Etiology:
Malaria is endemic throughout the tropical areas of the world and is acquired from the bite of the female nocturnal-feeding Anopheles mosquitoes.
The Plasmodium species infecting humans are P falciparum, P vivax, P ovale, and P malariae.
Life cycle:
In mosquito (sexual phase)
The Plasmodium species infecting humans are P falciparum, P vivax, P ovale, and P malariae.
Sporogony, or the sexual cycle, begins when the female mosquito ingests circulating gametocytes.
After fertilization, the zygote penetrates the gut walls and forms as oocyst.
Within the oocyst, sporozoites are formed, released into the stomach, and migrate to salivary glands.
Sporozoites are injected into humans at the next blood meal.
In human (asexual phase, Schizogony)
Sporozoites invade liver cells, replicate, and produce merozoites.
Rupture of infected hepatocytes releases merozoites into the blood strewn.
Merozoites enter red blood cells and appear as ring-shaped trophozoites.
Nuclear division occurs, producing a multinucleated schizont.
Cytoplasm condenses around each nucleus, forming merozoite daughter cells.
About 48 hours after invasion, infected erythrocytes rupture releasing merozoite, which invade new red cells. Some are transformed into sexual forms or gametocytes.
Plasmodia falaparium is not dormant in the liver, hence late relapses do not occur.
The most severe disease is produced by P. falciparum. This species can parasitize red cells in every state of development, resulting in a higher percentage of parasitemia.
Plasmodium, vivax will parasitize only the larger reticulocytes, leading to a lower degree of parasitemia.
Epidemiology:
Malaria is endemic throughout the tropical areas of the world and is acquired from the bite of the female nocturnal-feeding Anopheles mosquitoes.
The risk of malaria is
highest for travelers to sub-Saharan Africa, Papua New Guinea, the Solomon Islands, and Vanuatu;
intermediate in Haiti and the Indian subcontinent
low in most of Southeast Asia and Latin America
Transmission is possible in more temperate climates, including areas in the United States where Anopheles mosquitoes are present.
Nearly all of the reported cases in the United States are imported after infection acquired abroad.
The spread of chloroquine-resistant P falciparum strains throughout the world is of increasing importance
P. Falciparum infection in Zaire is chloroquine resistant.
Plasmodium vivax and P falciparum are the most common species worldwide.
Their geographical distribution is -
P. Falciparum- Central and South Africa, South America, South East Asia, Indian subcontinent
P. vivax - Indian subcontinent, South east Asia, Central and South Africa
P. ovale - rare, found mainly in Africa
P. malariae - rare, worldwide
Clinical Manifestations:
Fever: The classic symptoms are high fever with chills, rigor, sweats, and headache, which may be paroxysmal.
As the infection becomes synchronized, the fever and paroxysms generally occur in a cyclic pattern.
Depending on the infecting species, fever appears every other or every third day.
The fever, anemia, circulatory changes and immunopathologic phenomena are all the result of invasion of erythrocytes.
Anemia and thrombocytopenia are common, and pallor and jaundice caused by hemolysis may occur. Destruction of host red cells by the mature schizont as it liberates merozoites, TNF-alpha effect.
Hepatosplenomegaly may be present.
Infection by Plasmodium falciparum is potentially fatal and most commonly manifests as a febrile nonspecific influenza-like illness without localizing signs.
Complications include:
Cerebral malaria - altered mental states, confusion, coma, seizures and death. It is a metabolic encephalopathy produced when infected erythrocytes bind to cerebral vascular endothelium, resulting in increased glucose utilization, lactate production, and cerebral anoxia.
Renal failure - results from microvascular disease (oxygen and glucose deprivation in the renal cortex), and hemolysis with circulating free hemoglobin and malarial pigment in the kidneys. Massive hemoglobinuria results in black urine ('Blackwater fever').
Respiratory failure and metabolic acidosis, without pulmonary edema. Noncardiogenic pulmonary edema, which is difficult to manage and may be fatal .
Gastroenteritis - seen in young children with P. falciparum. Results from adherence of red cells to vascular endothelium in the GI tract.
Vascular collapse and shock associated with hypothermia and adrenal insufficiency
Children with asplenia are at high risk of death due to malaria.
Hypersplenism with danger of late splenic rupture
Nephrotic syndrome from the deposition of immune complexes in the kidney.
Chronic asymptomatic parasitemia for as long as several years after the last exposure
Congenital malaria secondary to perinatal transmission may occur rarely. Manifestations can resemble those of neonatal sepsis, including fever and nonspecific symptoms of poor appetite, irritability, and lethargy.
Severe malaria is defined as a
parasitemia greater than 5%
signs of central nervous system
other end-organ involvement
shock
acidosis
hypoglycemia.
Diagnostic Tests:
Treatment:
The choice of malaria chemotherapy is based on the infecting species, possible drug
resistance, and the severity of disease
Standard therapy:
Erythrocytic: Chloroquine, Mefloquine, Qinine/quinidine, Antifolates
Exoerythrocytic: Primaquine (vivax and ovale only)
Chloroquine resistance strains:
Chloroquine resistance is prevalent in Central and South Africa, South East Asia, the Indian sub-continent, and Central America.
The recommended regimens for Chloroquine resistance are
Quinine plus doxycycline
Quinine plus clindamycin
Quinine plus pyrimethamine-sulfadoxine.
Alternate regimens are Mefloquine, Halofantrine or Artesunate.
Severe malaria
Patients with severe malaria require intensive care and parenteral treatment until the parasite density falls below 1% and they are able to tolerate oral therapy.
Exchange transfusion may be warranted when parasitemia exceeds 10%.
For patients with P falciparum malaria, sequential blood smears are indicated to monitor treatment.
Control Measures:
What control measures are available to prevent its transmission?
Prevention of Relapses.
Primaquine phosphate should be considered.
Primaquine can cause hemolysis in patients with glucose-6-phosphate dehydrogenase deficiency
Patients should be screened for glucose-6-phosphate dehydrogenase deficiency before primaquine therapy is initiated.