Malaria causes symptoms that typically include fever, fatigue, vomiting and headaches. In severe cases it can cause yellow skin, seizures, coma or death.[2] These symptom usually begin ten to fifteen days after being bitten. In those who have not been appropriately treated disease may recur months later.[1] In those who have recently survived an infection, re-infection typically causes milder symptoms. This partial resistance disappears over months to years if there is no ongoing exposure to malaria.[2]

The signs and symptoms of malaria typically begin 8–25 days following infection;[8] however, symptoms may occur later in those who have taken antimalarial medications as prevention.[3] Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms,[9]and can resemble other conditions such as septicemia, gastroenteritis, and viral diseases.[3] The presentation may include headache, fever, shivering, joint pain, vomiting, hemolytic anemia,jaundice, hemoglobin in the urine, retinal damage, and convulsions.[10]

The classic symptom of malaria is paroxysm—a cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occurring every two days (tertian fever) in P. vivax andP. ovale infections, and every three days (quartan fever) for P. malariae. P. falciparum infection can cause recurrent fever every 36–48 hours or a less pronounced and almost continuous fever.[11]

Severe malaria is usually caused by P. falciparum (often referred to as falciparum malaria). Symptoms of falciparum malaria arise 9–30 days after infection.[9] Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturing, nystagmus, conjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonus, seizures, or coma.[9]

There are several serious complications of malaria. Among these is the development of respiratory distress, which occurs in up to 25% of adults and 40% of children with severe P. falciparum malaria. Possible causes include respiratory compensation of metabolic acidosis, noncardiogenic pulmonary oedema, concomitant pneumonia, and severe anaemia. Although rare in young children with severe malaria,acute respiratory distress syndrome occurs in 5–25% of adults and up to 29% of pregnant women.[12] Coinfection of HIV with malaria increases mortality.[13] Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.[9]

Infection with P. falciparum may result in cerebral malaria, a form of severe malaria that involves encephalopathy. It is associated with retinal whitening, which may be a useful clinical sign in distinguishing malaria from other causes of fever.[14] Splenomegaly, severe headache,hepatomegaly (enlarged liver), hypoglycemia, and hemoglobinuria with renal failure may occur.[9]

Malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight,[15] particularly in P. falciparum infection, but also with P. vivax.[16]

Symptoms of malaria can recur after varying symptom-free periods. Depending upon the cause, recurrence can be classified as either recrudescence, relapse, or reinfection. Recrudescence is when symptoms return after a symptom-free period. It is caused by parasites surviving in the blood as a result of inadequate or ineffective treatment.[29]

Relapse is when symptoms reappear after the parasites have been eliminated from blood but persist as dormant hypnozoites in liver cells. Relapse commonly occurs between 8–24 weeks and is commonly seen with P. vivax and P. ovale infections.[3] P. vivax malaria cases in temperate areas often involve overwintering by hypnozoites, with relapses beginning the year after the mosquito bite.[30]

Reinfection means the parasite that caused the past infection was eliminated from the body but a new parasite was introduced. Reinfection cannot readily be distinguished from recrudescence, although recurrence of infection within two weeks of treatment for the initial infection is typically attributed to treatment failure.[31] People may develop some immunity when exposed to frequent infections.[32]

DIAGNOSIS- Owing to the non-specific nature of the presentation of symptoms, diagnosis of malaria in non-endemic areas requires a high degree of suspicion, which might be elicited by any of the following: recent travel history, enlarged spleen, fever, low number of platelets in the blood, and higher-than-normal levels of bilirubin in the blood combined with a normal level of white blood cells.[3]

Malaria is usually confirmed by the microscopic examination of blood films or by antigen-based rapid diagnostic tests (RDT).[43][44] Microscopy is the most commonly used method to detect the malarial parasite—about 165 million blood films were examined for malaria in 2010.[45] Despite its widespread usage, diagnosis by microscopy suffers from two main drawbacks: many settings (especially rural) are not equipped to perform the test, and the accuracy of the results depends on both the skill of the person examining the blood film and the levels of the parasite in the blood. The sensitivity of blood films ranges from 75–90% in optimum conditions, to as low as 50%. Commercially available RDTs are often more accurate than blood films at predicting the presence of malaria parasites, but they are widely variable in diagnostic sensitivity and specificity depending on manufacturer, and are unable to tell how many parasites are present.[45]

In regions where laboratory tests are readily available, malaria should be suspected, and tested for, in any unwell person who has been in an area where malaria is endemic. In areas that cannot afford laboratory diagnostic tests, it has become common to use only a history of fever as the indication to treat for malaria—thus the common teaching "fever equals malaria unless proven otherwise". A drawback of this practice is overdiagnosis of malaria and mismanagement of non-malarial fever, which wastes limited resources, erodes confidence in the health care system, and contributes to drug resistance.[46] Although polymerase chain reaction-based tests have been developed, they are not widely used in areas where malaria is common as of 2012, due to their complexity.[3]

TREATMENT- Several medications are available to prevent malaria in travellers to areas where the disease is common. Occasional doses of the medication sulfadoxine/pyrimethamineare recommended in infants and after the first trimester of pregnancy in areas with high rates of malaria. Despite a need, no effective vaccine exists, although efforts to develop one are ongoing.[1]

The recommended treatment for malaria is a combination of antimalarial medications that includes an artemisinin.[1][2] The second medication may be either mefloquine, lumefantrine, or sulfadoxine/pyrimethamine.[4] Quinine along with doxycycline may be used if an artemisinin is not available.[4]

It is recommended that in areas where the disease is common, malaria is confirmed if possible before treatment is started due to concerns of increasing drug resistance. Resistance has developed to several antimalarial medications; for example, chloroquine-resistant P. falciparum has spread to most malarial areas, and resistance to artemisinin has become a problem in some parts of Southeast Asia.[1]

Malaria is treated with antimalarial medications; the ones used depends on the type and severity of the disease. While medications against fever are commonly used, their effects on outcomes are not clear.[76]

Uncomplicated malaria may be treated with oral medications. The most effective treatment for P. falciparum infection is the use of artemisininsin combination with other antimalarials (known as artemisinin-combination therapy, or ACT), which decreases resistance to any single drug component.[77] These additional antimalarials include: amodiaquine, lumefantrine, mefloquine or sulfadoxine/pyrimethamine.[78] Another recommended combination is dihydroartemisinin and piperaquine.[79][80] ACT is about 90% effective when used to treat uncomplicated malaria.[56] To treat malaria during pregnancy, the WHO recommends the use of quinine plus clindamycin early in the pregnancy (1st trimester), and ACT in later stages (2nd and 3rd trimesters).[81] In the 2000s (decade), malaria with partial resistance to artemisins emerged in Southeast Asia.[82][83]

Infection with P. vivax, P. ovale or P. malariae is usually treated without the need for hospitalization. Treatment of P. vivax requires both treatment of blood stages (with chloroquine or ACT) as well as clearance of liver forms with primaquine.[84]

Recommended treatment for severe malaria is the intravenous use of antimalarial drugs. For severe malaria, artesunate is superior to quinine in both children and adults.[85] Treatment of severe malaria involves supportive measures that are best done in a critical care unit. This includes the management of high fevers and the seizures that may result from it. It also includes monitoring for poor breathing effort, low blood sugar, and low blood potassium.[19]

Above Information from Wiki:

Florida Department of Health


Symptoms of malaria depend on the Plasmodiumspecies, but in most cases develop between seven and thirty days after the bite of an infected mosquito. P. vivax can develop up to a year after exposure and if not treated properly can cause additional attacks (“relapses”). Commonly, people experience flu-like symptoms such as fever, chills, sweats, headache, nausea and vomiting, body aches, and general malaise. P. falciparum can cause severe and life-threatening disease.


P. falciparum and P. vivax were previously present in Florida, but was eradicated from the state in the late 1940s. Local transmission has occurred only rarely in recent years, likely due to mosquito control measures, improved housing with screens, use of repellents, and drainage practices. A number of malaria cases are reported in immigrant and travelers to areas where malaria risk is high. There are 14 Anopheles mosquito species in Florida, all of which are potentially capable of transmitting malaria. An. quadrimaculatus and An. crucians have been major malaria vectors in the past. Since introduction from endemic areas occurs regularly and competent vectors exist in the state, local transmission is possible.

In Florida

The largest outbreak in recent Florida history occurred in Palm Beach County in 2003 where there were eight cases. In 2012, 65 cases of imported malaria were reported in Florida. Forty-five cases (69%) were diagnosed with P. falciparum, 16 (25%) with P. vivax, two (3%) with P. ovale, two with P. malariae (3 %). All 65 cases were associated with travel or immigration. Reasons given for traveling to a malaria endemic county included: 43% visiting friends and relatives (VFR), 29% for business (including missionary and military), 9% of cases were recent immigrants, 8% tourism, 5% students or teachers, and 6% unknown reason.