MALARIA

PRESENTED BY
DR KOMAL
JR2 MEDICINE
 ETIOLOGY

Malaria is a potentially life-threatening protozoan disease transmitted by

the bite of infected Female Anopheles mosquitoes.
• Six species of the genus Plasmodium
• 1. P. falciparum
• 2. P. vivax
• 3. Two species P. Ovale (curtisi and wallikeri)
• 4. P. malariae
• 5. P. knowlesi
• P. falciparum, P. knowlesi and occasionally P. vivax also
can cause severe illness.
• There are many vectors of malaria Anopheles
culicifacies is the main vector of malaria.
• Extensive breeding is generally encountered following
monsoon rains
• Most of the vectors, including Anopheles culicifacies,
start biting soon after dusk.
• Peak of transmission between July and November
• It is widespread in tropical and subtropical region.
EPIDEMIOLOGY
EPIDEMIOLOGY
• Malaria occurs throughout most of the tropical regions of the
world
• P. falciparum predominates in Africa, New Guinea, and Hispaniola
• P. vivax is more common in Central and South America.
• The prevalence of these two species is approximately equal on
the Indian subcontinent and in eastern Asia and Oceania.
• P. malariae is found in most endemic areas, especially throughout
sub-Saharan Africa, but is much less common.
• P. ovale is relatively unusual outside of Africa and in India it
comprises <1% of isolates.
• P. knowlesi causes human infections commonly on the island of
Borneo and, to a lesser extent, elsewhere in Southeast Asia.
STABLE AND NON-STABLE
TRANSMISSIONS

• Stable transmission: In areas where transmission Is

Constant, frequent, year-round infection.
• People infected repeatedly throughout their lives,
• Nonspecific host defense mechanisms stop the
infection’s expansion.
• Subsequent strain-specific immune response then
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,
“asymptomatic parasitemia “is common among adults
and older children But rates of morbidity and
mortality due to malaria are considerable during early
childhood
• Unstable transmission: areas where transmission is
low, erratic, or focal full protective immunity is not
acquired, and symptomatic disease
• may occur at all ages
PATHOPHYSIOLOGY
 LIFE CYCLE OF MALARIA
The life cycle of malaria involves two hosts: the human and the female Anopheles mosquito.
1. Sporozoite Stage:
o When an infected mosquito bites a human, it injects sporozoites into the bloodstream.
o These sporozoites travel to the liver and invade liver cells.
2. Liver Stage (Pre-Erythrocytic):
o In the liver, the sporozoites mature into schizonts, which then rupture, releasing thousands of
merozoites into the bloodstream.
3. Erythrocytic Stage:
o The merozoites invade red blood cells (RBCs) and multiply asexually.
o This leads to the formation of trophozoites, which develop into schizonts.
o Schizonts rupture, releasing more merozoites to infect new RBCs, causing cyclic symptoms of
malaria (fever, chills).
4. Gametocyte Formation:
o Some merozoites develop into male and female gametocytes in RBCs.
o These gametocytes are ingested by a mosquito when it bites the infected human.
5. Mosquito Stage (Sporogonic Cycle):
o Inside the mosquito’s gut, gametocytes develop into gametes and fuse to form zygotes.
o The zygotes become motile ookinetes, which penetrate the gut wall and form oocysts.
o Oocysts mature and release sporozoites, which migrate to the mosquito's salivary glands, ready to
infect a new human host during the next bite.
• Merozoites in the red blood cells (RBCs) and multiply six- to
twenty-fold every 48 h (P. knowlesi, 24 h; P. malariae, 72 h).
• By the end of the intraerythrocytic life cycle, the parasite
consume two thirds of the RBC’s hemoglobin and grow to
occupy most of the cell called a schizont.
• Initially, the host responds to plasmodial infection by
activating nonspecific defense mechanisms.
• Splenic immunologic and filtrate clearance functions are
augmented in malaria
• The spleen remove damaged ring-form parasites and return
the once infected erythrocytes to the circulation, where
their survival period is shortened
PATHOPHYSIOLOGY OF PLASMODIUM FALCIPARUM MALARIA

 Cytoadherence
• Seen mainly in P. falciparum malaria.
• Infected RBCs express parasite-derived proteins (e.g., PfEMP1) on their surface.
• These bind to endothelial receptors (ICAM-1, VCAM-1, CD36, E-selectin) → RBCs stick to
vascular endothelium.
• Leads to microvascular obstruction, impaired tissue perfusion, and severe disease (e.g.,
cerebral malaria).

 Rosetting
• Infected RBCs bind to uninfected RBCs via parasite ligands.
• Forms “rosettes” of one infected cell surrounded by several normal RBCs.
• Contributes to microcirculatory blockage and tissue hypoxia.

 Agglutination
• Clumping together of infected RBCs with other infected RBCs.
• Mediated by antibodies and parasite proteins.
• Further worsens microvascular flow and increases severity of anemia and organ dysfunction.

These processes are unique to P. falciparum and are key drivers of severe malaria
complications like cerebral malaria, renal failure, and multi-organ dysfunction.
CLASSIFICATION

Uncomplicated Malaria: symptomatic malaria without signs of

severity or evidence[clinical or laboratory] of vital organ dysfunction.
Signs and symptoms are nonspecific.

Severe Malaria : Evidence[clinical or laboratory]of vital organ

dysfunction . Usually due to falciparum or mixed infection.
 CLINICAL FEATURES –
UNCOMPLICATED MALARIA
• The first symptoms of malaria are nonspecific; the lack of
a sense of wellbeing, headache, fatigue, abdominal
discomfort, and muscle aches followed by fever are all
similar to the symptoms of a minor viral illness.
• The classic malarial paroxysms, in which fever spikes,
chills, and rigors occur at regular intervals
• The fever is usually irregular at first (that of falciparum
malaria may never become regular) in P. vivax or P. ovale.
• Mild anemia, mild jaundice
• In some cases, a palpable spleen and slight enlargement of
the liver
 MANIFESTATIONS OF SEVERE
FALCIPARUM MALARIA
Major
Unarousable coma / cerebral malaria:

• Most characteristic and ominous feature:Failure to localize or respond appropriately to

noxious stimuli; coma persisting for >30 min after generalized convulsion; a Glasgow
Coma Score <11, or in young children a Blantyre Coma Score of <3
• Associated with death rate of ~ 20% among adults and 15% among children.
• Onset: Gradual or sudden, sometimes following a convulsion.
• Neurological signs: Diffuse symmetric encephalopathy; focal deficits rare.
• Reflexes: Corneal reflexes preserved except in deep coma; tendon reflexes variable;
plantar flexor/extensor; abdominal and cremasteric reflexes absent; primitive reflexes
absent except pout reflex.
• Eye signs: Divergent eyes, bruxism; 15–40% have retinal hemorrhages, papilledema,
cotton wool spots, or vessel discoloration.
• Seizures: Generalized, often repeated; ~10% adults, 40–50% children; covert seizures
common in children.
• Neurologic sequelae: ~10% of children survivors may have hemiplegia, cerebral palsy,
cortical blindness, deafness, or cognitive impairment—often linked to hypoglycemia,
anemia, prolonged coma, or repeated seizures.
• Prognosis: Most deficits improve within 6 months, but ~10% may have persistent
language or learning deficits.
Acidemia / acidosis Arterial pH of <7.25, base deficit >8 meq/L, or
plasma bicarbonate level of <15 mmol/L; venous lactate level of ≥5 mmol/L;
manifests as labored deep breathing, often termed “respiratory distress.”

Severe normochromic, normocytic anemia Hematocrit of <15% or

hemoglobin level of <50 g/L (<5 g/dL) with parasite density of >10,000/µL

Renal failure:- Serum or plasma creatinine level of >265 µmol/L (>3

mg/dL) or blood urea level of >20 mmol/L

Pulmonary edema / adult respiratory distress syndrome:-

Noncardiogenic pulmonary edema, often aggravated by overhydration;
radiologically confirmed or oxygen saturation <92% on room air with a
respiratory rate >30/min, often with chest wall indrawing and crepitations
on auscultation.
Hypoglycemia :- Plasma glucose level of <2.2 mmol/L (<40 mg/dL). It is
associated with poor prognosis. It results from both a failure of hepatic
gluconeogenesis and increase in consumption of glucose by host.

Hypotension / shock :- Systolic blood pressure of <70 mmHg in children

1–5 years or <80 mmHg in adults; with evidence of impaired perfusion or
capillary refill >2 s.

Bleeding / disseminated intravascular coagulation:- Significant

bleeding and hemorrhage from the gums, nose, and gastrointestinal tract
and/or evidence of disseminated intravascular coagulation.

Convulsions :- More than two generalized seizures in 24 h; signs of

continued seizure activity, sometimes subtle (e.g., tonic-clonic eye
movements without limb or face movement).
Other
Hemoglobinuria:- Macroscopic black, brown, or red urine; not
associated with effects of oxidant drugs and red blood cell enzyme
defects (such as G6PD deficiency).

Extreme weakness :- Prostration; inability to sit unaided

Hyperparasitemia :- Parasitemia level of >5% in nonimmune patients

(>10% in any patient)

Jaundice :- Serum bilirubin level of >50 mmol/L (>3 mg/dL) if

combined with a parasite density of >100,000/µL or other evidence
of vital-organ dysfunction.
 DIAGNOSIS

Clinical Diagnosis:
• History of travel or residence in endemic areas.
• Symptoms: Fever, chills, sweating, headache, fatigue, nausea, and
vomiting. In severe cases, altered mental status, seizures, respiratory
distress, or jaundice.
Physical findings: Splenomegaly, hepatomegaly, pallor (due to anemia),
and in severe cases, signs of cerebral malaria or shock.
LABORATORY DIAGNOSIS
A. Microscopy:
Peripheral Blood Smear (Thick and Thin smears):
o The gold standard for malaria diagnosis.
o Thick smear: More sensitive for detecting the presence of parasites.
o Thin smear: Used for species identification and determining the level of parasitemia.
o Microscopy allows for quantification of parasite load, which helps determine the
severity of infection.
Findings:
o Plasmodium falciparum: Multiple ring forms, crescent-shaped gametocytes.
o Plasmodium vivax: Enlarged RBCs with amoeboid trophozoites, Schüffner's dots.

B. Rapid Diagnostic Tests (RDTs):

• Detect specific malaria antigens (such as Plasmodium HRP2, LDH, or aldolase) in the
blood.
• Provide results within 15-20 minutes.
• Useful in areas with limited laboratory facilities.
• Less sensitive than microscopy, especially for detecting low parasitemia or mixed
infections
[Link] Chain Reaction (PCR):
• Highly sensitive and specific method for detecting malaria parasites and
identifying species.
• Used mainly in research or for confirming cases in areas where malaria is not
common.
• Expensive and requires specialized equipment, making it less suitable for routine
diagnosis in endemic regions.

D. Serology:
• Detects antibodies against malaria parasites.
• Useful for epidemiological studies but not for diagnosing acute malaria because
antibodies take time to develop.

E. Quantitative Buffy Coat (QBC):

• A fluorescent microscopy technique that can detect parasites in the buffy coat
layer of a centrifuged blood sample
• Sensitive but requires specific equipment
Other Investigations:
• Complete Blood Count (CBC): May show anemia, thrombocytopenia,
and elevated leukocytes.
• Liver and Kidney Function Tests: To assess organ damage, especially
in severe malaria cases.
• Blood Glucose: To detect hypoglycemia, especially in severe
falciparum malaria.
• Lactate Levels: To detect metabolic acidosis, which may indicate
severe malaria.
PROGNOSIS
TREATMENT OF VIVAX MALARIA

• Plasmodium vivax malaria is generally less severe than Plasmodium

falciparum malaria but can cause relapses due to the presence of
dormant liver stages (hypnozoites) .
• Treatment involves two main phases:
1. Blood-stage treatment : To clear the parasites from the bloodstream
and resolve the symptoms.
2. Liver-stage (Hypnozoite) treatment : To prevent relapses by targeting
the dormant parasites in the liver.
NOTES

1. Primaquine Testing : Before initiating primaquine, patients should be tested

for Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency to avoid the risk of
hemolysis.

2. Chloroquine-resistant Vivax: In areas with known chloroquine resistance,

Artemisinin-based combination therapy (ACT) is recommended instead of
chloroquine.
o Example ACT regimen: Artemether-Lumefantrine for 3 days.

Special Considerations:
• Pregnancy : Primaquine is contraindicated due to potential risks to the fetus.
• G6PD deficiency : Lower-dose regimens or alternative treatments may be
required to avoid hemolysis
Monitoring and Follow-up:
• Ensure that the patient completes both the blood and liver-stage
treatments to avoid relapse.
• Monitor for side effects, especially with primaquine in G6PD-
deficient patients.
• Patients should be advised on the potential for relapse even after
treatment and to return for evaluation if symptoms recur.
TREATMENT OF FALCIPARUM
MALARIA
1. Uncomplicated Falciparum Malaria
• First-Line Treatment: Artemisinin-Based Combination Therapy (ACT)
• The WHO recommends ACTs as the first-line treatment for
uncomplicated P. falciparum malaria. These combination therapies
involve an artemisinin derivative paired with a longer-acting partner
drug to ensure complete clearance of parasites and reduce the risk of
resistance.
2. Severe Falciparum Malaria
• Severe malaria is a medical emergency and requires parenteral treatment
to reduce mortality. Treatment must begin immediately upon suspicion of
severe malaria, and once the patient can tolerate oral medications, they
should be switched to ACTs to complete the full treatment course.

• ALWAYS BE CAUTIOUS REGARDING WHAT NOT TO DO IN SEVERE MALARIA

Do not use
• adrenaline
• corticosteroids
• intravenous mannitol
• heparin (as anticoagulant)
• Do not overhydrate the patient.
SUPPORTIVE MANAGEMENT IN SEVERE
MALARIA
• Patients with severe malaria should preferably be managed in a critical
care unit
• Hyperpyrexia should be adequately managed as it may lead to coma and
convulsions
• Control of seizures should be achieved using intravenous
benzodiazepines, phenytoin sodium, or phenobarbital with careful
monitoring for respiratory depression
• Blood sugar should be routinely monitored as hypoglycemia is very
common
• Hypokalemia is also a common complication of severe malaria and often
becomes apparent on correction of acidosis. Careful, serial monitoring of
serum potassium with adequate supplementation is suggested
 • Bacterial co infection should always be suspected and treated
empirically with broad-spectrum antibiotics, until the results of cultures
are available.
• In patients with hypotension or signs of dehydration, volume expansion
corrects the hemodynamic abnormalities and is associated with
improved organ function
• Deteriorating respiratory status requires mechanical ventilation and
adequate management of the airway
• Early-positive pressure ventilation helps prevent the high mortality
associated with ARDS in severe malaria
• Patients with renal failure should initially be treated conservatively. Early
dialysis should be instituted if the urine output does not increase and
there is further deterioration of renal parameters
MALARIA IN PREGNANCY

Malaria in early pregnancy causes fetal loss.

It is associated with low birth weight ,congenital malarial infection,
fetal distress, premature labour, still birth and subsequently
increased infant mortality rate.
In areas with unstable transmission pregnant women are prone to
severe infection and likely to develop high Falciparum parasitaemia
complicated by anemia , hypoglycemia and acute pulmonary edema .
PREGNANCY CONSIDERATIONS

 First Trimester:
• Quinine plus Clindamycin for uncomplicated falciparum malaria.

 Second and Third Trimesters:

• ACTs are safe after the first trimester.
• IV Artesunate is the treatment of choice for severe malaria in
pregnancy at any stage
PROPERTIES OF ANTIMALARIAL
DRUGS – SUMMARY

1. Quinine
• CLASS - Quinoline Alkaloid
• PK: Good oral absorption; ↓ in malaria; t½ 16h (malaria).
• Activity : Blood schizonticide; kills P. vivax, P. falciparum gametocytes
• Minor toxicity: Cinchonism, hypotension, ECG changes- QT
prolongation
• Major toxicity: Hypoglycemia, arrhythmias, visual/auditory
disturbance, hypotension, hemolytic uremic syndrome.
[Link]
• CLASS - 4-Amino-quinoline
• PK : Good oral absorption; extensive distribution
• Activity : Blood schizonticide; not active on liver stages
• Minor toxicity : GI upset, pruritus, headache, bitter taste
• Major toxicity :
• Acute - Hypotensive shock, cardiac arrhythmias
• Chronic- Retinopathy, cardiomyopathy
[Link]

• PK : Good absorption; long t½ (~28 days)

• Activity : As chloroquine; active against chloroquine-resistant P. falciparum
• Minor toxicity : Epigastric pain, diarrhea, ECG changes
• Major toxicity : None

[Link]

• PK : Rapid oral absorption

• Activity : Blood schizonticide, chloroquine-resistant strains
• Minor toxicity: GI upset, headache, ECG changes
• Major toxicity: Agranulocytosis, hepatotoxicity
[Link]
• PK : Complete oral absorption; hepatic metabolism
• Activity : Radical cure – kills liver hypnozoites & gametocytes
• Minor toxicity : GI upset, methemoglobinemia
• Major toxicity: Severe hemolysis in G6PD deficiency

[Link]:Class: Arylaminoalcohol, antimalarial (related to

mefloquine).
 Pharmacokinetics:
• Highly variable oral absorption; enhanced with fatty meals.
• Long half-life(~3–4 days)
• Clinical Use :Used only in fixed-dose combination with artemether (ACT –
Artemisinin-based Combination Therapy) for uncomplicated P. falciparum
malaria, including chloroquine-resistant strains.
• Minor Toxicity : Gastrointestinal upset, headache, dizziness.
• Major: None identified.
[Link]
• PK : Good oral absorption; long t½ (14–20 days)
• Activity : Blood schizonticide (all species)
• Minor toxicity : GI upset, dizziness, mood changes
• Major toxicity : Neuropsychiatric effects, seizures

[Link] & Derivatives

• PK: Rapid absorption; short t½ - 1 hour
• Activity : Broad stage specificity; rapid parasite clearance
• Minor toxicity : Neutropenia, ECG changes
• Major toxicity : Rare – anaphylaxis
• The most commonly used in North India is Artemether+Lumefantrine (available
as a common brand name with Lumerax 80)
[Link]

• PK : Good oral absorption; slow elimination

• Activity : Blood stages ( folate antagonist)
• Minor toxicity: Well tolerated
• Majortoxicity : Megaloblastic anemia
[Link]-Proguanil Quinone derivative + Biguanide
• ACTION - Atovaquone inhibits mitochondrial electron transport;
Proguanil inhibits folate synthesis
• USE: Treatment and prophylaxis of P. falciparum
• Contraindications Severe renal impairment, pregnancy,
breastfeeding, hypersensitivity
• DOSAGE Adults : 250 mg atovaquone/100 mg proguanil once
daily for 3 days. *Children* : Weight-based dosing
• SIDE EFFECTS- Abdominal pain, nausea, vomiting, diarrhea,
headache, rash
[Link]: Tetracycline antibiotic Inhibits protein synthesis in
the parasite by binding to the 30S ribosomal subunit
• USE: Prophylaxis and treatment of malaria, often in combination
with quinine
• CONTRAINDICATIONS:
• Pregnancy, children under 8 years (due to risk of teeth discoloration),
hypersensitivity, severe liver disease
• DOSAGE:Adult : 100 mg daily for prophylaxis; 100 mg twice daily for
treatment for 7 days
• SIDE EFFECTS:Photosensitivity, GI upset, esophagitis, vaginal
candidiasis
MALARIA VACCINE -

Name: RTS,S/AS01 (trade name: Mosquirix ).

Type : Recombinant protein vaccine targeting Plasmodium falciparum.
Mechanism : Contains circumsporozoite protein of P. falciparum fused to
hepatitis B surface antigen; induces antibody and T-cell response to block
sporozoite entry into liver cells.
Efficacy : Around 30–40% reduction in clinical malaria and severe cases in
children; protection wanes over time, requiring booster doses.
Schedule ( WHO recommendation): 4 doses — at 5, 6, 7, and 18 months of
age in endemic regions.
Approval & Use : Piloted in Ghana, Kenya, Malawi since 2019; WHO
endorsed in 2021 for broader use in sub-Saharan Africa.
Limitations : Does not replace preventive measures (bed nets,
chemoprophylaxis); works best when combined with other malaria control
strategies.
WHO Recommendation:
• In 2021, the World Health Organization (WHO) recommended the
widespread use of Mosquirix for children in areas with moderate to
high Plasmodium falciparum malaria transmission.

Ongoing Research:
• Other malaria vaccines, including R21, which shows promising early
results with higher efficacy, are under development and clinical trials.
CHEMOPROPHYLAXIS IN MALARIA IN
PREGNANCY
 The choice of prophylaxis depends on local transmission intensity and drug
resistance.
WHO recommendations (high-transmission areas):
• Intermittent Preventive Treatment in Pregnancy (IPTp) with sulfadoxine–
pyrimethamine (SP):
• Start in 2nd trimester (≥13 weeks).
• One dose every 4 weeks until delivery (at least 3 doses).
• Each dose = SP 1500 mg sulfadoxine + 75 mg pyrimethamine, taken as a single oral
dose under supervision.

Low-transmission or travel to endemic area:

• Chloroquine 300 mg base weekly if sensitive area.
• If chloroquine-resistant P. falciparum → Mefloquine 250 mg weekly (can be used in
all trimesters).
• Atovaquone–proguanil is generally avoided unless no alternative, due to limited
safety data.

Doxycycline is contraindicated in pregnancy.

 CHEMOPROPHYLAXIS IN
• TRAVELLERS
Malaria prevention in travellers depends on destination, species prevalence, and
drug resistance patterns.
 General Principles
• Begin prophylaxis before travel to ensure drug tolerance.
• Continue for the recommended period after leaving endemic area to cover
incubation.
• Combine with mosquito bite prevention (bed nets, repellents, protective clothing).

Drug Options
• Chloroquine: 300 mg base weekly; only in chloroquine-sensitive areas. Start 1–2
weeks before travel, continue 4 weeks after leaving.
• Mefloquine: 250 mg weekly; for chloroquine-resistant areas. Start 2 weeks before,
continue 4 weeks after.
• Doxycycline: 100 mg daily; start 1–2 days before, continue 4 weeks after.
Contraindicated in pregnancy & children <8 yrs.
• Atovaquone–Proguanil: 250/100 mg daily; start 1–2 days before, continue 7 days
after leaving. Well tolerated; useful for short trips.
CHEMOPROPHYLAXIS IN CHILDREN
The approach depends on local epidemiology and resistance patterns.
• Intermittent Preventive Treatment in Infants (IPTi) – WHO recommendation in
some high-transmission areas:
• Drug: Sulfadoxine–pyrimethamine (SP).
• Schedule: Given at routine immunization visits (e.g., with DPT2, DPT3, measles
vaccine).
• Dose: Single age-appropriate dose under direct observation.

Seasonal Malaria Chemoprevention (SMC) – For children 3–59 months in Sahel &
similar seasonal areas:
• Drugs: Amodiaquine + SP.
• Schedule: Once monthly during peak transmission season (usually 3–4 months).

Continuous Chemoprophylaxis – For high-risk children (e.g., sickle cell anemia):

• Chloroquine 5 mg/kg base weekly in chloroquine-sensitive areas.
• Mefloquine 5 mg/kg weekly or Atovaquone–proguanil (weight-based daily) in
resistant areas.
 CHRONIC COMPLICATIONS OF
MALARIA
Hyperreactive malarial splenomegaly
(HMS), formerly termed tropical splenomegaly syndrome, arises
from an exaggerated immune response due to chronic or repeated
Plasmodium infections in malaria-endemic areas.
• It is marked by massive splenomegaly (palpable ≥10 cm below the costal
margin) and often accompanying hepatomegaly.
• Immunologically, HMS involves polyclonal hyper-IgM production and high
anti-malarial antibody titres, reflecting ongoing antigenic stimulation.
• Peripheral blood smear is frequently negative for malaria parasites despite
the severe clinical syndrome.
• The diagnosis relies on major criteria: persistent gross splenomegaly, raised
IgM (≥2 SD above local mean), elevated antimalarial antibodies, and
regression with antimalarial therapy.
• Management focuses on long-term antimalarial prophylaxis; chloroquine or
proguanil weekly is common, with alternatives in resistant areas.
Quartan Malaria Nephropathy (QMN) is a
chronic immune-mediated glomerular disease associated with
prolonged Plasmodium malariae infection. It is more common in
children in endemic areas. Persistent antigenemia leads to immune
complex deposition in glomeruli, causing membranoproliferative
glomerulonephritis. Clinically, it presents with proteinuria (often
nephrotic), hematuria, edema, and progressive renal failure.
Diagnosis is supported by malaria serology, renal biopsy, and
exclusion of other causes. Prognosis is poor, with many patients
developing chronic kidney disease despite antimalarial therapy.
BURKITTS LYMPHOMA AND EPSTEIN - BARR INFECTION :
• Malaria related immune dysregulation provokes infection
with lymphoma viruses .
• Childhood burkitt's lymphoma is associated with EBV and
with high transmission of p. falciparum.
 Chronic P. falciparum malaria drives large numbers of EBV-
infected cells through the lymph node germinal centers and
deregulates activation-induced cytidine deaminase, resulting
in DNA damage, c-myc translocations, and sometimes
lymphoma.
 MALARIA CONTROL STRATEGIES (NVBDCP)
[Link] case Detection and Prompt Treatment (EDPT)
2. Vector Control
[Link] Control
• Use of Indoor Residual Spray (IRS) with insecticides
• Use of chemical larvicides like Abate in potable water
• Aerosol space spray during day time
• Malathion fogging during outbreaks
[Link] Control
• Use of larvivorous fish in ornamental tanks, fountains etc
Personal Prophylatic Measures by individuals
• Use of mosquito repellent creams, liquids, coils, mats etc.
• Screening of the houses with wire mesh
• Use of bednets treated with insecticide
• Wearing clothes that cover maximum surface area of the body
THANK YOU