An 11-year-old male neutered Golden Retriever from Cañon City, Colorado, was brought to a local veterinary clinic in January 2010 for a 1-day history of lethargy and anorexia. The dog had traveled to Nevada approximately 2 months before it became sick. Physical examination was unremarkable apart from a rectal temperature of 103.8°F. Body weight was 35.4 kg. An in-house complete blood count (CBC) showed a hematocrit of 49.9%, mean corpuscular volume (MCV) of 79.9 fL (reference range [RR], 60–77 fL), 4430 neutrophils/μL (RR, 2000–12000 cells/μL), lymphopenia (500 cells/μL; RR, 500–4900 cells/μL), and 67,000 platelets/μL (RR, 175–500 × 103 platelets/μL). Thrombocytopenia was verified by smear evaluation. A serum biochemistry panel showed increased activity of serum ALT (797 U/L; RR, 10–100 U/L) and serum alkaline phosphatase (ALP) (232 U/L, RR 23–212 U/L). Serum total bilirubin, albumin, cholesterol, and glucose concentrations were within RR. Serum activity of creatine kinase (CK) was not measured. A presumptive diagnosis of immune-mediated thrombocytopenia was made. Treatment with prednisone (1.1 mg/kg PO q12h), amoxicillin (14 mg/kg PO q12h for 30 days), famotidine (0.6 mg/kg PO q12h), sucralfate (28 mg/kg PO q8h for 14 days), and S-adenosylmethionine (6.3 mg/kg PO q24h) was initiated.
The dog's lethargy and anorexia subsided, but CBCs performed 13 and 31 days after initiating treatment showed persistent thrombocytopenia (85,000 platelets/μL and 81,000 platelets/μL, respectively). The prednisone dosage was decreased (1.1 mg/kg PO q24h), but over the following week the dog became lethargic again, and weight loss (2 kg) was documented. A CBC showed neutrophilia (13365 cells/μL; RR, 3000–11500 cells/μL), 495 band neutrophils/μL (RR, 0), slightly toxic neutrophils, and clumped platelets. A biochemistry panel showed increased serum ALT activity (131 U/L). Serum CK activity was not measured. Thoracic radiographs were unremarkable. On day 38, the prednisone dosage was decreased further (20 mg PO q24h for 7 days, then q48h for 7 days) and tramadol was added (3.0 mg/kg PO q12h), but from day 51 the dog developed progressive pelvic limb weakness and anorexia.
Sixty-six days after onset of illness, the dog was examined by a board-certified veterinary neurologist. On physical examination, the dog was alert and interactive. Generalized muscle atrophy, a mild plantigrade stance in the pelvic limbs, stilted gait, and collapse with exercise were documented. Additional findings on neurologic examination were bilateral facial paresis, decreased conscious proprioception in all 4 limbs, delayed hopping reactions, and decreased segmental reflexes. Sciatic nerve sensation was decreased. The dog's rectal temperature fluctuated between 103.1 and 105.8°F over the next 24 hours. A CBC showed neutrophilia (20,114 cells/μL; RR, 2,060–10,600 cells/μL), monocytosis (904 cells/μL; RR, 0–840 cells/μL), nonregenerative anemia (34%) and a platelet count of 290,000/μL. A biochemistry panel showed hypoalbuminemia (2.5 g/dL; RR, 2.7–4.4 g/dL), increased serum activities of ALT (298 U/L; RR, 12–118 U/L), aspartate aminotransferase (AST) (197 U/L; RR, 15–66 U/L), CK (896 U/L; RR, 59–895 U/L), and hypomagnesemia (1.3 mEq/L; RR, 1.5–2.5 mEq/L). Treatment with ampicillin and enrofloxacin parenterally was initiated pending culture results. Aerobic and anaerobic bacterial blood cultures were negative. Aerobic bacterial urine culture yielded a broadly susceptible Escherichia coli. Urinalysis was not performed. Thoracic radiographs again showed no clinically relevant findings. Electromyography on day 67 showed spontaneous activity including increased insertional activity and fibrillation potentials in a generalized distribution. Motor nerve conduction velocities from the tibial and ulnar nerves were markedly decreased at 37 and 43 m/s, respectively (RRs, 68.2 ± 1.4 m/s and 58.9 ± 1.0 m/s, respectively). Compound motor unit amplitudes were decreased with dispersion. Biopsies were collected from the deep digital flexor muscle and left common peroneal nerve and processed as described previously. Cerebrospinal fluid collected from the lumbar cistern showed a normal cell count and protein concentration of 62 mg/dL (RR, ≤30 mg/dL). Immunofluorescent antibody serology12 for serum antibodies to N. caninum, Babesia canis, Bartonella henselae, Bartonella vinsonii, Ehrlichia canis, and Rickettsia rickettsii was negative. Results of serology using an in-house commercial diagnostic test13 for Borrelia burgdorferi, E. canis, Anaplasma spp., and Dirofilaria immitis also were negative. The dog was discharged from the hospital on day 69. Medications were enrofloxacin (5 mg/kg PO q12h for 10 days) for the urinary tract infection, clindamycin (11 mg/kg PO q8h) pending results of N. caninum serology and cyclosporine (5.6 mg/kg PO q12h), and dexamethasone (0.06 mg/kg PO q24h) for a possible immune-mediated polyneuropathy.
Histopathology of the muscle biopsies showed severe protozoal myositis. On day 75, cyclosporine was discontinued and the dexamethasone dosage tapered (0.06 mg/kg PO q72h). Eighty-four days after onset of illness, the dog became anorexic and collapsed, and was brought to an emergency clinic. On physical examination, the dog was weak and panting. Ptyalism was noted. Rectal temperature was 105.3°F, pulse 146 beats/min, and the dog was estimated to be 5–7% dehydrated. Body weight was 29.5 kg. A PCV was 35% and the serum biochemistry panel was normal apart from mild hypernatremia (163 mEq/L; RR, 144–160 mEq/L). Serum CK activity was not measured. The dog was treated with fluids (lactated Ringer's solution, 65 mL/h, IV), meropitant citrate14 (1 mg/kg, SC), dexamethasone sodium phosphate (0.07 mg/kg, IV, once), and clindamycin (12.7 mg/kg, IV, once), but died several hours after admission. Necropsy was not performed.
A 4-year-old female spayed Rottweiler from Greenough, in rural Montana, was brought to a local veterinary clinic in March of 2010 with a 1-day history of lethargy, ptyalism, anorexia, watery diarrhea, and increased panting. Three days before the onset of clinical signs, the dog was suspected to have contacted, and possibly ingested, carrion. On physical examination, the dog weighed 46.1 kg, had a rectal temperature of 104.2°F, heart rate of 124 beats/min, respiratory rate of 22 breaths/min, had tacky mucous membranes, and abdominal pain. Radiographs of the thorax and abdomen were unremarkable. A CBC showed a hematocrit of 50.8% (RR, 37–55%), 7,100 neutrophils/μL (RR, 3,000–10,500 cells/μL), lymphopenia (200 cells/μL; RR, 1,000–4,000 cells/μL), monocytopenia (0 cells/μL; RR, 150–1,200 cells/μL), and thrombocytopenia (99,000 platelets/μL; RR 200–500 × 103/μL). The thrombocytopenia was confirmed by microscopic examination of a blood smear. A serum biochemistry panel, performed on serum that had been separated from the clot without delay after collection, showed increased serum ALT activity (176 U/L; RR, 10–100 U/L) and hypoglycemia (58 mg/dL; RR, 74–143 mg/dL). Serum CK activity was not measured. Treatment with metronidazole (22 mg/kg PO q12h) and amoxicillin (22 mg/kg PO q12h) was initiated without clinical improvement. Two days later, the dog was taken to a local emergency clinic. At that time, the dog's rectal temperature was 102.9°F, and it was treated with lactated Ringer's solution (250 mL/h IV).
A CBC performed the next day at the local clinic showed an HCT of 38.4%, 7,900 neutrophils/μL (RR, 3,000–10,500 cells/μL), 600 monocytes/μL (RR, 150–1,200 cells/μL), 300 lymphocytes/μL (RR, 1,000–4,000 cells/μL), and clumped platelets. A serum biochemistry panel showed increased serum activities of ALP (2203 U/L; RR, 20–200 U/L), ALT (255 U/L; RR, 10–100 U/L), hyperbilirubinemia (3.5 mg/dL; RR, <0.4 mg/dL), and hypokalemia (3.3 mEq/L; RR 3.4–5.4 mEq/L). The dog was hospitalized and treated with enrofloxacin (2.2 mg/kg IV q12h), ampicillin (22 mg/kg IV q8h), and famotidine (0.43 mg/kg IV q12h). Abdominal ultrasound examination by a board-certified internist showed no clinically relevant findings. The next day, the dog began eating and was discharged from hospital. Treatment with amoxicillin and metronidazole was continued. Over the next week, the dog's appetite returned to normal and fever and ptyalism resolved. Although the dog's activity level improved, lethargy persisted.
At a recheck examination 28 days after the onset of illness, physical examination showed an stiff gait, reluctance to stand, and generalized muscle pain on palpation. A CBC and serum biochemistry panel was performed. The CBC showed an HCT of 44.5%. There were 4,700 neutrophils/μL (RR, 3,000–10,500 cells/μL), 300 monocytes/μL (RR, 150–1,200 cells/μL), 1,300 lymphocytes/μL (RR, 1,000–4,000 cells/μL), and 236,000 platelets/μL (RR 200–500 × 103/μL). Serum creatinine concentration was 1.1 mg/dL (RR, 0.4–1.4 mg/dL), and BUN concentration was 17 mg/dL (RR, 6–24 mg/dL). Serum ALT (294 U/L; (RR, 10–100 U/L) and AST (555 U/L; RR, 10–40 U/L) activities were increased, but serum ALP activity and total bilirubin concentration were within normal limits. Serum CK activity was increased (7,179 U/L; RR, 20–200 U/L). Serology for Leptospira spp. antibodies was negative.15 Serology for T. gondii IgM antibody was negative.16 Reciprocal antibody titers for T. gondii IgG antibody16 and Neospora caninum antibodies17 were positive at 64 and 40, respectively. Treatment with clindamycin (13 mg/kg PO q12h), prednisone (0.1 mg/kg PO q12h), and tramadol (2.2 mg/kg PO q6-8h) was initiated. This resulted in mild clinical improvement. Serum CK activity remained persistently increased (3,281 U/L on day 45 after onset of illness, and 5,406 U/L on day 50). Fifty-two days after the onset of illness, the dog was anesthetized and muscle biopsies were collected from the biceps femoris and triceps muscles, and histopathology of these tissues showed severe protozoal myositis.
Approximately 3 months after the onset of illness, protozoal serology was repeated. Serology for T. gondii was negative.16 The reciprocal antibody titer for N. caninum was 800.16 Treatment with clindamycin and tramadol was continued. An attempt was made to taper and discontinue the prednisone but the dog became painful again and so prednisone treatment was re-instituted. Serum CK activity remained increased almost 4 months after onset of illness (1,484 U/L), and the dog continued to exhibit generalized pain and muscle wasting.
Treatment with prednisone was discontinued and decoquinate (10–20 mg/kg PO q12h) was added. Over the next 3 months, the dog's muscle mass and energy level normalized and a 5 kg weight gain was recorded. Serum CK activity decreased to 474 U/L and the clindamycin was discontinued. The dog remains well at the time of writing, 9 months after initiating treatment with decoquinate.