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]
>> PubMed Abstract

Related articles:
Stockdale, H.D., et al., Tritrichomonas foetus infections in surveyed pet cats. Vet Parasitol, 2009. 160(1-2): p. 13-7.
>> PubMed Abstract

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.
>> PubMed Abstract

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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]
>> PubMed Abstract

Related articles:
Stockdale, H.D., et al., Tritrichomonas foetus infections in surveyed pet cats. Vet Parasitol, 2009. 160(1-2): p. 13-7.
>> PubMed Abstract

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.
>> PubMed Abstract

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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]
>> PubMed Abstract

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.
>> PubMed Abstract

Addie, D., et al., Feline infectious peritonitis ABCD guidelines on prevention and management. J Feline Med Surg, 2009. 11(7): p. 594-604.
>> Free full text article

More on cat health: Winn Feline Foundation Library
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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]
>> PubMed Abstract

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.
>> PubMed Abstract

Addie, D., et al., Feline infectious peritonitis ABCD guidelines on prevention and management. J Feline Med Surg, 2009. 11(7): p. 594-604.
>> Free full text article

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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)
>> PubMed Abstract

Related articles:
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.
>> PubMed Abstract

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.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library
Join us on Facebook

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)
>> PubMed Abstract

Related articles:
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.
>> PubMed Abstract

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.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library
Join us on Facebook

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