Inclusion-body hepatitis in day-old turkeys

Inclusion-body hepatitis was diagnosed in 1-day-old turkeys experiencing above-average mortality. At necropsy, turkeys appeared anemic and had pale yellow livers. Histopathologic examination of affected livers revealed diffuse hepatic degeneration and multifocal necrosis, with approximately 70% of the hepatocytes containing large, basophilic, intranuclear inclusion bodies. An adenovirus was isolated from affected livers and identified as a group I avian adenovirus by indirect immunofluorescence.     

Endometrial nitric oxide production and nitric oxide synthases in the equine endometrium: Relationship with microvascular density during the estrous cycle

Nitric oxide (NO) plays an important role in angiogenesis and in the regulation of the blood flow. This study was carried out to investigate (i) the effects of endogenous estrogens and progestins and exogenous progesterone (P₄) (5 ng/ml or 1 μg/ml) or estradiol 17β (E₂β) (50 pg/ml or 1 μg/ml) on in vitro endometrial NO synthesis; (ii) the presence of different isoforms of NO synthase; (iii) and their relationship to microvascular density in the equine endometrium during the estrous cycle. NOS expression was also evaluated in the myometrium. Expression of endothelial and inducible forms of NOS in the uterus was assessed by Western blot and immunocytochemistry. Vascular density in endometrial tissue was determined on histologic sections. In the luteal phase, compared to the follicular phase, endometrial NO production increased without exogenous hormones and with exogenous E₂β (1 μg/ml). Although immunocytochemistry revealed iNOS and eNOS expression in the endometrium, no positive signal for iNOS was detected by Western blot. Endothelial NOS was observed in endometrial glands, endothelial cells, fibroblasts, blood and lymphatic vessels. Endometrial eNOS expression was the highest in the follicular and mid-luteal phases while it was found to be the lowest in the early luteal phase. In the follicular phase, hyperplasia of endometrial tissue with respect to myometrium was detected. No difference in vascular density was present between phases. All together, NO may play some roles in both proliferative and secretory phases of endometrial development in the mare.     

Effects of treatment with omeprazole or ranitidine on gastric squamous ulceration in racing Thoroughbreds

OBJECTIVE: To compare the effects of oral administration of omeprazole and ranitidine on gastric squamous ulceration in Thoroughbreds in race training. DESIGN: Modified crossover study. ANIMALS: 60 Thoroughbreds in race training with gastric squamous mucosal ulceration. PROCEDURE: Horses were randomly allocated into 3 groups. Group 1 received no treatment for 28 days followed by administration of omeprazole (4 mg/kg [1.8 mg/lb], PO, once daily) for 28 days; group 2 received omeprazole (4 mg/kg, PO, once daily) for 28 days followed by no treatment for 28 days; and group 3 received ranitidine (6.6 mg/kg [3.0 mg/lb], PO, q 8 h) for 28 days followed by administration of omeprazole (4 mg/kg, PO, once daily) for 28 days. Ulceration was assessed endoscopically at days 0, 28, 42, and 56. Lesions were scored from 0 (no ulceration) to 3 (severe ulceration). RESULTS: After the initial 28 days of treatment, the decrease in ulcer severity was significantly greater after omeprazole treatment than after ranitidine treatment. Ulcer severity decreased significantly in group 3 horses after 14 days of treatment with omeprazole. Discontinuation of omeprazole resulted in worsening of ulcer scores; however, ulcer scores at completion of the study were less than at day 0. Horses that received omeprazole after 28 days of ranitidine treatment had a further reduction in ulcer severity. CONCLUSIONS AND CLINICAL RELEVANCE: Omeprazole was more effective than ranitidine in healing gastric squamous ulcers in Thoroughbreds in race training. Improvement was detected by 14 days and persisted in most of the group 2 horses for at least 28 days after omeprazole treatment was discontinued.     

Molecular characterization of canine coronavirus strains circulating in Brazil

To characterize canine coronavirus (CCoV) circulating in diarrheic puppies in Brazil, 250 fecal samples collected between 2006 and 2012 were tested. By using RT-PCR to partially amplify the M gene, CCoV RNA was detected in 30 samples. Sequence analysis of the M protein grouped eight strains with CCoV-I and another 19 with CCoV-II prototypes. To genotype/subtype the CCoV strains and assess the occurrence of single or multiple CCoV infections, RT-PCR of the S gene was performed, and 25/30 CCoV-positive strains amplified with one or two primer pairs. For 17/25 samples, single infections were detected as follows: six CCoV-I, nine CCoV-IIa and two CCoV-IIb. Eight samples were positive for more than one genotype/subtype as follows: seven CCoV-I/IIa and one CCoV-I/IIb. Sequence analysis revealed that the CCoV-I and IIa strains shared high genetic similarity to each other and to the prototypes. The Brazilian strains of CCoV-IIb displayed an aminoacid insertion that was also described in CCoV-IIb-UCD-1 and TGEV strains. Among the 25 CCoV-positive puppies, five had a fatal outcome, all but one of which were cases of mixed infection. The current study is the first reported molecular characterization of CCoV-I, IIa and IIb strains in Brazil.     

Genetic background of CTX‐M‐15‐producing Enterobacter hormaechei ST114 and Citrobacter freundii ST265 co‐infecting a free‐living green turtle (Chelonia mydas)

CTX‐M‐type extended‐spectrum β‐lactamase (ESBL)‐producing Enterobacteriaceae have become identified in marine ecosystem constituting a serious ecological issue. In this respect, although contamination of coastal waters and seafood, and even colonization of seabirds and fishes have been increasingly reported, molecular data are lacking to elucidate the clinical impact of ESBL producers in infected marine animals. In this study, using a genomic approach, we have analysed the genetic background of CTX‐M‐15‐producing Enterobacter hormaechei (belonging to the international human clone ST114) and Citrobacter freundii (ST265) co‐infecting a free‐living green turtle (Chelonia mydas) suffering from septic arthritis, which progressed to generalized coelomitis and death. Wide resistome of these pathogens contributed to treatment failure and death of the animal.