechial to ecchymotic hemorrhages were observed in various organs including the gastrointestinal tract (compartment 3 and colon), lungs, and heart. Fibrin thrombi in arterioles, capillaries, venules, and medium-sized veins were observed especially in the pulmonary interstitium, submucosa of the large intestine (ascending colon), deep dermis, and renal cortex. Furthermore, widespread hemorrhages and necrosis were constant histopathological lesions in parenchymatous organs. Based on clinical signs, hematology, blood biochemistry, and gross and microscopical findings, the cases were diagnosed as compartment 1 acidosis associated with hemorrhagic diathesis and endotoxicosis. Finally, compartment 1 acidosis associated with hemorrhagic diathesis is a serious fatal disease on the Arabian Peninsula in racing dromedaries causing multi-organ dysfunction and coagulopathy and disseminated hemorrhages.

Cellular infiltration, cytokines, and histopathology of skin lesions associated with different clinical forms and stages of naturally occurring lumpy skin disease in cattle.

Lumpy skin disease (LSD) caused by the Capripoxvirus LSD virus which infects cattle, leading to a serious disease characterized by fever and the eruption of skin nodules all over the surface of the body. Our understanding of the pathogenesis of this disease is still incomplete, particularly the immunopathological alterations occurring in the skin nodules of infected animals. Therefore, we collected skin nodules from naturally infected cattle with different forms of the disease, both in the early stage of clinical infection and after disease progression. The skin samples were examined both histopathologically and immunohistochemically using a variety of antibodies targeting immune cellular markers and cytokines. As a result, the dermatohistopathology revealed orthokeratotic hyperkeratosis, vasculitis, epidermal microvesicles, and cellules claveleuses of Borrel in the early stage of infection, with the severity of the lesions correlating with the severity of the clinical disease. Meanwhile, late-stage samples had epidermal hyperkeratosis as well as dermal lymphocytic and histiocytic infiltrations. The predominant cellular infiltrates in the cutaneous lesions of early-stage LSD samples were interferon (IFN)-γ+ cells and CD4+ T lymphocytes with few macrophage lineage cells. However, in the late-stage samples, numerous Iba-1+ macrophages, with few IFN-γ+ cells and CD4+ T lymphocytes, were detected. Our findings indicate that IFN-γ+ cells, CD4+ T lymphocytes, and macrophages play a key role in the immunity against natural LSD virus infection and imply that cutaneous vasculopathy associated with LSD virus infection is an immune-mediated lesion. The current study contributes to our understanding of the pathogenesis of LSD.

Protective potential of royal jelly against hydroxyurea -induced hepatic injury in rats via antioxidant, anti-inflammatory, and anti-apoptosis properties.

Hydroxyurea (HDU) is a widely used medication for various malignancies, thalassemia, and sickle cell anemia with reported side effects. The current study investigated HDU- induced hepatic injury and the protective potential of the royal jelly (RJ) against this hepatotoxic effect in the light of hepatic oxidative/ antioxidative status, pro-inflammatory cytokine, apoptosis signaling pathway, and histopathology. Sixty albino rats were used (n = 10/group) for 60 days: control, RJ (100 mg/kg body weight, orally), HDU (225 mg/kg body weight, orally), 2HDU (450 mg/kg body weight, orally), and HDU + RJ groups. HDU-treated rats showed significant elevation of liver function tests as aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, as well as malondialdehyde and nitric oxide (oxidative biomarkers) and significant decreased hepatic antioxidant molecules (reduced glutathione, superoxide dismutase, and glutathione peroxidase), compared to a control group, that more pronounced in the high dose of HDU. In addition, HDU induced significant upregulation of TNF-α and the Caspase-3 apoptotic pathway. Moreover, the liver of HDU treated groups showed various hepatic lesions from mild to severe necrotic changes related to the HDU dose. However, administration of RJ with HDU improved liver function tests, liver histology, and hepatic oxidative/antioxidative status concerning HDU groups. Furthermore, oral RJ administration with HDU significantly lessens the immune-expression area % of TNF-α and Caspase-3. Thus, the royal jelly has antioxidant, anti-inflammatory, and anti-apoptotic properties against HDU- induced hepatic injury and could be, therefore, used as adjuvant therapy in patients with long-term HDU medication.

Animal rabies situation in Sultanate of Oman (2017-2019).

Successful preventive and control measures of zoonotic diseases require updated epidemiological data. Sylvatic rabies is endemic in Oman since 1990. Studying of the prevalence of animal rabies in Oman (2017-2019) was the goal of the current study besides the clinical-histopathological investigations of rabies in different animal species. A total of 117 whole brains of different animal species from different regions of Oman were examined by fluorescent antibody test (FAT) and histopathology for rabies during 2017-2019. Sixty-four samples (54.7%) were positive for rabies by FAT. The most affected species were goat (53.1%) followed by camel (18.8%), which pose a great risk to farmers and veterinarians. Positive fox cases were (10.9%). Most confirmed cases of animal rabies were submitted from Northern regions of Oman. Rabies was reported recently in Al Wusta among wild ruminants, Central Oman. The seasonal cycle of animal rabies in Oman was year-round with the peak from December to April. The clinical signs and neuropathological findings were nearly similar in different animal species. Histopathology-positive cases had Negri bodies in pyramidal and purkinje neurons, non-suppurative encephalitis features, and neuronal degeneration and necrosis. The sensitivity and specificity of histopathological diagnosis of rabies in different animals were 76.47% and 100.00%, respectively. Finally, sylvatic rabies remains a major challenge to the public and animal health in Oman. Although of the value of histopathological diagnosis of rabies if no other technique is available, other complementary tests must be employed to confirm negative results.

Molecular characterization and diagnostic investigations of rabies encephalitis in camels (Camelus dromedaries) in Oman: a retrospective study.

The accurate and early diagnosis of rabies is critical for undertaking public health measures in animals. The aim of the current study was to identify the molecular characterization of the circulating rabies virus (RABV) among camels (Camelus dromedaries) in Oman and to evaluate the efficacy of the histopathology and reverse transcription polymerase chain reaction (RT-PCR) as diagnostic tools of acute rabies encephalitis in camels in comparison with direct fluorescent antibody test (dFAT). Of the forty-five brain samples from suspected camels submitted to the Animal Health Research Center in Oman (2009-2013), 22 cases were positive by dFAT and RT-PCR. Two positive samples were subjected for N gene nucleotide sequencing and phylogenetic analysis (accession numbers GU353156 and KC883998 for brain samples collected in 2009 and 2011, respectively). The specificity and sensitivity of histopathology were 100% and 81%, respectively, while in RT-PCR were 100% and 100%, respectively. The neuropathological changes were presence of intracytoplasmic inclusions (Negri bodies) in the pyramidal neurons of the hippocampus beside prominent cerebral and cerebellar congestion and hemorrhage. Neuronal necrosis with satellitosis and neuronophagia were also noticed in the cerebrum of affected brains. Conclusively, there was one genetic group of RABV with 99% homology circulating in Omani camels. Also, it is concluded that histopathological examination is a safe and reliable diagnostic tool when only formalin-fixed and paraffin-embedded material is available, but the negative results should be reaffirmed by dFAT or RT-PCR.

Natural Ehrlichia ruminantium infection in two captive Arabian tahrs (Arabitragus jayakari) in Oman.

This study was investigated the cause of death of two captive adult Arabian tahrs (Arabitragus jayakari) died within 2-3 days after onset of fever and neurologic signs in a private farm in northern Batinah Region of Oman. Blood counting revealed leukocytosis attributed to neutrophilia and serum chemistry showed hypoproteinemia, increased creatine kinase and BUN. Upon autopsy, the animals exhibited mild ascites and hydrothorax, prominent hydropericardium, with large pale-yellow clear fluid coagulum, prominent epicardial petechiation, as well as severe pulmonary edema associated with frothy fluid in airways. Brain edema with congestion of meningeal and parenchymal vessels was prominent. Histopathology revealed severe congestion and edema of both lung and brain as well as cardiac myopathy. Ehrlichia ruminantium colonies (the causative organism of cowdriosis; OIE-listed disease) were demonstrated in the capillary endothelium of fresh brain squash and lung macrophages. This is the first report of natural E. ruminantium infection in Arabian tahr, the highly endangered species, based on typical clinical signs of acute cowdriosis and demonstration of E. ruminantium colonies in the brain capillary endothelial cells.

Neurohepatic toxicity of subacute manganese chloride exposure and potential chemoprotective effects of lycopene.

Excess manganese (Mn) is potentially toxic resulting in a permanent neurodegenerative disorder, clinically known as "manganism" that is distinctive for hepaticencephalopathy. The present study was designed to explore the toxic impacts of subacute Mn exposure on brain and liver tissues, and the relative abilities of lycopene in averting such neurohepatic damage. Rats were daily injected with MnCl(2) (0 or 6mg/kg, i.p.) 20 days after lycopene administration (0 or 10mg/kg, p.o.), and killed 4 weeks after MnCl(2) exposure. MnCl(2)-induced lipid peroxidation and perturbation in antioxidant system, increase of acetylcholinesterase, aminotransferases, and decrease alkaline phosphatase, and lactate dehydrogenase activities with hyperglycemia as demonstrated by Alzheimer type II astrocytosis, and periportal hepatic necrosis and apoptosis were prevented by lycopene. However, lycopene did not prevent the increased body burden of Mn and the altered Fe and Cu homeostasis induced by MnCl(2). Glutathione S-transferase and catalase activities, and glutathione content were reduced in MnCl(2)-challenged rats, and sustained by lycopene. Our results indicate that although lycopene failed to reduce Mn concentration or retain disturbed elemental status; it appears to be a highly effective in alleviating its neurohepatic deleterious effects by preventing lipid peroxidation, hyperglycemia and changes in the activity of acetylcholinesterase and hepatobiliary enzymes, and antioxidant pathways.