Gross, microscopic, radiologic, echocardiographic and haematological findings in rats experimentally infected withAngiostrongylus cantonensis

Abstract

Although the gross and microscopic pathology in rats infected with Angiostrongylus cantonensis has been well described, corresponding changes detected using diagnostic imaging modalities have not been reported. This work describes the cardiopulmonary changes in mature Wistar rats chronically infected with moderate burdens of A. cantonensis using radiology, computed tomography (CT), CT angiography, echocardiography, necropsy and histological examinations. Haematology and coagulation studies were also performed. Thoracic radiography, CT and CT angiography showed moderately severe alveolar pulmonary patterns mainly affecting caudal portions of the caudal lung lobes and associated dilatation of the caudal lobar pulmonary arteries. Presumptive worm profiles could be detected using echocardiography, with worms seen in the right ventricular outflow tract or straddling either the pulmonary and/or the tricuspid valves. Extensive, multifocal, coalescing dark areas and multiple pale foci affecting the caudal lung lobes were observed at necropsy. Histologically, these were composed of numerous large, confluent granulomas and fibrotic nodules. Adult worms were found predominantly in the mid- to distal pulmonary arteries. An inflammatory leukogram, hyperproteinaemia and hyperfibrinogenaemia were found in most rats. These findings provide a comparative model for A. cantonensis in its accidental hosts, such as humans and dogs. In addition, the pathological and imaging changes are comparable to those seen in dogs infected with Angiostrongylus vasorum, suggesting rats infected with A. cantonensis could be a model for dogs with A. vasorum infection.

Anti-angiogenic effect of the combination of low-dose sorafenib and EGCG in HCC-induced Wistar rats

“…This can be explained by Kun MW et al, who discovered the other cause of Wistar rat's lung problem was lung infection due to A.Cantonensis. 35 M. Pulmonis causes a different type of infection, as explained by the study of Chawla et al, which showed gross and histopathological discoveries of severe congestion of the lungs with suppurative and necrotizing pneumonia. 36 Wang Y et al also evaluated the induction effect of DEN in a rat model.…”

Anti-angiogenic effect of the combination low-dose sorafenib and EGCG in HCC-induced Wistar rats

“…This can be explained by Kun MW et al, who discovered the other cause of Wistar rat's lung problem was lung infection due to A.Cantonensis. 28 M. Pulmonis causes a different type of infection as explained by the study of Chawla et al, which showed gross and histopathological discoveries of severe congestion of lungs with suppurative and necrotizing pneumonia. 29 Wang Y et al also evaluated the induction effect of DEN in a rat model and discovered that the induced rat had liver dysfunction and damage, which is characterized by diffuse lesions with extensive interstitial inflammatory cell infiltration, alveolar edema, and bleeding.…”

Successful Removal of Angiostrongylus cantonensis Larvae from the Central Nervous System of Rats 7- and 14-Days Post-Infection Using a Product Containing Moxidectin, Sarolaner and Pyrantel Embonate (Simparica Trio™) in Experimental Infections

“…A. cantonensis usually does not produce overt clinical signs in rats, unless the definitive host ingests a heavy dose of infective larvae over a short time. If this happens, verminous pneumonia develops, clinically manifested by dyspnoea and reduced exercise tolerance [ 1 , 2 , 3 , 4 ]. Rarely, transient neurological signs occur; although, usually despite extensive neural migration by larvae, neurological signs in rats are absent or unappreciated.…”

“…The most unusual aspect of the lifecycle involves an obligatory migration of L3 larvae in the rat central nervous system (CNS). Larvae migrate widely through the CNS, including the spinal cord, brain and optic nerves, growing, moulting and growing further until they are ready to leave the CNS via the arachnoid villi to make their way back to the right ventricle and pulmonary arteries [ 1 , 2 , 3 , 4 ].…”

“…In contradistinction to the situation in rats, the migration of infective L3 larvae can cause serious disease in accidental hosts such as dogs, wildlife (birds, possums, bats) and humans [ 1 , 2 , 3 , 4 , 5 ]. Rat lungworm disease (neuroangiostrongyliasis) is most often manifested as eosinophilic meningoencephalitis [ 3 , 4 ], and peripheral eosinophilia is often reported in canine and human dead-end hosts [ 2 ].…”