Malaria is a mosquito-borne disease caused by a parasite that is transmitted via the bites of infected Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms like fever and flu-like illness in cycles of 48-72 hours. It is a major global health problem in tropical and subtropical regions, causing over 2.7 million deaths per year. Treatment involves antimalarial drugs, while control relies on preventing mosquito bites through measures like indoor spraying, mosquito nets, and reducing mosquito breeding sites.

2. Definition
 Malaria is a mosquito-borne disease
that causes over 2.7 million deaths per
year according to estimates by the
World Health Organization.
 Quartan malaria; Falciparum malaria;
Biduoterian fever; Blackwater fever;
Tertian malaria; Plasmodium

4. Etiology
•Malaria is caused by a parasite that is
passed from one human to another by
the bite of infected Anopheles
mosquitoes.
•After infection, the parasites (called
sporozoites) travel through the
bloodstream to the liver, where they
mature and release another form, the
merozoites. The parasites enter the
bloodstream and infect red blood cells.

5. Etiology
•The parasites multiply inside the red
blood cells, which then break open
within 48 to 72 hours, infecting more red
blood cells. The first symptoms usually
occur 10 days to 4 weeks after infection,
though they can appear as early as 8
days or as long as a year after infection.
The symptoms occur in cycles of 48 to
72 hours.

6. Etiology
Malaria can also be transmitted from a mother to her
unborn baby (congenitally)and by blood transfusions.
Malaria can be carried by mosquitoes in temperate
climates, but the parasite disappears over the winter.The
disease is a major health problem in much of the tropics
and subtropics. The CDC estimates that there are 300-500
million cases of malaria each year, and more than 1 million
people die from it. It presents a major disease hazard for
travelers to warm climates.In some areas of the world,
mosquitoes that carry malaria have developed resistance to
insecticides. In addition, the parasites have developed
resistance to some antibiotics. These conditions have led to
difficulty in controlling both the rate of infection and
spread of this disease.

7. Malaria Life Sporogony
Cycle Oocyst
Life Cycle Sporozoites
Mosquito Salivary
Zygote Gland
Hypnozoites
Exo- (for P. vivax
and P. ovale)
erythrocytic
(hepatic) cycle
Gametocytes
Erythrocytic
Cycle
Schizogony

8. Clinical presentation
 Early symptoms
 Headache
 Malaise
 Fatigue
 Nausea
 Muscular pains
 Slight diarrhea
 Slight fever, usually not intermittent
 Could mistake for influenza or gastrointestinal
infection

9. Clinical presentation
 Acute febrile illness, may have periodic febrile
paroxysms every 48 – 72 hours with
 Afebrile asymptomatic intervals
 Tendency to recrudesce or relapse over months to
years
 Anemia, thrombocytopenia, jaundice,
hepatosplenomegaly, respiratory distress
syndrome, renal dysfunction, hypoglycemia,
mental status changes, tropical splenomegaly
syndrome

10. Malaria Transmission Cycle
Exo-erythrocytic (hepatic) Cycle:
Sporozoires injected Sporozoites infect liver cells and
into human host during develop into schizonts, which release
blood meal merozoites into the blood
Parasites
mature in
mosquito
midgut and Dormant liver stages
MOSQUITO HUMAN
migrate to (hypnozoites) of P.
salivary vivax and P. ovale
glands
Erythrocytic Cycle:
Merozoites infect red
blood cells to form
Some merozoites schizonts
Parasite undergoes
sexual reproduction in differentiate into male or
the mosquito female gametocyctes

11. Differential diagnosis
At the onset of the disease it may be very difficult to
differentiate malaria from viral fevers.
Jaundice and fever is also seen in viral hepatitis and
other forms of hepatitis, cholecystitis and hepatic
abscess.
Dengue, Leptospirosis and hemolytic anemia have the
common triad of pallor, icterus and splenomegaly.

12. As the disease progresses
The patient becomes more drowsy and breathless
suggesting ALI and ARDS.The O2 concentration
starts to drop and respiratory alkalosis sets in.
Eventually he may be started on mechanical
ventillation.
The kidneys start to fail and urine output lessens
signifying acute renal failure.
Shock,hypoglycemia, lactic acidosis and DIC
complete the picture of MOSF.

14.  The WHO publication, Drug resistance in malaria,
describes the state of knowledge about this problem
and outlines the current thinking regarding strategies to
limit the advent, spread and intensification of drug-
resistant malaria.

15.  Resistance of Plasmodium falciparum to choloroquine,
the cheapest and the most used drug is spreading in
almost all the endemic countries.

16. Treatment of Malaria
 sulfadoxine-pyrimethamine
 chloroquine
 quinine
 mefloquine
 Artemisinin compounds

17. sulfadoxine-pyrimethamine
 These drugs act by sequential inhibition of enzymes of
folate metabolism. Resistance to these drugs has
developed over the past 30 years and is now wide
spread. Resistance develops very rapidly and remains
stable due to a single point mutation.

18. chloroquine
 Chloroquine acts by getting accumulated in the food
vacuole where it inhibits heme polymerase. Resistant
strains are able to efflux the drug by an active pump
mechanism and release the drug at least 40 times faster
than sensitive strains, thereby rendering the drug
ineffective.

19. quinine
 Resistance has brought this drug back to the limelight.
Quinine remains quite effective even after extensive
use.

20. mefloquine
 Resistance develops when the parasite is able to efflux
the drug. Initially it was given at dose of 15mg/kg and
was combined with sulfadoxine/pyrimethamine to
reduce emergence of resistance.

21. Artemisinin compounds
 These are peroxide antimalarials which release carbon
centred free radicals when they come in contact with
heme.

22. Objectives of monitoring antimalarial drug
resistance
 Evaluate the efficacy of first- and second-line drugs
used in the treatment of malaria
 Provide information for action

23. Tools for Monitoring
1. Therapeutic efficacy tests
2. In vitro tests
3. Molecular markers

24. Methods of Control
 Methods used to prevent the spread of disease, or to
protect individuals in areas where malaria is endemic,
includeprophylactic drugs, mosquito eradication, and
the prevention of mosquito bites

25.  The continued existence of malaria in an area requires
a combination of high human population density, high
mosquito population density, and high rates of
transmission from humans to mosquitoes and from
mosquitoes to humans.

26.  Vector control
 Prophylactic drugs
 Indoor residual spraying
 Mosquito nets and bedclothes
 Vaccination

27. Vector control
 It is done by removing or poisoning the breeding
grounds of the mosquitoes or the aquatic habitats of
the larva stages, for example by filling or applying oil to
places with standing water.

28. Prophylactic drugs
 Several drugs, most of which are also used for
treatment of malaria, can be taken preventively.
Generally, these drugs are taken daily or weekly, at a
lower dose than would be used for treatment of a
person who had actually contracted the disease.

29. Indoor residual spraying
 Indoor residual spraying (IRS) is the practice of
spraying insecticides on the interior walls of homes in
malaria affected areas.

30. Mosquito nets and bedclothes
 Mosquito nets help keep mosquitoes away from people,
and thus greatly reduce the infection and transmission
of malaria.

31. Vaccination
 Vaccines for malaria are under development, with no
completely effective vaccine yet available. Presently,
there is a huge variety of vaccine candidates on the
table.

32. Other tests
Generally the complete blood counts and platelets counts
are of little benefit in the diagnosis but aid in
assessing the severity and complications of the
ongoing infection.
PfHRP2 dipstick or card test: monoclonal ab captures
the parasite antigens. Only for falciparum malaria.
LDH dipstick or card test

33. Drugs used to treat Malaria-
First group
 CHQ, Amiodaquine
 Quinine, Quinidine
 Mefloquine, Halofantrine
 Lumefantrine

34. First group-adverse
reactions
GI disturbances-nausea, vomiting, diarrhoea and
erosive or hemorrhagic gastritis with abdominal pain and
hematemisis at times.
Cardiovascular instability- Prolonged QTc ventricular
tachyarrythmia and hypotension
CNS-disorientation, abn behaviour, seizure
Metabolic- hypoglycemia
ALWAYS CHECK – K, MG, SUGAR before starting

35. Drugs used to treat malaria
 Doxy, Tetra – pregnancy, children, hepatic
 Sulfadoxine-Pyrimethamine – sulfa allergy, renal
failure
 Artemisin derivatives - safe

36. Drugs used to treat
Malaria-others
 Clindamycin
 Azithromycin
 Proguanil
 Dapsone
 Primaquine

37. Intravenous anti-malarial
therapy- Indications
Presence of vomiting
Inability to start oral therapy may also be due to altered
mental alertness and seizures.
Patients who are intubated and on ventillators.
Those who are critically ill.

38. Intra-venous therapy
Chloroquine: intravenous 10 mg/kg max 600mg over 6-8
hrs followed by 15mg/kg max 900mg over next 24 hrs
as slow infusion.
Quinine : intravenous 20mg/kg over 4 hrs; then
10mg/kg(max 600mg)three times a day.

39. Intra-venous therapy-severe
f.malaria
Artesunate 2.4mg/kg stat; followed by 2.4mg/kg at 12 hrs, 24hrs and
then daily. OR
Artemether 3.2mg/kg stat im; then 1.6mg/kg od im.
PLUS
Add quinine 20mg salt/kg over 4 hrs; followed by 10mg/kg over 2-8
hrs slow infusion thrice a day.
PLUS
Doxy 100mg bd / tetra 250mg (4mg/kg) qds

40. Other supportive therapy
 Maintain acid-base balance
 Maintain blood sugar
 Add folvite for hemolysis
 Blood transfusions
 Exchange transfusion

41. END