Abstract

Simple SummaryCanine leishmaniosis is responsible for pathological changes in the spleen. The main features detectable from ultrasound examination are splenomegaly and diffuse alterations of the echostructure. The study aimed to highlight whether these ultrasound changes are related to the severity of the disease or to a modification of splenic microvascularization that can be detected in vivo through contrast-enhanced ultrasonography. Bidimensional ultrasonography showed that splenomegaly and diffuse parenchymal changes were positively correlated with the severity of the disease, so they could be of prognostic value. Contrast-enhanced ultrasonography showed that a persistent heterogeneous distribution pattern appeared only in spleens with diffuse echostructure alterations, and quantitative parameters regarding volume and velocity of flow in three regions of interest did not show any differences between affected and control dogs. Diffuse splenic microvascular modifications evidenced by contrast-enhanced ultrasonography were reported for the first time in dogs with canine leishmaniosis. Canine leishmaniosis (CanL) is responsible for splenic pathological changes. The main features detectable from ultrasound examination are splenomegaly and diffuse alterations of the echostructure. The study aimed to highlight whether these ultrasound changes are related to the severity of the disease or to a modification of splenic microvascularization that can be detected in vivo through contrast-enhanced ultrasonography (CEUS). Twenty-five adult dogs tested for CanL were enrolled in this prospective, controlled study and staged according to LeishVet guidelines. Bidimensional ultrasonography revealed that splenomegaly was seen in 50% of the affected dogs, and diffuse parenchymal changes were seen in more than 60% of dogs with splenomegaly, showing a positive correlation with severity of the disease; therefore, splenomegaly could be of prognostic significance. CEUS showed that a persistent heterogeneous distribution pattern appeared only in spleens with diffuse echostructure alterations. The evaluation of quantitative CEUS parameters regarding the volume and velocity of flow in three regions of interest did not show differences between affected and control dogs. Diffuse spleen microvascular modifications evidenced by CEUS were reported for the first time in dogs with CanL. In endemic areas, CanL could be included in the differential diagnoses list when detecting splenic alterations in dogs.

Highlights

  • Canine leishmaniosis (CanL) is a globally distributed zoonosis responsible for potentially serious fatal diseases in both dogs and humans [1,2,3,4]

  • The aims of the present study were (i) to investigate splenic abnormalities via the bidimensional ultrasonography in dogs affected by CanL, (ii) to perform contrast-enhanced ultrasonography (CEUS) exams to understand whether the reported anatomical vascular alterations were responsible for an in vivo modification of the diffusion of the contrast agent, and (iii) to evaluate the relationship between ultrasonographic splenic abnormalities, the clinical stage of CanL, and the spleen parasite load

  • We grouped the data of the dogs in stages with a low numerosity and similar prognosis together [1]: infected clinically healthy (ICH) dogs with dogs with mild disease and severe disease dogs with those in stage 4

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Summary

Introduction

Canine leishmaniosis (CanL) is a globally distributed zoonosis responsible for potentially serious fatal diseases in both dogs and humans [1,2,3,4]. Leishmania infantum is the most important Leishmania spp. worldwide and the main reported species in Europe [4]. Female sand flies from the genera Phlebotomus in the Old World are responsible for the vector-borne transmission of Leishmania, other non-vectorial ways (transplacental, venereal, and by blood transfusion) can occur [2]. The development of clinical signs in dogs is mainly related to the adaptive immune response with a predominant T helper 2 (Th2) and compromised T helper 1 (Th1) response that evolves into immune exhaustion [1,5]. The most commonly reported clinical signs in

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