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Introduction
Malaria is a serious and sometimes fatal disease caused by a parasite called
Plasmodium that commonly infects a certain type of mosquito which feeds on humans. In
the human body, the parasites multiply in the liver, and then infect red blood cells.
People who get malaria are typically very sick with high fevers, shaking chills, and flu-like
illness and usually appear between 10 and 15 days after the mosquito bite.. Although
malaria can be a deadly disease, illness and death from malaria can usually be
prevented. In many parts of the world, the parasites have developed resistance to a
number of malaria medicines.
About 1,500 cases of malaria are diagnosed in the United States each year. The
vast majority of cases in the United States are in travelers and immigrants returning from
countries where malaria transmission occurs, many from sub-Saharan Africa and South
Asia.
Epidemiology
Malaria is responsible for approximately 1-3 million deaths per year, typically in
children in sub-Saharan Africa infected with P falciparum. Populations at an increased risk
for mortality due to malaria include primigravida individuals, travelers without immunity,
and young children aged 6 months to 3 years who live in endemic areas.
Young children aged 6 months to 3 years who live in endemic areas are at an
increased risk of death due to malaria. Travelers without immunity are at an increased
mortality risk, regardless of age.
In Indonesia, the endemic of Malaria is still high. Malaria is concentrated on the
outer islands of Papua, Maluku, Nusa Tenggara, Sulawesi, Kalimantan and Sumatra. It
occurs with low frequency or is absent on the islands of Java and Bali where
approximately 70% of the population live. All species of human malaria parasites are
found in Indonesia. Formerly, P. malariae and P. ovale were mostly found in the eastern
part of Indonesia, Nusa Tenggara Timur and Papua. Around 107 million people are at
varied degrees of risk. Malaria transmission in Indonesia is perennial. P. vivax and P.
falciparum are the most common types of malaria species prevalent in the country.
Most West Africans and people with origins in that region carry the Duffy-negative FyFy
phenotype and are therefore resistant to P. vivax Malaria.During the early stage of
intraerythrocytic development, the small "ring forms" of the four parasitic species appear
similar under light microscopy. As the trophozoites enlarge, species-specific
characteristics become evident, pigment becomes visible, and the parasite assumes an
irregular or ameboid shape. By the end of the 48-h intraerythrocytic life cycle (72 h for P.
malariae), the parasite has consumed nearly all the hemoglobin and grown to occupy
most of the RBC. It is now called a schizont. Multiple nuclear divisions have taken place
(schizogony or merogony), and the RBC then ruptures to release 630 daughter
merozoites, each potentially capable of invading a new RBC and repeating the cycle. The
disease in human beings is caused by the direct effects of RBC invasion and destruction
by the asexual parasite and the host's reaction. After a series of asexual cycles (P.
falciparum) or immediately after release from the liver (P. vivax, P. ovale, P. malariae),
some of the parasites develop into morphologically distinct, longer-lived sexual forms
(gametocytes) that can transmit Malaria. After being ingested in the blood meal of a
biting female anopheline mosquito, the male and female gametocytes form a zygote in
the insect's midgut. This zygote matures into an ookinete, which penetrates and encysts
in the mosquito's gut wall. The resulting oocyst expands by asexual division until it bursts
to liberate myriad motile sporozoites, which then migrate in the hemolymph to the
salivary gland of the mosquito to await inoculation into another human at the next
feeding.
Host Response
Initially, the host responds to plasmodial infection by activating nonspecific
defense mechanisms. Splenic immunologic and filtrative clearance functions are
augmented in Malaria, and the removal of both parasitized and uninfected erythrocytes
is accelerated. The parasitized cells escaping splenic removal are destroyed when the
schizont ruptures. The material released induces the activation of macrophages and the
release of proinflammatory mononuclear cellderived cytokines, which cause fever and
exert other pathologic effects. Temperatures of 40C damage mature parasites; in
untreated infections, the effect of such temperatures is to further synchronize the
parasitic cycle, with eventual production of the regular fever spikes and rigors that
originally served to characterize the different malarias. These regular fever patterns
(tertian, every 2 days; quartan, every 3 days) are seldom seen today in patients who
receive prompt and effective antimalarial treatment.
The geographic distributions of sickle cell disease, ovalocytosis, thalassemia, and
glucose-6-phosphate dehydrogenase (G6PD) deficiency closely resemble that of Malaria
before the introduction of control measures. This similarity suggests that these genetic
disorders confer protection against death from falciparum Malaria. For example, HbA/S
heterozygotes (sickle cell trait) have a sixfold reduction in the risk of dying from severe
falciparum Malaria. This decrease in risk appears to be related to impaired parasite
growth at low oxygen tensions. Parasite multiplication in HbA/E heterozygotes is reduced
at high parasite densities.
In Melanesia, children with -thalassemia appear to have more frequent Malaria
(both vivax and falciparum) in the early years of life, and this pattern of infection appears
to protect against severe disease. In Melanesian ovalocytosis, rigid erythrocytes resist
merozoite invasion, and the intraerythrocytic milieu is hostile.
Nonspecific host defense mechanisms stop the infection's expansion, and the
subsequent specific immune response controls the infection. Eventually, exposure to
sufficient strains confers protection from high-level parasitemia and disease but not from
infection. As a result of this state of infection without illness (premunition), asymptomatic
parasitemia is common among adults and older children living in regions with stable and
intense transmission (i.e., holo- or hyperendemic areas). Immunity is mainly specific for
both the species and the strain of infecting malarial parasite. Both humoral immunity and
cellular immunity are necessary for protection, but the mechanisms of each are
incompletely understood. Immune individuals have a polyclonal increase in serum levels
of IgM, IgG, and IgA, although much of this antibody is unrelated to protection. Antibodies
to a variety of parasitic antigens presumably act in concert to limit in vivo replication of
the parasite. In the case of falciparum Malaria, the most important of these antigens is
the surface adhesinthe variant protein PfEMP1 mentioned above. Passively transferred
IgG from immune adults has been shown to reduce levels of parasitemia in children;
although parasitemia in very young infants can occur, passive transfer of maternal
antibody contributes to the relative (but not complete) protection of infants from severe
Malaria in the first months of life. This complex immunity to disease declines when a
person lives outside an endemic area for several months or longer.
Several factors retard the development of cellular immunity to Malaria. These
factors include the absence of major histocompatibility antigens on the surface of
infected RBCs, which precludes direct T cell recognition; Malaria antigenspecific immune
unresponsiveness; and the enormous strain diversity of malarial parasites, along with the
ability of the parasites to express variant immunodominant antigens on the erythrocyte
surface that change during the period of infection. Parasites may persist in the blood for
months (or, in the case of P. malariae, for many years) if treatment is not given. The
complexity of the immune response in Malaria, the sophistication of the parasites'
evasion mechanisms, and the lack of a good in vitro correlate with clinical immunity have
all slowed progress toward an effective vaccine.
Clinical Features
Malaria is a very common cause of fever in tropical countries. The first symptoms
of Malaria are nonspecific; the lack of a sense of well-being, headache, fatigue,
abdominal discomfort, and muscle aches followed by fever are all similar to the
symptoms of a minor viral illness. In some instances, a prominence of headache, chest
pain, abdominal pain, arthralgia, myalgia, or diarrhea may suggest another diagnosis.
Although headache may be severe in Malaria, there is no neck stiffness or photophobia
resembling that in meningitis. While myalgia may be prominent, it is not usually as
severe as in dengue fever, and the muscles are not tender as in leptospirosis or typhus.
Nausea, vomiting, and orthostatic hypotension are common. The classic malarial
paroxysms, in which fever spikes, chills, and rigors occur at regular intervals, are
relatively unusual and suggest infection with P. vivax or P. ovale. The fever is irregular at
first (that of falciparum Malaria may never become regular); the temperature of
nonimmune individuals and children often rises above 40C in conjunction with
tachycardia and sometimes delirium. Although childhood febrile convulsions may occur
with any of the malarias, generalized seizures are specifically associated with falciparum
Malaria and may herald the development of cerebral disease. Many clinical abnormalities
have been described in acute Malaria, but most patients with uncomplicated infections
have few abnormal physical findings other than fever, malaise, mild anemia, and (in
some cases) a palpable spleen. Anemia is common among young children living in areas
with stable transmission, particularly where resistance has compromised the efficacy of
antimalarial drugs. In nonimmune individuals with acute Malaria, the spleen takes several
days to become palpable, but splenic enlargement is found in a high proportion of
otherwise healthy individuals in Malaria -endemic areas and reflects repeated infections.
Slight enlargement of the liver is also common, particularly among young children. Mild
jaundice is common among adults; it may develop in patients with otherwise
uncomplicated falciparum Malaria and usually resolves over 13 weeks. Malaria is not
associated with a rash like those seen in meningococcal septicemia, typhus, enteric
fever, viral exanthems, and drug reactions. Petechial hemorrhages in the skin or mucous
membranesfeatures of viral hemorrhagic fevers and leptospirosisdevelop only rarely
in severe falciparum Malaria.
Thin smear
Thick smear
PHRP2 dipstick
Prognosis
Good if patient get early treatment and poor in late case.
Complication
Anemia
Renal failure
Pulmonary edema
Hyperpyrexia
Jaundice
References :
1. WHO. Malaria. 2011. http://www.who.int/topics/malaria/en/
2. CDC. Malaria. 2010.http://www.cdc.gov/malaria/about/index.html
3. CDC. Where Malaria Occur. 2010.
http://www.cdc.gov/malaria/about/distribution.html
4. Fauce et al. Harrison's Internal Medicine. 2008. Chapter 203. Malaria
5. Jorge, EVP.
Malaria.
overview#a0199
2011.
http://emedicine.medscape.com/article/221134-
6. WHO.
2005.
Acces
http://www.searo.who.int/LinkFiles/Malaria_in_the_SEAR_ende_indo05.pdf
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