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DIFFERENTIAL SLIDES LEGEND
CYCLE 40 SLIDE 3
MALARIA
The term malaria originates from the Italian word Mal’aria, meaning bad air. The Romans knew about malaria 2,000
years ago. They believed that malaria was caused by foul air that resulted from fermentation that seeped out of
marshes and swamps. It is now known that malaria is spread by Anopheles mosquitoes. The disease is caused by a
protozoan, a single-celled endoparasite of the genus Plasmodium.
There are more than 50 species of Plasmodium, only four of which cause human malaria: Plasmodium falciparum,
Plasmodium malariae, Plasmodium ovale, and Plasmodium vivax. Plasmodium vivax is the most common. It usually causes a
mild and very rarely fatal form of malaria. Similarly, Plasmodium ovale causes a mild infection. Plasmodium malariae
causes a severe fever, but it is not usually life threatening. In contrast, Plasmodium falciparum causes severe infection
that kills millions of people every year worldwide. Plasmodium Falciparum is the organism that causes the form of
malaria that is classically thought of whenever the disease is mentioned.
The Plasmodium life cycle is described as an alternation of generations. This means an asexually reproducing generation,
which reproduces by splitting in two, alternates with a generation that reproduces by forming sex cells that fuse with
one another and produce individuals with new combination of traits.
When an infected mosquito bites a person, the plasmodium parasites enter the blood and head immediately for the liver.
Within 30 minutes to one hour, all of the parasites have penetrated the liver; none remain in the circulating blood. Once
inside the liver, the organisms multiply asexually, which means that each one divides into two identical copies of itself.
They continue this reproduction in the liver cells for nine to 16 days, after which they emerge from the liver and invade
red blood cells. The parasites mature in the red blood cells, where they feed on hemoglobin and continue to reproduce
asexually. Eventually they burst out of the blood cells, rupturing them in the process. After the first few reproductive
cycles in the red blood cells, the maturation of all of the parasites becomes more or less co-ordinated, and the blood
cells begin to rupture quite simultaneously. As the blood cells burst, the parasite becomes more or less coordinated, and
the blood cells begin to rupture quite simultaneously. As the blood cells burst, the parasites and their waste products
are released. The newly liberated parasites quickly infect new cells. This series of events repeats several times.
Eventually, however, the asexual stage of the malaria cycle comes to an end, and the final generation of parasites
emerges from the blood cells. Most of them reinvade the liver, where they may remain for a long time.
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Signs and symptoms
Symptoms of malaria include fever, shivering, arthralgia (joint pain), vomiting, anemia (caused by hemolysis), jaundice,
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, and every three days 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. Cerebral malaria is associated with retinal whitening, which may be a useful clinical
sign in distinguishing malaria from other causes of fever.
Severe malaria is almost exclusively caused by Plasmodium 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 is a feature of 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.
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The mainstay of malaria diagnosis has been the microscopic examination of blood using blood films. Although blood is the
sample most frequently used to make a diagnosis, both saliva and urine have been investigated as alternative, less
invasive specimens.
More recently, modern techniques using antigen tests or polymerase chain reaction have been discovered, though these
are not widely implemented in malaria-endemic regions. Areas that cannot afford laboratory diagnostic tests often use
only a history of subjective fever as the indication to treat for malaria.
Ring-forms and gametocytes of
Plasmodium falciparum in human blood
Treatment
When properly treated, a patient with malaria can expect a complete recovery. The treatment of malaria depends on the
severity of the disease; whether patients can take oral drugs or must be admitted depends on the assessment and the
experience of the clinician. Uncomplicated malaria is treated with oral drugs. The most effective strategy for P.
falciparum infection recommended by WHO is the use of artemisinins in combination with other antimalarials
artemisinin-combination therapy (ACT) to avoid the development of drug resistance against artemisinin-based therapies.
Severe malaria requires the parenteral administration of anti malarial drugs. Until recently the most used treatment for
severe malaria was quinine but artesunate has been shown to be superior to quinine in both children and adults.
Treatment of severe malaria also involves supportive measures.
Infection with P. vivax, P. ovale or P. malariae is usually treated on an outpatient basis. Treatment of P. vivax requires
both treatment of blood stages (with chloroquine or ACT) as well as clearance of liver forms with primaquine.
References
1. Malaria; By Bernard A. Marcus, I. Edward Alcamo, David Heymann
2. http://en.wikipedia.org/wiki/malaria
3. http://www.millerandlevine.com/chapter/20/fig-20-7.html
Questions
1. Discuss the life cycle of Plasmodium.
2. Discuss the signs and symptoms of malaria.
3. Discuss the treatment of malaria.
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