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An Introduction
Malaria since its fatal disease,is the
most difficult of all to encouneter.Because of the habit of increasing
resistance to the insecticides ,of the female anopheline species.Its highly
endemic in nature and is charecerised by imminent dangers and
complications.Its turning into a growing hazard in the developing
countries.Being a common communicable disease with increased morbidity and
mortality,it’s the focus of concern and included in the IDSP diseases as
well.
Problem
statement
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Internationally: Malaria is a major health
problem in Africa, Asia, Central America, Oceania, and South America.
About 40% of the world's population lives in areas where malaria is
common. Approximately 300-500 million cases of malaria occur every year,
and 1-2 million deaths occur, most of them in young children.
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Nationally:Among all the states Chennai is the
most endemic,for the disease.About 1000 cases are recorded per year in the
country.40% of all the cases end up in mortality.
Host Factors
Race: People of all races are affected,
with some exceptions. People of West African origin who do not have the
Duffy blood group are not susceptible to P vivax malaria.
Sex: Malaria affects females and males
equally.
Age: Children of all ages living in
nonmalarious areas are equally susceptible to malaria. In endemic areas,
children younger than 5 years have repeated and often serious attacks of
malaria. The survivors develop partial immunity. Thus, older children and
adults often have asymptomatic parasitemia, ie, presence of plasmodia in the
bloodstream without clinical manifestations of malaria. Most deaths
resulting from malaria occur in children younger than 5 years.
Agent
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Malaria can be transmitted through blood transfusion.
Among people living in malarious areas, semi-immunity to malaria allows
donors to have parasitemia without any fever or other clinical
manifestations. The malaria transmitted is by the merozoites, which do
not enter the liver cells. Because the liver stage is not present,
curing the acute attack results in complete cure.
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Transplacental malaria (ie, congenital malaria) can
be significant in populations who are semi-immune to malaria. The mother
may have placental parasitemia, peripheral parasitemia, or both, without
any fever or other clinical manifestations. Vertical transmission of
this infestation may be as high as 40% and is associated with anemia in
the baby.
Aetiopathogenesis
The bite of an infected mosquito
introduces asexual forms of the parasite, called sporozoites, into the
bloodstream. Sporozoites enter the hepatocytes and form schizonts, which are
also asexual forms. Schizonts undergo a process of maturation and
multiplication known as preerythrocytic or hepatic schizogony. In
Plasmodium vivax and Plasmodium ovale infection, some
sporozoites convert to dormant forms called hypnozoites, which can cause
disease after months or years.
Preerythrocytic schizogony takes 6-16 days, and results
in the host cell bursting and releasing thousands of merozoites into the
blood. Merozoites enter the erythrocytes and initiate another asexual
reproductive cycle, known as erythrocytic schizogony. The parasite passes
successively through the stages of trophozoite and schizont, ultimately
giving rise to several merozoites. On maturation of these merozoites, the
erythrocyte ruptures, releasing the merozoites and multiple antigenic and
pyrogenic substances into the bloodstream. These merozoites again infect new
erythrocytes. After a few cycles of this erythrocytic schizogony, some
merozoites differentiate into the sexual forms: the male and female
gametocytes. A mosquito that takes a blood meal from a patient with
gametocytemia acquires these sexual forms and plays host to the sexual stage
of the plasmodial life cycle.
Rupture of a large number of erythrocytes at the same
time releases a large amount of pyrogens, which causes the paroxysms of
malarial fever. The periodicity of malarial fever depends on the time
required for the erythrocytic cycle and is definite for each species.
Plasmodium malariae needs 72 hours for each cycle, leading to the name
quartan malaria. The other 3 species each take 48 hours for one cycle and
cause fever on alternate days (tertian malaria). However, this periodicity
requires all the parasites to be developing and releasing simultaneously; if
this synchronization is absent, periodicity is not observed.
Clinical Features
Young
children manifest this disease in many different ways, but the classic
picture of malaria, with periodic fever, shivering, and sweating, is not
observed. Malaria can mimic any febrile illness and should be suspected in
any febrile child who has been in a malarious area recently. Older children
may manifest the classic periodicity of fever with chills and shivering.
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Prodrome: After the mosquito bite, children are
asymptomatic while the parasites complete the liver cycle and one
erythrocytic cycle, which takes 8-18 days, depending on the species.
Children then become restless, drowsy, apathetic, and anorexic. Older
children may report aching body, headache, and nausea.
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Gastrointestinal symptoms: Vomiting is very common in
children with malaria, and it may make oral therapy ineffective. Mild
diarrhea is often observed, with dark green mucoid stools. Occasionally,
profuse diarrhea with dehydration and circulatory failure is observed.
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Congenital malaria: Parasitemia in neonates within 7
days of birth implies transplacental transmission. This congenital malaria
is usually associated with placental parasitemia, which sometimes persists
even after adequate treatment with antimalarial drugs. Babies have fever,
are irritable, refuse feeds, and often develop anemia, jaundice, and
hepatosplenomegaly.
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Malaria in immune children: Children living in an area
where malaria is endemic have repeated frequent infections and develop and
maintain partial immunity. These children often develop only a low-grade
fever, anemia, poor appetite, and malaise. Tiredness, restlessness, cough,
and diarrhea are other symptoms that may occur.
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Relapses and recrudescences: Depending on the species
of Plasmodium involved, relapses and recrudescences vary in their
effects. P vivax and P ovale both give rise to hypnozoites
in the liver. P vivax malaria may relapse for up to 3 years and
P ovale for 1-1.5 years. P falciparum and P malariae do
not form hypnozoites, so they do not have true relapses. However, the
disease recrudesces because of surviving erythrocytic forms. While P
falciparum can recrudesce for up to 1 year, P malariae may
continue to cause clinical malarial attacks even 20 years after the
original infection. Only the sporozoites (introduced by the mosquitoes
themselves) can penetrate the liver cells. Thus, if malaria is acquired by
blood transfusion or transplacentally, no infection of the liver occurs
and relapses do not occur.
Physical:
Lab Studies:
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Various techniques to enhance the diagnostic utility
of the peripheral blood smear examination are in use. Fluorescent
staining and microscopy, centrifugation, selective magnetic separation
techniques, and other techniques have been used but have only a moderate
effect.
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Serological tests provide confirmation of past
malaria in patients and are valuable for epidemiological studies. These
tests are also useful for screening donated blood and diagnosing
hyperactive malarial splenomegaly. Among the tests used are the indirect
fluorescent antibody test (IFAT), indirect hemagglutination antibody (IHA)
test, enzyme-linked immunosorbent assay (ELISA), and the immuno-chromatographic
test (ICT) for filariasis.
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The test has high sensitivity and specificity,
requires no special equipment or training, and produces results rapidly.
Findings remain positive for a week or more after treatment and cure,
creating false-positive results in this situation.
Procedures:
Histologic Findings: The appearance of
the parasite varies in the thick and thin films. The thick unfixed film
shows only leucocytes and parasites; erythrocytes are destroyed in the
staining process. The parasites themselves are also altered. Young
trophozoites appear as incomplete rings or spots of blue cytoplasm with
discrete red nuclei. In mature trophozoites, the cytoplasm may be
fragmented, and the various characteristics of the different species are
often indistinct. Gametocytes and schizonts usually retain their
characteristic appearances. Thin film examination is essential for the
accurate identification of plasmodial species, which has an important
bearing on treatment.
Medical Care:
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Oral paracetamol (acetaminophen) is safe and effective
for fever and should be used in doses of 10 mg/kg. This dose can be
repeated 3-6 times a day, as required. If the child has hyperpyrexia,
tepid sponging can bring the temperature down rapidly.
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Many children with malaria develop anemia. Because
onset is gradual, the child withstands a low level of hemoglobin quite
well, and blood transfusions are rarely needed. Standard hematinic therapy
is effective.
Diet:
Management
Blood
schizonticides are the first-line drugs for the treatment of malaria and
must be started as soon as the diagnosis is made or even suspected. They act
on the asexual forms in the erythrocytes and interrupt clinical attacks.
Delay in treatment of P falciparum malaria can lead to development
of severe malaria, which has a poorer prognosis than uncomplicated malaria.
Chloroquine, quinine, quinidine, mefloquine, halofantrine, and artemisinin
compounds are the rapidly acting drugs that can terminate an acute malaria
attack. While chloroquine acts rapidly, resistance is widespread and an
accurate travel history should be obtained before choosing the antimalarial
drug.
P vivax and P ovale
have dormant stages (hypnozoites) in the liver, and the treatment of an
episode of malaria requires eradication of these forms also. The classic
treatment is a 3-day course of chloroquine, followed by a 14-day course of
primaquine. A shorter course of 5 days of primaquine, started with
chloroquine, has been described but is associated with higher relapse rates. |