Margaret Stalker
Animal Health Laboratory, University of Guelph, ON
AHL Newsletter 2019;23(4):16-17.
There are few things more traumatic for a pet owner than witnessing the completely unexpected death of a family pet, or finding a pet lying dead in the home, yard or neighborhood. Determining the cause of sudden unexpected death is one of the main reasons companion animals are submitted to the Animal Health Laboratory for postmortem examination. Perhaps not surprisingly, the history often includes the owner’s query if this could be a case of malicious poisoning, particularly for animals with access to the outdoors. Thankfully, this scenario appears to be the notable exception, rather than the rule. As part of the OAHN Companion Animal disease surveillance network, causes of sudden unexpected death or animals found dead were tabulated from Sept 2015 to Sept 2019. Sudden death was defined as unexpected death occurring in less than 1 hour with no observed or recognized antecedent clinical signs.
For dogs (n =150 cases), the most frequent cause of death was underlying occult neoplasia (42 cases). The majority of these were hemangiosarcoma (33 cases), often with catastrophic pericardial, thoracic or abdominal hemorrhage as the cause of death. Cardiac disease was the second most frequent diagnosis (36 cases), including various forms of cardiomyopathy, and 4 cases of congenital aortic stenosis. Respiratory disease (16 cases including 9 cases of acute onset choking/asphyxia due to aspirated food), gastrointestinal accidents (11 cases including 9 cases of gastric dilation/volvulus and 2 cases of gastrointestinal foreign bodies with perforation), and trauma (14 cases including suspected motor vehicle trauma and 1 likely predator attack) were also common causes of unexpected death. Two cases of acute pancreatic necrosis, 10 cases of miscellaneous infectious diseases (including septicemia, pyelonephritis and hemolytic anemia due to Babesia canis infection), and 3 cases of miscellaneous inflammatory conditions (including idiopathic hemorrhagic enterocolitis and exertional rhabdomyolysis) were diagnosed, as well as a single case of juvenile Addison’s disease. There was a single case of chocolate toxicosis and a single case of bromodiolone toxicosis, as well as 5 additional cases of suspected anticoagulant rodenticide toxicity. Note that a definitive diagnosis was sometimes not reached due to limitations in the amount of testing allowed by the owner for various reasons. In 8 cases, no detectable lesions or cause of death was found.
For cats (n = 71 cases), the most frequent cause of death was underlying cardiac disease (44 cases), the majority of which were various forms of cardiomyopathy (42 cases). Trauma (including presumed predator attack), miscellaneous inflammatory conditions (ranging from anaphylaxis to chronic cholangiohepatitis with sepsis), and cases with no detectable lesions or cause of death each accounted for 6 cases, while miscellaneous infectious conditions (including panleukopenia, Salmonella typhimurium sepsis and cerebral cuterebriasis) accounted for 5 cases. Neoplasia (2 cases) and urethral obstruction/FLUTD (2 cases) were the least frequent diagnoses, the reverse of the trend in the dog population where neoplasia was the most frequent diagnosis.
While this list is likely not surprising to the experienced practitioner, it underscores the utility of postmortem examination in these highly emotional cases, and can help owners come to a place of closure without lingering suspicions of foul play.
Murray Hazlett
Animal Health Laboratory, University of Guelph, ON
AHL Newsletter 2019;23(4):18-19.
A one-year-old DSH cat was left alone for a weekend and the owners returned to find the cat dead on the bed where it had been left, with some signs of struggle and urine and feces present. The cat was an indoor/outdoor cat and there were concerns about toxicosis.
Submission to the Animal Health Laboratory for autopsy showed two foci of acute hemorrhage on the rostral/dorsal aspect of both cerebral cortices (Fig. 1A), with meningeal hemorrhage and a hemorrhagic tract in the grey matter of the right hemisphere (Fig. 1B). Two adjacent histology sections of cerebral cortex showed a large migrating parasite compatible with a Cuterebra spp. larva.
Most cases of cuterebriasis in cats occur from July to September, and they have been associated with parasitic tracks, laminar cerebrocortical necrosis, cerebral infarction and gliosis. There is evidence that at least some cases of feline ischemic encephalopathy are caused by these larvae.
Cuterebra spp. flies lay eggs near openings to rodent nests where the larvae enter hosts (normally rodents, but sometimes cats and dogs) and most commonly cause parasite-containing cutaneous nodules with fistulas through which the larva breaths. Aberrant migration can occur and is recognized especially in cats. Examination of AHL pathology records for feline CNS disease from 2008 to present revealed a total of 11 cases in which the pathologist felt that Cuterebra spp. was a possible etiology (Table 1). This was based on the lesions (idiopathic encephalomalacia, encephalitis with eosinophils) and the time of year (8 in July to September). In only one case (the present one) was the larva actually found in the brain.
Figure 1. Cuterebra spp. migration in a cat brain. A. Foci of hemorrhage in dorsal-rostral cerebral cortex (arrows). B. Hemorrhagic tract in cortex (arrow). C, D. Migrating larva in brain, H+E.
Table 1. Pathology coded cases of Cuterebra spp., all host species, all body sites.
Species |
Month |
Diagnosis/Location |
Dog (1 Pug) |
September |
peritracheal cuterebriasis |
Cat (5 cases) |
July to September |
3 brain, 2 skin, |
Rabbit (2 cases) |
July to August |
1 skin, 1 ocular |
Mouse (1 case) |
August |
skin |
Reference
Williams, KJ et al. Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. Vet Pathol 1998;35:330-343.
Kris Ruotsalo
Animal Health Laboratory, University of Guelph, Guelph, ON
AHL Newsletter 2019;23(4):19-20.
Blastomycosis is a systemic mycotic infection caused by the dimorphic fungus Blastomyces dermatitidis. This organism grows in acidic soil in proximity to water and within decaying organic matter as a saprophytic mycelial form that reproduces sexually, producing infective spores. Resident environmental organisms are thought to restrict the survival of Blastomyces, with a special set of environmental conditions required for proliferation of the organism; rain or heavy dew appears to facilitate the release of infectious spores. Blastomycosis is primarily a disease of North America, and is considered endemic to the Mississippi, Missouri, and Ohio River valleys, the Mid-Atlantic States, Manitoba, Ontario, Quebec, and southern Saskatchewan.
Most cases of blastomycosis are acquired by inhalation of spores. The spores enter the terminal airway and establish a primary infection in the lungs. At body temperature in tissues, the organism transforms into the yeast form and replicates asexually. The budding yeast forms are 5 to 20 um in diameter and have a thick, refractile, double-contoured cell wall. The yeast forms are too large to enter the terminal airway in an aerosol, thus transmission through coughing is unlikely. Following establishment of infection in the lungs, the yeast disseminates throughout the body via the lymphatics and vasculature. Preferred sites of infection in the dog include the lung, eyes, and skin, but many other sites including lymph nodes, bones, and subcutaneous tissues may be affected. In dogs, subclinical blastomycosis infection is unlikely.
Direct inoculation of Blastomyces into a wound from the soil may also occur, but is considered less likely. Because of this, cutaneous blastomycosis is usually considered a manifestation of disseminated disease.
Clinical signs of blastomycosis in dogs can include, but are not restricted to, anorexia, weight loss, cough, dyspnea, ocular disease, lameness, pyrexia, and skin lesions. These signs may have been apparent for days to weeks (occasionally longer) and are of varying severity. CBC and serum biochemistry usually reveal nonspecific findings of mild anemia, leukocytosis, and hyperglobulinemia. Diagnosis is typically made by identification of Blastomyces yeast through cytological or histological preparations. The site of sampling depends upon the clinical presentation, but when appropriate, evaluation of bronchoalveolar lavage fluid, aspiration of enlarged lymph nodes, and impression smears of skin lesions typically reveal a marked inflammatory response (suppurative to mixed inflammation), along with low numbers of characteristic yeast. Serology may occasionally be required to help establish a diagnosis if identification of organisms is not rewarding. Culture is not indicated due to the risk to laboratory personnel from inhalation of the mycelial form of the organism.
It is important to note that the yeast phase of Blastomyces cannot be transmitted from animals to people, or from person to person through aerosols. Care should be taken to avoid bites when handling a dog infected with blastomycosis, and contaminated knives or needles can accidently inoculate veterinarians during biopsy or postmortem procedures.
Recently, two cases of canine infection with Blastomyces dermatitidis were identified in samples submitted to the AHL Clinical Pathology Laboratory. The first case involved a 1-year-old female spayed mixed breed dog that initially presented with a history of lameness. Subsequently she developed respiratory signs and interdigital skin lesions with enlargement of draining lymph nodes. The second case was a 3-year-old, female spayed Boxer with a month-long history of dyspnea that apparently resolved without treatment. She then developed multiple draining cutaneous lesions on the hind limbs and the flank. Fine needle aspiration of lymph nodes and impression smears of skin lesions from both patients revealed marked suppurative inflammation with numerous extracellular yeast. Modified Wright’s-stained smears obtained from an affected lymph node illustrate the classic refractile, deeply basophilic, thick-walled structure of these yeast (Fig. 1A), along with evidence of broad-based budding (Fig. 1B).
Figure 1. A Blastomyces dermatitidis yeast in a fine aspirate of a lymph node (arrow) (modified Wright’s). B Broad-based budding of Blastomyces dermatitidis yeast (arrow) (modified Wright’s).
Photos courtesy of Dr. Felipe Reggeti
References
1. Legendre AM. Blastomycosis. In: Greene CE ed. Infectious Diseases of the Dog and Cat, 4th ed. St. Louis, MO: Elsevier, 2012.
2. Davies JF et al. Prevalence and geographic distribution of canine and feline blastomycosis in the Canadian prairies. Can Vet J 2013;54:753-760.
3. Brown et al. Epidemiology and geographic distribution of blastomycosis, histoplasmosis, and coccidiomycosis, Ontario, Canada 1990-2015. Emerg Infect Dis 2018;24:1257-1266.