Alterations in the Mitochondrial Physiology of Biomphalaria glabrata (Mollusca: Gastropoda) After Experimental Infection by Angiostrongylus cantonensis (Nematoda: Metastrongylidae). 
Angiostrongylus cantonensis is a metastrongylid nematode that has a heteroxenous cycle, where snails act as intermediate hosts and the rodents Rattus rattus and Rattus novergicus are the definitive hosts.  However, humans may act as accidental hosts presenting an atypical form of parasitism.  This fact has motivated research to better understand systems of relationships involving A. cantonensis, targeting the control of species of gastropods that act as intermediary hosts.  For this, six groups were formed: three control groups (uninfected) and three infected groups, exposed to approximately 1200 L1 larvae of A. cantonensis.  At the end of each week (1, 2, and 3 weeks), snails were dissected without anesthesia and the gonad-digestive gland (DGG) complex was separated for determination of oxygen consumption through high-resolution titration-injection respirometer (Oroboros, Oxygraph; Innsbruck, Austria).  The results indicate suppression of mitochondrial oxidative metabolism of the host and compromised in different mitochondrial respiratory states.  This effect, mainly observed in the group exposed to 1 week of infection, showed a decrease of approximately 38% (2.78 ± 0.37 pmol O2/mg of tissue; P < 0.05), 41% (2.76 ± 0.34 pmol O2/mg of tissue; P < 0.05) e 46% (2.91 ± 0.36 pmol O2/mg of tissue; P < 0.05) in the basal oxygen consumption after sequential addition (P + M), succinate and (ADP) in the respiratory medium, differing significantly from the control group.  The results presented indicate that the prepatent infection by this metastrongylid impairs the aerobic oxidative metabolism of its host, causing a reduction in basal oxygen consumption.  This effect, observed at the start of development of the parasites, indicates that this stage is the most critical for the success of the infection, and can be explained by a reduction of the mitochondrial density of the tissue analyzed, or also by suppression of enzyme centers related to the oxidative reactions.