Pathology in Practice

Robert J. Ossiboff Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Robert J. Ossiboff in
Current site
Google Scholar
PubMed
Close
 DVM, PhD
,
Laura L. Coffee Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Laura L. Coffee in
Current site
Google Scholar
PubMed
Close
 DVM, MS
, and
Ricardo de Matos Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

Search for other papers by Ricardo de Matos in
Current site
Google Scholar
PubMed
Close
 LMV

Click on author name to view affiliation information

Table 1—Blood glucose concentrations in blood samples collected simultaneously from the right lateral saphenous vein and the left cephalic vein of a 7-year-old ferret (Mustela putorius furo) that was evaluated because of acute right hind limb lameness that progressed within 1 week to persistent dragging of the limb with an absence of deep pain sensation and motor function and coolness to the touch, compared with all other limbs.

Table 1—

Blood glucose concentrations in blood samples collected simultaneously from the right lateral saphenous vein and the left cephalic vein of a 7-year-old ferret (Mustela putorius furo) that was evaluated because of acute right hind limb lameness that progressed within 1 week to persistent dragging of the limb with an absence of deep pain sensation and motor function and coolness to the touch, compared with all other limbs.

VariableLeft cephalic veinRight lateral saphenous veinReference interval
Blood glucose concentration (mg/dL)995180–117

History

A 7-year-old castrated male ferret (Mustela putorius furo) was evaluated at the Cornell University Hospital for Animals because of acute lameness of the right hind limb. The owner first noted the lameness 1 week prior, when the ferret was still able to ambulate with use of the affected limb. The lameness progressed to a non–weight-bearing stage suddenly on the day of the evaluation. Past medical history included a mid-diaphyseal fracture of the right tibia, which had been successfully repaired with placement of an intramedullary pin 2 years prior; hyperadrenocorticism of 3 years’ duration, which had been initially treated with monthly leuprolidea injections and later with left adrenalectomy; and prostatic cysts.

Clinical and Clinicopathologic Findings

On evaluation, the ferret was non–weight bearing in the right hind limb; there were periods when the right hind pes would be knuckled and dragged and periods when it was held in a normal position. The affected limb initially felt slightly cooler than did the left hind limb and forelimbs. There was minor bruising on the lateral and medial surfaces of the distal portion of the right hind limb, and a withdrawal reflex was present. As the day progressed, the affected limb became markedly cool to the touch and the withdrawal reflex decreased; the ferret's dragging of the limb became persistent. Palpation of the proximal portion of the right hind limb elicited a painful response not evident on palpation of the other limbs. Abdominal palpation revealed an enlarged right kidney, splenomegaly, distended urinary bladder, and presumptively enlarged prostate. Findings of auscultation of the thorax were considered normal. The remainder of the physical examination findings were unremarkable.

Radiography confirmed the presence of an intramedullary pin in the right tibia, with no evidence of pin migration. The tibia was well aligned, and a smooth bridging callous was present in the mid-diaphyses of the tibia and fibula. Color Doppler ultrasonography was used to attempt to visualize blood flow through the femoral artery in both the right and left hind limbs, but flow could not be detected in either limb, possibly because of the small size of the vessels in ferrets. A neurologic examination was performed and revealed an absence of deep pain sensation and motor function in the right hind limb, with apparently normal findings in all other limbs. Blood samples were collected simultaneously from the right lateral saphenous vein and the left cephalic vein, and the blood glucose concentration in each sample was measured separately by means of the same methodb (Table 1). Owing to a poor prognosis, the owner elected euthanasia and postmortem evaluation.

Formulate differential diagnoses from the history, clinical findings, and Table 1—then turn the page →

Gross and Histopathologic Findings

At necropsy, the ferret weighed 725 g (1.6 lb) and was in thin body condition. The right iliac vasculature was congested, but a definitive cause of the unilateral hind limb paresis was not identified. The heart weighed 6.2 g (0.014 lb [0.9% of body weight]); no gross abnormalities were noted. Other notable necropsy findings included a round, thin-walled, 4-cm-diameter, fluid-filled prostatic cyst; fibrosis of the parenchyma of the left kidney; and enlargement of the mesenteric lymph nodes.

Histopathologic analysis of sections of the abdominal aorta and internal and external iliac arteries revealed a dense, pale, eosinophilic lamellar coagulum composed of erythrocytes, leukocytes, and fibrin (consistent with an acute thrombus) at the origin of the right internal and external iliac arteries from the common iliac artery (Figure 1); the thrombus extended a short distance down the lumina of both the right internal and external iliac arteries. No abnormalities in the endothelium surrounding the thrombus were identified. Within the wall of the left ventricle and a left ventricular papillary muscle, there were multifocal areas of myocardial degeneration and myocyte loss with fibrosis and infiltration by adipocytes (Figure 2). The parenchyma of the left kidney was replaced by dense fibrous connective tissue with complete absence of viable nephrons and multifocal areas with moderate numbers of hemosiderin-laden macrophages. In the right kidney, there were multifocal acute and chronic infarcts with extensive interstitial fibrosis and mild lymphoplasmacytic inflammation. There was no evidence of active thrombosis in either kidney. Other histologic findings included a pancreatic islet cell tumor, lymphoid hyperplasia of the mesenteric lymph nodes, and mild, segmental lymphocytic gastroenteritis.

Figure 1—
Figure 1—

Photomicrograph of a section of the right iliac artery at the level of its bifurcation into the internal and external iliac arteries in a 7-year-old ferret (Mustela putorius furo) that was evaluated because of acute right hind limb lameness that progressed within 1 week to persistent dragging of the limb with an absence of deep pain sensation and motor function and coolness to the touch, compared with all other limbs. A thromboembolus (T) occludes the lumina (L) of the vessels. The arterial walls are highlighted (asterisks). H&E stain; bar = 1 mm.

Citation: Journal of the American Veterinary Medical Association 248, 5; 10.2460/javma.248.5.501

Figure 2—
Figure 2—

Photomicrograph of a section of the left ventricular myocardium in the ferret in Figure 1. Notice the locally extensive area of myocyte loss and replacement by fibrous connective tissue and adipocytes. Individual myocytes have variable amounts of sarcoplasmic vacuolation, and occasional myocytes have hypereosinophilic sarcoplasm. H&E stain; bar = 200 μm.

Citation: Journal of the American Veterinary Medical Association 248, 5; 10.2460/javma.248.5.501

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: severe acute thromboembolism of the right common iliac artery, subacute to chronic multifocal myocardial degeneration with interstitial fibrosis, and acute and chronic multifocal renal infarcts.

Case summary: unilateral iliac artery thromboembolism in a ferret.

Comments

To the authors’ knowledge, this is the first report of acute arterial thromboembolism associated with acute pelvic limb paresis in a ferret. Pelvic limb paresis in ferrets develops frequently, often in animals with hypoglycemia, cardiac disease, anemia, signs of severe pelvic or caudal abdominal pain, intervertebral disk disease, traumatic injury, neoplasia, toxicosis, or primary neurologic disease.2 In ferrets, several infectious diseases, such as infection with rabies virus, canine distemper virus, or Aleutian disease virus, may also result in hind limb paresis, paralysis, or ataxia.3,4 In ferrets with cardiac disease, hind limb paresis is thought to be associated with either generalized weakness or congestive heart failure5; thromboembolic disease associated with cardiomyopathies in ferrets has not been documented.

The clinical signs in the ferret of this report were similar to those observed in domestic cats with aortic thromboembolism (saddle thrombus) secondary to hypertrophic, restrictive, or otherwise unclassified cardiomyopathies. In cats, severe left atrial enlargement, blood stasis, and endocardial fibrosis are all risk factors for thromboembolus formation.6 Cats with embolization most commonly develop unilateral or bilateral hind limb paresis as a result of saddle thrombi at the distal aortic trifurcation. In affected animals, signs of pain are common, and the affected limbs are often firm and cool to the touch. Disruption of arterial blood flow can be confirmed by Doppler ultrasonography or comparison of blood glucose concentration in a blood sample from the affected limb or limbs with that in a blood sample from an unaffected limb. Coronary, renal, mesenteric, or pulmonary embolization may also occur and can be rapidly fatal.6

In ferrets, heart disease is relatively common, particularly in middle-aged and geriatric animals. Both dilated and hypertrophic cardiomyopathies in ferrets have been reported.5,7 In dilated cardiomyopathy, 1 or both ventricles are dilated because of global systolic dysfunction. Ferrets with hypertrophic cardiomyopathy have impaired diastolic function as a result of impaired filling of the left ventricle. Unlike cats, left ventricular hypertrophy secondary to hypertension or hyperthyroidism has not been reported for ferrets.7 Cardiomyopathies in ferrets are histologically characterized by myocyte degeneration, myofiber loss, and occasional inflammatory infiltrates, with progression to fibrosis and myocardial dysfunction.5 Valvular heart disease, arrhythmias, myocardial inflammation, and dirofilariasis are also important causes of cardiac disease in ferrets.

Postmortem examination of the ferret of this report revealed an acute thromboembolus that occluded the right common iliac artery as well as acute and chronic infarcts in both kidneys. Histologic changes in the heart, characterized by myocyte degeneration and loss and multifocal areas of mild fibrosis, were consistent with cardiomyopathy. Although abnormalities were not identified during gross examination of the heart, the weight of the heart (6.2 g [0.9% of total body weight]) was abnormally high. In a study8 by Truex et al, male black-footed ferrets (Mustela nigripes) had a mean body weight of 1,102 g (2.43 lb) and a mean heart weight of 5.0 g (0.011 lb [0.45% of total body weight]), and female black-footed ferrets had a mean body weight of 780.8 g (1.72 lb) and a mean heart weight of 3.7 g (0.008 lb [0.47% of total body weight]). Although no heart dimensions were obtained during the postmortem examination of the ferret of the present report, the noted cardiomegaly was suggestive of hypertrophic cardiomyopathy. The other antemortem clinical diagnoses and postmortem findings, including an islet cell tumor, prostatic cysts, and hyperadrenocorticism, were notable but unlikely to have contributed to the formation of arterial thromboemboli.

The geriatric ferret of the present report had unilateral pelvic limb paresis secondary to acute occlusion of the common iliac artery associated with cardiomegaly and cardiomyopathy. Thromboembolic disease should be considered as a differential diagnosis for ferrets with hind limb paresis or paralysis, particularly if there is clinical or radiographic evidence of cardiac disease.

Footnotes

a.

Lupron Depot, AbbVie Inc, Chicago, Ill.

b.

Assure 4, Arkray USA, Edina, Minn.

References

  • 1. Quesenberry KE, Orcutt C. Basic approach to veterinary care. In: Quesenberry KE, Carpenter JW, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. 3rd ed. St Louis: Elsevier, 2012;1326.

    • Search Google Scholar
    • Export Citation
  • 2. Antinoff N, Giovanella CJ. Musculoskeletal and neurologic diseases. In: Quesenberry KE, Carpenter JW, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. 3rd ed. St Louis: Elsevier, 2012;132140.

    • Search Google Scholar
    • Export Citation
  • 3. Niezgoda M, Briggs DJ, Shaddock J, et al. Pathogenesis of experimentally induced rabies in domestic ferrets. Am J Vet Res 1997; 58: 13271331.

    • Search Google Scholar
    • Export Citation
  • 4. Oxenham M. Aleutian disease in the ferret. Vet Rec 1990; 126: 585.

  • 5. Wagner RA. Ferret cardiology. Vet Clin North Am Exot Anim Pract 2009; 12: 115134.

  • 6. Fox PR. CVT update: therapy for feline myocardial diseases. In: Bonagura KD, ed. Kirk's current veterinary therapy XIII: small animal practice. Philadelphia: Saunders, 2000;762767.

    • Search Google Scholar
    • Export Citation
  • 7. Morrisey JK, Kraus MS. Cardiovascular and other diseases. In: Quesenberry KE, Carpenter JW, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. 3rd ed. St Louis: Elsevier, 2012;6277.

    • Search Google Scholar
    • Export Citation
  • 8. Truex RC, Belej R, Ginsberg LM, et al. Anatomy of the ferret heart: an animal model for cardiac research. Anat Rec 1974; 179: 411422.

All Time Past Year Past 30 Days
Abstract Views 161 0 0
Full Text Views 1086 1008 204
PDF Downloads 159 92 19
Advertisement