Migrating Porcupine Quills: Sudden Death of a Yearling American Black Bear (Ursus americanus) at a Wildlife Rehabilitation Center.

A yearling, intact, apparently healthy male American black bear (Ursus americanus) died peracutely at a rehabilitation facility in Ontario, Canada while overwintering, after recovery from porcupine quilling a few months previously. The postmortem examination findings support that porcupine quill migration should be a differential for cause of sudden death in wildlife.

Sudden death caused by Aeromonas hydrophila in a Crab-eating Macaque (Macaca fascicularis) associated with captivity stress.

Aeromonas hydrophila is a facultative anaerobic gram-negative bacterium regarded as an opportunistic pathogen in animals. A 17-year-old female crab-eating macaque (Macaca fascicularis) died after experiencing anorexia and depression for several days. The carcass was severely emaciated, and the sternum was exposed under subcutaneous lesions in the thorax. Many abnormal pathological lesions were found, including tracheal inflammation, pulmonary inflammatory emphysema, yellowish discoloration of the liver, enlargement of the gall bladder, necrosis of the heart, congested bilateral kidneys, and enlargement of the adrenal glands. The stomach was empty, mucosal ulcerations were found, and the duodenum was congested. Giemsa staining revealed rod-shaped organisms in the whole blood smear and major organs, which were identified as A. hydrophila. The animal had experienced stress, and decreased immune system function possibly contributed to the infection.

Fifteen risk factors associated with sudden death in Thoroughbred racehorses in North America (2009-2021).

OBJECTIVE: To identify risk factors associated with race-related sudden death in Thoroughbred racehorses in the US and Canada. ANIMALS: 4,198,073 race starts made by 284,387 Thoroughbred horses at 144 racetracks in the US and Canada between 2009 and 2021. PROCEDURES: Study data were extracted from the Equine Injury Database, which contains detailed records of 92.2% of all official race starts made in the US and Canada during the study period. Forty-nine potential risk factors were analyzed using univariable and multivariable logistic regression. Cases were defined as race starts that resulted in fatality within 3 days of racing, in which at least 1 of 5 codes relating to sudden death was recorded. Fatalities due to catastrophic musculoskeletal injury were omitted from the study cohort. RESULTS: 536 race starts resulted in sudden death, an incidence rate of 0.13/1,000 starts. Fifteen risk factors were significantly associated with sudden death, including horse age and sex, season and purse of race, race distance, and horses' recent history of injury and lay-up. Horses racing while on furosemide medication were at 62% increased odds of sudden death. CLINICAL RELEVANCE: Associations found between previous injury and sudden death suggests preexisting pathology could contribute in some cases. The association between furosemide and sudden death prompts further study to understand which biological processes could contribute to this result.

Should we be screening cats for cardiomyopathy? If so, how?

Occult feline hypertrophic cardiomyopathy (HCM) can result in unexpected sudden death or congestive heart failure (CHF) following routine interventions such as anesthesia, fluid administration, or, potentially, administration of corticosteroids. Consequently, clinicians would like to be able to screen at-risk cats to detect occult HCM and either avoid the risky intervention or attempt to reduce the risk of death or CHF. Currently, the feline N-terminal-proBrain natriuretic peptide test is the only potential screening test for detecting occult HCM. However, some cardiologists have pointed out the poor sensitivity of the test precludes its use as a screening test. This interpretation appears somewhat flawed. Using the current rapid test will allow clinicians to correctly identify half of the cats with moderate-to-severe occult HCM. A small number of cats without HCM will also test positive, necessitating an ultimately needless echocardiographic evaluation to demonstrate their disease-free status. However, the low prevalence of HCM in the general cat population and the apparently much lower rate of adverse events than would be predicted brings into question whether clinicians should bother screening. Therefore, until a more sensitive and accurate screening test becomes available, clinicians will have to decide for themselves whether identifying half of the at-risk cats of sudden death and CHF with this test is better than identifying none of them.

Parvoviral enteritis and salmonellosis in raccoons with sudden death.

Eight of 9 juvenile raccoons at a rehabilitation center died without obvious prior clinical signs. Gross changes were unremarkable except for mildly distended intestines. Microscopically, crypt loss, distension, necrosis, and regeneration with intranuclear viral inclusions were observed in the small intestine, with marked lymphoid depletion and necrosis in Peyer patches and mesenteric lymph nodes. Immunohistochemistry with a canine parvovirus antibody showed intensive signals of parvoviral antigens in the crypts and lymphoid germinal centers. Metagenomic sequencing allowed assembly of a complete parvoviral genome with >99% identity to canine parvovirus 2a, as well as Salmonella enterica subsp. enterica. Also, S. enterica subsp. enterica serovar Thompson with multiple antimicrobial resistance was isolated from the intestinal contents. Concurrent infection with parvovirus and Salmonella should be included as a differential diagnosis in raccoons with sudden death.

Sudden death caused by spinal cord injury associated with vertebral fractures and fetlock failure in a Thoroughbred racehorse.

The most prevalent causes of death in racehorses are musculoskeletal injuries, causing ~83% of deaths within the racing industry in California and elsewhere. The vast majority of these injuries have preexisting lesions that predispose to fatal injury. A 4-y-old Thoroughbred colt suffered an acute suspensory apparatus failure, including biaxial proximal sesamoid bone fractures of the right front fetlock, causing loss of support of the fetlock joint and consequent fall with fractures of the cervical and sacral spine. Cervical fracture caused spinal cord damage that resulted in sudden death. A preexisting lesion in the medial proximal sesamoid bone likely predisposed to complete fracture of this bone and fetlock breakdown. Interestingly, a comparable osteopenic lesion was present in the intact medial proximal sesamoid bone of the left forelimb, which is consistent with bilateral repetitive overuse injury in racehorses. The morphologic features of the cervical and sacral spine fractures were compatible with acute injury; no evidence of preexisting lesions was seen. Most likely, these acute vertebral fractures occurred as a result of the horse falling. This case emphasizes the importance of performing a detailed autopsy in horses that suffer an appendicular musculoskeletal injury, particularly in fatal cases when the horse dies following a leg injury.

Role of cardiac hypoxia in the pathogenesis of sudden death syndrome in broiler chickens - A metabolic and molecular study.

Sudden death syndrome (SDS) is an economically important disorder in broiler chickens with unknown aetiology. The aim of the present study was to evaluate the metabolic and molecular alterations related to hypoxia in the myocardium of broiler chickens with SDS. Samples from the cardiac muscle of internal control broiler chickens (ICs) (n = 36) and chickens having died of SDS (n = 36) were obtained during the rearing period. The activities of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) and the concentration of lactate were measured in the cardiac tissue using available commercial kits. The expression of hypoxia-inducing factor 1α (HIF1α), glucose transporter 1 (GLUT1), pyruvate dehydrogenase kinase 4 (PDHK4) and monocarboxylate transporter 4 (MCT4) genes was determined in the myocardium by real-time PCR analysis. The results showed the elevation of lactate level and activities of LDH and CPK in the cardiac muscle of SDS-affected chickens compared with the IC birds (P < 0.05). The cardiac muscle expression of HIF1α, MCT4 and GLUT1 genes was increased, while the PDHK4 mRNA level was decreased in the SDS-affected group compared to those in the IC chickens (P < 0.05). Our results showed that metabolic remodelling associated with hypoxia in the cardiac tissues may have an important role in the pathogenesis of cardiac insufficiency and SDS in broiler chickens.

Sudden death due to acute hemoabdomen and hypovolemia from a ruptured splenic hemangiosarcoma in a German shepherd dog.

A 12-year-old neutered male German shepherd dog was evaluated after dying suddenly at home. A few hours prior to the unexpected death the dog displayed anorexia and lethargy. Post-mortem examination and histopathology led to a diagnosis of marked hemoabdomen and hypovolemia due to a single ruptured splenic hemangiosarcoma.

Mort subite due à un hémo-adomen aigu et une hypovolémie à la suite de la rupture d'un hémangiosarcome splénique chez un chien berger allemand. Un chien berger allemand mâle castré âgé de 12 ans fut évalué à la suite de son décès soudain à la maison. Quelques heures avant ce décès inattendu, le chien montra des signes d'anorexie et de léthargie. L'examen post-mortem et histopathologique ont mené à un diagnostic d'hémoabdomen marqué et d'hypovolémie due à la rupture unique d'un hémangiosarcome splénique.(Traduit par Dr Serge Messier).

Sudden Death by Ovarian Hemorrhage and Hemoperitoneum in a Pregnant Miniature Mare.

This report describes a case of sudden death of a pregnant miniature mare due to an acute ovarian hemorrhage leading to fatal hemoperitoneum. The miniature horse was a 12-year-old female, 60 days pregnant, with a body condition score of 7 (1-9), with a history of obesity and laminitis. Necropsy revealed hemoperitoneum due to an ovarian capsule rupture and hemorrhage after a physiological supplementary ovulation and luteinization. Ovarian rupture after ovulation is uncommon in mares.

Exercise-induced Acute Abdominal Haemorrhage due to Iliopsoas Trauma in Racing Greyhounds.

Post-mortem examination of 74 racing greyhounds with sudden, unexpected death was undertaken at the Veterinary School, University of Nottingham, UK, from 2015 to 2019. These investigations revealed severe, acute haemoabdomen with extensive retroperitoneal haemorrhage and an underlying severe, unilateral iliopsoas tear in four cases (5.4%). In all four cases, unilateral trauma and haemorrhage affecting the right iliopsoas muscle was common near the caudal insertion. Despite the acute clinical event, three cases demonstrated histological evidence of previous muscle damage with muscular regeneration, fibrosis and evidence of chronic haemorrhage. To our knowledge, this is the first detailed description of exercise-induced trauma to the iliopsoas muscle leading to extensive haemoretroperitoneum and haemoabdomen with subsequent hypovolaemic shock and death in racing greyhounds.

Characterization of Clostridium novyi isolated from a sow in a sudden death case in Korea.

BACKGROUND: Multifocal spherical nonstaining cavities and gram-positive, rod-shaped, and endospore-forming bacteria were found in the liver of a sow that died suddenly. Clostridium novyi type B was identified and isolated from the sudden death case, and the isolate was characterized by molecular analyses and bioassays in the current study. RESULTS: C. novyi was isolated from the liver of a sow that died suddenly and was confirmed as C. novyi type B by differential PCR. The C. novyi isolate fermented glucose and maltose and demonstrated lecithinase activity, and the cell-free culture supernatant of the C. novyi isolate exhibited cytotoxicity toward Vero cells, demonstrating that the isolate produces toxins. In addition, whole-genome sequencing of the C. novyi isolate was performed, and the complete sequences of the chromosome (2.29 Mbp) and two plasmids (134 and 68 kbp) were identified for the first time. Based on genome annotation, 7 genes were identified as glycosyltransferases, which are known as alpha toxins; 23 genes were found to be related to sporulation; 12 genes were found to be related to germination; and 20 genes were found to be related to chemotaxis. CONCLUSION: C. novyi type B was isolated from a sow in a sudden death case and confirmed by biochemical and molecular characterization. Various virulence-associated genes were identified for the first time based on whole-genome sequencing.

Blackleg without skeletal muscle involvement as a cause of sudden death in unvaccinated calves.

Nine, 5-month-old unvaccinated black Angus calves died in less than 48 hours of each other. The calves expressed minimal or no clinical signs prior to death. On-farm post-mortem examinations were carried out on 3 of the deceased calves, and findings included: necrotizing and fibrinosuppurative myositis of the diaphragm muscle, and fibrinosuppurative pleuritis and epicarditis. Fluorescent antibody testing for pathogenic clostridia identified Clostridium chauvoei and a diagnosis of blackleg was made. The remainder of the herd were then vaccinated.

Charbon symptomatique sans implication des muscles squelettiques comme cause de mort subite chez des veaux non-vaccinés. Neuf veaux non-vaccinés de race Angus âgés de 5 mois sont morts en moins de 48 heures l'un de l'autre. Les veaux ne présentèrent que peu ou pas de signes cliniques avant la mort. Des examens post-mortem réalisés à la ferme ont été effectués sur trois des veaux décédés, et les trouvailles incluaient: myosite nécrosante et suppurative du muscle diaphragmatique, et pleurésie fibrino-suppurative et épicardite. La recherche de clostridies pathogènes à l'aide d'anticorps fluorescents permis d'identifier Clostridium chauvoei et un diagnostic de charbon symptomatique fut posé. Le restant du troupeau fut alors vacciné.(Traduit par Dr Serge Messier).

iTRAQ-based proteomic analysis reveals key proteins affecting cardiac function in broilers that died of sudden death syndrome.

Sudden death syndrome (SDS), which is a cardiac-related condition commonly observed in chickens selected for rapid growth, causes significant economic losses to the global poultry industry. Its pathogenesis in broilers is poorly understood, and little is known about the proteome of the heart tissue of SDS broilers. A quantitative proteomic approach using isobaric tags for relative and absolute quantification labeling of peptides was used to characterize the protein expression profiles in the left ventricle of SDS broilers. These proteins were further analyzed by bioinformatics, and two proteins were validated by western blot analysis. We identified 186 differentially expressed proteins (DEPs), of which 72 were upregulated, and 114 were downregulated in the SDS group. Functional annotation suggested that 7 DEPs were related to cardiac muscle contraction, and another 7 DEPs were related to cardiac energy metabolism. Protein interaction network predictions indicated that differences in cardiac muscle contraction between SDS and healthy groups were regulated by troponin T, tropomyosin alpha-1 chain, fast myosin heavy chain HCIII, myosin-1B, coronin, and myoglobin, whereas differences in cardiac energy metabolism and biosynthesis of amino acids were regulated by gamma-enolase, phosphoglycerate mutase, NADH-ubiquinone oxidoreductase chain 2, serine/threonine-protein kinase, myoglobin, and alpha-amylase. Our expression profiles provide useful information and new insights into key proteins to elucidate SDS for further studies.

Prognostic value of coupling interval, prematurity index and heart rate variability in Boxer dogs / Valor prognóstico do intervalo de acoplamento, índice de prematuridade e variabilidade da frequência cardíaca em cães da raça Boxer

Boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC) can experience sudden cardiac death regardless of presence/absence of clinical signs. The aims of this retrospective study were two-fold: 1) to investigate the coupling interval (CI) and prematurity index (PI) of ventricular arrhythmias (VA), and the heart rate variability (HRV) in Boxers, and 2) to evaluate their impact on overall survival time. The first 24-hour Holter 36 client-owned Boxer dogs meeting inclusion/exclusion criteria were evaluated for the number, morphology, site of origin, complexity, CI and PI, of ventricular premature complexes (VPCs), and time domain HRV. The effect on survival was assessed, considering the presence/absence of ventricular tachycardia (VT), and syncope. All-cause mortality was considered as the end-point, with median survival times being obtained by Kaplan-Meier analyses and compared by log-rank test. Polymorphic VPCs were more common in symptomatic dogs than asymptomatic. VPCs in dogs with VT were less premature, due to the influence of heart rate on PI despite comparable CI. The PI and mean heart rate (HRme) were significantly different between VT and non-VT dogs but did not discriminate adequately between groups as standalone tests. Median survival time was shorter in Boxer dogs with VT (463 vs 1645 days, HR: 4.31, P=0.03). The HRV parameters, SDNN and SDANN, were both associated with prognosis. The CI and PI were not demonstrated to be prognostic surrogates in Boxer dogs with VA. HRme≥112bpm is 100% sensitive but only 46% specific for detecting VT in Boxers on the 24-hour Holter. Presence of VT, SDNN≤245ms, or SDANN≤134ms at the time of the first 24-hour Holter was associated with a shorter survival.(AU)

Cães da raça Boxer com cardiomiopatia arritmogênica do ventrículo direito (CAVD) podem apresentar morte súbita independentemente da presença/ausência de sinais clínicos. Os objetivos desse estudo retrospectivo foram: 1) investigar o intervalo de acoplamento (IA) e o índice de prematuridade (IP) das arritmias ventriculares e a variabilidade da frequência cardíaca (VFC) em Boxers, e 2) avaliar o impacto de tais características sob o tempo de sobrevida global. O primeiro Holter de 24 horas de 36 Boxers selecionados para os critérios de inclusão/exclusão foram avaliados para o número, morfologia, local de origem, complexidade, IA e IP dos complexos ventriculares prematuros (CVPs) e da VFC no domínio do tempo. O efeito na sobrevida foi avaliado, considerado a presença/ausência de taquicardia ventricular (TV), e síncope. O desfecho final foi a mortalidade global, com o tempo de sobrevida mediano sendo obtido pela análise de Kaplan-Meier e comparado pelo teste de log-rank. CVPs polimórficos foram mais comuns em cães sintomáticos. Os CVPs em Boxers com TV foram menos prematuros, devido à influência da frequência cardíaca (FC) sobre o IP, apesar de IA comparáveis. O IP e a FC média diferiram entre os cães com TV e os sem, mas não discriminam adequadamente os grupos como variáveis isoladas. A sobrevida global foi menor nos cães com TV (463 dias vs 1645 dias, HR=4,31, P=0,03). Os parâmetros da VFC, SDNN e SDANN, foram associados ao prognóstico. O IA e o IP não possuem valor prognóstico em Boxers com arritmias ventriculares. A FC média ≥112bpm é 100% sensível, mas apenas 46% específica para detectar Boxers com TV no Holter de 24 horas. A presença de TV, SDNN≤245ms, ou SDANN≤134ms no momento do primeiro Holter de 24 horas estão associados a menor sobrevida global no Boxer.(AU)

The R9H phospholamban mutation is associated with highly penetrant dilated cardiomyopathy and sudden death in a spontaneous canine model.

Causative mutations for familial dilated cardiomyopathy (DCM) have been identified in the phospholamban gene. There are many poorly understood aspects about familial DCM (variable penetrance, expression) which may be studied in natural animal models. We characterized genetic aspects of familial DCM in a canine model with a high incidence of sudden death. A missense G > A mutation in exon 1 of the phospholamban gene that changed an amino acid from arginine to histidine was identified in affected dogs. This variant was predicted to be deleterious. We describe a spontaneous canine model of familial DCM and sudden death with the R9H mutation. In comparison to a reported human family, the variant was highly penetrant and resulted in sudden death. Genetic penetrance of this mutation may be influenced by genetic or environmental modifiers. The dog provides an excellent model in which to study complex aspects of familial DCM.