Plasmodium malariae: Quartan Malaria Symptoms & Treatment
Discover the unique characteristics of *Plasmodium malariae*, a malaria parasite known for its 72-hour fever cycle and potential for long-term, chronic infection.
Discover the unique characteristics of *Plasmodium malariae*, a malaria parasite known for its 72-hour fever cycle and potential for long-term, chronic infection.
Plasmodium malariae is a protozoan parasite that causes a form of human malaria known as quartan malaria. This species is found in tropical and subtropical regions, often alongside more prevalent Plasmodium parasites. While considered a “benign malaria” because it is less immediately dangerous than infections from P. falciparum, it presents unique long-term health challenges. Its global distribution contributes to the overall burden of malaria worldwide.
The transmission of Plasmodium malariae to humans begins with the bite of an infected female Anopheles mosquito. The mosquito injects sporozoites, a motile stage of the parasite, into the person’s bloodstream. These sporozoites travel to the liver, where they invade liver cells and begin an asexual reproductive phase known as the exo-erythrocytic cycle, with an incubation period of 18 to 40 days.
Inside the liver cells, the parasites mature into schizonts. When these schizonts rupture, they release thousands of merozoites into the bloodstream, marking the start of the erythrocytic, or blood, stage. The merozoites invade red blood cells for another phase of asexual reproduction. A distinguishing feature of P. malariae is its 72-hour erythrocytic cycle, longer than the 48-hour cycle of most other human malaria parasites.
Within red blood cells, parasites develop from a ring stage to a trophozoite and then a schizont containing 6 to 12 new merozoites. At the end of the 72-hour period, the infected cell ruptures, releasing merozoites to infect new cells. Some parasites also develop into male and female gametocytes, which can be ingested by another mosquito, continuing the transmission cycle.
The clinical hallmark of a Plasmodium malariae infection is the quartan fever, a pattern where fever episodes recur every 72 hours. This rhythm directly corresponds to the parasite’s cycle of rupturing red blood cells. These fever episodes begin with a sudden feeling of intense cold and shivering chills, followed by a high fever with a rapid pulse, headache, and muscle aches. After several hours, the fever subsides, and the individual experiences profuse sweating.
In the initial stages, the fever may be irregular before it settles into the 72-hour pattern. Individuals may also experience an enlarged spleen (splenomegaly) as the body works to clear infected red blood cells. While the acute illness is less severe than that caused by P. falciparum, the infection still leads to considerable discomfort and weakness.
The standard method for diagnosing Plasmodium malariae is the microscopic examination of a blood sample. A blood smear is prepared and stained with Giemsa stain to visualize the parasites. Microscopists look for specific features that distinguish P. malariae, including “band-form” trophozoites and compact schizonts with 6 to 12 merozoites in a “rosette” pattern. Infected red blood cells remain their normal size.
Rapid Diagnostic Tests (RDTs), which detect parasite antigens in the blood, are another tool. However, their utility for P. malariae can be limited, as some tests may not detect the lower parasite densities seen in these infections or differentiate P. malariae from other species.
For a more sensitive diagnosis, Polymerase Chain Reaction (PCR) is used. This molecular technique amplifies the parasite’s DNA, allowing for detection even when parasite levels are very low. PCR is useful for identifying mixed infections and for confirming the species when microscopic identification is uncertain.
Treatment for uncomplicated Plasmodium malariae infections involves the drug chloroquine. Unlike P. falciparum, P. malariae has largely remained sensitive to chloroquine in many parts of the world. The choice of medication, however, should always consider local drug resistance patterns to ensure effective treatment.
If chloroquine is ineffective or unavailable, artemisinin-based combination therapies (ACTs) are an effective alternative. These therapies are the standard of care for other forms of malaria and work well against P. malariae. Patients must complete the full course of treatment to ensure all parasites are cleared from the blood, preventing a recurrence.
P. malariae does not have a dormant liver stage (hypnozoites), which are characteristic of P. vivax and P. ovale infections. Therefore, treatment specifically targeting the liver stage, such as with primaquine, is not necessary. The goal of therapy is the complete eradication of parasites from the bloodstream.
A unique aspect of Plasmodium malariae is its ability to persist in the body for extended periods, causing chronic, low-level infections. These infections can last for many years, sometimes for an individual’s lifetime, often with few or no symptoms. This persistence creates the risk of recrudescence, where symptoms reappear decades after the initial infection if the person’s immune system weakens.
One of the most serious complications is quartan malarial nephropathy, a form of kidney disease. This condition results from the long-term deposition of immune complexes in the glomeruli, the filtering units of the kidneys. This can lead to structural damage and the development of nephrotic syndrome, characterized by protein in the urine and body swelling.
Another consequence of chronic infection is tropical splenomegaly syndrome, also known as hyperreactive malarial splenomegaly. This involves a massive enlargement of the spleen due to an overactive immune response to the parasite. The continuous, low-grade destruction of red blood cells can also contribute to chronic anemia.