Langenmayer M C, Jung S, Majzoub-Altweck M, Trefz F M, Seifert C, Knubben-Schweizer G, Fries R, Hermanns W, Gollnick N S
Institute of Veterinary Pathology at the Centre for Clinical Veterinary Medicine, LMU Munich, Munich, Germany.
Institute for Infectious Diseases and Zoonoses, LMU Munich, Munich, Germany.
J Vet Intern Med. 2018 Mar;32(2):853-859. doi: 10.1111/jvim.15040. Epub 2018 Feb 9.
Zinc deficiency-like (ZDL) syndrome is an inherited defect of Fleckvieh calves, with striking similarity to bovine hereditary zinc deficiency (BHZD). However, the causative mutation in a phospholipase D4 encoding gene (PLD4) shows no connection to zinc metabolism.
To describe clinical signs, laboratory variables, and pathological findings of ZDL syndrome and their utility to differentiate ZDL from BHZD and infectious diseases with similar phenotype.
Nine hospitalized calves with crusting dermatitis and confirmed mutation in PLD4 and medical records from 25 calves with crusting dermatitis or suspected zinc deficiency.
Prospective and retrospective case series.
The 9 calves (age: 5-53 weeks) displayed a moderate to severe crusting dermatitis mainly on the head, ventrum, and joints. Respiratory and digestive tract inflammations were frequently observed. Zinc supplementation did not lead to remission of clinical signs in 4 calves. Laboratory variables revealed slight anemia in 8 calves, hypoalbuminemia in 6 calves, but reduced serum zinc concentrations in only 3 calves. Mucosal erosions/ulcerations were present in 7 calves and thymus atrophy or reduced thymic weights in 8 calves. Histologically, skin lesions were indistinguishable from BHZD. Retrospective analysis of medical records revealed the presence of this phenotype since 1988 and pedigree analysis revealed a common ancestor of several affected calves.
ZDL syndrome should be suspected in Fleckvieh calves with crusting dermatitis together with diarrhea or respiratory tract inflammations without response to oral zinc supplementation. Definite diagnosis requires molecular genetic confirmation of the PLD4 mutation.
类锌缺乏(ZDL)综合征是弗莱维赫犊牛的一种遗传性缺陷,与牛遗传性锌缺乏(BHZD)极为相似。然而,磷脂酶D4编码基因(PLD4)中的致病突变与锌代谢并无关联。
描述ZDL综合征的临床症状、实验室指标及病理结果,以及它们在鉴别ZDL与BHZD及具有相似表型的传染病方面的作用。
9头住院的患有结痂性皮炎且PLD4基因确诊突变的犊牛,以及25头患有结痂性皮炎或疑似锌缺乏的犊牛的病历。
前瞻性和回顾性病例系列研究。
9头犊牛(年龄:5 - 53周)表现出中度至重度结痂性皮炎,主要位于头部、腹部和关节处。常观察到呼吸道和消化道炎症。4头犊牛补充锌后临床症状未缓解。实验室指标显示,8头犊牛有轻度贫血,6头犊牛有低白蛋白血症,但只有3头犊牛血清锌浓度降低。7头犊牛存在黏膜糜烂/溃疡,8头犊牛有胸腺萎缩或胸腺重量减轻。组织学上,皮肤病变与BHZD难以区分。对病历的回顾性分析显示自1988年以来就存在这种表型,系谱分析揭示了几头患病犊牛有一个共同祖先。
对于患有结痂性皮炎且伴有腹泻或呼吸道炎症且口服补锌无反应的弗莱维赫犊牛,应怀疑ZDL综合征。确诊需要对PLD4突变进行分子遗传学确认。