Immunity and Feline Infectious Peritonitis

Giordano, A. and S. Paltrinieri (2009). "Interferon-gamma in the serum and effusions of cats with feline coronavirus infection." Vet J 180(3): 396-8.

Investigators from the University of Milan studied and compared the quantity of interferon-gamma concentrations in the serum of clinically normal cats infected with feline coronavirus (FCoV) with the concentrations in the sera and effusions of cats with feline infectious peritonitis (FIP), a disease associated with infection with a mutated form of FCoV. Interferon-gamma is a cytokine and an important modulator of cell mediated immunity. Cats with strong cell mediated immunity (CMI) either do not become infected with FCoV or develop the non-effusive form of FIP. Investigators divided cases into two major groups: Group A included cats with clinical FIP and Group B included FCoV infected clinically normal animals. Group A was further subdivided into two groups, those with non-effusive FIP (A1) and effusive FIP (A2). Group B was also subdivided into 2 groups where subgroup B1 included cats from catteries with a high prevalence of FIP and group B2 included cats from catteries with a low prevalence of FIP. Clinically normal FCoV-infected cats from catteries with a high prevalence of FIP had the highest level of serum interferon-gamma. The serum concentration of interferon-gamma was not significantly different in cats with FIP and the clinically normal FCoV-infected cats from catteries with a low prevalence of FIP. The effusions from cats with FIP had a significantly higher level (40 fold) of interferon-gamma than the serum in these cats. This suggests that cells within FIP lesions produce the interferon-gamma present in effusions. The investigators believe the results indicate that CMI is also likely to be involved in the pathogenesis of FIP, and interferon-gamma prevents the onset of FIP in some instances and could contribute to development of disease in others. [VT]
>> PubMed Abstract

Related articles:
Kipar, A., M. L. Meli, et al. (2006). "Natural feline coronavirus infection: differences in cytokine patterns in association with the outcome of infection." Vet Immunol Immunopathol 112(3-4): 141-55.
>> PubMed Abstract

Paltrinieri, S., C. Metzger, et al. (2007). "Serum alpha1-acid glycoprotein (AGP) concentration in non-symptomatic cats with feline coronavirus (FCoV) infection." J Feline Med Surg 9(4): 271-7.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library

Giordano, A. and S. Paltrinieri (2009). "Interferon-gamma in the serum and effusions of cats with feline coronavirus infection." Vet J 180(3): 396-8.

Investigators from the University of Milan studied and compared the quantity of interferon-gamma concentrations in the serum of clinically normal cats infected with feline coronavirus (FCoV) with the concentrations in the sera and effusions of cats with feline infectious peritonitis (FIP), a disease associated with infection with a mutated form of FCoV. Interferon-gamma is a cytokine and an important modulator of cell mediated immunity. Cats with strong cell mediated immunity (CMI) either do not become infected with FCoV or develop the non-effusive form of FIP. Investigators divided cases into two major groups: Group A included cats with clinical FIP and Group B included FCoV infected clinically normal animals. Group A was further subdivided into two groups, those with non-effusive FIP (A1) and effusive FIP (A2). Group B was also subdivided into 2 groups where subgroup B1 included cats from catteries with a high prevalence of FIP and group B2 included cats from catteries with a low prevalence of FIP. Clinically normal FCoV-infected cats from catteries with a high prevalence of FIP had the highest level of serum interferon-gamma. The serum concentration of interferon-gamma was not significantly different in cats with FIP and the clinically normal FCoV-infected cats from catteries with a low prevalence of FIP. The effusions from cats with FIP had a significantly higher level (40 fold) of interferon-gamma than the serum in these cats. This suggests that cells within FIP lesions produce the interferon-gamma present in effusions. The investigators believe the results indicate that CMI is also likely to be involved in the pathogenesis of FIP, and interferon-gamma prevents the onset of FIP in some instances and could contribute to development of disease in others. [VT]
>> PubMed Abstract

Related articles:
Kipar, A., M. L. Meli, et al. (2006). "Natural feline coronavirus infection: differences in cytokine patterns in association with the outcome of infection." Vet Immunol Immunopathol 112(3-4): 141-55.
>> PubMed Abstract

Paltrinieri, S., C. Metzger, et al. (2007). "Serum alpha1-acid glycoprotein (AGP) concentration in non-symptomatic cats with feline coronavirus (FCoV) infection." J Feline Med Surg 9(4): 271-7.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library

Read More

Cats and Toxoplasmosis

Malmasi, A., B. Mosallanejad, et al. (2009). "Prevention of shedding and re-shedding of Toxoplasma gondii oocysts in experimentally infected cats treated with oral clindamycin: a preliminary study." Zoonoses Public Health 56(2): 102-4.

Researchers from the University of Tehran investigated the effect of oral clindamycin on shedding of Toxoplasma organisms in infected cats. Toxoplasma gondii is an important protozoal parasite that infects many mammalian species, including cats and humans. Infected cats shed millions of oocysts, which can then infect contact animals, including humans, with potentially serious consequences. While numbers of animals evaluated in this study were small (twelve infected cats, six treated, and six untreated), and clindamycin administration was given for 24 days beginning 3 days prior to and continuing through 3 weeks post-infection (this timing would not likely occur in natural infections), shedding did not occur in the treated cats. In contrast, treated cats shed for over one week. Following immunosuppression through administration of dexamethasone 45 days post-infection, the previously-treated cats again demonstrated no shedding of the organism in contrast to non-treated cats. Giving clindamycin prophylactically to cats made them oocyst-free and as long as they were receiving the medication, and they did not shed oocysts even under severe immunosuppression. This study is a model for future studies with larger groups. [MK]
>> PubMed Abstract

Related articles:
Lloyd, S. and J. Smith (2001). "Activity of toltrazuril and diclazuril against Isospora species in kittens and puppies." Vet Rec 148(16): 509-11.

Vollaire, M., S. Radecki, et al. (2005). "Seroprevalence of Toxoplasma gondii antibodies in clinically ill cats in the United States." Am J Vet Res 66(5): 874-877.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library

Malmasi, A., B. Mosallanejad, et al. (2009). "Prevention of shedding and re-shedding of Toxoplasma gondii oocysts in experimentally infected cats treated with oral clindamycin: a preliminary study." Zoonoses Public Health 56(2): 102-4.

Researchers from the University of Tehran investigated the effect of oral clindamycin on shedding of Toxoplasma organisms in infected cats. Toxoplasma gondii is an important protozoal parasite that infects many mammalian species, including cats and humans. Infected cats shed millions of oocysts, which can then infect contact animals, including humans, with potentially serious consequences. While numbers of animals evaluated in this study were small (twelve infected cats, six treated, and six untreated), and clindamycin administration was given for 24 days beginning 3 days prior to and continuing through 3 weeks post-infection (this timing would not likely occur in natural infections), shedding did not occur in the treated cats. In contrast, treated cats shed for over one week. Following immunosuppression through administration of dexamethasone 45 days post-infection, the previously-treated cats again demonstrated no shedding of the organism in contrast to non-treated cats. Giving clindamycin prophylactically to cats made them oocyst-free and as long as they were receiving the medication, and they did not shed oocysts even under severe immunosuppression. This study is a model for future studies with larger groups. [MK]
>> PubMed Abstract

Related articles:
Lloyd, S. and J. Smith (2001). "Activity of toltrazuril and diclazuril against Isospora species in kittens and puppies." Vet Rec 148(16): 509-11.

Vollaire, M., S. Radecki, et al. (2005). "Seroprevalence of Toxoplasma gondii antibodies in clinically ill cats in the United States." Am J Vet Res 66(5): 874-877.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library

Read More