Porcine epidemic diarrhoea virus (PEDV) infection causes watery diarrhoea, vomiting, anorexia, and weight loss, especially among neonatal piglets, inflicting on them morbidity and mortality potentially reaching 90%–100%. Despite it being known that certain mammalian cell phases are arrested by PEDV, the mechanisms have not been elucidated, and PEDV pathogenesis is poorly understood. This study determined the effect of an epidemic PEDV strain on cell cycle progression. We observed the effect of the PEDV SHpd/2012 strain on an infected Vero cell cycle through flow cytometry and Western blot, investigating the interrelationships of cell-cycle arrest, the DNA damage–signalling pathway caused by PEDV and the phosphorylation levels of the key molecules Chk.2 and H2A.X involved upstream and downstream in this pathway. PEDV induced Vero cell-cycle arrest at the G1/G0 phase. The phosphorylation levels of Chk.2 and H2A.X increased with the prolongation of PEDV infection, and no significant cell-cycle arrest was observed after treatment with ATM or Chk.2 inhibitors. The proliferation of PEDV was also inhibited by treatment with ATM or Chk.2 inhibitors. PEDV-induced cell-cycle arrest is associated with activation of DNA damage–signalling pathways. Our findings elucidate the molecular basis of PEDV replication and provide evidence to support further evaluation of PEDV pathogenesis.

Introduction: Chronic gastritis is a common diagnosis in dogs with signs of chronic vomiting. However, there is no data concerning endoscopic and histopathological agreement in dogs with chronic gastritis. Thus, a question should be raised whether taking gastroduodenal biopsies in dogs with chronic gastritis is necessary or not. Consequently, the purpose of the study was to compare the endoscopic and histopathological agreement in dogs with chronic gastritis. Material and Methods: A total of 22 non-pregnant client-owned dogs with the signs of chronic gastritis were enrolled in this prospective study. Procedures including clinical examination, blood analysis, and diagnostic imaging were performed before anaesthesia. Biopsies obtained from gastroduodenal sites were histopathologically evaluated. A total of 110 gastroduodenal samples were examined. Results: Sixtyeight samples had abnormal histopathology and endoscopy while 11 showed normal histopathological and endoscopic evidence. Conclusion: The obtained data demonstrated that it is not necessary to take extra gastroduodenal biopsies in dogs with evidence of endoscopic gastroduodenitis. We also believe that further prospective studies, including cost and time effectiveness and more specific comparison between endoscopic appearance and histopathology, are necessary to make final recommendations regarding the need of using both procedures for definitive diagnosis.

Porcine epidemic diarrhoea (PED) is a highly contagious and devastating enteric disease of pigs caused by porcine epidemic diarrhoea virus (PEDV), an enveloped, single-stranded RNA virus belonging to the Alphacoronavirus genus of the Coronaviridae family. The disease is clinically similar to other forms of porcine gastroenteritis. Pigs are the only known host of the disease, and the occurrence of PED in wild boars is unknown. The virus causes acute diarrhoea, vomiting, dehydration, and high mortality in suckling piglets reaching 100%. Heavy economic losses in the pig-farming industry were sustained in the USA between 2013 and 2015 when PEDV spread very quickly and resulted in epidemics. The loss in the US pig industry has been estimated at almost seven million pigs. The purpose of this review is a description of the current status of porcine epidemic diarrhoea in European pigs and the risk presented by the introduction of PEDV to Poland in comparison to the epidemics in the USA.

A study was conducted inthe Teaching Veterinary Clinical Complex,College of Veterinary Animal Sciences,Mannuthy to evaluate the efficacy ofclindamycin as potential monotherapytreatment plan for Babesia gibsoni infectionin dogs during the period from January2013 to March 2014. Dogs of variousbreeds and age groups belonging to bothsexes diagnosed of having Babesia gibsoniinfection by blood smear examination andconfirmed by PCR were selected for thestudy. These animals were treated withclindamycin @ 11mg/kg bw IV q24hr for10 days and supported with haematinics.All animals showed clinical cure withimprovement in appetite and physicalactivity, increase in haematologicalparameters including platelet count andimprovement in serum chemistry values.

Objective—To determine dose dependency of tranexamic acid–induced emesis and the time course of the antifibrinolytic potency of tranexamic acid in dogs. Animals—10 Beagles. Procedures—In a dose-escalating experiment, ascending doses of tranexamic acid (10, 20, and 30 mg/kg, IV) were administered at 5-minute intervals until vomiting was observed. In a separate single-dose experiment, ascending doses of tranexamic acid (20, 30, 40, and 50 mg/kg, IV) were administered at 1-week intervals until vomiting was observed. Time to onset of vomiting and number of vomiting episodes were measured in both experiments. In a coagulation experiment, a single 50 mg/kg bolus of tranexamic acid was administered, and blood was obtained 1 hour before and 20 minutes, 3 hours, and 24 hours after administration. Antifibrinolytic potency of tranexamic acid was evaluated by use of a modified rotational thromboelastography method. Results—Tranexamic acid induced vomiting in a dose-dependent manner. Vomiting frequency was < 2 episodes, and vomiting concluded < 250 seconds after administration. Antifibrinolytic potency of tranexamic acid was significantly higher at 20 minutes following administration, but not different by 24 hours, when compared with the potency measured before administration. No adverse effects were observed in any experiment. Conclusions and Clinical Relevance—IV administration of tranexamic acid induced emesis in a dose-dependent manner. The antifibrinolytic potency of tranexamic acid decreased in a time-dependent manner and was resolved < 24 hours after administration. Further studies are warranted to investigate the emetic and other adverse effects of tranexamic acid in dogs of various breeds and ages.

Objective-To determine whether tepoxalin alters kidney function in dogs with chronic kidney disease (CKD). Animals-16 dogs with CKD (International Renal Interest Society stage 2 or 3) and osteoarthritis. Procedures-Kidney function was assessed via serum biochemical analysis, urinalysis, urine protein-to-creatinine concentration ratio, urine γ-glutamyl transpeptidase-to-creatinine concentration ratio, iohexol plasma clearance, and indirect blood pressure measurement twice before treatment. Dogs received tepoxalin (10 mg/kg, PO, q 24 h) for 28 days (acute phase; n = 16) and an additional 6 months (chronic phase; 10). Recheck examinations were performed weekly (acute phase) and at 1, 3, and 6 months (chronic phase). Kidney function variables were analyzed via repeated-measures ANOVA. Results-There was no difference over time for any variables in dogs completing both phases of the study. Adverse drug events (ADEs) resulting in discontinuation of tepoxalin administration included increased serum creatinine concentration (1 dog; week 1), collapse (1 dog; week 1), increased liver enzyme activities (1 dog; week 4), vomiting and diarrhea (1 dog; week 8), hematochezia (1 dog; week 24), and gastrointestinal ulceration or perforation (1 dog; week 26). Preexisting medical conditions and concomitant drug use may have contributed to ADEs. Kidney function was not affected in the latter 5 dogs. Discontinuation of tepoxalin administration stabilized kidney function in the former dog and resolved the ADEs in 4 of the 5 latter dogs. Conclusions and Clinical Relevance-Tepoxalin may be used, with appropriate monitoring, in dogs with International Renal Interest Society stage 2 or 3 CKD and osteoarthritis.

Objective—To determine the Helicobacter spp present in the oral cavity of dogs and the relationship of those organisms with gastric Helicobacter spp to better define the potential for dog-human and dog-dog transmission. Sample—Saliva and dental plaque from 28 dogs and gastric biopsy specimens from a subset of 8 dogs. Procedures—PCR-based screening for Helicobacter spp was conducted on samples obtained from the oral cavity of 28 dogs. Comparative analysis was conducted on Helicobacteraceae 16S rDNA clone libraries from the oral cavity and stomach of a subset of 8 dogs (5 vomiting and 3 healthy) that had positive PCR results for Helicobacter spp. Results—Helicobacteraceae DNA was identified in the oral cavity of 24 of 28 dogs. Analysis of cloned 16S rDNA amplicons from 8 dogs revealed that Wolinella spp was the most common (8/8 dogs) and abundant (52/57 [91%] clones) member of the Helicobacteraceae family in the oral cavity. Only 2 of 8 dogs harbored Helicobacter spp in the oral cavity, and 1 of those was coinfected with Helicobacter heilmannii and Helicobacter felis in samples obtained from the stomach and saliva. Evaluation of oral cavity DNA with Wolinella-specific PCR primers yielded positive results for 16 of 20 other dogs (24/28 samples were positive for Wolinella spp). Conclusions and Clinical Relevance—Wolinella spp rather than Helicobacter spp were the predominant Helicobacteraceae in the oral cavity of dogs. The oral cavity of dogs was apparently not a zoonotically important reservoir of Helicobacter spp that were non–Helicobacter pylori organisms.

Four healthy cats were given clindamycin orally in daily doses of 25 or 50 mg/kg of body weight for 6 weeks. Significant change in Factor-VII activity was not found, compared with pretreatment values. In 2 cats tested, toxin produced by Clostridium difficile was not detected in fecal samples obtained before treatment and at 6 weeks after treatment, suggesting that intestinal overgrowth by C difficile did not develop. Results of the study seemed to indicate that orally administered clindamycin does not measurably reduce synthesis of vitamin K-dependent clotting factors in healthy cats.

A comprehensive study was conducted on the clinical observationsincluding clinical history, physical examination along with haematobiochemical alteration on 41 naturally occurring cases of canine babesiosis from Punjab state, India. Examination of 964 dogs revealed 4.25 percent (41/964) prevalence of the disease including 3.84 percent (37) B. gibsoni and 0.41 percent (4) B. canis infected cases. Clinical and parasitological diagnosis was finally confirmed by polymerase chain reaction. A large variation of clinical anifestations including rare findings of paraplegia, blindness, ocular bleeding, immune mediated haemolytic anaemia (IMHA), ascites and skin lesions were observed among the affected animals. Bloodfilms showed anisocytosis and nucleated erythrocytes indicating regenerative anaemia. Blood parameters of the affected dogs revealed significant decrease in Hb, TEC, PCV and thrombocytes. Significantdecrease in lymphocytes was found in B. gibsoni affected animals. The affected dogs showed significant increase in serum bilirubin, ALT, AKP, BUN and creatinine. Haemato-biochemical observations wereindicative of severity of babesiosis in dogs.

The objective of this study was to investigate the effects of intravenous alfaxalone with and without premedication on intraocular pressure (IOP) in healthy dogs. Thirty-three dogs were randomized to receive 1 of 3 treatments: acepromazine [0.03 mg/kg body weight (BW)] with butorphanol (0.2 mg/kg BW) intramuscularly (IM), followed by intravenous (IV) alfaxalone (1.5 mg/kg BW); dexmedetomidine (0.002 mg/kg BW) with hydromorphone (0.1 mg/kg BW) IM, followed by alfaxalone (1 mg/kg BW) IV; and saline 0.9% (0.02 mL/kg BW) IM, followed by alfaxalone (3 mg/kg BW) IV. Intraocular pressure (IOP) was measured at baseline, 15 min, and 30 min after premedication, after pre-oxygenation, after administration of alfaxalone, and after intubation. After induction and after intubation, the IOP was significantly increased in all groups compared to baseline. While premedication with acepromazine/butorphanol or dexmedetomidine/hydromorphone did not cause a significant increase in IOP, the risk of vomiting and the associated peak in IOP after dexmedetomidine/hydromorphone should be considered when selecting an anesthetic protocol for dogs with poor tolerance for transient increases in IOP.