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


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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


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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

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Tritrichomonas Infection in the Uterus of a Cat

Dahlgren, S. S., B. Gjerde, et al. (2007). "First record of natural Tritrichomonas foetus infection of the feline uterus." J Small Anim Pract 48(11): 654-7.

Tritrichomonas foetus is an emerging intestinal parasite of cats, causing chronic large bowel diarrhea. In cattle, this protozoan parasite is a sexually transmitted pathogen, infecting the uterus of cows and the preputial cavity and urethral orifice of bulls. In this case report, the first feline record of T. foetus infection of the uterus is described in a 17-month old Exotic Shorthair queen in Norway with pyometra. This queen had no history of diarrhea. Three other cats in the cattery were diagnosed with T. foetus infection using PCR on fecal samples: a 4.5-year old Persian male with intermittent diarrhea, a 22-month old male Exotic Shorthair with normal feces, and a 2.5-year old female Persian with normal feces. Interestingly, T. foetus has never been identified in cattle in Norway, although it is a reportable disease.
>> PubMed abstract


Related articles:
Winn funded research
Kather, E. J., S. L. Marks, et al. (2007). "Determination of the in vitro susceptibility of feline Tritrichomonas foetus to 5 antimicrobial agents." J Vet Intern Med 21(5): 966-70.
>> PubMed abstract


More on cat health: Winn Feline Foundation Library

Dahlgren, S. S., B. Gjerde, et al. (2007). "First record of natural Tritrichomonas foetus infection of the feline uterus." J Small Anim Pract 48(11): 654-7.

Tritrichomonas foetus is an emerging intestinal parasite of cats, causing chronic large bowel diarrhea. In cattle, this protozoan parasite is a sexually transmitted pathogen, infecting the uterus of cows and the preputial cavity and urethral orifice of bulls. In this case report, the first feline record of T. foetus infection of the uterus is described in a 17-month old Exotic Shorthair queen in Norway with pyometra. This queen had no history of diarrhea. Three other cats in the cattery were diagnosed with T. foetus infection using PCR on fecal samples: a 4.5-year old Persian male with intermittent diarrhea, a 22-month old male Exotic Shorthair with normal feces, and a 2.5-year old female Persian with normal feces. Interestingly, T. foetus has never been identified in cattle in Norway, although it is a reportable disease.
>> PubMed abstract


Related articles:
Winn funded research
Kather, E. J., S. L. Marks, et al. (2007). "Determination of the in vitro susceptibility of feline Tritrichomonas foetus to 5 antimicrobial agents." J Vet Intern Med 21(5): 966-70.
>> PubMed abstract


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Quality of Life for Cats Receiving Chemotherapy

Tzannes, S., M. F. Hammond, et al. (2008). "Owners 'perception of their cats' quality of life during COP chemotherapy for lymphoma." J Feline Med Surg 10(1): 73-81.


Lymphoma is one of the most common feline cancers and many owners opt for chemotherapy as a treatment option. Most owners are concerned about quality of life for feline cancer patients, both with and without chemotherapy. Questionnaires on quality of life (QOL) were completed by the owners of 31 cats undergoing treatment for lymphoma between 2002 and 2006. All cats were treated with cyclophosphamide, vincristine, and prednisolone (COP). QOL scores were significantly higher in cats before the onset of cancer than after, but before the start of chemotherapy. During chemotherapy, QOL scores were also lower than before the onset of cancer, but were significantly higher than prior to starting treatment. The majority of cats (87%) experienced adverse effects during treatment. Most pet owners (83%) were happy they treated their cats and most (87%) would treat another cat. The results of this questionnaire survey indicate that COP chemotherapy is well tolerated by cats according to owner perceptions of QOL.
>> PubMed abstract


Related articles:
Teske, E., G. van Straten, et al. (2002). "Chemotherapy with cyclophosphamide, vincristine, and prednisone (COP) in cats with malignant lymphoma: new results with an old protocol." J Vet Intern Med 16(2): 179-186.
>> PubMed abstract


More on cat health: Winn Feline Foundation

Tzannes, S., M. F. Hammond, et al. (2008). "Owners 'perception of their cats' quality of life during COP chemotherapy for lymphoma." J Feline Med Surg 10(1): 73-81.


Lymphoma is one of the most common feline cancers and many owners opt for chemotherapy as a treatment option. Most owners are concerned about quality of life for feline cancer patients, both with and without chemotherapy. Questionnaires on quality of life (QOL) were completed by the owners of 31 cats undergoing treatment for lymphoma between 2002 and 2006. All cats were treated with cyclophosphamide, vincristine, and prednisolone (COP). QOL scores were significantly higher in cats before the onset of cancer than after, but before the start of chemotherapy. During chemotherapy, QOL scores were also lower than before the onset of cancer, but were significantly higher than prior to starting treatment. The majority of cats (87%) experienced adverse effects during treatment. Most pet owners (83%) were happy they treated their cats and most (87%) would treat another cat. The results of this questionnaire survey indicate that COP chemotherapy is well tolerated by cats according to owner perceptions of QOL.
>> PubMed abstract


Related articles:
Teske, E., G. van Straten, et al. (2002). "Chemotherapy with cyclophosphamide, vincristine, and prednisone (COP) in cats with malignant lymphoma: new results with an old protocol." J Vet Intern Med 16(2): 179-186.
>> PubMed abstract


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Spironolactone in Cats With Heart Disease

Macdonald, K. A., M. D. Kittleson, et al. (2008). "Effect of spironolactone on diastolic function and left ventricular mass in Maine Coon cats with familial hypertrophic cardiomyopathy." J Vet Intern Med 22(2): 335-41.

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease affecting the left ventricle. Some of the pathologic abnormalities found in HCM are myocardial fibrosis and concentric hypertrophy. Treatments that would reverse these pathologic changes would be beneficial. In a rat model of HCM, spironolactone reversed interstitial fibrosis, decreased myocyte disarray by 50%, and improved diastolic function within 10 weeks of treatment. The goal of this study was to evaluate spironolactone treatment of Maine Coon cats with HCM for its ability to improve diastolic function and reduce left ventricular mass. The study enrolled 26 Maine Coon cats with familial HCM and randomized them into two groups. One group received spironolactone (2 mg/kg, PO, BID) and the other group received placebo for 4 months. No significant treatment effect on cardiac function or left ventricular mass was identified. Severe facial dermatitis developed in 4 of the 13 cats receiving spironolactone, requiring discontinuation of therapy.

>> PubMed abstract

Related articles:

Winn funded research

Meurs, K., X. Sanchez, et al. (2005). "A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy." Hum Mol Genet 14(23): 3587-3593.

>> PubMed abstract

More on cat health: Winn Feline Foundation Library

Macdonald, K. A., M. D. Kittleson, et al. (2008). "Effect of spironolactone on diastolic function and left ventricular mass in Maine Coon cats with familial hypertrophic cardiomyopathy." J Vet Intern Med 22(2): 335-41.

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease affecting the left ventricle. Some of the pathologic abnormalities found in HCM are myocardial fibrosis and concentric hypertrophy. Treatments that would reverse these pathologic changes would be beneficial. In a rat model of HCM, spironolactone reversed interstitial fibrosis, decreased myocyte disarray by 50%, and improved diastolic function within 10 weeks of treatment. The goal of this study was to evaluate spironolactone treatment of Maine Coon cats with HCM for its ability to improve diastolic function and reduce left ventricular mass. The study enrolled 26 Maine Coon cats with familial HCM and randomized them into two groups. One group received spironolactone (2 mg/kg, PO, BID) and the other group received placebo for 4 months. No significant treatment effect on cardiac function or left ventricular mass was identified. Severe facial dermatitis developed in 4 of the 13 cats receiving spironolactone, requiring discontinuation of therapy.

>> PubMed abstract

Related articles:

Winn funded research

Meurs, K., X. Sanchez, et al. (2005). "A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy." Hum Mol Genet 14(23): 3587-3593.

>> PubMed abstract

More on cat health: Winn Feline Foundation Library

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Cytauxzoonosis in Domestic Cats

Reichard, M. V., K. A. Baum, et al. (2008). "Temporal occurrence and environmental risk factors associated with cytauxzoonosis in domestic cats." Vet Parasitol 152(3-4): 314-20.

Cytauxzoonosis is caused by Cytauxzoon felis, a protozoan parasite of domestic and wild cats that is transmitted by ticks. The disease is seen in the south-central and southeastern U.S. Cytauxzoonosis is typically a severe disease in domestic cats, with fever , anorexia, anemia, and icterus. Most affected cats die within 3 weeks. This study determined the temporal occurrence and risk factors associated with C. felis infection in domestic cats in Oklahoma with a retrospective search of electronic medical records from the Oklahoma Animal Disease Diagnostic Laboratory and the Boren Veterinary Medical Teaching Hospital. From 1995 to 2006, a total of 232 cytauxzoonosis cases were identified and analyzed. The number of cases remained constant from year to year. Diagnosis of the disease followed a bimodal pattern, with most cases diagnosed in April-June and a smaller number in August-September. In cases where a client address was known, the majority occurred in low density residential areas. Cytauxzoonosis cases were significantly associated with more wooded cover and closer proximity to natural or unmanaged areas than control sites. More cases can be expected in domestic cats living in close proximity to environments that support both ticks and bobcats.
>> PubMed abstract

Related articles:
Haber, M. D., M. D. Tucker, et al. (2007). "The detection of Cytauxzoon felis in apparently healthy free-roaming cats in the USA." Vet Parasitol 146(3-4): 316-20.
>> PubMed abstract

Birkenheuer, A., J. Le, et al. (2006). "Cytauxzoon felis infection in cats in the mid-Atlantic states: 34 cases (1998-2004)." J Amer Vet Med Assoc 228(4): 568-571.
>> PubMed abstract

More on cat health: Winn Feline Foundation Library

Reichard, M. V., K. A. Baum, et al. (2008). "Temporal occurrence and environmental risk factors associated with cytauxzoonosis in domestic cats." Vet Parasitol 152(3-4): 314-20.

Cytauxzoonosis is caused by Cytauxzoon felis, a protozoan parasite of domestic and wild cats that is transmitted by ticks. The disease is seen in the south-central and southeastern U.S. Cytauxzoonosis is typically a severe disease in domestic cats, with fever , anorexia, anemia, and icterus. Most affected cats die within 3 weeks. This study determined the temporal occurrence and risk factors associated with C. felis infection in domestic cats in Oklahoma with a retrospective search of electronic medical records from the Oklahoma Animal Disease Diagnostic Laboratory and the Boren Veterinary Medical Teaching Hospital. From 1995 to 2006, a total of 232 cytauxzoonosis cases were identified and analyzed. The number of cases remained constant from year to year. Diagnosis of the disease followed a bimodal pattern, with most cases diagnosed in April-June and a smaller number in August-September. In cases where a client address was known, the majority occurred in low density residential areas. Cytauxzoonosis cases were significantly associated with more wooded cover and closer proximity to natural or unmanaged areas than control sites. More cases can be expected in domestic cats living in close proximity to environments that support both ticks and bobcats.
>> PubMed abstract

Related articles:
Haber, M. D., M. D. Tucker, et al. (2007). "The detection of Cytauxzoon felis in apparently healthy free-roaming cats in the USA." Vet Parasitol 146(3-4): 316-20.
>> PubMed abstract

Birkenheuer, A., J. Le, et al. (2006). "Cytauxzoon felis infection in cats in the mid-Atlantic states: 34 cases (1998-2004)." J Amer Vet Med Assoc 228(4): 568-571.
>> PubMed abstract

More on cat health: Winn Feline Foundation Library

Read More