Case Description—A 21-month-old spayed female Border Collie was examined because of progressive right forelimb lameness, signs of pain, and subcutaneous edema. The dog lived in a fenced yard in Tampa, Fla, that contained a small area of marshy terrain.
Clinical Findings—The subcutis and intermuscular fascia contained multiple cystic cavities filled with larval cestodes (plerocercoids or spargana) and cloudy red fluid. Parasites were identified morphologically and by DNA sequence analysis as pseudophyllidean cestodes, most likely Sparganum proliferum. The dog developed a progressively worsening fever, dyspnea, mature neutrophilia, and hypoproteinemia. Septic pleuritis and peritonitis complicated the later stages of the disease.
Treatment and Outcome—Treatment with praziquantel, fenbendazole, and nitazoxanide failed to control the proliferation and dissemination of larval cestodes. The dog was euthanatized after 133 days of treatment. At necropsy, numerous parasitic tissue cysts were present in the subcutis and intermuscular fascia; these cysts were most abundant in the soft tissues of the forelimbs and cervical musculature. The pleural and peritoneal cavities contained multiple larval cestodes and were characterized by neutrophilic inflammation and secondary bacterial infection.
Clinical Relevance—Findings indicated that clinical signs associated with proliferative sparganosis in dogs may be rapidly progressive and that the condition may be refractory to antiparasitic treatment. Veterinarians should be aware of this zoonotic, water-borne agent.
Objective—To determine clinical and pathologic findings before and after short-term (group 1) and longterm (group 2) treatment in dogs with Hepatozoon americanuminfection.
Animals—53 dogs with H americanuminfection.
Procedure—Medical records of dogs that were treated for hepatozoonosis diagnosed on the basis of meront or merozoite stages in skeletal muscle were reviewed.
Results—Circulating gametocytes of H americanum were identified in 12 of 53 dogs. Dogs were treated with various drugs, including toltrazuril, trimethoprimsulfadiazine, clindamycin, pyrimethamine, and decoquinate. Mean WBC counts prior to treatment were 85,700 and 75,200 cells/µl in groups 1 and 2, respectively, and 1 month after initiation of treatment were 12,600 and 14,600 cells/µl, respectively. Initial response to treatment was excellent in all dogs. Twenty-three of 26 dogs in group 1 relapsed at least once and died within 2 years; mean (± SD) survival time was 12.6 ± 2.2 months. Twenty-two of 27 group-2 dogs survived; 11 dogs had no clinical signs and were still receiving decoquinate (mean duration of treatment, 21 months), 11 dogs had no clinical signs after treatment for 14 months (range, 3 to 33 months; mean survival time, 39 months [range, 26 to 53 months]), 2 dogs were lost to follow-up, and 3 dogs were euthanatized because of severe disease.
Conclusions and Clinical Relevance—Although no treatment effectively eliminated the tissue stages of H americanum, treatment with trimethoprim-sulfadiazine, clindamycin, and pyrimethamine followed by long-term administration of decoquinate resulted in extended survival times and excellent quality of life. ( J Am Vet Med Assoc 2001;218:77–82)