In their competition for hosts, parasites with antigens that are novel to the host immune system will be at a competitive advantage.
Plasmodium vivax and Hepatitis B virus (HBV) are globally outspread in similar geographic regions. The concurrence of both infections and its association with some degree of protection against symptomatic and/or severe vivax malaria has been already described. Nevertheless, data on how host response to both pathogens undermines the natural progression of the malarial infection are scarce. Here, a large cohort of vivax malaria and HBV patients is retrospectively analyzed in an attempt to depict how inflammatory characteristics could be potentially related to the protection to severe malaria in coinfection.
Breakdown of the blood brain barrier (BBB) is a feature of cerebral malaria (CM), a manifestation of infection with Plasmodium falciparum parasites that currently has a 20% fatality rate and disproportionately affects children under 5 years old.
The Plasmodium vivax Duffy binding protein region II (DBPII) is a vital ligand for the parasite’s invasion of reticulocytes, thereby making this molecule an attractive vaccine candidate against vivax malaria.
Campylobacter jejuni is among the most common causes of diarrheal disease worldwide and efforts to develop protective measures against the pathogen are ongoing.
The human malaria parasite Plasmodium falciparum causes disease as it replicates within the host’s erythrocytes.
Malaria caused by Plasmodium vivax requires treatment of the blood‐stage infection and treatment of the hypnozoites that develop in the liver. This is a challenge to effective case management of P vivax malaria, as well as being a more general substantial impediment to malaria control. The World Health Organization (WHO) recommends a 14‐day drug course with primaquine, an 8‐aminoquinoline, at 0.25 mg/kg/day in most of the world (standard course), or 0.5 mg/kg/day in East Asia and Oceania (high‐standard course). This long treatment course can be difficult to complete, and primaquine can cause dangerous haemolysis in individuals with glucose‐6‐phosphate dehydrogenase (G6PD) deficiency, meaning that physicians may be reluctant to prescribe in areas where G6PD testing is not available. This Cochrane Review evaluated whether more patient‐friendly alternative regimens are as efficacious as the standard regimen for radical cure ofP vivax malaria.
Basic blue 3 is a promising anti-malarial lead compound based on the π-delocalized lipophilic cation hypothesis. Its derivatives with nitrogen atoms bonded to carbon atoms at the 3- and 7-positions on the phenoxazine ring were previously shown to exert potent antiprotozoal activity against Plasmodium falciparum, Trypanosoma cruzi, Trypanosoma brucei rhodesiense, and Leishmania donovani parasites in vitro. However, compounds with nitrogen modification at the 10-position on the phenoxazine ring were not evaluated.
Malaria caused by Plasmodium vivax and Plasmodium falciparum is among the major public health problems in most endemic areas of the world. Artemisinin-based combination therapy (ACT) has been recommended as a first-line treatment for uncomplicated Plasmodium falciparum malaria almost in all endemic regions. Since ineffectively regulated medicines in resource limited settings could favour infiltration of poor quality anti-malarial medicines into pharmaceutical supply chain and jeopardize a positive treatment outcome, regular monitoring of the quality of anti-malarial medicines is critical. Thus, the aim of this study was to assess the quality of fixed dose combination (FDC) artemether (ART)/lumefantrine (LUM) tablets available in Jimma zone, Ethiopia.