DR INAYAT ULLAH
PGY-1 PEDIATRICS.
Shifa International Hospital islamabad.11/17/2014 1
 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,
11/17/2014 2
 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.
11/17/2014 3
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
11/17/2014 4
 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.
11/17/2014 5
 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
11/17/2014 6
 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
11/17/2014 7
 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
11/17/2014 8
 A fifth species,
Plasmodium
knowlesi, causes
malaria in
macaques but
can also infect
humans.
 Discovered in
2004.
11/17/2014 9
 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 .
11/17/2014 10
 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)
11/17/2014 11
11/17/2014 12
11/17/2014 13
 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
 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.
11/17/2014 15
 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
11/17/2014 16
 P.vivax
 P.malariae Infectes only young or
 P.ovale Old Erythocytes maximal
parasitemia is 2 percent
 P.falciparum Infects all age groups
11/17/2014 17
 Liberated
Merozoites
penetrate RBC
 Three stages occur
1Trophozoites
2 Schizont
3 Merozoite
11/17/2014 18
 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
11/17/2014 19
 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.
11/17/2014 20
11/17/2014 21
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.
11/17/2014 22
11/17/2014 23
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.
11/17/2014 24
 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.
11/17/2014 25
 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.
11/17/2014 26
 Tertian Malaria: 48h
between fevers (P.
vivax and ovale)
 Quartan Malaria: 72h
between fevers (P.
malariae)
 Tropical Malaria: 48h
irregular high fever
(P. falciparum)
11/17/2014 27
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
11/17/2014 28
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)
11/17/2014 29
11/17/2014 30
 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
11/17/2014 31

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.
11/17/2014 32
 Present with
Hyperpyrexia
 Can lead to Coma
 Paralysis and other
complications.
 Brain appears
congested
11/17/2014 33
 Can produce Nephrotic
syndrome in rare
instances
 Affects mainly children
of years age
 Nephrotic syndrome of
this type is usually
steroid resistant.
11/17/2014 34
 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)
11/17/2014 35
11/17/2014 36
Ask the patient number
of questions concerning:
•Current symptoms such as
fever.
•Current medications.
•Recent travel history to
endemic area
11/17/2014 37
 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.
11/17/2014 38
 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
11/17/2014 39
 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.
11/17/2014 40
 Gives more information about the parasite
morphology and, therefore, is used to
identify the particular infecting species of
Plasmodium.
11/17/2014 41
 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
11/17/2014 42
 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.
11/17/2014 43
 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.
11/17/2014 44
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.
11/17/2014 45
11/17/2014 46
 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
11/17/2014 47
 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
11/17/2014 48
 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
11/17/2014 49
 Parenteral
 Quinidine gluconateSame as for
chloroquine-sensitive P. Falciparum
 or
 Quinine dihydrochlorideSame as for
chloroquine-sensitive P. falciparum
11/17/2014 50
 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])
11/17/2014 51
 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.
11/17/2014 52
 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.
11/17/2014 53
11/17/2014 54
 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.
11/17/2014 55
• 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
11/17/2014 56
• 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
11/17/2014 57
11/17/2014 58
 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.
11/17/2014 59
11/17/2014 60
 Protective clothing,
 Mosquito repellants (containing DEET),
 Insect vaporizers (coils containing
pyrethroids),
 Insecticide treated bed nets (most effective),
 Airconditioning
11/17/2014 61
 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
11/17/2014 62
 Residual spray: Spraying indoor surface of
house with DDT/malathion.
11/17/2014 63
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.
11/17/2014 64
11/17/2014 65

Malaria pediatric

  • 1.
    DR INAYAT ULLAH PGY-1PEDIATRICS. Shifa International Hospital islamabad.11/17/2014 1
  • 2.
     Name isderived 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, 11/17/2014 2
  • 3.
     Malaria isa 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. 11/17/2014 3
  • 4.
    Malaria is anacute 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 11/17/2014 4
  • 5.
     Malaria killsin 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. 11/17/2014 5
  • 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 11/17/2014 6
  • 7.
     1955 -WHOstarts world wide malaria eradication programme using DDT  1970 – Mosquitos develop resistance to DDT Programme fails  1976 –Trager and Jensen in vitro cultivation of parasite 11/17/2014 7
  • 8.
     Malaria iscaused 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 11/17/2014 8
  • 9.
     A fifthspecies, Plasmodium knowlesi, causes malaria in macaques but can also infect humans.  Discovered in 2004. 11/17/2014 9
  • 10.
     Falciparum accountsfor 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 . 11/17/2014 10
  • 11.
     Vector transmission:-biteby 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) 11/17/2014 11
  • 12.
  • 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 developemtnalphase 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. 11/17/2014 15
  • 16.
     P. malariaeor 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 11/17/2014 16
  • 17.
     P.vivax  P.malariaeInfectes only young or  P.ovale Old Erythocytes maximal parasitemia is 2 percent  P.falciparum Infects all age groups 11/17/2014 17
  • 18.
     Liberated Merozoites penetrate RBC Three stages occur 1Trophozoites 2 Schizont 3 Merozoite 11/17/2014 18
  • 19.
     Ruptured redcells 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 11/17/2014 19
  • 20.
     The tissueschizont 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. 11/17/2014 20
  • 21.
  • 22.
    Sexual phase Some merozoitesdifferentiate 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. 11/17/2014 22
  • 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. 11/17/2014 24
  • 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. 11/17/2014 25
  • 26.
     Stage 3 Patientstarts 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. 11/17/2014 26
  • 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) 11/17/2014 27
  • 28.
    Congenital malaria isan 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 11/17/2014 28
  • 29.
    The first signor 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) 11/17/2014 29
  • 30.
  • 31.
     On fewoccasions 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 11/17/2014 31
  • 32.
     Malignant malaria can affectthe brain and the rest of the central nervous system. It is characterized by changes in the level of consciousness, convulsions and paralysis. 11/17/2014 32
  • 33.
     Present with Hyperpyrexia Can lead to Coma  Paralysis and other complications.  Brain appears congested 11/17/2014 33
  • 34.
     Can produceNephrotic syndrome in rare instances  Affects mainly children of years age  Nephrotic syndrome of this type is usually steroid resistant. 11/17/2014 34
  • 35.
     It isa 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) 11/17/2014 35
  • 36.
  • 37.
    Ask the patientnumber of questions concerning: •Current symptoms such as fever. •Current medications. •Recent travel history to endemic area 11/17/2014 37
  • 38.
     Identify signsconsistent 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. 11/17/2014 38
  • 39.
     Malaria parasitescan 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 11/17/2014 39
  • 40.
     Used fordetecting 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. 11/17/2014 40
  • 41.
     Gives moreinformation about the parasite morphology and, therefore, is used to identify the particular infecting species of Plasmodium. 11/17/2014 41
  • 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 11/17/2014 42
  • 43.
     PCR basedtechniques:- 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. 11/17/2014 43
  • 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. 11/17/2014 44
  • 45.
    The management ofmalaria 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. 11/17/2014 45
  • 46.
  • 47.
     Oral Drugof 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 11/17/2014 47
  • 48.
     Parenteral Drugof 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 11/17/2014 48
  • 49.
     Oral Regimenof 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 11/17/2014 49
  • 50.
     Parenteral  QuinidinegluconateSame as for chloroquine-sensitive P. Falciparum  or  Quinine dihydrochlorideSame as for chloroquine-sensitive P. falciparum 11/17/2014 50
  • 51.
     Plasmodium vivaxand Plasmodium ovale Only  Primaquine phosphate  0.3 mg base/kg/24 hr for 14 days (maximum: 15 mg base [26.3 mg salt]) 11/17/2014 51
  • 52.
     Artemisinin derivativesclear 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. 11/17/2014 52
  • 53.
     The standarddosing 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. 11/17/2014 53
  • 54.
  • 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. 11/17/2014 55
  • 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 11/17/2014 56
  • 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 11/17/2014 57
  • 58.
  • 59.
     Preventing themosquitoes 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. 11/17/2014 59
  • 60.
  • 61.
     Protective clothing, Mosquito repellants (containing DEET),  Insect vaporizers (coils containing pyrethroids),  Insecticide treated bed nets (most effective),  Airconditioning 11/17/2014 61
  • 62.
     Using theanti 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 11/17/2014 62
  • 63.
     Residual spray:Spraying indoor surface of house with DDT/malathion. 11/17/2014 63
  • 64.
    Are expected tobecome 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. 11/17/2014 64
  • 65.

Editor's Notes