Malaria - Causes, Symptoms and Treatment
Malaria, an acute infectious disease, is caused by protozoa of the genus Plasmodium: P.falciparum, P. vivax, P. malariae, and P.ovale, all of which are transmitted to humans by mosquito vectors. P.Faleiparum malaria is the most severe form of the disease. When treated, malaria is rarely fatal; untreated, it's fatal in 10% of victims, 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 for several years. Susceptibility to the disease is universal. Malaria is a tropical and subtropical disease and is most prevalent in Asia, Africa, and Latin America, with highly endemic areas being Southeast Asia and Sub-Sahara Africa. Incidence of malaria in the United States during the last 25 years has ranged from a high of 4,230 cases in 1970 (when the disease occurred mainly among military personnel returning from Vietnam) to a low of 222 cases in 1973. Since 1940, very few cases of malaria have actually been contracted in the United States; most of these were transmitted by blood transfusions or the use of contaminated needles by drug addicts.
Causes of Malaria
Malaria literally means "bad air" and for centuries was thought to result from the inhalation of swamp vapors. It is now known that 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 by blood circulation to parenchymal cells of the liver; there they form cyst-like structures containing thousands of merozoites. Upon release, each merozoite invades an erythrocyte and feeds on hemoglobin. Eventually, the erythrocyte ruptures, releasing malaria pigment, cell debris, and more merozoites, which, unless destroyed by phagocytes, enter other erythrocytes. At this point, the infected person becomes a reservoir of malaria who infects any mosquito that feeds on him, thus beginning a new cycle of transmission. Hepatic parasites (P. vivax, P. ovale, and P. malariae) may persist for years in the liver. These parasites are responsible for the chronic carrier state. Because blood transfusions and street-drug paraphernalia can also spread malaria, drug addicts have a higher incidence of the disease. Malaria is a worldwide health problem that continues to impede the development of many countries.
Signs and Symptoms of Malaria
After an incubation period of 12 to 30 days, malaria produces chills, fever, headache, and myalgia interspersed with periods of well-being (the hallmark of the benign form of malaria). Acute attacks (paroxysms) occur when erythrocytes rupture and have three stages:
Paroxysms occur every 48 to 72 hours when malaria is caused by P. malariae and every 42 to 50 hours when malaria is caused by P. vivax or P. ovale. All three types have low levels of parasitosis and are self-limiting as a result of early acquired immunity. P. vivax and P. ovale also produce hepatosplenomegaly. Hemolytic anemia occurs in all but the mildest infections. The most severe and only lifethreatening form of malaria is caused by P.falciparum. This species produces persistent high fever, orthostatic hypotension, and red blood cell (RBC) sludging that leads to capillary obstruction at various sites. Signs and symptoms of obstruction at these sites include the following:
During blackwater fever (a complication of P. falciparum infection), massive intravascular hemolysis causes jaundice, hemoglobinuria, a tender and enlarged spleen, acute renal failure, and uremia. This dreaded complication is fatal in about 20% of patients.
Diagnosis for Malaria
A history showing travel to endemic areas, recent blood transfusion, or drug abuse in a person with high fever of unknown origin strongly suggests malaria. But because symptoms of malaria mimic other diseases, unequivocal diagnosis depends on laboratory identification of the parasites in RBC's of peripheral blood smears.
The Centers for Disease Control and Prevention can identify donors responsible for transfusion malaria through indirect fluorescent serum antibody tests. These tests are unreliable in the acute phase because antibodies can be undetectable for 2 weeks after onset.
Supplementary laboratory values that support this diagnosis include decreased hemoglobin levels, normal to decreased leukocyte count (as low as 3,000/ul), and protein and leukocytes in urine sediment. In falciparum malaria, scrum values reflect DIC: reduced number of platelets (20,000 to 50,000/ul), prolonged prothrombin time (18 to 20 seconds), prolonged partial thromboplastin time (60 to 100 seconds), and decreased plasma fibrinogen.
Treatment for Malaria
Malaria is best treated with oral chloroquine in all forms except chloroquine-resistant P. falciparum. Unfortunately, chloroquine-resistant malaria exists in most parts of the world. Studies are in progress to treat resistance with newer drugs. Symptoms and parasitemia decrease within 24 hours after chloroquine therapy begins, and the patient usually recovers within 3 to 4 days. If the patient is comatose or vomiting frequently, chloroquine is given I.M. Toxic reactions, which rarely occur, include GI upset, pruritus, headache, and visual disturbances.
Malaria caused by P.falciparum, which is resistant to chloroquine, requires treatment with oral quinine for 10 days, given concurrently with pyrimethamine and a sulfonamide, such as sulfadiazine. Relapses require the same treatment, or quinine alone, followed by tetracycline.
The only drug effective against the hepatic stage of the disease that is available in the United States is primaquine phosphate, given daily for 14 days. This drug can induce hemolytic anemia, especially in patients with glucose-6-phosphate dehydrogenase deficiency.
Special Considerations and Prevention Tips for Malaria
1. Obtain a detailed patient history, noting any recent travel, foreign residence, blood transfusion, or drug addiction. Record symptom pattern, fever, type of malaria, and any systemic signs.
2. Assess the patient on admission and daily thereafter for fatigue, fever, orthostatic hypotension, disorientation, myalgia, and arthralgia. Enforce bed rest during periods of acute illness.
3. Protect the patient from secondary bacterial infection by following proper hand washing and aseptic techniques.
4. Protect yourself by wearing gloves when handling blood or body fluids containing blood.
5. Discard needles and syringes in an impervious container designated for incineration.
6. Double-bag all contaminated linens, and transport them according to hospital policy.
7. To reduce fever, administer antipyretics, as ordered. Document onset of fever and its duration, and symptoms before and after episodes.
8. Fluid balance is fragile, so keep a strict record of intake and output. Monitor I.V. fluids closely. Avoid fluid overload (especially with P.falciparum) because it can lead to pulmonary edema and aggravate cerebral symptoms. Observe blood chemistry levels for hyponatremia and increased blood urea nitrogen, creatinine, and bilirubin levels. Monitor urine output hourly, and maintain at 40 to 60 ml/hour for an adult and at 15 to 30 ml/hour for a child. Immediately report any decrease in urine output or the onset of hematuria as a possible sign of renal failure; be prepared to do peritoneal dialysis for uremia caused by renal failure. For oliguria, administer furosemide or mannitol I.V., as ordered.
9. Slowly administer packed RBCs or whole blood while checking for crackles, tachycardia, and shortness of breath.
10. If humidified oxygen is ordered because of anemia, note the patient's response, particularly any changes in rate or character of respirations, or improvement in mucous membrane color.
11. Watch for and immediately report signs of internal bleeding, such as tachycardia, hypotension, and pallor.
12. Encourage frequent coughing and deep breathing, especially if the patient is on bed rest or has pulmonary complications. Record the amount and color of sputum.
13. Watch for adverse effects of drug therapy, and take measures to relieve them.
14. If the patient is comatose, make frequent, gentle changes in his position, and give passive range-of-motion exercises every 3 to 4 hours. If the patient is unconscious or disoriented, use restraints, as needed, and keep an airway or padded tongue blade available.
15. Provide emotional support and reassurance, especially in critical illness. Explain the procedures and treatment to the patient and his family. Listen sympathetically, and answer questions clearly. Suggest that other family members be tested for malaria. Emphasize the need for follow-up care to check the effectiveness of treatment and to manage residual problems.
16. Report all cases of malaria to local public health authorities.
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