malaria in children

1. Malaria
Dr S C Majhi

2. Malaria
 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

3. 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.

4.  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.

5. 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)

6. 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

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

9. Human cycle of plasmodium
1. Pre erythrocytic schizogony
 Development of sporozoites in liver parenchyma
 Liberated merozoites are called as cryptozoites
 No clinical manifestion; 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

10. 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’

11. 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.

12. 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

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

15.  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

16.  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.
 Signs- splenomegaly (common), hepatomegaly, and pallor due to anemia.
 Typical laboratory findings include anemia, thrombocytopenia, and a normal
or low leukocyte count.
 The erythrocyte sedimentation rate (ESR) is often elevated

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

18. 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
Severe malaria

19.  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

20. Parasite and RBCs
 P. falciparum -immature and mature erythrocytes
 P. ovale and P. vivax - immature erythrocytes
 P. malariae- only mature erythrocytes.

21. 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.
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

22. 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.

23. 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

24. 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.

25. 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.

26. 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.

27. 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.

29. New malaria treatment guidelines in
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
India

30. 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

31. 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.

32. 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)

33. Thank you