Malaria is a life-threatening disease caused by parasites that are transmitted via mosquito bites. The most common malaria parasites that infect humans are Plasmodium falciparum, vivax, ovale, malariae, and knowlesi. Malaria symptoms include fever, headache, fatigue, and in severe cases can lead to organ damage or death. Diagnosis involves examining blood smears under a microscope for parasites. Treatment depends on the parasite species and disease severity, with artemisinin-based combination therapies recommended by the WHO. Prevention focuses on avoiding mosquito bites through protective clothing, bed nets, and insect repellents.

1. Malaria

2. What is malaria?
 Malaria is a life-
threatening disease
caused by parasites of
the genus Plasmodium,
that are transmitted to
people through the bites
of infected mosquitoes.
Five species of the genus
Plasmodium that cause
nearly all malarial
infections in humans:
 Falciparum
 Vivax
 Ovale
 Malariae
 Knowlesi

3.  Malaria is spread by
vectors (carriers). In
malaria a mosquito serves
as the vector that carries
and transfers the
infectious agent
(Plasmodium), injecting it
with a bite.
 Transmitted exclusively
though the bite of a
Female Anopheline
Mosquito

4. Epidemiology
 3.3 billion people at risk
worldwide
 98% of Malarial deaths in
Africa
 Second leading cause of
death from infectious
diseases after HIV/AIDS in
Africa
 WHO estimates a
child dies every 45
seconds from
Malaria
 Makes up 20% all
childhood deaths
 50 million women
become pregnant in
Malaria endemic
areas yearly
 Half in areas where
P. falciparum
endemic

6.  Hepatic schizont The
actively dividing,
multinucleated, parasite
form in hepatocytes;
produces no
inflammatory response.
 Trophozoite
Metabolically active
form of the malaria
parasite living within the
RBC; sometimes called
the ring form.

7.  Erythrocytic schizont: multinucleated stage in a
RBC resulting from asexual multiplication of
trophozoite. Each schizont contains a species
determined number of meroziotes.
 Merozoite: the name given to infective schizont
components (see within the schizonts above) that
break out of RBC or hepatocyte and then adhere to
and penetrate a new RBC.

8.  Gametocyte: morpholo
gically distinctive sexual
(male or female) form of
the parasite which
develops from some
trophozoites in RBCs. It
is infective to mosquito.
 Sporozoite: the
morphological form
which develops in the
mosquito salivary gland
and is injected when the
mosquito feeds,
infecting humans.

9. Incubation period
Generally depends on the type of parasite:
 P. falciparum - 9 to 14 days
 P. vivax - 12 to 18 days
 P. ovale - 12 to 18 days
 P. malariae - 18 to 40 days
However, incubation periods can vary from as short
as 7 days, to several months for P. vivax and P.
ovale

10. Life cycle
 Exoerythrocytic cycle:
(hepatic cycle) asexual
reproduction within
hepatocytes producing
schizonts, which break out
of the hepatocytes and
invade other hepatocytes;
occurs as a complete cycle
only in P. vivax and P. ovale.
 Intraerythrocytic cycle: (er
ythrocytic cycle) asexual
reproduction within RBC's.
Involves trophozoite to
schizont, rupture of schizont,
release of merozoites,
invasion of new RBC, and
production of new
trophozoite.

11.  The incubation period is
both species and strain
dependent: e.g. P.
falciparum 8-42 days; P. vivax 5
days to years
 Only gametocytes infect
mosquito
 Only female Anopheles
sp. mosquitos are
vectors (no animal
reservoir)
Sporozoites
Liver
Asexual Reproduction
Single Sporozoite
eventually 10,000 to
>30,000 Daughter
Merozoites
Liver cell eventually bursts

12. Pathophysiology
 Only RBC trophozoites and schizonts cause disease
- no liver pathology caused by hepatic schizonts
or sporozoites
- disease caused by:
1. RBC destruction: - by parasite
- immune hemolysis
- splenic pooling
2. Antigen-antibody complexes in kidney
3. Schizonts of P. falciparum sticking to post-capillary
venules (esp. cerebral) endothelial cells
4. Cytokines and other ill-defined shock,
proinflammatory and capillary leakage producing
products

13. Clinical Manifestations
 First symptoms of malaria are nonspecific
 Lack of a sense of well-being
 Headache
 Fatigue
 Abdominal discomfort
 Muscle aches
 followed by Fever
 similar to the symptoms of a minor viral illness

14. Shortly accompanied by
 Headache
 Chest pain
 Abdominal pain
 Arthralgia (joint pain)
 Myalgia (muscle pain)
 Diarrhea
 Nausea
 Vomiting
 Orthostatic hypertension

15. Classic paroxysms
 Fever spikes
 Chills and rigors
occur at regular intervals, are relatively unusual and
suggest infection with P. vivax or P. ovale
 Childhood febrile convulsions
 Generalized seizures (associated with p. falciparum)

16. Physical findings
 Fever
 Malaise
 Mild Anemia
 Mild jaundice
 Palpable Spleen (in some cases)

17. Severe Malaria
Pathogenesis Clinical features
Cerebral Sluggish flow caused by sticky
knobs on parasitized red cells
leading to stagnant hypoxia
and vascular damage.
Impaired level of
consciousness.
Hyperpyrexia. Convulsions.
Generalized and localized
neurological signs.
Anemia Destruction of parasitized and
nonparasitized red cells by
immune complexes, bone
marrow suppression and
splenic pooling.
Pallor and jaundice. High
output cardiac state.
Renal Acute tubular necrosis
resulting from sluggish blood
flow and hypotension.
Hemoglobinuria.
Oliguria. Haemoglobinuria.
Acute renal failure.
Gastro-intestinal Unknown Diarrhea.

18. Pathogenesis Clinical features
Respiratory Increased pulmonary capillary
permeability.
Cough. Crepitations,
pulmonary edema,
iatrogenic fluid overload,
bronchopneumonia.
Hepatic Unknown. ? Partially due to
haemodynamic changes.
Jaundice (mainly
attributable to haemolysis).
Elevated serum enzyme
levels, impaired elimination
of drugs, prolonged
prothrombin time, bleeding.
Fluid &
electrolyte
balance
Unknown. ? Partially due to
inappropriate release of
antidiuretic hormone.
Increased intravascular
volume. Electrolyte
changes, hypoglycemia,
hyperkalemia and
hemolysis.
Obstetric Sluggish blood flow in
placental vessels leading to
vascular damage.
Fetal death. Premature
labour.

19. Diagnosis
Examination of both thick & thin smears:
 Use shape and size of: trophozoite, schizont and
gametocyte
 Percentage of RBCs with parasites (very rarely over >1%
parasitemia in P. vivax, ovale or malariae)
 Metabolic debris in RBC around parasite (called
Schuffner's dots in P. vivax infection)
 Size of RBCs which contain parasites (P. vivax and ovale
infect younger (larger) RBCs)

20. RDTs or Dipstick/Malaria Rapid
Diagnostic Devices (MRDD) PCR (no-go)
 Rapid, simple, sensitive,
and specific antibody-
based diagnostic stick or
card tests that detect P.
falciparum–specific, in
finger-prick blood samples
 RDTs are replacing
microscopy in many areas
because of their simplicity
and speed, but they are
relatively expensive and
do not quantify
parasitemia
 Antibody and PCR
tests have NO role in
the diagnosis of
malaria except that
PCR is increasingly
used for genotyping
and speciation in
mixed infections

21.  There may be a
persistent
gametocytemia
 Phagocytosed malarial
pigment is sometimes
seen inside peripheral-
blood
 Normochromic,
normocytic anemia is
usual
 WBC count is generally
normal (may be raised in
severe infections)
 Monocytosis,
lymphopenia, eosinopenia,
lymphocytosis and
eosinophilia (after the
acute infection)
 ESR, CRP are high
 Trombocytopenia may
occur

23. Complications
 Acute Renal Failure
 Acute Pulmonary Edema (ARDS)
 Hypoglycemia
 Spontaneous Bleeding
 Convulsions
 Aspiration pneumonia
 Bacterial Sepsis

24. Who is at risk?
 Young children
 Non-immune pregnant women
 Semi-immune pregnant women
 Semi-immune HIV-infected pregnant women
 People with HIV/AIDS
 International travellers from non-endemic areas
 Visiting immigrants from endemic areas and their
children

25. Treatment
 According to WHO, in areas where Malaria is common
treatment should start as soon as signs and symptoms
appear, ideally within 24 hours.
 People with uncomplicated malaria can be treated as
outpatients, while those with severe malaria need to be
hospitalized.
 In non-endemic areas WHO recommends that patients
with uncomplicated or severe malaria should be kept
under clinical observation if possible.
 Patients with P. falciparum infection and severe
symptoms who cannot take their medications orally
should receive them intravenously.
 The best available treatment, particularly for P.
falciparum malaria, is artemisinin-based combination
therapy (ACT)

26.  Clinical cure - eradication of RBC trophoziotes and
schizonts
 Radical cure - eradication of RBC trophozoites and
schizonts and hepatic schizonts (primaquine for 14
days, chloroquine for pregnant women)
 Different drugs required for different stages of life
cycle (eg. primaquine and Malarone for hepatic
schizonts and gametocytes) (mefloquine, quinine
and chloroquine for RBC schizonts and trophozoites)

27. Drug resistance
Resistance to antimalarial medicines is a recurring
problem. Resistance of P. falciparum to previous
generations of medicines, such as chloroquine and
sulfadoxine-pyrimethamine (SP), became
widespread in the 1970s and 1980s. Instead
nowadays WHO recommends ACT.

29. Malaria Control Framework

30. Prevention
 No safe, effective, long lasting vaccine available
 Avoidance of exposure to mosquitoes (dusk and
dawn)
 Insect repellents containing 10–35% DEET (or 7%
Picaridin)
 Suitable Clothing
 Insecticide-impregnated bed nets or other materials