Hematological and histopathological changes in Rattus norvegicus (Wistar) experimentally infected by Angiostrongylus cantonensis (Chen, 1935).

Eosinophilic meningitis caused by Angiostrongylus cantonensis is a zoonosis endemic to Southeast Asia and the Pacific islands. It is considered an emerging disease because it has been expanding both geographically and in terms of the range of hosts. In South America, the first cases were reported in Brazil and were attributed to eating infected snails. In this study, 70 adult females of Rattus norvegicus (Wistar) were used to evaluate hematology, blood gases, cardiac markers and lung histopathology changes caused by this parasite. Of them, 60 were individually infected by orogastric gavage with 100 L(3) larvae and 10 uninfected animals formed the control group. The results obtained demonstrate that infection caused by A. cantonensis in R. norvegicus promotes significant hematological changes induced in the vertebrate host, manifested mainly in the form of regenerative anemia, thrombocytopenia and eosinophilia. Additionally, histopathological changes in the lung parenchyma demonstrated in rodents reveal the occurrence of areas of necrosis and extensive fibrosis, being directly related to the development of cellular hypoxia and enzyme cardiac changes. This study can contribute to a better understanding of the relationship between A. cantonensis and R. norvegicus.

Metabolic and histopathological profile of Rattus norvegicus (Wistar) experimentally infected by Angiostrongylus cantonensis (Chen, 1935).

Eosinophilic meningitis is a disease characterized by increased eosinophils in the cerebrospinal fluid (CSF), which is the most commonly caused by invasion of the central nervous system by helminths, as occurs in Angiostrongylus cantonensis infections. The rodent Rattus norvegicus is the definitive natural host and humans act as accidental hosts and can become infected by eating raw or undercooked snails or food contaminated with infective L3 larvae. Recently in Brazil there have been four cases of eosinophilic meningitis due to ingestion of infected Achatina fulica. To evaluate biochemical and histopathological changes caused by this parasite, R. norvegicus were experimentally infected with 100 L3 larvae of A. cantonensis. After the anesthetic procedure, serum from the rodents was collected from the inferior vena cava for evaluation of the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALKP), gamma-glutamyl transferase (GGT), total protein and its fractions. During the necropsy, the liver was collected and weighed. Then a 1-g fragment was extracted from the major lobe to quantify the hepatic glycogen and fragment remainder was taken from the same lobe and fixed in Milloning's formalin for histopathological examination. Additionally, helminths were collected from the brain and lungs of the rodents. The activities of AST, ALT, ALKP and GGT in the serum and hepatic glycogen increased in response to infection, while the levels of globulin and total protein increased only in the eighth week of infection and there was a reduction in the levels of serum glucose. Albumin and bilirubin concentrations remained stable during the experiment. Infection with A. cantonensis caused metabolic and histopathological changes in the rodents. This study can contribute to a better understanding of the relationship between A. cantonensis and R. norvegicus.