Heartworm in Cats

Litster, A. L. and R. B. Atwell (2008). "Feline heartworm disease: a clinical review." J Feline Med Surg 10(2): 137-44.

Heartworm disease is caused by Dirofilaria immitis and is transmitted by mosquitoes in heartworm-endemic areas around the world. Dogs and other canids are the definitive hosts, but cats can also be infected. In endemic areas, it is estimated that the feline infection rate is about 5-10% of the canine infection rate. While many cats infected with heartworm have no signs of disease, others may have chronic respiratory signs similar to asthma, or chronic vomiting, or acute death. Diagnosis of feline heartworm is challenging, as there is no single perfect test methodology. Treatment is also problematic as there are no adulticides judged to be safe and effective in cats. Most infected cats are managed with supportive care. A number of safe and effective drugs are available for prevention of heartworm infection in cats, in both oral and topical formulations.
>> PubMed abstract

Related articles:
Hoch, H. and K. Strickland (2008). "Canine and feline dirofilariasis: life cycle, pathophysiology, and diagnosis." Comp Contin Edu Vet 30(3): 133-141.
>> PubMed abstract

Hoch, H. and K. Strickland (2008). "Canine and feline dirofilariasis: prophylaxis, treatment, and complications of treatment." Comp Contin Edu Vet 30(3): 146-151.
>> PubMed abstract

KNOW Heartworms

More on cat health: Winn Feline Foundation

Litster, A. L. and R. B. Atwell (2008). "Feline heartworm disease: a clinical review." J Feline Med Surg 10(2): 137-44.

Heartworm disease is caused by Dirofilaria immitis and is transmitted by mosquitoes in heartworm-endemic areas around the world. Dogs and other canids are the definitive hosts, but cats can also be infected. In endemic areas, it is estimated that the feline infection rate is about 5-10% of the canine infection rate. While many cats infected with heartworm have no signs of disease, others may have chronic respiratory signs similar to asthma, or chronic vomiting, or acute death. Diagnosis of feline heartworm is challenging, as there is no single perfect test methodology. Treatment is also problematic as there are no adulticides judged to be safe and effective in cats. Most infected cats are managed with supportive care. A number of safe and effective drugs are available for prevention of heartworm infection in cats, in both oral and topical formulations.
>> PubMed abstract

Related articles:
Hoch, H. and K. Strickland (2008). "Canine and feline dirofilariasis: life cycle, pathophysiology, and diagnosis." Comp Contin Edu Vet 30(3): 133-141.
>> PubMed abstract

Hoch, H. and K. Strickland (2008). "Canine and feline dirofilariasis: prophylaxis, treatment, and complications of treatment." Comp Contin Edu Vet 30(3): 146-151.
>> PubMed abstract

KNOW Heartworms

More on cat health: Winn Feline Foundation

Read More

Continuous Glucose Monitoring for Diabetic Cats

Wiedmeyer, C. E. and A. E. Declue (2008). "Continuous glucose monitoring in dogs and cats." J Vet Intern Med 22(1): 2-8.


Continuous glucose monitoring systems originally designed for human diabetic patients have been adapted for use in dogs and cats. Sensors continually measure glucose in subcutaneous interstitial fluid (ISF), rather than in blood. A small, flexible sensor is inserted through the skin into the subcutaneous space, secured to the skin, and attached to a recording device. The ISF glucose is recorded and stored every 5 minutes (288 readings per 24 hours). After the device is removed, the data are downloaded to a computer for analysis. The instrument can remain in place for several days, hospitalization of the patient is not necessary, and the normal daily routine of the animal can be maintained. This review from the University of Missouri-Columbia is designed to describe the technology behind the continuous glucose monitoring system, describe the clinical use of the instrument, provide clinical examples in which it may be useful, and discuss future directions for continuous glucose monitoring in dogs and cats.
>> PubMed abstract


Related articles:
Ristic, J. M., M. E. Herrtage, et al. (2005). "Evaluation of a continuous glucose monitoring system in cats with diabetes mellitus." J Feline Med Surg 7(3): 153-62.
>> PubMed abstract


More on cat health: Winn Feline Foundation Library

Wiedmeyer, C. E. and A. E. Declue (2008). "Continuous glucose monitoring in dogs and cats." J Vet Intern Med 22(1): 2-8.


Continuous glucose monitoring systems originally designed for human diabetic patients have been adapted for use in dogs and cats. Sensors continually measure glucose in subcutaneous interstitial fluid (ISF), rather than in blood. A small, flexible sensor is inserted through the skin into the subcutaneous space, secured to the skin, and attached to a recording device. The ISF glucose is recorded and stored every 5 minutes (288 readings per 24 hours). After the device is removed, the data are downloaded to a computer for analysis. The instrument can remain in place for several days, hospitalization of the patient is not necessary, and the normal daily routine of the animal can be maintained. This review from the University of Missouri-Columbia is designed to describe the technology behind the continuous glucose monitoring system, describe the clinical use of the instrument, provide clinical examples in which it may be useful, and discuss future directions for continuous glucose monitoring in dogs and cats.
>> PubMed abstract


Related articles:
Ristic, J. M., M. E. Herrtage, et al. (2005). "Evaluation of a continuous glucose monitoring system in cats with diabetes mellitus." J Feline Med Surg 7(3): 153-62.
>> PubMed abstract


More on cat health: Winn Feline Foundation Library

Read More

Pyruvate Kinase Deficiency in Abyssinian & Somali Cats

Kohn, B. and C. Fumi (2008). "Clinical course of pyruvate kinase deficiency in Abyssinian and Somali cats." J Feline Med Surg 10(2): 145-53.

Pyruvate kinase (PK) is one of the key regulatory enzymes for energy generation in red blood cells (RBCs). A deficiency in one PK isoenzyme leads to energy deprivation within the RBCs, resulting in a shortened survival time and hemolysis. PK deficiency has been described in several species, including humans and dogs. The first case of feline PK deficiency was identified in 1992 in an Abyssinian cat. The disease has since been identified in the related Somali breed, as well as in a few domestic shorthair cats. PK deficiency is transmitted as an autosomal recessive trait. The molecular defect has been identified and a genetic screening test has been developed. The objective of this study performed in Berlin, Germany was to examine the clinical signs, laboratory parameters, and course of disease in Abyssinian and Somali cats with PK deficiency. Over a period ranging from under 1 year to over 11 years (median 4.3), the disease was monitored in 25 PK-deficient cats. According to the owners, 11 cats did not show signs of disease. In the other 14 cats, clinical signs included lethargy, diarrhea, pale mucous membranes, anorexia, weight loss, among others. Laboratory abnormalities included anemia, increased aggregated reticulocyte counts, hyperglobulinemia, hyperbilirubinemia, and increased liver enzymes. PK deficiency shows variation in age of onset and severity of signs. Abyssinian and Somali cats destined for breeding should be tested as PK-deficient cats can be asymptomatic.
>> PubMed abstract


Josephine Deubler Genetic Disease Testing Laboratory, University of Pennsylvania


More on cat health: Winn Feline Foundation Library

Kohn, B. and C. Fumi (2008). "Clinical course of pyruvate kinase deficiency in Abyssinian and Somali cats." J Feline Med Surg 10(2): 145-53.

Pyruvate kinase (PK) is one of the key regulatory enzymes for energy generation in red blood cells (RBCs). A deficiency in one PK isoenzyme leads to energy deprivation within the RBCs, resulting in a shortened survival time and hemolysis. PK deficiency has been described in several species, including humans and dogs. The first case of feline PK deficiency was identified in 1992 in an Abyssinian cat. The disease has since been identified in the related Somali breed, as well as in a few domestic shorthair cats. PK deficiency is transmitted as an autosomal recessive trait. The molecular defect has been identified and a genetic screening test has been developed. The objective of this study performed in Berlin, Germany was to examine the clinical signs, laboratory parameters, and course of disease in Abyssinian and Somali cats with PK deficiency. Over a period ranging from under 1 year to over 11 years (median 4.3), the disease was monitored in 25 PK-deficient cats. According to the owners, 11 cats did not show signs of disease. In the other 14 cats, clinical signs included lethargy, diarrhea, pale mucous membranes, anorexia, weight loss, among others. Laboratory abnormalities included anemia, increased aggregated reticulocyte counts, hyperglobulinemia, hyperbilirubinemia, and increased liver enzymes. PK deficiency shows variation in age of onset and severity of signs. Abyssinian and Somali cats destined for breeding should be tested as PK-deficient cats can be asymptomatic.
>> PubMed abstract


Josephine Deubler Genetic Disease Testing Laboratory, University of Pennsylvania


More on cat health: Winn Feline Foundation Library

Read More

Feline Dysautonomia in the United States

Kidder, A. C., C. Johannes, et al. (2008). "Feline dysautonomia in the Midwestern United States: a retrospective study of nine cases." J Feline Med Surg 10(2): 130-6.


Dysautonomia in domestic animals results in clinical signs related to dysfunction or failure of the sympathetic and parasympathetic nervous systems. The disease was first reported in cats in 1982 in the United Kingdom, where it is often called Key-Gaskell syndrome. The disease remains uncommon in the United States. Common clinical findings include depression, anorexia, dysphagia, regurgitation or vomiting, constipation, dilated unresponsive pupils, prolapsed nictitating membranes, dry nose and mouth, reduced tear production, bradycardia, and megaesophagus. No etiology is known for this disease in any species although a neurotoxin or an infectious agent has been suggested. This study reports on 9 cases of feline dysautonomia in eastern Kansas and western Missouri. Interestingly, most cases of canine dysautonomia have occurred in eastern Kansas and western and southern Missouri. Unfortunately, feline dysautonomia is associated with a poor prognosis. Only 1 cat in this study could be classified as making a recovery.
>> PubMed abstract


Related articles:
Nunn, F., T. Cave, et al. (2004). "Association between Key-Gaskell syndrome and infection by Clostridium botulinim type C/D." Vet Rec 155(4): 111-115.
>> PubMed abstract


Cave, T., C. Knottenbelt, et al. (2003). "Outbreak of feline dysautonomia (Key-Gaskell syndrome) in a closed colony of pet cats." Vet Rec 153(13): 387-392.
>> PubMed abstract


More on cat health: Winn Feline Foundation Library

Kidder, A. C., C. Johannes, et al. (2008). "Feline dysautonomia in the Midwestern United States: a retrospective study of nine cases." J Feline Med Surg 10(2): 130-6.


Dysautonomia in domestic animals results in clinical signs related to dysfunction or failure of the sympathetic and parasympathetic nervous systems. The disease was first reported in cats in 1982 in the United Kingdom, where it is often called Key-Gaskell syndrome. The disease remains uncommon in the United States. Common clinical findings include depression, anorexia, dysphagia, regurgitation or vomiting, constipation, dilated unresponsive pupils, prolapsed nictitating membranes, dry nose and mouth, reduced tear production, bradycardia, and megaesophagus. No etiology is known for this disease in any species although a neurotoxin or an infectious agent has been suggested. This study reports on 9 cases of feline dysautonomia in eastern Kansas and western Missouri. Interestingly, most cases of canine dysautonomia have occurred in eastern Kansas and western and southern Missouri. Unfortunately, feline dysautonomia is associated with a poor prognosis. Only 1 cat in this study could be classified as making a recovery.
>> PubMed abstract


Related articles:
Nunn, F., T. Cave, et al. (2004). "Association between Key-Gaskell syndrome and infection by Clostridium botulinim type C/D." Vet Rec 155(4): 111-115.
>> PubMed abstract


Cave, T., C. Knottenbelt, et al. (2003). "Outbreak of feline dysautonomia (Key-Gaskell syndrome) in a closed colony of pet cats." Vet Rec 153(13): 387-392.
>> PubMed abstract


More on cat health: Winn Feline Foundation Library

Read More

Renal Failure Associated with Tainted Pet Food

Brown, C. A., K. S. Jeong, et al. (2007). "Outbreaks of renal failure associated with melamine and cyanuric acid in dogs and cats in 2004 and 2007." J Vet Diagn Invest 19(5): 525-31.

Contaminated pet food caused the death or illness of an unknown number of cats and dogs, most recently in 2007. Initial reports of the cause were confusing and contradictory, but over time, the toxicity was traced to food adulterated with melamine and cyanuric acid. This study from the University of Georgia evaluated histopathologic, toxicologic, and clinicopathologic changes in 16 animals (6 dogs and 10 cats) affected in outbreaks of pet food-associated renal failure in 2004 and 2007. All affected animals had evidence of uremia with anorexia, vomiting, lethargy, polyuria, azotemia and hyperphosphatemia. All animals either died or were euthanized due to severe renal failure. Lesions were found in the distal tubules of the kidneys of all animals at necropsy. Unique crystals were found in the distal tubules or collecting ducts of the kidneys in all animals. Renal tissue from all animals contained melamine and cyanuric acid. This study provides further evidence that melamine and cyanuric acid causes renal failure in cats and dogs.
>> PubMed abstract

Related articles:
Puschner, B., R. H. Poppenga, et al. (2007). "Assessment of melamine and cyanuric acid toxicity in cats." J Vet Diagn Invest 19(6): 616-24.
>> PubMed abstract

More on cat health: Winn Feline Foundation Library

Brown, C. A., K. S. Jeong, et al. (2007). "Outbreaks of renal failure associated with melamine and cyanuric acid in dogs and cats in 2004 and 2007." J Vet Diagn Invest 19(5): 525-31.

Contaminated pet food caused the death or illness of an unknown number of cats and dogs, most recently in 2007. Initial reports of the cause were confusing and contradictory, but over time, the toxicity was traced to food adulterated with melamine and cyanuric acid. This study from the University of Georgia evaluated histopathologic, toxicologic, and clinicopathologic changes in 16 animals (6 dogs and 10 cats) affected in outbreaks of pet food-associated renal failure in 2004 and 2007. All affected animals had evidence of uremia with anorexia, vomiting, lethargy, polyuria, azotemia and hyperphosphatemia. All animals either died or were euthanized due to severe renal failure. Lesions were found in the distal tubules of the kidneys of all animals at necropsy. Unique crystals were found in the distal tubules or collecting ducts of the kidneys in all animals. Renal tissue from all animals contained melamine and cyanuric acid. This study provides further evidence that melamine and cyanuric acid causes renal failure in cats and dogs.
>> PubMed abstract

Related articles:
Puschner, B., R. H. Poppenga, et al. (2007). "Assessment of melamine and cyanuric acid toxicity in cats." J Vet Diagn Invest 19(6): 616-24.
>> PubMed abstract

More on cat health: Winn Feline Foundation Library

Read More