Introduction
Renal transplantation has been a treatment option for cats with chronic renal disease since the first surgery was performed in 1987 and remains the only potential cure.1 To prevent allograft rejection following the procedure, cats are maintained on lifelong immunosuppressive therapy including the calcineurin inhibitor cyclosporine in combination with prednisolone. Unfortunately, long-term immunosuppressive therapy is known to have potential complications, including predisposing recipients to opportunistic infectious agents such as Toxoplasma gondii.2
Toxoplasma gondii is an obligate intracellular coccidian parasite that can infect all mammalian hosts and for which cats serve as the definitive host. Currently, seroprevalence of T gondii infection in cats in the United States has been estimated to be between 31.6% and 62%, therefore affecting a large portion of the potential donor and recipient populations.3,4,5 Although T gondii infection is a rare complication in human renal transplantation, opportunistic infections associated with T gondii resulting in both morbidity and death have been reported in feline renal transplant recipients following chronic immunosuppressive therapy.6,7 In 1 report, 3 cats developed fatal complications associated with disseminated toxoplasmosis 3 to 6 weeks following commencement of immunosuppressive therapy and renal transplantation.8
Potential recipients undergo rigorous preoperative screening to identify cats free of systemic disease not related to their renal function. This screening has led to either the exclusion of cats that are seropositive for T gondii as renal transplant recipients at some facilities or the recommendation that cats seropositive for T gondii be closely monitored for possible reactivation of infection following commencement of immunosuppressive therapy and renal transplantation. From 1998 until 2001, routine screening for T gondii was not performed at our institution for this population of patients. During that time, 3 recipients acutely deteriorated and died 2 to 13 months following transplantation from confirmed reactivation of latent T gondii infections. On the basis of this experience, routine testing was initiated, and all cats that were seropositive for T gondii were placed on lifelong prophylactic treatment of T gondii infection in conjunction with their immunosuppressive therapy. The purposes of the study presented here were to evaluate the effects of T gondii infection in feline renal transplant recipients with a preoperative SN-UKN for T gondii and evaluate the efficacy of lifelong prophylactic treatment of T gondii infection in feline renal transplant recipients with a preoperative serostatus of seropositive for T gondii.
Materials and Methods
Case selection criteria
Medical records of 170 cats that had undergone renal transplantation at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania from 1998 through 2018 were retrospectively reviewed, and 2 groups of cats were identified.
The first group included cats that were seronegative for T gondii or had an unknown serostatus for T gondii (ie, SN-UNK group cats) before renal transplantation. Cats in the SN-UNK group were not maintained on prophylactic treatment of T gondii and developed T gondii infections after initiation of immunosuppressive therapy and renal transplantation. The second group included cats that were seropositive for T gondii (ie, SP group cats) prior to initiation of immunosuppressive therapy and renal transplantation and were managed before and after surgery with lifelong prophylactic treatment of T gondii. Data on cats in each group were described and compared.
Medical records review
Information obtained from the medical record for both groups included signalment, date of renal transplantation, preoperative and postoperative serum antibody titers against T gondii, start date of immunosuppressive therapy and dose of immunosuppressive drugs, survival time (in days) after renal transplantation, and cause of death. Additional information was obtained for cats in the SN-UNK group as follows: clinical signs associated with T gondii infection, date when clinical signs of T gondii infection developed, method of diagnosis, treatment initiated, and pertinent necropsy findings (if available). Additional information was obtained for cats in the SP group as follows: start date of prophylactic treatment of T gondii, prophylactic drug administered, and dose of prophylactic drug. Cats with incomplete medical records or those that received allograft kidneys from donor cats of unknown T gondii infection serostatus were excluded from the study.
Procedures
For all cats that underwent renal transplantation, treatment with cyclosporine (2 to 3 mg/kg [0.9 to 1.36 mg/lb], PO, q 12 h) began days (23 cats) to months (1 SP group cat) before surgery. Trough blood concentrations of cyclosporine were measured by means of high-pressure liquid chromatography, and cyclosporine dosage was adjusted to maintain a trough blood concentration within the therapeutic range of 300 to 500 ng/mL8 for approximately 2 to 3 months following surgery. Thereafter, the amount of cyclosporine administered was tapered to maintain a blood concentration of approximately 250 ng/mL.
In addition, for all cats that underwent transplantation, treatment with prednisolone (0.4 to 1 mg/kg [0.18 to 0.45 mg/lb], PO, q 12 h) began the morning of surgery or 1 to 4 days prior to surgery. Renal transplantation was performed as previously described.9 Cats were recovered in the intensive care unit and discharged from the hospital when graft function was evident.
For recipient cats that underwent serologic testing for antibodies against T gondii, serum IgM and IgG antibody titers were determined by use of an ELISA performed at a commercial diagnostic laboratory. In the present study, all donor cats were seronegative for T gondii before surgery.
Results
SN-UNK group cats
Four cats with unknown serostatus and 4 seronegative cats that developed clinically apparent T gondii infections after renal transplantation were included in the SN-UNK group. Cats in the SN-UNK group ranged from 6.6 to 14.6 years of age at the time of renal transplantation (mean, 10.2 years; median, 9.6 years) and included 6 castrated male cats and 2 spayed female cats. All cats were domestic shorthair cats, except for 1 Abyssinian cat.
Cats in the SN-UNK group began cyclosporine treatment a mean ± SD of 3 ± 1.5 days prior to renal transplantation. Oral administration of prednisolone began the morning of transplantation in 5 cats and 4 days prior to surgery in 3 cats at a mean dosage of 0.65 ± 0.19 mg/kg (0.30 ± 0.09 mg/lb; range, 0.4 to 0.9 mg/kg [0.18 to 0.41 mg/lb]) every 12 hours. Median survival time for cats in the SN-UNK group that died was 203 days (range, 27 to 409 days) after surgery. One cat was alive 440 days after surgery.
Within 2 months prior to renal transplantation surgery, all 4 cats that underwent serologic testing for T gondii infection were seronegative. Three of these seronegative cats died 27, 53, and 147 days following renal transplantation as a result of T gondii infections. Treatment was initiated in the fourth cat, and this cat was alive 440 days after surgery.
The first seronegative cat in the SN-UNK group was brought to the primary veterinarian 22 days following renal transplantation for clinical signs of lethargy and anorexia. No treatment was initiated at that time, and the cat was brought to the authors’ institution 5 days later because of dyspnea. Thoracic radiography showed a diffuse alveolar infiltrate, and treatment was initiated for possible pneumonia. Two doses of ampicillin (22 mg/kg [10 mg/lb]) were administered IV; however, the cat died of respiratory arrest that evening. Necropsy revealed multifocal necrosis of the liver, both native kidneys, spleen, lung, pancreas, heart, and brain. Both T gondii tachyzoites and protozoal cysts were present in all of these organs as well as the bone marrow.
The second seronegative cat in the SN-UNK group was brought to the authors’ institution 146 days following renal transplantation for a 3- to 4-day history of progressive lethargy and anorexia. Thoracic radiography revealed an alveolar pattern. A single dose of clindamycin (15 mg/kg [6.8 mg/lb], IV) was administered on the day of hospital admission; however, the patient underwent respiratory arrest and died the following day. Tachyzoites were noted on cytologic examination of an endotracheal wash sample that was obtained during hospitalization.
The third seronegative cat in the SN-UNK group was brought to the authors’ institution 41 days following renal transplantation for lethargy and anorexia; subsequently, postrenal azotemia was diagnosed secondary to a mass at the neoureterocystostomy site. The mass was resected, and ureteral reimplantation was performed. Histologic examination of the mass revealed periureteral and pericystic pyogranulomatous cellulitis with numerous intralesional T gondii bradyzoite cysts. Serologic testing for antibodies against T gondii was performed at the time of mass resection and ureteral reimplantation and revealed an IgG titer of 1:1,024. The cat was discharged from the hospital and was prescribed clindamycin (17 mg/kg [7.7 mg/lb], PO, q 12 h); however, the cat was brought back 7 days later with marked dyspnea and was euthanized per the owner's request. The donor cat of this recipient cat was seronegative prior to renal transplantation, as was true for all donor cats, but was serologically retested given the T gondii bradyzoite–containing mass found in the recipient cat. Recheck serologic testing revealed that the donor cat remained seronegative with an IgG titer of < 1:64.
The fourth seronegative cat in the SN-UNK group was brought to the authors’ institution 79 days after renal transplantation because of inappetence and gastrointestinal signs. At the time of hospital admission, an elevation in serum concentration of renal values was noted (BUN, 56 mg/dL [reference range, 15 to 32 mg/dL]; creatinine, 1.6 mg/dL [reference range, 1 to 2 mg/dL]), compared with serum concentration of renal values 1 week earlier (BUN, 17 mg/dL; creatinine, 0.8 mg/dL). The cat also had neutrophilia with a left shift (21,240 mature neutrophils/μL and 210 band neutrophils/μL). Serum anti–T gondii antibody titers were obtained at this time, revealing an IgM titer of 1:64. Serum IgG antibodies against T gondii were not detected. The patient was started on treatment with clindamycin (10 mg/kg [4.5 mg/lb], IV, q 12 h) and was discharged from the hospital to continue oral administration of clindamycin every 12 hours. Clinicopathologic analysis performed 7 days following initiation of antimicrobial treatment revealed resolution of azotemia and neutrophilia. On repeated testing for serum IgM and IgG against T gondii performed 176 days following renal transplantation, the cat was seronegative. At approximately 440 days following renal transplantation (ie, at the time of manuscript preparation), the cat was still alive.
Four cats in the SN-UNK group underwent renal transplantation prior to the time when serologic testing for T gondii became a routine screening test and thus had an unknown preoperative serostatus. Three of the 4 cats with an unknown serostatus died secondary to complications associated with reactivation of a latent T gondii infection at 194, 199, and 409 days following renal transplantation. Two of the 3 cats that died were brought to referral hospitals at 195 and 405 days after renal transplantation because of the development of dyspnea. Thoracic radiography revealed diffuse alveolar infiltrates with pleural effusion in one cat and a diffuse interstitial pattern in the other cat.
In the first of the 4 cats with an unknown preoperative serostatus, T gondii tachyzoites were found on cytologic evaluation of both a pleural effusion sample and a sample obtained by endotracheal wash. Treatment was initiated with administration of enrofloxacin (10 mg/kg, IV, q 24 h), trimethoprim-sulfamethoxazole (15 mg/kg, IV, q 12 h), clindamycin (10 mg/kg, IV, q 8 h), and pyrimethamine and folinic acid (1 mg/kg, PO, q 24 h). The cat immediately required mechanical ventilation and died within 12 hours of hospitalization. Toxoplasma gondii tachyzoites were present within the lungs, retropharyngeal lymph nodes, and allograft kidney at necropsy. At the time of death, the cat had an IgG titer of 1:1,024.
In the second cat with an unknown preoperative serostatus, cytologic examination of a pulmonary aspirate revealed T gondii trophozoites, and the cat died of respiratory arrest. Necropsy revealed multifocal necrosis and cysts in the lungs, liver, kidney, spleen, pancreas, and brain with T gondii tachyzoites.
The third cat with an unknown preoperative serostatus had a subtherapeutic blood cyclosporine trough concentration of 169 ng/mL at 144 days after renal transplantation; the cat received an additional dose of cyclosporine orally. The following week, the cat became lethargic, anorexic, and azotemic (BUN, 86 mg/dL; creatinine, 6.1 mg/dL) and was treated for an acute allograft rejection episode with IV administration of cyclosporine (6.6 mg/kg [3 mg/lb]) and 2 doses of methylprednisolone (10 mg/kg, IV, q 12 h). Improvement in azotemia (BUN, 34 mg/dL; creatinine, 1.9 mg/dL) was initially noted 24 hours following treatment, and the allograft rejection protocol was repeated. The cat's azotemia worsened (BUN, 83 mg/dL; creatinine, 5.2 mg/dL), and the cat's clinical state deteriorated further. Abdominal ultrasonography revealed mild renal pelvic dilation and perirenal effusion. An aspirate of the perirenal effusion was obtained; on cytologic examination, the sample contained T gondii tachyzoites. Serologic testing was performed, and the T gondii IgG titer was 1:64. Treatment with ticarcillin-clavulanate (50 mg/kg [22.7 mg/lb], IV, q 6 h) was initiated; however, the cat died 24 hours later following the development of dyspnea. At necropsy, T gondii tachyzoites were present within the heart, lungs, liver, spleen, and pancreas.
The final cat with an unknown preoperative serostatus survived recrudescence of infection. This cat developed anorexia and azotemia (BUN, 53 mg/dL; creatinine, 2.9 mg/dL) 60 days after renal transplantation. Abdominal ultrasonography revealed perirenal fluid, and serum anti–T gondii antibody titers were consistent with an active T gondii infection (IgM titer, 1:400; IgG titer, 1:1,200). Treatment was initiated with clindamycin (10 mg/kg, IV, q 8 h), pyrimethamine (0.5 mg/kg [0.22 mg/lb], PO q 24 h), and trimethoprim-sulfadiazine (15 mg/kg, IV, q 12 h). The patient was discharged from the hospital 9 days later and maintained on clindamycin (15.3 mg/kg [6.9 mg/lb], PO, q 12 h) for the remainder of its life. Four months later, the serum anti–T gondii antibody titers were consistent with exposure and not active infection (IgM titer, antibodies not detected; IgG titer, 1:400). This patient died 392 days following renal transplantation from multicentric lymphosarcoma with no clinical signs associated with a T gondii infection.
SP group cats
Sixteen seropositive cats that underwent successful renal transplantation while receiving prophylactic treatment of T gondii were included in the SP group. Only 1 cat developed a nonfatal clinical T gondii infection after renal transplantation. Cats in the SP group ranged from 4.4 to 13 years of age at the time of renal transplantation (mean ± SD, 9.3 ± 2.8 years) and included 8 castrated male cats and 8 spayed female cats. All cats were domestic shorthairs.
For 15 cats in the SP group, cyclosporine administration was initiated 1 to 15 days (median, 5 days) before renal transplantation. One SP group cat had already been receiving cyclosporine for several months prior to renal transplantation for treatment of plasma cell pododermatitis. Prednisolone (0.75 to 1 mg/kg [0.34 to 0.45 mg/lb], PO, q 12 h) was administered starting the morning of renal transplantation in 14 cats and 4 days prior to surgery in the remaining 2 cats.
Median survival time for cats in the SP group was 667 days (range, 11 to 1,940 days). Preoperative serum anti–T gondii IgG antibody titers were available for all SP group cats and ranged from < 1:64 to 1:4,096, whereas preoperative serum IgM antibody titers against T gondii were available for 13 cats and ranged from < 1:64 to 1:256. Twelve cats began prophylactic treatment of T gondii with clindamycin a mean of 4.8 days (range, 0 to 18 days) prior to initiation of immunosuppressive therapy, and 3 cats started receiving clindamycin 1 day following initiation of cyclosporine administration. The remaining cat received prophylactic treatment of T gondii approximately 3 months before renal transplantation; however, clindamycin administration was discontinued for approximately 2 weeks and restarted 1 day prior to initiation of immunosuppressive therapy. Clindamycin was orally administered every 12 hours for 13 cats and every 8 hours for 2 cats. For cats that received twice-daily clindamycin administration, the mean ± dosage was 7.6 ± 2 mg/kg (3.5 ± 0.9 mg/lb). For prophylactic treatment of T gondii, 1 cat received trimethoprim-sulfadiazine (28 mg/kg [12.7 mg/lb], PO, q 12 h) after developing gastrointestinal upset following clindamycin administration. For all SP group cats, serum anti–T gondii antibody titers were measured as needed on the basis of health and the identification of clinical signs that could be associated with T gondii reactivation.
Discussion
Toxoplasma gondii is an obligate intracellular coccidian parasite that affects numerous warmblooded species, including both domestic cats and humans.3,5,10 Cats can be infected by 3 modes of transmission, including congenital infection, oocyst contamination within the environment, and ingestion of meat from an intermediate host infected with tissue cysts, the latter being the most common. Following ingestion, because cats are the definitive host, the parasite can undergo either an enteroepithelial life cycle, resulting in the shedding of oocysts, or extraintestinal life cycle, resulting in tissue encysted bradyzoites. The encysted organism usually persists for the lifetime of the host and, in most cats following an appropriate immune response, leads to subclinical disease.10 The seroprevalence of the disease in cats in the United States has been reported to be between 31.6% and 62%, therefore affecting a large portion of the feline population.3,4,5 These numbers may be further inflated because the prevalence of seropositive cats increases with age as a result of increased potential exposure.3 Although 1 study1 reports a mean age of 7.8 years in cats undergoing renal transplantation, an even higher percentage of potential seropositive recipient cats could exist. Because active T gondii infections in immunosuppressed recipients are typically fatal, as demonstrated by the findings in the present study, this high prevalence requires that either seropositive cats be removed as potential renal transplant recipients or a suitable method of monitoring and prevention be instituted.
Initially, following the establishment of the renal transplant program in 1998 at the authors’ institution, serologic testing for T gondii was not performed for potential recipients. In the present study, medical records from 1998 to 2001 included 4 cats in the SN-UNK group that underwent renal transplantation with unknown T gondii serostatus and later developed clinical disease. Three of the 4 cats died 194, 199, and 409 days following renal transplantation because of T gondii infections. The fourth cat had clinical signs of T gondii infection 60 days following renal transplantation and was treated aggressively with trimethoprim-sulfadiazine, pyrimethamine, and clindamycin and survived. This cat died 392 days following renal transplantation of multicentric lymphosarcoma, with no clinical signs associated with T gondii infection. In the present study, 4 cats in the SN-UNK group were seronegative for T gondii. Three of these cats died 27, 53, and 147 days following renal transplantation as a result of T gondii infections. Treatment was initiated in the fourth cat, which was alive at approximately 440 days following renal transplantation. It is unclear whether there were false-negative serologic test results for T gondii with the original preoperative serologic testing or whether these cats became exposed following the surgery. Alternatively, the parasitic burden in these cats may have been too low for detection by traditional serologic testing. Acute postoperative infections are unlikely because cats that undergo renal transplantation are required to live indoors following the procedure and are activity restricted through confinement to a small room or crate for the first month following renal transplantation. Carnivorous feeding and subsequent tissue cyst ingestion are therefore limited by lack of exposure to an outdoor environment. Beginning in 2001 at the authors’ institution, all potential recipients were screened for T gondii, and if these cats were seropositive for T gondii (as determined by IgG titers, IgM titers, or both), prophylactic treatment with clindamycin was initiated prior to renal transplantation.
Toxoplasma gondii infection, as a complication following transplantation in human medicine, is commonly seen when a seronegative recipient receives a seropositive donor heart, as this muscle is a common area of tissue encystment.11,12,13,14,15,16,17 Donor transmission is unlikely for the recipient cats described in the present study because all donor cats were seronegative for T gondii. Comparatively, T gondii infections are a rare complication of renal transplantation in humans, with only 44 reported cases in the literature, of which 21 were considered a reactivation of a latent infection.18,19 Routine administration of trimethoprim-sulfamethoxazole for the prevention of a commonly encountered opportunistic fungal pathogen, Pneumocystis jiroveci, in these patients has been thought to play some role in the prevention of donor-to-recipient transmission of T gondii; however, this remains unclear.20,21
The risk of infection in the recipient is related to the synergy of 2 factors, epidemiological exposure and the patient's net immunosuppression.22 Posttransplantation infections can result from reactivation of the disease, primary infection, donor-to-recipient transmission, and rarely from contaminated blood transfusions.7 In human transplant recipients, infectious complications are usually divided into 3 time frames to help define their etiology: the first month, 1 to 12 months, and > 12 months after transplantation.20,22,23 In the first month, infections are less common and are usually donor derived, were present in the recipient before transplantation, or were secondary to the surgical procedure itself. One cat in the SN-UNK group died because of T gondii infection during the first month following surgery. The most common time frame for infectious complications from opportunistic organisms is 1 to 12 months after transplantation. During this time, the degree of immunosuppression is high and infections usually result from residual surgical infections, viral infections, and opportunistic infections, including T gondii.22 Seven of the 8 cats in the SN-UNK group in the present study died during the first 409 days following surgery. In these cats, whether reactivation of a previously latent disease or opportunistic infections secondary to environmental exposure were the cause of the fatal infection is unknown.
Prior to 2001, donor cats were not regularly screened for T gondii at the authors’ institution because donor cats were obtained from a pathogen-free laboratory and thus assumed to be seronegative. Since 2001, all donor cats have undergone serum antibody screening for T gondii and were seronegative prior to transplantation. Although it is conceivable that the serologic testing may have missed an acutely T gondii–infected donor cat, donor transmission seems unlikely on the basis of the timing of infections and the fact that this is a rare cause of T gondii infection in human renal transplant recepients.20,22,23,24 Currently at our facility, donor cats that are seropositive for T gondii are not used in renal transplantation because the potential effects on the recipient cat are unknown. Mismatched transplantation in human medicine is a cause for extended prophylactic treatment of T gondii. In solid organ transplantation, the kidney is a low-risk organ because it is not a common site of parasite encystment.6
Clindamycin has been the most common therapeutic chosen for prophylactic treatment of T gondii infection in feline renal transplant recipients that are seropositive for T gondii. The drug is a member of the antimicrobial class of lincosamides.25 Although these antimicrobials are bacteriostatic through inhibition of the 50S ribosomal unit, they have also shown limited activity against fungal and protozoal organisms, including T gondii.26 In both human HIV patients and cardiac transplant recipients, sulfadiazine in combination with other therapeutics is the mainstay of both treatment and prophylactic regimens. However, sulfadiazine has been reported to be increasingly associated with hypersensitivity reactions, which have also been reported in veterinary medicine.27,28 This information has led to the increased use of clindamycin in the cats described in the present study. Although other drugs, including sulfadiazine, pyrimethamine, and folinic acid, have been used in the treatment of active infections when clindamycin did not seem to be effective, it remains the mainstay of prophylactic treatment of T gondii for cats that are seropositive for T gondii prior to renal transplantation. Of the 16 seropositive cats in the present study that were maintained on lifelong administration of clindamycin, only 1 cat experienced a suspected nonfatal reactivation. The mechanism of action of clindamycin against T gondii has been shown to be a delayed death effect when the parasite leaves the first infected host cell to begin division in the second parasitophorous vacuole.29 This is likely related to abnormal protein synthesis in the apicoplast, an organelle that directly affects survival.26 Additionally, other feline renal transplant programs use similar clindamycin prophylactic treatment in T gondii–seropositive cats with promising results.1 Prophylactic treatment must be lifelong, as clindamycin is effective against only the tachyzoite stage and will not clear the encysted bradyzoite stage, allowing chronic subclinical infections.
In the present study, of the 6 cats in the SN-UNK group that died of T gondii infection, 5 had similar signs of generalized lethargy that quickly progressed to fatal dyspnea. Thoracic radiography in all 5 cats revealed similar patterns of diffuse interstitial to alveolar patterns with or without pleural effusion. Diagnoses of T gondii infections were made on the basis of cytologic evidence of tachyzoites on an endotracheal wash in 2 cats, an aspirate of perirenal fluid surrounding the graft kidney in 1 cat, a pulmonary parenchymal aspirate in a fourth cat, and multiple organs during necropsy in the final cat. A study30 of histologically confirmed T gondii infections in cats showed that 97.7% of infected cats had T gondii pneumonia at the time of necropsy.
Reactivation of T gondii infection has also been seen in human patients following acute increases in immunosuppressive medications for allograft rejection episodes, primarily prednisone.7 In the present study, 1 cat in the SN-UNK group was treated for an allograft rejection episode and died 7 days later of a fatal T gondii infection. Additionally, the only cat in the SP group to develop a potential reactivation of infection while undergoing clindamycin treatment experienced this while being treated for an allograft rejection episode. In a previous report8 of 3 cats and 1 dog that developed T gondii infections after renal transplantation, 2 developed clinical signs following treatment for acute allograft rejection.
In conclusion, on the basis of our experience, cats that are seropositive for T gondii remain suitable candidates for renal transplantation if maintained on lifelong prophylactic treatment of T gondii. Clindamycin appears to be a well-tolerated and effective antiprotozoal medication in this population of cats. Regardless of preoperative serostatus, all cats undergoing renal transplantation and accompanying lifelong immunosuppressive therapy should be monitored closely for T gondii infection long-term. At the authors’ institution, frequent reevaluation of serum anti–T gondii antibody titers in seronegative patients for the first year after surgery has been instituted. In addition, clinicians should have a high index of suspicion for T gondii infection in any immunosuppressed cat that presents with pulmonary signs, especially if signs developed following an increase in medication for immunosuppressive therapy. Unfortunately, once pulmonary signs develop, the infection is often fatal.
Acknowledgments
No third-party funding or support was received in connection with this study or the writing or publication of the manuscript.
Presented in part as an abstract at the American College of Veterinary Surgeons Veterinary Symposium, Chicago, November 2011.
Abbreviations
| SN-UNK | Seronegative or unknown serostatus |
| SP | Seropositive serostatus |
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