Journal of Veterinary Diagnostic Investigation最新文献

Bovine botulism is a lethal disease caused by Clostridium botulinum neurotoxins (BoNT). In cattle, the most frequent form of this disease in several South American countries and elsewhere is caused by BoNT type D, which has been associated with phosphorus deficiency, leading to pica and osteophagy. An outbreak of botulism occurred in a fully vaccinated 600-steer herd of cattle. The cattle were grazing on native pasture in a paddock in which several decomposing animal carcasses were found; the animals had performed osteophagy. The first 2 deaths were recorded in November 2016, and the number of fatalities increased to 84 through April of 2017. All the cases had similar clinical signs, which were consistent with botulism. The affected animals had hypophosphatemia and rear-leg weakness, ataxia, progressive flaccid paralysis of several muscles, recumbency, and death. Autopsies were performed on 3 animals; gross findings included hydropericardium, congestion of the cerebellum, and bone fragments and stones in the rumen and reticulum. Botulism was confirmed in the 3 animals by detecting BoNT type D by mouse bioassay. A large outbreak of botulism in vaccinated cattle associated with phosphorus deficiency and osteophagy has not been reported previously in Argentina, to our knowledge. Our case demonstrates that, even in vaccinated herds, rigorous carcass management is essential to reduce the risk of environmental contamination and to prevent fatal botulism outbreaks, especially in phosphorus-deficient areas. Improved reporting of similar cases is vital to refine prevention strategies and reduce the economic impact of the disease.

A 12-y-old, 654-kg, Santa Gertrudis cow was presented to the veterinary hospital with acute abdominal distension and a large mass on the left side of the neck. Upon presentation, the patient was bright and alert, with a corticosteroid stress leukogram, hyperglycemia, and mildly increased blood urea nitrogen and creatine kinase activity. A firm, 15 x 10-cm, non-painful left-sided proximal cervical mass and ruminal tympany were appreciable. A fine-needle aspirate of the mass was performed, and cytological findings were consistent with a neuroendocrine neoplasm. Given the large size of the mass and poor prognosis, the owner elected euthanasia. At autopsy, a firm 15 x 12 x 8-cm mass effaced the left lobe of the thyroid gland. Histological examination confirmed a thyroid follicular-compact carcinoma with metastasis to the deep cervical lymph nodes. Neoplastic cells showed immunolabeling for thyroglobulin, 10% of the neoplastic cells exhibited immunolabeling for thyroid transcription factor 1 (TTF1), and none of the neoplastic cells showed immunolabeling for synaptophysin. Although the cytological features were typical of neuroendocrine neoplasia, immunohistochemistry excluded a thyroid medullary neoplasm. Unlike C-cell and ultimobranchial neoplasms, thyroid follicular carcinomas are rarely reported in cattle. The thyroid follicular-compact carcinoma described herein was associated with acute tympany.

Disorders of the intestinal vasculature in animals include arteriovenous malformations, telangiectasia (ectasia, angiodysplasia), hamartomas, and neoplasia (hemangiomas, hemangiosarcomas). Two, 2-d-old, female Nigerian dwarf goat kids born to different dams on the same farm had severe and progressive abdominal distension and were euthanized. The autopsies revealed segmental circumferential dark-red areas that caused focal constriction of the mid-jejunum. The constriction led to obstruction of the intestinal lumen and proximal dilation of the jejunum and duodenum in both cases. Clostridium perfringens type D enterotoxemia was also diagnosed in one case. Histologic examination in both cases revealed a focal, moderately well-demarcated proliferation of medium- to small-caliber vascular channels with luminal erythrocytes, lined by morphologically normal endothelial cells, that expanded the tunica muscularis and serosa of the jejunum and compressed the mucosa and the lumen. The congenital nature of these lesions favors a diagnosis of vascular hamartomas; however, the histologic findings were indistinguishable from those of intestinal hemangiomas reported in young humans, horses, a pig, and a dog. The age of the affected goats, the location of the lesions in the same segment of the jejunum, and the presence of only one buck on the farm were suggestive of a genetic origin for these lesions. It is speculated that intestinal obstruction was the predisposing factor for C. perfringens type D enterotoxemia in one of the goats.

Bovine interstitial and bronchointerstitial pneumonias are common and important diseases of cattle, caused by several infectious and non-infectious causes. Here, we review the roles of bovine respiratory syncytial virus, bovine parainfluenza virus 3, bovine alphaherpesvirus 1, bovine viral diarrhea virus, bovine coronavirus, influenza D virus, malignant catarrhal fever virus, and bovine adenovirus in interstitial or bronchointerstitial pneumonia. We describe the possible causes, pathogenesis, and diagnosis of bacterial septicemias that result in interstitial pneumonia, including E. coli, Salmonella, and Pasteurella multocida septicemias. We also review the parasitic causes of interstitial or bronchointerstitial pneumonia, primarily Dictyocaulus viviparus. Reaching a definitive postmortem etiologic diagnosis of interstitial or bronchointerstitial pneumonia can be challenging because infectious and non-infectious causes may look very similar grossly. Moreover, other conditions-that do not cause interstitial or bronchointerstitial pneumonia but rather pulmonary edema, congestion, and hemorrhage-can resemble interstitial pneumonia grossly. To guide the process of diagnosing interstitial and bronchointerstitial pneumonia, we offer an algorithm that integrates findings obtained from postmortem examination and ancillary laboratory testing. Our algorithm includes details on the gross characteristics of the lungs with interstitial or bronchointerstitial pneumonia, and we discuss other disease processes that may grossly resemble interstitial pneumonia. We highlight the key histologic features for differentiating specific causes and describe the most common ancillary laboratory tests to detect infectious and non-infectious causes.

Interstitial lung disease refers to lesions involving primarily any of the 3 layers of the alveolar wall (endothelium, basement membrane, alveolar epithelium) and the contiguous bronchiolar interstitium. Toxic agents are a significant cause of interstitial lung disease in cattle, primarily interstitial pneumonia. We review the most important substances associated with interstitial lung disease in cattle, addressing their epidemiology, clinical signs, pathogenesis, and lesions. These include the amino acid L-tryptophan (ingested with lush green forages), the toxin 4-ipomeanol (produced by moldy sweet potatoes infected with Fusarium solani), toxic plants such as Perilla frutescens and Zieria arborescens, and nitrogen dioxide (NO₂) released from recently filled silos. The diagnosis of these disorders may be challenging because the clinical signs and lung lesions often overlap regardless of the cause. Thus, a definitive diagnosis typically relies on a thorough epidemiologic investigation and confirmation of exposure of affected cattle to the potential cause. Laboratory confirmation of specific toxins is often limited because many are rapidly metabolized and unstable after ingestion, making their detection difficult.

Monocytes are key cells of the immune system; various cell subsets have distinct phenotypic characteristics and functions. We characterized canine monocyte subsets in different hematologic disorders by analyzing peripheral blood cells for their expression of CD14 and major histocompatibility complex class II (MHCII). Flow cytometry data of canine blood samples were evaluated retrospectively. We assigned 132 total cases to one of the following categories: healthy, inflammatory, T-zone lymphoma/leukemia (TZL), T-cell chronic lymphocytic leukemia (CLL), B-cell CLL, T-cell stage V lymphoma (SVL), B-cell SVL, acute lymphoblastic or undifferentiated leukemia (ALL/AUL), or acute myeloid leukemia (AML). We analyzed age, sex, breed, light scatter properties, WBC count, CD14^pos cells, CD14^posMHCII^pos cells, CD14^posMHCII^neg cells, and the CD14^posMHCII^pos/CD14^posMHCII^neg ratio. All groups were compared with the healthy group. In healthy dogs, CD14^posMHCII^pos cells were larger and had a more complex internal structure than CD14^posMHCII^neg cells. Absolute numbers of CD14^posMHCII^neg cells were significantly increased in all groups except the TZL and B-cell SVL groups. Absolute numbers of CD14^posMHCII^pos cells were significantly increased in the T-cell CLL, B-cell CLL, and T-cell SVL groups, mildly increased in the inflammatory and TZL groups, and decreased in the ALL/AUL group. The CD14^posMHCII^pos/CD14^posMHCII^neg ratio was markedly decreased in both acute leukemia groups, being <1 in all cases and usually close to 0. We found significant changes in canine monocyte subsets in different hematologic conditions. To our knowledge, a decreased CD14^posMHCII^pos/CD14^posMHCII^neg ratio has not been identified previously as a hallmark of acute leukemia in dogs.

In domestic species, the characterization and categorization of interstitial pneumonias have been limited, and non-infectious causes of such diseases are reported infrequently. A 6-y-old, castrated male French Bulldog with a history of brachycephalic obstructive airway syndrome and chronic regurgitation was evaluated because of respiratory distress. The dog was diagnosed antemortem with a heart-base mass and right-sided congestive heart failure via trans-thoracic echocardiography; euthanasia was elected, followed by postmortem examination. Gross findings included a large heart-base mass and diffusely dark-purple, firm, and heavy lungs, with the greatest severity in the caudal lung lobes. Histology findings confirmed that the heart mass was a chemodectoma. Lung was consolidated by organizing fibrin aggregates in alveoli, as well as organizing polypoid aggregates of fibrin and/or variably mature connective tissue partially or completely filling and obscuring bronchioles and alveolar ducts, findings consistent with acute fibrinous and organizing pneumonia (AFOP). AFOP, a debilitating condition with a wide variety of underlying causes, has features similar to, yet distinct from, other interstitial lung diseases, including diffuse alveolar damage and organizing pneumonia. AFOP is rarely and only recently reported in humans, and, to our knowledge, has not been reported previously in a dog.

Junctional epidermolysis bullosa (JEB) is a congenital blistering skin disorder with clefting within the lamina lucida of the basement membrane zone. We describe the clinical and morphologic features of JEB in a 4-mo-old domestic shorthair kitten and identify the underlying genetic variant. The kitten was presented with blistering lesions affecting friction-prone areas of haired skin, mucocutaneous junctions, and oral mucosa. Histopathology revealed extensive subepidermal cleft formation in affected tissues. Periodic acid-Schiff (PAS) staining showed a thin, PAS-positive line along the dermal side of the cleft, consistent with retention of the lamina densa. Transmission electron microscopy confirmed separation at the level of the lamina lucida with intact basal keratinocytes. Whole genome sequencing identified a homozygous 2-bp deletion in exon 7 of COL17A1, predicted to result in loss of function and disrupted binding domains. Our findings support a diagnosis of JEB associated with a novel COL17A1 variant.

Ovine pulmonary adenocarcinoma (OPA), caused by Jaagsiekte sheep retrovirus (JSRV; family Retroviridae, taxon species Betaretrovirus ovijaa), is a viral oncogenic lung disease in sheep. Its metastatic potential remains under-evaluated. We investigated macrometastases (MACs), micrometastases (MICs), and isolated tumor cells (ITCs) in regional draining lymph nodes (DLNs) using histopathology and immunohistochemistry (IHC). Samples from 41 lung tumors and their regional DLNs were obtained from slaughtered Țurcană sheep. Histologically, all cases were diagnosed as OPAs. The classical or mixed OPA was observed in 37 of 41 (90%) cases; the remaining tumors were the atypical form. In 10 cases, myxoid growths were also detected. For IHC, anti-multicytokeratin, thyroid transcription factor 1, and JSRV antibodies were used to detect metastatic cells within DLNs. Neoplastic cells were identified in 16 of 41 (39%) DLNs, including 2 MAC, 7 MIC, and 7 ITC cases. Lung tumors >7 cm were significantly associated with lymph node metastasis (p < 0.05). A random forest model incorporating tumor volume, necrosis, mitotic count, and Ki67 index achieved the best performance (AUC = 0.70; accuracy = 62.5%; F1 = 0.57) for metastasis prediction. A benign epithelial inclusion was found within a DLN in one case, which has not been reported previously, to our knowledge. We found that OPA has a higher metastatic potential than previously recognized, particularly in larger tumors. Multivariate analysis, including additional tumor markers, likely would improve metastasis prediction. Our findings advance our understanding of OPA progression and its relevance as a comparative model for human lung adenocarcinoma.

Interstitial lung diseases of sheep and goats, which are caused by a range of infectious, parasitic, and toxic agents, have substantial negative health and welfare impacts globally. Within this category of pulmonary disease, entities such as peste des petits ruminants (PPR) can undermine the livelihood of farming communities in sub-Saharan Africa and Southeast Asia; enzootic pneumonia, maedi, and ovine pulmonary adenocarcinoma compromise the productivity of farm enterprises where sheep are housed for prolonged periods. I detail the pathogenesis and lesions caused by a range of viral, bacterial, parasitic, and toxic agents that target the pulmonary interstitium in small ruminants, ultimately resulting in parenchymal damage and clinical disease. These lesions range from the progressive distortion of alveolar walls by infiltrating lymphocytes and macrophages following small ruminant lentiviral infection, to the acute impact of alveolar septal thromboembolism in Bibersteinia trehalosi infection, and eosinophil-mediated necrosis of alveolar walls triggered during the migratory larval stages of parasitism by Dictyocaulus filaria. In addition, I review the pathologic impact of neoplastic type II pneumocytes extending over the interstitial scaffold in cases of sheep pulmonary adenocarcinoma (jaagsiekte) and the toxic injury induced by plants (Trema and Crotalaria sp.) and other toxins (carbolic dips, 3-methyl indole) on the pulmonary interstitium.