DIRECTORATE OF LEARNING SYSTEMS
DISTANCE EDUCATION PROGRAMME
COMMUNICABLE DISEASES COURSE
Unit 11
Unit 5: Diseases of Faecal-oral Contamination
Allan and Nesta
Ferguson Trust
Unit 5: Diseases of Faecal-oral Contamination
A distance learning course of the Directorate of Learning Systems (AMREF)
© 2007 African Medical Research Foundation (AMREF)
This course is distributed under the Creative Common Attribution-Share Alike 3.0 license.
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address any correspondence to:
The African Medical and Research Foundation (AMREF)
Directorate of Learning Systems
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Tel: +254 (20) 6993000
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Writer: Dr Peter Ngwatu
Chief Editor: Anna Mwangi
Cover design: Bruce Kynes
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The African Medical Research Foundation (AMREF wishes to acknowledge the contributions
of the Commonwealth of Learning (COL) and the Allan and Nesta Ferguson Trust whose
financial assistance made the development of this course possible.
Contents
INTRODUCTION .................................................................................................................................. 1
SPECIFIC OBJECTIVES ......................................................................................................................... 1
SECTION 1: OVERVIEW OF FAECAL - ORAL DISEASES ......................................................... 2
NATURAL DEFENCES ........................................................................................................................... 4
Gastric Acid ...................................................................................................................................... 5
Natural Bowel Motility ..................................................................................................................... 5
Normal Intestinal Bacterial Flora .................................................................................................... 5
CLINICAL PRESENTATION OF FAECAL-ORAL DISEASE ...................................................................... 5
DIAGNOSIS............................................................................................................................................ 6
TREATMENT ......................................................................................................................................... 6
Oral Rehydration Salts ..................................................................................................................... 7
PREVENTION AND CONTROL ............................................................................................................... 8
CHECK-POINTS FOR SOURCES OF WATER BORNE DISEASES ........................................................... 11
Kiosks and Food Shops................................................................................................................... 11
Hotels.............................................................................................................................................. 12
Private Homes ................................................................................................................................ 12
Irrigation Furrows.......................................................................................................................... 12
Health Facilities ............................................................................................................................. 13
SECTION 2: FAECAL-ORAL DISEASES CAUSED BY BACTERIAL INFECTION ............... 13
ACUTE GASTROENTERITIS ................................................................................................................ 13
Epidemiology .................................................................................................................................. 14
Management ................................................................................................................................... 15
Prevention and Control .................................................................................................................. 15
BACILLARY DYSENTERY ................................................................................................................... 16
Epidemiology .................................................................................................................................. 17
Pathology........................................................................................................................................ 17
Clinical Picture .............................................................................................................................. 17
Diagnosis ........................................................................................................................................ 18
Management ................................................................................................................................... 18
Prevention and Control .................................................................................................................. 19
CAMPYLOBACTER JEJUNI INFECTIONS............................................................................................. 20
Pathology........................................................................................................................................ 20
Clinical Picture .............................................................................................................................. 21
Diagnosis ........................................................................................................................................ 21
Management ................................................................................................................................... 21
Prevention and Control .................................................................................................................. 22
CHOLERA ........................................................................................................................................... 23
Epidemiology .................................................................................................................................. 23
Clinical Picture .............................................................................................................................. 25
MANAGEMENT ..................................................................................................................................... 25
Prevention and Control .................................................................................................................. 26
ENTERIC FEVER ................................................................................................................................. 29
Epidemiology .................................................................................................................................. 29
Clinical Picture .............................................................................................................................. 30
Diagnosis ........................................................................................................................................ 30
Management ................................................................................................................................... 31
Prevention and Control .................................................................................................................. 31
SECTION 3: FAECAL-ORAL DISEASES CAUSED BY PROTOZOAL INFECTION .............. 31
GIARDIASIS ........................................................................................................................................ 32
Pathology........................................................................................................................................ 32
Clinical Picture .............................................................................................................................. 32
Diagnosis ........................................................................................................................................ 33
Management ................................................................................................................................... 33
Prevention and Control .................................................................................................................. 33
AMOEBIASIS ....................................................................................................................................... 33
Epidemiology .................................................................................................................................. 34
Pathology........................................................................................................................................ 34
Clinical Picture .............................................................................................................................. 35
Diagnosis ........................................................................................................................................ 36
Extra-Intestinal Manifestations of Amoebiasis ............................................................................... 36
Diagnosis ........................................................................................................................................ 37
Management ................................................................................................................................... 38
Prevention and Control .................................................................................................................. 39
SECTION 4: FAECAL-ORAL DISEASES CAUSED BY TOXINS ............................................... 40
FOOD POISONING ............................................................................................................................... 41
Epidemiology .................................................................................................................................. 41
Clinical Picture .............................................................................................................................. 41
Management ................................................................................................................................... 42
Prevention and Control .................................................................................................................. 42
SECTION 5: FAECAL-ORAL DISEASES CAUSED BY VIRAL INFECTION .......................... 43
Clinical Picture .............................................................................................................................. 45
Management ................................................................................................................................... 46
Prevention and Control .................................................................................................................. 46
VIRAL HEPATITIS .............................................................................................................................. 48
Hepatitis A ...................................................................................................................................... 48
Hepatitis E ...................................................................................................................................... 50
ROTAVIRUS ........................................................................................................................................ 50
Clinical Picture .............................................................................................................................. 50
Diagnosis ........................................................................................................................................ 51
Management ................................................................................................................................... 51
Prevention and Control .................................................................................................................. 51
TUTOR MARKED ASSIGNMENT .................................... ERROR! BOOKMARK NOT DEFINED.
ii
ABBREVIATIONS
ALT
Alanine aminotransferase
AST
Aspartate aminotransferase
EBV
Epstein-Barr virus
HIV
Human immunodeficiency virus
Ig
Immunoglobulin
IPV
Inactivated polio vaccine
OPV
Live attenuated orally administered polio vaccine
ORS
Oral re-hydration salts
DMO
District Medical Officer
WHO
Would Health Organization
iii
INTRODUCTION
Welcome to the eleventh unit of this course on communicable diseases. In the last three
units, you learnt about vector borne as well as emerging and re-emerging diseases. More
specifically, we focussed on their distribution, clinical manifestations, management and
how to prevent and control infections in the community. In this unit, we shall discuss
faecal-oral diseases that are of viral, bacterial and protozoal origin. We shall also look at
diseases caused by toxins but will leave out those that are caused by worms as these will
be covered in Unit 12 on helminthes.
For each of the diseases, we shall study the epidemiology, clinical manifestations,
diagnosis, treatment and how to prevent each one of them. As we go through this unit,
you will realize that the concepts you learnt in the first unit of this course need to be at the
back of your mind at all times, as many of them are applicable in this unit as well. Before
we begin, let us go through the objectives of this unit.
Specific Objectives
By the end of this unit you should be able to:

List the diseases acquired through the faecal-oral route;

Describe the epidemiology of the faecal-oral transmitted diseases;

Differentiate the clinical presentation for the various faecal-oral diseases;

Make a diagnosis for the different faecal-oral transmitted diseases;

Manage a patient with dehydration;

Manage the different faecal-oral transmitted diseases;

Discuss prevention and control of the diseases spread by the faecal-oral route.
Let us start off with a general overview of faecal-oral diseases.
1
Section 1: Overview of Faecal-Oral Diseases
As the name suggests, faecal-oral diseases are diseases that occur when the causative
organisms which are excreted in the stools of infected persons (or less commonly animals)
gain entry into the human host via the mouth. Therefore, the organisms have to pass
through the environment from the faeces of an infected person to the digestive system of a
susceptible person. This is known as the faecal-oral transmission route.
Faecal-oral transmission of organisms causing disease occurs mostly through faecal
contamination of food, water, and hands which is not at all apparent. Very small amounts
of faeces can carry enough organisms to establish infection. Seemingly sparkling clear
water may be dangerously polluted. Contaminated food may smell, look and taste normal
and yet harbour infective organisms. Clean-looking hands may carry and transmit enough
micro-organisms to spread disease. The diagram below summarizes the faecal-oral
transmission route.
Figure1: The faecal- oral transmission route
As shown in Figure 1, food plays a central role in transmitting diseases because it can be
directly or indirectly contaminated via polluted water, dirty hands, contaminated soil, flies,
animals and animal products. Water can be polluted directly by faeces or faecal material
may be washed into it from the polluted soil along river banks. The hands are usually
contaminated after defecation or by touching contaminated objects.
2
The house fly is very likely to carry faecal material because of its habit of starting a meal
on faeces and finishing it off on human food. The fly can transfer organisms from faeces
to food by carrying them on its body, by vomiting on solid food in order to liquefy the food
and by defecating on food. The faeces and vomitus of the fly may contain viable infective
organisms from human faeces.
Take Note

There are many diseases that are transmissible through faeces but not all of them
are strictly faecal-oral in transmission.
For instance, the polio virus may also be transmitted by droplet infection, especially during
epidemics while anthrax which is caused by the bacterium Bacillus anthracis may also be
transmitted by inhalation of spores and direct skin contact with infected hides. The eggs of
intestinal worms are excreted in the faeces but the portal of entry for infections is not
always the mouth. For example, Schistosoma mansoni is acquired through the skin.
Food poisoning is not always due to faecal contamination but certainly belongs to the
food-borne group of diseases. Many types of salmonella other than Salmonella typhi
come from animals and can cause diarrhoea in humans, while Campylobacter from poultry
can also be transmitted to humans. In these diseases infection is acquired by eating
infected meat or eggs or from contaminated kitchen utensils and surfaces. Table 1 below
shows the diseases acquired through the oral route.
Table 1: Diseases acquired via oral route
Viral
Polio
Bacterial
Typhoid and
paratyphoid
Protozoa
Worms
Amoebiasis Ascariasis
Hepatitis A, E
Giardiasis
Enterobiasis
Cholera
Viral diarrhoeas
such as rotavirus
and adenovirus
Toxins
Botulism
Staphylococcal
food poisoning
Trichuriasis
Bacillary dysentery
Taeniasis
Anthrax
Hydatidosis
Bacteria diarrhoeas
such as Yersinia,
Campylobacter, E. coli
3
Enterotoxigenic
coli diarrhea
We shall discuss the diseases that are shown in Column 4 (worms) in the next Unit. Here
we shall focus on the diseases that are shown in the other columns, that is, viral, bacterial,
protozoa and toxins.
The marked difference in the infectivity of these organisms is their susceptibility to lysis by
gastric acid in the stomach.
Take Note

Gastric acid is capable of killing many organisms thus preventing infection in
some cases. This natural defence mechanism is most effective against
organisms such as Vibrio cholera and Salmonella typhi.
As a result, very large doses of vibrio cholera or salmonella typhi have to be ingested in
order to cause disease. This makes accidental infection with typhoid or cholera by contact
or contamination of food by flies very unlikely. Thus both diseases are almost exclusively
water and food-borne.
When only a very small number of organisms is required to cause infection, as in bacillary
or amoebic dysentery, this is very easily done accidentally by the fingers or by
contamination of food and eating utensils by flies. Indeed, usually there is an increase of
dysentery cases during the season when flies are plentiful. Of course, infections through
contaminated water occur as well. Contamination of fingers and eating utensils is most
likely to occur when water for hand washing and cleaning is in short supply.
Diarrhoeal diseases are often associated more with an inadequate supply of water than
contamination of water and will usually disappear when the amount of water available is
increased. It is the quantity rather than its quality which appears to be more important in
relation to diarrhoeal disease transmission and control.
Natural Defences
Give 3 examples of natural defenses the body has against infection.
4
Gastric Acid
We already mentioned this first line of defence – the gastric acid. Due to its acidic nature,
the gastric acid prevents infections in some instances by killing ingested organisms
through lysis.
Natural Bowel Motility
The natural bowel motility acts as a cleaning mechanism. Diarrhoea is usually
accompanied by increased bowel movements and it can be regarded as a normal body
response for flushing out harmful substances from the body. Thus it should not be
surprising that suppression of bowel motility may be harmful in diarrhoeal diseases as you
tend to hold the infective organism much longer in the digestive tract and this will lead to a
delay in the recovery process.
Normal Intestinal Bacterial Flora
These bacteria form an important protective barrier against pathogenic bacteria. As long
as they live and multiply in the bowel, pathogenic organisms have less chance of thriving.
This is called bacterial competition. One way to predispose both animals and humans to
bowel infection is to treat them with broad spectrum antibiotics which kill their normal
intestinal flora.
Clinical Presentation of Faecal-oral Disease
Diarrhoea is the commonest manifestation for the majority of the faecal-oral diseases.
Diarrhoea causes loss of body fluids, leading to dehydration. In mild dehydration the child
presents with thirst and on physical examination will be alert or restless. However, with
moderate to severe dehydration, the child may present with:

Thirst, lethargy and irritability or even drowsiness;

Rapid and weak pulse due to poor perfusion;

Anterior fontanel sunken (it closes at about 18months of age). This reflects
depletion in cerebrospinal fluid;

Skin retracts slowly on being pinched due to decreased interstitial fluid;

Sunken eyes, reflecting decreased vitreous humor;

Mucus membranes are dry, reflecting reduced trans-cellular fluids;

Urine flow is reduced;

Poor capillary refill >2 seconds.
5
Take Note

Death from diarrhoeal diseases is largely due to dehydration and
disturbance of the electrolytes balance.
Diagnosis
Stools are examined under the microscope, using direct saline preparations (with eosin
and iodine stains as required), dark field microscopy, concentration methods and modified
Ziehl-Nielsen staining.
Stool culture and sensitivity of the sample is important, especially in those with severe
dehydration, those with very high fevers accompanying the gastroenteritis and in
dysentery or diarrhoea of more than 2 weeks (chronic/persistent diarrhoea) and where
there is history of blood stained stools.
Additional tests available include testing for Rotavirus and Adenovirus in the stool
samples. This is a reagent test and is available in a number of institutions in the country.
Treatment
Whatever the cause of diarrhoea or while waiting for the investigations, re-hydration must
be started. Children, because of their smaller size and dependence on caretakers to give
them fluids, are highly susceptible to rapid dehydration. Children with mild dehydration
have a history compatible with dehydration but few physical signs on examination, while
those with severe dehydration have marked physical signs which were listed on page 5
under clinical presentation.

Take Note
Re-hydration is the first priority!
6
Oral Rehydration Salts
Oral re-hydration salts (ORS) which can be obtained in packets from the nearest health
facility or purchased from local shops is the best fluid for preventing and treating all forms
of dehydration. The solution must be made up according to the instructions of the packet
using clean, boiled water which has been allowed to cool. As a guide for oral re-hydration,
50ml/kg of the ORS should be given within 4 hours to the child with mild dehydration and
100ml/kg over 6 hours for those with moderate-severe dehydration. The amounts and
rates should be increased if the patient continues to have diarrhoea or if re-hydration does
not appear complete. The ORS should be decreased if the patient appears fully hydrated
earlier than expected or develops peri-orbital oedema.
Vomiting may occur during the first two hours of ORS administration but it usually does not
prevent successful oral re-hydration. To reduce vomiting, the ORS should be given
slowly, 1 teaspoon (5 ml) every 1-2min. If the volumes are tolerated in the next 2 hours,
then you can increase to 2 teaspoons (10 ml) every 5-10min. Eventually you may
increase the volumes and reduce the frequency since it is a laborious activity. If severe
vomiting persists, intravenous re-hydration therapy should be started.
When re-hydration is complete, maintenance therapy should be started. Patients with mild
dehydration usually can then be treated at home using 100ml/kg/24 hr ORS until the
diarrhoea stops. Additional volume of ORS is given at 10ml/kg for every loose stool to
cover ongoing losses and if the child vomits you give a break of 5-10min and still give the
volumes but this time more slowly than previously at the same time, monitoring the
hydration state progress. The reconstituted ORS solution should be discarded after 24
hours from the time of reconstitution if not used.
Mothers must continue breastfeeding and giving additional fluids to babies and also give
other foods if the baby has already been started on them. Due to the difficulties in
preparing home-made re-hydration fluids, they are no longer recommended and it is better
to give other readily available fluids if ORS is not available.
Figure 2 illustrate how to prepare oral re-hydration salts at home.
7
Figure 2: Preparation of ORS at home

Take Note
Anti-diarrhoeal medication is sometimes given as first line treatment for all patients with
diarrhoea. As we saw earlier, this is not recommended as it may prolong the infection
period as the organisms take a longer time in the intestinal tract.
It is better to concentrate the energies on oral re-hydration as prevention and early
treatment of dehydration and electrolyte disturbances even without knowing the cause of
the diarrhoea. In this way many deaths would be prevented.
When dehydration is severe, blood circulation is poor and fluids given intra-osseously or in
to the peritoneum are not absorbed rapidly. Therefore, intravenous re-hydration is best for
severe forms of dehydration.
Prevention and Control
Prevention depends on breaking through the faecal-oral transmission cycle. Control of
diarrhoeal diseases, including dysentery, is only possible when the methods of stool
8
disposal are improved by the use of properly constructed pit latrines in rural areas, or flush
toilets. Hand washing facilities including soap and water should be provided immediately
outside all toilet and latrines. Preferably, there should be some facilities for washing the
hands with soap and clean running water, such as a metal container with a tap. Wash the
hands after using the toilet and always wash before cooking or eating. See Figure 3.
Figure 3: Actions that can be taken to break the transmission cycle.
Control flies by proper refuse and faecal disposal. This can be done by constructing
ventilated and improved pit latrines sited at proper distance from the living areas;
screening kitchens and food stores; storing food where flies cannot reach it; proper
disposal of refuse in a pit away from the living areas; and spraying with insecticides.
Food should always be properly cooked. Raw vegetables and fresh fruits without intact
skins should only be eaten if they can be thoroughly washed in clean drinking water.
Fresh intact fruits should be washed and then peeled at the time of eating. Milk should be
boiled or pasteurized. Eating utensils should be inspected to ensure that the processing,
preparation and serving of food is done in a hygienic manner.
The protection, purification and chlorination of public water supplies is of utmost
importance. Water from wells can be made safe with chlorine or lime. Water from deep
9
wells is usually uncontaminated if the well-head is protected and if there are no pit latrines
nearby. Drinking water from other sources should be boiled.
Piped water near each house would contribute greatly to general and personal cleanliness
and diminish the risk of infection from contaminated water.
Health education is always a helpful preventive measure. Educate people about the
dangers of bottle-feeding and encourage prolonged breastfeeding. Explain sources of
infectious diarrhoea and encourage the use of latrines and proper disposal of children
stools. Explain the importance of hand washing and cleaning utensils. Demonstrate
prevention of dehydration by giving ORS solution and other available fluids. Encourage
antenatal attendance and immunization of infants. Educate mothers about growth
monitoring and preparation of good weaning foods (while continuing to breastfeed) and
extra meals for a child after any illness in order to improve nutrition and “catch- up growth”.
Figure 4: Long term control of diarrhoeal diseases
As a health worker, you can participate in ensuring that water sources are safe for human
consumption. The points listed below will guide you as you check the water sources in
your community.
10
Check-points for Sources of Water Borne Diseases
Give at least 5 examples of places that could be primary sources for water borne
diseases.
Primary Schools
Primary schools may serve as a starting point for the spread of various infectons.
Therefore, you must check the:

Drinking water sources; how and where is the water prepared and stored for
drinking?

Latrines or toilets: are they sufficient for number of children attending the school?
Are they maintained and clean?

Facilities for washing hands; Is there soap and clean, preferably running, water
outside latrines? Also, ensure that the children actually practice hand washing
after toilet use and prior to eating.

If the school provides food, check on the cleanliness of the cooks, kitchen,
equipment and utensils; also check the place where children eat food brought from
home. Ensure the kitchen staffs have undergone their annual food handler
medical examination and have their medical certificates.

Disposal: Site and method of disposal of food and waste?
Kiosks and Food Shops
Kiosks and food shops could be another primary source of infection. Therefore, you
should visit such places and check the following:

The source of water; possible contamination and whether water is boiled or filtered
for drinking and stored in clean vessels;

The food preparation process: cleanliness of equipment, hygiene of the process
and disposal of waste materials;

Staff: personal hygiene, septic sores, and should undergo medical examination for
food handlers annually;

Consumption: care of drinking cups and other utensils;

Check for rats, cockroaches as a sign of cleanliness of the working environment;

Disposal: site and method of disposal of food and waste.
11
Hotels
In the hotels, check:

Food: water source; preparation and storage of water. How is the food stored and
for how long? Are there any rats and mice around?

Food preparation: Cleanliness of kitchen and utensils;

Where is waste food discarded ?

Staff: personal hygiene and medical examination for food handlers annually;

Customers’ facilities: Latrines, washing facilities including the cleanliness of towels
Private Homes
When visiting private homes check on the following:

Water supplies: from where and what distance must the water be collected? Is the
supply enough throughout the year? Is water for animals drawn from a separate
source? Is there a slab for washing clothes?

Water collection: private or common buckets? Who takes care of the cleanliness
of the bucket? Pump? Tap?

Water storage in the house: tins or pots covered and cleaned regularly; emptied
before refilling; protected against animals; advise the family on the three-pot
system (using a system of three pots used daily in rotation so that water stands for
three days before use); boiling or filtering of drinking water.

Latrines: each private home should have a latrine; look for the care of each latrine
and whether it is used by each member of the family;

Are there bathing and washing facilities?
Irrigation Furrows
Check for:

Site: chance of contamination; possibility of protection along its course.

Use: speed and volume of water; fluctuations of amount of water during various
periods of the year; use for humans and/or animals; maintenance.

Quality of water: is water used for drinking, washing?
Fields or Gardens

Where do people working in the fields get water for drinking?

Where do people in the fields go to relieve themselves?

Where is waste and refuse from the garden put?
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Health Facilities

Source of water: possible contamination and how water is stored ;

Toilets or latrines: separate facilities for patients and staff;

Facilities for washing hands: soap and clean water outside toilets and in
examination rooms;

Bathing facilities for patients;

Food preparation: cleanliness of kitchen and utensils;

Disposal: proper disposal of infectious waste and waste food from the health
facility.
We have now come to the end of Section 1, where we had a general overview of faecaloral diseases. In the next four sections we shall focus on the individual diseases and we
shall look into their epidemiology, clinical features, diagnosis and management. We shall
group the diseases into four sections, depending on their causative agent. We shall start
with faecal-oral diseases caused by bacteria.
Section 2: Faecal-Oral Diseases Caused By Bacterial Infection
Which faecal-oral diseases are of bacterial
origin?
Do you still remember Table 1 on page 3? In it we listed, typhoid and paratyphoid,
cholera, bacillary dysentery, anthrax, and bacterial diarrhoeas such as yersinia,
campylobacter and E. coli as faecal-oral diseases of bacterial origin. We shall now
discuss some of these diseases in more detail. We shall start with acute gastro-enteritis
Acute Gastroenteritis
Acute gastroenteritis is a clinical syndrome of diarrhoea, nausea and vomiting with or
without fever. Diarrhoea (change in bowel habit for the individual child resulting to more
frequent and/or looser stools) alone, without vomiting, is referred to as enteritis while
13
vomiting alone is referred to as gastritis. Diarrhoea is often more frequent in hot, dry
periods clearly associated with a shortage of water.
Acute gastroenteritis may affect any member of the population but severity varies in
different age groups. Dehydration occurs more rapidly in children and is a common cause
of morbidity and mortality. Especially at risk are infants, weanlings, bottle-fed children,
travellers and the malnourished child.
The malnourished child has a low immunity and hence the resistance to infections is also
low. Such children are quite prone to diseases, especially diarrhoeal diseases. During
infancy the immunity is still developing, so basically this is a high risk age for infections,
including gastroenteritis. During the weaning period of the child, malnutrition is common
due to lack of knowledge about the best weaning foods and this exposes the child to
gastroenteritis.
Bottle feeding is particularly dangerous in families of low socioeconomic status or
financially constrained families, since they do not have the facilities to clean the bottle
properly and often the money is not enough to buy sufficient amounts of milk/formula. The
child gets fed with poorly prepared diluted feeds and inevitably gets diarrhoea.
Breastfeeding is always the preferred mode of feeding the baby, because it’s not affected
by availability of water or the socioeconomic status of the family and has many properties
protective to the child against infections.
Traveller’s diarrhea occurs in people who are exposed to a new environment. This can
arise from natural disasters, human –caused disasters or among migrants and holiday
makers. Travellers’ diarrhoea is usually due to enterotoxic E.coli, a bacterial infection of
the bowel acquired through faecal-oral contact, but other factors such as changes in food
may also contribute. The diarrhoea is self-limiting and rarely requires antibiotic treatment.
Acute gastroenteritis is endemic in areas where sanitation is poor. Diarrheal diseases are
important because they are the leading cause of infant morbidity and mortality through
dehydration. Numerous episodes of diarrhoea interfere with nutrition and so they are an
important cause of malnutrition. Diarrhoea often accompanies measles and so contributes
to measles death, secondary to dehydration.
Epidemiology
Many organisms can cause diarrhoea, and it may be difficult to prove that any particular
organism is responsible. Even when sophisticated techniques are used, in many cases,
14
no organism can be found. In most cases of acute diarrhoea it is not important to identify
the cause as the treatment is the same, that is rapid and adequate re-hydration.
In infants, diarrhoea may be caused by bacteria such as enteropathic E.coli, or by viruses
such as rotavirus and other enteroviruses. All these organisms are transmitted by the
faecal-oral route apart from rotavirus where the mode of transmission is not quite definite
so far as the prevalence is not determined by the level of hygiene or availability of safe
water and it is similar in all socioeconomic levels.
In children, diseases like malaria, urinary tract infections and ear infections may cause
diarrhoea and this is referred to as parenteral diarrhoea. Therefore, it is vital that children
with acute gastroenteritis and fever are properly examined to rule out other local infections
that can cause diarrhoea and in malarial areas a blood slide is performed to rule out
malaria.
Management
The treatment of choice in the management of gastroenteritis is re-hydration. The degree
of dehydration should be carefully assessed. Continue feeding and give extra meals on
recovery to improve catch-up growth. Give an antibiotic only if there is an indication of
blood in the stool or after receiving indicators on investigation. If there is fever, treat it and
at the same time look for the cause, but bear in mind also that all infections can result in
fever. Do not give anti-diarrhoeals because they are not really useful. They tend to hold
the infecting organism much longer in the intestinal tract and hence prolong the infection.
Teach the mother how to prepare oral re-hydration fluid and how to give it to the child at
home and give her enough ORS to take home. Educate the mother about diarrhoea
prevention.
Prevention and Control
Prevent malnutrition in the weaning period by being vigilant in monitoring the babies
growth and weight gain. Provide nutrition education to the mother/caretaker, encouraging
breastfeeding, and while at the same time discouraging bottle-feeding.
Control of diarrhoeal diseases is an integral part of the Ministry of Health and the activities
include;

Growth monitoring during the first five years of life;

Oral re-hydration therapy to reduce diarrhoeal deaths;
15

Sustained breastfeeding;

Immunization against measles;

Improvement of water and sanitation to reduce transmission and number of
episodes of diarrhoea;

Improved weaning practices and nutrition of children ;

Investigation of diarhoeal outbreaks;

Vigilant antenatal care.
What have we learnt
Diarrhoeal diseases are very common in developing countries and children are especially
at risk. Causative organisms are difficult to identify. Spread is by faecal-oral transmission
route. Correction of dehydration is paramount in treatment. Control is by improvement of
sanitation, nutrition and health education.
Bacillary Dysentery
Bacillary dysentery is an acute diarrhoeal disease characterized by bloody stools, fever,
vomiting and abdominal cramps. It is also known as shigellosis. It is especially common
in areas where sanitary conditions are poor. The main factors influencing its occurrence
are the methods used in disposal of faeces, availability of water, fly population, seasonal
changes, overcrowding, and nutrition.
In the dry season the amount of water available for cleaning purposes decreases.
Cleaning of utensils and washing of hands gets low priority. The available water sources
may be contaminated and increase in dysentery cases can be expected. The number of
house flies is dependent on many factors, including methods of waste disposal and
whether any animals are kept close to the dwelling. House flies are very likely to transmit
dysentery. When the number of house flies increases, the incidence of dysentery also
increases. During the rainy season, a lot of faecal material deposited outside the latrines
will be washed into ponds and rivers. This results in heavy contamination of water
sources and increases the incidence of diarrhoeal diseases. Malnutrition lowers general
resistance against all diarrhoeal diseases, including dysentery. Shigella infections will
occur more readily, resulting into attacks of frank dysentery. Poorly nourished children
and old people are therefore, especially at risk. Other undernourished groups living in
poor and crowded conditions such as prisoners and refugees are also at risk.
16
In children diarrhoea or dysentery easily causes dehydration and this accounts for the high
rate of diarrhoeal diseases in this age group.
Epidemiology
Bacillary dysentery is caused by non-motile gram negative bacilli of the Shigella species.
Those most frequently responsible for outbreaks are S. sonnei, S. dysenteriae and S
flexneri. Humans are the only reservoirs for outbreaks. Following infection, people may
be asymptomatic carriers for up to 3 months. Transmission is by the faecal oral route.
Contaminated food, (often salads or other items requiring extensive handling of the
ingredients) and water are important vectors. Shigella multiply in food.
Although infection can occur at any age, it is most common between 2-3 years of age.
Infection in the first six months of life is rare for reasons that are not clear.
However, person to person transmission is probably the major mechanism of infection in
most areas of the world. The fact that it spreads within families, prisons, and day care
centres demonstrates the ability of low numbers of the organism to cause disease on
person to person contact.
Pathology
The target organ for shigella is primarily the colon where there is a resultant grossly diffuse
or localized ulceration and bleeding, as well as oedema of the mucosa/lining of the colon
due to the inflammatory response to the infection. Shigella might penetrate through the
intestinal lining into the blood circulation to cause bacteremia and sepsis, especially in the
infant and the malnourished child.
Clinical Picture
After ingestion of shigellae there is an incubation period of 1-4 days before symptoms
manifest. Asymptomatic infection of adults and children occurs but is uncommon. In the
well nourished, infection with shigella may result only in mild diarrhoea and in the
malnourished it may result in a fulminating and fatal disease and the diarrhoea may even
last for more than 10 days.
Mild cases are often not recognized and are regarded as non-specific gastroenteritis. The
diarrhoea may be watery and of large volume initially evolving into frequent small volumes
bloody mucoid stools.
17
In classical cases the onset is sudden with fever, colicky abdominal pains and painful
defecation and tenesmus (painful contractions of the sphincter ani), producing an almost
continuous and irresistible urge to defecate, but only small quantities of purulent mucus
and blood coming. Physical examination may elicit abdominal distension and tenderness,
hyperactive bowel sounds and a tender rectum on digital rectal examination
Some children never progress to the stage of bloody stools whereas in other, the first
stools are bloody. Dehydration is common and dangerous as it may cause muscular
cramps, oliguria and shock. Rectal prolapse may occur in infants.
Diagnosis
The laboratory is not always able to confirm the diagnosis and the clinical features can be
confused with those caused by infections like Campylobacter jejuni, Salmonella spp,
Enteroinvasive E.coli, and Entamoeba histolytica.
The stools appear dark red (blood) with much mucus. Microscopy shows numerous white
blood cells and many erythrocytes. Macrophages which contain red blood cells (after
phagocytosis) are easily mistaken for trophozoites of Entamoeba histolytica. The nucleus
of a macrophage is, however, more clearly visible and s irregularly shaped. The diagnosis
is confirmed by a positive stool culture or rectal swab for Shigella. Stools are best
transferred to the reference laboratory for culture in Cary Blair medium.
The total white cell count is usually 5,000-15,000 cells/ml. Anaemia is common, especially
with S.dysenteriae.
In children who appear toxic, blood cultures should be obtained, especially in very young
or malnourished children because of their increased risk of bacteremia.
Management
Prevention or treatment of dehydration is all that is necessary in mild infections as the
disease is self limiting. In severe infections re-hydration must be combined with
appropriate antibiotics because death is usually due to a combination of dehydration and
toxaemia. Oral re-hydration can be started as soon as possible. This is always useful as
an aid to parenteral re-hydration and carries less danger of disturbing the electrolytes
balance.
The next concern is a decision about the use of antibiotics. Many practitioners are against
the use of antibiotics in shigellosis, considering the high cost of antibiotics, the risk of
18
emergence of drug resistance and the fact that it is a self-limiting disease. But there is a
persuasive logic in favour of antibiotic use for all children in whom shigellosis is suspected
and that is what is generally practised currently. This practice is based on the argument
that the untreated illness may cause the child to be quite ill for 2 weeks or more and that
chronic or recurrent diarrhoea may ensue. Furthermore, the risk of malnutrition
developing or worsening during the period of prolonged illness, as well as the risk of
continued excretion and subsequent infection of contacts and the difficulties of culturing
shigella in the laboratory are strong enough arguments against the withholding of
antibiotics.
Cefixime and Ceftriaxone are effective alternatives in areas where Cotrimoxazole
resistance is common. First and second generation oral Cephaloporins are ineffective and
Ampicillin is more effective than Amoxicillin.
Take Note

Re-hydration is the priority in treatment for dysentery
Faeces of patients are highly infectious and should be handled with care. Required
measures include rigid personal precaution by attendants, proper disposal of faeces and
elimination of fly contact with faeces. Patients and contacts should not be employed as
food handlers until any danger of spread is no longer present.
Prevention and Control
Prevention of bacillary dysentery depends on stopping the oral-faecal transmission.
Whenever there is an outbreak of bacillary dysentery or other diarrhoeal disease, check
the water supply. Find out if there is a localized pattern in the spread of the disease. Is it
in families/villages, etc? Is water the vehicle of transmission? Are food or flies
transmitters? Examine all points on the checklist at the beginning of this chapter. Direct
your actions to possible causes. Give health education on preparation of oral re-hydration
fluids; use of safe water (boiling); use of safe food (preparation and storage); washing of
hands with water and soap; and proper disposal of faeces and refuse.
With endemic bacillary dysentery, give health education on the use of latrines, safe water,
and safe food, refuse disposal and personal hygiene. Stress the importance of prolonged
19
breastfeeding. Attend the village development committee meetings and stress the
importance of improvement of water supply with protected wells or piped water. Stress in
the same committee the importance of constructing and using latrines. With your health
assistant, inspect public eating houses, markets and boarding institutions.
What have we learnt?
Bacillary dysentery is an acute diarrhoeal condition which may vary from a mild diarrhoea
to a severe toxic and fatal disease. It is common and severe in the malnourished and
infants. Re-hydration is the mainstay of management. Resistance of shigella to antibiotics
is a common entity. Control depends on proper disposal of faeces and improvement of
water supply.
Campylobacter Jejuni Infections
Some infections are due to an enteric gram-negative micro-aerophilic bacterium known as
Campylobacter jejuni, initially considered an animal pathogen only. Campylobacter
infections are among the most common causes of bacterial gastroenteritis worldwide. It
presents with various symptoms ranging from mild gastroenteritis to severe dysentery.
The gastrointestinal tract of many domestic and wild animals is the main reservoir of
infection. This includes poultry, cats, dogs, sheep, cattle and raw milk. Transmission from
animals to persons occurs most often by the faecal-oral route by ingestion of contaminated
food, untreated water, undercooked poultry and unpasteurized milk. Person-to-person
transmission occurs but is much less common. Outbreaks of campylobacter diarrhoea are
common in day care centres and nurseries. Chronic carriage is uncommon.
Pathology
Symptoms and signs are related to dose and bacterial virulence, as well as host factors.
Low gastric pH kills many of the bacteria. Once through the stomach, the bacteria
colonize the distal small intestine and the colon, often producing inflammatory diarrhoea.
During this period large numbers of bacteria are shed into the stool. The invasion of the
mucosa by campylobacter bacteria results in mucus, pus and blood present in the gut
lumen with a friable ulcerated lining left behind and in addition transient blood invasion. In
some strains of C jejuni which produce a cholera-like toxin, there is minimal damage to the
mucosa lining and the patient only presents with watery diarrhoea. Symptoms are related
to the time taken for the bacteria to be cleared from the intestines and usually last 1-3
20
weeks, coinciding with the onset of increasing antibody titres. The incubation period
ranges from 1 to 7 days with a mean of 2-4 days.
Clinical Picture
What is the most common presentation of
campylobacter jejuni infecton?
Diarrhoea is the most common presentation of campylobacter infection. It may consist of
loose water stools or blood and mucus-containing stools. Blood appears in the stools 2-4
days after the onset of symptoms. Fever, vomiting and abdominal pain are common.
Fever may be the only initial complaint and abdominal pain in a large proportion of older
children is per-iumbilical, intermittent and may precede other symptoms or persist after the
stools return to normal. Most patients recover in less than a week, but a few have a
relapse, prolonged or severe illness.
When campylobacter invades the mucosa and gets into the blood, bacteremia results.
Bacteremia without localized infection is the commonest systemic infection caused by
campylobacter. This presents with fever, headache and malaise. The feve may be
relapsing or intermittent and is associated with night sweats and chills.
Focal campylobacter infections, such as meningitis, urinary tract infections, arthritis or
peritonitis occur mainly in neonates or immuno-compromised persons.
Diagnosis
Because campylobacter jejuni grows best in an environment of 5% oxygen at a
temperature of 42 and is slow growing, special media such as Skirrow´s or Batzler´s are
necessary to isolate it. Stool culture is the only way to confirm the diagnosis. Presumptive
evidence is seeing motile bacteria under dark-field microscopy.
Management
Fluid replacement, correction of electrolyte imbalances and supportive care are the
mainstay in management of campylobacter gastroenteritis.
21
Take Note

Antimotility medications may cause prolonged or fatal disease and should
not be used.
Controversy exists regarding the use of antibiotics in patients with uncomplicated
gastroenteritis since many studies showed no improvement in clinical symptoms or
shortening of the course of the disease.
Antibiotics are, however, recommended for patients with the dysenteric form of
campylobacter disease, high fever, or a severe course of illness as well as children
attending childcare centres or other institutions and children who are immuno-suppressed
or have underlying disturbances.
Erythromycin in a dose of 50 mg/kg/day in four divided doses for 5 days is effective. For
those with bacteremia, empirical parenteral Gentamicin is recommended until blood
culture and sensitivity results are obtained and treatment is for 3 weeks.
Prevention and Control
Prevention largely depends on reducing household contamination by domestic animals.
Improved food hygiene techniques are also important.
Take stool culture from the patient but specify the possibility of campylobacter. If seriously
ill, treat with erythromycin. Environmental control includes reducing the number of animals
and poultry coming into houses and yards. Cook all poultry very well; wash utensils after
preparation and expose them to the sun on a drying table. Regard all purchased chicken
as potentially infected and observe good hygienic preparation and cooking methods.
Summary
Campylobacter infections are now a more common cause of diarrhoea and dysentery.
The source is often domestic animals, especially poultry.
22
Cholera
What is your own definition of
cholera?
Cholera is an acute intestinal disease characterized by sudden onset of profuse watery
stools, vomiting, rapid dehydration and circulatory collapse. The clinical spectrum includes
asymptomatic infection, mild watery diarrhoea and severe watery diarrhoea with vomiting.
Both adults and children are affected but in endemic areas cholera mainly affects children
2-15 years of age and breastfeeding may be protective in the first 2 yrs of life from severe
cholera.
A rapidly increasing incidence of acute diarrhoea with dehydration in young population
should lead to a suspicion of cholera.
Epidemiology
Cholera is caused by Vibrio cholerae, the comma bacillus, a Gram negative, very small
curved motile organism. The two biotypes are classified as classic and El Tor, based on
hemolysin, haemagglutination, susceptibility to polymyxin B, and susceptibility to
bacteriophages. The organism survives in warm salty water with nutrients and oxygen.
Direct person-to-person transmission is rare. Because Vibrio cholerae are very sensitive
to gastric acid, a large number of the organisms have to be ingested for an infection to set
in. For this reason cholera is not a very infectious disease.
Transmission is through the faecal-oral route but almost all cholera infections are water
borne. Vibrio cholerae can live in water for 2 weeks and prefer salty water. In sea water
they may survive for longer periods. Vibrio cholerae can survive and multiply in shell fish
such as crab and shrimp. Vibrios also readily multiply in certain foods such as milk and
boiled rice. The reservoir of infection is formed mainly by carriers. These carriers excrete
vibrios in smaller numbers than the patients but because of their freedom of movement
and the fact that they far outnumber the patients they form the greatest danger to the
community.
23
Vibrios must colonize the small intestine to establish infection and cause disease. They
attach to the intestinal lining and multiply, producing an enterotoxin (cholera toxin). The
cholera toxin causes a prolonged elevation of cyclic adenosine monophosphate levels in
villous cells and this results into a decrease of the active absorption of sodium and
chloride in the villous cells and an increase of the active secretion of chloride by crypt
cells. The result is massive fluid secretion into the intestinal lumen and this is what is seen
as diarrhoea and vomiting in either end.
Take Note

Most cholera infections are asymptomatic or cause only simple self-limiting
diarrhoea.
Figure 5 illustrates the transmission of cholera by the faecal-oral route.
Fig 5: Transmission of cholera by the faecal-oral route
24
Clinical Picture
The incubation period is usually 2 - 3 days. Cholera is not a systemic infection, and
therefore, fever is generally low grade or absent. The vibrios are confined to the intestinal
tract. The clinical syndrome of cholera is caused by water and electrolyte losses.
In typical cases of severe cholera, the disease develops in three stages. The first stage
lasts for 3 - 12 hours. Profuse watery stools pour from the patient. Soon faecal matter
disappears from the stools which become almost clear fluid with flakes of mucus, giving
them the classical rice-water appearance. Vomiting follows the diarrhoea. At first food is
vomited but soon only rice water is vomited. Severe cramps in the abdomen and limbs
develop from salt loss.
In the second stage, there is collapse from dehydration. The body becomes cold, the skin
is dry and inelastic. The blood pressure is low or unrecordable, the pulse is rapid and
feeble. Urine production stops and the patient may die of shock.
The third stage is the stage of recovery, either spontaneously or with treatment. The
diarrhoea decreases; the patient is able to take fluids orally and the general condition
rapidly improves.
Cholera should be suspected in any outbreak of diarrhoeal disease. The diagnosis is
made on clinical grounds. Do not refer patients to confirm diagnosis but send a rectal
swab or stool specimen in transport medium if available to the next equipped laboratory.
The best transport medium for all enteric bacteria is the Cary Blair.
Management
Patients can be admitted to a temporary hospital such as an adapted school or church.
Strict isolation is not necessary as only the vomitus and stools are infective. These should
be properly disposed into a pit latrine or a septic tank system or flushed in the toilet.
Hospital equipment can be cleaned with a disinfectant while any instruments used should
be cleaned in disinfectant or sterilized. The patients should be made comfortable by
treating them on cholera beds. These are beds with a central hole through which the
continuous stools can pass into a bucket.
The essential cure of cholera is re-hydration, which if started on time, will save many
cholera cases even without any drug treatment.
25
Patients of all ages who are strong enough to drink will voluntarily ingest the volumes of
ORS needed for re-hydration and maintenance. Patients in shock or too weak to drink,
require intravenous fluids until they are able to take orally. Vomiting is caused by acidosis
and fluid loss. It may last for a few hours but the volume is usually small and continuous
drinking should replace the loss.
Oral re-hydration should be given in frequent small amounts by mouth or by naso-gastric
tube in children. Disturbance of electrolyte balance is less common with oral re-hydration
and intravenous fluids can be reserved for those with severe dehydration. A mother can
give a child a teaspoon of fluid every 1 - 2 minute. With every vomiting or loose motion
passed, the mother should add 5-10ml/kg body weight to the total fluids the child is to take
in 4-6 hours. The total fluids are calculated at 50-100ml/kg body weight, depending on
the degree of dehydration, as replacement of ongoing losses.
Tetracycline will speed up the cure and prevent the convalescent carrier stage and Cotrimoxazole can also be used with good effect. A stool culture will assist in the selection of
the most sensitive antibiotic.

Take Note
Re-hydration will save almost all cholera cases.
Prevention and Control
Surveillance is the key to a successful cholera control programme. Surveillance is the
continuous watching of all aspects of a disease. It includes collection of morbidity and
mortality reports, field investigation of epidemics or individual cases and laboratory
investigations such as culturing. Once an outbreak of a disease under surveillance is
noted in a certain area, immediate action must be taken. Surveillance depends on
reporting suspected cases of cholera. It is obligatory to report any case immediately to the
District Medical Officer (DMO) by any rapid means.
26

Take Note
Cholera is an internationally notifiable disease.
Three factors influence reporting of new cases by the public. Reporting is greatly inhibited
when repressive measures are taken once a case is identified. Repressive measures can
be quarantining a family, hospital, community or an area. Such measures will increase the
hysteria among the people and will hinder surveillance, as people will not come forward to
report cases. Saving lives should be the top priority in the control of cholera. Fear and
panic occur in the community when deaths occur. If cases are recognized and treatment is
given without delay, fear will disappear and families will report their cases. Treatment
centres should not be quarantined.
Reluctance to report cases and fear of the disease can be overcome by allowing visits to
the patients. A parent should stay with a paediatric case to assist in oral fluid therapy and
nursing. These means are important because they stress the relatively benign nature of
the disease and show that it is not very infectious.
As cholera is mainly a water-borne disease, it cannot spread when water is made safe.
This can be done by chlorination of the public water supply or by boiling or treating
supplies for individuals. In case of emergency, large quantities of water can be treated
with chloride or lime.
Only certain foods can transmit cholera, under special circumstances and for a limited
period of time. Milk products should be pasteurized. Uncooked food should be avoided or
washed in safe water. Left-over food should be protected against contamination by flies.
Markets should be inspected.
Improvement of sanitation facilities will result in a lower incidence of all diarrhoeal
diseases including cholera. Emergency measures in case of epidemics are impracticable
and not the first priority.
Tetracycline can prevent cholera in households where there is a cholera case if it is given
to close contacts, but administration of tetracycline to the entire population is impracticable
and inadvisable. Mass chemoprophylaxis only results in indiscriminate use of drugs and
increases the danger of drug-resistance and development of drug reactions.
27
Cholera vaccine is of low potency. It gives 50 % protection for 3 - 6 months only. The
vaccine will give some individual protection against clinical cholera but mass immunization
will increase the number of asymptomatic carriers. As a general measure to stop an
epidemic from spreading immunization is of no value. The public should be informed of
the limited value of immunization because in an epidemic they will demand protection and
they may panic when they find that vaccine is not available. On the other hand, pressure
may make the authorities start an immunization programme and so neglect the more
important protection and purification of the water supply. People who are immunized may
have a false sense of security and may be encouraged to consume unsafe water or food.
Improved vaccines are under development.

Take Note
Prevent cholera with a clean water supply!
Some funeral ceremonies may be conducive to the spread of the disease. If this is the
case, communities need further education about burials.
What have we leant?
Cholera is an acute intestinal disease characterized by rice-water stools, vomiting, and
rapid dehydration with shock. It is spread through contaminated water. Most cases are
sub-clinical infections resulting in the carrier stage. Control depends on surveillance. In
an outbreak the first priority is to improve the water supply. Existing vaccines have low
potency. Re-hydration is the mainstay of management.
28
Enteric Fever
Which bacteria cause the enteric
fever?
Enteric fever is a systemic clinical syndrome produced by certain Salmonella organisms
and includes typhoid fever caused by S. typhi, and paratyphoid fever caused by S.
paratyphi A and S. paratyphi B. Typhoid fever is a systemic infectious disease
characterized by high continuous fevers, malaise and involvement of lymphoid tissues and
spleen. Typhoid fever is the most frequent and more severe than the other forms.
Diarrhoea is not a common symptom in typhoid fever. Paratyphoid fever may present like
typhoid fever, but most cases present as gastroenteritis or transient diarrhoea.
Epidemic outbreaks can occur when a source of water or food used by many people is
contaminated.
Epidemiology
Humans are the only source and reservoir of S. typhi and thus direct or indirect contact
with an infected person is necessary for infection. Transmission is by the faecal-oral
route. Salmonellae are passed out in faeces and urine of carriers and actively infected
persons. The main ways of spread are through contaminated water and food. It is usually
most common at the end of the dry season and at the start of the rains. Contamination of
food usually occurs from the hands of carriers or undiagnosed patients. It is common in
areas where there is insufficient water for washing hands.
Stomach acidity is an important determinant of susceptibility to salmonella. Those that
survive the gastric acidity, escape into the small intestine where they attach onto the lining,
invade into the lympahtics and reach the bloodstream via the thoracic duct, causing a
transient bacteremia. Circulating salmonella reach mainly the liver, spleen and bone
marrow. In these organs the salmonellae multiply and the bacteria are then poured back
into the bloodstream, resulting in bacteremia. The gallbladder is particularly infected from
the bloodstream or through the biliary system. Proliferation in the gallbladder walls
produces a large number of salmonellae which is then emptied into the intestines and out
into the environment through faeces for a very long time if the patient is not treated to
29
eradicate the S. typhi. Urinary carriers are seen particularly in areas where Schistosoma
haematobium infection is common.
Clinical Picture
The incubation period is 2 - 3 weeks, depending on the amount of ingested innoculum,
and the clinical picture depends on age.
Over 5 years Old Patients
With patients who are over 5years old, the onset is gradual and initial symptoms include
fever, malaise, loss of appetite, headache and abdominal pains. In the early course of the
infection, diarrhoea may be present but this gives way to constipation which becomes a
more prominent symptom. The fever which rises in a step-ladder manner becomes
intermittent and high within 1 week, often reaching 40°C.
In the 2nd week of illness the fever is sustained and fatigue, loss of appetite and abdominal
pain increase in severity. The affected organs, mainly the liver and spleen enlarge and
are tender. This may be picked out on clinical examination. The abdomen also becomes
distended and tender due to ulcers in the lymphatic tissues of the intestine. These ulcers
may cause bleeding and perforation in the 3rd week of the disease.
If no complications occur, the symptoms and physical findings gradually subside within 2 4 weeks.
Under 5 years Old Patients
Enteric fever rarely inflicts the age group of under five years old, and if it does, it is a mild
disease with diarrhoea occurring more frequently than in the other age group. Usually,
there is mild fever and malaise, which can be misdiagnosed as a viral infection.
Diagnosis
The best way to prove typhoid fever is to culture the salmonellae. Blood cultures are
positive early in the course of the infection and because of the intermittent and low-level
bacteremia, repeated blood cultures should be obtained. Stool and urine cultures are
positive after the 1st week of infection and sometimes in chronic carriers. Bone marrow
culture is the most sensitive method of diagnosis.
The Widal test becomes positive by the end of the 1st week and a rising titer shown by two
tests performed 4 - 5 days apart may indicate active infection. The interpretation of Widal
30
tests is, however, full of difficulties and in many cases it is of little use in the diagnosis of
typhoid, especially in endemic areas and in people who have had the vaccine
Management
Antibiotic therapy is important in treating typhoid infection and due to the emergence of
increasing drug resistance, the choice of antibiotic is left to sensitivity and resistance
patterns in different areas. Quinolones are still much in use for typhoid in addition to
Chloramphenicol.
Prevention and Control
General prevention is as for the other diarrhoeal diseases. It is important to identify
carriers who work as food handlers as they are especially likely to transmit typhoid fever.
Patients and family contacts should not be employed as food handlers until the danger of
transmission is over.
A typhoid vaccine is available and is given at 2years of age, with a booster at 5years and
10 years for children. The vaccine only gives partial protection but the number of infecting
organisms necessary to cause typhoid fever is higher in the immunized than in the nonimmunized persons. If used, immunization should be repeated yearly.
However, good water supply and improved food hygiene are the best control measures.
What have we learnt?
The enteric fevers are systemic diseases. Typhoid fever is characterized by high
continuous fever and malaise. Paratyphoid fever may resemble typhoid fever or
gastroenteritis .both diseases are spread by infected water and contaminated food through
the faecal-oral transmission route. Control depends mainly on sanitary disposal of faeces
and improvement of water supply.
Section 3: Faecal-Oral Diseases Caused By Protozoal Infection
In the previous section we discuss some diseases caused by bacterial infection. In this
section we are going to focus on diseases where the causative agent is protozoa.
31
Do you still remember Table 1 on p. 3? Which two
diseases were listed there under protozoal infection?
That’s right! The diseases mentioned in Table 1 are amoebiasis and giardiasis. Let us
first focus on giardiasis.
Giardiasis
Giardiasis is an infection of the small intestine caused by a flagellated protozoal parasite,
Giardia lamblia resulting in a clinical picture ranging from asymptomatic colonization to
acute or chronic diarrhoeal illness. It is common in areas with poor levels of sanitation,
day-care centres and residential institutions for the mentally handicapped. Waterborne
outbreaks have been linked to the ingestion of surface water treated by faulty or
inadequate water purification systems. Person-to-person and food-borne transmission
also occurs resulting in sporadic cases as well as epidemics.
Giardia lamblia is also a significant pathogen in people with malnutrition, immunodeficiencies, or cystic fibrosis. Chronic illness results in malabsorption and weight loss.
Asymptomatic carriers among people are common and infection can spread from person
to person, especially within families.
Symptoms develop 1-3 weeks after exposure to the parasite but the majority of infected
individuals are probably asymptomatic.
Pathology
Giardia infects humans through ingestion of the cysts, whose viability is not affected by the
normal concentrations of chlorine used to treat water for drinking. Cysts are activated by
the acid of the stomach and release the trophozoites upon reaching the upper small
intestine, each cyst releasing four trophozoites. The trophozoites attach themselves to the
mucosal lining, divide and multiply. The mature cysts are passed in the stools of infected
individuals and may remain viable for as long as 2 months.
Clinical Picture
In those who are ill, the symptoms range from mild diarrhoea to debilitating malabsorption
and weight loss. Lactose intolerance due to reversible lactase deficiency and
malabsorption of fat and vitamin B12 may occur as complications.
32
Most of the symptoms are a result of the malabsorption and include abdominal discomfort,
cramps, nausea, sensation of bloating, frequent loose, bulky, foul and urgent stools;
malaise and/or weight loss. The disease may be self-limiting or prolonged. The acute
stage lasts for about 4 days on average but may persist for months or years. The mean
duration of symptoms is 6-7 weeks.
Diagnosis
Diagnosis is often difficult to establish. Stool examination rarely reveals motile
trophozoites, but approximately 60% of samples will show cysts. Three separate stool
specimens can bring this sensitivity to 90% because cyst excretion is irregular; the
concentration method also increases the chance of finding cysts. If symptoms persist for
weeks, and there is a strong suspicion of giardiasis in spite of negative stool examination,
a treatment trial may be warranted.
Management
Most cases of Giardiasis are probably self-limiting. When Giardia causes symptoms it
should be treated because of the potential for chronic or intermittent symptoms.
Metronidazole at 5mg/kg/ day eight hourly for 7 days is effective. Tinidazole, Furazolidine
and Paromomycin have been used with good effect.
Prevention and Control
The cysts of Giardia lamblia are highly susceptible to heat. Cooking food or boiling
drinking water kills the cysts early. The cysts are not affected by chlorine treatment of
water or by iodine. Required action is to improve food hygiene, avoid eating raw
vegetables from endemic areas and improve water and sanitation.
Amoebiasis
Amoebiasis is an infection caused by a pathogenic amoeba, Entamoeba histolytica.
Infection with amoeba in most cases is asymptomatic. In a small proportion of individuals
the amoeba may invade the bowel wall causing amoebic dysentery or may disseminate to
other organs, especially the liver where it causes an abscess.
33
Take Note

Clinical amoebiasis is endemic in areas where sanitary conditions
are poor.
Epidemiology
Entamoeba histolytica is the only pathogenic one of several Entamoeba species that can
parasitize humans. It is distinguished from the others by its size and the fact that it has 4
nuclei in the cyst form. It is activated when cysts are ingested. The cysts are resistant to
environmental conditions such as low temperature as well as to the normal concentration
of chlorine commonly used in water purification. The parasite can, however, be killed by
heating food or water to 55°C before consumption. Food or water contaminated with
E.histolytica cysts and faecal-oral contact are the main means of infection. Untreated
water and human faeces used as fertilizer are important sources of infection. Food
handlers passing amoebic cysts play a role in spreading the infection. Direct person-toperson transmission also occurs when one comes into contact with infected human
faeces.
Pathology
The cyst is resistant to gastric acidity and digestive enzymes, and upon ingestion it excysts in the small intestines releasing 8 trophozoites. The emerging trophozoites take up
residence in the ascending large bowel where they can live as a commensal
(asymptomatic carrier) or begin penetrating the intestinal wall, causing small mucosal
ulcerations which result in dysentery. The parasite penetrates through the sub-mucosa
and into the muscularis layer of the colon. If the muscularis layer becomes extensively
involved scarring can result (amoeboma). Invasion of the bloodstream by the trophozoites
may lead to infection of the liver, especially the right lobe, lungs and brain. After a variable
incubation period, a liver abscess may develop. Lung and brain metastasis are rare (see
Figure 7).
The only infective form of E .histolytica is the cyst. A patient with amoebic dysentery is
unlikely to spread the disease because of only passing out trophozoites, which if ingested
34
are destroyed in the stomach by the gastric acid. It is the asymptomatic cyst-passer who
forms the main reservoir for the spread of amoebiasis. Cysts are passed from person-toperson by the faecal-oral route, by fingers soiled with faeces directly into the mouth or via
food. Amoebiasis can occur in families or spread through institutions but usually does not
occur in epidemics, unlike bacillary dysentery. Although infections may occur from
drinking water, amoebiasis is not really a water-borne disease. It can be endemic in a
population in which many individuals are asymptomatic cyst-passers with only a few
getting the disease.
Figure 6: The life cycle of Entamoeba histolytica
Clinical Picture
Most infected individuals are asymptomatic and cysts are found in their faeces. The most
common clinical manifestations are due to local invasion of the intestinal lining and spread
to the liver.
35
When the amoeba penetrate the intestinal wall, they multiply in the sub-mucosa, causing
bottle-shaped ulcers. From these ulcers, the amoeba may be transported to the liver. An
amoeboma or amoebic granuloma may result from repeated invasion in the colon. An
amoeboma may become very large, forming a hard swelling which is difficult to
differentiate clinically from carcinoma.
Usually the onset of amoebic dysentery is insidious and associated with abdominal
discomfort. There may be mildly loose stools or frank diarrhoea with or without blood and
mucus. Tenderness may develop over the caecum area. Generalised constitutional
symptoms and signs are characteristically absent with fever only noted in about a third of
the patients on clinical examination. The dysentery occurs in attacks lasting a few days to
several weeks and recurrence is very common in untreated patients. Intestinal
amoebiasis may occur in about 2 weeks of infection or be delayed for months.
In severe cases the onset is more sudden. The patient is ill and toxic with fever and signs
of dehydration. The faeces contain a lot of dark altered blood and blood streaked mucus.
Trophozoites are present in large numbers.
Diagnosis
Chronic amoebiasis is difficult to diagnose. Alternating diarrhoea and constipation is often
seen. The colon may be distended. Chronic amoebiasis may resemble duodenal ulcer,
gall bladder disease or carcinoma of the colon.
Extra-Intestinal Manifestations of Amoebiasis
Earlier on we mentioned that when the amoeba penetrate the intestinal wall, they multiply
in the sub-mucosa, where it will cause ulcers, and then from these ulces it may be
transported to other organs of the body, such as the liver, skin or even the brain. When
the amoeba invade the liver, they cause an amoebic live abscess.
Amoebic Liver Abscess
The most common findings of the amoebic liver abscess are fever, leukocytosis, enlarged
and tender liver and elevation and fixation of the right diaphragm on radiographs/x-ray.
Although diffuse liver enlargement has been associated with intestinal amoebiasis, liver
abscess may appear in individuals with no indicators of intestinal disease. An amoebic
liver abscess may perforate into the chest cavity (see Figure 7) or the peritoneal cavity,
causing acute abdomen.
36
When a liver abscess breaks through into the chest cavity, a lung abscess (which may
perforate into a bronchus) or empyema may occur. When a liver abscess is close to the
diaphragm, the diaphragm will not move and the right lower lobe will not be well ventilated.
As a result, liver abscess is often accompanied or masked by bronchopneumonia in the
right lower lobe. Pleurisy dry or with effusion may occur if the pleura covering the
diaphragm is jammed
Figure 7: Elevation of the diaphragm in amoebic liver abscess
.Amoebiasis of the Skin
Amoebiasis of the skin may occur where amoeba breaks through the skin, resulting in
cutaneous amoebiasis. Another site could be where it comes into contact with the skin
that is around the anus and perineum, or around the incision wounds after
appendicectomy or drainage of a liver abscess or around a fistula from a liver abscess
which perforated. This opening may be far away from the liver.
An amoebic skin ulcer is irregular and painful. The ulcer enlarges continually because of
necrosis of the edges.
Amoebiasis of the Brain
Rarely an amoebic brain abscess may complicate severe amoebiasis.
Diagnosis
The presence of cysts in stools does not prove that symptoms are caused by entamoeba.
Trophozoites of E. histolytica must be differentiated from those of Escherishia coli and
may also be seen in diarrhoea stools caused by another organism. The presence of
ingested erythrocytes in the E histolytica indicates an active infection.
37
Cysts must also be differentiated from those of E. coli. Cysts are differentiated when a
stool specimen is stained with Lugol´s solution to demonstrate the nuclei. E. histolytica
cysts have four nuclei. See Figure 8.
Figure 8: Differentiation of E. histolytica and Escherichia coli
Management
The luminal amoebicides such as Diloxanide Furoate, Furazolidine or Paromomycin are
primarily effective in the gut lumen, while Metronidazole, Chloroquin and Dihydroemetine
are effective in the treatment of invasive amoebiasis.
All individuals with E. histolytica trophozoites or cysts in their stools whether symptomatic
or not, should be treated. Diloxanide Furoate is the drug of choice for asymptomatic cyst
passers.
Invasive amoebiasis of the intestine, liver, or other organs requires the use of
Metronidazole, a tissue amoebicidal drug. It is administered orally in a daily dose of
50mg/kg/day for 10 days. Metronidazole is also a luminal amoebicide but less effective
38
than Diloxanide Furoate. Patients with invasive amoebiasis should thus receive an
additional course of the latter drug following Metronidazole therapy.
Chloroquin is useful in the treatment of amoebic liver abscess because it is concentrated
in the liver. Aspiration of large lesions may be necessary if rupture is imminent or if the
patient shows poor clinical response 4 - 6 days after administration of amoebicidal drugs.
Stool examination should be repeated 2 weeks following completion of therapy as of cure.
Prevention and Control
The cyst passers are responsible for the spread of amoebic dysentery in the community.
They are usually asymptomatic and will not report for treatment. People employed as food
handlers should be screened before and during employment. Water cannot be made safe
by ordinary chlorination. Boiling of drinking water kills the cysts.
The most important control method is proper faeces disposal and ensuring that food
handlers are not carriers.
In your notebook, summarize the differences between
bacillary dysentery and amoebic dysentery and then
compare your answer with Table 2 below.
Table 2: Differences between bacillary and amoebic dysentery
Features
Bacillary dysentery
Amoebic dysentery
Incubation period
Short < 1 week
Long: 3 weeks or more
Onset
Acute
Insidious
Occurrence
Epidemic
Endemic
Fever
Common
Only in complications
Clinical picture
“Lying down dysentery”
“Walking dysentery”
39
Tenderness
Whole abdomen
More localized in sigmoid region
Tenesmus
Very severe
Not usual
Stools
Mucous and blood only
Stools with blood and mucous
Macroscopic
Numerous red blood cells
Numerous clumped red cells
Microscopic
Numerous polymorphs
Scanty polymorphs
Few bacteria
Many bacteria
Macrophages
E. histolytica trophozoites with
ingested red cells
What have we learnt?
Amoebiasis is an infection with potentially pathogenic amoebae. Infection occurs through
the faecal-oral transmission route. Infection is usually asymptomatic but may result in
attacks of dysentery and /or liver abscess. Treatment covers both tissue parasites and
parasites in the bowel lumen. Control depends on proper disposal of faeces.
Asymptomatic carriers are difficult to trace.
Section 4: Faecal-Oral Diseases Caused By Toxins
In the previous section we discussed diseases caused by protozoa. We are now going to
focus on some conditions that are caused by toxins.
Go back to Table 1 on page 3 and remind yourself what diseases are caused by
toxins.
40
Food Poisoning
Food poisoning is a term applied to an acute intestinal disease acquired by the
consumption of food or water. The cause may be intoxication with chemicals, toxins
produces by bacterial growth and a variety of organic substances that may present in
natural food, for example, mushrooms. Acute salmonellosis and intestinal anthrax are
often regarded as food poisoning although these are more of acute enteric infections than
intoxication.
Food poisoning occurs in small outbreaks; mortality is very low. Members of one family or
an institution are usually affected. A good number of cases reported as gastroenteritis
may well be due to a form of food poisoning. Food poisoning is usually recognized when
all members sharing the same food, usually members of one household, customers eating
in one restaurant or travellers on an aeroplane, fall sick within a short time.
Epidemiology
Food poisoning may be real intoxication or an infection. Intoxication may be caused by
ingestion of food contaminated with toxin-producing staphylococci from purulent
discharge, for example, the septic finger of an infected person. The staphylococci multiply
when food is allowed to stand for several hours before serving. Infection may be caused
by ingestion of salmonellae in food contaminated by infected faeces of humans, or
ingestion of meat containing anthrax bacilli.
Humans are the only reservoir for staphylococci. Domestic and wild animals are the
reservoirs for salmonellae. Cattle and game are reservoirs for anthrax.
Clinical Picture
The incubation period is short: staphylococci food poisoning takes 1 - 6 hours while
salmonella food poisoning takes 12-14 hours. There is acute onset of vomiting, abdominal
pains and diarrhoea after ingestion of made-up food. Usually a number of cases occur
together. There may be moderate fever, seldom over 38 C. Complications are rare but
children with sickle cell disease may develop a salmonella osteomyelitis after salmonella
food poisoning.
Gastrointestinal anthrax has an incubation period of 2 - 5 days when vomiting, abdominal
pains, haematemesis, bloody diarrhoea and toxaemia develop.
41
Management
Treatment is symptomatic. Correct dehydration. Antibiotics are not indicated except for
anthrax.
Prevention and Control
Serve meals immediately after preparing them so as to avoid growth of accidentally
introduced staphylococci. Note that the toxin produced by staphylococci is heat – sable,
so cooking of already prepared food will kill the staphylococci but will not break down the
toxin unless the food is heated to over 140 C.
Contrast the differences in the clinical features of food poisoning and cholera.
Compare your answer to the features given in Table 3.
Table 3: Distinguishing between cholera and food poisoning
Cholera
Food poisoning
Diarrhoea
Precedes vomiting
Follows vomiting
Vomiting
Watery and projectile; causes
Violent and distressing, vomit
no distress
consists of food
Nausea
Absent
Common
Abdominal pain
Not usually severe
Constant
Tenesmus
Absent
Common
Stools
Rice-water, not offensive
Liquid, feacal, offensive
Urination
May be completely suppressed Usually not suppressed
Muscular cramps
Constant, severe
In very severe cases, extremities
only
42
Headache
Absent
Frequent
Fever
Absent
Only present in salmonella
infection
Thorough cooking of food will prevent all cases of salmonella food poisoning. Exclude
people with pyogenic skin infections from food handling. In case of an outbreak search for
them and identify them. Thoroughly cook foodstuffs derived from animals and avoid the
use of raw eggs. Rat-proof all food stores. Give health education to all food handlers
about the necessity of refrigerating foods, washing hands and maintaining a clean kitchen.
Educate communities about not eating animals that have died after an illness.
If food poisoning is suspected, trace all persons who ate the infected meal and treat them
if necessary. Try to establish the cause of the food poisoning. Watch out for neurological
symptoms suggesting insecticide or mushroom poisoning.
What have we learnt?
Food poisoning occurs among people who share the same meal. Causes are intoxication
or infection. Re-hydration management is the first priority.
We have so far discussed three of the four major causes of faeco-oral diseases. We are
now going to turn our attention to viral infections.
Section 5: Faecal-Oral Diseases Caused By Viral Infection
Did you know that the polio virus,
too, inhabits the digestive tract?
43
Poliomyelitis
Poliomyelitis is an acute viral disease of the nervous system with a wide range of clinical
presentation, from asymptomatic infection to paralytic disease. It is also known as infantile
paralysis or polio. The polio virus belongs to a large group of viral agents that inhabit the
digestive tract known as enteroviruses.
Passive antibodies transferred across the placenta from mother to foetus in the womb
persist up to about 6 months of age. Active immunity after infection probably gives a
lifelong immunity. Infection below the age of 3 years rarely results in paralysis. The
degree of functional recovery depends upon the adequacy and promptness of therapy as
related to proper body positioning, active motion, use of assistive devices, and of great
importance, the psychological motivation of the patient to return to as full and normal life
as soon as possible.
In an unimmunised person the risk of paralysis increases with age. People who get
infected after the age of 20 are at a greater risk of getting paralysis. With an increasing
polio immunization coverage, vigilant lookout for new cases of acute flaccid paralysis and
contact tracing, Kenya is working hard towards the goal of being declared polio free by the
World Health Organization (WHO).
After ingestion of the virus in faecally contaminated food, it settles in the digestive tract.
Within one day the infection extends to the regional lymph nodes. On about the third day
the polio virus invades the bloodstream involving the target organs which are the nerve
endings, the meninges and the brain. Multiplication of the polio virus in the regional lymph
nodes coincides with the onset of clinical symptoms. Major viraemia occurs during the
period of multiplication of the polio virus in the target sites, usually lasting from the third to
the seventh day of the infection. The injury to the nerves results in paralysis and the
resultant muscular atrophy is due to disuse of the affected muscle. In 90 - 95% of those
infected with polio no symptoms are noted, while the remainder can present as abortive,
nonparalytic or paralytic poliomyelitis. Persons with asymptomatic infection, mostly
children are the reservoirs of polio infection.
44
Clinical Picture
Asymptomatic Poliomyelitis
In cases of asymptomatic poliomyelitis, there is infection with the polio virus but there are
no symptoms, not even of the febrile illness. These cases are the main the reservoirs of
the infection.
Abortive Poliomyelitis
Abortive poliomyelitis infection with the polio virus results in a mild general reaction.
There is fever, headache, malaise, sore throat and gastrointestinal disturbance lasting 1-2
days. The gastrointestinal disturbances include anorexia, vomiting, constipation and
unlocalized abdominal pains. This minor illness cannot be differentiated from other mild
viral infections and is only recognizable during an epidemic of polio. After the minor
illness, the disease sometimes progresses into the major illness, that is, the central
nervous phase, with a recurrence of fever.
Non-paralytic Poliomyelitis
In non-paralytic poliomyelitis the symptoms are similar to those of abortive poliomyelitis.
However, in addition, there is soreness and stiffness of the posterior muscles of the neck,
trunk and limbs. The headache, nausea and vomiting are more intense. After 1 or 2 days
the symptoms disappear. The patient may recover or may go on to paralysis. Physical
activity at the time of temporary improvement may aggravate the degree of subsequent
paralysis.
Paralytic Poliomyelitis
As the temperature settles down, the paralysis appears in the paralytic poliomyelitis.
Paralysis can appear at any site of the body and is asymmetrical. The lower limbs are
more often affected than the upper. The spread of paralysis is usually completed in 24
hours. The paralyzed muscles are painful.
Post Paralytic Stage
The post paralytic stage is the stage of residual disability. Paralysis or weakness of
muscles will lead to deformity and contractures. A severely affected limb will show effects
of abnormalities in blood circulation such as coldness and cyanosis. There may be
retardation of bone growth resulting in shortening of the affected limb.
45
Management
No specific drug is available as poliomyelitis is a viral infection. Absolute bed rest is
necessary in the pre-paralytic stage until it is certain that paralysis will not develop. All
injections should be avoided for fear of precipitating paralysis. In the paralytic stage,
mobility by passive movements of the affected limb must be maintained to prevent
contractures. In the post-paralytic stage of the disease, active physiotherapy should be
started. Physiotherapists can help in assessment of disability and deformity, with active
exercises and passive stretching of contractures and by measuring for braces and gait
training. It is important to immunize all contacts and ensure high coverage in the
community.
Health workers in a community have responsibility to help mothers with the rehabilitation
of polio-crippled children. A disability should not be allowed to progress into a social
handicap. Every effort should be made to bring up the child in as normal a way as
possible. This includes play with others, walking upright and going to school. Health
workers need to teach families how to construct low cost aids such as wooden parallel
bars, supporting seats and crutches.
Prevention and Control
Vaccination is the only effective method of preventing poliomyelitis. Vaccination is
necessary to control transmission in older age groups while hygienic steps help to limit the
spread of poliomyelitis infection in the young children.
The polio vaccines available are the live attenuated orally administered polio vaccine OPV
and the inactivated polio vaccine IPV as an intramuscular injection. Both vaccines induce
production of antibodies against the three strains of polio virus
The OPV stimulates pharyngeal as well as intestinal secretory Ig A production, preventing
virus replication at these sites, which is unlike the case in IPV given via an intramuscular
injection. Transmission of the wild-type virus by faecal spread is thus limited in OPV
recipients.
The OPV, being a live vaccine may undergo reversion to a virulent state as it multiplies in
the digestive tract and cause vaccine associated polio in the recipient of the vaccine or in
their contacts. This risk is very low; no incident has yet been reported in Kenya while
hundreds of millions of doses have been given worldwide without incident.
46
The polio vaccine is given routinely to all under fives, starting the immunization at birth and
then at 6 weeks, again at 10 weeks and at 14 weeks of age. Booster vaccinations at 18
months and 5 years are recommended. In Kenya, this is the practice in private health
care, with the public institutions yet to catch up. The 6, 10 and 14 weeks polio vaccine is
given together with DPT.
In 2006, Kenya had sporadic outbreaks of poliomyelitis and this was thought to be due to
emigration of unvaccinated children from Somalia. This necessitated emergency mass
polio immunization of all under fives in the country in a bid to boost up the immunity of the
population. Polio surveillance is on high alert in Kenya as it works to a declaration of a
polio free country by the World Health Organization.

Take Note
Poliomyelitis is a notfiable disease. Inform your DMO when you suspect any new
paralytic case.
Any new suspected case must be investigated to confirm the diagnosis. This is done by
sending fresh stool samples for viral studies to a special referral centre.
General action is to check your MCH clinic to see if polio immunizations are carried out
routinely. Is the refrigerator working as it should? Are there wasted opportunities to
complete each infant’s full immunization? In an outbreak of polio do the following:

Inform your DMO;

Confirm cases by sending fresh stool samples immediately to the nearest
reference laboratory;

Ensure immunization of all under fives;

Postpone other immunizations (injections);

Restrict use of injections;

Advise people, especially teachers, to postpone sports activities and other
exercises;

Refer paralytic patients for physiotherapy as soon as the acute stage (pain and
fever) is over.
47
What have we learnt?
Poliomyelitis is an acute viral disease which can be complicated by central nervous
system involvement. Transmission is by close contact. Previously most children were
infected at a young age resulting in relatively few cases of paralysis. Now almost all
children have been immunized.
Paralytic cases need physiotherapy. Polio can be prevented by immunization. Each
suspected case requires detailed investigation and laboratory confirmation.
Let us now turn our attention to another disease of viral origin that is becoming a major
health problem.
Viral Hepatitis
Viral hepatitis is a systemic disease predominantly affecting the liver and is a major health
problem in both developed and developing countries. It is characterized by a
constitutional upset, followed by jaundice, although there are many asymptomatic cases.
Hepatitis A, B, C, D, E viruses cause hepatitis as their primary disease manifestation,
while other viruses such as HIV, Epstein-Barr virus (EBV), Cytomegalovirus and many
others also cause hepatitis but as a component of a multi-systemic disease.
Hepatitis A and E are transmitted via the faecal-oral route and never lead to chronic liver
disease unlike B, C, and D which are transmitted through blood products and may lead to
chronic liver infection and cirrhosis.
Hepatitis A
Hepatitis A only causes acute hepatitis. It occurs in slowly spreading epidemics in families
and institutions. Epidemics can be traced to contaminated food, water or milk. Poor
personal hygiene, overcrowding and poor sanitation increase the transmission which is
mainly via the faecal oral route. Most infections in children younger than 5 years are
asymptomatic or have mild non-specific manifestations, including gastroenteritis without
jaundice. The resulting immunity is long-lasting. When children escape infection at an
early age they are more likely to develop jaundice and more severe infections when they
are infected later in life. Most cases of infectious hepatitis are, therefore, diagnosed in
older children and young adults.
The infectious agent is excreted in faeces and urine and occurs late in the incubation
period, reaches its peak just before the onset of symptoms and is minimal in the week
48
after the onset of jaundice. The mean incubation period for hepatitis A infection is about 4
weeks. Most probably it is also present in nasal and pharyngeal discharges. The main
way of transmission is, however, by faecal contamination of water or food.
Clinical Picture
The incubation period is 1 - 4 weeks. In the pre-icteric (pre-jaundice) phase, the disease
presents like gastroenteritis with sudden onset of fever, malaise, anorexia, nausea and
abdominal discomfort. Children often do not go into the next phase. In the icteric phase
after a few days, jaundice appears. The jaundice is partly of the hepatocellular type and is
partly obstructive because the swollen liver cells block the bile flow in the bile capillaries.
Itching is not usually present. Complete recovery in about 2 weeks is the rule, but a long
period of extreme tiredness with depression may occur after the jaundice has
disappeared.
Diagnosis
Hepatitis A infection should be considered when a history of jaundice exists in family
contacts, friends, school mates, day care playmates or school personnel. The acute
phase of the infection is diagnosed by the presence of IgM anti Hepatitis A virus which is
present for 3 -12 months, and thereafter IgG anti-hepatitis A virus is found.
Stools are usually pale. The urine is dark and contains bilirubin. White cell count total and
differential are normal. There is no albuminuria. In blood, both direct and indirect bilirubin
are raised in addition to alanine aminotransferase (ALT) and aspartate aminotransferase
(AST) but all these do not help in differentiating the many causes of hepatitis. A blood
slide should be taken to exclude other causes of jaundice such as malaria and relapsing
fever.
Management
No specific treatment is available, therefore, there is no strict reason for admission to
hospital. Bed rest at home is best and will prevent spread of the disease. If admission for
one or other reason is indicated, there should be careful disposal of excreta. Fat can be
restricted when there is nausea and a high calorie diet is indicated.
Prevention and Control
Improvement of sanitation will diminish transmission of hepatitis A. Injection of pooled
gamma-globulin can protect susceptible individuals for periods of about 3 months.
49
Hepatitis A vaccine is available and is given as 2 injections 6 months apart. Its use is
slowly picking up but the biggest problem at the moment is its high cost.
What have we learnt?
Viral hepatitis A is characterized by abdominal discomfort and malaise, most often
followed by jaundice. No specific treatment is available. Environmental sanitation,
personal hygiene and food hygiene are important.
Hepatitis E
Hepatitis E is transmitted via the faecal-oral route and causes outbreaks of hepatitis with
similar signs and symptoms to hepatitis A. The incubation period for hepatitis E is 3 -12
weeks. Children have a lower rate of infection so that it appears that more adults are
affected. Most people with hepatitis E recover fully and there is no progression to chronic
liver disease
Rotavirus

Take Note
Rotavirus infection is the single most important cause of severe dehydrating
diarrhoea in the first 2 years of life and in some by 5 years of age.
The rotavirus spread via the faecal-oral route and outbreaks are common in children’s
hospitals and day care centres. It is shed in the faeces at very high concentrations before
and for days after the clinical illness.
Clinical Picture
The infection starts with mild to moderate fever and vomiting, followed by an onset of
frequent watery stools after an incubation period of up to 48 hours. The vomiting and
fever subside 48 - 72 hours after the onset, but the diarrhoea often continues for 5-7 days.
Dehydration is common with the rotavirus diarrhoea.
50
Diagnosis
Stool test for rotavirus (latex test) is the main mode of diagnosis available. In stool
microscopy, the specimens are usually free of blood and leukocytes but in a few cases
might be positive for blood in microscopy.
Management
The mainstay of treatment is management of dehydration. There is no cure at the moment
for rotavirus infection.
Prevention and Control
A rotavirus vaccine is now available and is given as 2 doses. The first dose can be given
as early as a few weeks of age, with the booster 4 weeks later. This seems to be the only
protecting mechanism available at the moment.
Summary
We have now come to the end of this unit. It was quite a long one but we learnt many
important things. We covered diseases transmitted through the faecal-oral route that are
caused by viral, bacterial or protozoal organisms and their toxins. In the next unit, you will
learn about helminthes and the diseases they cause. Before you proceed, I suggest you
attempt the self test questions to assess your understanding of the content covered in this
unit. The answers are provided at the end of this unit.

Self Test
Please, try to answer all the questions without looking for the answers in the text.
1. The insect associated with faecal-oral transmission is:
a. Phlebotomous fly
b. Sand fly
c. House fly
d. Tse tse fly
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2. Which of the following does NOT offer protection against the pathogenic bacteria
that causes faecal-oral diseases:
a. Antimotility drugs
b. Intestinal bacterial flora
c. Gastric acid
d. Normal bowel motility
3. Bacillary dysentery is caused by:
a. Adenoviruses
b. Shigella spp
c. Rotavirus
d. Salmonella spp
4. The campylobacter jejuni bacteria is a:
a. Gram negative micro-aerophillic bacteria
b. Gram positive anaerobic bacteria
c. Gram positive micro-aerophillic bacteria
d. An acid fast bacteria
5. Giardiasis infection in man results after ingestion of
a. Trophozoites of giardia
b. Cysts of giardia
c. Adult giardia
6. The organism that causes bottle shaped ulcers in the intestines is:
a. Escherichia Coli
b. Giardia Lamblia
c. Shigella Flexneri
d. Entamoeba histolytica
7. In which of the following is fever not a major symptom?
a. Cholera
b. Campylobacter Jejuni infection
c. Bacillary dysentery
d. Rotavirus infection
8. The diarrhoea passed by a Cholera patient is:
a. Mucoid and bloody with no feaces
b. Feaces mixed with blood and mucous
52
c. Rice water in appearance
d. Feaces mixed with blood
9. Which of the following pair of viruses is transmitted through the faecal oral route?
a. Hepatitis A and B
b. Hepatitis C and D
c. Hepatitis A and D
d. Hepatitis A and E
10. The monthly statistics for your district show that the prevalence of amoebic
dysentery is on the rise. Describe
a. The clinical manifestations of a person with amoebiaisis;
b. How you would diagnose Amoebiasis;
c. Complications associated with Amoebiasis;
d. How you would manage the patients;
e. The measures you would institute in the district to prevent and control this
disease.

Check your answers to the Self Test
1. D
2. A
3. B
4. A
5. B
6. D
7. A
8. C
9. D
10.
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a) Clinical manifestations :

Abdominal discomfort;

mildly loose stools or frank diarrhoea with or without mucous,

abdominal tenderness.

Severe cases present with fever and dehydration
b) Diagnosis
By identifying cysts and trophozoites in stool. These must be differentiated from those of
E.Coli.
c) Complications:

Amoebic liver disease,

bottle shaped ulcers,

amoeboma formation,

Amoebiasis of skin
d) Management
Luminal amoebicides such as diloxanide furoate, furazolidine, paromomycin are primarily
effective in the gut lumen,
Metronidazole chloroquin, dihydroemetine are effective in the treatment of invasive
amoebiasis.
Diloxanide furoate is the drug of choice for asymptomatic cyst passers.
Chloroquin is useful in the treatment of amoebic liver abscess.
e) Prevention and control

Screen food handlers before and during employment;

Make drinking water safe by chlorination or boiling,

proper faeces disposal
How well did you do? I hope you did quite well and are now ready to do your tutor marked
assignment before you start work on Unit 12. But take a well-deserved break first!

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DIRECTORATE OF LEARNING SYSTEMS
DISTANCE EDUCATION COURSES
Student Number: ________________________________
Name: _________________________________________
Address: _______________________________________
_______________________________________________
COMMUNICABLE DISEASES COURSE
Tutor Marked Assignment
Unit 11: Diseases Caused By Faecal-oral Contamination
Instructions: Answer all the questions in this assignment.
1. What are the common diseases spread by the faecal-oral route in your area?
Approximately how many cases did you see last month?
Disease
Number of cases
______________________
_______________________
______________________
_______________________
______________________
_______________________
2. What are the main ways of breaking the transmission cycle of diseases spread by the
faecal-oral route?
_____________________________________________________________________
_________________________________________________________________
___________________________________________________________________
___________________________________________________________________
___________________________________________________________________
___________________________________________________________________
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3. What practical steps could you take in your area to prevent attacks of diarrhoea in
children?
________________________________________________________________________
______________________________________________________________
________________________________________________________________________
______________________________________________________________
___________________________________________________________________
___________________________________________________________________
4. Fill in the table below with “yes’ or “no”.
Amoebic dysentery
Bacillary dysentery
White cells in stool
Trophozoite in stool
May involve the liver
Mainstay of treatment is
hydration
Metronidazole is used in
treatment
5. From the monthly statistics in the district, you have noticed that the number of patients
with a diagnosis of amoebiasis is on the rise. What is the causative organism?
____________________________________________________
6. What signs and symptoms are patients with amoebiasis likely to present with?
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
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7. List four complications that can result from amoebiaisis
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
__________________________________________________________________
8. What action would you institute to prevent and control the spread of amoebiasis?
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
_____________________________________________________________________
9. What clinical features would raise your suspicions that a patient may be having
cholera?
___________________________________________________________________
___________________________________________________________________
___________________________________________________________________
__________________________________________________________________
10. Apart from treating the patient what other things would you do?
___________________________________________________________________
___________________________________________________________________
___________________________________________________________________
________________________________________________________________________
______________________________________________________________
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Congratulations! You have now come to the end of this unit. Remember to indicate your
Student Number, names and address before sending the assignment. Once you complete
this assignment, post or bring it in person to AMREF Training Centre. We will mark it and
return it to you with comments.
Our address is:
AMREF Distance Education Project
P O Box 27691-00506
Nairobi, Kenya
Email: amreftraining@amrefhq.org
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