MALARIA

INTRODUCTION

Malaria is a major public health concern in Zambia. Malaria affects people of all ages, but is

more dangerous to pregnant women and children under five years. It spreads from person to

person through an infected female anopheles mosquito bite.

It can also be transmitted through blood transfusion of infected blood, tissue transplants and

transplacentally from mother to foetus. It is a leading cause of morbidity and mortality in

Zambia, accounting for about three million clinical cases annually with 50,000 cases resulting in

death. Malaria accounts for 36.7% of all OPD attendances in Zambia, with 10% pregnant

women, 49% of under five OPD cases attributed to malaria. Malaria is also a major cause of

admission to health facilities in Zambia today with an average of 62.1% of in-patient cases

(CBoH, MOH and RBM 2001).

DEFINITION OF MALARIA

Malaria is a protozoa infection of the blood (red blood cells) but with general effect

on the body caused by a genus plasmodium species that is transmitted by an

infected anopheles mosquito, characterized by regular cycles of chills and fever

(Marcia and Jeanette, 2004).

ETIOLOGY

Malaria is caused by protozoa of the genus plasmodium species. There are four types of

plasmodium that are capable of causing infection in human. These are plasmodium falciparum,

plasmodium vivax, plasmodium ovale, and plasmodium malariae. All these plasmodia infect and

destroy human erythrocytes, produce chills, fever, and anaemia and splenomegaly. Plasmodium

falciparum causes more severe disease than the other plasmodium species and accounts for

malaria deaths (Rubin and Farber1999).

The incubation period varies according to the type of plasmodium specie i.e.

1. Plasmodium Falciparum – 7-14 days

Plasmodium Vivax – 12-17 days

Plasmodium Ovale – 15-18 day

Plasmodium Malariae – 18-40 days

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EPIDEMIOLOGY

Malaria has been eradicated in most developed countries. The disease is found throughout the

tropical and subtropical regions of the world and causes 300 million acute illnesses and at least

one million deaths each year. 99% of these deaths occur among children below the age of five in

sub-Saharan Africa. It kills an African child every 30 minutes. Those who survive an episode of

severe malaria may suffer from a range of physical and mental disabilities. The rural poor,

infants, children, malnourished persons and pregnant women are all especially susceptible to

infection. All inhabitants of hyper-endemic regions are presumed to harbour malaria parasites

even though they may have no clinical symptoms.

TYPES OF MALARIA PARASITES

There are four types of plasmodium that are capable of causing infection in human. These are

Plasmodium Falciparum, Plasmodium Vivax, Plasmodium Ovale and Plasmodium

Malariae. All these plasmodia infect and destroy human erythrocytes, produce chills, fever, and

anaemia and spleenomegally. Plasmodium falciparum causes more severe disease than the other

plasmodium species and accounts for malaria deaths (Rubin and Farber1999).

Plasmodium falciparum and ovale are the predominant species in Africa, while plasmodium

malariae is the least common. And coming to the Zambian perspective, plasmodium falciparum

still remains the commonest cause of malaria cases. It accounts for about 95% of all malarial

cases in Zambia (RBM 2001).

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LIFE CYCLE OF MALARIA PARASITE

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THE MALARIA LIFE CYCLE

The life cycle has two phases; a sexual cycle known as sporogony which takes place within the

intestinal tract of a mosquito and the asexual cycle known as schizogony, the infective form for

human, is found in the saliva of an infected mosquito. Saliva containing infective sporozoites is

injected into the blood stream of humans through the mosquito proboscis. After circulating in the

peripheral blood for about 20-30 minutes, the sporozoites enter the parenchyma cells of the liver,

where they begin to multiply (the exoerythrocytic stage). In about 6-14 days, multiple small

forms called merozoites, break out of the liver cells and are released into the circulation, where

they seek out and penetrate erythrocytes.

Within the erythrocytes (erythrocytic stage), a series of developmental stages occur. These

organisms develop into a “ring form” known as the trophozoites, which depending on the

species, enlarge and divide into a segmented state known as the schizont. The individual

segments of the schizonts rapture the erythrocytes and merozoites are released in the circulation.

These merozoites then seek out uninfected erythrocytes and the cycle continues.

After several erythrocytic cycles have taken place, some of the merozoites transform into sexual

macrogametocyte (female) and microgametocyte (male). When a plasmodium free anopheles

female mosquito bites a human infected with plasmodia parasites these gametocytes are ingested

along with the trophozoite infected erythrocytes as part of the blood meal.

In the stomach of the mosquito the microgametocyte develop six to eight flagella. This

microgametocyte breaks free to penetrate the female macrogametocyte and produce fertilized

zygote. This new zygote will penetrate the wall of the mosquito midgut; it then becomes

encysted and known as an oocyst. The oocyst finally bursts to liberate sporozoites into the

coelic cavity of the mosquito. These sporozoites then move to the salivary gland in readiness to

inject or inoculate the next human host during feeding and initiate the pre-erythrocytic

development.

When the mosquito bites a new host, sporozoites are squeezed from the salivary glands and

injected through the proboscis into the human host (koneman et al 1997).

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PATHOPHYSIOLOGY OF MALARIA

The malaria pathogenesis starts with injection of sporozoites into human host which develop into

merozoites that invade red blood cells. This invasion is specific, ordered and sequential process.

The Pathophysiological changes results from destruction of erythrocytes (both infected and

uninfected), the consequent liberation of parasites and erythrocyte material into the circulation

and the host reaction to these events (Guerrant et al, 2006).

The merozoites released from the ruptured hepatocytes will invade the red blood cells by

attachment to the erythrocyte surface mediated by a specific erythrocyte receptor.

Within the red blood cells the parasites digest the red cell protein primarily the hemoglobin. As

the hemoglobin is digested the break down products are toxic to the parasite and thus hemazoin

(a polarizable crystal) is formed in the food vacuole.

The intracellular parasites modify the erythrocyte in several ways. They derive energy from

anaerobic glycolysis of glucose to lactic acid which may contribute to clinical manifestation of

hypoglycemia and lactic acidosis. They also make the red cell membrane less deformable

resulting in hemolysis and accelerated splenic clearance which ultimately contribute to anaemia

and splenomegaly.

The parasites induce release of cytokines, the tumor necrosis factor alpha (TNF-a) in particular.

These cytokines are responsible for many symptoms and signs of infection particularly fever and

malaise.

The falciparum malaria infected erythrocytes specifically sequester in the microcirculation of

the vital organs e.g. the brain, kidney, eyes, liver by attachment or cytoadherence interfering with

microcirculatory flow and host tissue metabolism. This process is called sequestration and it is

specific to falciparum malaria.

Clinical signs and symptoms of malaria are caused by the asexual forms of the parasites as they

destroy the red blood cells (Guerrant, et al, 2006).

PREDISPOSING FACTORS

These include:

Stagnant water in ditches, ponds, dambos, agricultural fields, boreholes and standpipes.

Tall grass and bushes near houses make it conducive for mosquito to breed.

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Hot weather making people to sleep at night without covering themselves and leaving

windows and doors open, thus, exposing themselves to mosquito bites.

Low socio-economic status; most people cannot afford to buy electric fans, insecticides,

and mosquito repellents or buy mosquito nets to sleep in to prevent the mosquitoes from

biting them.

Pregnancy; this is due to susceptibility of this woman to infections due to her lowered

immunity.

HIVAIDS; this lowers the immunity of an individual.

SIGNS AND SYMPTOMS OF MALARIA

For easy recognition the signs and symptoms have been categorized into symptoms of

uncomplicated malaria, moderately severe malaria, severe and complicated malaria and general

signs and symptoms in children.

1. Uncomplicated malaria.

Fever is the commonest

General malaise

Loss of appetite

Headache

Joint pains

Sweating and chills

Body pains

Acute gastroenteritis

2. Moderately severe malaria.

This is usually presented with the following: nausea, vomiting, dehydration, diarrhea and

extreme weakness.

3. Severe and complicated malaria.

Fever of 38 t0 40 degrees centigrades

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Severe headache

Generalised aches

Severe anaemia

Jaundice usually as an early sign

Drowsiness or lethargy

Prostration (in ability to seat or stand without support)

Respiratory distress

Unconsciousness or coma

Change in behavior

Hepatosplenomegally

Abnormal bleeding.

4. Children’s general signs and symptom of malaria

poor appetite

restlessness

cough

diarrhea

Loss of interest in the surrounding.

Rigor is a common manifestation of malaria and the following are some of the stages involved in

a rigor:

Cold stage

It is characterized by shivering, intense feeling of cold, lips and fingers are cyanotic, dry and

pale. In children there may be seizures. This stage takes about 15 minutes to 60 minutes.

Hot stage

This stage last about 2-6 hours and it is caused by temperature which could be above 41c. It is

characterized by full bound pulse, dry burning skin, intense headache, and nausea and vomiting.

Sweating stage

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This stage lasts about 2-4 hours and it is characterized by profuse sweating, temperature falls

rapidly below normal, patient falls into a deep sleep and on waking up the patient feels weak, but

normal (Koneman 1997).

MANAGEMENT

1. Investigations/Diagnosis

The diagnosis of malaria is divided into two, Rapid Diagnostic Test (RDT) at first contact and

laboratory diagnosis. Before RDT is done a careful medical history should be taken from the

patient. This should be supplemented by a careful clinical examination.

Malaria RDTs rely on the detection of parasite specific antigens (proteins) circulating in the

bloodstream. The most common antigens for RDTs are P. Falciparum histidine-rich Protein-

2(pfHRP2) and Plasmodium spp. lactose dehydrogenase (pLDH). Tests based on the pfHRP2

antigen are specific to P. falciparum, the most dangerous species of malaria, and are more

readily available and less expensive. Tests based on pLDH come in two varieties:  pan-malarial

tests which detect all malaria species, or species specific tests that detect malaria species other

than P. falciparum. Pan-malarial tests are also available which detect the Aldolase antigen.

The laboratory diagnosis of malaria involves blood slide examination (both thick and thin film

slide) to check for the presence of parasites in the peripheral blood by the use of a microscope.

Other methods of checking for the presence of parasites include Rapid Testing Technique using a

strip.

The other supportive investigations done include:

Blood glucose estimation for patients with altered consciousness.

Heamatocrit or haemoglobin estimation.

Lumber puncture to rule out meningitis.

Urine examination.

2. Treatment

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Based on available evidence, the Zambian government decided to change the first line treatment

of malaria from chloroquine to artemensin-based combination such as Artemether Lumefantrine

(Coartem®) – an Artemisinin based combination therapy except for children less than 5kg body

weight. Therefore, the following is the treatment policy of malaria in Zambia.

FIRST LINE TREATMENT OF UNCOMPLICATED MALARIA

Artemether 20mg – Lumefantrine 120mg (coartem) is the first line treatment choice for

uncomplicated malaria. However, children with weight less than 5kg body weight and pregnant

women are not recommended for this drug, therefore it means that they have to be started on the

second line drug of choice which is Quinine. Pregnant women in the first trimester with malaria

should be treated with quinine as the first line treatment of uncomplicated malaria as Fansidar is

contraindicaed.

Treatment

First line treatment for uncomplicated malaria according to the new Zambian government policy

is Artemisin based combination therapy e.g. Atermether 20mg + Lumefantrine 120mg tablets

is given according to the body weight as follows:

The dosages are as follows;

Table 1: First line treatment of malaria

Age(years) Weight (kg) Number of tablets

per dose 0h, 8h, 24h,

36h, 48h, 60h

Atermether (A) +

Lumefantrine (L)

per dose

<1 <5 Not recommended -

1 – 5 5 – 14 1 20mg A + 120mg L

6 – 8 15 – 24 2 40mg A + 240mg L

9 – 12 25 – 34 3 60mg A +360mg L

Over 12 >35 4 80mg A + 480mg L

Source: MOH, 2009.

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Children, >5 kg-14 kg get one tablet stat, then one tablet after 8hours, then one tablet 12

hourly

15 kg-24 kg, get two tablets per dose (taken as above)

25 kg – 34 kg, get three tablets per dose (taken as above)

35 kg and above, get four tablets per dose (taken as above)

SECOND LINE TREATMENT

The second line treatment of malaria is quinine.

Dosage of quinine

Quinine can be administered orally, intramuscularly and intravenously.

Orally 10mg/kg body weight every 8 hours for 5-10 days.

Intramuscularly 10mg/kg body weight, diluted with equal volume of water-for-injection

( no need for a loading dose )

Intravenously 20mg/kg body weight in 1 litre of 5% dextrose loading dose (infused over

4 hours), followed by a maintenance dose 10mg/kg body weight in 500mls of 5%

dextrose 8 hour

Table 3: oral quinine 300mg tablet dosage schedule

Age(years) Number of tablets per dose

<1 0.25

1 – 3 0.5

4 – 6 0.75

7 – 11 1

12 – 15 1.5

15+ 2

Source: MOH, 2009

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NURSING CARE

Aims

o To relieve symptoms

o To promote comfort

o To prevent complications

ENVIRONMENT

o Well ventilated and clean environment with adequate lightng

o Nursed in acute bay for close observations.

o Equipment such as drip stands, fluids should be readily available

o Environment be quite to promote rest.

POSITION

o Nurse in position that the patient is comfortable with

o Nurse on a railed paddled bed as patient may convulse.

o Patient may be nursed according to stages as follows.

COLD STAGE

o Provide extra linen to war m patient.

o Provide warm/hot drink to warm patient.

o Close nearby windows to prevent cold air from entering the room.

HOT STAGE

o Remove extra linen as patient can tolerate.

o Offer cool drink to provide a cooling effect to patient

o Allow patient to wear light clothes as excess clothes may cause temperature rise .

o If necessary, tepid sponging can be done to provide a cooling effect.

o Give antipyretics as prescribed –Aspirin 600mg x 3days

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o Encourage bed rest because patient may be weak

o Open nearby windows to allow cool air to rush in.

THE SWEATING STAGE

o Continue reassuring the patient

o Change linen if wet due profuse sweating.

o Open nearby windows.

o Wipe excessive sweat with clean cloth or using patient’s face towel.

o If available, a fan may be useful protocol the patient

o A warm bath or shower can be provided. This may have a cooling effect.

o Encourage patient to take plenty of fluids to prevent dehydration which can be caused by

excessive sweating.

OBSERVATIONS

o Observe general condition of the patient. Patient with severe malaria may progress into

unconsciousness cardinal indication of cerebral malaria.

o Vomits –for frequency, color and consistence. Check urine output – to rule out renal failure

that my results from increased haemolysis

o Look out for side effects of medication e.g. hypoglycaemia, Tinnitus etc.

VITAL SIGNS—

o Temperatures—patient tend to have rigors which progress through the named stages. Steady

reduction in temperature can be an indication of good response to treatment.

FLUIDS AND NUTRITION

- In acute Stage provide IV Fluids as prescribed e.g. Ringers lactate and 5%

o Dextrose for fluid replacement and provision of energy respectively.

o 5%Dextrose prevents patient from going into hypoglycemia when on IV

o quinine

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- Provide highly nutritious foods that would promote recovery and

- Healing of patient. The diet should be rich in proteins, carbohydrates and vitamins

- Serve meals in small amounts but frequently and attractively. This

- Promotes appetite.

SEVERE MALARIA

This is mainly caused by plasmodium falciparum which occur as a result of:

i. Delay in treatment of uncomplicated malaria

ii. Misdiagnosis

iii. May occur rapidly

FEATURES INDICATING SEVERE MALARIA

- confusion,

- Hallucinations (psychosis).

- Coma,

- hypoglycemia,

- acute renal failure,

- severe anaemia,

- shock,

- haemoglobinuria (black water fever)

- Jaundice

- extreme weakness

PATHOPHYSIOLOGY OF SEVERE MALARIA

Anaemia is due top destruction of red blood cells by the malaria parasites and malfunctioning the

bone marrow.

Renal failure; there is acute tabular necrosis which leads to shock.

Hypoglycaemia due to impaired gluconegenesis in liver since parasites consumes large

quantities of glucose.

TREATMENT

If patient could not respond to coartem and is able to take drugs orally, oral quinine is given as

the second line of treatment.

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QUININE ORAL

Presentation: 300 milligrams tablets.

Dosage is given according to age and is taken 3 times daily for 7 days.

Table of dosages for oral quinine by age

AGE IN YEARS NUMBR OF TABLETS PER DOSE

Less than 1 1/4

1-3 1/2

4-6 3/4

7-11 1

12-15 1 1/2

15 and above 2

Children:

Quinine 10 milligrams per kilogram (mg/kg) body weight intramuscularly diluted in saline or

water for injection (to a concentration of 60 – 100mg per milliliter).

Repeated after 4 hours and then 12 hourly. A loading dose not recommended by this route.

By intravenous injection

Quinine loading dose of 20 milligrams / kg bwt diluted 10 ml of 5% or 10 % dextrose( or

isotonic fluid if hypoglycaemia is excluded ) per kg body weight by intravenous infection over 4

hours.

After 12 hours , maintenance dose of 10mg / kg bwt given over 2 hours , repeated 12 hourly

until patient swallow , then oral Quinine 10mg / kg body weight 8 hours to complete 7 days

course or treatment

ADULTS

By intramuscular injection

Quinine 10mg / kg body weight diluted in saline or water for injection to a concentration of 60 –

100m salt / ml, repeated after 4 hours and then 8 hourly. A loading dose is not recommended by

this rout.

By intravenous injection

Loading dose of Quinine 20mg / kg bwt dilute in 10 ml of 5% or 10% dextrose (or isotonic

fluid if hypoglyceaemia is excluded) per kg body weight by intravenous infusion over 4 hours

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After 8 hours maintenance dose of 10 milligram per /kg body wt given over 4 hours repeated 8

hours until patent can swallow or after coma resolution , then oral quinine 10mg/ kg body weight

8 hrly to complete7 days of treatment.

Quinine is sometimes used in combined with tetracycline or clindamycin or Doxycline in places

where reduced sensitivity to quinine is.

In Zambia Quinine sensitivity is still very high and there is no justification for using the

combination

MALARIA IN PREGNANCY

Intermittent presumptive treatment (IPT)- sulphadoxine +pyrimethamine (sp) is the drug of

choice for prevention of malaria in pregnancy . Three tables of sulphadoxine + pyrimethamine

are giving after 16 weeks following the last 4 weeks apart during the second and third trimester.

A total of 3 doses should be given during the entire duration of pregnancy.

Pregnant women diagnosed with malaria are given quinine and not Coartem. Individuals who are

intolerant to sp should be counseled about personal preventive measures to reduce contact with

mosquitoes.

Severe

Hypoglyceamia – 50% dextrose

Convulsions – diazepam o.2 mg / bwt

- Adult 10ms

- Phenobarbitone 10 – 12 mg / kg bwt

NURSING MANAGEMENT

The objectives of nursing care are to relieve pain, minimize the signs and symptoms of malaria,

prevent complication and avoid a disease from developing into severe or cerebral malaria.

CARE DURING COLD STAGE

Care is given according to the problems identified during this stage of fever in malaria.

When a patient is shivering due to cold, the following will be done to warm the patient.

o Give extra linen to prevent heat loss.

o Give a warm drink to warm the patient.

o Put a hot water bottle rapt in a towel to avoid burning the patient.

Pain killers will be given to relieve headache and join pains.

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CARE DURING HOT STAGE

Since during this stage, the patient is feeling hot, the temperature is high and skin is dry, the

following will be done to reduce the temperature.

Open nearby windows to allow cool fresh air into the room.

Remove extra linen from the patient.

Provide light bed wear to increase heat loss.

Lower room temperature by using air conditioner.

Give a cold drink to help cool the body.

Do tepid sponging and check the temperature to avoid sudden drop of temperature.

ENVIRONMENT

The patient will be admitted medical room away from a busy bay to provide privacy and

promote rest.

The place should not have a lot of other equipment around the bed to make the place look

tidy and avoid bumping into equipment when getting out of bed since malaria patients are

usually weak.

The room will be well ventilated to promote free air circulation during.

POSITION

Since a malaria patient can be nursed in any position, nurse patient in the position they

are comfortable with, to promote comfort and avoid straining.

If the patient is unconscious, or semiconscious, do 4 hourly turnings to prevent him / her

from developing pressure sores.

PSYCHOLOGICAL CARE

Explain the nature of the disease and procedures to the patient and relatives to allay

anxiety.

Attend to the patients’ questions and worries, those that need Doctor’s clarification will

be referred to the Doctor to build confidence and trust in the health care team.

Allow relatives to visit the patient during visiting hours so that they don’t feel cut off

from the family.

Explaining the treatment to the patient, the side effects of the drugs will be done to help

patient co-operate during his treatment.

REST

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Procedures will be done collectively to avoid disturbing the patient and encourage rest.

Maintain visiting hours to avoid noise from visiting relatives to allow him / her to rest to

promote recovery.

Administer prescribed drugs like panadol 500 milligrams to 1g depending on age 3 times

a day to promote rest and comfort.

OBSERVATION

Do 4 hourly checking of temperature, pulse, respiration and blood pressure in acute stage

to act as baseline data. This will help me monitor the patient’s response to treatment. If

temperature is high Open nearby windows to allow cool fresh air into the room, remove

extra linen from the patient, provide light bed wear to increase heat loss.

If the patient is shivering due to cold, the following will be done to warm the patient.

o Give extra linen to prevent heat loss.

o Give a warm drink to warm the patient.

o Put a hot water bottle rapt in a towel to avoid burning the patient.

If the patient is sweeting room remove wet and soiled line to promote comfort and rest.

Observe the general condition of the patient, whether it’s deteriorating or improving.

If the patient is unconscious, monitor the level of consciousness using a Glascocoma

scale to assess if patient’s condition is improving or not.

Palpation of the spleen and liver will be done to rule out organomegally.

If patient is having diarrhea and vomiting, observe the colour, amount and consistence to

assess severity and abnormalities.

NUTRITION

Provide meals rich in carbohydrates for energy since the body is weak but with low fat to

prevent nausea.

If patient is not able to eat, insert a nasal gastric tube feeding for feeds.

Increase fluid intake by encouraging plenty of oral fluid to rehydrate the patient since

there is vomiting and diarrhea.

If the patient cannot tolerate oral fluids due to vomiting, an intravenous infusion with

normal saline alternating with 5% dextrose will be maintained to rehydrate and provide

energy for the patient.

HYGIENE

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Provide a bath depending of the condition, bed bath or assisted bath everyday and when

necessary especially after profuse sweating.

Do oral care when having a bath and after meals to keep mouth fresh and improve the

appetite.

Keep the bed linen clean and wrinkle free to make patient comfortable to prevent

pressure sore.

Hair care will be done to provide feeling of wellbeing.

Proved a clean emesis bowl with a cover and clean it with disinfectant after use.

Provide a bed pan with a cover to avoid patient from messing up the bed.

I do pressure area care frequently to prevent pressure sores.

ELIMINATION

The patient is losing water through profuse sweat, vomiting and record.

If the patient is unconscious. put up a urinary catheter to empty the bladder and record on

the fluid balance chart.

Record the fluid intake and output then balance in 24 hours using a fluid balance chart.

This also help me assess dehydration in case of reduced output.

Maintaining a fluid balance chart and monitoring of urine output will also help detect

renal failure / impairment as a complication of malaria.

EXERCISE

After patient has recovered a bite, allow him / her to do working exercises to increase

blood circulation which promotes healing.

If confined to bed, assist with passive exercise to prevent complications like deep vein

thrombosis contractures and ankylosis (joint stiffness).

MEDICATION

Give the patient the drugs prescribed by the doctor and make sure that he / she takes the

right drugs, at the right time, the right dose.

HEALTH EDUCATION ON PREVENTION OF MALARIA

Educate the patient of the following:

Encourage the patient seek treatment early whenever they have s/s of malaria before

before complications develops.

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Provide health education information on malaria prevention by using of treated

insecticide bed nets every night to prevent mosquito btes.

Using mosquito repellents to avoid being bitten by mosquitoes.

Reducing mosquito bleeding grounds like clearing of Vegetation around the house.

Burring of ditches with stagnant water or pouring oil on top to prevent mosquito

bleeding.

Residual spraying of houses to kill mosquitoes at least twice a year.

Encourage patient to be wearing long clothes during the night to protect him / her from

mosquito bites.

Intermittent Presumptive Treatment (IPT)

All pregnant women should receive anti-malaria prophylaxis. Following this, it has been

recommended that all pregnant women should receive IPT which is 3 adult treatment

doses with fansidar starting in the second trimester, at least once a month. This approach

should be accompanied by the provision of ITNs at a highly subsidized price through the

antenatal clinics.

COMPLICATIONS

Cerebral Malaria – This is unarousable coma not attributed to any other cause, with

Glasgow coma scale equal or less than 9 due to cerebral sequestration and is caused by

the adherence of parasitised red blood cells to the walls of the small blood vessels in the

brain. In children it carries 10-40% mortality and most deaths occur within the first 24

hours. It causes cerebral dysfunction, convulsions (+50% generalized), focal

neurological signs, coma, brainsterm failure.

Hypoglycemia – (whole blood glucose <2.2mmol/L or <40mg/dl) may be due to reduced

hepatic function or Quinine induced hyperinsulinaemia. Hepatic glycogen in children

only lasts for 12 hours. It contributes to nervous system dysfunction, and in cerebral

malaria is associated with residual neurologic deficit in survivors.

Hypoglycemia presents with anxiety, sweating, breathlessness, dilated pupils, oliguria,

and hypothermia, tachycardia eventually leading to decrease consciousness, convulsions

and coma. Hypoglycemia is common in children 1 to 3 years old.

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JAUNDICE is common in adult patients and is the result a number of mechanisms including

hemolysis, hepatocellular damage, and cholestasis.

BLACK WATER FEVER is massive haemoglobinuria (the urine becomes very dark) in the

context of severe malaria.

HYPOGLYCAEMIA due to impaired liver function or quinine induced hyperinsulinaemia

(Pregnant women are particularly prone. Characterized by sweating, breathlessness, dilated

pupils, oliguria, hypothermia and tachycardia.

HYMOLYTIC ANAERMIA

This results from excessive break down of red blood cells by malaria parasites.

SPLEENOMEGALLY

As a result of many blood cells being broken down, the spleen can be enlarged as a result of over

working.

RENAL FAILURE

CONGESTIVE HEART FAILURE

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FILARIASIS

DEFINITION

Filariasis is a parasitic and infectious tropical disease, that is caused by thread-like filarial

nematode worms in the superfamily Filarioidea, also known as "filariaet". This infection with

filarial worms results in blocking of the lymphatic causing swelling of the surrounding tissue.

CAUSES

There are 9 known filarial nematodes which use humans as the definitive host. These are divided

into 3 groups according to the niche within the body that they occupy:

Lymphatic Filariasis,

Subcutaneous Filariasis,

Serous Cavity Filariasis.

LYMPHATIC FILARIASIS

Lymphatic Filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi, and Brugia

timori. These worms occupy the lymphatic system, including the lymph nodes, and in chronic

cases these worms lead to the disease Elephantiasis.

SUBCUTANEOUS FILARIASIS

Subcutaneous Filariasis is caused by Loa loa (the African eye worm), Mansonella streptocerca,

Onchocerca volvulus, and Dracunculus medinensis (the guinea worm). These worms occupy the

subcutaneous layer of the skin, the fat layer.

SEROUS CAVITY

Serous Cavity Filariasis is caused by the worms Mansonella perstans and Mansonella ozzardi,

which occupy the serous cavity of the abdomen. In all cases, the transmitting vectors are either

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blood sucking insects (fly or mosquito) or Copepod crustaceans in the case of Dracunculus

medinensis.

PATHOLOGY

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Lymphatic Filariasis

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This illustration depicts the life cycle of Brugia malayi, one of the parasitic worms that cause the

tropical disease lymphatic filariasis. Credit: CDC.

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Human filarial nematode worms have a complicated life cycle, which primarily consists of five

stages. After the male and female worm mate, the female gives birth to live microfilariae by the

thousands. The microfilariae are taken up by the vector insect (intermediate host) during a blood

meal. In the intermediate host, the microfilariae molt and develop into 3rd stage (infective)

larvae. Upon taking another blood meal the vector insect injects the infectious larvae into the

dermis layer of the skin. The larva enters circulation and reaches the lymphatic system. The

lymphatic system of the groins is mainly affected.Fertilisation then occurs and the female worm

passes large number of micro-filaria into the blood stream. After approximately one year the

larvae molt through 2 more stages, maturing into to the adult worm.

Individuals infected by filarial worms may be described as either "microfilaraemic" or

"amicrofilaraemic," depending on whether or not microfilaria are found in their peripheral blood.

Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of

microfilaria in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases

based on clinical observations and, in some cases, by finding a circulating antigen in the blood.

INCIDENCE

Any age group can be affected but common in tropical and forest areas, North Africa, West and

North Southern Africa. Filariasis is endemic in tropical regions of Asia, Africa, Central, South

America and Pacific Island nations.

INCUBATION PERIOD

3 months-3 years

CLINICAL FEATURES

The most spectacular symptom of lymphatic Filariasis is elephantiasis—edema with

thickening of the skin and underlying tissues—which was the first disease discovered to

be transmitted by mosquito bites. Elephantiasis results when the parasites lodge in the

lymphatic system.

NYIRONGO (C) 2012 25

Lymphangitis of the affected vessels-pain, tenderness along the coarse of the lymphatic

vessels

Elephantiasis affects mainly the lower extremities, while the ears, mucus membranes, and

amputation stumps are affected less frequently.

Wuchereria bancrofti can affect the legs, arms, vulva, and breasts.

Epidydimitis,orchitis and may develop a hydrocele

Inflammation of ankles,leges,femoral regions

Brugia timori rarely affects the genitals.

Those who develop the chronic stages of elephantiasis are usually amicrofilaraemic, and

often have adverse immunological reactions to the microfilaria as well as the adult worm.

The subcutaneous worms present with skin rashes, urticarial papules, and arthritis, as

well as hyper- and hypopigmentation macules.

Onchocerca volvulus manifests itself in the eyes causing "river blindness"

(onchocerciasis), the 2nd leading cause of blindness in the world.

Serous cavity Filariasis presents with symptoms similar to subcutaneous Filariasis, in

addition to abdominal pain because these worms are also deep tissue dwellers.

INVESTIGATIONS

Presenting signs and symptoms

Blood slide- Blood must be drawn at night, since the microfilaria circulate at night

(nocturnal periodicity), when their mosquito vector is most likely to bite. Filariasis is

usually diagnosed by identifying microfilariae on a Giemsa stained thick blood film.

X-ray of the limbs affected may reveal dead worms

Blood count- increased white blood cell count

In loiasis-exam of the eye may reveal keratitis

Lymph fluid for aspiration-. Lymph Node aspirrate, Chylus fluid may also yield

Microfilriae

Polymerase chain reaction (PCR) and antigenic assays are also available for making the

diagnosis. The latter are particularly useful in amicrofilaraemic cases

Imaging like CT, MRI may reveal "Filarial Dance Sign" in Chylus fluid. X-ray can show

calcified adult worm in lymphatics.

NYIRONGO (C) 2012 26

DEC provokation test is performed to obtain satisfying number of parasite in day-time

samples.

Circulating Filarial Antigen (CFA) may be detected by PCR.

Xenodiagnosis is now obsolete EOsinophilia is a non-specific primary sign.

TREATMENT

Complete bed rest

The recommended treatment for killing adult filarial worms in patients outside the United

States is albendazole (a broad spectrum anthelmintic) combined with ivermectin. A

combination of diethylcarbamazine (DEC) and albendazole is also effective.

In 2003 the common antibiotic doxycycline was suggested for treating elephantiasis.

Filarial parasites have symbiotic bacteria in the genus Wolbachia, which live inside the

worm. When the symbiotic bacteria are killed by the antibiotic, the worms themselves

also die. Clinical trials in June 2005 by the Liverpool School of Tropical Medicine

reported that an 8 week course almost completely eliminated microfilaraemia.

Diethylcarbamazine

Dose-3-6mg/kg body weight daily for 21 days

Side effects-fever, nausea, headache, urticaria, prostration

Inerimectin

Dose-150mg in a single dose

Suramin-macrofilariendal but is liable to cause severe toxic effects and has no action on

micofilariae

COMPLICATIONS

NYIRONGO (C) 2012 27

Hydrocele-accumulation of fluids

Irreversible elephantiasis

Blindness on loiasis (when loaloa worm penetrate eye ball)

Ascites caused by blockage of lymphatic vessels of the abdomen

NYIRONGO (C) 2012 28