TABLE OF CONTENT
1.1.1 Anopheles Mosquito
1.1.2 TRANSMISSION OF MALARIA
& LIFE CYCLE
220.127.116.11 Sporogony within the
18.104.22.168 ASEXUAL CYCLE
phase (schizogony in the liver)
1.1.3 PATHOGENESIS OF MALARIA
1.1.4 CLINICAL FEATURES OF
22.214.171.124b. Body ache, back ache
and joint pains:
1.1.5 OCULAR EFFECTS OF
126.96.36.199 Retinal manifestations
1.2 DEFINATION OF TERMS
1.2.1 ACCOMMODATION&LITUDE OF ACCOMMODATION
1.2.2 NEAR POINT OF CONVERGENCE
1.2.3 SEVERE MALARIA
1.2.4 VISUAL ACUITY
1.3 AIM OF STUDY
1.4 OBJECTIVES OF STUDY
1.5 SIGNIFICANCE OF STUDY
2.0 LITERATURE REVIEW
2.1 EPIDEMIOLOGY OF MALARIA
2.2 GENERAL SYMPTOMS OF MALARIA
2.3 OCULAR SYMPTOMS OF MALARIA
3.1. RESEARCH DESIGN
3.2. STUDY POPULATION
3.2.1 Inclusion Criteria
3.2.2 Exclusion Criteria
3.3. RESEARCH MATERIALS
3.4 DESCRIPTION OF PROCEDURES
3.4.1 Case History
3.4.2 Visual Acuity
3.4.3 External exam Using
3.4.4 Ocular Motility Test
3.4.5 Amplitude of Accommodation
3.5 DATA ANALYSIS
3.6. LIMITATIONS OF STUDY
6.0 CONCLUSION AND RECOMMENDATION 6.1
Malaria is probably one of the oldest diseases known to man,
that has affected social, economic and mental development. The history of
malaria is as ancient as civilization. Malaria was linked with poisonous vapours
of swamps or stagnant water on the ground since time immemorial. This probable
relationship was so firmly established that it gave the two most frequently
used names to the disease mal'aria, later shortened to one word malaria. The
term malaria (from the Italian mala "bad" and aria "air")
was used by the Italians to describe the cause of intermittent fevers
associated with exposure to marsh air or miasma. The word was introduced to
English by Horace Walpole, who wrote in 1740 about a "horrid thing called
mal’aria that comes to Rome every summer and kills one." The term malaria,
without the apostrophe, evolved into the name of the disease only in the 20th
century. Up to that point the various intermittent fevers had been called
jungle fever, marsh fever, paludal fever, or swamp fever.
1.1 BACKGROUND INFORMATION
Malaria is a vector-borne infectious disease caused by
protozoan parasites. It is widespread in tropical and subtropical regions,
including parts of America, Asia and Africa (Barat, 2006). Despite intensive
efforts over the last century to understand and control malaria, to date it
remains the greatest cause of debility and mortality through-out the world.
Malaria has remained a great worldwide problem despite its eradication in
Northern America and most parts of Europe towards the Second World War. In
Africa sub-regions such as Nigeria, malaria remains endemic. Over 40 per cent
of the world’s population live in the regions where malaria is most prevalent,
around the equatorial zone, although climate change may be promoting the spread
of malaria to adjacent regions (UNICEF, 2007).
Country-level burden estimates available for 2010 show that an
estimated 80% of malaria deaths occur in just 14 countries. Together, the
Democratic Republic of the Congo and Nigeria account for over 40% of the
estimated total of malaria deaths globally (W.H.O., 2013). Malaria is a major
public problem in Nigeria; Nigeria contributes a quarter of malaria burden in
Africa. Over 90 per cent of the country’s 167 million people are at risk. It is
estimated that malariarelated illnesses and mortality cost Africa’s economy
about $12 billion annually (Vanguard, 2013).
The malaria situation in Nigeria is no different from the
African regions. Due to its endemic nature, it is cliché to attribute any
pyrexia to malaria in the absence of differential laboratory tests. This high
rate of occurrence of malaria has made people to result to self-medication of
anti-malaria drugs upon the onset of fever and headache, or even malaise and occasionally
dizziness. Some of the malaria drugs are of the class
artemether&lumefantrine, quinine and Artesunate. Though it is gradually
reducing, but it is still worthy to note that some persons still resort to
herbal remedies which comprises of extract of roots, barks and leaves of trees
such as Azadrichata indica (‘Dogonyaro’). These herbal remedies does have
anti-malaria properties, but it pose a danger to the patient due to the
inadequate knowledge of its pharmacological properties such as the active
constituents, therapeutic dosage and side effects.
The most prevalent plasmodia species in Africa is plasmodium falciparum which
unfortunately causes the highest mortality rate.
Children under age five are most likely to suffer from the
severe effects of malaria because they have not developed sufficient naturally
acquired immunity to the parasite.
Malaria during pregnancy can range from an asymptomatic
infection to a severe lifethreatening illness depending on the epidemiological
setting. In areas of stable malaria transmission most adult women have
developed enough natural immunity that infection does not usually result in
symptoms, even during pregnancy. In such areas the main impact of malaria
infection is malaria- related anaemia in the mother and the presence of
parasites in the placenta, contributing to low birth weight, a leading cause of
impaired development and infant mortality. In areas of unstable malaria
transmission women have acquired little immunity and thus at risk of severe
malaria and death.
Malaria is caused by intra-erythrocytic protozoa of the genus Plasmodium, with humans being infected
by one or more of the following species: Plasmodium
falciparum, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, and
Plasmodium knowlesi. Plasmodia are primarily transmitted by the bite of an
infected female Anopheles mosquito. (Zaki and Shanbag, 2011). Infections
can also occur through exposure to infected blood products and by congenital
1.1.1 Anopheles Mosquito
Malaria is transmitted from man to man by the female anopheles
mosquito. This genus of mosquito was first described and named by J.W Meigen in
1818. About 460 species has been recognized; while over 100 can transmit human
malaria, only 30-40 commonly transmit parasites of the genus plasmodium, which cause malaria in
humans in endemic regions. Anopheles
gambiae is best known, because of its predominant role in the transmission
of the most dangerous malaria parasite specie to humans-plasmodium falciparum.
The genome of A.gambiae
has now been cracked and the effort is expected to help in future research into
mosquito control strategies.
The female mosquito has a specialised
apparatus to penetrate the skin of its victim.
Once through the skin, the mosquito's proboscis begins probing
for a tiny blood vessel. Inside the proboscis are two hollow tubes, one that
injects saliva into the microscopic wound and one that withdraws blood. The
mosquito's saliva includes a combination of antihemostatic and anti-
inflammatory enzymes that disrupt the clotting process and inhibit the pain
reaction. (Park, 2007; Paniker, 2007).
Mosquito need human blood because female mosquito lays 30-150
eggs every 2-3 days. Human blood is needed to nourish these eggs and Anopheles
shows the most regular cycles of blood feeding and egg laying. The average life
span of a mosquito is 2-3 weeks. (Paniker, 2007). It can be longer in ideal
Anopheles mosquitoes breed in clean water collections.
Therefore, breeding increases dramatically in the rainy season because many
artificial water collections occur. During the rains, water collects in
bottles, tins, tender coconut shells, buckets, tyres etc., that are thrown out
in the open and these provide ample breeding ground. Also wells, ponds, water
tanks, etc., act as breeding grounds. Usually it takes about a week for the
eggs to develop into adults.
1.1.2 TRANSMISSION OF MALARIA & LIFE
Principal mode of spread of malaria is by the
bites of female anopheles mosquito.
Other modes of transmission
Rarely malaria can
spread by the inoculation of blood from an infected person to a healthy person.
In this type of malaria, asexual forms are directly inoculated into the blood
and preerythrocytic development of the parasite in the liver does not occur.
Therefore, this type of malaria has a shorter incubation period and relapses do
not occur. Others include
Blood transfusion (Transfusion malaria).
Mother to the growing fetus (Congenital malaria)
Needle stick injury (Paniker, 2007; Zaki and
The malaria parasite has a complex, multistage life cycle
(fig.1.1.2) occurring within two living beings, the vector mosquitoes and the vertebrate
hosts. The parasite passes through several stages of development such as the:
Sporozoites (Gr. Sporos = seeds; the infectious form injected by the mosquito)
Merozoites (Gr. Meros = piece; the stage invading the erythrocytes),
Trophozoites (Gr. Trophes = nourishment; the form multiplying in
Gametocytes (sexual stages) and all these stages
have their own unique shapes and structures and protein complements. The
surface proteins and metabolic pathways keep changing during these different
stages thus help the parasite to evade the immune clearance, while also
creating problems for the development of drugs and vaccines.
(Floren et al, 2002).
Figure 1.1.2: Plasmodium life cycle. Image courtesy Centre for Disease
188.8.131.52 Sporogony within the Mosquito
Mosquitoes are the definitive hosts for the malaria parasites,
wherein the sexual phase of the parasite's life cycle occurs. The sexual phase
is called sporogony and results in the development of innumerable
infecting forms of the parasite within the mosquito that induce disease in the
human host following their injection with the mosquito bite.
When the female Anopheles
draws a blood meal from an individual infected with malaria, the male and
female gametocytes of the parasite find their way into the gut of the mosquito.
The molecular and cellular changes in the gametocytes help the parasite to
quickly adjust to the insect host from the warm-blooded human host and then to
initiate the sporogonic cycle. The male and female gametes fuse in the mosquito
gut to form zygotes, which subsequently develop into actively moving ookinetes
that burrow into the mosquito mid-gut wall to develop into oocysts. Growth and
division of each oocyst produces thousands of active haploid forms called
sporozoites. After the sporogonic phase of 8–15 days, the oocyst bursts and
releases sporozoites into the body cavity of the mosquito, from where they
travel to and invade the mosquito salivary glands. When the mosquito thus loaded
with sporozoites takes another blood meal, the sporozoites get injected from
its salivary glands into the human bloodstream, causing malaria infection in
the human host. It has been found that the infected mosquito and the parasite
mutually benefit each other and thereby promote transmission of the infection.
The Plasmodium-infected mosquitoes
have a better survival and show an increased rate of bloodfeeding, particularly
from an infected host. (Park, 2007, Paniker 2007, Fauci et al., 2008).
184.108.40.206 ASEXUAL CYCLE
220.127.116.11.1 Pre-erythrocytic phase (schizogony in the liver)
Man is the intermediate host for plasmodium, and it is man the
asexual cycle is completed. With the mosquito bite, tens to a few hundred
invasive sporozoites are introduced into the skin. Following the intradermal
deposition, some sporozoites are destroyed by the local macrophages, some enter
the lymphatics, and some others find a blood vessel. (Ashley M., 2008; Lucy M.,
2007). The sporozoites that enter a lymphatic vessel reach the draining lymph
node wherein some of the sporozoites partially develop into exo-erythrocytic
stages and may also prime the T cells to mount a protective immune response.
(Michael & Denise, 2007). The sporozoites
that find a blood vessel reach the liver within a few hours. It has recently
been shown that the sporozoites travel by a continuous sequence of
stick-and-slip motility, using the thrombospondin-related anonymous protein
(TRAP) family and an actin–myosin motor. (Sylvia M et al 2009; Baum J. et al 2006). The sporozoites then
negotiate through the liver sinusoids, and migrate into a few hepatocytes, and
then multiply and grow within parasitophorous vacuoles. Each sporozoite develop
into a schizont containing 10,000–30,000 merozoites (or more in case of P. falciparum). The pre-erythrocytic
phase remains a “silent” phase, with little pathology and no symptoms, as only
a few hepatocytes are affected. (Ashley M. et
al, 2008). This phase is also a single cycle, i.e. it occurs just once.
The merozoites that develop within the hepatocyte are
contained inside host cell-derived vesicles called merosomes that exit the
liver intact, thereby protecting the merozoites from phagocytosis by Kupffer
cells. These merozoites are eventually released into the blood stream at the
lung capillaries and initiate the blood stage of infection thereon. (Maria M et
18.104.22.168.2 Erythrocytic Schizogony
The merozoites released from the liver cells attach onto the
red blood cell membrane and by a process of invagination, enter the red cell.
Within the red blood cell, the asexual division starts and the parasites
develop through the stages of rings, trophozoites, early schizonts and mature
schizonts; each mature schizont consisting of thousands of erythrocytic merozoites.
These merozoites are released by the lysis of the red blood cell and they
immediately invade uninfected red cells. This repetitive cycle of invasion -
multiplication - release - invasion continues. The intra erythrocytic cycle
takes about 48 hours in P. vivax, P.
ovale and P. falciparum infections and 72 hours in case of P. malariae infection.
The process of attachment, invasion, and establishment of the
merozoite into the red cell is made possible by the specialized apical
secretory organelles of the merozoite, called the micronemes, rhoptries, and
dense granules. The initial interaction between the parasite and the red cell
stimulates a rapid “wave” of deformation across the red cell membrane, leading
to the formation of a stable parasite–host cell junction. Following this, the
parasite pushes its way through the erythrocyte bilayer with the help of the
actin–myosin motor, proteins of the thrombospondin-related anonymous protein
family (TRAP) and aldolase, and creates a parasitophorous vacuole to seal
itself from the host-cell cytoplasm, thus creating a hospitable environment for
its development within the red cell. At this stage, the parasite appears as an
intracellular “ring”. (Cowman and Crabb, 2006).
The content of the infected cells are released with the lysis
of RBC that stimulate Tumor Necrosis Factor and other cytokines, which results
in the characteristic clinical manifestation of the disease.
A small proportion of asexual parasites do not undergo
schizogony but differentiate into the sexual stage gametocytes. These male or
female gametocytes are extracellular and nonpathogenic and help in transmission
of the infection to others through the female anopheles mosquitoes, wherein
they continue the sexual phase of the parasite's life cycle.
1.1.3 PATHOGENESIS OF MALARIA
Pathology associated with all malarial species is related to
the rupture of infected erythrocytes, release of parasite material and
metabolites and cellular debris. The growing parasite consumes and degrades the
intracellular proteins, mainly haemoglobin (fig.1.1.3). The transport
properties of the erythrocyte cell membranes are altered and new parasite
derived proteins are inserted. P.falciparum has some unique adhesive
characteristics that no other strains possess. Erythrocytes containing mature
forms of P.falciparum adhere to microvascular endothelium (cytoadherence) and
disappear from the circulation. This is called sequestration. Sequestration can
be increased when adherent infected erythrocytes bind to other infected
erythrocytes (autoagglutination) or non-infected erythrocytes (rosetting) or
use platelets to bind to other infected erythrocytes (platelet-mediated
clumping). The major advantage of sequestration for the parasite is avoidance
of the spleen and subsequent elimination from the body. In addition, the low
oxygen tensions in deep tissues may provide a better metabolic environment.
Sequestration within the blood vessels reduces microvascular flow. In addition,
the presence of parasites inside erythrocytes decreases the ability of the
cells to deform so that they have more difficulty passing through the
microvasculature, causing rupture. (Dondorp et
This occurs predominantly in the venules of vital organs. The
consequence of microcirculatory obstruction are activation of the vascular endothelium
and reduced oxygen and substrate supply, which leads to anaerobic glycolysis,
lactic acidosis and cellular dysfunction. Once the mirocirculatory flow is
affected, a range of manifestations can occur including hypoxia, release of
toxic and pharmaco-active substances (free radicals, nitric oxide etc.), and
disruption of capillary flow. (Rahul S, 2011).
fig.1.1.3: pathogenesis of
malaria. Courtesy nature Reviews.
1.1.4 CLINICAL FEATURES OF MALARIA
Malaria infection covers a wide spectrum from
asymptomatic infection to fulminant disease.
Important determinants of the clinical
of the parasite
degree of malaria endemicity. (Rahul S, 2011).
The hallmark of all forms of malaria is fever, which can occur
at regular 2 to 3 day intervals in P.vivax and P.malariae, or more irregularly
with P.falciparum. Fever is associated with lassitude, loss of appetite and
vague pains in bones and joints. Other symptoms include tachycardia,
hypotension, cough, headache, back pain, nausea, abdominal pain, vomiting,
diarrhea and altered consciousness. (Rahul S., 2011). In highly endemic areas,
malaria may present with various atypical manifestations listed below, with or
without the presence of fever. 22.214.171.124a.
Headache: headache maybe a presenting feature of malaria with or without
fever. It can be unilateral or bilateral. Sometimes the headache could be so
intense that it may mimic intra-cranial infections or intra-cranial space
occupying lesions. It may also mimic migraine, .sinusitis etc. Presence of
projectile vomiting, papilloedema, neck stiffness and focal neurological signs
would suggest other possibilities.
126.96.36.199b. Body ache, back ache and joint
These symptoms are fairly common in malaria. These can occur
even during the prodromal period and at that stage these are generally ignored
and diagnosis of malaria is impossible owing to lack of peripheral parasitemia.
They are also common accompaniments of the malaria paroxysm. Sometimes, malaria
may present only with these symptoms, particularly in cases of recurrent
188.8.131.52c. Dizziness, vertigo:
Some patients may present with dizziness or vertigo, with or
without fever. They may also have associated vomiting and/or diarrhoea. This
may mimic labyrinthitis, Menniere's disease, vertebro-basilar insufficiency
etc. Rarely patients may present with swaying and cerebellar signs. Drugs like
chloroquine, quinine, halofantrine and mefloquine can also cause dizziness,
vertigo, and tinnitus.
184.108.40.206d. Convulsions, coma:
Patients with cerebral malaria present with generalised
seizures and deep unarousable coma. Sometimes one single fit can precipitate
deep, unarousable coma. These could also be due to hypoglycemia and all
patients presenting with these manifestations should be administered 2550%
dextrose immediately. Drugs like chloroquine, quinine, mefloquine and
halofantrine may also trigger convulsions.
Cough maybe a presenting feature of malaria especially P.falciparum. The present may present
with pharyngeal congestion and features of mild bronchitis. Patients that have
persistent cough and/or fever even after clearance of parasitemia should be
evaluated for secondary bacterial pneumonias/ bronchopneumonia and bronchitis.
Sometimes patients may present with history of weakness,
malaise and prostration. On examination they may have significant pallor,
hypotension, dehydration etc. the patient may not have fever at all.
Chloroquine is also known to cause profound muscular weakness and a new disease
called macrophagicmyofacitis has been described in patients receiving
Patients may present with history of yellowish discoloration
of eyes and urine. Mild jaundice is fairly common in malaria and may be seen in
20-40% of the cases.
Deeper jaundice with serum bilirubin of more than 3 mg/dL is
seen in severe P. falciparum malaria and is associated with anemia,
hyperparasitemia and malarial hepatitis with elevated serum enzymes. Malaria
must be considered as a differential diagnosis for all cases of jaundice in a
220.127.116.11j.Puffiness of lids:
Occasionally patients may present with
puffiness of lids, with or without renal dysfunction.
18.104.22.168k. Secondary infections:
Malaria produces significant immune suppression and this can
result in secondary infections. Common among them are pneumonia, aspiration
bronchopneumonia (in the elderly), urinary tract infection, colitis etc.
Meningitis and enteric fever have also been reported. In falciparum malaria,
severe infection can lead to septicaemic shock (algid malaria). Persistence of
fever, neutrophilic leucocytosis and focal signs of infection should always
alert the clinician to this possibility of secondary infections.
(Harris V.K. et al, 2001; Sen R. et al, 1994; Bruneel F. et
al, 2003; Gayathri K. et al, 2000; Oh M.D. et al, 2001; Song H.H et al, 2003).
1.1.5 OCULAR EFFECTS OF MALARIA
Many patients with uncomplicated malaria have no significant
intraocular abnormalities. (Lewallen, 1997). However, malaria patients may
develop oedema and hyperaemia of the eyelids, chemosis of the conjunctiva,
conjunctival haemorrhage and anterior uveitis (Biswas J. et al 1996; Hidayat A.A. et
However, the scenario with complicated malaria is different.
The eye “acts as a window to the brain” and therefore looking at the retina in
the eyes of patients with cerebral malaria can provide a vital insight into why
malaria infection in the brain is so deadly. This is because retinal and
cerebral tissues are embryologically the same (neuro-ectodermal) in origin and
therefore share structural and functional similarities. (White V.A et al, 2001).
22.214.171.124 Neuro-ophthalmic manifestations
These occur primarily in a patient with cerebral malaria and
are due to anaemia, vascular occlusion, inflammation and increased intracranial
pressure. As a result, patients may develop a variety of visual sensory
disorders during the course of the disease such as visual field defects,
cortical blindness, optic neuritis, papilloedema and opticatrophy. Papilloedema
is caused by raised intracranial pressure, which in patients with cerebral
malaria has been hypothesised to be a result of increased intravascular blood
volume arising from the presence of sequestered biomass (Rahul S., 2011).
Cortical blindness is a neurological sequelae of cerebral malaria and because
it is reversible, its pathogenesis has been attributed to transient ischaemia.
(Idro R. et al, 2010). Occasionally,
patients develop brainstem infarcts and these may produce disturbances of
ocular motility related to the location and extent of the infarct. Common signs
include changes in pupillary size and reaction, and disorders of conjugate gaze
and eye movements. Absence of corneal and oculocephalic reflexes are associated
with increased mortality. (Molyneux M.E., 1989).
126.96.36.199 Retinal manifestations
Malarial retinopathy is characterized by retinal whitening,
vessel changes and/or haemorrhages (figure188.8.131.52).
Retinal whitening consists of irregular patchy areas that may
be localised or diffused in all segments of the retina. The retinal colour of
the affected portion varies from subtle pallor to dense white. The pattern of
retinal whitening is distinctive in its distribution, affecting both the
central macula (sparing the foveola) and peripheral retina, although it can
occur independently of each other.
Retinal whitening is similar in appearance to that observed in
patches in ischaemic central retinal vein occlusion (CRVO), but has a different
retinal distribution.Vessel changes manifest as discolouration (white or
orange) and occur mainly in the peripheral fundus. Discrete sections of vessels
or peripheral trees can be involved or larger vessels and capillaries can be
involved with distinctive features (Looareesuwan S. et al, 1983). This discoloration occurs due to the absence of
haemoglobin in parasitized erythrocytes, which are sequestered within the
retinal vasculature and cannot reflect the normal red colour. Changes in larger
vessels are commonly segmental, affecting variable lengths of scattered
arterioles and venules but capillary whitening can affect large area of the
fundus, often co-localizing with retinal whitening. (Rahul S., 2011) While
retinal haemorrhages can occur in other conditions causing coma, in malaria
(particularly when white centred) it is highly suggestive of a diagnosis of
cerebral malaria. (Beare N.A., et al,
2009). It has also been observed that the number of retinal haemorrhages
correlates with the number of brain haemorrhages in patients who die from
Fig184.108.40.206: Retinal manifestations of
malaria. Image courtesy of White N. (2000).
1.2 DEFINITION OF TERMS
1.2.1 ACCOMMODATION&LITUDE OF ACCOMMODATION
Accommodation is a process where the crystalline lens
increases its converging power so that diverging rays of light emanating from
an object of regard is brought to focus on the retina. The amplitude of
accommodation (AOA) measured in Dioptres (D) represents the maximal
accommodative level, or closest near focusing response, that can be produced
with maximal voluntary effort in the fully corrected eye.
1.2.2 NEAR POINT OF CONVERGENCE
point of convergence (NPC) measured in centimetres (cm) is defined as the
amplitude of convergence (punctum proximum of convergence), or the closest
point in space where the patient can hold fusion when the two eyes move-in to
see one target (Borish,
1975). People with inadequate NPC may complain of eyestrain,
binocular vision problems and difficulty performing near work. As a result, NPC
findings are used as a screening for obvious convergence insufficiencies
(Brinkley and Walonker, 1983).According to literatures, the normal value for
NPC varies, and this may be due to the measuring technique used. Von Noorden,
(1990) noted that the normal NPC should be 8-10cm.
1.2.3 SEVERE MALARIA
For many years, severe malaria was pictured as essentially two
major syndromes, with relatively simple underlying pathogenic processes:
Severe anaemia caused by the destruction of red
blood cells (RBCs); and
Cerebral malaria (CM) caused by obstruction of
small vessels of the brain by sequestered parasites. (Mackintosh et al, 2004).
A major change in
recent years has been the recognition that severe malaria is a complex
multisystem disorder with many similarities to sepsis syndromes. At the
clinical level, this is evident in the recognition of metabolic acidosis
(leading to the clinical picture of respiratory distress) as the strongest
predictor of death in severe malaria. (Taylor et al, 1993).The pathogenesis of
metabolic acidosis is poorly understood. Hypovolaemiais a major feature of
severe malaria and, when further exacerbated by anaemia and micro-vascular
obstruction from sequestered parasites, is likely to lead to decreased delivery
of oxygen to tissues, anaerobic metabolism and lactic acidosis.
1.2.4 VISUAL ACUITY
Visual acuity is the resolving power of the eye, or the
ability to see two separate objects as separate (Grosvenor, 2007). There are
various measuring instruments or chart for visual acuity, e.g are snellen
chart, Cardiff acuity chart, LogMAR acuity chart etc.
1.3 AIM OF STUDY
determine the ocular complications of malaria.
1.4 OBJECTIVES OF STUDY
determine the ocular complications of malaria with its relationship with the
determine if these complications are dependent on the severity of malaria
1.5 SIGNIFICANCE OF STUDY
This study will be able to help us find out the retina and
ocular adnexa signs that are common in children with malaria in our environment.
Also it will help us to assess the burden of malaria in our environment and on
H10: There are no known ocular complications
associated with malaria parasitaemia in the paediatric population. H1o=HA.
H1A: There are ocular complications associated with
malaria parasitaemia in the paediatric population. H1o≠H1A.
H20: Malaria ocular complications
are not dependent on the severity of malaria parasitaemia.
H2A: Malaria complications are
dependent on the severity of malaria parasitaemia. H2o≠H2A