Auscultation and echocardiographic findings in Bull Terriers with and without polycystic kidney disease

OBJECTIVE: To investigate a possible association between Bull Terrier polycystic kidney disease (BTPKD) and cardiac disease, to determine the prevalence of mitral valve disease (MVD) and left ventricular outflow tract obstruction (LVOTO) in the Australian Bull Terrier population, and to compare auscultation and echocardiography in detection of cardiac disease in Bull Terriers. DESIGN: Ninety-nine Bull Terriers, ranging in age from 8 weeks to 13 years and 11 months were auscultated and examined using renal ultrasonography; 86 were also examined using echocardiography. The prevalence and severity of heart defects in dogs with BTPKD was compared with that in dogs without BTPKD. RESULTS: Nineteen of these 99 dogs were diagnosed with BTPKD. Forty-two percent of Bull Terriers with BTPKD and 28% of those without BTPKD had murmurs characteristic of mitral regurgitation or LVOTO. How recently an animal was descended from an ancestor with BTPKD was associated with presence (P = 0.008) and loudness of a murmur (P = 0.009). Overall, echocardiography detected MVD in 39% of Bull Terriers, with increased prevalence in older animals (P = 0.003). Mitral stenosis was found in eight cases. Fifty-three percent of dogs in this study had evidence of LVOTO, with obstruction consisting of a complex of lesions including dynamic or fixed subvalvular LVOTO, significantly narrowed left ventricular outflow tract or valvular aortic stenosis. Dogs with BTPKD, or those descended from dogs with BTPKD, were more likely to have MVD (P = 0.006), and while LVOTO was not more common in these dogs, if they did have LVOTO, they were more likely to have severe obstruction than dogs with no ancestors with BTPKD (analysed in three ways P = 0.028 to 0.001). In this study, 46% of Bull Terriers without a murmur or arrhythmia had cardiac disease detected on echocardiographic examination. CONCLUSION: Cardiac disease, especially MVD and LVOTO, was common in Bull Terriers in this study, and those with BTPKD had an increased risk of cardiac abnormalities. Auscultation did not detect a significant number of Bull Terriers with cardiac disease.     

Polycystic kidney disease in bull terriers: an autosomal dominant inherited disorder

The prevalence, mode of inheritance and urinalysis findings in Bull Terriers with polycystic kidney disease were assessed by screening 150 clinically normal dogs. The disorder was diagnosed in 39 dogs on the basis of renal ultrasound results and family history of the disease. In equivocal cases confirmation required gross and histopathological renal examination. Necropsy was performed on nine affected dogs and the kidneys from another five affected animals were also examined. Renal cysts were usually bilateral, occurred in cortex and medulla and varied from less than 1 mm to over 2.5 cm in diameter. Cysts were lined by epithelial cells of nephron origin. Abnormal urine sediment and proteinuria were common in affected dogs. The disease appears to be inherited in a highly penetrant autosomal dominant manner.     

Familial progressive nephropathy in young Bull Terriers

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes.

The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.     

Familial progressive nephropathy in young Bull Terriers

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes. The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.     

Echocardiographic parameters in 14 healthy English Bull Terriers

OBJECTIVE: To determine the range of various cardiac parameters using echocardiography in apparently normal, healthy English Bull Terriers. DESIGN: Fourteen English Bull Terriers were selected for study. Cardiac auscultation of the parents of these dogs was normal. Echocardiographic examination of one parent of each animal showed: no mitral or aortic valve abnormalities; no myocardial lesions; no two dimensional evidence of fixed or dynamic left ventricular outflow tract obstruction; and no systolic aortic or left ventricular outflow tract turbulence on colour flow Doppler examination. The 14 selected dogs did not have arrhythmias or murmurs, and on echocardiographic examination had similar findings to their parents. Systolic blood pressure was measured in all dogs and they had no clinical evidence of Bull Terrier polycystic kidney disease or Bull Terrier hereditary nephritis. PROCEDURE: All dogs were auscultated and subjected to a sequential global echocardiographic assessment of the heart, including two dimensional long and short axis, and colour flow Doppler interrogation of the mitral and aortic valves. Dimensional measurements, including those from the left atrium, aortic annulus and left ventricle, were taken from a right parasternal window, and derived values such as fractional shortening, stroke volume and left atrial to aortic annulus ratio were calculated. Peak systolic aortic velocity was measured from the left parasternal window using two dimensional-guided pulsed wave Doppler with angle correction. Systolic blood pressure was measured using a Doppler monitor. The absence of Bull Terrier polycystic kidney disease was determined using renal ultrasonography, and of Bull Terrier hereditary nephritis using urinary protein to creatinine ratio. RESULTS: These 14 dogs had greater left ventricular wall thickness and smaller aortic root diameters than those reported as normal for other breeds of comparable body size. Left atrial dimensions were also larger, however this may have been due to the "maximising" method of measurement. These apparently normal English Bull Terriers also had higher aortic velocities than those reported for other breeds, possibly due to a smaller aortic root diameter or other anatomic substrate of the left ventricular outflow tract, lower systemic vascular resistance, or breed-specific "normal" left ventricular hypertrophy. While these dogs were selected to be as close to normal as possible, the breed may have a particular anatomy that produces abnormal left ventricular echocardiographic parameters. CONCLUSION: These echocardiographic parameters may be used to diagnose left ventricular outflow tract obstruction and left ventricular hypertrophy, and inaccurate diagnoses may result if breed-specific values are not used.     

Blood, Bull Terriers and Babesiosis: further evidence for direct transmission of Babesia gibsoni in dogs

This study reports on the epidemiology of Babesia gibsoni in American Pit Bull Terriers living in a region of western Victoria in southern Australia. Both American Pit Bull Terriers (n = 100) and other dog breeds (n = 51) were screened for B gibsoni using immunofluorescent antibody testing (IFAT) and/or polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). A questionnaire was also completed by each dog owner, ascertaining the husbandry and habits of the dogs sampled. Fourteen dogs were positive for B gibsoni using IFAT and/or PCR-RFLP and all were American Pit Bull Terriers. Dogs that were male and/or had been bitten by or were biters of other American Pit Bull Terriers were more likely to be B gibsoni positive, thus suggesting that blood-to-blood transmission contributes to the spread of this disease between dogs.     

Babesia gibsoni infection among dogs in the southeastern United States

OBJECTIVE: To identify subclinical Babesia gibsoni infection in American Pit Bull Terriers from the southeastern United States and to determine the genetic sequence of parasite DNA isolated from these dogs. DESIGN: Case series. ANIMALS: 33 American Pit Bull Terriers and 87 dogs of various other breeds. PROCEDURE: Blood smears were examined for microscopic evidence of the parasite, and DNA was extracted from blood samples and used in a polymerase chain reaction (PCR) assay designed to amplify the small subunit ribosomal RNA gene sequence of B. gibsoni. Amplification products of the expected size were sequenced, and sequences were compared with published sequences for B. gibsoni isolates. Hematocrit, platelet count, mean platelet volume, WBC count, and eosinophil count were compared between dogs with positive PCR assay results and dogs with negative results. RESULTS: Results of the PCR assay were positive for 18 of the 33 (55%) American Pit Bull Terriers, including all 10 dogs with microscopic evidence of parasitemia. Only 1 of these dogs was clinically ill at the time blood samples were collected. Results of microscopic evaluation of blood smears and of the PCR assay were negative for the 87 other dogs. Hematocrit and platelet count were significantly lower in dogs with positive PCR assay results than in dogs with negative results. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that American Pit Bull Terriers in the southeastern United States may be subclinically infected with B. gibsoni. However, subclinical infection was not identified in dogs of other breeds from the same geographic area.     

Inherited congenital extrahepatic portosystemic shunts in Cairn terriers

The pathogenesis of congenital portosystemic shunt (CPSS) in dogs still is incompletely understood. In Irish Wolfhounds and Yorkshire Terriers, CPSS is reported to be hereditary. The aim of this study was to investigate a possible genetic basis and the mode of inheritance of CPSS in Cairn Terriers. Between July 1990 and July 2001, 6-week-old pups of the Dutch Cairn Terrier population were screened by measuring venous ammonia concentrations and in the presence of hyperammonemia by ultrasonography, autopsy, portal vein angiography, or exploratory celiotomy. The same successfully operated female was used 3 times in test matings with an unrelated affected male, her unaffected sire, and an affected offspring. The prevalence of CPSS in the general Cairn Terrier population, the direct progeny of frequently used males, and the offspring of the test matings were tested for significant differences. In total, 6,367 Cairn Terriers were screened; 32 males and 26 females had CPSS. In 3 large family groups, significantly higher prevalences were found compared with the general population (P < .0001, P < .0001, and P < .044). The prevalence of CPSS in the offspring of the test matings was significantly higher (P < .002) than in the general population. No sex predisposition occurred among the affected dogs. The higher prevalence of CPSS in the test matings and the 3 family groups compared with the general population indicates that CPSS in Cairn Terriers is a genetic disease. The inheritance is autosomal and most likely polygenic or monogenic with variable expression.     

A KCNJ10 mutation previously identified in the Russell group of terriers also occurs in Smooth-Haired Fox Terriers with hereditary ataxia and in related breeds

Background

Hereditary ataxias with similar phenotypes were reported in the Smooth-Haired Fox Terrier, the Jack Russell Terrier and the Parson Russell Terrier. However, segregation analyses showed differing inheritance modes in these breeds. Recently, molecular genetic studies on the Russell group of terriers found independent mutations in KCNJ10 and CAPN1, each associated with a specific clinical subtype of inherited ataxia. The aim of this study was to clarify whether or not Smooth-Haired Fox Terriers with hereditary ataxia and dogs of other related breeds harbor either of the same mutations. A sub goal was to update the results of KCNJ10 genotyping in Russell group terriers.

Findings

Three Smooth-Haired Fox Terriers with hereditary ataxia and two Toy Fox Terriers with a similar phenotype were all homozygous for the KCNJ10 mutation. The same mutation was also found in a heterozygous state in clinically unaffected Tenterfield Terriers (n = 5) and, in agreement with previous studies, in Jack Russell Terriers, Parson Russell Terriers, and Russell Terriers.

Conclusions

A KCNJ10 mutation, previously associated with an autosomal recessive spinocerebellar ataxia in Jack Russell Terriers, Parson Russell Terriers, and Russell Terriers segregates in at least three more breeds descended from British hunting terriers. Ataxic members of two of these breeds, the Smooth-Haired Fox Terrier and the Toy Fox Terrier, were homozygous for the mutation, strengthening the likelihood that this genetic defect is indeed the causative mutation for the disease known as “hereditary ataxia” in Fox Terriers and “spinocerebellar ataxia with myokymia, seizures or both” in the Russell group of terriers.     

Assessment of retinal function and characterization of lysosomal storage body accumulation in the retinas and brains of Tibetan Terriers with ceroid-lipofuscinosis

OBJECTIVE: To characterize lysosomal storage body accumulation in the retina and brain of Tibetan Terriers with ceroid-lipofuscinosis and determine whether the disease in these dogs is accompanied by impaired retinal function and retinal degeneration. ANIMALS: Three 7- to 10-year-old Tibetan Terriers with ceroid-lipofuscinosis and 1 healthy 5-year-old Tibetan Terrier. PROCEDURE: Owners completed a questionnaire to identify behavioral and physical signs indicative of ceroid-lipofuscinosis. Neurologic, behavioral, and ophthalmologic evaluations, including full-field electroretinograms, were performed on each dog. Fluorescence, light, and electron microscopy were performed on specimens of retina, cerebral cortex, and cerebellum of all dogs postmortem. RESULTS: Behavioral assessments of the affected dogs revealed moderate visual impairment in low-light conditions but good vision in bright light. On funduscopic evaluation of these dogs, abnormalities detected ranged from none to signs of moderately advanced retinal degeneration. Compared with findings in the control dog, electroretinography revealed depressed rod cell function with some impairment of cone cell function in the affected dogs. Morphologically, disease-specific storage bodies were detected in retinal Müller cells and neurons, particularly in ganglion cells, and in cells of the cerebral cortex and cerebellum in affected dogs. Substantial photoreceptor cell loss and disruption of photoreceptor outer segment morphology appeared to develop late in the disease. IMPLICATIONS FOR HUMAN MEDICINE: The similarities between ceroid-lipofuscinosis in Tibetan Terriers and some forms of ceroid-lipofuscinosis in humans suggest that the canine disease may have a genetic and biochemical basis similar to that of one of the ceroid-lipofuscinosis disorders in humans.     

Topical flea and tick pesticides and the risk of transitional cell carcinoma of the urinary bladder in Scottish Terriers

OBJECTIVE: To determine whether use of topical flea and tick products increases the risk of transitional cell carcinoma (TCC) of the urinary bladder in Scottish Terriers. DESIGN: Case-control study. ANIMALS: 87 adult Scottish Terriers with TCC (cases) and 83 adult Scottish Terriers with other health-related conditions (controls). PROCEDURE: Owners of study dogs were recruited through private veterinary practices and the Scottish Terrier Club of America. History of exposure to flea and tick products 1 year prior to diagnosis of TCC for case dogs and during a comparable period for control dogs was obtained through a questionnaire. Risk of TCC associated with exposure to flea and tick products was determined by means of univariate and multiple logistic regression analysis. RESULTS: After adjustment for host factors, Scottish Terriers treated with topical spot-on flea and tick products containing fipronil or imidacloprid did not have an increased risk of TCC, compared with Scottish Terriers that had never been exposed to any flea and tick products. The risk of TCC associated with use of older topical flea and tick products such as shampoos, dips, powders, sprays, and collars could not be evaluated because of the low number of owners in the study population that had used such products. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that use of topical spot-on flea and tick products does not increase the risk of TCC in Scottish Terriers.     

Dog sperm swimming parameters analysed by computer‐assisted semen analysis of motility reveal major breed differences

Dogs have undergone an intensive artificial selection process ever since the beginning of their relationship with humans. As a consequence, a wide variety of well‐defined breeds exist today. Due to the enormous variation in dog phenotypes and the unlikely chance of gene exchange between them, the question arises as to whether they should still be regarded as a single species or, perhaps, they be considered as different taxa that possess different reproductive traits. The aim of this study was therefore to characterize some male reproductive traits, focusing on kinematic characteristics of dog spermatozoa from several breeds. Thirty‐seven dogs from the following breeds were used: Staffordshire Bull Terrier, Labrador Retriever, Spanish Mastiff, Valencian Rat Hunting Dog, British Bulldog and Chihuahua. Semen samples were obtained via manual stimulation and diluted to a final sperm concentration of 50 million/ml, and they were subsequently analysed by the computer assisted semen analysis (CASA‐Mot) ISAS^®v1 system. Eight kinematic parameters were evaluated automatically. All parameters showed significant different values among breeds and among individuals within each breed. The fastest sperm cells were those of Staffordshire Bull Terriers and the slowest were recorded in Chihuahuas. The intra‐male coefficient of variation (CV) was higher than the inter‐male CV for all breeds with the Staffordshire Bull Terrier showing the lowest values. When taking into consideration the cells by animal and breed, discriminant analyses showed a high capability to predict the breed. Cluster analyses showed a hierarchical classification very close to that obtained after phylogenetic studies with genome markers. In conclusion, future workers on dog spermatozoa should bear in mind major differences between breeds and realize that results cannot be extrapolated from one to another. Because sperm characteristics are associated with breed diversity, dogs may represent a good model to examine changes in reproductive parameters associated with selection processes.     

Hypomagnesemia and hypocalcemia associated with protein-losing enteropathy in Yorkshire terriers: five cases (1992-1998)

OBJECTIVE: To determine clinical and laboratory findings associated with protein-losing enteropathy, hypomagnesemia, and hypocalcemia in Yorkshire Terriers. DESIGN: Retrospective study. ANIMALS: 5 purebred or crossbred Yorkshire Terriers with protein-losing enteropathy, hypomagnesemia, and hypocalcemia. PROCEDURE: Medical records were reviewed for dogs with protein-losing enteropathy, hypomagnesemia, and hypocalcemia. RESULTS: Of 8 dogs with these signs, 5 had Yorkshire Terrier breeding. Common findings were diarrhea, abdominal effusion, leukocytosis, neutrophilia, hypocalcemia (ionized calcium), hypomagnesemia, hypoproteinemia, hypoalbuminemia, hypocholesterolemia, and increased serum activity of aspartate aminotransferase. CONCLUSIONS AND CLINICAL RELEVANCE: Yorkshire Terriers are at increased risk for development of protein-losing enteropathy with hypomagnesemia and decreased ionized calcium concentration. Hypomagnesemia and hypocalcemia may have a related pathogenesis involving intestinal loss, malabsorption, and abnormalities of vitamin D and parathyroid hormone metabolism. Serum electrolyte replacement may be required to avoid neurologic and metabolic problems.     

Evaluation of haplotypes associated with copper toxicosis in Bedlington Terriers in Australia

OBJECTIVE: To evaluate the haplotype distribution associated with the copper toxicosis gene and the segregation of the mutated allele in a Bedlington Terrier population in Australia. ANIMALS: 131 Bedlington Terriers. PROCEDURE: Samples of DNA and RNA were obtained from each dog. Genetic status of each dog was evaluated by use of the DNA markers C04107; single nucleotide polymorphism (SNP), which was adjacent to exon 2 of Murr1; and a deletion marker for exon 2. A subgroup of the study population was evaluated by use of biochemical and histologic techniques to elucidate the correlation between genotype and phenotype. RESULTS: We identified a recombination between the C04107 marker and Murr1 and a variation in a nucleotide in the splice site of exon 2 in our Bedlington Terrier cohort. Furthermore, we identified a novel haplotype associated with copper toxicosis in this cohort. CONCLUSIONS AND CLINICAL RELEVANCE: Our findings indicate that the deletion of exon 2 was not the sole cause of copper toxicosis, although only exon 2 deletion of Murr1 has been responsible for copper toxicosis in Bedlington Terriers. Although we failed to find a novel mutation in our cohort, we identified an affected dog family with an intact exon 2. Furthermore, we found that an SNP in the 5' splicing site of exon 2 may or may not be associated with a novel mutation of the Murr1 gene or other genes. Loss of linkage between the C04107 marker and the Murr1 gene was also identified in a certain family of dogs.     

Modified rib pivot lateral thoracotomy: a case series

Objective

To describe a modified rib pivot thoracotomy and its clinical application in client‐owned dogs and cats.

Study design

Case series of 24 dogs and 1 cat requiring a thoracotomy.

Methods

A lateral thoracic incision over the required thoracic segment was made. The latissimus dorsi muscle was reflected dorsally. The predetermined rib was identified and the periosteum overlying the rib was elevated circumferentially, avoiding the intercostal neurovascular structures. Holes were pre‐placed above and below the proposed osteotomy site. The rib was osteotomised and pivoted cranially. The pleura was incised and the required intrathoracic procedure was then performed. The thoracic cavity was closed by pre‐placement of a suture through the pre‐placed holes within the osteotomised rib. The pleura and intercostal musculature were closed, avoiding the intercostal neurovascular structures. The rib was re‐apposed and the lateral approach was closed. The cases included were reviewed for both the rib pivoted as per the procedure required and postoperative complications.

Results

The study group comprised 8 Staffordshire Bull Terriers, 2 Poodles, 2 German Shepherd Dogs, 1 each of Basset Hound, Rhodesian Ridgeback, Golden Retriever, Australian Shepherd, Vizsla, Bull Mastiff, Schnauzer, Jack Russell Terrier, Bulldog, Deerhound, Labrador Retriever and Australian Terrier, and 1 cat. A modified rib pivot thoracotomy was performed for lung lobectomy (n = 11), oesophagectomy (7), subtotal pericardectomy (5), patent ductus arteriosus ligation (1) and thoracic duct ligation (1). Follow‐up ranged from 2 to 40 weeks postoperatively. Postoperative complications included seroma formation in two dogs.

Conclusion

A modified rib pivot thoracotomy should be considered as an alternative lateral thoracic approach with good exposure, minimal complications and low morbidity.     

Canine zinc-responsive dermatosis.

Zinc is important in a multitude of biological functions, including regulation of the immune response, modulation of keratogenesis and wound healing, maintenance of normal reproductive function, and acuity of taste and smell. Zinc-responsive dermatosis is an uncommon disease of dogs resulting from either an absolute or relative deficiency in zinc. Dermatological lesions are characterized by erythema, alopecia, scales, and crusts that primarily affect the head. Two forms of the disease exist: a familial form affecting Alaskan Malamutes and Siberian Huskies and a form that affects growing puppies fed zinc-deficient or oversupplemented diets. The history, clinical signs, and skin biopsy results are typically diagnostic. Life-long zinc supplementation is usually necessary in the familial form of the disease, although dietary correction alone may be curative in the second form. Lethal acrodermatitis is a rare inherited disorder of Bull Terriers that does not respond to zinc supplementation and is invariably fatal.     

Surgical management of suspected congenital luxation of the radial head in three dogs

Abstract

CASE HISTORIES: Three dogs, aged between 11 and 20 weeks, were presented with unilateral forelimb lameness, with an associated bony prominence on the lateral elbow.

CLINICAL FINDINGS AND DIAGNOSIS: Radiographs revealed a caudolateral luxation of the radial head in all cases, consistent with a diagnosis of suspected congenital luxation of the radial head. Surgical reduction and stabilisation involved open reduction of the radial head, and in two cases the use of a trans articular pin.

CLINICAL RELEVANCE: Congenital luxation of the radial head is an uncommon condition that has conflicting reports in the literature regarding its cause, heritability, breed predisposition, treatment and prognosis. The three cases here occurred in young dogs of English Bull Terrier, Jack Russell Terrier, and Staffordshire Bull Terrier breeds. Surgical reduction and stabilisation provided successful outcomes, in all cases. Only six cases of congenital luxation of the radial head managed surgically have previously been reported in the literature.     

Dwarfism in Tibetan Terrier dogs with an LHX3 mutation

Canine pituitary dwarfism in German Shepherd and related dog breeds has been reported to be associated with a 7-bp deletion mutation in intron 5 of the LHX3 gene. This mutation is transmitted as an autosomal recessive trait that results in dwarf dogs with significantly smaller stature and abnormal haircoat, and potentially early death. Phenotypically, affected adult dogs are proportionally dwarfs. These dwarfs also have a soft, woolly puppy coat that fails to transition into the typical adult hair coat, and marked hair loss occurs in some dogs. We report a similar manifestation of dwarfism in Tibetan Terriers with the same LHX3 mutation. Dwarf Tibetan Terrier puppies were born physically normal but failed to gain weight or to grow at the same rate as their normal littermates. The 7-bp deletion mutation of the LHX3 gene was identified in both alleles of 3 Tibetan Terrier dwarfs from 3 litters, which were biologically related. All parents of these dogs are carriers, confirming transmission of dwarfism in an autosomal recessive manner. Recognition and detection of this mutation will help in guiding future breeding plans to eventually eliminate this trait from Tibetan Terriers.     

Nodular dermatofibrosis and cystic renal disease in three mixed-breed dogs and a Boxer dog

Three mixed-breed dogs and a Boxer dog with nodular dermatofibrosis are described. The three mixed breed dogs had concurrent renal epithelial cysts ( n  = 2) or renal cystadenomas ( n  = 1); these lesions were visualized antemortem on ultrasonographic examination. One of these dogs was a 7-year-old Labrador Retriever-Gordon Setter mixed breed which survived 5 years after diagnosis, and was euthanized for unrelated causes. The Boxer dog had renal cystic adenomatous hyperplasia and renal cystadenocarcinomas which were not visualized on ultrasonographic examination but were diagnosed at necropsy.