兽研摘要
已知肉孢子虫属（Sarcocystis sp.）引起的疾病主要见于马，其中 S. neurona 是美洲马原虫性脊髓脑炎的主要病原体。虽然马是异常宿主，但易感物种范围包括海洋哺乳动物、浣熊和猫。犬临床疾病的报道罕见，在南美洲尚未见报道。本研究描述了巴西一例由肉孢子虫属自然发生的致死性犬脑膜脑脊髓炎和肌炎的临床、病理及免疫组化表现。一只5岁混种母犬表现为急性不能行走的四肢轻瘫、全身性肌肉萎缩和失明。尽管给予支持治疗，患犬病情恶化并被安乐死。大体检查发现淋巴结肿大、中度脾肿大和肝肿大，肝被膜有多灶性轻度纤维蛋白沉积，胰腺伴多灶性轻度出血。组织病理学显示严重的多灶性坏死性脑膜脑脊髓炎、肌炎、脾炎、淋巴结炎和间质性肺炎，病变内可见原虫裂殖体。免疫组化支持与肉孢子虫属一致的免疫标记，同时排除了刚地弓形虫和犬新孢子虫。据作者所知，这是南美洲首例经组织病理学和免疫组化证实的、具有如此严重程度的犬临床肉孢子虫病的报道。这些发现支持肉孢子虫属应被列为犬进行性神经系统疾病的鉴别诊断之一，并突显了野生动物储存宿主在该病流行病学中的潜在作用。
关键词：犬；免疫组化；脑膜脑脊髓炎；原虫；南美洲；顶复门
背景
肉孢子虫属是一属顶复门寄生虫，包括 S. neurona，它是美洲马原虫性脑膜脑炎的主要病原（de Lahunta et al. 2021; Dubey et al. 2015）。虽然负鼠（Didelphis spp.）是终末宿主，但该寄生虫可感染多种中间宿主和异常宿主，包括海獭、浣熊、猫，以及罕见的犬（Abdolahi et al. 2025; Dubey et al. 2000; Gondim et al. 2021; Nawshirwan et al. 2023; Rosenthal 2021）。
在犬中，肉孢子虫相关疾病的报道罕见（Allison et al. 2006; Dubey et al. 1991, 2006, 2014; Gerhold et al. 2014; Sykes et al. 2011; Trasti et al. 1999）。然而，该病可表现为严重的多灶性神经功能缺损、全身性炎症或两者兼有（Dubey et al. 2014; Irvine et al. 2016）。已记录的临床病例稀少，限制了对该病在犬中的致病性和流行病学意义的认识，尤其是在终末宿主普遍存在的南美洲（Gondim et al. 2021）。
本报告旨在描述巴西一例犬自然获得的、与肉孢子虫属相关的致死性感染的临床、解剖病理学和免疫组化特征。我们强调了原虫性脑炎的诊断挑战、向多器官系统的播散，以及将该病原体与其他嗜神经原虫相鉴别的重要性。
病例介绍
一只5岁未绝育雌性混种犬因侧卧和急性视力丧失六天病史，被送至一家兽医教学医院的神经内科和神经外科服务处。该患犬生活在一个有家畜和其他健康犬的乡村环境中。疫苗接种和驱虫程序未按时进行。
体格检查显示体况评分为5/9，轻度脱水，弥漫性肌肉萎缩，以骨盆肢更为明显。眼科检查显示双侧白内障和角膜混浊。骨科触诊可引发左胸肢疼痛，肘部周围可见软组织肿胀。
神经系统检查显示精神状态沉郁、不能行走的四肢轻瘫以及右侧颞肌局灶性肌阵挛。脑神经评估显示咽反射减弱和双侧威胁反应缺失。四肢脊髓反射和肌张力均降低。神经解剖定位为多灶性，涉及前脑、脑干和脊髓节段（C6-T2和L4-S3），并伴有周围神经系统成分。
初始诊断检查包括全血细胞计数（CBC）、血清生化（肌酐和丙氨酸氨基转移酶[ALT]）、腹部超声检查以及犬瘟热抗原免疫层析试验（尿液）。CBC显示绝对中性粒细胞增多（14,863/mm³；参考区间：3,000–11,500/mm³），白细胞总数正常，轻度红细胞大小不均和缗钱状形成。血清生化无异常。犬瘟热抗原试验为阴性。腹部超声显示肝肿大、脾结节性增生以及主动脉-腰椎淋巴结增大伴退化性回声结构。左前肢X线片显示与炎症一致的软组织肿胀。建议进行磁共振成像（MRI）和脑脊液（CSF）分析，但因经济限制和患犬病情不稳定，畜主拒绝。
该患畜住院接受支持性治疗，包括液体疗法（乳酸林格氏液）、镇痛（美沙酮0.3 mg/kg 肌内注射 每6小时一次；安乃近25 mg/kg 静脉注射 每8小时一次）和抗生素治疗（氨苄西林20 mg/kg 静脉注射 每8小时一次）。由于48小时后未见改善，抗生素方案升级为氨苄西林-舒巴坦（20 mg/kg 静脉注射 每8小时一次），并在调整后的镇痛方案中加入曲马多（4 mg/kg 肌内注射 每8小时一次）。尽管进行了重症监护，患畜的神经学状态仍进行性恶化。畜主选择安乐死，并授权进行完整尸体剖检。
大体检查显示黏膜苍白。右侧腋窝淋巴结增大且质地坚硬。肝脏增大，边缘圆钝，可见小叶图案，多灶性瘀点，以及被膜上轻度纤维素沉积。观察到淋巴结肿大，累及肝淋巴结、胃淋巴结和肠系膜淋巴结。脾脏中度增大，伴弥漫性白髓增生。肺脏后叶可见多灶性红色区域，气道内有泡沫状渗出物。尸体剖检时，组织采集于10%中性缓冲福尔马林中，常规处理用于组织病理学检查，并进行苏木精-伊红（HE）染色。
对大脑（包括额叶、顶叶和枕叶皮质、脑桥、小脑）以及颈段、胸段、腰段和骶段脊髓切片的组织病理学评估显示，随机分布的多灶性液化性坏死区域，在脑桥中累及高达50%的实质，在皮质和脊髓的显著部分亦有累及（图1）。坏死区域内混杂有严重的炎症浸润，由巨噬细胞、淋巴细胞、浆细胞和中性粒细胞组成，并伴有多灶性中度胶质增生和水肿。类似的炎症浸润可见于血管周围间隙和脑膜的扩张。坏死灶内可见大量原虫结构，特征为薄壁裂殖体，直径可达20 μm，内含大量椭圆形嗜碱性裂殖子，大小为2 × 3 μm（图1）。裂殖子也可见于坏死区域内游离分布。骨骼肌和舌表现为淋巴浆细胞性和组织细胞性肌炎，伴肌纤维坏死和病灶内原虫。
[图：犬肉孢子虫中枢神经系统感染的组织病理学和免疫组织化学（IHC）切片。A：脑，大量原虫]
原虫结构也见于脾脏、淋巴结和肺脏，伴有 多灶性重度组织细胞性脾炎和淋巴结炎，以及多灶性中度间质性肺炎。此外，肝脏表现为多灶性中度小叶中央性大泡性变性和多灶性轻度出血，肾脏表现为多灶性中度膜增生性肾小球肾炎。
对大脑和脊髓切片按先前所述方法（Henker et al. 2020）进行免疫组织化学（IHC）检测，针对刚地弓形虫、犬新孢子虫和肉孢子虫属。抗神经肉孢子虫抗体为非商业化兔多克隆一抗，由JP Dubey（美国马里兰州贝尔茨维尔）提供，按Hamir et al.（1993）的方案制备。病灶内寄生虫对肉孢子虫属显示强烈的阳性免疫反应性（图1），而对刚地弓形虫和犬新孢子虫 consistently 阴性，支持该诊断。
讨论
本报告描述了一例罕见的与肉孢子虫属感染相关的致死性犬脑膜脑脊髓炎和肌炎病例。据作者所知，这是拉丁美洲首例经组织病理学和IHC证实的犬如此严重全身性和神经性肉孢子虫病的报道。
不能行走的四肢轻瘫和多灶性神经功能缺损的临床表现与其他常见犬传染病（如犬瘟热、利什曼病、新孢子虫病和弓形虫病）高度重叠（Platt and Olby 2013）。在本病例中，病变的快速进展和严重程度（以广泛液化性坏死为特征）值得注意。类似的组织病理学模式在EPM中有充分记录（Dubey et al. 2015; Henker et al. 2020; Paixão et al. 2007; Saville et al. 2004），但在犬中以如此强度报道较少（Cooley et al. 2007; Dubey et al. 2006; Gerhold et al. 2014; Trasti et al. 1999）。
在犬中，脑膜脑脊髓炎病例主要报道于美国，而肌肉或内脏表现则报道于南美洲（Chapman et al. 2005; Cooley et al. 2007; Dubey et al. 2006, 2014; Gerhold et al. 2014; Mouser et al. 2009; Vashisht et al. 2005）。在巴西，此前唯一一例与神经肉孢子虫感染相关的伴侣小动物脑膜脑炎报道涉及一只猫（Hammerschmitt et al. 2020），而一项使用有神经症状犬的冷冻脑样本的研究在十一份样本中仅鉴定出一例PCR阳性病例（Ries et al. 2025）。这种病例的明显稀少可能归因于该地区的诊断不足，因为大多数诊断实验室并不常规进行肉孢子虫属的确认性辅助检测。
由于形态学相似，使用常规HE染色与犬新孢子虫和刚地弓形虫的鉴别具有挑战性。使用IHC标记物结合裂殖体的形态有助于这一鉴别任务（Dubey et al. 2006; Henker et al. 2020）。
在南美洲，与肉孢子虫属相关的主要临床表现是由S. neurona引起的马原虫性脑膜脑炎，其流行病学与终末宿主Didelphis albiventris（白耳负鼠）存在内在联系（Dubey et al. 2000, 2001; Gondim et al. 2021）。巴西负鼠中已报道高感染率（Gondim et al. 2021）。本报告中的犬生活于已确认存在野生动物的农场，提示环境污染或捕食感染中间宿主可能是传播途径（Freitas et al. 2018; Ridgway 2021）。尽管肉孢子虫属感染最常见的临床表现与胃肠道或肌肉系统相关，但临床症状、组织病理学发现、IHC结果及流行病学特征的结合支持本病例为Sarcocystis neurona感染的怀疑。
本报告的局限性在于，由于患者临床状态不稳定及经济限制，无法进行先进的生前诊断，如MRI和CSF分析。此外，由于没有冷冻或新鲜组织样本，且福尔马林固定石蜡包埋组织的PCR结果为阴性（与其他类似研究一样，可能由于DNA降解）（Henker et al. 2020），因此无法进行分子特征分析（PCR）。虽然免疫印迹或免疫荧光试验等额外确认方法可进一步加强诊断，但由于没有额外样本可用，这些分析无法进行。然而，诊断是通过特征性组织病理学发现和免疫组化试验的结合实现的。裂殖体的独特形态，加上肉孢子虫属阳性免疫反应性以及T. gondii和N. caninum阴性结果（犬原虫性脑膜脑脊髓炎的主要鉴别诊断），支持该诊断（Dubey et al. 2015; Henker et al. 2020）。
据我们所知，这是犬中报道的少数自然发生的肉孢子虫属神经系统和全身性肉孢子虫病病例之一，为兽医文献提供了有价值的临床和病理信息。本病例强调拉丁美洲的兽医临床医生需要在多灶性神经症状犬的鉴别诊断中考虑肉孢子虫属，尤其是在农村环境中。
致谢
作者感谢国家科学技术发展委员会（CNPq，巴西利亚，巴西）为第一作者提供奖学金。
作者贡献
作者对本文的贡献如下。Ítalo Henrique do Nascimento Iara：写作；分析；原稿准备。Ana Flávia Goveia Martins：数据管理；组织病理学分析；Luana de Sousa Ribeiro：临床支持；数据管理；文本审阅和编辑。Fabiana Marques Baobaid：组织病理学和免疫组化分析，以及文本审阅。Luiz Gustavo Schneider de Oliveira：尸体剖检、组织病理学和免疫组化分析；文本审阅。Emanoelly Machado Sousa da Silva：组织病理学和免疫组化分析。David Driemeier：组织病理学和免疫组化分析；Bruno Benetti Junta Torres：临床支持；监督；文本审阅和编辑。所有作者审阅了最终稿件。
资助
本研究发表的文章处理费（APC）由Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil（CAPES）资助（ROR标识符：00x0ma614）。本研究发表的文章处理费（APC）由Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil（CAPES）资助（ROR标识符：00×0ma614）。
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声明
伦理批准
本病例报告不需要研究伦理委员会批准，因为它涉及在所有者同意下提交用于诊断性尸体剖检的安乐死患者。
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脚注
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参考文献
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Abstract
Sarcocystis sp.-induced disease is known especially in horses, in which S. neurona is the primary causative agent of Equine Protozoal Myeloencephalitis in the Americas. While horses are aberrant hosts, the range of susceptible species includes marine mammals, raccoons, and cats. Reports of clinical disease in dogs are rare, remaining unreported in South America. This study describes the clinical, pathological, and immunohistochemical findings of a naturally occurring, fatal case of meningoencephalomyelitis and myositis caused by Sarcocystis sp. in a dog in Brazil. A 5-year-old mixed-breed bitch presented with acute non-ambulatory tetraparesis, generalized muscle atrophy, and blindness. Despite supportive therapy, the patient deteriorated and was euthanized. Gross findings included enlarged lymph nodes, moderate splenomegaly and hepatomegaly, with multifocal mild fibrin deposition on the liver capsule, accompanied by multifocal mild hemorrhages in the pancreas. Histopathology demonstrated severe, multifocal necrotizing meningoencephalomyelitis, myositis, splenitis, lymphadenitis and interstitial pneumonia, associated with intralesional protozoal schizonts. Immunohistochemistry supported immunolabelling consistent with Sarcocystis sp. while excluding Toxoplasma gondii and Neospora caninum. To the authors’ knowledge, this represents the first report of clinical canine sarcocystosis with this severity in South America supported by histopathological and immunohistochemical findings. These findings support that Sarcocystis sp. should be considered a differential diagnosis for canine progressive neurological disease, highlighting the potential role of wildlife reservoirs in the disease’s epidemiology.
Keywords: Canine, Immunohistochemistry, Meningoencephalomyelitis, Protozoa, South America, Apicomplexa
Background
Sarcocystis is a genus of apicomplexan parasites that includes S. neurona, the primary etiological agent of equine protozoal meningoencephalitis (EPM) in the Americas (de Lahunta et al. 2021; Dubey et al. 2015). Although opossums (Didelphis spp.) are the definitive hosts, the parasite can infect a wide range of intermediate and aberrant hosts, including sea otters, raccoons, cats, and rarely, dogs (Abdolahi et al. 2025; Dubey et al. 2000; Gondim et al. 2021; Nawshirwan et al. 2023; Rosenthal 2021).
In dogs, Sarcocystis-related disease is rarely reported (Allison et al. 2006; Dubey et al. 1991, 2006, 2014; Gerhold et al. 2014; Sykes et al. 2011; Trasti et al. 1999). However, it can manifest as severe multifocal neurological deficits, systemic inflammation, or a combination of both (Dubey et al. 2014; Irvine et al. 2016). The scarcity of documented clinical cases has limited the understanding of its pathogenicity and epidemiological significance in canine, especially in South America where the definitive host is prevalent (Gondim et al. 2021).
This report aims to describe the clinical, anatomopathological, and immunohistochemical features of a naturally acquired, fatal infection associated with Sarcocystis sp. in a dog in Brazil. We highlight the diagnostic challenges of protozoal encephalitis, the dissemination to multiple organ systems, and the importance of differentiating this agent from other neurotropic protozoa.
Case presentation
A 5-year-old, intact female mixed-breed dog was presented to the Neurology and Neurosurgery Service of a Veterinary Teaching Hospital with a six-day history of lateral recumbency and acute vision loss. The patient lived on a rural property with livestock and other healthy dogs. Vaccination and deworming protocols were not up to date.
Physical examination revealed a body condition score of 5/9, mild dehydration, and diffuse muscle atrophy, which was more pronounced in the pelvic limbs. Ophthalmic inspection showed bilateral cataracts and corneal opacity. Orthopedic palpation elicited pain in the left thoracic limb, where soft tissue swelling was noted around the elbow.
Neurological examination demonstrated a depressed mental status, non-ambulatory tetraparesis, and focal myoclonus of the right temporal muscle. Cranial nerve assessment revealed a reduced gag reflex and bilateral absence of menace response. Spinal reflexes and muscle tone were reduced in all four limbs. Neuroanatomic localization was multifocal, involving the forebrain, brainstem, and spinal cord segments (C6-T2 and L4-S3), with a peripheral nervous system component.
Initial diagnostic workup included a complete blood count (CBC), serum biochemistry (creatinine and alanine aminotransferase [ALT]), abdominal ultrasonography, and a distemper antigen immunochromatography test (urine). CBC revealed absolute neutrophilia (14,863/mm³; RI: 3,000–11,500/mm³) with normal leukocyte counts, mild anisocytosis, and rouleaux formation. Serum biochemistry was unremarkable. The distemper antigen test was negative. Abdominal ultrasonography revealed hepatomegaly, splenic nodular hyperplasia, and enlarged aortic-lumbar lymph nodes with degenerative echotexture. Radiographs of the left forelimb showed soft tissue swelling consistent with inflammation. Magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis were recommended but were declined by the owner due to financial constraints and the patient’s unstable condition.
The patient was hospitalized for supportive care, receiving fluid therapy (Lactated Ringer’s solution), analgesia (methadone 0.3 mg/kg IM q6h; metamizole 25 mg/kg IV q8h), and antibiotic therapy (ampicillin 20 mg/kg IV q8h). Due to a lack of improvement after 48 h, the antibiotic protocol was escalated to ampicillin-sulbactam (20 mg/kg IV q8h) and tramadol (4 mg/kg IM q8h) was added to adjusted analgesia. Despite intensive care, the patient’s neurological status progressively deteriorated. The owner elected for humane euthanasia, and a full necropsy was authorized.
Gross examination revealed pale mucous membranes. The right axillary lymph node was enlarged and firm. The liver was enlarged with rounded edges, evidenced lobular pattern, multifocal petechiae, and mild fibrin deposition on the capsule. Lymphadenomegaly was observed affecting hepatic, gastric, and mesenteric nodes. The spleen was moderately enlarged with diffuse white pulp hyperplasia. The lungs showed multifocal reddish areas in the caudal lobes and frothy exudate in the airways. During necropsy the tissues were collected in 10% neutral buffered formalin, routinely processed for histopathology and stained with hematoxylin and eosin (HE).
Histopathologic evaluation of the brain, including the frontal, parietal and occipital cortex, pons, cerebellum, and sections of the cervical, thoracic, lumbar and sacral spinal cord revealed randomly distributed multifocal areas of liquefactive necrosis, compromising up to 50% of the parenchyma in the pons and significant portions of the cortex and spinal cord (Fig. 1). Intermingled in areas of necrosis was a severe inflammatory infiltrate of macrophages, lymphocytes, plasma cells and neutrophils, with multifocal moderate gliosis and edema. Similar inflammatory infiltrate was seen expanding the perivascular spaces and meninges. Within the necrotic foci were numerous protozoan structures characterized as thin-walled schizonts, up to 20 μm in diameter, containing numerous oval basophilic merozoites, measuring 2 × 3 μm (Fig. 1). Merozoites were also found free within areas of necrosis. Skeletal muscles and tongue exhibited lymphoplasmacytic and histiocytic myositis with myofiber necrosis and intralesional protozoa.
[图：Histopathology and immunochemistry (IHC) slides of canine sarcocystosis in central nervous system. A: Brain, numerous pr]
The protozoal structures were also identified in the spleen, lymph nodes and lungs, accompanied by multifocal severe histiocytic splenitis and lymphadenitis, as well as multifocal moderate interstitial pneumonia. Additionally, the liver presented multifocal moderate centrilobular macrovacuolar degeneration and multifocal mild haemorrhage and the kidney exhibited multifocal moderate membranoproliferative glomerulonephritis.
Sections of the brain and spinal cord were subjected to immunohistochemistry (IHC) testing for Toxoplasma gondii, Neospora caninum, and Sarcocystis sp. as previously described (Henker et al. 2020). The anti- Sarcocystis neurona antibody was a non-commercial rabbit polyclonal primary antibody, provided by JP Dubey (Beltsville, MD, USA), produced according to the protocol by Hamir et al. (1993). Intralesional parasites showed intense positive immunoreactivity for Sarcocystis sp. (Fig. 1) and were consistently negative for T. gondii and N. caninum, supporting the diagnosis.
Discussion
This report describes a rare case of fatal canine meningoencephalomyelitis and myositis associated with Sarcocystis sp. infection. To the authors’ knowledge, this represents the first reported description supported by histopathology and IHC of such severe systemic and neurological sarcocystosis in a dog in Latin America.
The clinical presentation of non-ambulatory tetraparesis and multifocal neurological deficits overlaps significantly with other common canine infectious diseases, such as distemper, leishmaniosis, neosporosis, and toxoplasmosis (Platt and Olby 2013). In this case, the rapid progression and severity of the lesions, characterized by extensive liquefactive necrosis, were remarkable. Similar histopathological patterns are well-documented in EPM (Dubey et al. 2015; Henker et al. 2020; Paixão et al. 2007; Saville et al. 2004) but are infrequently reported in dogs with this intensity (Cooley et al. 2007; Dubey et al. 2006; Gerhold et al. 2014; Trasti et al. 1999).
In dogs, meningoencephalomyelitis cases have been reported predominantly in the United States, whereas muscular or visceral manifestations have been reported in South America (Chapman et al. 2005; Cooley et al. 2007; Dubey et al. 2006, 2014; Gerhold et al. 2014; Mouser et al. 2009; Vashisht et al. 2005). In Brazil, the only previous report of meningoencephalitis associated with Sarcocystis neurona infection in small domestic animals involved a cat (Hammerschmitt et al. 2020), and a study using frozen brain samples from dogs with neurological signs identified a single PCR-positive case out of eleven samples (Ries et al. 2025). This apparent scarcity of cases may be attributed to underdiagnosis in the region, as confirmatory ancillary techniques for Sarcocystis sp. are not routinely performed in most diagnostic laboratories.
Differentiation from N. caninum and T. gondii is challenging using routine H&E staining due to morphological similarities. The employment of IHC markers combined with the morphology of the schizonts is helpful for this task (Dubey et al. 2006; Henker et al. 2020).
The main clinical manifestation associated with Sarcocystis sp. in South America is equine protozoal meningoencephalitis by S. neurona, whose epidemiology is intrinsically linked to the definitive host, Didelphis albiventris (Dubey et al. 2000, 2001; Gondim et al. 2021). High infection rates have been reported in Brazilian opossums (Gondim et al. 2021). The dog in this report lived on a farm with confirmed wildlife presence, suggesting environmental contamination or predation of infected intermediate hosts as likely transmission routes (Freitas et al. 2018; Ridgway 2021). Despite the most common clinical manifestations of Sarcocystis sp. infections being associated with the gastrointestinal or muscular systems, the combination of clinical signs, histopathological findings, IHC results, and epidemiological features supports the suspicion of Sarcocystis neurona infection in this case.
A limitation of this report was the inability to perform advanced ante-mortem diagnostics, such as MRI and CSF analysis, due to the patient’s clinical instability and financial constraints. Furthermore, molecular characterisation (PCR) was not possible as frozen or fresh tissue samples were not available and PCR from formalin fixed paraffin embedded tissue was negative, like other similar studies, probably due to DNA degradation (Henker et al. 2020). Although additional confirmatory methods, such as immunoblotting or immunofluorescence assays, could further strengthen the diagnosis, these analyses could not be performed because no additional samples were available. However, the diagnosis was achieved through the combination of characteristic histopathological findings and immunohistochemistry tests. The distinct morphology of the schizonts, coupled with positive immunoreactivity for Sarcocystis sp. and negative results for T. gondii and N. caninum, the primary differential diagnoses for protozoal meningoencephalomyelitis in dogs, supports the diagnosis (Dubey et al. 2015; Henker et al. 2020).
To our knowledge, this is one of the few naturally occurring cases of neurological and systemic sarcocystosis by Sarcocystis sp. reported in a dog, contributing valuable clinical and pathological information to the veterinary literature. This case highlights the need for veterinary clinicians in Latin America to consider Sarcocystis sp. in the differential diagnosis of dogs with multifocal neurological signs, especially in rural settings.
Acknowledgements
The authors would like to thank the National Council for Scientific and Technological Development (CNPq, Brasília, Brazil) for the first author’s scholarship.
Author contributions
The authors contributed to this paper as it follows. Ítalo Henrique do Nascimento Iara: Writing; Analysis; Original draft preparation. Ana Flávia Goveia Martins: Data curation; Histopathological analysis; Luana de Sousa Ribeiro: Clinical support; Data curation; Text review and editing. Fabiana Marques Baobaid: Histopathological and immunohistochemical analyses, and Text reviewing. Luiz Gustavo Schneider de Oliveira: Necropsy, histopathological and immunohistochemical analyses; Text reviewing. Emanoelly Machado Sousa da Silva: Histopathological and immunohistochemical analyses. David Driemeier: Histopathological and immunohistochemical analyses; Bruno Benetti Junta Torres: Clinical support; Supervision; Text review and editing. All authors reviewed the final manuscript.
Funding
The Article Processing Charge (APC) for the publication of this research was funded by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) (ROR identifier: 00x0ma614). The Article Processing Charge (APC) for the publication of this research was funded by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) (ROR identifier: 00×0ma614).
Data availability
No datasets were generated or analysed during the current study.
Declarations
Ethical approval
This case report did not require approval from a research ethics committee, as it involved a euthanized patient submitted for diagnostic necropsy with owner consent.
Competing interests
The authors declare no competing interests.
Footnotes
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References
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Associated Data
Data Availability Statement
No datasets were generated or analysed during the current study.