MALARIA

• Epidemiology
• Etiology
• Lifecycle
• Pathogenesis
• Clinical Presentations
• Laboratory Diagonosis
• Complications
• Treatment and management
• Prevention and control
 Epidemiology
• More than 200 million people worldwide have malaria, and more
than 1 million die of it each year, making it the most common lethal
infectious disease. It occurs primarily in tropical and subtropical
areas, especially in Asia, Africa, and Central and South America.
• Malaria in the United States is seen in Americans who travel to areas
of endemic infection without adequate chemoprophylaxis and in
immigrants from areas of endemic infection. It is not endemic in the
United States. Certain regions in Southeast Asia, South America, and
east Africa are particularly affected by chloroquine-resistant strain
ETIOLOGY

• Malaria is the most frequent tropical parasitosis

• Malaria is caused by obligate intracellular protozoa of the genus
Plasmodium, including;
• P. falciparum,
• P. malariae,
• P. ovale,
• P. vivax,
• P. knowlesi.
Life cycle of plasmodium species

• There are two major phases in the life cycle, an asexual phase
(schizogony) in humans and a sexual phase (sporogony) in mosquitoes.
• The life cycle in humans begins with the introduction of
sporozoites into the blood from the saliva of the biting mosquito.
• The sporozoites are taken up by hepatocytes.This exoerythrocytic phase
consists of cell multiplication and differentiation into merozoites.
 Plasmodium vivax and P.ovale produce a latest form(hypnozoites) in the
liver, this form is the cause of relapses seen with vivax and ovale malaria
 Merozoites are released from liver cells and infect red blood cells.
• During the erythrocytic phase, the organism differentiates into a ring-
shaped trophozoite.
• The ring form grows into an ameboid form and then differentiates
into a schizont filled with merozoites. After release, the merozoites
infect other erythrocytes. This cycle in the red blood cell repeats at
regular intervals typical for each species.
• The periodic release of merozoites causes the typical recurrent
symptoms of chills, fever and sweats seen in malaria patient
Pathogenesis of Malaria
Most of the pathologic findings of malaria result from the destruction
of red blood cells. Red cells are destroyed both by the release of the
merozoites and by the action of the spleen to first sequester the
infected red cells and then to lyse them. The enlarged spleen
characteristic of malaria is due to congestion of sinusoids with
erythrocytes, coupled with hyperplasia of lymphocytes and
macrophages.
Malaria caused by P. falciparum is more severe than that caused by
other plasmodia. It is characterized by infection of far more red cells
than the other malarial species and by occlusion of the capillaries with
aggregates of parasitized red cells.
This leads to life-threatening hemorrhage and necrosis, particularly in
the brain (cerebral malaria). Furthermore, extensive hemolysis and
kidney damage occur, with resulting hemoglobinuria. The dark color of
the patient’s urine has given rise to the term “blackwater fever.” The
• . The timing of the fever cycle is 72 hours for P. malariae and 48 hours for the other
plasmodia. Disease caused by P. malariae is called quartan malaria because it recurs
every fourth day, whereas malaria caused by the other plasmodia is called tertian
malaria because it recurs every third day. Tertian malaria is subdivided into malignant
malaria, caused by P. falciparum, and benign malaria, caused by P. vivax and P. ovale.
• Plasmodium falciparum causes a high level of parasitemia because it can infect red
cells of all ages. In contrast, P. vivax infects only reticulocytes and P. malariae infects
only mature red cells; therefore, they produce much lower levels of parasites in the
blood.
• Individuals with sickle cell trait (heterozygotes) are protected against malaria because
their red cells have too little ATPase activity and cannot produce sufficient energy to
support the growth of the parasite. People with homozygous sickle cell anemia are
also protected but rarely live long enough to obtain much benefit.
• The receptor for P. vivax is the Duffy blood group antigen. People who
are homozygous recessive for the genes that encode this protein are
resistant to infection by P. vivax. More than 90% of black West
Africans and many of their American descendants do not produce the
Duffy antigen and are thereby resistant to vivax malaria
• People with glucose-6-phosphate dehydrogenase (G6PD) deficiency
are also protected against the severe effects of falciparum malaria.
G6PD deficiency is an X-linked hemoglobinopathy found in high
frequency in tropical areas where malaria is endemic. Both male and
female carriers of the mutated gene are protected against malaria
Clinical presentation
• The clinical manifestations of malaria range from asymptomatic infection to fulminant
illness and death, depending on the virulence of the infecting malaria species and the
host immune response.
• Common symptoms/signs of uncomplicated malaria
• Fever:above37.5°C(taken from theaxilla)orhistoryofever.
• Loss of appetite, mild vomiting, diarrhea
• Weakness,headache, joint andmuscle pain
• Mildanaemia(mildpallorofpalmsandmucous membranes);occurs commonly inchildren.
• Milddehydration
• Enlarged spleen (in acute malaria it may be minimally enlarged,soft and mildly tender)
Complications/ severe malaria
• Cerebral Malaria
• Splenic rupture
• Renal failure
• Severe anemia
• Severe hemolysis
• Pulmonary edema
• Hypoglycemia
• Respiratory distress
• Liver Failure
• Jaundice
• Shock
Laboratory diagonosis
• The diagnosis of malaria is established by the identification of organisms
on stained smears of peripheral blood using both thick and thin Giemsa-
stained smears. The thick smear is used to screen for the presence of
organisms, and the thin smear is used for species identification.
• It is important to identify the species because the treatment of different
species can differ. Ring-shaped trophozoites can be seen within infected
red blood
• RDTs(Rapid Diagnostic tests) detect malaria antigen (not whole parasites
like the blood slide) and remain positive for 2 to 3 weeks after effective
treatment.
• RDT do not become negative if the patient has already taken
antimalarials
Treatment and management
 For uncomplicated malaria
• All patients: including children <4months of age and pregnant women in 2nd and 3rd trimesters
• First line medicine
Artemether/Lumefantrine
• First line alternative
Artesunate/Amodiaquine
• Second line medicine
Dihydroartemisin/
Piperaquine
If not available:quininetablets
• Pregnant women 1st trimester
ACT currently used
• Severe Malaria
• First line
IV Artesunate
• First line alternative
IV Quinine or Artemether injection
Supportive treatment
Hyperpyrexia ; Give paracetamol 1g every 6hours Child:10mg/kg+tepid sponging + fanning
Convulsions; Give diazepam 0.2 mg/kg (max 10 mg) slow IV or(in adults)IMor0.5 mg/kg rectally.
Hypoglycemia; Adult:dextrose25%2ml/kg by slow IV bolus over 3-5 min
Child:dextrose10%5ml/kg by slow IV bolus over 5-7 min
Pulmonary edema; Regulate the IV infusion(don't over load with IV fluids), Give oxygen, Give
furosemide 1-2 mg/kg
Shock; If systolic BP < 80mmHg(adult) or <50 mmHg (child) or if peripheral
pulse absent and capillary refill is slow (>2seconds)
Raise the foot of the bed ,Give sodium chloride 0.9%byfast IV infusion bolus 20 ml/kg in 15 min
Prevention and control
• There are two components of malaria prevention: reduction of
exposure to infected mosquitoes and chemoprophylaxis
• Chemoprophylaxis is not recommended for all those living in a highly
endemic area like Uganda . However , it is recommended for certain
high-risk groups but is not 100% effective eg pregnant mothers ,
sticklers ,non immune travelers , HIV patients
Reduce human-mosquito contact
• Use insecticide-treated materials(e.g. bed nets)
• Destroy adult mosquitoes by indoor residual spraying of dwellings with
insecticide or use of knock down sprays
• Screen houses
• Carefully select house sites avoiding mosquito infested areas
• Wear clothes which cover the arms and legs and use repellent mosquito coils
and creams/sprays on the skin when sitting outdoors at night
Control mosquito breeding sites
• Eliminate collections of stagnant water where mosquitoes breed, e.g. in empty
cans/ containers, potholes, old car tyres ,plastic bags, and footprints by
disposal, draining, or covering with soil or sand
• Destroy mosquito larvae by dosing stagnant water bodies with larvicides or
with biological methods (e.g. larvae- eating fish)
• Give public health education on the above measures include the need for self
testing (selfcare) using RDT before any medication