Feline Spongiform Encephalopathy

Hilbe MM, Soldati GG, Zlinszky KK, Wunderlin SS, Ehrensperger FF. Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy. BMC Vet Res. Mar 31 2009;5(1):11.

Two domestic shorthair cats presenting with progressive hind-limb ataxia and increased aggressiveness were examined at necropsy and a diagnosis of feline spongiform encephalopathy (FSE) was made. A wide spectrum of tissue samples was collected and evaluated histologically and immunohistologically for the presence of prion protein. FSE is a prion-induced disease affecting most members of the cat family (Felidae). FSE belongs to the group of transmissible spongiform encephalopathies (TSE) that also occur in humans, cattle and sheep. To date, 89 cases of FSE have been reported in domestic cats in Great Britain and a few cases additionally found in other European countries. The disease is characterized by progressive onset of clinical signs including abnormal behavior such as increased timidity or aggression, ataxia and hyperesthesia. The main histopathological lesions are vacuolation of the neuropil in the grey matter of the brain and spinal cord (also referred as spongiosis), vacuolation of neuronal perikarya, and a diffuse astrocytic reaction. The condition in cats is believed to result from ingestion of bovine spongiform encephalopathy (BSE)-contaminated food. In the two cats necropsied, heavy prion protein immunostaining was detected in brain, retina, adrenal gland and the nerve plexus of the intestines. Some studies postulate a possible excretion of prions through urine (prionuria) and that this may play a role in the horizontal transmission of TSEs. Immunostaining was found in the kidneys of both an infected and a control cat. The two FSE cases described here had essentially the same histological lesions and prion protein distribution in the brain and the peripheral tissues as reported in earlier FSE cases. The source of infection for one cat could have been due to exposure to canned food contaminated with nervous tissue of BSE infected cattle from before the ban. In summary, the distribution of prion protein in FSE is similar to BSE but different from classical scrapie (sheep). Therefore, horizontal prion transmission in FSE appears to be unlikely. [VT]

Related articles:
Iulini B, Cantile C, Mandara MT, et al. Neuropathology of italian cats in feline spongiform encephalopathy surveillance. Vet Pathol. 2008 Sep;45(5):626-33.

Salvadori C, Lossi L, Arispici M, et al. Spongiform neurodegenerative disease in a Persian kitten. J Feline Med Surg. 2007 Jun;9(3):242-5.

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Hilbe MM, Soldati GG, Zlinszky KK, Wunderlin SS, Ehrensperger FF. Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy. BMC Vet Res. Mar 31 2009;5(1):11.

Two domestic shorthair cats presenting with progressive hind-limb ataxia and increased aggressiveness were examined at necropsy and a diagnosis of feline spongiform encephalopathy (FSE) was made. A wide spectrum of tissue samples was collected and evaluated histologically and immunohistologically for the presence of prion protein. FSE is a prion-induced disease affecting most members of the cat family (Felidae). FSE belongs to the group of transmissible spongiform encephalopathies (TSE) that also occur in humans, cattle and sheep. To date, 89 cases of FSE have been reported in domestic cats in Great Britain and a few cases additionally found in other European countries. The disease is characterized by progressive onset of clinical signs including abnormal behavior such as increased timidity or aggression, ataxia and hyperesthesia. The main histopathological lesions are vacuolation of the neuropil in the grey matter of the brain and spinal cord (also referred as spongiosis), vacuolation of neuronal perikarya, and a diffuse astrocytic reaction. The condition in cats is believed to result from ingestion of bovine spongiform encephalopathy (BSE)-contaminated food. In the two cats necropsied, heavy prion protein immunostaining was detected in brain, retina, adrenal gland and the nerve plexus of the intestines. Some studies postulate a possible excretion of prions through urine (prionuria) and that this may play a role in the horizontal transmission of TSEs. Immunostaining was found in the kidneys of both an infected and a control cat. The two FSE cases described here had essentially the same histological lesions and prion protein distribution in the brain and the peripheral tissues as reported in earlier FSE cases. The source of infection for one cat could have been due to exposure to canned food contaminated with nervous tissue of BSE infected cattle from before the ban. In summary, the distribution of prion protein in FSE is similar to BSE but different from classical scrapie (sheep). Therefore, horizontal prion transmission in FSE appears to be unlikely. [VT]

Related articles:
Iulini B, Cantile C, Mandara MT, et al. Neuropathology of italian cats in feline spongiform encephalopathy surveillance. Vet Pathol. 2008 Sep;45(5):626-33.

Salvadori C, Lossi L, Arispici M, et al. Spongiform neurodegenerative disease in a Persian kitten. J Feline Med Surg. 2007 Jun;9(3):242-5.

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Phimosis in Cats

May LR, Hauptman JG. Phimosis in cats: 10 cases (2000-2008). J Am Anim Hosp Assoc. Nov-Dec 2009;45(6):277-283.

Medical records for ten cats diagnosed with phimosis were reviewed at Michigan State University Veterinary Teaching Hospital. Phimosis is a condition defined by the inability of the penis to be extruded beyond the preputial orifice due to either the absence of an opening or an abnormally small orifice. The problem can either be congenital or acquired. Causes of acquired phimosis included neoplasia, edema, inflammation or scarring secondary to trauma. Signs can vary from asymptomatic changes to narrowing severe enough to cause urine retention and death. The most common signs noted in this review were stranguria and pollakiuria, found in eight of ten cats. The median age of the cats was 18.6 weeks and diagnosis was made by physical examination alone. Surgical correction by widening the preputial orifice was performed in eight of the ten cats. Follow-up communications with owners indicated that surgical correction resolved the pre-operative clinical signs attributed to phimosis. [VT]

Related articles:
Bright SR, Mellanby RJ. Congenital phimosis in a cat. J Feline Med Surg. Dec 2004;6(6):367-370.

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May LR, Hauptman JG. Phimosis in cats: 10 cases (2000-2008). J Am Anim Hosp Assoc. Nov-Dec 2009;45(6):277-283.

Medical records for ten cats diagnosed with phimosis were reviewed at Michigan State University Veterinary Teaching Hospital. Phimosis is a condition defined by the inability of the penis to be extruded beyond the preputial orifice due to either the absence of an opening or an abnormally small orifice. The problem can either be congenital or acquired. Causes of acquired phimosis included neoplasia, edema, inflammation or scarring secondary to trauma. Signs can vary from asymptomatic changes to narrowing severe enough to cause urine retention and death. The most common signs noted in this review were stranguria and pollakiuria, found in eight of ten cats. The median age of the cats was 18.6 weeks and diagnosis was made by physical examination alone. Surgical correction by widening the preputial orifice was performed in eight of the ten cats. Follow-up communications with owners indicated that surgical correction resolved the pre-operative clinical signs attributed to phimosis. [VT]

Related articles:
Bright SR, Mellanby RJ. Congenital phimosis in a cat. J Feline Med Surg. Dec 2004;6(6):367-370.

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Characterization of FIP Mutants

Pederson N, Liu H, Dodd K, Pesavento P. Significance of coronavirus mutants in feces and diseased tissues of cats suffering from feline infectious peritonitis. Viruses. 2009;1(2):166-184.

This article describes viral characterization of the feline coronavirus found in feces versus diseased tissues of cats with feline infectious peritonitis (FIP). The researchers found that within a single cat, the viruses found in the intestinal tract and diseased tissue were almost 100% identical genetically. Minor differences were found in several of the genes of feline coronaviruses. Notably, the gene encoding a virus protein whose function remains unknown, the 3c protein, was almost always mutated in viruses found in FIP lesions. These mutations, while minor, are predicted to lead to a dysfunctional protein product. Viruses from the feces of these same cats however, almost always had intact, functional 3c genes. While the 3c mutation is not universal among FIP virus isolates, it does occur in the majority, and is speculated to play a significant role in FIP development. From this study, it also appears that the FIP mutants arose separately in each affected cat, rather than spreading cat-to-cat. Thus, horizontal transmission of FIP does not readily occur. More research into the function of the 3c gene product is needed to define its role in FIP. [MK]

Related articles:
Pedersen NC. A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine & Surgery. 2009;11(4):225-258.

Vennema H, Poland A, Foley J, Pedersen NC. Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses. Virology. Mar 30 1998;243(1):150-157.

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Pederson N, Liu H, Dodd K, Pesavento P. Significance of coronavirus mutants in feces and diseased tissues of cats suffering from feline infectious peritonitis. Viruses. 2009;1(2):166-184.

This article describes viral characterization of the feline coronavirus found in feces versus diseased tissues of cats with feline infectious peritonitis (FIP). The researchers found that within a single cat, the viruses found in the intestinal tract and diseased tissue were almost 100% identical genetically. Minor differences were found in several of the genes of feline coronaviruses. Notably, the gene encoding a virus protein whose function remains unknown, the 3c protein, was almost always mutated in viruses found in FIP lesions. These mutations, while minor, are predicted to lead to a dysfunctional protein product. Viruses from the feces of these same cats however, almost always had intact, functional 3c genes. While the 3c mutation is not universal among FIP virus isolates, it does occur in the majority, and is speculated to play a significant role in FIP development. From this study, it also appears that the FIP mutants arose separately in each affected cat, rather than spreading cat-to-cat. Thus, horizontal transmission of FIP does not readily occur. More research into the function of the 3c gene product is needed to define its role in FIP. [MK]

Related articles:
Pedersen NC. A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine & Surgery. 2009;11(4):225-258.

Vennema H, Poland A, Foley J, Pedersen NC. Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses. Virology. Mar 30 1998;243(1):150-157.

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Feline Leukemia Virus

Stutzer B, Muller F, Majzoub M, et al. Role of latent feline leukemia virus infection in nonregenerative cytopenias of cats. J Vet Intern Med. Nov 17 2009.

Nonregenerative cytopenias such as nonregenerative anemia, neutropenia, and thrombocytopenia are a common finding in cats infected with feline leukemia virus (FeLV). The objective of this study was to assess the role of latent FeLV infection in bone marrow in cats with nonregenerative cytopenias that had a negative FeLV antigen blood test. Thirty-seven cats were included in the patient group meeting inclusion criteria of a nonregenerative cytopenia of unknown origin and a negative FeLV antigen test result. The group’s results were compared to two control groups that also totaled 37 cats. Whole blood and bone marrow samples were tested for FeLV using two different PCR assays. Results indicated that PCR from bone marrow could be considered a more sensitive method to detect FeLV latency than PCR of whole blood. Two of the 37 cats (5.4%) in the patient groups were positive on bone marrow PCR results and were considered infected with FeLV. The latent FeLV infection in those two cats was the possible cause of the observed nonregenerative cytopenia. [VT]

Related articles:
Herring ES, Troy GC, Toth TE, Forrester SD, Weigt LA, Herring IP. Detection of feline leukaemia virus in blood and bone marrow of cats with varying suspicion of latent infection. J Feline Med Surg. Sep 2001;3(3):133-141.

Torres AN, Mathiason CK, Hoover EA. Re-examination of feline leukemia virus: host relationships using real-time PCR. Virology. Feb 5 2005;332(1):272-283.

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Stutzer B, Muller F, Majzoub M, et al. Role of latent feline leukemia virus infection in nonregenerative cytopenias of cats. J Vet Intern Med. Nov 17 2009.

Nonregenerative cytopenias such as nonregenerative anemia, neutropenia, and thrombocytopenia are a common finding in cats infected with feline leukemia virus (FeLV). The objective of this study was to assess the role of latent FeLV infection in bone marrow in cats with nonregenerative cytopenias that had a negative FeLV antigen blood test. Thirty-seven cats were included in the patient group meeting inclusion criteria of a nonregenerative cytopenia of unknown origin and a negative FeLV antigen test result. The group’s results were compared to two control groups that also totaled 37 cats. Whole blood and bone marrow samples were tested for FeLV using two different PCR assays. Results indicated that PCR from bone marrow could be considered a more sensitive method to detect FeLV latency than PCR of whole blood. Two of the 37 cats (5.4%) in the patient groups were positive on bone marrow PCR results and were considered infected with FeLV. The latent FeLV infection in those two cats was the possible cause of the observed nonregenerative cytopenia. [VT]

Related articles:
Herring ES, Troy GC, Toth TE, Forrester SD, Weigt LA, Herring IP. Detection of feline leukaemia virus in blood and bone marrow of cats with varying suspicion of latent infection. J Feline Med Surg. Sep 2001;3(3):133-141.

Torres AN, Mathiason CK, Hoover EA. Re-examination of feline leukemia virus: host relationships using real-time PCR. Virology. Feb 5 2005;332(1):272-283.

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Bacterial Peritonitis in Cats

Ruthrauff CM, Smith J, Glerum L. Primary bacterial septic peritonitis in cats: 13 cases. J Am Anim Hosp Assoc. Nov-Dec 2009;45(6):268-276.

Primary septic peritonitis is an abdominal infection without a primary focus, such as a perforated bowel. The most common cause in cats is feline infectious peritonitis. Little is known about primary bacterial septic peritonitis in cats. The investigators examined the medical records of twelve cats diagnosed with primary bacterial septic peritonitis and identified significant characteristics associated with this condition. The overall mortality rate was 31%, and cats that experienced clinically significant decreased heart rates and hypothermia did not survive. Other clinical findings were similar to cats with septic peritonitis from identifiable causes (e.g., fever, abdominal pain, elevated white blood cell counts, elevated serum bilirubin). All cats had anaerobic bacteria isolated from the infection; these microbes are common in the gastrointestinal tract. This would indicate that in these cases, antibiotic treatment directed against anaerobes should be effective. All but two of the organisms identified in these cases are common oral flora, but gingival disease was not found to be a contributor. For primary bacterial septic peritonitis, a mechanism for inoculation of the bacteria into the abdomen has yet to be determined, but an oral source is suggested. The investigators concluded that cats with primary bacterial septic peritonitis have a fair to good prognosis if they are treated aggressively prior to development of shock. This treatment should include surgical intervention, nutritional support, and appropriate antibiotic therapy. [MK]

Related Articles:
King LG. Postoperative complications and prognostic indicators in dogs and cats with septic peritonitis: 23 cases (1989-1992). J Am Vet Med Assoc. Feb 1 1994;204(3):407-414.

Bonczynski JJ, Ludwig LL, Barton LJ, Loar A, Peterson ME. Comparison of peritoneal fluid and peripheral blood pH, bicarbonate, glucose, and lactate concentration as a diagnostic tool for septic peritonitis in dogs and cats. Vet Surg. Mar-Apr 2003;32(2):161-166.

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Ruthrauff CM, Smith J, Glerum L. Primary bacterial septic peritonitis in cats: 13 cases. J Am Anim Hosp Assoc. Nov-Dec 2009;45(6):268-276.

Primary septic peritonitis is an abdominal infection without a primary focus, such as a perforated bowel. The most common cause in cats is feline infectious peritonitis. Little is known about primary bacterial septic peritonitis in cats. The investigators examined the medical records of twelve cats diagnosed with primary bacterial septic peritonitis and identified significant characteristics associated with this condition. The overall mortality rate was 31%, and cats that experienced clinically significant decreased heart rates and hypothermia did not survive. Other clinical findings were similar to cats with septic peritonitis from identifiable causes (e.g., fever, abdominal pain, elevated white blood cell counts, elevated serum bilirubin). All cats had anaerobic bacteria isolated from the infection; these microbes are common in the gastrointestinal tract. This would indicate that in these cases, antibiotic treatment directed against anaerobes should be effective. All but two of the organisms identified in these cases are common oral flora, but gingival disease was not found to be a contributor. For primary bacterial septic peritonitis, a mechanism for inoculation of the bacteria into the abdomen has yet to be determined, but an oral source is suggested. The investigators concluded that cats with primary bacterial septic peritonitis have a fair to good prognosis if they are treated aggressively prior to development of shock. This treatment should include surgical intervention, nutritional support, and appropriate antibiotic therapy. [MK]

Related Articles:
King LG. Postoperative complications and prognostic indicators in dogs and cats with septic peritonitis: 23 cases (1989-1992). J Am Vet Med Assoc. Feb 1 1994;204(3):407-414.

Bonczynski JJ, Ludwig LL, Barton LJ, Loar A, Peterson ME. Comparison of peritoneal fluid and peripheral blood pH, bicarbonate, glucose, and lactate concentration as a diagnostic tool for septic peritonitis in dogs and cats. Vet Surg. Mar-Apr 2003;32(2):161-166.

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Feline Red Blood Cell Parasites

Tasker S, Peters IR, Papasouliotis K, et al. Description of outcomes of experimental infection with feline haemoplasmas: copy numbers, haematology, Coombs' testing and blood glucose concentrations. Vet Microbiol. Nov 18 2009;139(3-4):323-332.

Feline hemoplasma infections are caused by three separate organisms that infect red blood cells, but only one of these, Mycoplasma haemofelis, causes hemolysis with significant disease. However, investigation of clinical parameters following experimental infection with each of the three organisms has not been done. The investigators studied ten cats infected with Mycoplasma haemofelis (“HF” group), three cats infected with candidatus M. haemominutum (“HM” group), and three cats infected with candidatus M. turicensis (“TU” group). The cats were followed for 85 days post infection. Using quantitative PCR, they found the TU cats had significantly lower amounts of organisms in their blood than the other groups, and were negative for the organism by 45 days after infection. All HF cats developed significant anemias. While HM and TU group cats did not have anemia or clinical signs, both groups experienced a drop in red blood cell levels for the first three weeks post infection. Only the HF cats had positive results on the Coombs assay, indicating the presence of antibodies to red blood cells. Severe hypoglycemia has been reported in some animals other than cats following hemoplasma infections. In this study, blood glucose levels for all three groups remained in the normal range. While the size of the groups was small, particularly the HM and TU groups, this study does demonstrate the increased pathogenicity of M. haemofelis compared to the other hemoplasmas. [MK]
>> PubMed Abstract

Related articles:
Peters IR, Helps CR, Willi B, Hofmann-Lehmann R, Tasker S. The prevalence of three species of feline haemoplasmas in samples submitted to a diagnostics service as determined by three novel real-time duplex PCR assays. Vet Microbiol. 2008;126(1-3):142-150.
>>PubMed Abstract

Sykes JE, Terry JC, Lindsay LL, Owens SD. Prevalences of various hemoplasma species among cats in the United States with possible hemoplasmosis. J Am Vet Med Assoc. Feb 1 2008;232(3):372-379.
>>PubMed Abstract

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Tasker S, Peters IR, Papasouliotis K, et al. Description of outcomes of experimental infection with feline haemoplasmas: copy numbers, haematology, Coombs' testing and blood glucose concentrations. Vet Microbiol. Nov 18 2009;139(3-4):323-332.

Feline hemoplasma infections are caused by three separate organisms that infect red blood cells, but only one of these, Mycoplasma haemofelis, causes hemolysis with significant disease. However, investigation of clinical parameters following experimental infection with each of the three organisms has not been done. The investigators studied ten cats infected with Mycoplasma haemofelis (“HF” group), three cats infected with candidatus M. haemominutum (“HM” group), and three cats infected with candidatus M. turicensis (“TU” group). The cats were followed for 85 days post infection. Using quantitative PCR, they found the TU cats had significantly lower amounts of organisms in their blood than the other groups, and were negative for the organism by 45 days after infection. All HF cats developed significant anemias. While HM and TU group cats did not have anemia or clinical signs, both groups experienced a drop in red blood cell levels for the first three weeks post infection. Only the HF cats had positive results on the Coombs assay, indicating the presence of antibodies to red blood cells. Severe hypoglycemia has been reported in some animals other than cats following hemoplasma infections. In this study, blood glucose levels for all three groups remained in the normal range. While the size of the groups was small, particularly the HM and TU groups, this study does demonstrate the increased pathogenicity of M. haemofelis compared to the other hemoplasmas. [MK]
>> PubMed Abstract

Related articles:
Peters IR, Helps CR, Willi B, Hofmann-Lehmann R, Tasker S. The prevalence of three species of feline haemoplasmas in samples submitted to a diagnostics service as determined by three novel real-time duplex PCR assays. Vet Microbiol. 2008;126(1-3):142-150.
>>PubMed Abstract

Sykes JE, Terry JC, Lindsay LL, Owens SD. Prevalences of various hemoplasma species among cats in the United States with possible hemoplasmosis. J Am Vet Med Assoc. Feb 1 2008;232(3):372-379.
>>PubMed Abstract

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Recurrence of Feline Uroliths

Albasan H, Osborne C, Lulich J, et al. Rate and frequency of recurrence of uroliths after an initial ammonium urate, calcium oxalate, or struvite urolith in cats. J Am Vet Med Assoc. 2009;235(12):1450-1455.

This case-controlled study was performed through the Minnesota Urolith Center. The objective was to determine the frequency of and interval until recurrence after initial ammonium urate, calcium oxalate and struvite uroliths in cats and whether breed, age, or gender was associated with increased risk for recurrence. In 1998, 4,435 cats were evaluated for an initial urolith episode and between 1998 and 2003 for recurrence episodes. Ammonium urate uroliths were found in 221 cats and 13.1% had an initial recurrence with a mean interval to recurrence of 22 months. Calcium oxalate uroliths were found in 2,393 cats and 7.1% had an initial recurrence with a mean interval of 25 months. Of 1,821 cats with struvite uroliths, 2.7% had a recurrence with a mean interval of 29 months. In all three types of uroliths, the largest percentage was located in the lower urinary tract. The study noted a low frequency of recurrence after struvite uroliths. The authors also noted it is likely that calcium oxalate and purine uroliths require at least 6 months to recur. Infection-induced struvite uroliths constitute an estimated 1 to 2% of uroliths retrieved from cats. An association was found in this study between recurrent episodes after initial calcium oxalate and struvite uroliths and older cats. The study also indicated a possible association between Persians and ammonium urate uroliths. Norwegian Forest Cats and Manx cats are at an increase risk for development of calcium oxalate uroliths, yet the number of these cats was small in this study. The majority of the uroliths (94%) found in the first recurrent episodes were identical to that of the initial urolith. Therefore, the composition of an initial urolith may be used as an estimate of the composition of subsequent uroliths. [VT]
>> PubMed Abstract

Related articles:
Osborne CA, Lulich JP, Kruger JM, Ulrich LK, Koehler LA. Analysis of 451,891 canine uroliths, feline uroliths, and feline urethral plugs from 1981 to 2007: perspectives from the Minnesota Urolith Center. Vet Clin North Am Small Anim Pract. 2009;39(1):183-197.
>> PubMed Abstract

Lulich JP, Osborne CA. Changing paradigms in the diagnosis of urolithiasis. Vet Clin North Am Small Anim Pract. 2009;39(1):79-91.
>> PubMed Abstract

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Albasan H, Osborne C, Lulich J, et al. Rate and frequency of recurrence of uroliths after an initial ammonium urate, calcium oxalate, or struvite urolith in cats. J Am Vet Med Assoc. 2009;235(12):1450-1455.

This case-controlled study was performed through the Minnesota Urolith Center. The objective was to determine the frequency of and interval until recurrence after initial ammonium urate, calcium oxalate and struvite uroliths in cats and whether breed, age, or gender was associated with increased risk for recurrence. In 1998, 4,435 cats were evaluated for an initial urolith episode and between 1998 and 2003 for recurrence episodes. Ammonium urate uroliths were found in 221 cats and 13.1% had an initial recurrence with a mean interval to recurrence of 22 months. Calcium oxalate uroliths were found in 2,393 cats and 7.1% had an initial recurrence with a mean interval of 25 months. Of 1,821 cats with struvite uroliths, 2.7% had a recurrence with a mean interval of 29 months. In all three types of uroliths, the largest percentage was located in the lower urinary tract. The study noted a low frequency of recurrence after struvite uroliths. The authors also noted it is likely that calcium oxalate and purine uroliths require at least 6 months to recur. Infection-induced struvite uroliths constitute an estimated 1 to 2% of uroliths retrieved from cats. An association was found in this study between recurrent episodes after initial calcium oxalate and struvite uroliths and older cats. The study also indicated a possible association between Persians and ammonium urate uroliths. Norwegian Forest Cats and Manx cats are at an increase risk for development of calcium oxalate uroliths, yet the number of these cats was small in this study. The majority of the uroliths (94%) found in the first recurrent episodes were identical to that of the initial urolith. Therefore, the composition of an initial urolith may be used as an estimate of the composition of subsequent uroliths. [VT]
>> PubMed Abstract

Related articles:
Osborne CA, Lulich JP, Kruger JM, Ulrich LK, Koehler LA. Analysis of 451,891 canine uroliths, feline uroliths, and feline urethral plugs from 1981 to 2007: perspectives from the Minnesota Urolith Center. Vet Clin North Am Small Anim Pract. 2009;39(1):183-197.
>> PubMed Abstract

Lulich JP, Osborne CA. Changing paradigms in the diagnosis of urolithiasis. Vet Clin North Am Small Anim Pract. 2009;39(1):79-91.
>> PubMed Abstract

More on cat health: Winn Feline Foundation Library
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