Leishmaniasis is a zoonotic disease that affects humans, dogs, and other mammals. Although endemic to certain areas of the world, it is not endemic to the United States, where prevalence among companion animals has been historically low. However, case numbers have been increasing in North America. Therefore, it is imperative that U.S. veterinarians be able to identify and treat leishmaniasis in their patients.<\/p>\n
This article reviews canine leishmaniasis and provides a case study of a dog with infection that was imported from China. The case study highlights the complexity of this zoonotic infection and the wide range of its clinical manifestations, from asymptomatic infection to potentially fatal disease. This review should raise awareness and provide guidance for U.S. veterinarians on how to recognize, diagnose, treat, and manage imported and autochthonous leishmaniasis in dogs.<\/p>\n
Take-Home Points<\/strong><\/p>\n Leishmaniasis is a major zoonotic disease caused by the intracellular protozoa Leishmania<\/i>, transmitted primarily by the bite of infected female phlebotomine sand flies.1,2<\/sup> It is widespread in tropical and subtropical areas and found in 99 countries and territories in the Mediterranean basin, Africa, central and southwestern Asia, and Central and South America, where sand flies are endemic.1,3<\/sup> In humans, leishmaniasis is one of the world\u2019s most significant emerging infectious diseases.4<\/sup><\/span><\/p>\n Leishmaniasis has not been considered a significant concern to veterinarians in the United States because the sand flies capable of transmitting the parasite have been documented in only a few isolated parts of the country and prevalence of leishmaniasis in dogs native to the United States has been relatively low. However, the number of cases of canine leishmaniasis has increased, from both importation of dogs from Leishmania<\/i>-endemic areas and local acquisition (autochthonous cases); autochthonous cases have been reported in California,5<\/sup> Georgia, Maryland, New York, North Dakota, Oklahoma, and Texas.6<\/sup> Contributions to the rise of canine leishmaniasis in the United States include vertical transmission, international travel and animal transportation, and climate change.7<\/sup> Like people, dogs and cats (along with other animals) can be infected by a variety of species of Leishmania<\/i>; the main reservoir hosts, however, are dogs, susceptible to different forms of disease, ranging from self-limiting cutaneous lesions to severe visceral disease that can be fatal if untreated.8<\/sup> As incidence of leishmaniasis diagnoses in dogs increases in the United States, veterinarians should be familiar with the clinical signs and consider it as a potential diagnosis for dogs in North America, especially ill dogs that have been to or bred to any dog from a Leishmania<\/i>-endemic region.<\/span><\/p>\n This article describes a case of canine leishmaniasis in a 5-year-old spayed female Australian shepherd recently imported to the United States from a shelter in the Henan province of China.<\/span><\/p>\n The\u00a0Parasitology series<\/a>\u00a0is brought to you by Merck Animal Health, the makers of Bravecto\u00ae (fluralaner) and Sentinel\u00ae (milbemycin oxime\/lufenuron).<\/span><\/p>\n Initial Examination in China<\/b><\/p>\n On initial examination in China, the patient appeared healthy, except for being underweight and having moderate to severe dental tartar. Basic veterinary care <\/span>was provided, including core vaccinations and occasional doses of <\/b>flea protection. She progressively lost weight, and lameness developed and worsened over the 9\u00a0months preceding her transport to the United States.<\/span><\/p>\n Routine laboratory tests (<\/span>TABLE 1<\/b><\/span>), including several complete blood counts (CBCs), most notably indicated initial hemoconcentration, which progressed over 9\u00a0months to mild nonregenerative anemia. Initial biochemistry results indicated mild hypoalbuminemia and hyperglobulinemia, which progressed to significant hypoalbuminemia and hyperglobulinemia, and creatinine and blood urea nitrogen (BUN) progressed from normal ranges to elevated values. No urinalysis was performed. A fecal flotation<\/a> result was negative.<\/span><\/p>\n One month before transport, progressively worsening lameness was noted. Radiographs showed marked soft tissue swelling around the right elbow with normal <\/span>appearing carpi and long bones. No cause was identified. Immediately before transport, non\u2013weight-bearing lameness developed on the left forelimb. Radiographs showed increased soft tissue swelling of the right elbow and mild right carpal soft tissue swelling (left carpus not seen). A chondroitin supplement was started. Because of the dog\u2019s clinical decline, she was taken to a veterinarian immediately after arrival in the United\u00a0States. <\/span><\/p>\n Initial Examination in the United States <\/b><\/p>\n During initial examination (<\/span>FIGURE 1<\/b><\/span>), the patient was quiet, alert, and slightly dehydrated. Her mucous membranes were pale pink. She had a temperature of 39.9\u00a0\u00b0C (103.8\u00a0\u00b0F). <\/span><\/p>\n Figure 1. Patient at initial examination in the United States.<\/p><\/div>\n She had mild alopecia and scaling around both eyes and on the bridge of the nasal planum, small crusts on the tip of the nares, and bilateral blepharitis. The anterior carpi and caudal tarsi had mild, diffuse alopecia and large white scales. There was large flaky white crusting on all paw pads and diffuse sarcopenia (<\/span>FIGURE 2<\/b><\/span>). The patient was unwilling to rise without assistance, but once standing, she was able to walk with lameness noted in multiple limbs. Swelling and moderate palpable effusions were noted on the right elbow, left carpus, and both tarsi. Submandibular, prescapular, and popliteal lymph nodes were mildly enlarged and firm. Fundic and neurologic examinations<\/a> were unremarkable.<\/span><\/p>\n\n
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\nCase Report<\/h2>\n
History and Clinical Findings<\/h3>\n
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