CHAPTER 1

1.0: INTRODUCTION.

The causative agent of amoebiasis is the intestinal protozoa of the order amoebida.

Dysentry was first described by Hippocrates but it was not until 1875 that losch characterized
motile trophozoite from stool of a Russian farmer. Later actual relationship between the
organism and the disease was established in 1891 as a result of the investigation of councilman
and lafler.(Monica cheesbrough).

It was a world wide distribution and it is the most common widespread in man, apes, monkeys,
dogs, cats, and rats.

Who (1979) showed that up to 10% of the world population was infected with entamoeba
histolytica resulting to a morbifity second only to that of malaria and schistosomiasis.

The same report shows that less than 5% incidence of amoebic infection in developed countries
occur, but survey in homosexual have documented isolation of entamoeba histolytica from
upto 30% of stool specimen. (WHO,1979).

Infection occur mainly through the faecal oral route. Man is the resevoir host of infection.

Entamoeba is endemic in many parts of tropical and sub tropical africa, asia, mexico, south
america and china.

Distribution is more related to inadequate environmental sanitation and poor hygiene than to
climate. (Monica cheesbrough).

10% of those with amoebiasis develop amoebic disease and that 40000-110000 people die from
invasive amoebiasis worldwide (WHO, 1981).

The organism (entamoeba histolytica) invades the wall of large intestine of man, multiply in the
sub mucosa causing low abdominal pain and acute attacks of dysentery with blood and mucus
in faeces, forming large flask shaped walls .

Some lesions remain small and discrete but others expand undermining ulcer margin.

Transmission and lifecycle of entamoeba histolytica occurs when infection cysts are ingested in
food, water through hands contaminated with faeces.

Lack of perional hygiene among cysts carriers contribute to spread of infection.

Also vectors loke flie transmit by feeding on faeces contaning cysts and sub sequent containing
food.

Encysted and the infective cysts panes faeces to environment which causes contamination and
cycle start again. (Gilmans AL, 1990).

Human infection is derived directly from other humans (carriers) although dogs, cats and rats
may occasionally be a source of infection. It's likely that the non human reservois are more
often infected from man.

Most infected people are symptomatic cysts passers and may act as reservoirs host especially if
they are food handlers.

Insects may help to disseminate the infection to a small extent by mechanical carrying of cysts
on their feet from faeces on to the food. (Carter j and O.Leuma 1994).

1.1: HOST

Man remains the reservoir host of the entamoeba histolytica. It's believed that man can create
a good environment suitable for invasion by entamoeba histolytica by taking irritating food
such as hot spices, tropical fruits as well as expensive alcohol which may irritate the intestinal
mucosa hence the invasion. This account for high incidence of amoebiasis among visitors to
tropical areas.

Women are less frequently affected especially with repeat to acute amoeba colitis and liver
abscess also preschool children show lower infections than those in old age groups.

Peak of infections occur in twenty four to twenty ninth year of age and this may be due to
chances of exposure than sex and age.

1.2: TRANSMISSION.

Infection occur through faecal oral route after ingestion of infective cysts in food or drinking
water contaminated with sewage or hands contaminated with faeces. Also may occur by eating
raw vegetables and fruits which are not properly washed (Gilmans AL, 1990).

1.3: LIFECYCLE.

The resistant infective cysts formed in the lumen of the large intestine are passed out in the
faeces and are ingested by a new host through contamination of food and water, since the
mature cysts are resistant to the acidic digestive juice of the stomach, pass to the lower part of
the small intestine.
Under influence of the neutral or alkaline digestive juice, the cysts wall disintegrates liberating a
four nucleated meta cystic amoeba.

The small immature amoebae move downward to the large intestine where encystation takes
place giving mature cyst which are voided out through faecal material.

1.4: OBJECTIVES.

1. To determine the age group mostly affected.

2. To identify the predisposing factor of the disease.
3. To asses the possible ways of prevention and control of amoebiasis in the region.

1.6: PROBLEM STATEMENT.

The research on amoebiasis has been widely done especially in underdeveloped countries
(Elaine,2017) but none has been done in Miathene sub county hospital. According to the center
for disease control and prevention (CDC,2019) when symptoms occur they tend to appear one
to four weeks after ingestion.

When the amoebiasis is located outside the intestines it can not be traced in the stool (Elaine,
2017).

It has been found that one the trophozoite have breached the intestinal wall, they can enter
the blood stream and travel to various internal organs example liver, heart,lungs,brain, and
other organs. This can potentially cause; absecesse, infectio, severe illness or death (Elaine,
2017).

1.7: STUDY AREA.

The research was carried out in Miathene sub county hospital. The hospital is situated in
Tigania west sub county in Meru county and is a sub county hospital that takes care of many
people in the area.

The hospital is located several kilometers from meru town in a small village called Miathene.

Miathene is located in a somehow flat area but near a hill called Nyambene hills. The area
receives maximum rainfall in the months October- December.

The main tribe in the area are Merians and the common language is Kimeru.

The infrastructure of the area is of an average standard the main road has been tarmarked
recently and clean water in the households is being adopted.

The habitants are mostly business people who mainly deal with vegetables, fruits and cereals. A
lot of people also engage in grazing which indirectly contribute to the spread of amoebiasis in
that the milk is sold in kiosks, which at times is not properly milked due to carelessness and lack
of personal hygiene of some milkers.

The drainage systems are not well managed. This contributes to the increase of the infection to
the people living in the area.

CHAPTER 2

2.0: LITERATURE REVIEW.

2.1 MORPHOLOGY AND IDENTIFICATION.

Amoebiasis is caused by a parasite that belong to phylum protozoa, sub phylum sarcodina and
genus entamoeba.

Amoeba protozoa consist of s shapeless mass of moving cytoplasm which is divided into
granules endoplasma and clear ectoplasm.

They move by pushing out the ectoplasm to form pseudopodia into which the endoplasm then
flows (lewis, 1870)

Amoeba produces asexual by simply dividing into two (binary fission). It lives in the large
intestine as trophozite. It produces resistant cysts by which it is transmitted. It is spherical and
occasionally void in shape. It is formed in the lumen of the intestines and it develops up to four
nuclei each nucleus contains antennally placed endosome with chromatin granules around the
nucleus inner edge (Monica cheesbrough 1990).

Diagram of entamoeba histolytica trophozoite

 10-50um in diameter
 Cytoplasm clearly differentiated into ectoplasm and endoplasm.
 Nucleus vesicular with small karyosome and fine peripheral granules of chromatin.(J.
Carter and O. Leuma)
Diagram of the entamoeba histolytica cyst

Features of the cyst

 10-20um in diameter
 Spherical with nuclei when mature
 Chromatoid bar stain blue
 Chromatoidal bodies have rounded edge (Jane carter and orgene leuma, 1994).
2.2: PATHOGENESIS

The infection occurs mainly through the feacal oral route. Man is the reservoir host of infection,
although other primates can harbour entamoeba histolytica.

The infection is endemic in many parts of tropical and sub tropical africa, asia, Mexico, south
america and China.

Distribution is more related to inadequate environmental sanitation and poor hygiene than to
climate. (Monica cheesbrough)

Who report between(1975-1981) shows that 10% of those with amoebiasis develop amoebic
disease and that annually probably, 40000-110000 people die from invasive amoebiasis world
wide.

The organism (entamoeba histolytica) invades the wall of the large intestine of man, multiply in
the sub mucosa causing low abdominal pain and acute attacks of dysentery with blood and
mucus in faeces, forming large flask shaped ulcers. (Gillespie JA, 1967)

Some lesion remain small and discrete but others expand undermining ulcer margin. Patients
have mild and intermittent diarrhoea with passage of 4-6 bulky foul smelling blood stained
stool with acidic pH since the amoeba digest red blood cells from damaged capillaries.

Colicky pain experienced in the right and left illiac forral, pelvic colon and caecum maybe tender
on palpation entamoeba histolytica also causes extra intestinal amoebiasis, which affects the
liver, pericardium and occasionally brain, bladder, cervix and spleen causing absasess (Monica
cheesbrough).

Amoeba may also invade the blood and be carried to the liver where they can cause hepatic
amoebiasis, with abscess formation where there is leukocytosis with a left shift of the
neletrophils, anaemia, a marketly raised erythrocytes sedimentation rate a low serum albumin
and an increase in alkaline phosphate level, patients with large or multiple abscess may be
jaundiced (cruickshrik el, 1976)

Finally amoebiasis causes two types of dysentery that is amoebic dysentery and bacillary
dysentery. (Gilmans Al, 1990)

Distinguish features of amoebic dysentery and bacillary.

Microscopy Amoebic dysentery Bacillary dysentery

 Ingested red blood  Many pus cells

 cells  Large macrophages
 Few pus cells and  Red blood cells
macrophage cells present.

Reaction of stool  Often dark red  Alkaline pH

with blood and  Often bright red with
mucus mixed with blood clots and mucus
faeces  Stool is odourless
 Stool has offensive
odour

(Councilman antlafleur, 1891).

2.3: LABORATORY DIAGNOSIS.

Laboratory diagnosis involved collection of faecal specimen where patients were given wide
mouthed polypot for collection of faeces. For clinical purposes a fresh faecal specimen was
required.

The container of collection had to be clean, leak proof and free from any traces of antiseptic
and disinfectant.

Method involved included macroscopic examination and microscopic examination.

2.4: MACROSCOPIC EXAMINATION.

After receiving the specimen in the laboratory the following was noted and reported

I. Colour
II. Consistency whether the stool was formed, semi formed or watery.
III. Smell either odourless, offensive odour etc.
IV. Presence of blood, mucus or pus

2.5: MICROSCOPIC EXAMINATION.

Microscopic examination is the method of choice in identification of various intestinal parasites.

The specimen was examined immediately by the methods below;

a) Wet preparation
b) Concentration method
a) Wet preparation.
Materials; microscope

Slides and coverslips

Applicator sticks

Normal saline

Disinfecting container

1% iodine

Procedure

 A drop of normal saline was placed on one end of a slide and a drop of eosin on the
other end
 A small amount of stool was picked using an applicator stick and emulsified on the
above preparations.
 The preparations were then covered by a cover glass
 On the microscope stage the slide was examined first with x10 objective with the
condenser closed sufficiently to give good contrast
 Then x40 objective was removed and put in a disinfecting container different from that
of coverslips.
 Results obtained were recorded and dispatched.

b. Concentration method.

The method was necessary because it helped in detecting parasites which were not easily found
in direct preparation yet there were symptoms of intestinal parasites infection.

The method mostly used was;

Formal ether concentration technique

PRINCIPLE: Parasites are sedimented by centrifugal force and ether dissolves faecal fat and
separate faecal matter from sedimented fat.

REQUIREMENTS:

 Formal water 10%

 Diethylether
 Sieve (strainer) with small hole preferably 400-450 um in size
METHOD:

i. Using an applicator stick an estimated 1g of faeces was emulsified in about 4ml of 10%
formal water contained in a tube.
ii. A further 4ml of 10% formal water was added and the bottle stoppered, mixed by
sharking about 20seconds.
iii. The emulsified faeces were sieved and the sieved suspension was collected in a beaker
iv. The suspension was then transferred into a centrifuge tube and an equal volume of
ethyl ether was added.
v. The centrifuge tube was stoppered and the suspension with ethyl ether was mixed for
one minute and left for 5 minutes.
vi. With a piece of cloth, the stopper was woseved then centrifuged at 3000 rpm
vii. The supernatant was discarded leaving the sediments
viii. The tube was put in an upright position which allows the fluids on the sides of the tube
to be drained to the bottom of the tube.
ix. Sediments were mixed with a pasteur pipette and a drop was transfered to a slide and
covered with a coverslip.
x. The preparation was examined microscopically with x10 and then with x40 objective,
with condenser sufficiently closed to give a good contrast.
xi. Invade the cysts were present, iodine was run to confirm diagnosis.

2.6: TREATMENT

In treatment of intestinal amoebiasis and other invasive forms of the infection, a number of
amoebicides are used. The treatment of intestinal amoebiasis is directed at eradicating the
cysts with luminal amobicides which include;

 Diloxamide furoate
 Paromomycin (aminoside)
 Iodoquinone (iodohydroxy quinone)

Tissue invading (bupatic) amoebiasis is treated with tissue amoebicides which are active against
invading trophozoite and are absorbed into systemic circulation to reach tissues. The drugs
include;

 Metronidazole
 Secnidazole
 Tinidazole
 Dihydroemetine
 Chloroquine
In severe cases of tissue invading amoebiasis the use of tetracycline (eg doxycycline) to lessen
the risk of opportunistic or concurrent bacterial infection is recommended.

Treatment with hepatic amoebicides should be followed by a course of luminal a.oebicide to

eradicate the source of infection. There is also use of drug combinations containing more than
one drug which are synergistic and have both tissue and luminal activity eg metronidazole and
diloxamide furoate (entamizole) ( British national fomularly, 2001).

SOME OF THE INDIVIDUAL DRUGS.

2.6.1: Metronidazole

Metronidazole is a drug of choice for acute invasive amoebic dysentery since it is very effective
against vegetative forms of entamoeba histolytica in ulcers;

It is given in an adult dose of 800mg three times daily for 5 days.

For amoebic abscess of the liver, it is effective in doses of 400mg three times daily for 5-10
days.

It causes various side effects e.g nausea, vomiting, metallic taste, gastrointestinal disturbances,
darkening of urine, e.t.c. (BNF, march 2001)

2.6.2: Diloxamide Furoate

Diloxamide furoate is the drug of choice for asymptomatic patients with entamoeba histolytica
cysts in the faeces;

Its relatively free from toxic effects and the visual course is of 10 days, its given alone for
chronic infections or following metronidazole and tinidazole treatment.

It's usually contraindicated in pregnancy and breast feeding mothers.

It's main side effect include; flatulence, vomiting, uticarria and pruritus (BNF, 2001).

Diloxamide furoate is not effective against hepatic amoebiasis but a 10day course should be
given at the completion of metronidazole or tinidazole treatment to destroy any amoebae in
the gut (BNF,2001)

2.6.3: Paromomycin.

Paromomycin is an aminoglycoside antibiotic, it's active against luminal amoebiasis but has no
effect against extra intestinal infection.

2.7: PREVENTION AND CONTROL.

For proper prevention of infections then water, food and other contaminated liquours or
beverages should be avoided at all cost.

Drinking water should be boiled. This will mainly kill infective cysts of the parasite which may
have contaminated the water in the water supplies.

There should be proper food coverage and storage to avoid contamination from vectors
carrying infective cysts.

Food should be properly cooked before being eaten, for vegetables and fruits they should be
thoroughly washed before being eaten to avoid contamination by the parasite cysts, for the
green salads soak in vinegar for 30 minutes to kill the cysts since the parasite are killed at
temperature of 53degree celcius.

There should be proper faecal disposal, this is mainly by digging of pit latrines and use of toilet
to avoid faecal contamination of water in natural sources.

Water should be treated by super chlorination before being distributed to the consumers in
order to kill the infective cysts of entamoeba histolytica which may have contaminated the
water.

CHAPTER THREE

3.0: METHODOLOGY.

3.1: RESEARCH DESIGN.

The method of data collection was mainly through obtaining vital information from treatment
sheets and laboratory results which were later analyzed.

3.2: Location of the study.

The study was conducted in Miathene sub county hospital since the hospital handles such
common cases.

The hospital is located in Meru county in Tigania west a place accessible and convenient for
study of patients in hospital and it's vicinity.

3.3: Population of the study.

The target population was all attending the hospital in the year 2019 from 1st September to
20th December with complications resulting from amoeba infection. The sample size of 800
patients was used for the study following the objectives of the study
3.4: Sampling procedure.

The procedure which was employed here is random sampling, sampling was done by picking
treatment sheets and laboratory results, the data contained was then collected and then
recorded. It was analyzed by considering the age groups and sex of the patients.

CHAPTER FOUR

4.0: RESULTS AND PRESENTATION.

The patients who attended Miathene sub county hospital ranged from 1-62years.

Out of 800 samples examined in the laboratory between the months of September and
December 2016, 346 samples were positive.

4.1: TABLES

Table 1 below shows the positive cases in different age groups.

Table 1.

FEMALE MALE

MONTH 0-20 21-41 42-62 0-20 21-41 42-62 TOTAL

September 14 21 9 13 20 6 83

October 17 27 11 17 17 7 96

November 20 20 7 10 23 11 91

December 13 18 9 19 11 6 76

TOTAL 64 86 36 59 71 30 346

From the data obtained, table 1, it was clear that the incidence of infection were high in the
months of October and November.

Female patients recorded the highest number of infections according to the research.

The ages between 21-41 in female patients recorded the highest number of infections, while
ages between 42-62 recorded the lowest with 36 cases.

Ages between 0-20 were relatively high but not more than 21-41.
In male patients ages between 21-41 also recorded the highest number of infections, while ages
between 42-62 recorded the lowest with 30 infected patients.

Ages between 0-20 in male patients recorded 59 cases of the infection.

The total number of infections were 346 between the months of September to December.

Table 2;

PREVALENCE OF ENTAMOEBA IN PATIENTS AGED 1-20 YEARS.

SEX NUMBER OF POSITIVE NEGATIVE

PATIENTS

MALES 80 59 21

FEMALE 95 64 31

TOTAL 175 123 52

In comparison, according to the research at this ages 1-20 females are more infected than
males.

Research showed that most people between the ages of 1-20 that had the symptoms of the
infection after diagnosis were found infected.

Table 3;

PREVALENCE OF AMOEBIASIS IN PATIENTS AGED 21-41 YEARS.

SEX NUMBER OF POSITIVE NEGATIVE

PATIENTS

MALES 101 71 30

FEMALES 146 86 70

TOTAL 247 157 100

Most patients in this ages 21-41 are infected. So many cases were reported and tested positive.

Females are more infected than males.

 Table 4;

PREVALENCE OF AMOEBIASIS IN PATIENTS AGED 42-62 YEARS

SEX NUMBER OF POSITIVE NEGATIVE

PATIENTS

MALES 62 30 32

FEMALES 58 36 22

TOTAL 120 66 54

Females are still more than males according to the table above.

Not so many reported cases between this ages 42-62 in comparison to other ages.

In tables 2,3 and 4, there were more female 54% as compared to males 46% affected.

This may be due to the reason they they handle children who may have faecal contamination.

Table 5;

PERCENTAGE DISTRIBUTION OF ENTAMOEBA HISTOLYTICA IN PATIENTS AGED 1-20

SEX NUMBER OF POSITIVE NEGATIVE % DISTRIBUTION

PATIENTS

MALES 80 59 21 73.75%

FEMALES 95 64 31 67.37%

TOTAL 175 123 52 70.3%

Table 6;

PERCENTAGE DISTRIBUTION OF ENTAMOEBA IN PATIENTS AGED 21-41 YEARS.

SEX NUMBER OF POSITIVE NEGATIVE % DISTRIBUTION

PATIENTS

MALES 101 71 30 70.3%

FEMALES 146 86 70 58.9%

TOTAL 247 157 100 63.6%

Table 7;

PERCENTAGE DISTRIBUTION OF ENTAMOEBA IN PATIENTS AGED 42-62 YEARS.

SEX NUMBER OF POSITIVE NEGATIVE % DISTRIBUTION

PATIENTS

MALES 62 30 32 48.4%

FEMALES 58 36 22 62%

TOTAL 120 66 54 55%

In relation to the age groups, the data shows female of age between 21-41 years had the
highest percentage of infections.

This may be due to lack of toilets in the rural areas and poor hygiene.