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Malaria Dr S C Majhi

Malaria in children- nelson

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Page 1: Malaria in children- nelson

MalariaDr S C Majhi

Page 2: Malaria in children- nelson

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

Malaria

Page 3: Malaria in children- nelson

Malaria is an acute and chronic illness characterized byparoxysms of fever, chills, sweats, fatigue, anemia, andsplenomegaly.

Malaria is of overwhelming importance in the developing worldtoday, with an estimated 300 to 500 million cases and morethan 1 million deaths each year.

Most malarial deaths occur among infants and young children.

Know malaria and why

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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.

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Season: most common in July-November

Definitive host: Anopheles mosquito

Intermediate host: Man

Vector: Anopheles culicfacies(rural) and

Anopheles stephensi (urban)

Epidemiology of malaria in india

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)

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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

Modes of malaria transmission

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Man Female anopheles mosquito

Secondary host Primary host

Intermediate host Definitive host

Asexual cycle Sexual cycle

Schizogony Sporogony

Hosts involved in transmission of malaria

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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

Human cycle of plasmodium

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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’

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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.

Mosquito cycle of plasmodium

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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

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

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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

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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

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Symptoms Signs lab

Fever Splenomegaly Anemia

Headache hepatomegaly Thrombocytopenia

Drowsiness Pallor Normal/ low TLC

Anorexia Elevated ESR

Nausea

Vomiting

Diarrhea

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WHO has identified 10 complications of P. falciparum malaria that define severe malaria

1. Impaired consciousness 2. Prostration3. Multiple seizures4. Respiratory distress5. Pulmonary edema6. Jaundice7. Hemoglobinuria8. Abnormal bleeding9. Severe anemia10. Circulatory collapse

123 CNS45 RS6789 hematological10 CVS

Severe malaria

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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

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P. falciparum -immature and mature erythrocytes

P. ovale and P. vivax - immature erythrocytes

P. malariae- only mature erythrocytes.

Parasite and RBCs

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The diagnosis of malaria Giemsa-stained smears of peripheral blood or rapid immunochromatographic assay.

Stains used for diagnosisGiemsa 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 speciesand determination of the percentage of infected erythrocytes and is useful in following the response to therapy

Diagnosis

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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.

Diagnosis

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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

Differential diagnosis

Page 24: Malaria in children- nelson

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.

Complications

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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 Supportivetreatment of seizures and hypoglycemia.

Cerebral malaria

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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. Nephroticsyndrome associated with P. malariae infection is poorly responsive to steroids.

Facts to remember

Page 27: Malaria in children- nelson

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.

Terminology

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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

New malaria treatment guidelines in India

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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

Complicated malaria

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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.

Prevention

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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)

Chemoprophylaxis

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Thank you