A. Definition
Malaria is a contagious infectious disease caused by parasites of the genus Plasmodium, transmitted through the bite of Anopheles mosquitoes with a picture of a disease that is often periodic fever, anemia, enlarged spleen and various collection of symptoms by its effects on several organs such as brain, liver and kidney. (Http://medicafarma.blogspot.com)
Malaria is an acute disease becomes chronic and can be caused by a protozoan (genus Plasmodium) that intra living cells (Iskandar Zulkarnain, 1999). Malaria is an infectious disease that can be acute or chronic, caused by protozoa of the genus plasmodium characterized by fever, anemia and splenomegaly.
B. Etiology
Plasmodium are parasites that includes vilum Protozoa, sporozoa class. There are four species of Plasmodium in humans, namely: Plasmodium vivax causes vivax malaria (malaria tertiana light). Falcifarum Plasmodium cause malaria falsifarum (malaria tertiana weight), and Blackwater faver pernicious malaria. Plasmodium malariae malaria kuartana cause, and cause malaria, Plasmodium ovale ovale. (Nelson, 1999)
The four species of Plasmodium can be distinguished by comparing the shape schizont morphology, trofozoit form, the form contained gametocytes in the peripheral blood and pre-eritrositik form of schizont contained in liver parenchymal cells.
C. CLINIC manifestations
1. Plasmodium vivax (malaria tertiana)
a. Fell dizzy
b. Chills chills / fever (8 to 12 hours, can occur two days after symptoms first occur can happen for 2 weeks after infection)
c. Cold sweat
d. Convulsions
e. Feelings of weakness, no appetite, pain in bones and joints.
2. Falcifarum Plasmodium (malaria, tropical)
a. Fell dizzy
b. Chills chills / fever (more than 12 hours, can occur two days after symptoms first occur can occur for 2 miggu setela infection)
c. Cold sweat
d. Convulsions
e. Feelings of weakness, no appetite, pain in bones and joints.
3. Plasmodium malariae (malaria kuartana)
a. Fell dizzy
b. Chills chills / fever (not the first symptoms occur between 18 to 40 days after infection. The symptoms are then likely to recur every 3 days)
c. Cold sweat
d. Convulsions
e. Feelings of weakness, no appetite, pain in bones and joints
4. Plasmodium ovale (rarely found)
Where similar clinical manifestations of malaria tertiana:
a. Fell dizzy
b. Chills chills / fever (8 to 12 hours, can occur two days after symptoms first occur can happen for 2 weeks after infection)
c. Cold sweat
d. Convulsions
e. Feelings of weakness, no appetite, pain in bones and joints.
D. Pathogenesis / Pathophysiology
The occurrence of infection by the Plasmodium parasite into the human body can occur through two ways:
1. Naturally through the bite of female Anopheles mosquitoes containing malaria parasites
2. Namely if the stage asexual induction in erythrocytes get into human blood, for example through blood transfusions, injections, or the newborn via the placenta-infected mothers (congenital).
Pathophysiology of malaria is very complex and may relate to matters as follows:
a. Destruction of erythrocytes which occurs because of:
Rupture of erythrocyte-containing parasites
Phagocytosis of erythrocyte-containing and not containing parasites
The result is anemia and anoksia network and intravascular hemolysis
b. Endotoxin-macrophage release of mediators
In the process of releasing skizoni endotoxin, macrophages release various mediators endotoxin.
c. The release of TNF (tumor necrosis factor necrosing factor or tumor)
It is a monokin released by the malaria parasite. TNF is responsible for the fever, hypoglycemia, ARDS.
d. Sekuetrasi erythrocytes
Infected erythrocytes to form a knob on its surface. Knob contain malaria antigens, which then reacts with the antibody. Infected erythrocytes will stick to the capillary endothelium in the tool and forming clots causing dam. (Http://medicafarma.blogspot.com)
E. SUPPORTING DATA
1. Laboratories
Anemia in malaria can be acute or chronic, the acute objec rapid decline of Hb. The cause of anemia is destruction of erythrocytes by malaria parasites, emphasis eritropoesis and may be very important is the hemolysis by immunological processes. In acute malaria also occur eritropoesis inhibition on bone marrow, but when parasitaemia disappeared, the bone marrow into hiperemik, pigmentation active with hyperplasia of normoblast. In the peripheral blood can be found poikilositosis, anisositosis, polikromasia and basophilic spots resembling pernisioasa anemia. Thrombocytopenia can also be found that can interfere with the process of coagulation.
In severe tropical malaria, the plasma fibrinogen may decrease due to increased consumption of fibrinogen due to the occurrence of coagulation intravskuler. Mild jaundice occurs with indirect bilirubin increased more and abnormal liver function tests such as increased transaminase, sefalin flocculation tests positive, glucose and alkaline phosphatase decreased. Plasma proteins, especially albumin decreased, despite increased globulin. This change not only caused by fever alone but also because of increasing liver function. Hipokolesterolemia also can occur in malaria. Glucose is essential for respiration of plasmodia and the increase in blood glucose are found in tropical and tertiana malaria, may be associated with suprarenalis gland. Potassium in plasma increased at the time of fever, probably due to destruction of red blood cells. ESR is increased in malaria but returned to normal after being given treatment.
2. Diagnosis
Diagnosis of malaria often require proper diagnose the patient whether the patient about the origin of the malaria endemic region, history of travel to malaria areas, and preventip Portfolio kuratip treatment.
a. Examination drops of blood for malaria
Microscopic examination of peripheral blood for the detection of malaria parasites is essential for diagnosis. Examination one time with a negative result does not rule out the diagnosis of malaria. Peripheral blood examination three times and a negative result then the diagnosis of malaria can be excluded. The peripheral blood examination can be done through:
1) thick droplets of blood preparations
Is the best way to find malaria parasites because the blood drop quite a lot compared to thin blood preparations. Preparations are easy to make, especially for studies in the field. Thickness in making the preparations necessary to facilitate the identification of parasites. Parasite examinations performed for 5 minutes (an estimated 100 visual field with powerful magnification). Preparations declared negative when 200 of visual field after being reviewed by 700-1000 times magnification can not find the parasite. Calculate the parasite can be carried out in thick drops by counting the number of parasites per 200 leukocytes. When the leukocyte count parasites 10.000/ul then multiplied by 50 is the number of parasites is the number of parasites per micro-liter of blood.
b). A thin trickle of blood preparations. Used to identify the types of plasmodium, if the thick blood preparations difficult to determine. Parasite density expressed as arithmetic parasite (parasite count), it can be done based on the number of erythrocytes containing parasites per 1000 red blood cells. When the number of parasites> blood 100.000/ul indicate a severe infection. Calculate the parasite is important for determining the prognosis of malaria patients. Painting is done by staining Giemsa, or Leishman's, or Field's and also Romanowsky.
Giemsa staining is commonly used in several laboratories and is a painting that is easy with good results.
b. Antigen Test: p-f test
Which detects an antigen of P.falciparum (histidine rich protein II). Detection of very fast just 3-5 minutes, requires no special training, good sensitivity, requires no special equipment. Antigen detection for vivaks already circulating in the market that is by the method of ICT. Similar test by detecting lactate dehydrogenase from Plasmodium (pLDH) by immunochromatographic tests have been marketed under the name OPTIMAL. Optimal to detect than 000-200 parasites / ul blood and can distinguish whether or P.vivax P.falciparum infection. Sensitivity to 95% and false positive results is lower than the HRP-2 detection test. This test is now known as a rapid test (Rapid Test).
c). Serology Tests
Serology was introduced since 1962 by using indirect fluorescent antibody test technique. This test is useful to detect the existence of specific antibodies against malaria or in circumstances where the parasite is very minimal. This test is less useful as a diagnostic tool for a new antibody occurred after several days of parasitemia. Benefits of serologic tests, especially for epidemiological studies or blood donor screening tool. Titer> 1:200 is considered as a new infection, and test> 1:20 tested positive. Serologic test methods include indirect haemagglutination test, immunoprecipitation techniques, ELISA test, the radio-immunoassay.
d). PCR (Polymerase Chain Reaction) ---> examination of infection
This examination is considered to be extremely sensitive to DNA amplification technology, when used fairly fast and high sensitivity and specificity. The advantages of this test, although the number of parasites is very little to give positive results. This test is only used as a means of research and not for routine examination.
F. COMPLICATIONS
Complications of malaria is generally caused by P.falciparum and is often called pernicious manifestasions. Often occur suddenly without symptoms sebeumnya, and often occurs in people who are not immune as in the newcomers and pregnancy. Complications occur in 5-10% of all patients who were treated in hospital and 20% of them are fatal cases.
Malaria patients with kompikasi generally classified as severe malaria according to WHO defined as P.falciparum infection with one or more complications as follows:
1. Cerebral malaria (coma) that are not caused by other diseases or more than 30 minutes after a seizure, the degree of impairment of consciousness should be evaluated based on the GCS (Glasgow Coma Scale) was below 7 or equal to the clinical situation soporous.
2. Acidemia / acidosis, blood pH <> respiratory distress.
3. Severe anemia (Hb <> 10.000/ul; when anemianya hipokromik or miktositik must set aside the iron deficiency anemia, thalassemia / hemoglobinopathy other.
4. Acute renal failure (urine less than 400 ml/24 hours in adults or 12 ml / kg in children) after rehydration, with creatinine> 3 mg / dl.
5. Non-kardiogenik/ARDS pulmonary edema (adult respiratory distress syndrome).
6. Hypoglycemia: Blood sugar <>
7. Failed circulation or shock: systolic blood pressure <> C: 8). 10
8. Spontaneous bleeding from the nose or gums, gastrointestinal tract and laboratory abnormalities accompanied by intravascular coagulation disturbances
9. Recurrent seizures over 2 hour kali/24
10. Macroscopic hemoglobinuri because of acute malaria infection (not because of anti-malarial drugs / erythrocyte abnormalities (lack of G-6-PD)
11. Diagnosis of post-mortem with the discovery of parasites in the dense network of capillaries in the brain.
G. MEDICAL MANAGEMENT
Treatment of malaria can be done by giving the drug antimalari. Antimalarial drugs can be divided in 9 groups, namely:
1.kuinin (quinine)
2.mepakrin
3.klorokuin, amodiakuin
4.proguanil, klorproguanil
5.Primakuin
6.pirimetamin
7.sulfon and sulfonamide
8.kuinolin methanol
9.antibiotic
Based on the susceptibility of various stages of the malaria parasite to antimalarial drugs, the antimalarial drug can also be divided into 5 groups, namely:
1 Skizontisida primary tissue that can kill parasites in the liver praeritrositik stage so as to prevent the parasite into the erythrocyte, so it is used as a causal prophylactic drug. Medicine are proguanil, pyrimethamine.
2 Skizontisida secondary networks can kill the parasite cycle eksoeritrositik P. vivax and P. ovale and used for radical treatment as anti-relapse drug, medicine adala primaquine.
3 Skizontisida that kill blood stage parasites eritrositik, which is associated with acute illness accompanied by clinical symptoms. These drugs are used for suppressive treatment for the four Plasmodium species and also to kill the stage gametocytes of P. vivax, P. malariae and P. ovale, but not effective for the gametocytes of P. falcifarum. Medicine are quinine, chloroquine or amodiakuin; or proguanil and pyrimethamine which have a limited effect.
4 Gametositosida that destroys all sexual forms including gametocytes of P. falcifarum. Medicine are primaquine as gametositosida for four species, and quinine, chloroquine or amodiakuin as gametositosida to P. vivax, P. malariae and P. ovale.
5 Sporontosida that can prevent or inhibit the gametocytes in the blood to form oocysts in the mosquito Anopheles and sporozoit. Drugs - drugs that include this group is primaquine and proguanil.
