Anaplasma phagocytophilum infection associated with strong inflammatory response in 3 cats.

Anaplasmosis is a vector-borne disease caused by Anaplasma (A.) spp. which currently is still rarely diagnosed in cats. This article describes 3 independent cases of anaplasmosis in cats from different regions of Germany presented to veterinarians in 2021. All cats showed unspecific clinical signs, such as fever, reduced general condition, and decreased appetite. One cat additionally had generalized limb pain, another showed reluctance to move as well as vomiting. On complete blood cell count, only 1 of 3 cats showed mild thrombocytopenia. A. phagocytophilum was detected in blood samples of all 3 cats by polymerase chain reaction. Additionally, in 2 cats (in which blood smears were evaluated) morulae could be detected within neutrophilic granulocytes. Initially, all 3 cats had highly elevated serum amyloid A (SAA) concentrations. Treatment with doxycycline caused a rapid improvement of clinical signs, followed by a decrease of SAA concentrations to normal levels as well as negative PCR results after a treatment duration of at least 28 days. In cats with fever, otherwise unspecific clinical signs with only mild or no hematological changes, elevated SAA concentrations, and previous exposure to ticks, attending veterinarians should consider anaplasmosis as differential diagnosis.

Case series: Heinz body formation in 13 multimorbid dogs following metamizole administration.

Background: Heinz Body (HB) anemia is a result of oxidative damage and is an uncommon condition in dogs relative to cats. In this retrospective case series, clinical features, laboratory values, concurrent diseases, and outcomes of 13 multimorbid dogs that developed HBs after receiving metamizole are reported. Case description: Of the 13 dogs in this case series that developed HBs, 10 were older and multimorbid, but the only feature that all the dogs had in common was receiving metamizole. HBs were detected in 7 out of 13 dogs within a few days (3-10 days) after starting metamizole treatment. The metamizole dose was 38-159 mg/kg/day. The highest percentage of HBs detected was 28-95% (mean, 46%). There was no correlation between the percentage of HBs and the daily dose of metamizole. All but 1 dog had mild-to-severe anemia at the time of the highest HB appearance. The number of HBs did not correlate with the hematocrit at that time. In 8/12 dogs, no stress leukogram was present. Approximately half of the dogs with HBs also had evidence of gastrointestinal hemorrhage, which could have masked additional oxidative damage. Conclusion: In multimorbid dogs that develop regenerative anemia after receiving metamizole, hemolysis due to HB development caused by oxidative damage should be considered as an important differential diagnosis.

Hemostatic and thromboelastographic parameters in dogs with renal azotemia.

Background and Aim: Humans and dogs with azotemia can develop coagulation disorders. Therefore, this study aimed to evaluate the coagulation profiles and thromboelastographic parameters in dogs with acute kidney injury (AKI) and chronic kidney disease (CKD). Materials and Methods: In this prospective study, 31 client-owned dogs with renal azotemia (creatinine >220 µmol/L) were enrolled. Clinical signs of hemostatic disorders, complete blood count, coagulation profile, D-dimers, thromboelastography, and 28-day survival data were obtained and analyzed using the t-test, Mann-Whitney U test, and Chi-square test. Statistical significance was set at p < 0.05. Results: Seventeen dogs with AKI, 10 with CKD, and four with acute-on-chronic kidney injury (AoC) were enrolled. Ten dogs (AKI, 8/17; CKD, 2/10) had thrombocytopenia. Prothrombin time was prolonged in four dogs with AKI and longer in dogs with AKI than in dogs with CKD (p = 0.004). The activated partial thromboplastin time was prolonged in 23 dogs (AKI, 14/17; CKD, 7/10; AoC, 3/4) and was longer in azotemic dogs than in healthy control dogs (p = 0.003). Thromboelastographic tracings were hypocoagulable in three dogs with AKI and hypercoagulable in 16 dogs (AKI 4/17, CKD 9/10, AoC 3/4). The thromboelastographic values for maximum amplitude (p < 0.001) and global clot strength (p < 0.001) were lower in dogs with AKI than in those with CKD. Conclusion: Hypercoagulable thromboelastographic tracings were observed in dogs with CKD, whereas coagulation times were prolonged in dogs with AKI. However these findings should be validated by further studies.

Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.

[Disseminated protothecosis with ulcerative granulomatous colitis in a Rhodesian Ridgeback from Germany]. / Ulzerative granulomatöse Kolitis durch Prototheca spp. bei einem Rhodesian Ridgeback in Deutschland.

A 10-month-old male Rhodesian Ridgeback was presented to the Clinic of Small Animal Medicine, LMU, Germany, with a 6-month history of chronic diarrhea and hematochezia. The dog lived in Germany and had never traveled abroad. Complete blood count and serum biochemistry performed by the referring veterinarian revealed neutrophilia, hyperkalemia, and hyponatremia, with a basal cortisol of 4.3 µg/dl, which excluded hypoadrenocorticism. Since antibiotic treatment had not resulted in any improvement, a 2 week course of prednisolone administration had been initiated, leading to a marked deterioration of intestinal signs and a significant weight loss of 6 kg. At the time of referral, the patient was markedly emaciated, dehydrated, hypovolemic and had a rectal temperature of 39.6 °C. Abdominal ultrasound showed a thickened and irregular colonic wall. On colonoscopy, an irregular colonic mucosa with ulcerations was observed. Histopathologic examination revealed an ulcerative granulomatous colitis, and on Periodic acid-Schiff reaction (PAS) numerous organisms consistent with Prototheca spp. were identified. Prototheca zopfii infection was confirmed by culture and MALDI-TOF MS. In order to test for an underlying immunodeficiency, immunoglobulin levels in serum were determined. IgM was decreased, while IgG and IgA levels were within the reference interval. Due to deterioration of general condition, grave prognosis and costs of a treatment trial, the patient was euthanized one week later, and necropsy was performed. Prototheca spp. were detected on histopathologic examination in the lymphnodes, however not in the eyes or the central nervous system. Protothecosis should be considered an differential diagnosis in dogs with chronic diarrhea and ulcerative granulomatous colitis even in dogs living in Germany. Histopathologic examination of colonic biopsies with special stains such as PAS is recommended in every dog with signs of chronic large bowel disease in order to avoid missing this rare infectious disease.

Toxoplasma gondii-associated cholecystitis in a cat receiving immunosuppressive treatment.

A 9-year-old female neutered domestic shorthair cat diagnosed with immune-mediated thrombocytopenia that was treated with prednisolone and cyclosporine, was presented for anorexia, vomiting, increased liver enzymes, and hyperbilirubinemia. Abdominal ultrasound revealed a markedly thickened gallbladder and common bile duct wall. Bile cytology detected severe neutrophilic inflammation and protozoal zoites. Suspected Toxoplasma gondii infection was confirmed by real-time PCR of bile. The cat was treated with clindamycin and ursodeoxycholic acid for 6 weeks, recovered and remained stable for 2 years despite ongoing immunosuppressive treatment. Thereafter, the cat was presented with suspicion of intestinal lymphoma, and recurrence of toxoplasmosis was diagnosed. Following treatment with clindamycin and prednisolone over 4 weeks the cat was euthanized. This is the first report of Toxoplasma gondii zoites detected in bile fluid from a cat with cholecystitis. Pathogenesis of toxoplasmosis in cats is still not fully understood. Although immunosuppression can represent a relevant predisposing factor, other factors, such as virulence of the parasite and genetic polymorphism of the host, can also play an important role. Toxoplasmosis should be included as a differential diagnosis in cats developing clinical signs of an inflammatory disease while receiving immunosuppressive treatment.