1) Malaria is a major health problem in many parts of the world, infecting over 3 billion people. It poses significant risks during pregnancy, especially for primigravida women. 2) Malaria in pregnancy can cause maternal complications like anemia, hypoglycemia, acute pulmonary edema, and immunosuppression as well as fetal complications like low birth weight, intrauterine growth retardation, and congenital malaria. 3) Proper diagnosis and treatment are needed to prevent adverse outcomes for both mother and baby.

1. MALARIA in
PREGNANCY
Prof.M.C.Bansal.
Founder principal & Controller ;
Jhalawar Medical college And Hospital, Jhalawar.
Ex. Principal & collenter;
Mahatma Gandhi Medical College And Hospital,
Sitapura, Jaipur

2. INTRODUCTION
• Malaria is a protozoal disease transmitted by
bite of infected female Anopheles mosquito.
• It is Most important parasitic infestation in
humans with a transmission in 109 countries
containing 3 billion people and responsible for
1 – 3 million deaths per year.

3. EPIDEMIOLOGY
There were an estimated 247 million malaria
cases among 3.3 billion people at risk in 2006,
causing nearly a million deaths, mostly of
children under 5 years.
Nearly 2.48 million malaria cases are reported
annually from South Asia of which 75% cases are
contributed by India alone.
. In Africa, perinatal mortality due to malaria is at
about 1500/day.

4. Plasmodium vivax is the predominant malarial
parasite in India accounting for 50.4- 56.4%
cases in the last five years.
Falciparum malaria is the more severe variant
of malaria in the region.
The states most affected in INDIA are UP,
Bihar, Karnataka, Orissa, Rajasthan, Madhya
Pradesh & Pondicherry

6. Malaria in pregnant women
• >50 million pregnant women exposed to
malaria each year.
• ~3.5 million pregnant women infected
Poor birth outcomes
Poor maternal outcome.
• Pregnant women constitute the main adult
risk group for malaria.

7. Gravidity and malaria
• Primigravida have no pre-existing immunity to
placental parasites and are highly susceptible.
• In high transmission areas, primigravida
develop immunity to placental parasites and
are protected in subsequent pregnancies.
• In low transmission areas, multigravida are
unexposed and unprotected

9. ANOPHELES
Mosquito
THE VECTOR…
ANOPHELES CULICIFACIES (RURAL)
ANOPHELES STEPHENSI (URBAN)

11.  They choose their victim by odor.
 Males are more frequently bitten.
 Most common time of bite is late evening to early
morning with peak at midnight.
 Stylets cut & proboscis probe for tiny blood vessels
in the skin. If it does not strike blood proboscis is
withdrawn and struck again at different angle.
 They can fly for few Km.
 Their life span is 2–3 weeks.
 Human blood is needed to lay eggs and nourish
eggs.
SOME FACTS ABOUT ANAPHELES…..

12. Transmission…
Bite of infected mosquito.
Congenitally acquired disease.
Blood transfusion.
Sharing of contaminated needles.
Organ transplantation.

13. CAUSATIVE ORGANISM…
Plasmodium
Apicomplexa group of protozoa, have
specialized complex of apical organelles
involved in host cell invasion.
More than 120 species are present but only 4
are capable of causing HUMAN MALARIA.
p. Vivax
p. falciparum
p. Malariae
p. oval

14. LIFE CYCLE OF PLASMODIUM
• PRIMARY / DEFINITIVE HOST – MOSQUITO
• SECONDARY / INTERMEDIATE HOST - HUMAN

16. Malaria in Pregnancy : Double
Trouble
• Malaria is more common in pregnancy
compared to the general population.
• Malaria in pregnancy tends to be more
atypical in presentation. This could be due to
the hormonal, immunological and
hematological changes of pregnancy.
• The parasiteamia tends to be 10 times higher.
• P. falciparum malaria in pregnancy being
more severe, the mortality is also double (13
%) compared to the non-pregnant population
(6.5%).

17. Pathogenesis of malaria in pregnancy
• During normal pregnancy, the cellular immune
response (Th1) is suppressed to prevent fetal
rejection.
• Malaria stimulates the Th1 response  intrauterine
growth retardation.
• Malaria stimulates expression of an HIV co-receptor
(CCR5) in the placenta.
• Various hypotheses have been put forth to explain
the pathophysiology of malaria in pregnancy.

18. The general immunosupression of pregnancy
Reduced lymph proliferative response
Elevated levels of serum cortisol
To prevent the fetal rejection
Renders the pregnant woman
susceptible to infestations
(This does not explain the diminished susceptibility to
malaria experienced by multigravid women.)
HYPOTHESIS -1

19. HYPOTHESIS - 2
• Placenta is a new organ in the primigravida and
allows the parasites to by-pass the existing host
immunity or allows placenta specific phenotypes of P.
falciparum to multiply.
• Development of placenta specific immunity may thus
explain the decreased susceptibility in multigravida.
• It has been discovered that multigravida women can
form strain-independent antibodies against CSA-
specific parasites, and they demonstrate greatly
diminished parasite load.

20. Hypothesis - 3
• Pregnant women display a bias towards type- 2 cytokines
and are therefore susceptible to diseases requiring type 1
responses for protection like TB, malaria, leishmaniasis etc.
• In infected pregnant women a change of balance of the
local placental environment from TH2 to TH1 has been
observed, consistent with large number of monocytes in
infected placenta. IL-10 levels are decreased, while IFN-g ,
IL-2, and TNF-α levels-hallmarks of a type-1 cytokine
response-are elevated.
• These pro-inflammatory cytokines account for the
pathology of maternal malaria: Elevated levels of TNF-
α are associated with severe maternal anemia;
symptomatology of malaria and localized cytokine elevation
contributes to adverse pregnancy outcomes.

21. Effects of malaria on
pregnant women
MATERNAL EFFECTS:
• Hyperpyrexia
• Hemolytic anemia
• Lactic acidosis
• Folate deficiency
• Bleeding disorders including DIC
• Hypoglycemia
• Acute renal failure
• Acute pulmonary edema
• Cerebral malaria:seizures,delirium
• Jaundice
• Hepatitis
• Hepatic failure
• Post partum haemorrhage
• Circulatory collapse
• Fluid and electrolyte imbalance
• Blackwater fever
• Yellow fever
• Death

22. FETAL AND PERINATAL EFFECTS:
• High risk of abortion
• Higher incidence of preterm delivery
• Intrauterine growth retardation
• Low birth weight
• Intrauterine fetal demise
• Congenital malaria
• Failure to thrive
• High perinatal morbidity and mortality

23. EFFECT OF PREGNANCY ON
MALARIA
• Pregnancy is an immunocompromised state
therefore the hazards of malaria increases.
• Frequency of infection is high during advanced
pregnancy.
• Severity of infection is higher in primigravida.
• Higher morbidity because of complications
following malaria during pregnancy.

24. Role of Placenta, the NEW
ORGAN of pregnancy:
• Incidence of placental involvement during pregnancy in women
living in endemic areas varies between 16 to 60%.
• P. falciparum has the unique ability of cytoadhesion.
• Chondroitin sulfate A and hyaluronic acid have been identified as
the adhesion molecules for parasite attachment to placental cells.
• The parasites sequester along the surface of the placental
membrane, specifically the trophoblastic villi, extravillous
trophoblasts, and syncytial bridges.
• Intervillous spaces are filled with parasites and macrophages,
interfering with oxygen and nutrient transport to the foetus.
• All the placental tissues exhibit malarial pigments (with or even
without parasites).
• These changes impede oxygen-nutrient transfer and can cause
general hemorrhaging.
• These changes contribute to the complications experienced by both
mother and child.

25. Placental malaria

26. CLINICAL
MICROSCOPY
IMMUNOLOGY
MOLECULAR
SEROLOGY
DIAGNOSIS
OF
MALARIA

27. PROGNOSTIC PARAMETERS
• Parasitemia >5%
• Packed cell volume <30%
• Hemoglobin <7.1 gm%
• Hypoglycemia :blood glucose <40 mg%
• Low levels of glucose in cerebrospinal fluid
• Raised venous lactic acid >60 m.mol/L
• Low level of antithrombin 3
• Peripheral schizontemia
• Increased plasma S-nucleotides
• Serum creatinine >3.0mg%
• Blood urea >60.0mg%

28. CLINICAL FEATURE
• Atypical manifestations of malaria are more common
in pregnancy, particularly in the 2nd half of pregnancy.
• Severity of the disease depends on the species of
invading Plasmodium parasite ,the intensity of
parasitemia , the extent of host resistance & the speed
of diagnosis and implement of effective therapy.
• The three stages.
The cold stage
The hot stage
The sweating stage
It is followed by another similar attack in 24-48 hours.

29. • Fever: -Patient may have different patterns of fever - from
afebrile to continuous fever, low grade to hyper pyrexia. In
2ndhalf of pregnancy, there may be more frequent
paroxysms due to immunosuppression.
• Anemia: Most common feature of malaria in pregnancy.
• Splenomegaly: Enlargement of the spleen may be variable.
It may be absent or small in 2nd half of pregnancy.
• Other symptoms besides fever with rigors include
headache,malaise,nausea and vomiting,delirium,hemolytic
jaundice,cachexia.

30. MICROSCOPIC DIAGNOSIS
Light microscopy of thick and thin films by a skilled microscopist
– gold standered
Thick film- diagnosis of malaria, more sensitive
Thin film- species identification
Sample can be collected any time irrespective of fever but
before administration of antimalarials
For best results film should be made soon after collection and in
case of anticoagulant within 2 hrs
Smear should be examined with 100x oil immersion objective
lense 3 times before concluding it negative

31. BENEFITS OF MICROSCOPY
1) Skilled microscopist pick up 5-10 parasite/ml of
blood.
2) species identification along with stage of parasite.
3) determines parasite density.
4) Malarial pigment in neutrophil & monocytes (in
profound anemia).

32. DISADVANTAGES OF MICROSCOPY
1) Time consuming .
2) Skilled technician & infrastructure required.
3) Deep sequestered parasite not deleted.
4) In mixed infection often one species suppresses.
other making detection of suppressed one difficult.

33. RAPID DIAGNOSTIC TESTS ( RDTs )
Immunochromatographic tests to detect plasmodium specific
antigens in blood
Employ monoclonal antibodies directed against targeted parasite
antigens
Currently available rapid Diagnostic Tests are as follows –
Histidine rich protein ii ( HRP-II ) : asexual stages and young
gametocytes of p.Falciparum
Parasite lactate dehydrogenase (pLDH) : p.Vivex , p.Falciparum ,
all 4 plasmodia
Plasmodium aldolase – all 4 plasmodia

34. Performance characteristic of RDTs Sensitivity
WHO- A MINIMUM STANDARD OF 95% SENSITIVITY FOR
P.FALCIPARUM DENSITIES OF 100 PARASITES/L OF BLOOD
AND A SPECIFICITY OF 95%
HRP-II with parasite density 100/ml of blood -90% -
with 10/ml -75%
HRP-II remain positive for 1-3wk.
p LDH remain positive for 5 days.

35. BENEFITS OF RDTs
NOT MUCH TRAINING REQUIRED
EASY TO INTERPRIT
DOES NOT NEED ELECTRICITY
RAPID RESULT
GOOD FOR FAR REACH HEALTH CARE FACILITIES WHERE
MICROSCOPIC DIAGNOSIS IS NOT POSSIBLE
IN SEVERE COMPLICATED MALARIA WITH NEGATIVE PERIPHERAL
PARASITAEMIA DUE TO SEQUESTRATION

36. DISADVANTAGES OF RDTs
1)Cannot distinguish new infection from old
2) Do not quantify parasite load .
3) Detection threshold 40-60 parasites/ml.
4) Storage problem.
5) cost.
6) Cross-reactions with autoantibodies
7) False positive & false Negative results

38. MOLECULAR METHODS
DNA PROBES .
DOT BLOT ASSAY .
PCR AMPLIFICATION.
MASS SPECTROMETRY
FLOW CYTOMETRY

39. SEROLOGICAL TEST
INDIRECT IMMUNOFLUROSCENCE
(using quantitative buffy coat – QBC )
Detect I'm, Gig, IgA.
Indirect haem agglutination .
ELISA
RIA

40. Complications
• Anemia:-
• Malaria can cause or aggravate anemia. It could be due to the following causes:
• Hemolysis of parasitised red blood cells.
• Increased demands of pregnancy.
• Profound hemolysis can aggravate folate deficiency.
• It is more common and severe between 16-29 weeks. It can develop suddenly, in
case of severe malaria with high grades of parasitemia. Pre existing iron and folate
deficiency can exacerbate the anemia of malaria and vice versa.
• Anemia increases perinatal mortality and maternal morbidity and mortality. It also
increases the risk of pulmonary oedema.
• Risk of post-partum haemorrhage is also higher.
• Significant anemia (Hemoglobin <7-8 g%) may have to be treated with blood
transfusion. In view of the increased fluid volume in pregnancy, it is better to
transfuse packed cells than whole blood. Rapid transfusion, particularly whole
blood, may cause pulmonary oedema.

41. Acute pulmonary oedema:-
• It may be the presenting feature or can develop suddenly
after several days.
• More common in 2nd and 3rdtrimesters.
• It can develop suddenly in immediate post-partum period
due to auto transfusion of placental blood with high
proportion of parasitised RBC’s and sudden increase in
peripheral vascular resistance after delivery.
• Aggravated by pre existing anemia and hemodynamic
changes of pregnancy.
• It carries a very high mortality.

42. Hypoglycemia:
• It is also more common in pregnancy.
• Contributing factors:
- Increased demands of hyper catabolic state and infecting parasites.
- Hypoglycemic response to starvation.
- Increased response of pancreatic islets to secretory stimuli (like quinine) leads to
hyper insulinemia and hypoglycemia..
- Hypoglycemia in these patients can remain asymptomatic and may not be detected.
This is because, all the symptoms of hypoglycemia are also caused by malaria viz.
tachycardia, sweating, giddiness etc. Some patients may have abnormal behaviour,
convulsions, altered sensorium, sudden loss of consciousness etc.-
- These symptoms of hypoglycemia may be easily confused with cerebral malaria.
Therefore, in all pregnant women with falciparum malaria, particularly those
receiving quinine, blood sugar should be monitored every 4-6 hours.
- Hypoglycemia can be recurrent and therefore constant monitoring is needed.
- In some, it can be associated with lactic acidosis and in such cases mortality is very
high. Maternal hypoglycemia can cause fetal distress without any signs.

43. Immuno suppression:-
• It makes malaria more common and more severe.
• malaria itself suppresses Immune response.
• Hormonal changes of pregnancy, reduced synthesis of
immunoglobulins, reduced function of reticulo endothelial
system are the causes for immunosuppression in pregnancy.
• This results in loss of acquired immunity to malaria, making
the pregnant more prone for many infection and also
malaria.
• Secondary infections (UTI and pneumonias) and algid
malaria (septicaemic shock) are more common in pregnancy
due to immunosuppression.

44. Congenital malaria:
• It is due to transplacental or peripartal infection of the fetus is being
increasingly reported in 8–33% of pregnancies from both malaria-
endemic and non endemic areas.
• Most cases are following P. falciparum or P. vivax malaria.
• Infants born to non immune mothers with malaria at the time of
labour may develop parasitemia and illness in the first few weeks of
life.
• Congenital malaria usually manifests between the second and eighth
weeks of life (as early as 1 day or delayed by weeks or months) with
symptoms such as fever, anorexia, lethargy, anemia, and
hepatosplenomegaly etc.
• Features suggestive of neonatal sepsis such as irritability, poor
feeding, regurgitation, loose stools, jaundice, and occasionally
drowsiness, restlessness, and cyanosis, may also be seen.

45. Management of Malaria in
Pregnancy:
Management of malaria in pregnancy involves
the following three aspects and equal
importance should be attached to all the three.
• Treatment of malaria
• Management of complications
• Management of labour

46. Treatment of malaria:
Treatment of malaria in pregnancy should be energetic, anticipatory and
careful.
• Energetic:
Don't waste any time.
It is better to admit all cases of P. falciparum malaria.
Assess severity- General condition, pallor, jaundice, BP,
temperature, hemoglobin, Parasite count, SGPT, S. bilirubin, S.
creatinine, Blood sugar.
• Anticipatory:
one should always be looking for any complications by regular
monitoring.
Monitor maternal and fetal vital parameters 2 hourly.
RBS 4-6 hourly; hemoglobin and parasite count 12 hourly; S.
creatinine; S. bilirubin and Intake / Output chart daily.

47. Careful:
• The physiologic changes of pregnancy pose special
problems in management of malaria.
• Certain drugs are contraindicated in pregnancy or may
cause more severe adverse effects. All these factors should
be taken into consideration while treating these patients.
• Choose drugs according to severity of the disease/
sensitivity pattern in the locality.
• Avoid drugs that are contraindicated.
• Avoid over / under dosing of drugs
• Avoid fluid overload / dehydration
• Maintain adequate intake of calories.

48. ANTIMALARIAL IN PREGNANCY
• All trimester –
Chloroquine,Quinine,Artesunate,Artemether,
Artether.
• Second trimester-Mefloquine,Sulfadoxin.
• Third trimester-Mefloquine,Sulfadoxin.
• Contraindication-
Primaquine,Tetracycline,Doxycycline,
Maloprim,Paludrin,Mefloquine,Halofentrin,
Artemesinine.

49. TREATMENT OF UNCOMPLICATED
MALARIA

50. SEVERITY INDICATION DOSES
UNCOMPLICATE
D MALARIA
P.FALCIPARUM Oral quinine 600
mg 8hourly and
oral Clindamycin
450 mg 8 hourly
for 7 days (can
be given
together)
Or Atovaquone –
Proguanil 4 tab
daily for 3 days

51. • Chloroquine -10mg base /kg perorally
followed by 10mg/kg at 24 hours and 5.0 mg
base /kg at 48 hrs.
• For radical care Primaquine is prescribed after
delivery .
• Alternatively,Quinine 10 mg/kg po every 8
hours for 7 days.

52. TREATMENT OF COMPLICATED
MALARIA

53. SEVERITY INDICATION DOSES
SEVERE OR COMPLICATED
MALARIA
ANY PLASMODIUM ARTESUNATE iv 2.4mg/kg at
0,12,24 hr than daily artether
when patient is well enough
to take oral medication.She
can be switched to oral
artesunate 2mg/kg once a day
plus clindamycin or quinine
and clindamycin 450 mg TDS
for 7 days.
ANY SPECIES QUININE iv 20mg/kg loading
dose(no loading dose if
patient took oral quinine or
mefloquine)in 5%Dextrose
over 4 hours than 10 mg/kg iv
over 4 hours in every 8 hours
and Clindamycin 450 mg in
every 8 hours(max dose of
quinine is 1.4 gms).
When the patient is well
enough to take orally switch
on 600 mg oral quinine TDS to
complete 5-7 days and oral
clindamycin 450 mg TDS for 7
days.

54. TREATMENT OF COMPLICATED
MALARIA
• Chloroquine -10mg base/kg iv over
8hrs,followed by 15 mg base/kg over 24
hours.
• Alternatively consider Quinine salt 20 mg/kg
iv infusion over 4 hrs every 8 hrly until oral
intake become permissible.
• Complete 7 days treatment in all.
• Patient with severe anaemia(Hct <20)require
packed cell transfusions.

55. MANAGEMENT OF
COMPLICATION

56. Pulmonary Oedema: Careful fluid management; back
rest; oxygen; diuretics; ventilation if needed.
Hypoglycemia: 25-50% Dextrose, 50-100 ml I.V., followed
by 10% dextrose continuous infusion. If fluid overload is a
problem, then Inj. Glucagon 0.5-1 mg can be given intra
muscularly. Blood sugar should be monitored every 4-6
hours for recurrent hypoglycemia.
Anemia: Packed cells should be transfused if hemoglobin
is <5g%.
Renal failure: Renal failure could be pre-renal due to
unrecognised dehydration or renal due to severe
parasitemia. Treatment involves careful fluid
management, diuretics, and dialysis if needed.

57. Septicaemic shock: Secondary bacterial infections like urinary
tract infection, pneumonia etc. are more common in
pregnancy associated with malaria. Some of these patients
may develop septicaemic shock, the so called 'algid malaria'.
Treatment involves administration of 3rd generation
cephalosporins, fluid replacement, monitoring of vital
parameters and intake and output.
Exchange transfusion: Exchange transfusion is indicated in
cases of severe falciparum malaria to reduce the parasite
load. Patient’s blood is removed and it is replaced with
packed cells. It is especially useful in cases of very high
parasitemia (helps in clearing) and impending pulmonary
oedema (helps to reduce fluid load).

58. Management of labour
• Pregnant women with severe malaria are better managed in
an intensive care unit.
• Falciparum malaria induces uterine contractions, resulting
in premature labour. The frequency and intensity of
contractions appear to be related to the height of the fever.
• Fetal distress is common and often unrecognised.
• Only monitoring of uterine contractions and fetal heart rate
may reveal asymptomatic labour and foetal tachycardia,
bradycardia or late deceleration in relation to uterine
contractions, indicating fetal distress.

59. • All efforts should be made to rapidly bring the temperature
under control, by cold sponging, anti pyretics like
paracetamol etc.
• Careful fluid management is also very important.
Dehydration as well as fluid overload should be avoided,
because both could be detrimental to the mother and/or
the foetus.
• In cases of very high parasitemia, exchange transfusion may
have to be carried out.
• If the situation demands, induction of labour may have to
be considered. Once the patient is in labour, foetal or
maternal distress may indicate the need to shorten the
2nd stage by forceps or vacuum extraction.
• If needed, even caesarian section must be considered

60. SUPPORTIVE MANAGEMENT

61. Household spraying
• Anophelies rest on walls
and ceiling after blood
meal
• DDT is best:
– Affordable, effective, safe
• Requires too much
infrastructure for poor
countries

62. Insecticide Treated Nets
• Bednets impregnated
with permethrin
insecticide.
– Need retreatment every 6
months
– New “permanets” do not
need retreatment
• Act as human-baited
mosquito traps and are
better with high coverage

63. THANK YOU

64. Pathophysiology
• The pathophysiology of malaria in pregnancy
is greatly due to the altered immunity and
availability of a new organ called placenta in
pregnancy. A dramatic breakdown of acquired
immunity occurs in pregnancy, especially in
primigravidae. (Paradoxically, fully effective
ant malaria immunity is transferred to the
child!) Various hypotheses have been put
forth to explain the pathophysiology of
malaria in pregnancy.

65. • Some anti malarial are contra indicated in pregnancy
and some may cause severe adverse effects. Therefore
the treatment may become difficult, particularly in
cases of severe P. falciparum malaria.
• Management of complications of malaria may be
difficult due to the various physiological changes of
pregnancy. Careful attention has to be paid towards
fluid management, temperature control, etc. Also
decisions regarding induction of labor may be difficult
and complex. Fetal loss, IUGR, and premature labor are
common.

66. Pregnancy- malaria and
intensity of transmission:
• Clinical presentation and severity of malaria in pregnancy differ in areas of high transmission
and low transmission due to differences in the level of immunity.
• In high endemic areas, acquired immunity is high, mortality is less common, asymptomatic
and incidental parasitemia are not uncommon.
• Sequestration of MP in the placenta and long standing placental malaria occur and peripheral
blood may be negative for MP.
• Higher parasitemia, particularly in II and III trimester; anemia and altered placental integrity
result in less nutritional support leading to LBW, abortion, stillbirth, premature birth and low
birth weight, and excess infant mortality/morbidity.
• These problems are more common in first and second pregnancies as the parasitemia level
decreases with increasing number of pregnancy.
• HIV infection extends this to all pregnancies and makes it worse.
• The strategy for management of malaria in pregnant population in areas of high transmission
include intermittent treatment and use of insecticide treated bednests.
In areas of low transmission, the problems are dramatically different.
The risk of malaria infection during pregnancy is greater and can result in maternal death and
spontaneous abortion in up to 60% of cases.
Low birth weight can occur even in cases of treated malaria; however, silent malaria rather rare.
The strategy involves measures to avoid malaria by ITMs/chemoprophylaxis and early diagnosis
and prompt treatment of cases.