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Although tick infestation is a significant health problem in livestock, there are limited studies on the dermatopathological aspects of natural tick infestation in cattle. This study aimed to describe the gross and histologic aspects of cutaneous lesions caused by tick infestation in cattle. Thirteen cases were selected based on necropsy data from a 10-year retrospective study. Predispositions were observed in beef cattle (P =.049) and the Angus breed (P =.012), and lesions occurred mainly in the fall (P =.007). Gross lesions included hypotrichosis (13/13; 100%), scales (12/13; 92%), alopecia (11/13; 85%), ulcers (7/13; 54%), crusts (7/13; 54%), and erosions (2/13; 15%). These gross lesions were mainly located in the thorax (12/13; 92%), head (11/13; 85%), abdomen (10/13; 77%), neck (9/13; 69%), limbs (9/13; 69%), and perineum (9/13; 69%). Histologically, all cases had ticks adhered to the epidermis with erosions (13/13; 100%), ulcers (11/13; 85%), orthokeratotic hyperkeratosis (13/13; 100%), irregular acanthosis (13/13; 100%), intraepidermal pustules (13/13; 100%), crusts (10/13; 77%), and ballooning degeneration (4/13; 31%). In the dermis, just below the tick insertion site, there was coagulation necrosis, fibrin deposition, and inflammatory infiltrate composed of mixed cells (neutrophils, lymphocytes, plasma cells, macrophages, and few eosinophils) (9/13; 69%), neutrophils (3/13; 23%), or eosinophils (1/13; 8%). This study reinforces the different patterns of cutaneous lesions caused by tick infestation in cattle, which should be considered as a potential cause of dermatitis in this species. [ABSTRACT FROM AUTHOR]

Primary pulmonary neoplasms in cattle are rare. There are few studies on the pathological findings of these neoplasms in this species. This study aimed to describe the histological and immunohistochemical findings of primary and metastatic pulmonary carcinomas in cattle. We conducted a retrospective study of 19 cases of epithelial neoplasms with pulmonary involvement. Histologically, most of the neoplasms were classified as primary pulmonary neoplasms, including different adenocarcinoma subtypes (4/19, 21%) and adenosquamous carcinomas (3/19, 16%), followed by squamous cell carcinoma (6/19, 32%), metastatic uterine adenocarcinoma (4/19, 21%), metastatic hepatocellular carcinoma (1/19, 5%), and metastatic cholangiocarcinoma (1/19, 5%). By immunohistochemistry, all neoplasms were positive for pancytokeratin, and 4/19 (21%) were positive for vimentin. Primary pulmonary neoplasms had immunoreactivity for thyroid transcription factor-1 (6/7), while only 2 of these cases were positive for napsin A. All cases with squamous differentiation (9/9) had immunoreactivity for cytokeratin (CK) 5/6, while only 7 of these cases were positive for p40. CK20, CK7, and CK8/18 showed varied immunoreactivity in the primary and metastatic pulmonary carcinomas but were important markers to confirm the diagnosis of primary mucinous adenocarcinoma and metastatic cholangiocarcinoma. HepPar-1 was only positive in the metastatic hepatocellular carcinoma. The limited number of cases of metastatic uterine adenocarcinomas in this study precluded identification of a specific immunophenotype for this tumor. Immunohistochemistry proved to be an important tool to confirm the proper classification of these neoplasms. [ABSTRACT FROM AUTHOR]

Monensin poisoning is uncommon and has been rarely reported in birds. This work aimed to described clinical-pathological aspects of an outbreak of monensin poisoning in captive and free-ranging birds. Thirty-seven of 600 captive birds fed a diet containing 893.19 mg/kg of monensin died within 10 days (mortality 6.17%). There was no ionophore antibiotics on the feed label supplied to captive birds, which established an error in feed production. Necropsies were performed on twelve animals: Muscovy duck (Cairina moschata) (2/12), greater rhea (Rhea americana) (2/12), black-necked swan (Cygnus melancoryphus) (2/12), garganey (Anas querquedula) (1/12), ostrich (Struthio camelus) (1/12), and common pigeon (Columbus livia) (4/12). These four common pigeons were free-ranging birds and died after eating the same contaminated feed. Birds were mainly found dead, however in animals which clinical signs were observed (Columba livia, Rhea americana, Cairina moschata, Anas querquedula, and Struthio camelus), they included incoordination, inability to stand, and intense prostration, that ranged from 24 to 72 h until death. Grossly, five birds had focally extensive pale firm areas in the myocardium and two had in the skeletal muscles, one being concomitant lesions. Histologically, muscle necrosis and degeneration were observed in striated musculature (skeletal and/or heart) in all birds analyzed. Monensin poisoning outbreaks can affect free-ranging birds that are fed on external feeders, as well as captive birds, due to an error in the feed formulation. [ABSTRACT FROM AUTHOR]

Simple Summary: Chromium is a heavy metal often utilized in industrial applications in its hexavalent form, which is particularly toxic. It also serves as a trace mineral to organisms in its trivalent form. In humans, accidental or intentional ingestion of high amounts of hexavalent chromium leads to corrosive lesions in the gastrointestinal tract, potentially resulting in death due to extensive areas of necrosis and hemorrhage in the stomach and intestines. In a swine farm, pigs housed in bedding of pine wood shavings containing chromium died secondarily to ulcerative gastritis with subsequent perforation of the glandular stomach. This study marks the first description of natural acute oral chromium poisoning in animals. Heavy metal poisoning poses a challenge in diagnostic practices and environmental safety. This study describes the epidemiological, clinical, and pathological aspects of a chromium (Cr) poisoning outbreak in growing/finishing pigs housed in pens with bedding of pine wood shavings containing Cr. A visit to the affected farm was conducted. Epidemiological data were collected, and necropsy and histopathological examinations and heavy metal quantifications were performed. Up to 30% of the animals from the affected pens displayed clinical signs 48 h after housing, characterized by apathy, rigid gait, distended abdomen, pain to abdominal palpation, fever, vomiting, and skin cyanosis. The lethality rate reached 76.6%. Main postmortem findings consisted of ulcerative gastritis with perforation of the glandular stomach in all necropsied swine. Heavy metal analysis revealed a higher concentration of Cr in the bedding of the affected pens, along with elevated levels of Cr in the livers of the affected swine. Given that Cr is a known cause of poisoning in humans (with acute oral exposure resulting in corrosive lesions in the gastrointestinal tract), this study marks the first diagnosis of acute oral natural Cr poisoning in animals. This diagnosis was established through the association of epidemiological, pathological, and heavy metal quantification data. [ABSTRACT FROM AUTHOR]

This report describes 2 events of degenerative myelopathy in 4- to 27-day-old piglets, with mortality rates reaching 40%. Sows were fed rations containing low levels of pantothenic acid. Piglets presented with severe depression, weakness, ataxia, and paresis, which were more pronounced in the pelvic limbs. No significant gross lesions were observed. Histologically, there were degeneration and necrosis of neurons in the spinal cord, primarily in the thoracic nucleus in the thoracic and lumbar segments, and motor neurons in nucleus IX of the ventral horn in the cervical and lumbar intumescence. Minimal-to-moderate axonal and myelin degeneration was observed in the dorsal funiculus of the spinal cord and in the dorsal and ventral nerve roots. Immunohistochemistry demonstrated depletion of acetylcholine neurotransmitters in motor neurons and accumulation of neurofilaments in the perikaryon of neurons in the thoracic nucleus and motor neurons. Ultrastructurally, the thoracic nucleus neurons and motor neurons showed dissolution of Nissl granulation. The topographical distribution of the lesions indicates damage to the second-order neurons of the spinocerebellar tract, first-order axon cuneocerebellar tract, and dorsal column-medial lemniscus pathway as the cause of the conscious and unconscious proprioceptive deficit, and damage to the alpha motor neuron as the cause of the motor deficit. Clinical signs reversed and no new cases occurred after pantothenic acid levels were corrected in the ration, and piglets received parenteral administration of pantothenic acid. This study highlights the important and practical use of detailed neuropathological analysis to refine differential diagnosis. [ABSTRACT FROM AUTHOR]