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Review
. 2022 Aug 31;12(17):2257.
doi: 10.3390/ani12172257.

The Welfare of Fighting Dogs: Wounds, Neurobiology of Pain, Legal Aspects and the Potential Role of the Veterinary Profession

Affiliations
Review

The Welfare of Fighting Dogs: Wounds, Neurobiology of Pain, Legal Aspects and the Potential Role of the Veterinary Profession

Daniel Mota-Rojas et al. Animals (Basel). .

Abstract

Throughout history it has been common to practice activities which significantly impact on animal welfare. Animal fighting, including dogfighting, is a prime example where animals often require veterinary care, either to treat wounds and fractures or to manage pain associated with tissue and where death may even result. Amongst the detrimental health effects arising are the sensory alterations that these injuries cause, which not only include acute or chronic pain but can also trigger a greater sensitivity to other harmful (hyperalgesia) or even innocuous stimuli (allodynia). These neurobiological aspects are often ignored and the erroneous assumption made that the breeds engaged in organized fighting have a high pain threshold or, at least, they present reduced or delayed responses to painful stimuli. However, it is now widely recognized that the damage these dogs suffer is not only physical but psychological, emotional, and sensory. Due to the impact fighting has on canine welfare, it is necessary to propose solution strategies, especially educational ones, i.e., educating people and training veterinarians, the latter potentially playing a key role in alerting people to all dog welfare issues. Therefore, the aim of this review is to describe the risk factors associated with dogfighting generally (dog temperament, age, sex, nutrition, testosterone levels, environment, isolation conditions, socialization, education, or training). A neurobiological approach to this topic is taken to discuss the impact on dog pain and emotion. Finally, a general discussion of the format of guidelines and laws that seek to sanction them is presented. The role that veterinarians can play in advancing dog welfare, rehabilitating dogs, and educating the public is also considered.

Keywords: animal fight; dog aggression; dog fight; dog welfare; illegal sports; pain.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Search methodology.
Figure 2
Figure 2
Diverse lesions caused by fights with conspecifics. (A) A severe wound in the foot of the left pelvic limb of this patient after a fight with a Rottweiler. The site shows exposed bone (metatarsals, phalanges) and ligaments and the loss of tissue continuity with multiple exposed fractures. (B) Image of an exposed fracture of the distal portion of the femur caused by a fight with a stray dog. (C,D) Images of an English Bull Terrier brought for examination with diverse lesions caused by a spontaneous fight with a stray dog. There are evident scratches and penetrating bites in the muzzle, nasal plane, and left thoracic limb.
Figure 3
Figure 3
Lesions caused during a fight between two Pit Bulls (one male, one female). The female suffered the deepest wounds, shown in image (A,C). Obvious orifices in the skin of the mandibular region due to penetrating injuries inflicted by the other dog’s teeth (B). Lesions in the oral cavity, specifically the lower gum and lip (D). Deep lesions in the right thoracic limb that resulted from bites by the other dog. Most of these lesions required thorough washing and suturing to join the edges of the bites and prescriptions for antibiotics and analgesics.
Figure 4
Figure 4
Corporal regions and percentage of the incidences of the principal lesions that occur during dogfights. 1. Dorsal and lateral area of the head with an incidence of 57–94%. 2. Ocular and periorbital region with an incidence of 18%. 3. Pinnae, incidence = 55%. 4. Muzzle and oral mucosa, incidence = 51–89%. 5. Dorsal and lateral aspects of the neck, incidence = 73%. 6. Ventral neck and thoracic region, incidence = 58%. 7. Scapular region, incidence = 44%. 8. Thoracic limbs, incidence = 63–97%. 9. Thoracic and lumbar vertebral region, incidence = 10%. 10. Lateral thoracic and abdominal region, incidence = 27%. 11. Ventral thoracic and abdominal region, incidence = 21%. 12. Pelvic limbs, incidence = 52%. 13. Pelvis and tail, incidence = 15% (Miller et al. [15] and Intarapanich et al. [5]).
Figure 5
Figure 5
Route of nociceptive transmission from the peripheral nerves to the CNS, beginning with transduction of a nociceptive stimulus during a dogfight. Abbreviations: ASP: aspartate; BK: bradykinin; CA: catecholamines; CGRP: calcitonin-gene-related peptide; GLU: glutamate; H: histamine; H+: hydrogen; IL: interleukin; K+: potassium; LT: leukotrienes; NT: neurotrophins; PAF: platelet-activating factor; PC: prostacyclin; PG: prostaglandin; ROS: free radicals; SP: substance P; TNFα: tumoral necrosis factor; TRPV1: transient receptor potential vanilloid 1; TX: thromboxane; 5HT: serotonin Johnson et al. [50], Hernández-Avalos et al. [51], Imlan et al. [52], Youn et al. [53], and Mota-Rojas et al. [54]).
Figure 6
Figure 6
Sensitization of the nervous system. Inflammatory mediators (histamine, NGF) released after tissue injury (bites) bind to peripheral receptors located on first-order neurons. Activation of these receptors (TrkA, TRPV1, ASIC3, BR2) and ionic channels, such as Na+, Ca2+ and K+, modulates and enhance the excitability of the primary afferent nerve cells. When the nociceptive signal reaches the dorsal horn of the spinal cord, it causes the release of pronociceptive neurochemicals including GLU, SP, CGRP, and BDNF, from the primary neurons to the second-order neuron receptors, mainly AMPA, NMDA, NK1, CGRPR, and TrkB. These receptors promote the transmission of the excitatory signaling to the brain and cortical structures, where the perception of pain is consciously recognized. Abbreviations: AMPA: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic; ASIC3: acid-sensing ion channel 3; BDNF: brain-derived neurotrophic factor; BR2: bradykinin receptor 2; CGRP: calcitonin-gene-related peptide; DRG: dorsal root ganglion; GLU: glutamate; NGF: nerve growth factor; NK1: neurokinin 1 receptor; NMDA: N-methyl-D-aspartate; p75: neurotrophin receptor; SP: substance P; TrkA: tropomyosin kinase receptor A; TRPV1: transient potential receptor vanilloid 1. DeLeo [66], Verri et al. [67], Watkins et al. [68], and Enomoto et al. [69].

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