details of presentation of malaria signs symptoms diagnosis, and treatment in pediatric patients.

1. DR INAYAT ULLAH
PGY-1 PEDIATRICS.
Shifa International Hospital islamabad.11/17/2014 1

2.  Name is derived from Italian
Mal’ aria or bad air
Malaria continues to be most important cause
of fever and morbidity in theTropical world
Malaria has been eradicated from Europe,
Most of North America, USA South America
Korea and Japan,
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3.  Malaria is a vector-borne
infectious disease
caused by protozoan
parasites. It is
widespread in tropical
and subtropical regions,
including parts of the
Americas, Asia, and
Africa.
 Transmission: Via
female Anopheles
mosquito.
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4. Malaria is an acute and chronic illness
characterized by paroxysms of fever, chills,
sweats, fatigue, anemia, and splenomegaly.
 It has played a major role in human history,
having caused more harm to people than any
other infectious disease. Malaria is of
overwhelming importance in the developing
world today, with an estimated 300–500 million
cases and >1 million deaths each year
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5.  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.
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6.  1880 - Charles Louis Alphose Lavern
discovered malarial parasite in wet mount
 1883 - Methylene blue stain - Marchafava
 1891 - Polychrome stain- Romanowsky
 1898 - Roland Ross - Life cycle of parasite
transmission, wins Nobel Prize in 1902
 1948 - Site of Exoerythrocytic development
in Liver by Shortt and Garnham
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7.  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
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8.  Malaria is caused by an infection by one of
four single celled Plasmodia species, they are:
falciparum, vivax, malariae, and ovale.The
most dangerous of the four
is.P.falciparum
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9.  A fifth species,
Plasmodium
knowlesi, causes
malaria in
macaques but
can also infect
humans.
 Discovered in
2004.
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10.  Falciparum accounts for 90% of deaths due to
malaria and vivax is the most widely spread
species because it exists in both temperate
and tropical climates (Encarta).The malaria
life cycle is a complex system with both
sexual and asexual aspects .
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11.  Vector transmission:-bite by infective female
anopheles mosquitoes.
 Direct transmission
blood transfusion, the parasite can live for 14
days in blood bottles under -4*C.
The use of contaminated needles.
 CongenitalTransmission
Mother to newborn(via the placenta)
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13. 11/17/2014 13

14.  Man – Intermediate
host.
 Mosquito – Definitive
host
– Sporozoites are
infective forms
 Present in the salivary
gland of female
anopheles mosquito
 After bite of infected
mosquito sporozoites
are introduced into
blood circulation.11/17/2014 14

15.  Sprozoites undergo
developemtnal phase in the
liver cell
 Sprozoites are elongated
and spindle shaped
become rounded inside the
liver parenchyma
 Multiple nuclear divisions
develop to Schozonts
 A Schizont contains 20,000
– 50,000 merozoites.
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16.  P. malariae or P. falciparum sporozoites do
not form hypnotizes, develop directly into
pre-erythrocytic schizonts in the liver
 Pre-erythrocytic schizogeny takes 6-16 days
post infection
 Schizonts rupture, releasing merozoites
which invade red blood cells (RBC) in liver
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17.  P.vivax
 P.malariae Infectes only young or
 P.ovale Old Erythocytes maximal
parasitemia is 2 percent
 P.falciparum Infects all age groups
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18.  Liberated
Merozoites
penetrate RBC
 Three stages occur
1Trophozoites
2 Schizont
3 Merozoite
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19.  Ruptured red cells release
Merozoites which attack
new red cells
 Continue with Schizogony
 Repeated cycles will
continue
 In P.falciparum - infected
erythrocytes with
Schizonts aggregate in the
capillaries of brain and
other internal organs
 Only ring forms are seen in
the blood smears
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20.  The tissue schizont of
rupture once and
donot persist in the liver.
 While in case of and tissue
schizonts are of 2 types primary type rupture
in 6-9 days,and the secondary type remain
dormant in the liver cells for weeks,months
,or as long as 5 years and causing relapse of
infection.
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22. Sexual phase
Some merozoites differentiate into
male and female gametocytes, the
forms of Plasmodia infective to
mosquitoes. These are taken up by
a mosquito during another blood
meal. These fuse to form an
ookinette in the gut lumen of the
mosquito. The ookinette invades the
stomach wall to form the oocyst.
This in turn develops and releases
sporozoites which migrate to the
salivary gland of the mosquito. This
mosquito then goes on to infect
another human host.
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23. 11/17/2014 23

24. Incubation period: P. falciparum, 9-14 days; P.
vivax, 12-17 days; P. ovale, 16-18 days, and P.
malariae, 18-40 days.
The incubation period can be prolonged in
patients with partial immunity or incomplete
chemoprophylaxis and as long as 6-12 mo for
P. vivax.
Prodromal symptoms include headache,
fatigue, anorexia, myalgia, slight fever, and
pain in the chest, abdomen, or joints.
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25.  Stage 1
 Chills for 15 min to 1 hour
 Caused due to rupture from the host red cells
escape into Blood
 Present with nausea, vomiting,headache
 Stage 2
 Fever may reach upto 400c may last for
several hours starts invading newer red cells.
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26.  Stage 3
Patient starts sweating, concludes the episode
Cycles are frequentlyAsynchronous
Paroxysms occur every 48 – 72 hours
In P.malariae pyrexia may lost for 8 hours or
more and temperature my exceed 410c.
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27.  Tertian Malaria: 48h
between fevers (P.
vivax and ovale)
 Quartan Malaria: 72h
between fevers (P.
malariae)
 Tropical Malaria: 48h
irregular high fever
(P. falciparum)
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28. Congenital malaria is an important
cause of
 abortions,
 miscarriages,
stillbirths,
 premature births,
 intrauterine growth retardation,
and neonatal deaths
Congenital malaria usually occurs in a
nonimmune mother with P. vivax or P.
CONGENITAL MALARIA
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29. The first sign or symptom most commonly occurs
between 10-30 days of age .
Signs and symptoms include fever, restlessness,
drowsiness, pallor, jaundice, poor feeding, vomiting,
diarrhea, cyanosis, and hepatosplenomegaly.
 Malaria is often severe during pregnancy and may have
an adverse effect on the fetus or neonate owing to
maternal illness or placental infection even in the absence
of transmission from mother to child.
CONGENITAL MALARIA (CONT)
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31.  On few occasions life
threatening complications
can occur.
 Occurs in infections with
P.falciparum
 Associated with Heavy
parasitemia
 Grouped into three types
1. Cerebral Malaria
2 Algid malaria
3 Black water fever
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32. 
Malignant malaria
can affect the brain
and the rest of the
central nervous
system. It is
characterized by
changes in the level
of consciousness,
convulsions and
paralysis.
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33.  Present with
Hyperpyrexia
 Can lead to Coma
 Paralysis and other
complications.
 Brain appears
congested
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34.  Can produce Nephrotic
syndrome in rare
instances
 Affects mainly children
of years age
 Nephrotic syndrome of
this type is usually
steroid resistant.
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35.  It is a manifestation of infection with P.falciparum
occuring in persons who have been previously
infected and have had been inadequate dose of
quinine
 It is characterized by intravascular hemolysis fever,
and Haemoglobunuria
 Cardiovascular collapse and shock
 Abnormalities in blood coagulation and
thrombocytopenia (decrease in blood platelets)
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36. 11/17/2014 36

37. Ask the patient number
of questions concerning:
•Current symptoms such as
fever.
•Current medications.
•Recent travel history to
endemic area
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38.  Identify signs consistent with malaria:
 fever, pallor, jaundice, splenomegaly.
 Exclude other possible causes of fever (e.g.
signs of viral and bacterial infections)
 Examine rest of the systems to rule out any
potential infection causing fever.
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39.  Malaria parasites can be identified by
examining under the microscope a drop of
the patient's blood, spread out as a "blood
smear" on a microscope slide.
 Prior to examination, the specimen is stained
(most often with the Giemsa stain) to give to
the parasites a distinctive appearance.This
technique remains the gold standard for
laboratory confirmation of malaria
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40.  Used for detecting malaria: a larger volume
of blood is examined allowing detection of
even low levels of parasitaemia.
 Also used for determining parasite density
and monitoring the response to treatment.
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41.  Gives more information about the parasite
morphology and, therefore, is used to
identify the particular infecting species of
Plasmodium.
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42.  Antigen Detection
 Various test kits are available to detect antigens
derived from malaria parasites. Such immunologic
("immunochromatographic") tests most often use a
dipstick or cassette format, and provide results in 2-
15 minutes.These "Rapid DiagnosticTests" (RDTs)
offer a useful alternative to microscopy in situations
where reliable microscopic diagnosis is not
available. Malaria RDTs are currently used in some
clinical settings
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43.  PCR based techniques:- Detects DNA or RNA
sequences specific to Plasmodium.
 Fluorescent techniques:- Relatively low
specificity and sensitivity. Cannot identify the
parasite species.
 Serologic tests:-Based on
immunofluorescence detection of antibodies
against Plasmodium species. Useful for
epidemiologic and not diagnostic purposes.
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44.  influenza
 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.
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45. The management of malaria is based on the
clinical presentation.
 In severe malaria, anti malarial therapy must be
given Intravenously or Intramuscularly, oral
treatment should be substituted as early as
possible
 Doses must be calculated in on a mg/kg of body
weight.
 It is important to weigh the patient, and
administer the dose appropriate for weight.
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46. 11/17/2014 46

47.  Oral Drug of Choice
 Chloroquine phosphate10 mg base/kg
(maximum: 600 mg base)
 then 5 mg base/kg (maximum: 300 mg base),
6 hr later,
 and 5 mg base/kg/24 hr (maximum: 300 mg
base) at 24 and 48 hr
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48.  Parenteral Drug of Choice
 Quinidine gluconate10 mg/kg loading dose
(maximum: 600 mg) over 1-2 hr,
 then 0.02 mg/kg/min continuous infusion until
oral therapy can be started
 Or
 Quinine dihydrochloride (not available in the
USA)20 mg/kg loading dose over 4 hr,
 then 10 mg/kg over 2-4 hr q8h (maximum: 1,800
mg/24 hr) until oral therapy can be started
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49.  Oral Regimen of Choice
 Quinine sulfate 30 mg/kg/24 hr divided in three
doses for 3-7 days (maximum: 650 mg/dose) plus
Tetracycline 20 mg/kg/24 hr divided in four doses for
7 days (maximum: 250 mg/dose) or plus
Pyrimethamine-sulfadoxine (Fansidar) <1 yr, single
dose of 1/4 tablet
1-3 yr, single dose of 1/2 tablet
4-8 yr, single dose of 1 tablet
9-14 yr, single dose of 2 tablets
>14 yr, single dose of 3 tablets or Mefloquine
hydrochloride15 mg PO followed by 10 mg/kg PO 8-
12 hours later (maximum: 1,250 mg) for 1 day
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50.  Parenteral
 Quinidine gluconateSame as for
chloroquine-sensitive P. Falciparum
 or
 Quinine dihydrochlorideSame as for
chloroquine-sensitive P. falciparum
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51.  Plasmodium vivax and Plasmodium ovale
Only
 Primaquine phosphate
 0.3 mg base/kg/24 hr for 14 days (maximum:
15 mg base [26.3 mg salt])
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52.  Artemisinin derivatives clear parasitemia more
rapidly than quinine .They are active against a
broader life-cycle range of blood stage parasites
than quinine and they are active against
gametocytes .
 Artemisinin derivatives include artesunate ,
artemether and artemotil. Artesunate is the
preferred artemisinin; clinical experience with
artemether and artemotil drugs is limited and
they should not be used for treatment of severe
disease.
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53.  The standard dosing regimen for intravenous
artesunate consists of five doses:
2.4 mg/kg as the first dose, followed by
2.4 mg/kg at 12 and 24 hours, followed by
2.4 mg/kg once daily
Emergence of artemisinin resistance is an important
concern therefore combination is prefferred.
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55.  Supportive therapy
 PRBC transfusion(s) to maintain the hematocrit more
than 20%,
 Exchange transfusion in life-threatening P. falciparum
malaria with parasitemia more than 5%,
 Supplemental O2 and ventilatory support for
pulmonary edema or cerebral malaria,
 Intravenous rehydration for severe malaria,
 Intravenous glucose for hypoglycemia,
 Anticonvulsants for cerebral malaria with seizures,
 Dialysis for renal failure.
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56. • Chloroquine and
hydroxychloroquine
• Primaquine
• 1-2 weeks before travel,
weekly while in country,
and for 4 weeks
afterwards
• Only used for
prophylaxis in areas
with p. vivax, and for
terminal prophylaxis
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57. • Atovaquone-Proguanil
• Doxycycline
• Mefloquine
• 1-2 days before, daily while in
country and 7 days after
• 1-2 days before, daily in
country and 4 weeks
afterwards
• 2 weeks before, weekly in
country and weekly for 4
weeks afterwards
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59.  Preventing the mosquitoes from entering the
house – Close door / windows, especially
toilets.
 Well-constructed houses with window
screens
 Preventing the mosquitoes from hiding –
Avoid dark corners/ hanging clothes in rooms
 Mosquito Control – Avoid stagnant water,
insecticide spraying etc.
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61.  Protective clothing,
 Mosquito repellants (containing DEET),
 Insect vaporizers (coils containing
pyrethroids),
 Insecticide treated bed nets (most effective),
 Airconditioning
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62.  Using the anti larval measures such as oiling the
collection of standing water or dusting them with
paris green effectively controlled malaria
 Some moderm larvicides such as temephos which
confer long effect with low toxicity are more widely
used
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63.  Residual spray: Spraying indoor surface of
house with DDT/malathion.
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64. Are expected to become available toWHO
in 2014-2015.
Evaluated as an addition to, not a
replacement for, existing preventive,
diagnostic and treatment measures.
Finally, extensive efforts have been
made to develop a malaria vaccine but
results to date have been disappointing.
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