Murine schistosomiasis mansoni: process of blood coagulation at pre-patent, acute and chronic phases, and consequence of chemotherapeutic cure on the reversion of changes

Abstract

The present study aims to elucidate in a sequential manner the changes of the blood coagulation process at different phases of experimental schistosomiasis, comprising the pre-patent, acute, intermediate and chronic phases, and the effect of chemotherapeutic cure, at the acute and chronic phases, on reversion of changes related to the coagulation factors. Mice were infected with Schistosoma mansoni cercariae, and were divided into four groups. Blood samples from these groups were collected 32, 70, 100, and 140 days after infection, corresponding to the pre-patent, acute, intermediate and chronic phases, respectively. Simultaneously, other infected groups were given oxamniquine, 70 and 140 days after infection. At the same time as blood collection from infected and/or treated animal groups, other uninfected control animal groups were punctured and maintained under the same conditions as the infected animals. The vitamin-K-dependent clotting factors were found to be more sensitive to infection at different phases, while factors VIII and XI presented hyperactivity. Results obtained 90 days after chemotherapeutic treatment with oxamniquine, administered at the acute and chronic phases, presented noticeable reversion of the main alterations in the coagulation mechanism. The present study provides unquestionable data on the development of hemostatic changes throughout the course of S. mansoni infection.

The schistosome in the mammalian host: understanding the mechanisms of adaptation

“…Factors that may contribute to this lack of blood clotting around the parasite are the thrombocytopaenia occuring during infection (Ngaiza and Doenhoff, 1987; 1990; Stanley et al 2003 a ), inhibition of blood Factor XIIa (Tsang et al 1977; Foster et al 1992) and infection-induced increases in blood clotting times (Carvalho et al 2005). The worm surface nucleotide dihydrolase described by Vasconcelos et al (1993) may inhibit platelet activation by hydrolysing ADP and an anticoagulant peptide has been identified (Lin and He, 2006).…”

Interference with the Host Haemostatic System by Schistosomes

“…In contrast, studies on blood coagulation in hepatosplenic schistosomiasis patients (reviewed by Tanabe [24]) showed that patients have prolonged coagulation times [25]. In infected humans, major haemostatic abnormalities are only observed in hepatosplenic schistosomiasis patients, but murine studies observed changes in the activity of several coagulation factors already during the early phase of schistosomiasis [26]. Hepatosplenic schistosomiasis patients have a reduced activity or reduced levels of the coagulation factors II, VII, IX, X, XI, XII, fibrinogen, high–molecular-weight kininogen (HMWK), and prekallikrein, as well as the regulatory proteins antithrombin and protein C [27], [28].…”