Abstract
BackgroundEpigastric pain, vomiting, and other gastrointestinal problems are among the most important symptoms of malaria infection as they suggest the possibility that the condition is serious. Pathophysiologies such as gastric mucosal changes and delayed gastric emptying have been reported in serious cases of malaria infection. However, it is unclear whether or not pathophysiological involvement of the upper gastrointestinal tract occurs in Plasmodium berghei ANKA (PbA)-infected mice.MethodsPbA-infective Anopheles mosquitoes were used to infect mice via the natural route of infection. Fifteen PbA-C57BL/6 mice were used as a cerebral malaria model and the same numbers of PbA-BALB/c mice were used as a cerebral malaria-resistant model, and then we investigated the pathophysiological involvement of the stomach and small intestine.ResultsOn day 8 post infection, six PbA-C57BL/6 mice showed cerebral malaria and nine others had uncomplicated infection. All the PbA-C57BL/6 mice on that same day showed severe weight loss with multiple, red gastric patches and changes to the course of the small intestine with villus goblet cell enlargement. In addition, cerebral malaria cases showed gastric gas retention with submucosal edema and small intestinal shortening. In PbA-BALB/c mice, overextension of the stomach and gas retention were evident from week 2 after PbA infection, as well as changes to the course of the small intestine and mesenteric thinning with fragility.ConclusionsWe described the upper gastrointestinal pathophysiology representing new findings directly linked to malarial severity and subsequent death in PbA-infected mice as a mouse model of malaria infection.
Highlights
Epigastric pain, vomiting, and other gastrointestinal problems are among the most important symptoms of malaria infection as they suggest the possibility that the condition is serious
Shimada et al Tropical Medicine and Health (2019) 47:18 few studies have addressed the detailed course of the upper gastrointestinal pathophysiology of malaria infection in humans, and none has described the pathophysiology of the upper gastrointestinal tract, including the stomach, in mouse models of malaria
In Plasmodium berghei ANKA (PbA)-BALB/c mice, the average parasitemia exceeded 1% on day 6 (1.3% ± 1.0%) and 3.7% ± 0.8% on day 8, after which it rapidly increased to 32.5% ± 9.0% on day 12, 43.2% ± 8.1% on day 13, and 57.2% ± 11.8% on day 15 (Fig. 1)
Summary
Epigastric pain, vomiting, and other gastrointestinal problems are among the most important symptoms of malaria infection as they suggest the possibility that the condition is serious. Pathophysiologies such as gastric mucosal changes and delayed gastric emptying have been reported in serious cases of malaria infection. Malaria infection begins with the non-specific symptoms of acute high fever and severe headache When it reaches the severe stage, it causes cerebral malaria due to sequestration of parasites in the brain [2] and brain edema [3] and multiple organ dysfunction, including pulmonary edema and renal failure [4]. Shimada et al Tropical Medicine and Health (2019) 47:18 few studies have addressed the detailed course of the upper gastrointestinal pathophysiology of malaria infection in humans, and none has described the pathophysiology of the upper gastrointestinal tract, including the stomach, in mouse models of malaria
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