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来自北美一家动物园机构的9只非洲白腹穿山甲()的肝脏脂肪变性。

Hepatic lipidosis in nine African white-bellied pangolins () from a North American zoologic institution.

作者信息

Horgan Molly, Landolfi Jennifer, Stacy Nicole I, Watts Jennifer, Aitken-Palmer Copper

机构信息

Department of Comparative, Diagnostic, and Population Medicine, College of Veterinary Medicine, University of Florida, Gainesville, FL, United States.

Zoological Pathology Program, University of Illinois, Brookfield, IL, United States.

出版信息

Front Vet Sci. 2025 Jun 3;12:1562904. doi: 10.3389/fvets.2025.1562904. eCollection 2025.

DOI:10.3389/fvets.2025.1562904
PMID:40530035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12170562/
Abstract

INTRODUCTION

The African white-bellied pangolin () is an endangered species with a small population under managed care in the United States. Over the course of 4 years, nine pangolins at a single North American zoological institution died or were euthanized with necropsy findings consistent with hepatic lipidosis, representing 9 of 14 mortalities during this time period.

METHODS

This report describes hepatic lipidosis in these pangolins (clinical presentation, diagnostic imaging, clinicopathologic and postmortem findings) and summarizes clinically relevant predictors of disease.

RESULTS

The time from the onset of illness to death ranged from 2 to 75 days (median 23 days). Obesity was noted prior to clinical presentation for illness in 4/9 animals. All pangolins had anorexia and lethargy; other common clinical signs included constipation (6/9), vomiting or regurgitation (6/9), and/or dyspnea (5/9). Increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were observed in 7/9 animals, hyperbilirubinemia in 5/9, and increased bile acids in 5/9. Serum selenium was low in 3/9 animals, but vitamin E concentrations were normal. Hypertriglyceridemia was uncommon during illness (1/9). Evidence of renal dysfunction was also common, and included glucosuria (6/6), proteinuria (7/7), and azotemia (6/9). Ultrasound was the most reliable imaging technique at identifying hepatic lipidosis as evidenced by hepatomegaly and increased echogenicity. Despite variable treatment including assisted feeding, hepatoprotectants, fluid therapy, gastroprotectants, antibiotics, and/or antiemetics, all cases were ultimately fatal. Each of the animals had comorbidities or an inciting reason for anorexia that led to negative energy balance. In 5/9, resultant hepatic lipidosis was severe and deemed the primary cause of death or euthanasia.

DISCUSSION

This case series suggests that white-bellied pangolins are prone to developing hepatic lipidosis following a period of anorexia secondary to other underlying disease processes. Elevated AST, ALT, bilirubin, and bile acids in an anorectic and lethargic pangolin should provide a high index of suspicion for hepatic lipidosis. Further study is needed to evaluate pangolins for potential unique polyunsaturated fatty acid or other species-specific dietary requirements.

摘要

引言

非洲白腹穿山甲()是一种濒危物种,在美国人工饲养条件下数量稀少。在4年的时间里,北美一家动物园的9只穿山甲死亡或被实施安乐死,尸检结果显示符合肝脂肪变性,占该时间段内14例死亡病例中的9例。

方法

本报告描述了这些穿山甲的肝脂肪变性(临床表现、诊断性影像学检查、临床病理及尸检结果),并总结了该疾病的临床相关预测因素。

结果

从发病到死亡的时间为2至75天(中位数23天)。4/9的动物在出现临床疾病之前就已出现肥胖。所有穿山甲均有厌食和嗜睡症状;其他常见临床体征包括便秘(6/9)、呕吐或反流(6/9)和/或呼吸困难(5/9)。7/9的动物出现丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)升高,5/9出现高胆红素血症,5/9出现胆汁酸升高。3/9的动物血清硒水平较低,但维生素E浓度正常。疾病期间高甘油三酯血症并不常见(1/9)。肾功能不全的证据也很常见,包括糖尿(6/6)、蛋白尿(7/7)和氮质血症(6/9)。超声是识别肝脂肪变性最可靠的影像学技术,表现为肝脏肿大和回声增强。尽管采用了包括辅助喂食保肝剂、液体疗法、胃保护剂、抗生素和/或止吐药在内的多种治疗方法,但所有病例最终均死亡。每只动物都有合并症或导致厌食的诱因,进而导致能量负平衡。5/9的病例中,由此导致的严重肝脂肪变性被认为是死亡或安乐死的主要原因。

讨论

该病例系列表明,白腹穿山甲在因其他潜在疾病过程继发厌食一段时间后容易发生肝脂肪变性。厌食和嗜睡的穿山甲中AST、ALT、胆红素和胆汁酸升高应高度怀疑肝脂肪变性。需要进一步研究以评估穿山甲是否存在潜在的独特多不饱和脂肪酸或其他特定物种的饮食需求。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/c7f0d7d47b12/fvets-12-1562904-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/af598baa5e1d/fvets-12-1562904-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/1ef52e5a981d/fvets-12-1562904-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/c7f0d7d47b12/fvets-12-1562904-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/af598baa5e1d/fvets-12-1562904-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/1ef52e5a981d/fvets-12-1562904-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43f8/12170562/c7f0d7d47b12/fvets-12-1562904-g003.jpg

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