MALARIA

Oct 2012

Dr.kibruyisfaw zewdie

Introduction To Malaria

Malaria is an acute and chronic illness characterized by paroxysms of fever, chills, sweats, fatigue, anemia, and splenomegaly

It is protozoa d/se w/ch is mostly transmitted by a vector Anopheles mosquitoes.

The most important of the parasitic disease of humans =>107 countries, 3 billion people, 1-3 million deaths/yr

ETIOLOGY & PATHGENESIS

Malaria is caused by intracellular Plasmodium protozoa transmitted to humans by female Anopheles mosquitoes.

Four species of the genus plasmodium cause nearly all malarial infections in humans.

Almost all deaths are by P.falciparum.

The pathogensis in human is as a result of direct effects of RBC destruction.

Major Malaria Parasites P. falciparum ( 60%) P. vivax ( 40%) P. malariae (rare) < 1% P. ovale (rare)

Major Malaria Vectors An. arabiensis (family of An. gambiae

comlex) => primary vector An. funestus An. phareonsis An. nili

Life cycle of malaria Plasmodium species exist in a variety of forms

and have a complex life cycle that enables them to survive in different cellular environments in the human host (asexual phase) and the mosquito vector (sexual phase).

The exoerythrocytic phase begins with inoculation of sporozoites into the bloodstream by a female Anopheles mosquito.

Within minutes, the sporozoites enter the hepatocytes where they develop and multiply asexually as a schizont.

After 1–2 wk, the hepatocytes rupture and release thousands of merozoites into the circulation. The tissue schizonts of P. falciparum and P. malaria rupture once and do not persist in the liver.

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There are 2 types of tissue schizonts for P. ovale and P. vivax. The primary type ruptures in 6–9 days, while a secondary type remains dormant in the liver cell in the hypnozoite form for weeks, months, or as long as 5 yr before releasing merozoites, and thereby causing relapses of infection.

The erythrocytic phase of Plasmodium asexual development begins when the merozoites from the liver penetrate erythrocytes. Once inside the erythrocyte, the parasite transforms into the ring form, which then enlarges to become a trophozoite.

The trophozoite multiplies asexually to produce a number of small erythrocytic merozoites that are released into the bloodstream when the erythrocyte membrane ruptures, which is associated with fever.

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Over time, some of the merozoites develop into male and female gametocytes that complete the Plasmodium life cycle when they are ingested during a blood meal by the female Anopheline mosquito.

The male and female gametocytes fuse to form a zygote in the stomach cavity of the mosquito

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Life cycle

Female Anopheles mosquito (sexual cycle) Gametocytes Sporozoites injected

In man (Asexual cycle) Exo-erythocytic (hepatic) stage

Liver (schizogony) = Merozoites or Hypnozoites

Erythrocytic stage Merozoites and Gametocytes

Life cycle of malaria

Types of Clincal Features

Benign tertian malaria Paroxysim(AFI) of 48 hrs =>P. vivax and

ovale Malignant tertian malaria

Paroxysim of 48 hrs => P. falcipurum Quartan malaria

Paroxysim of 72 hrs => P. malarie

Malignacy of P. falcipurum High parasitemia(up to 60%), fatal

>25% Multiple parasites in RBC Endothelial adherence (sticky nobes) Children and new immigrants

EPIDEMOLOGY Malaria occurs throughout most of

the tropical regions of the world. Global distribution prevalence of 500 million people/yrly Two million death/yrly 40% of the world population living in

tropical/subtropical climates are exposed to malaria.

MALARIA IN ETHIOPIA Malaria is one of the leading public

health problems in Ethiopia 75% of the country is malarious

(<2000m), with about 68% of the population (50 million) at risk

Major impediment to socio-economic development, coincides with major planting and harvesting season

Malaria Epidemiology

Bimodal type of transmission: Major: Sep - Dec, following the main

rainy season from Jun to Aug Minor: Apr–May, following a short

rainy season from Feb to Mar Major epidemics occur every 5-8

years, focal outbreaks are common Distribution varies from place to

place depending on climate and altitude

Geographic Distribution of Malaria in Ethiopia

Malaria in Ethiopia is Unstable

Unstable malaria Seasonal Lack of

immunity Epidemic

common All age groups

affected

Malaria in Ethiopia

Stable malaria Intense,

perennial High immunity Epidemic

uncommon Children &

pregnant women more affected

Trend of an epidemic malaria in Adami Tulu District. Microscopically confirmed malaria cases at Zeway MCL, 1999-2004.

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Malaria in Ethiopia is Seasonal

Malaria Burden in Ethiopia

More than 600,000 confirmed and >9 million clinical cases each year

Cause about 70,000 deaths each year Health and health related indicator

(2005/06) of the FMOH: 18% of OPD cases (1st) 14% of admission (2nd) 9% of hospital deaths (2nd)

Poor health information system

ENDEMICITY

Endemicity is defined in terms of parasitemia rates or palpable-spleen rates in children 2-9 yrs of age as-hypo/meso/hyper/holo-endemic.

Infant parasite rate- most sensitive index of transmission of malaria to a locality

Epidemic can occur under some conditions

Clinical features

Malaria is a very common cause of

fever in tropical countries.

Non-specific symptoms

Predisposing factors for complications (1.) Extremes of age. (2.) Pregnancy, especially in

primigravidae and in 2nd half of pregnancy.

(3.) Immunosuppressed - patients on steroids, anti- cancer drugs, immunosuppressant drugs.

(4.) Immunocompromised - patients with advanced tuberculosis, HIV and cancers.

(5.) Splenectomy. (6.) Lack of previous exposure to

malaria (non-immune) or lapsed immunity

(7.) Pre-existing organ failure.

Complications of P. falciparum malaria Cerebral malaria ( coma ) Severe anemia Metabolic (Lactic) Acidosis renal failure Pulmonary odema & ARDS hypoglycemia Hypotention & shock Bleeding & clotting

disorder(DIC) Algid Malaria(CR-Collapse) Convulsions haemoglobinuria hyperparasitemia Hyperpyrexia Jaundice Prostration

Complications of P. vivax / P. malariae

Rupture of spleen Hepatic dysfunction Thrombocytopenia Severe anemia malarial nephropathy

…cerebral malaria

Cerebral malaria manifests as diffuse symmetrical encephalopathy

No meningial sign Primitive reflexes are absent Corneal reflexes are reserved muscle tone either increase or decrease Flexor or extensor posturing may be

seen. Approximately 15% of pts have retinal

haemorrhage

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coma is a characteristic and ominous feature (MR 15-20% despite treatment).

Any obtundation, delirium, or abnormal behaviour should be taken seriously.

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Generalized convulsion(50%) vs covert seizure

Neurological deficit in 3-15% 1o% of children has language deficit The incidence of epilepsy increase

Life expectancy decrease among these children.

HYPOGLACEMIA

Plasma glucose level of <2.2mmol/l(<40mg/dl)

Indicate poor prognosis Causes:

Failure in hepatic gluconeogensis Increase consumption drugs

Direct Diagnosis

Blood smears for asexual P.falciparom parasite is

the gold standard. Thick and thin blood films are made

on clear grease-free glass slides. Thick film is for parasite

identification. Thin film is for species identification.

Treatment of uncomplicated falciparum malaria: • Artemether-Lumefantrine:

(Coartem 20/120): is most widely used in Ethiopia.

Tablet containing 20 mg Artemether plus 120 mg Lumefantrine in a fixed dose combination.

Adult Dosage: < 35 kg: 3 tabs PO BID for 3 days

> 35 Kg: 4 tabs PO BID for 3 days

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b) Quinine: Adult dose : 600 mg PO TID for 5 – 7

days alone or in combination with + Tetracycline 500

mg PO QID or Doxycycline 100mg PO /day for the same period

Side effects: Cinchonism: Tinnitus, hearing loss,

dizziness, tremor, nausea, resteleness, blurring

Hypogycemia : is the commonest adverse effect

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The treatment of Malaria is supportive and specific Supportive treatment may include the

following:1. Reducing the temp. if hyperpyrexia is present

specially common with P.falciparum infection.2. Rehydration specially when vomiting and

diarrhea have been prominent and in acidosis. 3. Monitoring renal output and taking corrective

measures if necessary (such as hypovolemia and oliguria maintain careful flood balance.)

4. Monitoring the need for blood transfusion which may be life-saving.

5. Terminating convulsion with appropriate drugs-rectal diazepam or lorazepam, rectal or intramuscular paraldehyde, and intramuscular phenobarbital are some options.

6. Monitoring of blood glucose and correction of hypoglycaemia where necessary (10-40mL) of 50% dextrose diluted three times with saline and infused over 5-10min.)

7. Reducing acidaemia. Rehydration blood transfusion and anti malaria therapy are usually sufficient for this purpose

Treatment of Severe and complicated falciparum malaria: A) Drug Treatment: i) Quinine: is drug of choice for severe and complicated

malaria. Dosage and Adminstration: Where IV administration of quinine is possible Loading dose: Quinine 20 mg salt/kg of body weight by

infusion over 4 hours, in 5 % dextrose in saline (5-10 ml/kg of body weight depending on

the patient's overall fluid balance). Maintenance does: Twelve hours after the start of the

loading dose, give quinine 10 mg salt/kg of body weight in dextrose saline over 4 hours. Repeat

the same dose of quinine (i.e. 10 mg salt/kg) every 8 hours until the patient can take

oral medication.32

Thank u????

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