Malaria

Malaria, an acute infectious disease, is caused by protozoa of the genus Plasmodium— P. falciparum, P. vivax, P. malariae, P. ovale, and a more recent species, P. knowlesi—all of which are transmitted to humans by mosquito vectors. Falciparum malaria is the most severe form of the disease. When treated, malaria is rarely fatal; left untreated, it’s fatal in 10% of patients, usually as a result of complications such as disseminated intravascular coagulation (DIC).

Untreated primary attacks last from a week to a month or longer. Relapses are common and can recur sporadically over several years. Susceptibility to the disease is universal.

Causes

Malaria is transmitted by the bite of female Anopheles mosquitoes, which abound in humid, swampy areas. When an infected mosquito bites, it injects Plasmodium sporozoites into the wound. The infective sporozoites migrate through the blood to parenchymal cells in the liver; there they form cystlike structures containing thousands of merozoites.

Upon release, each merozoite invades a red blood cell (RBC) and feeds on hemoglobin. Eventually, the RBC ruptures, releasing heme (malaria pigment), cell debris, and more merozoites, which, unless destroyed by phagocytes, enter other RBCs. (See What happens in malaria.)

At this point, the infected person becomes a reservoir of malaria and infects any mosquito that feeds on him or her, thus beginning a new cycle of transmission. Each Plasmodium species has a specific incubation period: P. falciparum infection typically develops within 1 month of exposure but has been known to develop after a year, whereas P. vivax and P. ovale may emerge weeks to months after inoculation.

Because blood transfusions and street-drug paraphernalia can also spread malaria, there is a higher incidence of the disease in drug addicts. The outcome of infection depends on host immunity: Parasites are cleared spontaneously in those with immunity, while in those without immunity the parasites continue to expand the infection.

Complications

Complications of malaria include renal failure, liver failure, heart failure, pulmonary edema, DIC, seizures, hypoglycemia, splenic rupture, cerebral dysfunction, and death.

Assessment Findings

The patient history usually reveals travel to an area known to harbor malaria parasites. Some patients may present with only splenomegaly and no overt symptoms. An acute infection may present with flu-like symptoms, including chills, fever, fatigue, headache, and myalgia. Some may present with GI symptoms (diarrhea, nausea, vomiting), while others present with only anemia. Acute attacks (paroxysms) occur when RBCs rupture. There are three stages of paroxysms:

Cold stage, lasting 1 to 2 hours, ranging from chills to extreme shaking
Hot stage, lasting 3 to 4 hours, characterized by a high fever (up to 107° F [41.7° C])
Wet stage, lasting 2 to 4 hours and characterized by profuse sweating

The most severe form of malaria, which causes the most morbidity and mortality, is caused by P. falciparum. Severe malaria symptoms include seizures, delirium, and coma (cerebral malaria); pulmonary involvement (respiratory distress, pulmonary edema, nasal flaring, intercostal or subcostal chest retraction, use of accessory muscles, abnormally deep breathing); severe anemia; and renal failure (oliguria, anuria, and uremia).

Diagnostic Tests

Peripheral blood smears identify the parasites in RBCs. The immunochromatographic test ParaSight F, which detects monoclonal antibody to P. falciparum–specific histidine-rich protein 2, is an alternative sensitive and
specific test for laboratories that are not equipped to identify parasites in RBCs. A rapid dipstick test (OptiMAL) that detects the lactate dehydrogenase (LDH) of the parasite can distinguish P. falciparum from other species. Thrombocytopenia, elevated LDH levels, and atypical lymphocytes in a patient are suggestive of malarial infection.
Polymerase chain reaction and nucleic acid sequence-based amplification are more expensive but sensitive tests available for diagnosis.