Malaria is caused by Plasmodium parasites transmitted via mosquito bites. It is one of the oldest known diseases, described by Hippocrates. The parasite has a complex lifecycle between humans and mosquitoes. In humans, it causes cyclic fevers as the parasite reproduces in red blood cells. P. falciparum infection can cause severe complications like cerebral malaria. Diagnosis is by blood smear microscopy or rapid tests, looking for the parasite in red blood cells. While most malaria occurs in Africa and other tropical regions, travelers are still at risk if bitten in an endemic area.

1. Malaria
Dr. Shyam Kartikey Dwivedi
Moderator-Dr. Rohinie Dhokane

2. • History of malaria

3. Malaria
• History and Introduction
• Epidemiology of malaria in India
• Life cycle of plasmodium and pathophysiology of
malaria
• Clinical features and severe malaria
• Differential diagnosis
• Complications
• Diagnosis
• Treatment
• Prevention

4. Ancient History of Malaria
• Malaria parasites have been with us since the
dawn of time. They probably originated in
Africa (along with mankind), and fossils of
mosquitoes up to 30 million years old, show
that the malaria vector, the malaria mosquito,
was present well before the earliest history.

5. Malaria and Man

6. Hippocrates and Malaria
• Hippocrates, a physician
born in ancient Greece,
today regarded as the
"Father of Medicine",
was the first to describe
the manifestations of
the disease, and relate
them to the time of year
and to where the
patients lived.

7. Malaria
• Name is derived from Italian
• Mal’ aria or bad air
• Malaria continues to be most important
cause of fever and morbidity in the
Tropical world
•

8. History – Events on Malaria
• 1880 - Charles Louis Alphose Lavern
discovered malarial parasite in wet mount
• 1883 - Methylene blue stain - Marchafava
• 1898 - Roland Ross - Life cycle of parasite
transmission, wins Nobel Prize in 1902
• 1948 - Site of Exoerythrocytic development in
Liver by Shortt and Garnham

9. Major Developments in 20th Century
• 1955 - WHO starts world wide malaria
eradication programme using DDT
• 1970 – Mosquitos develop resistance to DDT
Programme fails
• 1976 – Trager and Jensen in vitro cultivation
of parasite

10. Lavern and Ronald Ross
Pioneered the Events on Malaria

11. Nobel Prizes in Malaria
• The discovery of this
parasite in mosquitoes
earned the British scientist
Ronald Ross the Nobel
Prize in Physiology or
Medicine in 1902. In 1907,
Alphonse Lavern received
the Nobel prize for his
findings that the parasite
was present in human
blood.

12. Introduction
• Malaria is probably one of the OLDEST DISEASES known to
mankind that has had profound impact on our history.
• It is a huge social, economical and health problem,
particularly in the tropical countries.
• Malaria is a vector-borne infectious disease caused by single-
celled PROTOZOAN PARASITES of the genus Plasmodium.
• Malaria is transmitted from person to person by the bite of
female mosquitoes.

13. Female Anopheles Mosquitos
transmit Malaria

14. Global problem

15. What causes Malaria
• Malaria is caused by a parasite called
Plasmodium, which is transmitted via the
bites of infected mosquitoes. In the human
body, the parasites multiply in the liver, and
then infect red blood cells.
• Transmission of Malaria do not occur <160c
and >330c
• Do not occur > 2000 meters altitude.

16. Malaria Kills more people than AIDS
• Malaria kills in one year what AIDS kills in 15
years. For every death due to HIV/AIDS there
are about 50 deaths due to malaria. To add to
the problem is the increasing drug resistance
to the established drug.

17. Who is at risk?
• young children
• pregnant women
• people with HIV/AIDS
• international travelers from non-endemic areas
• immigrants from endemic areas and their children

18. Know malaria and why
• Malaria is an acute and chronic illness characterized by
paroxysms of fever, chills, sweats, fatigue, anemia, and
splenomegaly.
• Malaria is of overwhelming importance in the developing
world today, with an estimated 300 to 500 million cases
and more than 1 million deaths each year.
• Most malarial deaths occur among infants and young
children.

19. • 4 species of Plasmodium were known to cause malaria in
humans:
P. falciparum,
P. malariae,
P. ovale, and
P. vivax.
• In 2004 P. knowlesi (a primate malaria species) was also
shown to cause human malaria.

20. Epidemiology of malaria in India
Season: most common in July-November
Definitive host: Anopheles mosquito
Intermediate host: Man
Vector: Anopheles culicfacies(rural) and
Anopheles stephensi (urban)
Type Incubation period
P vivax 8-17 days (14days)
P falciparum 9-14 days (12 days)
P malariae 18-40 days (28 days)
P ovale 16-18 days (17 days)

21. Modes of malaria transmission
• Bite of female anopheline mosquitoes: Infective
form: sporozoites
• Infection of blood of a malaria patient containing
asexual forms- ‘trophozoite’ induced malaria
1. Trasfusion malaria
2. Congenital malraia
3. Malaria in drug addicts

22. Hosts involved in transmission of malaria
Man Female anopheles mosquito
Secondary host Primary host
Intermediate host Definitive host
Asexual cycle Sexual cycle
Schizogony Sporogony

23. •Life Cycle of Malaria

25. Human cycle of plasmodium
1. Pre Erythrocytic Schizogony
– Development of sporozoites in liver parenchyma
– Liberated merozoites are called as cryptozoites
– No clinical manifestation; no pathological changes
– Blood is sterile
2. Erythorcytic schizogony
– Parasite resides inside RBCs; passes through stages of Trophozoite,
Shcizont, Merozoite
– Parasitic multiplication brings clinical attack of malaria

26. 3. Gametogony
– Some merozoites develop in RBCs of spleen and bone marrow to form
‘Gametocytes’
4. Exo Erythorocytic Schizogony
– Persistence of late tissue phase in liver
– Seen in P vivax and P ovale
– Cause relapses in Vivax and Ovale malaria
– Liberated merozoites are known as ‘Phanerozoites’

27. Mosquito cycle of plasmodium
1. Completion of gametogomy
• Exflagellation of microgamete and maturation of gametes
• Fusion of gametes form Zygote; Zygote matures to
Ookinite
2. Sporogony
• Ookinite develops into oocyst
• On 10th day of infection, oocyst ruptures, relasing
sporozoites; sporozoites reach salivary glands
• Mosquito at this stage is capable of transmitting infection.

28. Once inside the erythrocyte, the parasite
transforms into the ring form, which then
enlarges to become a trophozoite.
These latter 2 forms can be identified with
Giemsa stain on blood smear, the primary means
of confirming the diagnosis of malaria

30. Pathological process
• Fever
• Anaemia
• Immunogenic events
• Tissue anoxia
• Hypoglycemia and lacticacidemia due to
anaerobic metabolism of glucose

31. • Fever – due to rupture of infected
erythrocytes and release of
merozoites in the circulation
• Anaemia – due to sequestration of
infected erythrocytes into spleen and
other organs and bone marrow
supression

32. • Tissue anoxia – due to cytoadherence of
infected RBC in the capillary (p.
falciparum) , obstruction of capillary
• Immunogenic events – due to
proinflammatory mediators, TNF, and
polyclonal activation resulting hyper
gama globulinemia and the formation of
immunecomplex and immunosupression

33. • Cumulative effect of these
pathologic process leads to
cerebral, cardiac, pulmonary,
renal and hepatic failure

34. • Natural immune mechanism prevents
malaria,
Sickle cell, fetal hemoglobin
• New born has passive maternal
antibody and HbF
•

35. • The age between 3 months to 5
years is potentially fatal

36. Febrile paroxysms are characterized by high fever, sweats, and headache,
as well as myalgia, back pain, abdominal pain, nausea, vomiting, diarrhea,
pallor

37. • Paroxysms coincide with the rupture of schizonts
that occurs
 every 48 hr with P. vivax and P. ovale, resulting in fever
spikes every other day- tertian malaria
 every 72 hr with P. malariae, resulting in fever spikes every
3rd or 4th day- quartan marlaria
• Periodicity is less apparent with
 P. falciparum and mixed infections
 travelers from nonendemic regions

38. I. Children with malaria often lack typical paroxysms and have
nonspecific symptoms, including fever (may be low-grade but is
often greater than 104°F), headache, drowsiness, anorexia,
nausea, vomiting, and diarrhea.
II. Signs- splenomegaly (common), hepatomegaly, and pallor due
to anemia.
III. Typical laboratory findings include anemia, thrombocytopenia,
and a normal or low leukocyte count.
IV. The erythrocyte sedimentation rate (ESR) is often elevated

39. Symptoms Signs Lab
Fever Splenomegaly Anemia
Headache hepatomegaly Thrombocytopenia
Drowsiness Pallor Normal/ low TLC
Anorexia Elevated ESR
Nausea
Vomiting
Diarrhea

40. Severe malaria
WHO has identified 10 complications of P. falciparum malaria
that define severe malaria
1. Impaired consciousness
2. Prostration
3. Multiple seizures
4. Respiratory distress
5. Pulmonary edema
6. Jaundice
7. Hemoglobinuria
8. Abnormal bleeding
9. Severe anemia
10. Circulatory collapse
123 CNS
45 RS
6789 Hematological
10 CVS

41. • The most common serious complication is severe
anemia.
• Serious complications that appear unique to P.
falciparum include cerebral malaria, acute renal
failure, respiratory distress from metabolic
acidosis, algid malaria and bleeding diatheses.
• P. falciparum is the most severe form of malaria
and is associated with higher density parasitemia
and a number of complications

42. Unique complications of P.falciparum
• Cerebral malaria
• Algid malaria
• ARF
• Respiratory distress due to metabolic acidosis
• Bleeding diatheses

43. • P.vivax commonly occur with
P.falciparum
• P.malariae associated with
nephrotic syndrome

44. Congenital malaria
• Clinical features- symptoms appear within 10-30
days of life but average is 14hrs to several months
• Fever
• Poor feeding
• Restlessness
• Drowsiness
• Vomitting
• Diarrhoea

45. • Signs- pallor
Icterus
Cynosis
Hepatosplenomegaly

46. Complications
• Abortion
• Miscarriage
• IUGR
• Premature birth
• Neonatal death

47. Parasite and RBCs
• P. falciparum -immature and mature erythrocytes
• P. ovale and P. vivax - immature erythrocytes
• P. malariae- only mature erythrocytes.

48. Diagnosis
• Fever or unexplained systemic illness
• History of travel from endemic area with
previous year ,think about malaria untill
proven otherwise

49. Diagnosis
• The diagnosis of malaria
Giemsa-stained smears of peripheral blood or
rapid immunochromatographic assay.
• Stains used for diagnosis
Giemsa stain >Wright stain or Leishman stain.

50. Thick and Thin blood smears
• The concentration of erythrocytes on a thick
smear is 20-40 times that on a thin smear and is
used to quickly scan large numbers of
erythrocytes.
• The thin smear allows for positive identification
of the malaria species and determination of the
percentage of infected erythrocytes and is useful
in following the response to therapy

51. Diagnosis
• A single negative blood smear does not exclude
malaria.
• Most symptomatic patients with malaria will have
detectable parasites on thick blood smears within
48 hr.

52. Dignostic feature of malaria
• Ring stage- immature tropozyte
• Mature tropozyte
• Schizont
• Gametocyte

53. Differential diagnosis
• Viral infections such as influenza and hepatitis,
• Sepsis,
• Pneumonia,
• Meningitis, encephalitis,
• Endocarditis,
• Gastroenteritis,
• Pyelonephritis,
• Babesiosis, brucellosis, leptospirosis,
• Tuberculosis,
• Relapsing fever,
• Typhoid fever,
• Yellow fever,
• Amebic liver abscess,
• Hodgkin disease, and
• Collagen vascular disease

54. Complications
• Severe malarial anemia (hemoglobin < 5 g/dL) is the most
common severe complication of malaria in children.
• Anemia-
 hemolysis
 removal of infected erythrocytes by the spleen and
 impairment of erythropoiesis
• The primary treatment -blood transfusion.

55. Diagnosis for P.falciparum
• H/O travel within one month from endemic
area
• Parasitemia more then 2%
• Ring form with double chromatin dots
• Erythrocytes infected with more then one
parasite

56. Cerebral malaria
• Cerebral malaria is defined as the presence of coma in a child with P. falciparum
parasitemia and an absence of other reasons for coma.
• Cerebral malaria is associated with long-term cognitive impairment in children.
• Physical findings- high fever, seizures, muscular twitching, rhythmic movement of the
head or extremities, contracted or unequal pupils, retinal hemorrhages, hemiplegia,
absent or exaggerated deep tendon reflexes, and a positive Babinski sign.
• LP- increased pressure and cerebrospinal fluid protein with no pleocytosis and normal
glucose and protein concentrations.
• Treatment –
antimalarial medications
Supportive
treatment of seizures and hypoglycemia.

57. Facts to remember
• Severe disease and death from P. vivax are usually due to severe
anemia and sometimes to splenic rupture.
• P. ovale malaria is the least common type of malaria.
• P. malariae is the mildest and most chronic of all malaria infections.
• Nephrotic syndrome is a rare complication of P. malariae infection that
is not observed with any other human malaria species. Nephrotic
syndrome associated with P. malariae infection is poorly responsive to
steroids.

58. Terminology
Recrudescence after a primary attack may occur from the survival of
erythrocyte forms in the bloodstream.
• merozoites from an exoerythrocytic source in the liver- P. vivax and P.
ovale, or
• persistence within the erythrocyte -P. malariae, P. falciparum(rare).
Congenital malaria
• is acquired from the mother prenatally or perinatally.
• Causes-abortions, miscarriages, stillbirths, premature births, intrauterine
growth retardation, and neonatal deaths.
• Presentation- between 10 and 30 days of age (range 14 hr to several
months of age).
• Signs and symptoms - fever, restlessness, drowsiness, pallor, jaundice, poor
feeding, vomiting, diarrhea, cyanosis, and hepatosplenomegaly.

60. New malaria treatment guidelines in
India
Uncomplicated malaria
Uncomplicated P. vivax-
• Chloroquine for 3 days (Day 1: 10 mg/kg + Day 2: 10 mg/kg + Day 3: 5mg/kg)
• + Primaquine 0.25 mg/kg daily for 14 days
Uncomplicated P. falciparum-
• Artesunate (4 mg/kg body weight) daily for 3 days and
• sulfadoxine pyrimethamine (25 mg/kg + 1.25 mg/kg body weight) on Day 0;
• + Primaquine 0.75 mg/kg body weight single dose on day 2
Mixed Infections (P. vivax + P. falciparum)-
• Full course of artemisinin-based combination therapy (ACT) + Primaquine 0.25 mg/kg
daily for 14 days

61. 1. Treatment of severe falciparum malaria
Preferred regime Alternative regime
IV Artesunate (60mg): 2.4mg/kg on
admission, followed by 2.4mg/kg at 12h &
24h, then once daily for 7 days.
Once the patient can tolerate oral therapy,
treatment should be switched to a complete
dosage of Riamet (artemether/lumefantrine)
for 3 day.
IV Quinine loading 7mg salt /kg over 1hr
followed by infusion quinine 10mg salt/kg over
4 hrs, then 10mg salt/kg Q8H or IV Quinine
20mg/kg over 4 hrs, then 10mg/kg Q8H.
Plus
Adult & child >8yrs old: Doxycycline
(3.5mg/kg once daily)
or
Pregnant women & child < 8yrs old:
Clindamycin (10mg/kg twice daily). Both drug
can be given for 7 days.
Reconstitute with 5% Sodium Bicarbonate &
shake 2-3min until clear solution obtained.
Then add 5ml of D5% or 0.9%NaCl to create
total volume of 6ml.
Slow IV injection with rate of 3-4ml/min or
IM injection to the anterior thigh.
The solution should be prepared freshly for
each administration & should not be stored.
Dilute injection quinine in 250ml od D5%
and infused over 4hrs.
Infusion rate should not exceed 5 mg salt/kg
per hour.

62. 2. Treatment of uncomplicated p.falciparum
Preferred regime Alternative regime
Artemether plus lumefantrine(Riamet)
(1 tab: 20mg artemether/120mg lumefantrine)
Quinine sulphate (300mg/tab)
Weight
Group
Day 1 Day 2 Day3 Day 1-7: Quinine 10mg salt/kg PO
Q8H
Plus
*Doxycycline (3.5mg/kg once a day)
OR
*Clindamycin (10mg/kg twice a day)
*Any of these combinations should be
given for 7 days.
Doxycycline: Children>8yr
Clindamycin: Children<8yr
5-14kg 1 tab stat
then 8hr later
1 tab Q12H 1 tab
Q12H
15-24kg 2 tab stat
then 8hr later
2 tab Q12H 2 tab
Q12H
25-34kg 3 tab stat
then 8hr later
3 tab Q12H 3 tab
Q12H
>34kg 4 tab stat
then 8hr later
4 tab Q12H 4 tab
Q12H
Take immediately after a meal or drink containing at
least 1.2g fat to enhance lumefantrine absorption.
Add primaquine 0.75mg base salt/kg single dose if gametocyte is present at any time during
treatment.

63. Dosage and administration Plasmodium falciparum for young infant
Age Group
Weight
group
Artesunate or *Quinine
0 - 4
months
<5 kg
** IM first dose
Artesunate 1.2
mg/kg or IM
Arthemeter 1.6
mg/kg)
***Oral
Artesunate
2mg/kg/day
day 2 to day 7
Oral
Quinine 10
mg/kgTDS
for 4 days
then 15-20
mg/kg TDS
for 4 days
Source: Malaria in Children, Department of tropical Pediatrics, Faculty of Tropical Medicine, Mahidol
University.
** Preferably Artesunate/Artemether IM on day 1 if available
*** When Artesunate/Artemether IM is unavailable, give oral Artesunate from day 1 to day 7
* Treat the young infant with Quinine when oral Artesunate is not available
Children under 5 kg or below 4 months should not be given Riamet instead treat
with the following regimen (see table).

64. 3. Treatment of malaria caused by p.knowlesi & mixed
infection (p. falciparum + p. vivax)
• Treat as p. falciparum

65. Important notes
Riamet tablets should be taken with or after food.
Patient with acute malaria re frequently averse to food, the dose may be
taken with fluid and encourage patient to resume normal eating as soon as
food can be tolerated.
Watch all patients swallowing the first dose of Riamet® and observe for 1
hour after the intake. In the event of vomiting within one hour of
administration, a repeat dose should be taken.
For small children Riamet® can be crushed, diluted in water and then put
either directly into the mouth using a syringe or given with a spoon.
Riamet may cause fatigue and dizziness. Warn patient not to drive or use
machines.
Instruct patient to report signs/symptoms of QT interval prolongation.

66. 4. Treatment of of malaria caused by p.vivax, p. ovale or p. malariae.
CHLOROQUINE
(150 mg base/tab) 25 mg base/kg
divided over 3 days
PRIMAQUINE
(7.5 mg base/tab)
Day 1 Day 2 Day 3
Start concurrently with CHLOROQUINE 0.5
mg base/kg Q24H for 2 weeks
Take with food
Check G6PD status before start primaquine
In mild-to-moderate G6PD deficiency,
primaquine 0.75 mg base/kg body weight
given once a week for 8 weeks.
In severe G6PD deficiency, primaquine is
contraindicated and should not be used.
10mg
base/kg
stat,
then
5mg
base/kg
5mg
base/kg
Q24H
5mg
base/kg
Q24H
1 tab of chloroquine phosphate 250mg equivalent to 150mg base. Calculation of dose for
chloroquine is based on BASE, not SALT form. 1 tab of primaquine phosphate contains
7.5mg base.

67. Treatment in specific population & situations
Specific
populations
Preferred regime Alternative regime
Pregnancy Quinine plus clindamycin to be given for
7 day
Artesunate plus Clindamycin
for 7 days is indicated if first
line treatment fails
Lactating
women
Should receive standard antimalarial treatment (including ACTs) except for
dapsone, primaquine and tetracyclines, which should be withheld during
lactation
Hepatic
impairment
Chloroquine: 30-50% is modified by liver, appropriate dosage adjustment
is needed, monitor closely.
Quinine : Mild to moderate hepatic impairment-no dosage adjustment,
monitor closely.
Artemisinins : No dosage adjustment
Renal
Impairment
Chloroquine : ClCr<10ml/min-50% of normal dose.
Hemodialysis, peritoneal dialysis: 50% of normal dose.
Continuous Renal Replacement Therapy(CRRT) :100% of normal dose.
Quinine : .ClCr 10-50ml/min : Administer Q8-12H, CLCr<10ml/min :
administer Q24H,Severe chronic renal failure not on dialysis : initial dose:
600mg followed by 300mg Q12H, Hemo- or peritoneal dialysis: administer
Q24H ,Continuous arteriovenous or hemodialysis: Administer Q8-12H.
Artemisinin : no dosage adjustment.

68. Treatment of complications of malaria
• Severe & complicated falciparum or knowlesi
malaria is a medical emergency that requires
intervention and intensive care as rapidly as
possible.
• Fluid, electolyte glucose & acid-base balance
must be monitored.Intake & output should be
carefully recorded.

69. Immediate clinical management of severe manifestations and complications
of P. falciparum malaria
Definitive clinical features Immediate management/treatment
Come (Cerebral malaria) Monitor & record level of consciousness using Glaslow coma
scale, temperature, respiratory, and depth, BP and vital signs.
Hyperpyrexia (rectal body
temperature >40°C)
Treated by sponging, fanning &with an antipyretic drug.
Rectal paracetamol is preferred over more nephrotoxic drugs
(e.g. NSAIDs)
Convulsions A slow IV injection of diazepam(0.15mg/kg, maximum 20mg
for adults).
Hypoglycaemia (glucose
conc. <2.8mmol/L)
Correct with 50% dextrose (as infusion fluids). Check blood
glucose Q4-6H in the first 48hrs.
Severe anaemia (hb <
7g/dl)
Transfuse with packed cells. Monitor carefully to avoid fluid
overload. Give small IV dose of frusemide, 20mg, as
necessary during blood transfusion to avoid circulatory
overload.
Acute pulmonary oedema Prop patient upright (45°), give oxygen, give IV diuretic (but
most patient response poorly to diuretics), stop intravenous
fluids. Early mechanical ventilation should be considered.

70. Immediate clinical management of severe manifestations and complications
of P. falciparum malaria (cont.)
Definitive clinical features Immediate management/treatment
Acute renal failure (urine
output <400ml in 24hrs in
adults or 0.5ml/kg/hr,
failing to improve after
rehydration & a serum
creatinine of >265μmol/L)
Exclude pre-renal causes by assessing hydration status.
Rule out urinary tract obstruction by abdominal examination
or ultrasound.
Give intravenous normal saline
If in established renal failure add haemofiltration or
haemodialysis, or if unavailable, peritoneal dialysis.
Disseminated
intravascular
Coagulopathy (DIVC)
Transfuse with packed cell, clotting factors or platelet.
Usual regime: Cryoprecipitate 10units,platelets 4-8units,
fresh frozen plasma(10-15ml/kg).
For prolonged PT, give vitamin K, 10mg by slow IV injection.
metabolic acidosis Infuse sodium bicarbonate 8.4% 1mg/kg over 30min and
repeat if needed.
if severe, add haemodialysis.
Shock (hypotension with
systolic blood pressure
<70mmHg)
Suspect septicaemia, take blood for cultures; give parenteral
broad-spectrum antimicrobials, correct haemodynamic
disturbances.

71. Monitoring & follow-up
• Blood smear should be repeated daily
(twice daily in severe infection). Within 48-
72 hr after start of treatment, patients
usually become afebrile and improve
clinically except in complicated cases.
• All patients should be investigated with
repeated blood film of malarial parasite
one month upon recovery of malarial
infection, to ensure no recrudescence.

72. Prevention
•Avoid mosquito bites:
Wearing long sleeves, trousers.
Insecticide Treated Bednets
Repellent creams or sprays.

73. Chemoprophylaxis
• Indicated for travellers travel to
endemic areas in Malaysia.
• Mefloquinine 250mg weekly (up to 1
year) or doxycycline 100mg daily (up
to 3 month), to start 1 week before
and continue till 4 weeks after leaving
the area.

74. Dosing schedule for mefloquine
Weight Age No of tablets per
week
< 5 kg < 3 months Not
recommended
5 - 12 kg 3 - 23 months 1/4
13 - 24 kg 2 - 7 yrs 1/2
25 - 35 kg 8 - 10 yrs 3/4
36 and above 11 yrs and above 1

75. Dosing schedule for doxycycline
Weight in kg Age in years No of tablets
< 25 < 8 Contraindicated
25 - 35 8 - 10 ½
36 - 50 11 - 13 ¾
50+ 14+ 1

78. Tx failure of uncomplicated
• A failure to clear malarial parasitaemia and/or resolve clinical
symptoms despite the administration of an antimalarial. So
while drug resistance may lead to treatment failure, not all
treatment failures are caused by drug resistance.
• Treatment failure can also be the result of incorrect dosing,
problems of treatment adherence (compliance), poor drug
quality, interactions with other drugs, compromised drug
absorption, or misdiagnosis of the patient. Apart from leading
to inappropriate case management, all these factors may also
accelerate the spread of true drug resistance by exposure of
the parasites to inadequate drug levels.

79. Tx failure for uncomplicated malaria
• Treatment failures within 14 days of initial treatment
should be treated with a second-line antimalaria.
• the following second-line treatments are
recommended,
• in order of preference:
• ■ an alternative ACT known to be effective in the
region,
• ■ artesunate plus tetracycline or doxycycline or
clindamycin (given for a total of 7 days),
• ■ quinine plus tetracycline or doxycycline or
clindamycin (given for a total of 7 days).

80. Complicated malaria
Initial treatment
• Parenteral Artemisin derivatives (Artesunate, Artemether,
Arteether) or
• Parenteral Quinine
Once patient can take Oral therapy
• Those on parenteral Artemisin derivatives: oral ACT(full course)
ACT- Artesunate Sulfalene Pyrimethamine Combination Therapy
• Those on parenteral Quinine: oral quinine+Doxycycline 7 days
Complicated malaria in pregnancy
• I trimester: parenteral quinine
• II and III trimester: Parenteral Artemisin derivatives

81. Prevention
• Malaria prevention consists of
 Reducing exposure to infected mosquitoes and
 Chemoprophylaxis
• Chemoprophylaxis is necessary for
 all visitors to and
 residents of the tropics who have not lived there since
infancy, including children of all ages.
• Health care providers should consult the latest
information on resistance patterns before prescribing
prophylaxis for their patients.

82. Chemoprophylaxis
• Short term chemoprophylaxis (<6 weeks):
Doxycycline(2 days before to 4 weeks after
leaving area)
• Long term chemoprophylaxis (> 6 weeks):
Mefloquine (2 weeks before to 4 weeks after
leaving area)

84. Thank you