Malaria

Last November 2008 my brother went to East Kalimantan of Indonesia for worked. During 2 months worked nothing happent with his health.

One night after christmas, he got high fever and dizziness.
When he called me, i ask him to go to hospital, but unlucky there is no hospital there.
at that time i just thought he just tired, or got typus.
For prevent i just ask him to take vitamin B & C complex and take the generic medicine.

three days later, fever getting worse. he can't walk himself.
so, i suggest him to come to JAKARTA, where all family were here can help him.

When he arrived in JAKARTA after 2 days trip from kalimantan , my brother's body look so thin , no power and yellowish (eyes, skin).
Then we bring him to hospital, and the doctor give infusion, take his blood for laboratory check,
but the result from the laboratorium is after new year.
When doctor see result from lab, he said it's negative of typus. also negative Aedes dangue.

then my mom said: "please check malaria, i suspect he got malaria.".

Doctor said: "Malaria? , where he come from?"

my mother said : "Kalimantan"

Doctor : "oh i see, ok, we'll check the blood once again, tommorow we will see the result"

Oh my GOD, in my mind i am thinking indonesian doctor..... check and check waiting too long.
my brother is gonna be die. i saw the body getting worst.

when the lab result come, yes it's true my brother got malaria.

Eventhough doctor said my brother can back home, the malarie is not disappear.
Be careful of malaria, bacause small parasites malaria mosquitoes is can permanen in the body. when he get tired, stress, or late take lunch or dinner, will come fever, sweat, vomiting and dizzy .

Below i share a little bit about malaria.

Malaria has infected humans for over 50,000 years, and may have been a human panthogen for the entire history of the species. Close relatives of the human malaria parasites remain common in chimpanzees. References to the unique periodic fevers of malaria are found throughout recorded history, beginning in 2700 BC in China. The term malaria originates from Medieval Italian: mala aria — "bad-air; and the disease was formerly called ague or marsh fever due to its association with swamps and marshland.
Scientific studies on malaria made their first significant advance in 1880, when a French army doctor working in the military hospital of Constantine in Algeria named Charles Louis Aphonse Laveran observed parasites for the first time, inside the red blood cells of people suffering from malaria. He, therefore, proposed that malaria is caused by this protozoan, the first time protozoa were identified as causing disease
Although some patients died from malaria, this was preferable to the almost-certain death from syphilis. Although the blood stage and mosquito stages of the malaria life cycle were identified in the 19th and early 20th centuries, it was not until the 1980s that the latent liver form of the parasite was observed. The discovery of this latent form of the parasite finally explained why people could appear to be cured of malaria but still relapse years after the parasite had disappeared from their bloodstreams.

Malaria caused by a genus of mosquito that name "Anopheles "

Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Diptera
Family: Culicidae
Genus: Anopheles

(picture: larva anophelines)

Like all mosquitoes, anophelines go through four stages in their life cycle: egg, larva, and imago. The first three stages are aquatic and last 5-14 days, depending on the species and the ambient temperature. The adult stage is when the female Anopheles mosquito acts as malaria vector. The adult females can live up to a month (or more in captivity) but most probably do not live more than 1-2 weeks in nature.

Symptoms of malaria include fever, shivering, arthralgia (joint pain), vomiting, anemia, (caused by hemolysis), hemoglobinuria, retinal damage and convulsions. The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours, occurring every two days in P. vivax and P. ovale infections, while every three for P. malariae. P. falciparum can have recurrent fever every 36–48 hours or a less pronounced and almost continuous fever. For reasons that are poorly understood, but that may be related to high intracranial pressure , children with malaria frequently exhibit abnormal posturing, a sign indicating severe brain damage. Malaria has been found to cause cognitive impairments, especially in children. It causes widespread anemia during a period of rapid brain development and also direct brain damage. This neurologic damage results from cerebral malaria to which children are more vulnerable.

Severe malaria is almost exclusively caused by P. falciparum infection and usually arises 6–14 days after infection. Consequences of severe malaria include coma and death if untreated—young children and pregnant women are especially vulnerable. Splenomegaly (enlarged spleen), severe headache, cerebral ischemia, hepatomegaly, (enlarged liver), hypoglycemia, and hemoglobinuria with renal failure may occur. Renal failure may cause blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine. Severe malaria can progress extremely rapidly and cause death within hours or days. In the most severe cases of the disease fatality rates can exceed 20%, even with intensive care and treatment. In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria can be as high as one in ten.

Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. Chronic malaria is seen in both P. vivax and P. ovale, but not in P. falciparum. Here, the disease can relapse months or years after exposure, due to the presence of latent parasites in the liver. Describing a case of malaria as cured by observing the disappearance of parasites from the bloodstream can, therefore, be deceptive. The longest incubation period reported for a P. vivax infection is 30 years.

Approximately one in five of P. vivax malaria cases in temperate areas involve overwintering by hypnozoites (i.e., relapses begin the year after the mosquito bite).

Malaria parasites
Malaria is caused by protozoan parasites of the genus Plasmodium (phylum Apicomplexa). In humans malaria is caused by P.falciparum, P.malariae, P.ovale, P.vivac and P.knowlesi

P. falciparum is the most common cause of infection and is responsible for about 80% of all malaria cases, and is also responsible for about 90% of the deaths from malaria. Parasitic Plasmodium species also infect birds, reptiles, monkeys, chimpanzees and rodents. There have been documented human infections with several simian species of malaria, namely P. knowlesi, P.inui, P. cynomolgi, P.simiovale, P.brazilianum, P. schwetzi, P.simium; however, with the exception of P. knowlesi, these are mostly of limited public health importance.

Although avian malaria can kill chickens and turkeys, this disease does not cause serious economic losses to poultry farmers. However, since being accidentally introduced by humans it has decimated the endemic birds of Hawaii, which evolved in its absence and lack any resistance to it. Malaria in humans develops via two phases: an exoerythrocytic and an erythrocytic phase. The exoerythrocytic phase involves infection of the hepatic system, or liver, whereas the erythrocytic phase involves infection of the erythrocytes, or red blood cells. When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver.

Within 30 minutes of being introduced into the human host, the sporozoites infect hepatocytes, multiplying asexually and asymptomatically for a period of 6–15 days. Once in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blodd cells, thus beginning the erythrocytic stage of the life cycle. The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.
Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.
Some P. vivax and P. ovale sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (6–12 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in these two species of malaria.
The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen. This "stickiness" is the main factor giving rise to hemorrhagic complications of malaria.
High endothelial venules (the smallest branches of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the blood brain barrier possibly leading to coma.
Although the red blood cell surface adhesive proteins (called PfEMP1, for Plasmodium falciparum erythrocyte membrane protein 1) are exposed to the immune system, they do not serve as good immune targets because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and perhaps limitless versions within parasite populations. Like a thief changing disguises or a spy with multiple passports, the parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system.
Some merozoites turn into male and female gametocytes. If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut, thereby defining the mosquito as the definitive host of the disease. New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes, and malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight, particularly in P. falciparum infection, but also in other species infection, such as P. vivax.