Case 3 171208 (B1704482)
Conference Coordinator: Devinn Sinnott.
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7-year-old, MC, Boxer.
HistoryWhile being treated for cutaneous epitheliotropic T cell lymphoma, the dog developed vomiting and inappetance. Endoscopic biopsies of the stomach and biopsies of the skin were performed. The dog had lived in Pennsylvania for the past two years, and prior to that he had lived in Texas.
Ten endoscopic pinch biopsies of stomach were received.
N/A
Ten endoscopic pinch biopsies of gastric mucosa are examined. The lamina propria has multifocal areas of hemorrhage and is variably infiltrated with plasma cells, lymphocytes, and macrophages that occasionally form loosely aggregated nodules. Many macrophages contain multiple intracytoplasmic, round to oval, 2 to 4-um-diameter organisms with amphophilic cytoplasm and a round, basophilic nucleus. Multifocally the gastric glands are mildly hyperplastic.
CD18: Scrolls of this slide were positive for Leishmania infantum by PCR.
Stomach: moderate, chronic, multifocal, lymphoplasmacytic and histiocytic gastritis with intralesional, intrahistiocytic amastigotes (consistent with Leishmania sp.) and mild glandular hyperplasia.
Visceral leishmaniasis became a re-emerging disease in dogs in the United States after an outbreak occurred in a foxhound kennel in New York in 1999. Since then, cases have been reported in 22 states and 2 Canadian provinces (1). Visceral leishmaniasis is caused by Leishmania infantum, an obligate intracellular kinetoplastid parasite. Leishmania spp. infect many cell types, but have a tropism for macrophages. Leishmaniasis has been reported in several mammalian species including humans, and wild and domestic dogs serve as the reservoir hosts. Transmission predominantly occurs via sand flies in endemic regions. Sand flies inject the host with promastigotes while feeding, which are phagocytized by macrophages and distributed throughout the body. Phagocytosis by macrophages is mediated by multiple receptors, most importantly complement receptors 1 and 3 (2). Promastigotes undergo replication and form amastigotes within macrophages, which are consumed by feeding sand flies. Amastigotes then undergo replication and form promastigotes within the gut of sand flies (1). Cases of canine leishmaniasis in the United States are sporadically acquired abroad in endemic areas such as South America, the Mediterranean basin, and the Middle East. However, L. infantum is also maintained in the United States via vertical transmission including transplacental or transmammary infection, blood contamination from fight wounds, and blood transfusions (1). Potentially suitable vectors (Lutzomyia spp.) are present in the United States and there is evidence supporting the ability of these sand fly species to transmit L. infantum (3).
Clinical signs of visceral leishmaniasis include lethargy, fever, muscle atrophy, nasal discharge or epistaxis, brittle hair coat and nails, distended abdomen due to splenohepatomegaly, lymphadenomegaly, vomiting, diarrhea, and melena. Clinicopathologic findings may include anemia, thrombocytopenia, azotemia, increased ALT and ALP, hypergammaglobulinemia and hypoalbuminemia. Histologically, amastigotes can be seen in several different tissues due to dissemination throughout the body in macrophages, but are most commonly seen in the liver, spleen, lymph nodes, and bone marrow. Amastigotes are 1 to 3 um in diameter, round organisms with a round, dark basophilic nucleus and a rod-shaped, basophilic kinetoplast (1). Gastrointestinal involvement is not uncommon in cases of leishmaniasis. Amastigotes have been documented within macrophages in all layers and in all segments of the gastrointestinal tract, but are most consistently found within the lamina propria and in the cecum and colon (4). Gastrointestinal infection can be asymptomatic with minimal gross lesions (4), but has also been reported to cause chronic, lymphoplasmacytic and histiocytic, erosive gastritis and enterocolitis (5). Based on morphology, differential diagnoses include Trypanosoma cruzi and Histoplasma capsulatum. Other protozoal species are too large or involve tissue cysts forms that are inconsistent with the organisms seen in this case. This case was contributed by Dr. Kevin Woolard1. Petersen CA, Barr SC. Canine leishmaniasis in North America: emerging or newly recognized?. Veterinary Clinics of North America: Small Animal Practice. 2009. 39(6): 1065-1074. 2. Ueno N, Wilson NE. Receptor-mediated phagocytosis of Leishmania: implications for intracellular survival. Trends in Parasitology. 2012. 28(8): 335-344.
3. Schaut RG, Robles-Murguia M, Juelsgaard R, Esch KJ, Bartholomay LC, Ramalho-Ortigao M, Petersen CA. Vectorborne transmission of Leishmania infantum from hounds, United States. Emerging Infectious Diseases. 2015. 21(12): 2209-2212. 4. Pinto AJW, Figueiredo MM, Silva FL, Martins T, Michalick MSM, Tafuri WL, Tafuri WL. Histopathological and parasitological study of the gastrointestinal tract of dogs naturally infected with Leishmania infantum. Acta Veterinaria Scandinavica. 2011. 53(67): 1-8. 5. Ruiz G, Laloy E, Benchekroun G. Chronic gastritis and enterocolitis associated with Leishmania infection in an 18-month-old, intact female dog. Veterinary Quarterly. 2015. 35(4): 236-239.