Tritrichomonas in Cats in Italy

Holliday, M., D. Deni, and D.A. Gunn-Moore, Tritrichomonas foetus infection in cats with diarrhoea in a rescue colony in Italy. Journal of Feline Medicine & Surgery, 2009. 11(2): p. 131-134.

Tritrichomonus foetus is protozoan parasite causing diarrhea in cats. Clinical signs are those of large bowel diarrhea, and include increased frequency of defecation, semi-formed to liquid feces, foul-smelling feces with fresh blood and mucus, and fecal incontinence. Affected cats are typically well otherwise. There are various methods of diagnosing T. foetus infection in cats, such as PCR on feces and fecal culture. Most reports of T. foetus infection in cats have come from the U.S., but there are a few reports from other countries, such as the U.K. and Germany. In this report, fecal samples from 74 cats with chronic large bowel diarrhea living in a rescue colony in Tuscany were submitted for T. foetus diagnostics. Most were rescued street cats, but some were surrendered by owners. Of the 74 cats, almost 1/3 were found to be infected with T. foetus. The infected cats were predominantly over a year of age and were all neutered non-pedigreed, domestic cats. The investigators conclude that the prevalence of T. foetus may be more widely distributed than previously thought. [SL]
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Related articles:
Stockdale, H.D., et al., Tritrichomonas foetus infections in surveyed pet cats. Vet Parasitol, 2009. 160(1-2): p. 13-7.
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Frey, C.F., et al., Intestinal Tritrichomonas foetus infection in cats in Switzerland detected by in vitro cultivation and PCR. Parasitol Res, 2009. 104(4): p. 783-88.
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Pathogenesis of Feline Coronavirus Infection

Pedersen, N.C., C.E. Allen, and L.A. Lyons, Pathogenesis of feline enteric coronavirus infection. Journal of Feline Medicine & Surgery, 2008. 10(6): p. 529-541.

The importance of feline enteric coronavirus (FECV) as a primary intestinal pathogen is considered minimal. The importance of FECV is that this virus can mutate in vivo. At least one mutant form causes the highly fatal disease called feline infectious peritonitis (FIP). Initially, this study had been designed to demonstrate that resistance and susceptibility to FECV infection were under genetic control, just as genetics appear to play a significant role in FIP resistance. With more than 3 years of study results, it became apparent that genetics would not readily define this initial goal. The investigators made a decision to concentrate their efforts on what was learned about FECV pathogenesis. A distinct primary stage of infection was identified that lasted from 7 to 18 months, with the highest level of virus shedding during this phase. This primary stage resolved in one of the three following ways: 1) recovery, 2) persistent shedding, or 3) recurrent or intermittent shedding. During the primary phase, shedding levels were significantly higher in kittens than in adult cats. As kittens might be infected before their immune systems mature, FECV replication would be more frequent and increase the potential for FECV to FIP mutations. FIP is known to be more common in kittens than adult cats. The investigators also looked at the role of stress on reactivating latent or subclinical infection, or increasing virus shedding. They evaluated the role natural stress such as pregnancy, parturition, and lactation might play. Stress was also simulated by giving a series of corticosteroid injections using methylprednisolone acetate. No increase in virus shedding was reported in any of the scenarios. Virus shedding and serum antibody titers had a significant relationship to each other. Cats shedding virus usually had titers of 1:100 or higher. Cats that were not shedding virus usually had titers of 1:25 and lower. Additional observations on immunity to FECV infection found that immunity during the primary phase of infection was slow to develop, intermittent, and tenuous in duration. Immunity during re-infection tended to mirror that occurring during primary infection, indicating this immunity lacks memory. This pattern of infection and immunity is strongly influenced by environmental factors. [MK]
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Related articles:
Pedersen, N.C., A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine & Surgery, 2009. 11(4): p. 225-258.
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Addie, D., et al., Feline infectious peritonitis ABCD guidelines on prevention and management. J Feline Med Surg, 2009. 11(7): p. 594-604.
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Investigating the Genetic Causes of HCM

Meurs, K.M., et al., Analysis of 8 sarcomeric candidate genes for feline hypertrophic cardiomyopathy mutations in cats with hypertrophic cardiomyopathy. J Vet Intern Med, 2009. 23(4): p. 840-3.

The most common heart disease in cats is hypertrophic cardiomyopathy (HCM). A causative mutation has been identified in two breeds, the Maine Coon (MC) and Ragdoll that involve the cardiac myosin binding protein C gene (MYBPC3). HCM is thought to be inherited in other breeds as well. The objective of the study was to evaluate a subset of cats from additional breeds with HCM including the British Shorthair (BSH), Norwegian Forest Cat (NWF), Siberian, and Sphynx and to also examine MC cats known to be affected with HCM but lacking the known mutation. Fourteen affected cats among these breeds were evaluated. A causative mutation was not identified in the eight candidate genes studied, although several single nucleotide polymorphisms were detected. The study concluded that mutations within these cardiac genes do not appear to be the only cause of HCM in these breeds. Further evaluation of additional cardiac genes is considered warranted. (VT)
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Meurs, K.M., et al., A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy. Genomics, 2007. 90(2): p. 261-4.
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Meurs, K., et al., A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy. Hum Mol Genet, 2005. 14(23): p. 3587-3593.
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Cats and Dietary Sodium

Xu, H., D.P.L. Laflamme, and G.L. Long, Effects of dietary sodium chloride on health parameters in mature cats. Journal of Feline Medicine & Surgery, 2009. 11(6): p. 435-441.

High sodium diets are often used for cats to increase water intake and urine output, both beneficial goals for treatment of lower urinary tract disease. A study published in 2006 suggested that increased dietary sodium might have adverse effects on the kidneys. The objective of this controlled, prospective study was to evaluate the effect of different salt contents in diets fed to mature cats for a period of 6 months. No adverse effects were noted, including effects on food intake, body weight, hydration, blood pressure, and kidney function. These results are consistent with the
majority of other studies which indicate that sodium at 1.5% of the diet (DM) is not harmful to healthy cats. [SL]
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Kirk, C.A., D.E. Jewell, and S.R. Lowry, Effects of sodium chloride on selected parameters in cats. Vet Ther, 2006. 7(4): p. 333-46.
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Luckschander, N., et al., Dietary NaCl does not affect blood pressure in healthy cats. J Vet Intern Med, 2004. 18(4): p. 463-467.
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Understanding FIP

Regan, A.D., R.D. Cohen, and G.R. Whittaker, Activation of p38 MAPK by feline infectious peritonitis virus regulates pro-inflammatory cytokine production in primary blood-derived feline mononuclear cells. Virology, 2009. 384(1): p. 135-43.

Feline infectious peritonitis (FIP) is a fatal disease of cats associated with feline coronavirus (FCoV) infection, a common enteric virus of cats. How this virus leads to the lethal disease is not clear, as most infected cats do not develop disease. Cytokines are proteins secreted from cells, including cells of the immune system, that are important in mediating an effective immune response. Cats with FIP have abnormal cytokine production that may contribute to the disease FIP. In this study, the investigators examined the effects of the FIP virus on certain white blood cells collected from cats, in a laboratory environment. These cells are the target of the FCoV in cases of FIP. The investigators showed that an important cellular pathway responsible for inducing inflammation is activated by the virus, and is a key contributor to the disease observed in cats with FIP. The raises the possibility that inhibitors of this pathway may be beneficial in the treatment of FIP. [MK]
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Takano, T., et al., Neutrophil survival factors (TNF-alpha, GM-CSF, and G-CSF) produced by macrophages in cats infected with feline infectious peritonitis virus contribute to the pathogenesis of granulomatous lesions. Arch Virol, 2009.
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Giordano, A. and S. Paltrinieri, Interferon-gamma in the serum and effusions of cats with feline coronavirus infection. Vet J, 2009. 180(3): p. 396-8.
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Risk Factors for FIV Infection

Murray, J.K., et al., Risk factors for feline immunodeficiency virus antibody test status in Cats Protection adoption centres (2004). Journal of Feline Medicine & Surgery, 2009. 11(6): p. 467-473.

This study determined the prevalence of feline immunodeficiency virus (FIV) within a group of cats entering 10 United Kingdom adoption centres run by Cat Protection. All cats entering the facilities were tested for FIV using a rapid enzyme immunoassay antibody test. The overall prevalence of positive test results was 3.1%, while the prevalence at different adoption centres varied from 0.8% to 6.7%. Male cats were found to be approximately three times more likely than female cats to be FIV positive. The previous history of the cat was also shown to be associated with FIV status, where cats admitted from stray or feral backgrounds were approximately three times more likely to be FIV positive than those cats surrendered by their owners. Cats in poor health were four times more likely to be positive than those with fair to good health. There was no evidence found for an association between neuter status and FIV test results. The study may help adoption centres identify those cats with an increased risk of FIV for routine FIV testing. [VT]
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Levy, J.K., et al., Seroprevalence of feline leukemia virus and feline immunodeficiency virus infection among cats in North America and risk factors for seropositivity. J Am Vet Med Assoc, 2006. 228(3): p. 371-6.
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Macieira, D.B., et al., Prevalence and risk factors for hemoplasmas in domestic cats naturally infected with feline immunodeficiency virus and/or feline leukemia virus in Rio de Janeiro - Brazil. J Feline Med Surg, 2008. 10(2): p. 120-9.
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Treatment of Feline Diabetes with Diet and Insulin

Hall, T. D., O. Mahony, et al. (2009). "Effects of diet on glucose control in cats with diabetes mellitus treated with twice daily insulin glargine." Journal of Feline Medicine & Surgery 11(2): 125-130.

Diabetes mellitus is a common feline disease and is treated with a combination of dietary therapy and insulin. Insulin glargine (Lantus, Sanofi-Aventis) is a long-acting recombinant human insulin that is frequently used to treat diabetic cats. The purpose of this study, from Tufts Cummings School of Veterinary Medicine, was to compare a low carbohydrate/high protein (LCHP) diet to a non-prescription control diet in diabetic cats receiving insulin glargine twice daily. Over the 10-week trial, 6 cats were given the LCHP diet (DM Dietetic Management Feline Formula dry & canned, Nestle Purina) and 6 cats were given control diets (Pro Plan Adult Cat total Care Chicken and Rice dry, Nestle Purina and Friskies Special Diet Turkey & Giblets Dinner canned, Nestle Purina). Re-evaluations (blood glucose curves, serum fructosamine, and assessment of clinical signs) were performed at weeks 1, 2, 4, 6, and 10. Using insulin glargine twice daily and frequent monitoring, all cats in both groups did well. The main difference between the two groups was that the cats fed the LCHP diet had significantly lower serum fructosamine levels compared to the cats on the control diets. The clinical significance of this is unknown as all cats in both diet groups achieved good glycemic control. [SL]
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Marshall, R. D., J. S. Rand, et al. (2008). "Glargine and protamine zinc insulin have a longer duration of action and result in lower mean daily glucose concentrations than lente insulin in healthy cats." J Vet Pharmacol Ther 31(3): 205-212.
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Rios, L. and C. Ward (2008). "Feline diabetes mellitus: diagnosis, treatment, and monitoring." Compend Contin Educ Vet 30(12): 626-39; quiz 639-40.
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Feline Papillomavirus

Munday, J. S., L. Howe, et al. (2008). "Detection of papillomaviral DNA sequences in a feline oral squamous cell carcinoma." Res Vet Sci 86(2): 359-361.

Oral squamous cell carcinomas constitute 7.5% of all feline cancers, and often lead to death in affected cats. In humans, these tumors are associated with papillomavirus in about 25% of the cases. To investigate the association of papillomavirus with feline oral tumors, 40 oral lesions (20 cancerous, 20 non-cancerous) were examined for viral DNA. Papillomaviral DNA was detected in one oral tumor, but not in any non-cancerous lesion. Finding viral DNA in only one tumor did not indicate a causal relationship. The finding of viral DNA does however indicate additional research into the carcinogenic potential of these viruses in cats is warranted; the carcinogenic potential of papillomaviruses in general and the finding here of viral DNA in a feline oral tumor hints at a possible role. [MK]
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Munday, J. S., M. Kiupel, et al. (2007). "Detection of papillomaviral sequences in feline Bowenoid in situ carcinoma using consensus primers." Vet Dermatol 18(4): 241-5.
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Sundberg, J., M. Van Ranst, et al. (2000). "Feline papillomas and papillomaviruses." Vet Pathol 37(1): 1-10.
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Vitamin B12 Deficiency in Cats

Barron, P. M., J. T. Mackie, et al. (2009). "Serum cobalamin concentrations in healthy cats and cats with non-alimentary tract illness in Australia." Aust Vet J 87(7): 280-283.

The objective of this study was to determine a reference range for serum cobalamin (vitamin B12) concentration in healthy cats in Australia and prospectively investigate the prevalence of hypocobalaminemia in cats with non-alimentary tract disease. Blood samples were collected from 50 healthy cats and 47 cats with non-alimentary tract illness, and serum blood cobalamin concentrations were determined for each group. Cobalamin is a cofactor for several mammalian enzymatic reactions necessary for normal cellular function. Cats with low cobalamin levels have significant metabolic disturbances and clinical research into feline hypocobalaminemia has mostly involved cats with gastrointestinal disease. The reference range in the 50 clinically healthy cats was 345 to 3668 pb/mL. The median serum cobalamin concentration in the 47 cats with non-alimentary tract illness was not significantly different than the median concentration in the healthy cat group. The results indicate that hypocobalaminemia is uncommon in sick cats with non-alimentary tract illness in Australia, though its occurrence in this study still warrants further investigation. [VT]
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Ibarrola, P., L. Blackwood, et al. (2005). "Hypocobalaminaemia is uncommon in cats in the United Kingdom." J Fel Med Surg 7(6): 341-348.
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Ruaux, C., J. Steiner, et al. (2005). "Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia." J Vet Intern Med 19(2): 155-160.
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Diabetes in Burmese Cats

Lederer, R., J. S. Rand, et al. (2009). "Frequency of feline diabetes mellitus and breed predisposition in domestic cats in Australia." Vet J 179(2): 254-8.

Diabetes mellitus (DM) is defined as a group of metabolic disorders characterized by yperglycemia as a result of defects in insulin secretion, insulin action or both. In the United States, the reported prevalence of feline DM has increased over the past 30 years from 1 in 1250 in 1970 to 1 in 81 cats affected by the disease in 1999. A number of studies have looked at potential risk factors for the development of DM, and increasing age, being a neutered male, and being obese have been identified. In North America, no particular breed of cat appears to be associated with an increased risk for the development of DM, but this does not appear to be true in other countries. The frequency of DM in two large feline-only clinics in Brisbane, Australia over a 5-year study period is described in this report. Frequency was estimated using period prevalences (the proportion of the population at risk that was affected by diabetes at any point during a specified time period). The 5-year period prevalence of DM was 7.4 per 1000 cats. Period prevalence was significantly higher in Burmese cats (22.4 cats per 1000) than in domestic longhair or shorthair cats. There appears to be a predisposition of Burmese cats to DM in some countries, and further investigations are warranted. [SL]
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Related articles:
McCann, T. M., K. E. Simpson, et al. (2007). "Feline diabetes mellitus in the UK: the prevalence within an insured cat population and a questionnaire-based putative risk factor analysis." J Feline Med Surg 9(4): 289-99.
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Rand, J. S., L. M. Fleeman, et al. (2004). "Canine and feline diabetes mellitus: nature or nurture?" J Nutr 134(8 Suppl): 2072S-2080S.
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