Severe clinical presentation of visceral leishmaniasis in naturally infected dogs with disruption of the splenic white pulp.
In this work, we investigated the association between the disruption of splenic lymphoid tissue and the severity of visceral leishmaniasis in dogs. Clinical and laboratory data from 206 dogs were reviewed. Spleen sections collected during the euthanasia of these animals were analyzed, and the splenic lymphoid tissue samples were classified as well organized (spleen type 1), slightly disorganized (spleen type 2), or moderately to extensively disorganized (spleen type 3). Of 199 dogs with evidence of Leishmania infection, 54 (27%) had spleen type 1, 99 (50%) had spleen type 2, and 46 (23%) had spleen type 3. The number of clinical signs associated with visceral leishmaniasis was significantly higher in the animals with evidence of Leishmania infection and spleen type 2 or 3 than in the animals with spleen type 1. Alopecia, anemia, dehydration, dermatitis, lymphadenopathy, and onychogryphosis were all more frequent among animals with evidence of Leishmania infection and spleen type 3 than among the dogs with evidence of Leishmania infection and spleen type 1. The association between the severity of canine visceral leishmaniasis and the disorganization of the splenic lymphoid tissue was even more evident in the group of animals with positive spleen culture. Conjunctivitis and ulceration were also more common in the animals with spleen type 3 than in the animals with spleen type 1. The serum levels (median, interquartile range) of albumin (1.8, 1.4-2.3 g/dL) and creatinine (0.7, 0.4-0.8 mg/dL) were significantly lower and the serum levels of aspartate aminotransferase were significantly higher (57, 39-95 U) in animals with spleen type 3 than in animals with spleen type 1 (2.8, 2.4-3.4 g/dL; 0.9, 0.7-1.2 mg/dL and 23, 20-32 U, respectively). Our data confirm the hypothesis that disruption of the splenic lymphoid tissue is associated with a more severe clinical presentation of canine visceral leishmaniasis.
Fundação Oswaldo Cruz, Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil.
Isadora S
IS
Lima
Fundação Oswaldo Cruz, Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil.
Joselli S
JS
Silva
Fundação Oswaldo Cruz, Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil.
Valter A
VA
Almeida
Centro de Referência em Doenças Endêmicas Pirajá da Silva (PIEJ), Jequié, Bahia, Brazil.
Floriano G Leal
FG
Junior
Centro de Referência em Doenças Endêmicas Pirajá da Silva (PIEJ), Jequié, Bahia, Brazil.
Patrício An
PA
Souza
Universidade Federal da Bahia, Escola de Medicina Veterinária, Salvador, Bahia, Brazil.
Daniela F
DF
Larangeira
Universidade Federal da Amazônia, Faculdade de Ciências Farmacêuticas, Manaus, Amazonas, Brazil.
José P
JP
Moura-Neto
Fundação Oswaldo Cruz, Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil ; Universidade Federal da Bahia, Escola de Medicina Veterinária, Salvador, Bahia, Brazil.
Deborah B M
DB
Fraga
Fundação Oswaldo Cruz, Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil.
Luiz A R
LA
de Freitas
Fundação Oswaldo Cruz, Centro de Pesquisas Gonçalo Moniz, Salvador, Bahia, Brazil.
Washington L C
WL
dos-Santos
D000818:Animals; D015415:Biomarkers / Q000032:analysis*; D016054:DNA, Protozoan / Q000235:genetics; D004283:Dog Diseases / Q000276:immunology / Q000469:parasitology / Q000473:pathology*; D004285:Dogs; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D018314:Leishmania infantum / Q000235:genetics / Q000302:isolation & purification; D007898:Leishmaniasis, Visceral / Q000469:parasitology / Q000473:pathology* / Q000662:veterinary*; D008297:Male; D060888:Real-Time Polymerase Chain Reaction; D013154:Spleen / Q000469:parasitology / Q000473:pathology*
D015415:Biomarkers; D016054:DNA, Protozoan