Integrative review on biomarkers of stress-triggered cardiac, renal, and multi-organ dysfunction in wildlife and zoo species

Wildlife and zoo animals are frequently exposed to acute and chronic stressors, including capture, restraint, translocation, live stranding, predation attempts, environmental extremes, and human wildlife conflicts. These stressors can precipitate severe physiological responses culminating in cardiac injury, acute kidney injury (AKI), and multi organ failure. Stress related syndromes particularly capture myopathy represent a significant cause of morbidity and mortality across multiple taxa. This review synthesizes current evidence on the pathophysiology, clinical manifestations, biochemical and molecular biomarkers, species susceptibility, and management of stress induced organ damage in wildlife and zoological settings. Emphasis is placed on the mechanisms linking extreme stress to myocardial damage, myoglobinuric kidney injury, and systemic organ dysfunction. The review highlights common clinical features, the utility of emerging biomarkers such as cardiac troponins and creatine kinase, and the limitations posed by species heterogeneity and lack of standardized reference intervals. Evidence based strategies for prevention, monitoring, and intervention are discussed, with recommendations for future research aimed at improving conservation and clinical outcomes.

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Introduction

Stress responses in animals trigger a cascade of physiological adaptations that may be beneficial in the short term but deleterious if prolonged or extreme. In wildlife and zoo animals, stressors such as capture, handling, transportation, live-stranding, and confrontation with predators initiate heightened sympathetic activity and metabolic disturbances. When these stress responses exceed physiological tolerance, they can precipitate severe outcomes, including capture myopathy (CM) a systemic metabolic syndrome characterized by muscle damage, cardiac compromise, and renal dysfunction. CM has been described across a broad range of taxa, particularly in mammals and birds, and is increasingly recognized as analogous to human stress cardiomyopathy (e.g., Takotsubo syndrome) (Rogers et al., 2004, Arregui et al., 2020, Dinesh et al., 2020, Vera et al., 2024) [4,1,7,24] . Defining and diagnosing stress-related organ damage in wildlife is challenging due to limited access to diagnostic imaging and scarce baseline data for many species. Nonetheless, clinical and post-mortem studies have identified common features of cardiac and renal injury, including elevations in serum markers such as creatine kinase (CK), lactate dehydrogenase (LDH), cardiac troponin I (cTnI), blood urea nitrogen (BUN), and creatinine, along with histopathological evidence of muscle necrosis, myocardial degeneration, and renal tubular damage. The interrelation between cardiac injury and kidney failure in stressed animals reflects a form of animal cardiorenal syndrome, wherein damage to one organ system exacerbates dysfunction in another. This review aims to provide an integrative, evidence-based overview of stress-induced organ injury syndromes in wildlife and zoo animals, focusing on pathophysiology, clinical assessment, biomarker profiles, species-specific susceptibilities, and management strategies (Carramenha, 2012) [18] .

Pathophysiology of Stress-Induced Organ Injury 2.1 Capture Myopathy: Definition and Mechanisms

Capture myopathy (CM) is a metabolic disorder triggered by intense physical exertion or psychological stress during events such as pursuit, capture, restraint, transport, or live-stranding of wildlife. CM encompasses a spectrum of syndromes from hyper-acute (capture shock) to chronic forms and leads to severe muscle breakdown (rhabdomyolysis), metabolic acidosis, and multi-organ injury (Carramenha, 2012, Breed et al., 2019, Dinesh et al., 2020) [18,2,7] . The initial stress response involves sympathetic activation and catecholamine surge, causing increased heart rate, respiration, and muscle activity. If prolonged, this overwhelms cellular energy stores, leading to muscle cell membrane breakdown and release of intracellular contents such as myoglobin, CK, and troponins into circulation. These substances can be directly toxic to kidneys and other tissues, resulting in myoglobinuric nephrosis and acute kidney injury (Cebi et al., 2022) [20] . Cardiac involvement in CM resembles human stress cardiomyopathy, with myocardial necrosis, contraction band necrosis, and vascular changes. Histopathological studies in cetaceans demonstrated acute myocardial degeneration with depletion of cardiac proteins and inflammatory infiltrates following live-stranding and rehabilitation efforts. Elevated levels of cTnI and CK have been correlated with such cardiac damage in multiple wild species (Spraker et al., 2012, Arregui et al., 2020) [8,1] .

Renal Injury and Multi-Organ Dysfunction:

Myoglobin released from damaged skeletal and cardiac muscle causes myoglobinuric acute kidney injury by precipitating in renal tubules, inducing oxidative stress and tubular necrosis. Laboratory findings frequently show elevated blood urea nitrogen (BUN) and creatinine, indicating impaired renal filtration (Cebi et al., 2022) [20] . Beyond the heart and kidneys, systemic stress can produce multi-organ pathology, including hepatic congestion, adrenal insufficiency, and intestinal or pulmonary lesions. Histopathological examinations of CM cases show multifocal necrosis across many organs, reflecting the widespread impact of metabolic derangements and hypoxia resulting from prolonged stress (Cebi et al., 2022) [20] .

Clinical Manifestations and Biomarker Profiles 3.1 Cardiac Injury Markers & assessment

Cardiac injury in wild animals is most commonly assessed using biomarkers such as cardiac troponins (cTnI), which are highly specific indicators of myocardial cell damage. Elevated cTnI levels have been documented in live-stranded cetaceans and are correlated with histopathological evidence of stress cardiomyopathy (Spraker et al., 2012, Arregui et al., 2020) [8,1] . Creatine kinase (CK) and lactate dehydrogenase (LDH) are less specific but indicate broader muscle damage including cardiac muscle. In free-ranging deer (Campos, 2024) subjected to intense exertion, significant elevations in LDH, AST (aspartate aminotransferase), and CK were observed, highlighting their utility in diagnosing exertional myopathy (Landau et al., 2012) [13] . [20] . Systemic biomarkers such as metabolic acidosis (low blood pH) and electrolyte imbalances signal advanced organ dysfunction in stressed animals, often accompanying cardiac and renal compromise. [20] . [8,7,1] .

Species Susceptibility and

Species Susceptibility and

Terrestrial Ungulates

Ungulates including deer (Campos, 2024), antelopes, and giraffes show significant susceptibility to CM, likely due to evolutionary traits such as high running speed and social behavior that predispose them to intense stress responses (Atkinson, 2012) [14] . [16,9,14,4,24] . The fundamental pathology involves muscle cell membrane disruption due to inadequate oxygen delivery, anaerobic metabolism, and accumulation of toxic metabolites (e.g., lactic acid). This leads to rhabdomyolysis (Nueangphuet et al., 2022) [4] , where intracellular components such as myoglobin, creatine kinase (CK), and electrolytes are released into the bloodstream, causing widespread metabolic derangement.

Birds and Zoo Species

Birds and Zoo Species

Cardiac Injury Mechanisms

Cardiac involvement in stress-induced syndromes mirrors human stress cardiomyopathy (e.g., Takotsubo syndrome), characterized by myocardial degeneration, contraction-band necrosis, and hypercontracted myofibers. In marine mammals such as dolphins, elevated CK and cardiac troponin I (cTnI) during episodes of live-stranding and rehabilitation have been directly linked to myocardial compromise. Cardiac degeneration is further confirmed by histopathology showing wavy fibers, hypereosinophilia, vacuolization, and mononuclear infiltration within both atrial and ventricular myocardium following stress events (Arregui et al., 2020) [1] .

Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

Progression to Multi-Organ Failure

The integration of severe muscle damage, cardiac stress, and renal dysfunction can culminate in multi-organ failure (MOF). Histopathological evaluations frequently reveal multifocal necrosis across the central nervous system, liver, spleen, pancreas, and lungs, reflecting systemic ischemia and inflammatory responses. Electrolyte imbalances (e.g., hyperkalemia), acidosis, and inflammatory cytokine release further drive dysfunction across organ systems as stress intensifies (Cámara et al., 2019) [5] . [11,12] in wild species such as cervids.  Cardiac Troponin I (cTnI): This is considered more cardiospecific and a reliable biomarker of myocardial necrosis. Elevated cTnI levels have been documented in dolphins with stress cardiomyopathy and in CM across other taxa (Arregui et al., 2020) [1] .  Blood Urea Nitrogen (BUN) and Creatinine:

Clinical Assessment and

Elevations in these renal function markers are indicative of AKI and help distinguish prerenal from intrinsic renal injury.

Histopathological Confirmation

In many clinical studies and case reports, post-mortem histopathology remains the gold standard for confirming stress-induced organ injury. For example, cetaceans show contraction band necrosis in cardiac fibers, severe multifocal skeletal muscle degeneration, and renal tubular casts positive for myoglobin (Spraker et al., 2012) [8] . Microscopic findings also reveal multi-organ congestion, edema, and hemorrhage, corroborating the systemic impact of extreme physiological stress.

Management and Prevention Strategies 7.1 Acute Intervention

There are currently no universally effective treatments for capture myopathy once it develops. Acute management focuses on minimizing metabolic stress, maintaining hydration, correcting electrolyte imbalances, and supporting organ perfusion. Supportive care may include fluid therapy and careful monitoring, but outcomes remain poor once organ systems are deeply compromised (Zahid, 2018, Breed et al., 2019, Dinesh et al., 2020) [19,2,7] .

Minimizing Stress during Wildlife Handling

Preventive measures are crucial because once CM and related syndromes become clinically evident, prognosis is poor. Best practices include:

 Reducing chase and restraint durations during capture.  Providing adequate sedation/immobilization to minimize physical struggle.  Avoiding overheating and ensuring cool, shaded environments post-capture.  Rapid processing and release when possible.

Species Susceptibility and Conservation Implications 8.1 Ungulates and Large Mammals

Studies show that ungulates (Atkinson, 2012) [14] such as deer are particularly prone to CM due to their physiological adaptations for flight responses. Elevated CK and LDH levels correlate with muscle damage and exertional (Landau et al., 2012) [13] stress in these species.

Marine Mammals

Live-stranded dolphins and other marine mammals demonstrate severe rhabdomyolysis and cardiac necrosis, with renal failure often complicating outcomes (Cámara et al., 2019, Nueangphuet et al., 2022) [5,4] .

Birds and Other Wildlife

Birds, especially large birds like cranes and turkeys, experience capture myopathy marked by muscle stiffness, hyperthermia, and sometimes sudden cardiac collapse (Businga et al., 2007) [10] . [15,5,4] . Best practices recommended in wildlife management include:  Minimizing pursuit and handling time to reduce stress and metabolic demand.  Use of species-specific capture methods (e.g., appropriate sedation and restraint) based on biological and behavioral traits.  Reducing auditory and visual stimuli during capture by keeping noise low and using blindfolds when appropriate.  Efficient processing and rapid release where possible to limit duration of stress.

Preventative interventions have been shown to halve the incidence of CM in cervids when handling and processing are optimized (e.g., sedation, minimized noise) (Nueangphuet et al., 2022) [4] 10. [3,5,4] .

Environmental and Welfare Recommendations

For zoo and captive wildlife, enrichment and husbandry practices should minimize chronic stressors. Environmental stress, including inadequate space, social isolation, or unpredictable handling procedures, can predispose animals to stress responses that mimic capture myopathy upon acute challenges. Providing habitat enrichment, predictable daily routines, and minimizing unnecessary handling are integral to welfare-driven conservation (Nueangphuet et al., 2022) [4] . [2] .

Conservation Implications and Policy Considerations

13. Summary Tables Table 1: Comparison of Stress-Induced Organ Injury Mechanisms in Wildlife (Herráez et al., 2007) [3] Component Mechanism Biomarkers Outcomes

Component	Mechanism	Biomarkers	Outcomes
Muscle Injury	Rhabdomyolysis due to exertion/stress(Herráez et al., 2007) [3]	CK, LDH	Muscle necrosis, systemic metabolic acidosis
Cardiac Stress	Stress cardiomyopathy	cTnI, ECG changes	Myocardial degeneration & arrhythmias
AKI	Myoglobinuric nephrosis	BUN, creatinine	Tubular necrosis, oliguria
MOF	Combined organ dysfunction	Composite metabolic panels	Systemic shock, mortality

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Comparison of Stress-Induced Organ Injury Mechanisms in Wildlife (Herráez et al., 2007) [3]

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Cardiac Injury Assessment in Wildlife and Zoo Animals (Landau et al., 2012) [13]

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Muscle Injury

Rhabdomyolysis due to exertion/stress (Herráez et al., 2007) [3] CK

Concluding Remarks

Stress-induced organ injury in wildlife and zoo animals especially cardiac injury, acute kidney injury, and multi-organ failure is a critical pathology with implications for animal welfare, conservation outcomes, and veterinary practice. Although capture myopathy is often the central driver of these syndromes, the breadth of stressors that can precipitate similar pathophysiological cascades demands comprehensive monitoring and preventive strategies. Biomarker profiling plays an increasingly important role in identifying subclinical injury and guiding interventions. However, persistent gaps in species-specific data, validated diagnostic protocols, and effective therapeutic regimens underscore the need for targeted research. Advances in molecular diagnostics and species-tailored management protocols are essential for reducing mortality associated with stress responses in wildlife conservation and zoo medicine. Adopting evidence-based prevention and welfare practices has the potential not only to improve individual animal outcomes but also to support broader biodiversity conservation efforts.

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Comparative chart of Systemic Biomarker (Cebi et al., 2022) [20]

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Comparative chart of biomarker with commercial availability of diagnosis test in market (Hartup et al., 1999, Cattet et al., 2008,

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