Asli Mete

Evaluation of the efficacy and safety of single administration of 4.7-mg deslorelin acetate implants on egg production and plasma sex hormones in Japanese quail (Coturnix coturnix japonica)

OBJECTIVE To evaluate the effects of 4.7-mg deslorelin acetate implants on egg production and plasma concentrations of 17β-estradiol and androstenedione in Japanese quail (Coturnix coturnix japonica) over 180 days and assess safety of the implants in quail via gross and histologic examination. ANIMALS 20 female Japanese quail. PROCEDURES Following a 7-day period of consistent egg laying, quail were anesthetized and received a 4.7-mg deslorelin implant (treatment group; n = 10) or identical placebo implant (control group; 10) SC between the scapulae. Egg production was monitored daily. Plasma concentrations of 17β-estradiol and androstenedione were measured on days 0 (immediately prior to implant injection), 14, 29, 62, 90, 120, 150, and 180 via radioimmunoassay. Birds were weighed periodically and euthanized at day 180 for complete necropsy. RESULTS Egg production was significantly decreased in the treatment group, compared with the control group, from 2 to 12 weeks after implant injection. Egg production ceased in 6 of 10 quail in the treatment group (mean duration of cessation, 70 days). Plasma androstenedione and 17β　-estradiol concentrations were significantly lower on day 29 in the treatment group than in the control group. On day 180, 17β　-estradiol concentration was lower in control than in treated birds.No clinically relevant lesions were detected in either group at necropsy [corrected]. CONCLUSIONS AND CLINICAL RELEVANCE 4.7-mg deslorelin acetate implants reversibly decreased egg laying for approximately 70 days in most of the Japanese quail evaluated. Further studies evaluating implants containing different concentrations of the drug are needed in quail and other avian species.

Disease Associated with Equine Coronavirus Infection and High Case Fatality Rate

Background Equine coronavirus (ECoV) is associated with clinical disease in adult horses. Outbreaks are associated with a low case fatality rate and a small number of animals with signs of encephalopathic disease are described. Objectives The aim of this study is to describe the epidemiological and clinical features of two outbreaks of ECoV infection that were associated with an high case fatality rate. Animals 14 miniature horses and 1 miniature donkey testing fecal positive for ECoV from two related disease outbreaks. Methods Retrospective study describing the epidemiological findings, clinicopathological findings, and fecal viral load from affected horses. Results In EcoV positive horses, 27% (4/15) of the animals died or were euthanized. Severe hyperammonemia (677 μmol/L, reference range ≤60 μmol/L) was identified in one animal with signs of encephalopathic disease that subsequently died. Fecal viral load (ECoV genome equivalents per gram of feces) was significantly higher in the nonsurvivors compared to animals that survived (P = .02). Conclusions and Clinical Importance Equine coronavirus had a higher case fatality rate in this group of miniature horses than previously reported in other outbreaks of varying breeds. Hyperammonemia could contribute to signs of encephalopathic disease, and the fecal viral load might be of prognostic value in affected horses.

Necrotizing Enteritis and Hyperammonemic Encephalopathy Associated With Equine Coronavirus Infection in Equids

Equine coronavirus (ECoV) is a Betacoronavirus recently associated clinically and epidemiologically with emerging outbreaks of pyrogenic, enteric, and/or neurologic disease in horses in the United States, Japan, and Europe. We describe the pathologic, immunohistochemical, ultrastructural, and molecular findings in 2 horses and 1 donkey that succumbed to natural infection with ECoV. One horse and the donkey (case Nos. 1, 3) had severe diffuse necrotizing enteritis with marked villous attenuation, epithelial cell necrosis at the tips of the villi, neutrophilic and fibrinous extravasation into the small intestinal lumen (pseudomembrane formation), as well as crypt necrosis, microthrombosis, and hemorrhage. The other horse (case No. 2) had hyperammonemic encephalopathy with Alzheimer type II astrocytosis throughout the cerebral cortex. ECoV was detected by quantitative polymerase chain reaction in small intestinal tissue, contents, and/or feces, and coronavirus antigen was detected by immunohistochemistry in the small intestine in all cases. Coronavirus-like particles characterized by spherical, moderately electron lucent, enveloped virions with distinct peplomer-like structures projecting from the surface were detected by negatively stained transmission electron microscopy in small intestine in case No. 1, and transmission electron microscopy of fixed small intestinal tissue from the same case revealed similar 85- to 100-nm intracytoplasmic particles located in vacuoles and free in the cytoplasm of unidentified (presumably epithelial) cells. Sequence comparison showed 97.9% to 99.0% sequence identity with the ECoV-NC99 and Tokachi09 strains. All together, these results indicate that ECoV is associated with necrotizing enteritis and hyperammonemic encephalopathy in equids.

Causes of Mortality in Backyard Chickens in Northern California: 2007–2011

SUMMARY A 5-yr retrospective study was conducted to characterize the spectrum of diseases causing mortality in 1301 backyard chickens submitted to the California Animal Health and Food Safety laboratory in Davis, California. Infectious diseases were diagnosed in the majority (60.4%). Viral diseases comprised 50% of the infectious entities, followed by bacterial diseases with an incidence of 39%. Mareks disease in the viral group and Escherichia coli in the bacterial group were the most commonly diagnosed infectious diseases. Zoonotic agents including Aspergillus sp., Salmonella sp., Listeria sp., Mycobacterium sp., Candida sp., and Baylisascaris sp. were detected in 46 (3.5%) birds. Among noninfectious conditions, fatty liver hemorrhagic syndrome and reproductive tract adenocarcinoma were the leading causes of mortality. This analysis provides an overview of backyard chicken diseases for practitioners and avian pathologists working with backyard poultry. In addition, this study illustrates that backyard chickens do not seem to pose a major risk to public health, although zoonoses do comprise a notable portion (5.9% of all infectious cases) of isolated agents. RESUMEN Reporte de Caso—Causas de mortalidad en aves de traspatio en el norte de California entre los años 2007 al 2011. Se llevó a cabo un estudio retrospectivo de 5 años para caracterizar el espectro de enfermedades que causaron mortalidad en 1301 aves de traspatio enviadas al Laboratorio de Salud Animal e Inocuidad de los Alimentos de California, en Davis. En su mayoría se diagnosticaron enfermedades infecciosas (60.4%). Las enfermedades virales comprendieron 50% de las entidades infecciosas, seguido por enfermedades bacterianas, con una incidencia de 39%. La enfermedad de Marek en el grupo viral y Escherichia coli en el grupo de las enfermedades bacterianas fueron las enfermedades infecciosas más comúnmente diagnosticadas. Agentes zoonóticos como Aspergillus sp., Salmonella sp., Listeria sp., Mycobacterium sp., Candida sp., y Baylisascaris sp. se detectaron en 46 (3.5%) de las aves. Entre las condiciones no infecciosas, el síndrome del hígado graso y hemorrágico y el adenocarcinoma del tracto reproductivo fueron las principales causas de mortalidad. Este análisis proporciona una visión general de las enfermedades de pollo de traspatio para los profesionales y los patólogos que trabajan con aves de traspatio. Además, este estudio pone de manifiesto que los pollos de traspatio no parecen plantear un riesgo para la salud pública, a pesar de que las enfermedades zoonóticas las zoonosis comprenden una parte notable (5.9% de todos los casos infecciosos) de los agentes aislados.

Fatty Liver Hemorrhagic Syndrome in the Backyard Chicken: A Retrospective Histopathologic Case Series

Fatty liver hemorrhagic syndrome, characterized by sudden death in overconditioned hens due to hepatic rupture and hemorrhage, is one of the leading noninfectious idiopathic causes of mortality in backyard chickens. Nutritional, genetic, environmental, and hormonal factors, or combinations of these, have been proposed yet not proven as the underlying cause. In an attempt to characterize the hepatic changes leading to the syndrome, this retrospective case study examined 76 backyard chickens that were diagnosed with fatty liver hemorrhagic syndrome between January 2007 and September 2012 and presented for necropsy to the diagnostic laboratory of the California Animal Health and Food Safety Laboratory System. A majority of the birds were female (99%), obese (97.5%), and in active lay (69.7%). Livers were examined histologically, and the degree of hepatocellular vacuolation (lipidosis), the reticular stromal architecture, the presence of collagenous connective tissue, and vascular wall changes were evaluated and graded using hematoxylin and eosin, Gomori’s reticulin, oil red O, Masson’s trichrome, and Verhoeff-Van Gieson stains. Interestingly, there was no correlation between lipidosis and reticulin grades; hepatocellular lipidosis was absent in 22% of the cases and mild in 26% of the cases. Additionally, there was evidence of repeated bouts of intraparenchymal hemorrhage before the acute “bleed-out” in 35.5% of the cases. These data are not supportive of the previously proposed causes and provide a framework for future studies to elucidate the pathogenesis of this condition. Furthermore, the data shown in this study support hemorrhagic liver syndrome as a more accurate name, as hepatic lipidosis is absent in a significant proportion of ruptured livers.

Public health implications of lead poisoning in backyard chickens and cattle: four cases

Abstract Lead intoxication in livestock has historically been associated with cattle turned out to pasture and accidental ingestion of lead from drinking crankcase oil, licking grease from machinery, chewing on plumbing or batteries, or drinking water contaminated from leaching materials. Even with the decrease in manufactured items produced with lead, contaminants persist in the landscape and may enter the food supply through animal products. Changing patterns of open range herds moving to new pasture and the increased popularity of urban/suburban backyard chickens or other livestock necessitates public awareness about the clinical signs of lead intoxication, the potential for subclinical animals, public health concerns, particularly for exposure in children, and testing options available. Cases of lead intoxication in livestock demand a thorough case work-up to identify all sources of lead, address subclinical cases, evaluate risk to consumers, and make management suggestions for future prevention. We discuss four recent cases of confirmed lead poisoning in backyard chickens and open range cattle and assess the public health implications therein. Taken as a whole and considering the potential of the remaining herd or flock to be affected without necessarily showing signs, public health officials and veterinarians should be prepared to advise clients on case work-up and management and prevention considerations. Backyard chickens and cattle may not present for suspected lead poisoning as in several of the cases discussed herein yet may still contain concerning tissue or blood levels. The authors believe increased surveillance through heavy metal screens is crucial to adequately protect public health.

The pathology of enterotoxemia by Clostridium perfringens type C in calves.

The pathology of Clostridium perfringens type C infection has been described with detail only in foals and piglets. The current report describes the diagnostic workup and detailed pathology of 3 cases of C. perfringens type C infection in calves. A 2-day-old Jersey calf and fresh and fixed tissues from a 4-week-old Angus calf and from a 1-week-old Jersey calf were received at the California Animal Health and Food Safety Laboratory System with a history of digestive disease and death. The gross changes in the gastrointestinal tract of 1 calf consisted of multifocal subserosal hemorrhages of the rumen, diffuse congestion and multifocal hemorrhages of the small intestinal mucosa, and dilated cecum with bloody liquid contents. In a second calf, a large segment of small intestine was hemorrhagic. The small intestine of the third calf was dilated and filled with abundant yellow fluid content. Microscopically, all 3 calves had diffuse coagulation necrosis of the intestinal mucosa. Clostridium perfringens type A was isolated from the intestinal content of 2 calves. In addition, enzyme-linked immunosorbent assay for Bovine rotavirus was positive on colonic content of 1 calf. Small numbers of cryptosporidia were seen in smears of colonic content of 2 calves, and Salmonella sp. group E was detected in the small intestinal content of another calf. Clostridium perfringens beta toxin was detected in the intestinal content of the 3 animals. A diagnosis of C. perfringens type C infection was confirmed based on pathological findings and detection of beta toxin in the intestinal content of the 3 animals.

Clostridium piliforme encephalitis in a weaver bird (ploceus castaneiceps)

A juvenile Taveta golden weaver (Ploceus castaneiceps) bird housed in a zoo aviary developed a sudden onset of neurological signs. The bird demonstrated head tilt, rolling onto its back, and inability to perch. Euthanasia was elected due to lack of response to intensive care, and a necropsy was performed. There were no significant abnormal findings on gross examination. On histopathology, the remarkable findings were localized to the brain and consisted of multifocal cerebral microabscesses and rarefaction. Filamentous rod-shaped bacteria were present within and at the periphery of the necrotic foci, and dispersed throughout the neuroparenchyma and intracellularly in neurons. The bacteria were Gram negative, and Warthin–Starry stain demonstrated characteristic “hay stacking.” Real-time polymerase chain reaction analysis of the brain identified the agent as Clostridium piliforme. An additional microscopic finding was severe crypt enteritis; however, the bacteria were not observed in the intestinal sections.

Temporal and Geographic Clustering of Polyomavirus-Associated Olfactory Tumors in 10 Free-Ranging Raccoons (Procyon lotor)

Reports of primary nervous system tumors in wild raccoons are extremely rare. Olfactory tumors were diagnosed postmortem in 9 free-ranging raccoons from 4 contiguous counties in California and 1 raccoon from Oregon within a 26-month period between 2010 and 2012. We describe the geographic and temporal features of these 10 cases, including the laboratory diagnostic investigations and the neuropathologic, immunohistochemical, and ultrastructural characteristics of these tumors in the affected animals. All 9 raccoons from California were found within a localized geographic region of the San Francisco Bay Area (within a 44.13-km radius). The tight temporal and geographic clustering and consistent anatomic location in the olfactory system of tumor types not previously described in raccoons (malignant peripheral nerve sheath tumors and undifferentiated sarcomas) strongly suggest either a common cause or a precipitating factor leading to induction or potentiation of neuro-oncogenesis and so prompted an extensive diagnostic investigation to explore possible oncogenic infectious and/or toxic causes. By a consensus polymerase chain reaction strategy, a novel, recently reported polyomavirus called raccoon polyomavirus was identified in all 10 tumors but not in the normal brain tissue from the affected animals, suggesting that the virus might play a role in neuro-oncogenesis. In addition, expression of the viral protein T antigen was detected in all tumors containing the viral sequences. We discuss the potential role of raccoon polyomavirus as an oncogenic virus.

Diagnostic value of tissue monensin concentrations in horses following toxicosis

Two separate incidents of monensin exposure in horses resulting in toxicosis provided insight into the diagnostic value and interpretive criteria of various biological samples. In case 1, 25 horses broke into a shed and ingested feed that was supplemented with 800 g/ton (880 µg/g) of monensin. Within 48 hr, 1 horse had died, 2 developed cardiac arrhythmias, lethargy, and recumbency, and another was euthanized due to severe deterioration. Minimal histologic lesions were noted in the horse that died peracutely, while another showed characteristic lesions of acute cardiomyocyte degeneration and necrosis. Stomach content, heart, liver, urine, and serum revealed various detectable concentrations of monensin in clinically affected and unaffected horses with known exposure. In case 2, a pastured horse had access to a mineral mix containing 1,600 g/ton (1,760 µg/g) of monensin. Within 48 hr, the horse became symptomatic and was euthanized because of severe respiratory distress. Histologic cardiac lesions were minimal but detectable amounts of monensin were found in blood, heart, liver, and stomach contents. In both cases, monensin toxicosis was confirmed with toxicological analysis. These cases demonstrate an overall lack of correlation of monensin concentrations in various biological samples with clinical outcome. However, serum, urine, blood, liver, heart, and stomach content can be tested to confirm exposure. More importantly, the consistently higher concentrations found in heart tissue suggest this is the most useful diagnostic specimen for postmortem confirmation of toxicosis in horses especially in cases in which associated feed cannot be tested for monensin or in cases with no histologic lesions.