Malaria is a global parasitic disease caused by Plasmodium parasites transmitted via mosquito bites. It is most prevalent in Africa, where it is a leading cause of mortality and disease burden. The document discusses the global scope of malaria, its transmission and life cycle, clinical manifestations ranging from uncomplicated to severe malaria including cerebral malaria, diagnostic criteria, risk factors and prognostic indicators.

1. MALARIA
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2. Global burden of malaria
• Most important parasitic disease of humans
• Disease burden: 300 – 500 Mil. Cases; 90% in
Africa
• 103 countries in the world are malarious.
• 2 Bil. people exposed to the risk of infection
annually.
• Eliminated from north America, Europe and Russia
• Residents of non-endemic areas may also have
• Travel malaria
• Airport malaria
• Mortality very high in this group
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3.  Malaria transmission occurs in more than 100 countries. Majority of which,
possess tropical or subtropical zones where anopheles mosquito habitats
exist.
 A child dies every 5 seconds from malaria in Africa
 New methods estimate the number of malaria cases to be 243 million clinical
cases and 863 thousands deaths (2008 estimates)
 More than 85% of malaria cases and 90% of malaria deaths occur in Africa
south of the Sahara
 Responsible for 1 in 4 childhood deaths in Africa
 Accounts for 10% of Africa’s disease burden
 It is the leading cause of Under-5 mortality in Africa [20%]
 It accounting for about 40% of public health expenditure in many African
homes
 In Nigeria, N132 billion is lost annually from malaria.
Global burden of
malaria
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4. ETIOLOGY
• The parasite (Plasmodium) is introduced into the host through a
bite by a female Anopheles mosquito
• Plasmodium is an obligate intracellular blood protozoa with 100
species but only 4 [+1] species implicated in malaria.
• They are Plasmodium falciparum, vivax, ovale & malariae.
• Plasmodium falciparum is the most common and causes the most
lethal infection in the tropics and subtropics, as it destroys RBCs of
all ages and multiply infects red cells to a high degree
• Plasmodium malariae destroys the aged RBCs, causing a mild
infection.

5. • Plasmodia ovale and vivax destroy young RBCs, resulting in a
mild infection but relapse due to the presence of hypnozoites in
the hepatic tissues.
• Plasmodium falciparum is responsible for 80-90% of malarial
infection either alone or in combination.
• Plasmodium vivax is uncommon in Africa.
• Less common means of infection includes:
-Congenital acquisition through the placenta.
-Infected blood transfusion.
-Perinatally due to mingling of blood during birth.
ETIOLOGY

6. Endemicity and immunity to
malaria
Endemicity refers to the amount or severity of malaria in an area
or community.
 Measured by parasitaemia or palpable spleen rates:
A. Hypoendemicity - little transmission and the disease has little
effect on the population. (<10%)
B. Mesoendemicity - varying intensity of transmission; typically
found in rural communities of the sub-tropics. (10-50%)
C. Hyperendemicity - intense but seasonal transmission;
immunity is insufficient to prevent the effects of malaria on all
age groups. (51-75%)
D. D. Holoendemicity - intense transmission occurs throughout
the year. As people are continuously exposed to MPs they
gradually develop immunity to the disease. (>75%)

7. Endemicity and immunity to
malaria
Depending on the intensity of transmission,
malaria can be stable or unstable, reflecting
different epidemic scenarios.
• Stable malaria: Sustained incidence over several years.
Seasonal fluctuations in transmission may occur but
epidemics are unlikely.
• Unstable malaria: Marked variations in the incidence of
malaria over time. Population does not develop
immunity and people of all ages are susceptible to
severe disease when transmission increases.

8. Predisposition
 Malaria and hemoglobinopathies
• Geographical distribution of sickle-cell gene closely
follows that of endemic P. falciparum malaria
• Subjects with sickle cell trait (Hb AS) have less severe
malaria than individuals with AA genotype
 Susceptibility to malaria is increased by:
• Splenectomy
• Pregnancy (especially primigravidae)
• Malnutrition www.medrockets.com
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9. Pathogenesis
• P. falciparum causes most severe disease because it
can infect RBCs of any age
• Immunity can be natural or acquired
• Natural:
• Duffy-negative blood group-P. vivax (lacks receptor)
• Genotype AS
• Thalassemia
• G6PD deficiency
• Pyruvate Kinase deficiency
• Functional spleen
• Acquired: Following attack of malaria
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10. LIFE CYCLE

12. PATHOLOGY
• It is due to Haemolysis of infected RBCs and adherence of
infected RBCs to capillaries.
• Profound anaemia is seen in prolonged attack due to haemolysis
of RBCs.
• More severe haemolysis due to P. falciparum infection, as it
invades RBCs of all ages.
• Liberation of toxic haemozoin and antigenic substances upon
rupture of schizonts, which may further damage the capillaries.
• Adherence of parasitized cells to capillaries of major organs-
brain, kidney, lungs, gut, liver, could cause organ congestion and
anoxia.

13. OTHER GENETIC FACTORS.
• These factors influence the susceptibility to malaria by reducing the
ability of MP to penetrate the RBCs, thus reduce the severity of
acute malaria & prevalence of chronic malaria.
-HbS
-G-6-PD deficiency
-HbF
-HbE
-Thalassemia
-Duffy-negative genotype
-Well-nourished children (Malnutrition does not increase the severity
of malaria, as well-nourished children are more likely to suffer from
severe malaria)

14.  Innate or Acquired
 INATE- Red cell abnormalities –sickle cell trait, G6PD
deficiency, Thalassaemia trait, ovalocytosis etc. Duffy
antigen in W/Africans and vivax
 ACQUIRED-require repeated exposure. Neonates
protected by maternal Ig G in the first 6 months.
Antiparasite dx occurs at 10 yrs of age in area of stable
transmission.
 Well-nourished children (Malnutrition does not
increase the severity of malaria, as well-nourished
children are more likely to suffer from severe
malaria)
PROTECTION AGAINST MALARIA

15. The clinical course of P. falciparum
Following a bite by an infected mosquito, many people do
not develop any signs of infection. If infection does
progress, the outcome is one of three depending on host
and parasite factors:
A. Asymptomatic parasitaemia
(“clinical immunity”)
B. Acute, uncomplicated malaria
C. Severe malaria
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16. MALARIA – Clinical syndromes
Chronic Disease
Chronic or Recurrent
Asymptomatic
Infection
Placental Malaria
& AnaemiaAnaemia
Infection
During
Pregnancy
Developmental
Disorders
Transfusions
Death
Low
Birth weight
Increased
Infant
Mortality
Acute Disease
Non-severe
Acute Febrile
disease
Cerebral
Malaria
Death

17. ACUTE UNCOMPLICATED MALARIA
-Most cases in tropics and its clinical manifestation (symptoms) includes :
1.FEVER
-commonest symptom in childhood, though variable, showing remarkable
periodicity.
-bouts of fever corresponds to the maturation & rupture of erythrocytic
schizonts with subsequent discharge of merozoites into the
bloodstream.
-P.vivax , ovale .. 48hrs (tertian)
-P.malariae .. 72hrs (quartan)
-P. falciparum .. Irregular tertian (malignant tertian pattern)

18. Acute Uncomplicated contd
-Obscured periodicity is seen in younger children, who are non- or
semi- immune, as it corresponds to the level of parasitaemia.
-Malaria febrile paroxysms are preceded by 3 defined stages,
especially in older children viz the cold, hot & sweating stages.
2. HEADACHE..very common symptom in older children.
3.VOMITTING..bilious especially in the absence of diarrhoea.
4. PALLOR..usually mild to moderate from haemolysis.
5. PAIN & OTHER ACHES..commonly seen in children presenting with
acute malaria.
6. DIARRHOEA..P. falciparum in infants.
7. COUGH..atypical in younger children.
• OTHER SYMPTOMS- General malaise, anorexia,
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19. Clinical signs
-On examination;
• Fever
• Pallor
• Jaundice is not a feature except in haemoglobinuria or if there is
underlying pathology eg in sickle cell anaemia, sepsis, G-6-P-D
deficiency
• Hepatomegaly
• Splenomegaly
• Hepatosplenomegaly
• Tender enlarged spleen (rare cases).
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20. • It is a life threatening condition of P.falciparum malaria.
• It is diagnosed by the presence of asexual form of the
P.falciparum in the peripheral blood smear of a Patient who
presents with a potentially fatal complications of acute malaria,
provided all diagnosis in other systems have been excluded.
• The essential pathology is by deep microvasculature parasite
sequestration with obstruction of vascular flow resulting in
hypoxic-ischaemic injury to the tissues, with greatest affectation
to the brain.
SEVERE MALARIA
(Acute complicated malaria)

21. Types & Diagnostic features of severe
malaria.
• Prostration (generalized weakness)
• Hyperparasitaemia (5% of RBCs or 250,000 cu. ml)
• Cerebral malaria..altered sensorium ( 30minutes)
• Hyperpyrexia (rectal temp  40C)
• Severe anaemia (Hb5.0g/dl or PCV0.15 or Hb3.1mmol/L)
• Severe jaundice (Serum bilirubin  51 mol/L)
• Hypoglycaemia (RBS  2.2 mol/L)
• Renal failure (Oligouria or anuria & Serum creatinine  265mol/L.)
• Shock (hypotension, rapidly thready pulse, pallor)
• Pulmonary oedema (clinical & radiological diagnosis)
• Clotting disturbance (bleeding episodes)
• Electrolyte & Acid-base balance (clinically, low serum levels, pH7.2)

22. SEVERE MALARIA [any of these]
Clinical features:
• impaired consciousness or unrousable coma:
• prostration: generalised weakness so that the patient is unable walk or sit up
without assistance. Child is unable to feed.
• multiple convulsions – more than two in 24 hours
• deep breathing, respiratory distress: acidotic breathing
• circulatory collapse or shock: systolic blood pressure <70mmHg in adults and
<50mmHg in children
• jaundice
• haemoglobinuria: coke coloured urine
• abnormal spontaneous bleeding
• pulmonary oedema: clinical and radiological
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23. SEVERE MALARIA[any of these]
Laboratory findings
• hypoglycaemia: blood glucose <2.2mmol/L or <40mg/dl
• metabolic acidosis: plasma bicarbonate <15mmol/L
• severe anaemia: (Hb < 5g/dl, packed cell volume < 15%,)
• haemoglobinuria
• hyperparasitaemia: Parasite density >250,000/UL of blood or >5%
parasitised red blod cells
• hyperlactataemia: lactate >5mmol/L
• renal impairment: serum creatinine >265micromol/L
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24. CEREBRAL MALARIA
• It is a rapidly progressive encephalopathy due to sludging of the
cerebral capillaries by RBCs parasitized by asexual forms of P.
falciparum and leading to cerebral hypoxia, edema.
• It is the most serious complication of falciparum malaria in children &
occurs usually in children aged 6 mths to 5 yrs
• It is more prevalent in well-nourished children.
• Pathognomonic feature is the presence of ring haemorrhages
surrounding the capillaries & arterioles in a brain biopsy and excess
haemozoin (malarial pigment). Slatey grey appearance of brain
tissue.

25. CEREBRAL MALARIA contd
• The ‘Mechanical theory’ postulates a phenomenom of reduced
deformability and cyto-adherence in parasitized RBCs &
rosetting in unparasitised RBCs causing obstruction of the
cerebral capillaries & arterioles.
WHO diagnostic criteria are
• Asexual parasitaemia of P. falciparum on blood film
• Altered sensorium lasting > 30 minutes. There is either no
response or non-purposeful response to painful stimuli.
• Exclusion of other causes of encephalopathy eg meningitis
[normal CSF ], encephalitis, hypoglycemia

26. • Acute falciparum malaria which may be complicated by ARF &
rarely by AGN.
• Also known to cause Quartan malarial nephropathy as it is
caused by P. malariae. This is rarely reported in recent times.
• BLACKWATER FEVER
-Is a syndrome of intravascular haemolytic episode with
subsequent haemoglobinuria associated with falciparum malarial
infection.
-it is most likely due to hypersensitivity to incompletely killed
parasites & usually follows inadequately treated acute P.
falciparum infection or suppression by quinine.
MALARIAL NEPHROPATHY

27. • ANAEMIA IN MALARIA
Multifactorial causes. They include :
-Haemolysis
-Sequestration of RBCs in RES & deep tissues.
-Dyserythropoiesis
-Capillary haemorrhages
-Haemodilution due to expansion of plasma volume.
-Bone marrow suppression.
-Hypersplenism from hyperreactive splenomegaly
• ALGID MALARIA
-It is characterised by shock [circulatory collapse].
-Usually associated with gram negative sepsis

28. Poor Prognostic symptoms 1
• Clinical
• Marked agitation
• Hyperventilation (respiratory distress)
• Hypothermia (<36.5C)
• Bleeding
• Deep coma
• Repeated convulsions
• Anuria
• Shock

29. Poor Prognostic symptoms 2
• Laboratory
• Hypoglycemia (<2.2 mmol/L)
• Hyperlactatemia (>5 mmol/L)
• Acidosis (pH <7.3, serum HCO3 <15 mmol/L)
• Elevated serum creatinine (>265 mol/L)
• Elevated total bilirubin (>50 mol/L)
• Elevated liver enzymes (AST/ALT 3 times
upper limit of normal, 5-nucleotidase)
• Elevated muscle enzymes (CPK, myoglobin)
• Elevated urate (>600 mol/L)

30. Poor Prognostic symptoms 3
• Haematology
• Leukocytosis (>12,000/L)
• Severe anemia (PCV <15%)
• Coagulopathy
• Decreased platelet count (<50,000/L)
• Prolonged prothrombin time (>3 s)
• Prolonged partial thromboplastin time
• Decreased fibrinogen (<200mg/dL)
• Parasitology
• Hyperparasitemia
• Increased mortality at >100,000/L
• High mortality at >500,000/L
• >20% of parasites identified as pigment-containing trophozoites and
schizonts
• >5% of neutrophils with visible pigment

31. DIAGNOSIS
• In endemic regions, malaria should be considered a cause in of
fever in a febrile child.
• Confirmation is by microscopic demonstration of the parasite in
a thick & thin blood smear stained with Giemsa stain (gold
standard in developing countries)
• Finding of only the Ring forms (asexual forms) of P. falciparum is
diagnostic.
• The thick film reveals the presence and the count[load] of the
parasite while the thin film identifies the plasmodial spp.
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32. • Non-microscopic techniques are been developed and involves
the detection of plasmodial Ag, anti-plasmodial Abs or the
parasitic metabolic products.
• Examples include; paraSight, F-test, ICT malaria P.F test,
optiMal assay, PCR, ELISA,.
• Other investigations, depend on presentation.
DIAGNOSIS
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33. BLOOD FILM
• Thick smears
• Parasite density
• Thin smears
• Specie
identification

34. DIFFERENTIAL DIAGNOSIS
• This is very broad; in fact any “fever” in the tropics is assumed to
be malaria until proven otherwise.
• Viral ailments:
• Influenza, hepatitis & even common cold.
• Typhoid fever,
• Yellow fever,
• Tuberculosis,
• Pneumonia,
• Meningitis,
• Septicaemia.
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35. Aim Of Treating Malaria
• To fight an established infection, and this includes
• Elimination of the parasites.
• Supportive measures to overcome morbidity
associated with infection
• Monitoring to ensure early diagnosis and treatment
of complication that can lead to death within hours.
TREATMENT

36. Clinical Case Management &
Basic Supportive Care
• Rehydration
• Monitor Blood Sugar
• Anticonvulsants –to control seizures – rectal
diazepam.
• Dialysis in renal shut down.
• Blood transfusion for anaemia- PCV < 20%.
• Antibacterial for bacterial infections - aspiration
pneumonia and sepsis
• Exchange blood transfusion
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37. • WHO has recommended the use of Artemisinin Combination Therapy for the
treatment of uncomplicated malaria. The recommended ACTs include:
• Artemether-lumefantrine (Nigeria) 1.5/9 mg/kg twice daily for three days
• Artesunate+Amodiaquine Artesunate 4 mg/kg once dly for 3 days + Amodiaquine
10mg base/kg on days 1, 2, & 3
• Artesunate+Mefloquine Artesunate 4 mg/kg once daily for 3 days + mefloquine 25
mg base/kg (mefloquine 8.3mg/kg daily for 3 days)
• Dihydroartemisinin-piperaquine This a new ACT that has been shown to be safe and
equally effective
UNCOMPLICATED MALARIA

38. Specific Antimalarial Treatment
for Severe Malaria
• The recommended treatment for severe malaria is
Artesunate Injection
• Give 2.4 mg/kg IV bolus, repeat 1.2 mg/kg after 12 hours and
then 1.2 mg/kg daily until patient can tolerate oral medication
(or for a minimum of 48 hours). Thereafter given follow-on
treatment using a full 3-day course of ACT
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39. Possible alternatives if not available include
Intravenous quinine Give 20 mg/kg of Quinine dihydrochloride salt as
loading dose diluted in 10 ml/kg of 4.3% dextrose in 0.18% saline or 5%
dextrose over a period of 4 hours. Then 12 hours after the start of the loading
dose, give 10 mg salt /kg infusion over 2 hours every 12 hours until when
patient is able to take orally. Change oral ACT once patient can tolerate oral
medication
OR
Intramuscular Artemether:- 3.2 mg/kg IM on the first day and then 1.6
mg/kg daily for a maximum of 3 days until the patient can take oral
treatment, then give a full 3-day course of ACT.
Specific Antimalarial Treatment
for Severe Malaria

40. Advantages of ACT:
• High efficacy and rapid clearance of parasites
• Artemisinin reduces gametocyte carriage thus reduces
malaria transmission
• Artemisinin derivatives – most rapidly schizonticidal
antimalarial drugs known to date
• Used for >2 centuries in china and still effective
(artemisinin derivatives do not remain in the blood
stream for long)
• Relatively good safety profile despite initial anxiety
following pre-clinical findings
• Reduction in malaria transmission

41. Prevention & Control
• Good personal hygiene
• Environmental hygiene
• Good Nutrition and immunity
• Early diagnosis and treatment
• Presumptive treatment of severe cases. Make every effort to establish diagnosis in
the laboratory before treatment. However, this should not delay treatment in cases of
suspected severe malaria.
• Ensure compliance
• Protection against mosquito bites
• Chemoprophylaxis- indications
• Sickle cell anaemia
• Patients on immunosuppressive therapies or disease states
• Non-immune or semi-immune children
• Pregnant women
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42. MALARIA CONTROL-
WHAT IS RBM
• This is a global movement mobilizing support for local
initiative. It is a coordinated approach to strengthen public and
private health care. It involves multiple strategies targeted to
meet local malaria control needs. It was established 31st July
1998
• Six Principles of RBM
• Early detection
• Rapid diagnosis and Effective Treatment
• Multiple prevention
• Focused research
• Well coordinated actions
• Dynamic movement
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43. Reduce Contact Between Humans And Mosquitoes
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44. THANK YOU
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