Antler abnormalities with testicular atrophy in a wild roe deer (Capreolus pygargus): a case report

Article information

Korean J Vet Res. 2025;.e28

Publication date (electronic) : 2025 December 17

doi : https://doi.org/10.14405/kjvr.20250026

Dayoung Dayoung Choi¹, Da-Ye Nam¹, Jae-Hoon Kim¹, Jinho Jang^1,2, Youngmin Yun^1,2, Ji-Youl Jung^1,

¹College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju 63243, Korea

²Jeju Wildlife Rescue Center, Jeju National University, Jeju 63243, Korea

^*Corresponding author: Ji-Youl Jung College of Veterinary Medicine, Jeju National University, 102 Jejudaehak-ro, Jeju 63243, Korea Tel: +82-64-754-3364 E-mail: jungjy1982@jejunu.ac.kr

Received 2025 July 4; Revised 2025 November 17; Accepted 2025 December 4.

Deer antlers are unique mammalian appendages that undergo serial regeneration, a process which is primarily regulated by testosterone levels. Insulin-like growth factor 1, other hormones, and local factors also contribute to this complex biological phenomenon [1]. Testosterone plays a critical role in regulating seasonal antler growth patterns, mineralization, and casting in cervids. Antler initiation typically begins in spring as the day length increases, which is likely triggered by a transient rise in testosterone. However, persistently high testosterone levels inhibit angiogenesis and pedicle activity [2]. During summer, antlers grow under relatively low testosterone levels, remain unmineralized, and are vulnerable to trauma. In fall, testosterone levels rise significantly, exceeding approximately 1 ng/mL, which initiates mineralization and velvet shedding in preparation for the rutting season [3,4]. When testosterone production is disrupted, antler development becomes abnormal, resulting in persistent velvet coverage, shortened beams, and aberrant points, a condition collectively referred to as the “cactus buck” [5].

Antler abnormalities frequently arise from disruptions in testosterone production, often owing to testicular lesions, such as atrophy, hypoplasia, orchitis, or epididymitis [5]. Reported causes of testicular atrophy include heat stress, infectious agents (e.g., epizootic hemorrhagic disease virus [EHDV]), toxins, phytoestrogens, mycotoxins, nutritional deficiencies, heavy metals, organochlorine contaminants, and genetic factors; however, the etiology is often multifactorial and remains uncertain [5–8].

Abnormal antler development associated with testicular pathology has been extensively documented in mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus) populations, with histological findings of severe degeneration, fibrosis, chronic inflammation, and mineralization [5,7,8]. Hormonal imbalances involving the luteinizing hormone, follicle-stimulating hormone, and prolactin have also been observed in these cases [4,9].

Here, we report the fatal case of a wild male roe deer (Capreolus pygargus) in South Korea that is presented with antler abnormalities and testicular pathologies. To the best of our knowledge, this is the first report of a wild roe deer in South Korea presenting both cactus buck syndrome and capture myopathy.

A wild male roe deer, approximately 2 years old, weighing 20.7 kg, was discovered on July 3, 2024, in Hangyeong-myeon, Jeju-si, Jeju Island, with its left antler entangled in agricultural netting (Fig. 1A). The animal was rescued by the Jeju Wildlife Rescue Center and underwent a physical examination. The clinical examination revealed a mild nutritional deficiency and signs of mild dehydration. The left antler, which was entangled in the netting, was detached from the skull with a hemorrhage at the detachment site. Blood sample was collected; whole blood was used for hematological examination, while serum was used for biochemical and hormonal analyses. However, its prognosis was poor, and the animal eventually died. The carcass was subsequently submitted to the Laboratory of Veterinary Pathology at Jeju National University for postmortem examination to determine the exact cause of death.

Fig. 1.

Gross findings. (A) A wild roe deer with its left antler entangled in netting, (B) Velvet retention observed on the antlers, (C) Small testes (circle), (D) Red-brown urine found in the urinary bladder.

Grossly, both antlers were markedly enlarged with irregular and nodular surfaces. These were entirely covered with hair (Fig. 1B). Both testes were markedly small (length, 3.5 cm; weight, 2–2.3 g) (Fig. 1C). Additionally, red-brown urine was observed (Fig. 1D). After necropsy, the tissue samples were fixed in 10% neutral-buffered formalin for histopathological analysis. Routine histological procedures were performed: paraffin-embedded tissues were sectioned at 4 μm thickness, deparaffinized, rehydrated through graded alcohols, and stained with hematoxylin and eosin for microscopic examination. In addition, urinalysis was performed during necropsy to evaluate the urine characteristics. Microscopically, the seminiferous tubules were severely atrophied, and interstitial fibrosis was observed in both testes (Fig. 2A and B). The skeletal muscles of the hind limbs displayed degeneration and coagulative necrosis (Fig. 2C). Coagulative necrosis of the tubular epithelium and intraluminal eosinophilic casts were observed in the kidneys (Fig. 2D).

Fig. 2.

Histopathological findings. (A, B) Testis: seminiferous tubular atrophy, degeneration, and interstitial fibrosis. (C) Skeletal muscle: muscular degeneration and necrosis. (D) Kidney: renal tubular necrosis and intraluminal eosinophilic casts (arrows). Hematoxylin and eosin stain, scale bars: (A) 100 µm, (B–D) 20 µm.

Hormonal assays revealed a serum testosterone level of 0.032 ng/mL. The urine samples tested positive for blood on a dipstick analysis. Blood gas analysis revealed a decreased blood pH (7.143), low base excess in the extracellular fluid (BEecf, –10 mmol/L), elevated partial pressure of carbon dioxide (PCO₂, 56 mmHg), and low partial pressure of oxygen (PO₂, 23 mmHg). In addition, creatine kinase (CK) levels were not evaluated.

Based on the gross, histological, and hormonal results, we concluded that the antler deformity was associated with testicular atrophy. These morphological characteristics of the antler are consistent with those typically observed in cactus bucks. Hormonal assays revealed markedly decreased testosterone levels (0.032 ng/mL), considerably below the pre-rut reference range (0.88–4.59 ng/mL) reported in Capreolus capreolus (European roe deer) by Ventrella et al. [10]. Because no published data on baseline testosterone concentrations are available for C. pygargus, we referred to C. capreolus as the closest available reference. Although the present case involves C. pygargus, both species are sister taxa that diverged approximately 2 to 3 million years ago and exhibit about 4.9% mitochondrial DNA sequence divergence [11]. Due to their close phylogenetic relationship, reference values from C. capreolus can serve as a reasonable proxy for physiological interpretation. Nonetheless, interspecific physiological variations cannot be excluded, and further studies establishing hormonal reference ranges for C. pygargus are warranted. This hormonal deficiency was closely associated with the observed abnormal antler development, particularly the persistence of velvet and impaired ossification. Ultimately, the hormonal imbalance was likely secondary to the underlying testicular pathology identified at necropsy.

Environmental factors—such as habitat alteration, nutritional deficiencies, and potential exposure to pollutants or pathogens—are known to contribute significantly to endocrine disruptions in wildlife [6–8]. Although orchitis and epididymitis have been linked to infectious agents in cervids, the role of infectious diseases in causing chronic orchitis and subsequent testicular fibrosis warrants further investigation [5]. The previous study proposed a possible association between testicular atrophy and epizootic EHDV infection [5]; however, EHDV was not tested in the present case due to the absence of EHDV cases reported in South Korea. Furthermore, no histopathological lesions which are typically associated with EHDV—such as chronic vascular damage, inflammation, or tissue necrosis—were observed, making a viral etiology unlikely. In this case, due to the limited background information inherent to a wild animal, the exact cause of testicular atrophy could not be determined. Nevertheless, noninfectious factors—including heat stress, environmental toxins exposure, nutritional deficiencies, and genetic predisposition—were regarded as more likely contributors in this case.

In addition to endocrine and reproductive abnormalities, clinical pathology and histopathological findings strongly supported the capture myopathy diagnosis. Although the measurement of blood CK levels is a key diagnostic indicator of capture myopathy, CK was not assessed in this case, which is a limitation of the present study. However, a urinalysis revealed positive blood test results, suggesting the presence of myoglobinuria, which further supported the suspicion of rhabdomyolysis. In addition, the animal exhibited metabolic acidosis with low blood pH and base excess along with elevated PCO₂ and reduced PO₂, which are typical in cases of rhabdomyolysis [12]. Histologically, skeletal muscle necrosis and eosinophilic casts in renal tubules further supported the presence of myoglobinuria and muscle breakdown secondary to extreme stress.

This case represents the first documentation of severe endocrine and reproductive pathology in roe deer in South Korea, highlighting the importance of wildlife health monitoring for similar abnormalities. A detailed investigation of endocrine dysfunction and the associated histopathological lesions provide crucial insights into the antler abnormality pathophysiology and their systemic implications. Although antler deformities are not inherently fatal, they can impair physical performance, reduce reproductive competitiveness, and increase the susceptibility to environmental hazards.

In this case, the antler deformity likely contributed to the entanglement of the animal in the agricultural netting, which ultimately resulted in fatal capture myopathy. This emphasizes that even nonlethal morphological abnormalities can indirectly threaten survival, particularly under human-induced environmental pressures. These findings highlight the complex interplay between endocrine imbalance, environmental stress, and mortality risk in wild cervids, and emphasize the importance of comprehensive pathological investigations in wildlife conservation. Furthermore, understanding how antler morphology relates to reproductive ecology is essential for interpreting the broader biological significance of these abnormalities.

In cervids, antlers serve as key secondary sexual characteristics, functioning both as weapons in male-male competition and as visual signals of strength and genetic quality to potential mates. The size and symmetry of antlers are therefore closely associated with reproductive success and overall fitness [13]. In a study by Fox et al. [5], an apparent increase in cactus bucks in Colorado was attributed to recent changes in management practices that reduced male deer hunting. This led to a higher proportion of older males that survived to develop cumulative antler abnormalities. In South Korea, where the hunting of roe deer is currently limited, such population dynamics could similarly increase the likelihood of older males exhibiting endocrine-related antler deformities. This highlights a potential conservation concern, as the accumulation of hormonally compromised individuals may affect the overall health of wild populations.

Further research is warranted to identify the underlying causes, including environmental toxins and nutritional imbalances, to improve the conservation and health management strategies for roe deer and other cervid species in South Korea.