Found worldwide, it causes a so-called "benign malaria", not nearly as dangerous as that produced by P. falciparum or P. vivax.

[2] At any one time, an estimated 300 million people are said to be infected with at least one of these Plasmodium species and so there is a great need for the development of effective treatments for decreasing the yearly mortality and morbidity rates.

It is widespread throughout sub-Saharan Africa, much of southeast Asia, Indonesia, on many of the islands of the western Pacific and in areas of the Amazon Basin of South America.

[7] Along with bouts of fever and more general clinical symptoms such as chills and nausea, the presence of edema and the nephrotic syndrome has been documented with some P. malariae infections.

[2] It has been suggested that immune complexes may cause structural glomerular damage and that renal disease may also occur.

[2] Even with these techniques, however, it may still be impossible to differentiate infections, as is the case in areas of South America where humans and monkeys coexist and P. malariae and P. brasilianum are not easily distinguishable.

[2] P. malariae is the only human malaria parasite that causes fevers which recur at approximately three-day intervals (therefore occurring every fourth day, a quartan fever), longer than the two-day (tertian) intervals of the other malarial parasites.

[2] Following fertilization of the macrogamete, a mobile ookinete is formed, which penetrates the peritropic membrane surrounding the blood meal and travels to the outer wall of the mid-gut of the mosquito.

[2] A small number of sporozoites are introduced into the salivary duct and injected into the skin of the bitten human.

[2] P. vivax and P. ovale sitting in EDTA for more than 30 minutes before the blood film is made will look very similar in appearance to P. malariae, which is an important reason to warn the laboratory immediately when the blood sample is drawn so they can process the sample as soon as it arrives.

Failure to detect some P. malariae infections has led to modifications of the species-specific primers and to efforts towards the development of real-time PCR assays.

[2] The development of such an assay has included the use of generic primers that target a highly conserved region of the 18S rRNA genes of the four human-infecting species of Plasmodium.

[2] The immunofluorescent-antibody (IFA) technique can be used to measure the presence of antibodies to P. malariae..[2] A pattern has emerged in which an infection of short duration causes a rapidly declining immune response, but upon re-infection or recrudescence, the IFA level rises significantly and remains present for many months or years.

In a study by Müller-Stöver et al., the researchers presented three patients who were found to be infected with the parasite after taking anti-malarial medications.

According to Dr. William E. Collins from the Center of Disease Control (CDC), chloroquine is most commonly used for treatment and no evidence of resistance to this drug has been found.

The food vacuole is the specialized compartment that degrades hemoglobin during the asexual erythrocytic stage of the parasite.

[6] It is implied that effective drug treatments can be developed by targeting the proteolytic enzymes of the food vacuole.

In a paper published in 1997, Westling et al.[5] focused their attention on the aspartic endopeptidase class of enzymes, simply called plasmepsins.

[5] Another study by Bruce et al.[7] presented evidence that there may be regular genetic exchange within P. malariae populations.

A recent study shows that quartan malaria parasites are easily exchanged between humans and monkeys in Latin America.