MALARIA IN PREGNANCY
I. OBJECTIVES
At the end of the session you should be able to:
1. Outline the causes of malaria in pregnancy
2. Outline clinical features of malaria in pregnancy,
3. Describe maternal and fetal effects of malaria in
pregnancy
4. Describe the maternal fetal immunity for malaria in
pregnancy,
5. Describe treatment of malaria in pregnancy and
lactating mothers
6. Describe the WHO package for the prevention and
control of malaria during pregnancy
II. BACKGROUND
• Burden of the disease:
– 2 billion people affected worldwide.
– 1-2.5 million deaths annually (mostly pregnant
women, infants 0-5 years and HIV patients).
• Greatest challenge today is Resistance to
Drugs
– Incidences have risen in recent years, probably
due to increasing resistance to antimalarial
medicines.
III. CAUSES OF MALARIA
• Protozoa:
– Genus: Plasmodium.
– Species that infect humans are
–P. falciparum,
–P. vivax,
–P. ovale and
–P. malariae.
• Vector: Female anopheline mosquito
• Occasional infections with monkey malaria
parasites, such as P. knowlesi, also occur.
IV. CLINICAL FEATURES
I. Uncomplicated malaria
• Clinical features include:
– Headache, lassitude, fatigue, abdominal
discomfort and muscle and joint aches,
– Followed by fever, chills, anorexia, vomiting and
worsening malaise.
• Infection with P. vivax and P. ovale, more than
with other species, can be associated with welldefined malarial paroxysms, in which:
– Fever spikes, chills and rigors occur at regular
intervals.
CLINICAL FEATURES cont
II. Severe/complicated malaria
One or more of the following criteria + the
presence of asexual parasitaemia defines severe
malaria.
• Cerebral malaria/ unarousable coma
– at least for 30min
• Metabolic acidosis:
– Arterial pH < 7.25 or plasma bicarbonate level of <
15 mmol/l or Venous lactate level of > 15 mol/l.
• Severe haemolytic anaemia/black water fever
– Usually is normocytic normochromic anaemia.
CLINICAL FEATURES: complicated malaria cont
• Hypoglycaemia
– RBG < 40 mg/dl (2.2 mmol / l
• Acute renal failure
• Pulmonary oedema / adult respiratory distress
syndrome
• Disseminated intravascular coagulation (DIC),
• Hypotension
– 2°bacterial infections may → septicaemic shock
• Convulsions
NOTE: If untreated, severe malaria is almost always fatal.
Other manifestations of severe malaria, which
do not by themselves define the condition
• Impairment of consciousness less marked than
unarousable coma.
• Prostration and weakness
– Patient cannot sit or walk with no obvious
neurological explanation.
• Hyperparasitaemia:
• Hyperpyrexia:
– Rectal temperature above 40° C (104° F) in adults
and children.
V. MATERNAL EFFECTS OF MALARIA
1. Anaemia in pregnancy
•
More common and severe young primigravidae
•
Starts in mid trimester btn 16 – 24 th weeks of GA
Mechanisms:
a. Haemolysis and sequestration of infected
RBCs into the RES.
b. Haemolysis of non-parasitized RBCs
Non-parasitized RBCs may be may be opsonized
and develop auto-antibodies that make them prone
to haemolysis. Such opsonized RBCs are
sequestrated into the spleen and removed
from circulation by lympho-macrophages
Malarial anaemia in pregnancy cont
c. Bone marrow suppression and
dyserythropoiesis (ineffective
erythropoiesis):
•
Tumor necrosis factor (TNF) is thought to
mediate bone marrow suppression by inducing
dyserythropoiesis and reducing erythroid
proliferation.
d. Loss of appetite
VI. FETAL EFFECTS OF MALARIA
1. Pyrexia is associated with
– Induction of uterine contractions leading to
 Abortions, preterm labour,
–
IUFD and fetal distress.
2. Placental Parasitization:
• Presents with clogging of the intervillous spaces
with macrophages (Placental Reaction), which is
most marked during the second half of pregnancy:
•
Ultimate effect of placental parasitization:
– IUGR, LBW, IUFD, SB
VII. IMMUNITY IN ENDEMIC AREAS
1. Maternal immunity
• Generally, immunity declines in pregnancy
– Probably due to increased levels of cortisol,
hence increased susceptibility to falciparum
malaria in pregnancy
• Immunity for malaria decrease is more
marked in primes and younger women
particularly in the third trimester, than in
multips and older women.
2. Fetal immunity in endemic areas
Protective mechanisms of the fetus in utero
a. Immune mother transmit passive immunity
(antimalarial IgG) to the fetus.
The few parasites that succeed are destroyed by
the antimalarial IgG
b. The placenta greatly limits the number of
parasites gaining access into the fetal
circulation.
c. Falciparum parasites do not grow well in fetal
RBC containing Hb F.
Fetal immunity in endemic areas cont
IMPORTANT NOTE:
1. These protective mechanisms wane after
birth
2. In non endemic areas usually there is low
maternal immunity, hence no protection
against development of congenital
anaemia. Therefore, such babies may be
stillborn or suffer ENND
VIII. DIAGNOSIS OF MALARIA
1. Importance
– Help to reduce unnecessary use of antimalarials.
– High specificity can reduce unnecessary
treatment with antimalarials and improve
differential diagnosis of febrile illness.
2. Methods
• The diagnosis of malaria is based on:
– Clinical diagnosis - has very low specificity
– Detection of parasites in the blood.
DIAGNOSIS OF MALARIA cont
•
If blood results are not readily available,
– Weigh the risk of withholding antimalarial treatment
against the risk associated with antimalarial
treatment when given to a patient who does not
have malaria
•
Methods in use for parasitological diagnosis
i. Light microscopy
Low cost, high sensitivity and specificity when
used by well-trained staff.
ii. Rapid diagnostic tests (RDTs)
• Used to detection of parasite antigen
DIAGNOSIS OF MALARIA cont
• In areas of high stable malaria transmission,
– Under fives should be treated on the basis of a
clinical diagnosis.
– A parasitological diagnosis is recommended before
treatment is started in:
• Older children and adults
• Pregnancy
• All suspected cases of severe malaria,
• In the absence of or a delay in obtaining
parasitological diagnosis, patients should be
treated for severe malaria on clinical grounds.
IX. RESISTANCE TO ANTIMALARIAL DRUGS
• Resistance has arisen to all classes of
antimalarials except, as yet, to the artemisinin
derivatives.
• Resistance can be prevented, or its onset
slowed considerably,
– By combining antimalarials with different mechanisms
of action and ensuring very high cure rates through
full adherence to correct dose regimens
• Resistance to antimalarials has been
documented for P. falciparum, P. vivax and,
recently, P. malariae.
RESISTANCE TO ANTIMALARIALS cont
• In P. falciparum, resistance has been observed
to almost all currently used antimalarials
(amodiaquine, chloroquine, mefloquine, quinine
and sulfadoxine–pyrimethamine) except for
artemisinin and its derivatives.
• The geographical distributions and rates of
spread have varied considerably
• Impact of resistance
– Increased the global malaria burden and is a major
threat to malaria control.
X. ANTIMALARIALS IN PREGNANCY
• No sufficient information on the safety and
efficacy of most antimalarials in pregnancy,
particularly for exposure in the first trimester,
and so treatment recommendations are different
to those for non-pregnant adults.
ANTIMALARIALS IN PREGNANCY cont
• The antimalarials considered safe in the first
trimester of pregnancy are
– Quinine, chloroquine, proguanil, pyrimethamine and
sulfadoxine–pyrimethamine.
• Of these, quinine remains the most effective and
can be used in all trimesters of pregnancy
including the first trimester.
– Amodiaquine, chlorproguanil- dapsone, halofantrine,
lumefantrine and piperaquine
• Have not been evaluated sufficiently to permit
positive recommendations.
ANTIMALARIALS IN PREGNANCY cont
– Sulfadoxine–pyrimethamine
• Is safe but may be ineffective in many areas
because of increasing resistance.
– Primaquine and tetracyclines
• Should not be used in pregnancy.
NOTE:
Despite these many uncertainties, effective treatment
must not be delayed in pregnant women.
XII. TREATMENT OF MALARIA IN PREGNANCY
I. UNCOMPLICATED MALARIA
• First trimester:
– Quinine (orally) for 7 days.
– ACT should be used if it is the only effective
treatment available.
• Second and third trimesters:
– Artemether plus Lumefantrine (ALu)
TREATMENT OF MALARIA IN PREGNANCY cont
II. SEVERE MALARIA
• Quinine 10 mg/kg body weight
– Dilute in 5 – 10 ml/kg body weight of 5% Dextrose or
dextrose saline
– Infused over 4 hours and repeated every 8 hours
Drop rate per minute = amount of fluid to be infused x 20 (drop factor)
Time period to be infused (in minutes)
• Discontinue infusions once the patient is able to take oral
medication, alternatively a full course of Artemether plus
Lumefantrine (ALu) should be for 7 days
TREATMENT OF MALARIA IN PREGNANCY cont
• Dilution of quinine for i.m
– Dose: 10 mg/kg
– Dilute four –times in water for injection or
normal saline to a concentration of 60 mg/ml.
This dilution minimizes the risk of abscess
formation
XIII. WHO package of interventions for the
prevention and control of malaria during
pregnancy
1. Use of insecticide treated nets (ITNs) to
prevent infection
2. Intermittent Preventive Treatment (IPT)
To prevent asymptomatic infections among
pregnant women living in areas of moderate or high
transmission of P. falciparum
3. Effective management and prevention of
malaria illness and anaemia.
XIV. INTERMITTENT PRESUMPTIVE TREATMENT
Definition
Is the administration of drug therapy in a full
therapeutic doses at predetermined intervals
during pregnancy even if individuals do not
have symptoms or signs of malaria.
Purposes
Prevention of negative effects of malaria to
the mother, foetus and newborn
INTERMITTENT PRESUMPTIVE TREATMENT cont
• Drug of choice: Sulfadoxine/pyrimethamine (SP)
• Doses: 3 tablets twice during pegnancy
• First dose: between 20 – 24 weeks
• Second dose: between 28 – 32 weeks
• Preferably given as DOT