UNIT 11: DISEASES CAUSED BY FAECAL CONTAMINATION



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. Any part of this unit including the illustrations may be copied, reproduced or adapted to meet the needs of local health workers, for teaching purposes, provided proper citation is accorded AMREF. If you alter, transform, or build upon this work, you may distribute the resulting work only under the same, similar or a compatible license. AMREF would be grateful to learn how you are using this course and welcomes constructive comments and suggestions. Please address any correspondence to:

The African Medical and Research Foundation (AMREF)

Directorate of Learning Systems

P O Box 27691 – 00506, Nairobi, Kenya

Tel: +254 (20) 6993000

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Email: amreftraining@

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Writer: Dr Peter Ngwatu

Chief Editor: Anna Mwangi

Cover design: Bruce Kynes

Technical Co-ordinator: Joan Mutero

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 10

Kiosks and Food Shops 11

Hotels 11

Private Homes 12

Irrigation Furrows 12

Health Facilities 12

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 18

Diagnosis 18

Management 19

Prevention and Control 20

Campylobacter Jejuni Infections 20

Pathology 21

Clinical Picture 21

Diagnosis 22

Management 22

Prevention and Control 23

Cholera 23

Epidemiology 24

Clinical Picture 25

management 26

Prevention and Control 27

Enteric Fever 29

Epidemiology 29

Clinical Picture 30

Diagnosis 31

Management 31

Prevention and Control 31

Section 3: FAECAL-ORAL DISEASES CAUSED BY PROTOZOAL INFECTION 32

Giardiasis 32

Pathology 33

Clinical Picture 33

Diagnosis 33

Management 34

Prevention and Control 34

Amoebiasis 34

Epidemiology 34

Pathology 35

Clinical Picture 36

Diagnosis 37

Extra-Intestinal Manifestations of Amoebiasis 37

Diagnosis 38

Management 39

Prevention and Control 39

Section 4: FAECAL-ORAL DISEASES CAUSED BY TOXINS 41

Food Poisoning 41

Epidemiology 42

Clinical Picture 42

Management 42

Prevention and Control 42

Section 5: FAECAL-ORAL DISEASES CAUSED BY VIRAL INFECTION 44

Clinical Picture 45

Management 46

Prevention and Control 47

Viral Hepatitis 48

Hepatitis A 49

Hepatitis E 51

Rotavirus 51

Clinical Picture 51

Diagnosis 51

Management 51

Prevention and Control 52

Tutor Marked Assignment 56

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

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.

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.

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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.

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.

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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 |Bacterial |Protozoa |Worms |Toxins |

|Polio |Typhoid and paratyphoid |Amoebiasis |Ascariasis |Botulism |

|Hepatitis A, E |Cholera |Giardiasis |Enterobiasis |Staphylococcal food |

|Viral diarrhoeas such as |Bacillary dysentery | |Trichuriasis |poisoning |

|rotavirus and adenovirus |Anthrax | |Taeniasis |Enterotoxigenic coli |

| |Bacteria diarrhoeas such as | |Hydatidosis |diarrhea |

| |Yersinia, Campylobacter, E. coli | | | |

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.

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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

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| |Give 3 examples of natural defenses the body has against infection. |

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.

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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.

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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.

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Figure 2: Preparation of ORS at home

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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 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.

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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 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”.

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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.

Check-points for Sources of Water Borne Diseases

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| |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.

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?

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 faecal-oral 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

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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 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, 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;

• 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.

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.

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 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.

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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 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 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

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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.

Υ

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.

Cholera

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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.

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.

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Figure 5 illustrates the transmission of cholera by the faecal-oral route.

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Fig 5: Transmission of cholera by the faecal-oral route

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.

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 Co-trimoxazole can also be used with good effect. A stool culture will assist in the selection of the most sensitive antibiotic.

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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.

Υ

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.

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.

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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.

Enteric Fever

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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 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 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 non-immunized 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.

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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, immuno-deficiencies, 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.

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.

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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-to-person 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 ex-cysts 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 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-to-person 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. 

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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.

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.

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

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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.

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.

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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 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.

|[pic] |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” |

|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.

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| |Go back to Table 1 on page 3 and remind yourself what diseases are caused by toxins. |

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.

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.

|[pic] |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 no distress |Violent and distressing, vomit consists of food |

| |Absent |Common |

|Nausea |Not usually severe |Constant |

|Abdominal pain |Absent |Common |

|Tenesmus |Rice-water, not offensive |Liquid, feacal, offensive |

|Stools |May be completely suppressed |Usually not suppressed |

|Urination |Constant, severe |In very severe cases, extremities only |

|Muscular cramps | |Frequent |

| |Absent |Only present in salmonella infection |

|Headache |Absent | |

|Fever | | |

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

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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.

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.

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.

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.

Υ

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.

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 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.

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

Υ

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.

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

1. 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

1. Bacillary dysentery is caused by:

a. Adenoviruses

b. Shigella spp

c. Rotavirus

d. Salmonella spp

1. 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

1. Giardiasis infection in man results after ingestion of

a. Trophozoites of giardia

b. Cysts of giardia

c. Adult giardia

2. The organism that causes bottle shaped ulcers in the intestines is:

a. Escherichia Coli

b. Giardia Lamblia

c. Shigella Flexneri

d. Entamoeba histolytica

1. In which of the following is fever not a major symptom?

a. Cholera

b. Campylobacter Jejuni infection

c. Bacillary dysentery

d. Rotavirus infection

1. The diarrhoea passed by a Cholera patient is:

a. Mucoid and bloody with no feaces

b. Feaces mixed with blood and mucous

c. Rice water in appearance

d. Feaces mixed with blood

1. 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

1. 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.

Ρ 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.

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!

[pic]

DIRECTORATE OF LEARNING SYSTEMS

DISTANCE EDUCATION COURSES

|Student Number: ________________________________ |[pic] |

| | |

|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?

______________________________________________________________________________________________________________________________________

___________________________________________________________________

___________________________________________________________________

___________________________________________________________________

___________________________________________________________________

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? ______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________

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?

___________________________________________________________________

___________________________________________________________________

___________________________________________________________________

______________________________________________________________________________________________________________________________________

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@

-----------------------

Take Note

There are many diseases that are transmissible through faeces but not all of them are strictly faecal-oral in transmission.

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.

Take Note

Death from diarrhoeal diseases is largely due to dehydration and disturbance of the electrolytes balance.

Take Note

Re-hydration is the first priority!

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.

Which faecal-oral diseases are of bacterial origin?

What is the most common presentation of campylobacter jejuni infecton?

Take Note

Re-hydration is the priority in treatment for dysentery

Take Note

Antimotility medications may cause prolonged or fatal disease and should not be used.

Do you still remember Table 1 on p. 3? Which two diseases were listed there under protozoal infection?

Take Note

Clinical amoebiasis is endemic in areas where sanitary conditions are poor.

What is your own definition of cholera?

Take Note

Most cholera infections are asymptomatic or cause only simple self-limiting diarrhoea.

Take Note

Re-hydration will save almost all cholera cases.

Take Note

Cholera is an internationally notifiable disease.

Take Note

Prevent cholera with a clean water supply!

Which bacteria cause the enteric fever?

Did you know that the polio virus, too, inhabits the digestive tract?

Take Note

Poliomyelitis is a notfiable disease. Inform your DMO when you suspect any new paralytic case.

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.

[pic]

DIRECTORATE OF LEARNING SYSTEMS

DISTANCE EDUCATION PROGRAMME

Unit 11

Unit 5: Diseases of Faecal-oral Contamination

|[pic] | |

| |Allan and Nesta |

| |Ferguson Trust |

COMMUNICABLE DISEASES COURSE

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