1. Malaria is transmitted from person to person by mosquito vectors and rarely by blood transfusion. Malaria caused by Plasmodium falciparum is more acute and severe than malaria caused by other Plasmodium species.

2. Severe malaria is defined as acute malaria with levels of parasitemia >5% and/or major signs of organ dysfunction.

3. Malaria is endemic in most tropical countries.

1. After inoculation, sporozoites invade and replicate in hepatocytes. Infected hepatocytes rupture; merozoites enter the bloodstream and invade erythrocytes, causing fever and leading to the pathologic process of erythrocyte loss and sequestration in the microvascular bed.

1. Clinical manifestations are fever and rigors; this can progress to altered consciousness with seizures and multiorgan failure.

2. Routine laboratory findings are anemia, hyperbilirubinemia, hypoglycemia, and metabolic acidosis.

3. Definitive diagnosis is made by evidence of parasites on thin and thick smear; rapid diagnostic tests for malaria-specific antigens are now available, as are more expensive PCR assays.

1. Artesunate intravenously at dose 2.4 mg/kg at 0, 12, and 24 hours, followed by 2.4 mg/kg once a day for 3 to 5 days. In the USA, the drug is available under investigational protocol from the CDC, Malaria Hotline: (770) 488-7788 and (770) 488-7100.

2. Quinidine gluconate intravenously at loading dose 10 mg salt /kg over 1 to 2 hours (maximum 600 mg salt) followed by 0.02 mg salt/kg/min by continuous infusion. This agent must be administered in an intensive care setting. Criteria for switch to oral regimen are ability to tolerate PO and level of parasitemia <1%. Duration of treatment will vary depending on where the parasite was acquired.

3. Treatment with quinidine should be combined with doxycycline, tetracycline, or clindamycin.

1. West Nile virus (WNV) is a mosquito-borne disease caused by an RNA virus, genus Flaviviridae.

2. WNV is one of the most widely distributed arboviruses, affecting North America as well as parts of Europe, the Middle East, Asia, and Africa.

1. After inoculation, the virus replicates, leading to viremia that seeds various organs and tissues.

1. Clinical manifestations can range from asymptomatic to neuroinvasive disease, which can present as encephalitis, meningitis, or flaccid paralysis.

2. Routine laboratory findings are nonspecific. In patients with neuroinvasive disease, the cerebrospinal fluid (CSF) usually demonstrates pleocytosis with predominance of lymphocytes and an elevated protein concentration.

3. Serologic studies in serum or CSF, or nucleic acid testing (NAT) confirms the diagnosis.

Supportive treatment.

1. Tularemia is a potentially lethal zoonotic infection caused by a gramnegative bacterium, Francisella tularensis. Transmission to humans occurs from contact with contaminated animals or a biting insect. Transmission can also occur from airborne spread of contaminated materials.

2. Tularemia affects North America, most of the European countries, the Middle East, and part of Asia.

1. After multiplying at the site of inoculation, the organism spreads systemically via a lymphohematogenous route causing an inflammatory reaction and leading to tissue necrosis.

1. Clinical manifestations of rapid onset of fever and malaise; additional signs and symptoms depend on the portal of entry. Pneumonic tularemia results from direct inhalation of the organism into the lungs; typhoidal tularemia may result from any portal of entry. The ulceroglandular form of tularemia arising at the site of cutaneous inoculation is the most common form of tularemia.

2. Laboratory findings include thrombocytopenia, elevated liver enzymes, and hyponatremia but are often nonspecific.

3. Serologic testing is supportive of the diagnosis. A fourfold or greater rise in titer between acute and convalescent sample is usually needed for diagnostic confirmation. Cultures should be inoculated on supplemented media to confirm the diagnosis. Laboratory personal should be notified, as culture of the organism represents a potential danger.