Eliminação de larvas e histopatologia de camundongos Swiss infectados com diferentes inóculos de Angiostrogylus costaricensis

Abstract

Abdominal angiostrongiliasis (AA) is a disease caused by the nematode Angiostrongylus costaricensis, and was first described in Costa Rica. It is a zoonosis endemic to south Brazil. wild rodents as the final hosts of this nematode, and molluscs the intermediate hosts (Graeff-Teixeira et al., 1989). The man is accidentally infected by ingestion of the infecting form of the parasite (L3) in vegetables, vegetables and/or fruits and the characteristic symptoms are abdominal pain and palpable tumor mass, which can be confused with appendicitis or tumors. Correlations between infections and different doses of third stage larvae (L3), severity of clinical signs and surviva l of the animals has not been elucidated, as well as the relation with the shedding of first stage (L1) larvae. The study was performed at the laboratory animal facility of the Institute of Biological Sciences of Universidade de Passo Fundo (ICB/UPF) and thirty-two male Swiss mice (Mus musculus) infected with different doses of L3 from A. costaricensis were divided into four groups of eight animals: group 1: 5 L3; group 2: 15 L3; group 3: 30 L3 and group 4: control. Fecal sampling of the animals were collected individually, from the day 20 post infection (DPI) until death, and macro and microscopic analysis of them. Studies that help to better elucidate the disease are important for the understanding of the parasite and host relationship in the pathophysiology of the disease. We evaluated the elimination of L1 larvae in the feces with the survival and histopathological analysis of the rodents post mortem, relating the severity of the clinical signs with the different infective doses of the parasite. Our results showed that animals infected with a higher infective dose had a higher larval elimination rate. We also noticed that the majority of rodents died between day 20 and 40 post infection, presenting bronchopneumonia and hepatitis, highlighting the differences between the groups in relation to the presence of intestinal thrombi, splenitis, eggs / larvae and liver infarction. We conclude that different infective doses of L3 from A. costaricensis interfere with the shedding of L1, as well as alter the histopath ological aspects in the mice, with higher doses resulting in the abundant presence of eggs and larvae and liver infarction, splenitis and intestinal thrombosis but don’t alters the mortality of these rodents