Part 2-Cdc Feco Oral Disease

Mizan tepi university
College of Medicine and Health Science Department of

Nursing
For psychiatry students
By; Tsehaye G.(BSc N, MSc in adult health Nursing)
Prevention and control of feco - orally transmitted

diseases
April 2022
By, Tsehaye G. 05/31/2024
Objectives
 At the end of this lesson students will able to;

 Define typhoid fever
 Identify the five important “Fs” in oral-fecal disease
transmission.
 Describe the sign and symptom of communicable d/se
 Demonstrate the Diagnosis of CD
 Describe the management of CD
 Identify the preventation mechanism of CD
Brainstorming
 What do you know about feco- oral disease and the
mechanism of transmission?

Common features of feco oral Diseases
1.The agent are excreted in the stools
2.The portal of entry - mouth

 feces to the GIT of a susceptible host
 known as feco-oral transmission.
3. Fecal oral transmission- occurs mostly through unapparent
fecal contamination of food, water and hands.

The five “Fs” which play an important role in feco- oral disease
transmission are feces, finger, flies, fomites and food.
Water
Soil
Feces Food
Flies Mouth
Fomites
Finger

General prevention methods
1. Early case detection and appropriate Rx of cases
2. Safe human excreta disposal
3. Control of flies
4. Safe water supply
5. Hand washing and sanitary handling of food and utensils(kits)
6. Control and check up of food handlers
7. Avoid eating of uncooked foods

Classification of feco-orally transmitted disease
1.As a result of fecally contaminated water and food

 Diseases mainly transmitted through fecally contaminated
water rather than food
1.Typhoid fever
2. Amebiasis
3. Giardiasis
4. Cholera
5. Bacillary dysentery
6. Infectious hepatitis
2. As a result of fecally contaminated soil
 These infections are acquired through exposure to fecally

contaminated soil
1. Ascariasis
2. Hook worm
3. Trichuriasis
4. Enterobiasis
5. Stronglodiosis

3. As a result of direct contact with feces
 Diseases transmitted mainly through direct contact with

feces of the infected person.
1. Poliomyelitis
2. Hydatid disease or Echinococus

1. Typhoid Fever
 Definition: It is a systemic infectious disease characterized by

high & continuous fever, malaise and involvement of lymphoid
tissues.
 It is a bacterial infection that can spread throughout the body,
affecting many organs.
Etiology:
 Salmonella typhi
 Salmonella enteritis (rare cause)

Cont.…

Cont.….
 Epidemiology:- common in world wide, poor socioeconomic

areas
 Over 21.9 million cases annually
 Majority of the cases occurred age group between 5- 12 years.
 Reservoir:- human
 Mode of transmission:- feco oral
 Incubation period:- 1 – 3 weeks
Cont.…
 Period of communicability:
 As long as the bacilli appear in excreta, usually from the first
week throughout convalescence(recovery).
 About 10 % of untreated patients will discharge bacilli for 3
months after onset of symptoms.
 2- 5% become chronic carriers

Cont.….
 Susceptibility and resistance:-

 susceptibility is general and increased in individuals with
gastric achlorhydria(lack of HCL) or those who are HIV
positive.
 Relative specific immunity follows recovery from clinical dx.

Clinical Manifestations
 First Week:- mild illness x-zed by fever rising stepwise (ladder

type). i.e. fever rises one day, falls the subsequent morning, and
continues to form peaks and troughs with insidious onset.
 for 4 - 5 days with associated chills, myalgia, dry cough,
anorexia, lethargy, malaise and general aches.
 Dull and continuous frontal headache is prominent.
 Nose bleeding(epistaxis), vague abdominal pain and
constipation in 10% of pts.
Cont.…
 Second week:- sustained fever, weakness, mental dullness or

delirium, abdominal discomfort and distension.
 Diarrhea is more common than 1st week
 Rash on chest, upper abdomen, shoulder, and back
 slightly raised rose-red spots fade on pressure, not visible on
dark skinned person.
 Hepatospleenomegally may occur.

Cont.…
 Third week:- patients continue to be febrile and extremely

exhausted
 If no complications occur, patient begins to improve and
temperature decrease gradually.
 increased toxemia, ileus perforation, GI hemorrhage, melena,
rigid abdomen, coma, & death are also may occur

Clinical Manifestations suggestive of typhoid fever
1. Fever:- sustained fever (ladder fashion)
2. Rose spots:- small pallor, blanching, slightly raised macules

usually seen on chest and abdomen in 75% of white people.
3. Relative bradycardia:- slower than expected from the level

of temperature
4. Leucopenia:- WBC count is less than 4000/mm3 of blood

Diagnosis
 Based on clinical manifestation

 Widal reactions against somatic & flagella antigens
 Blood culture (1st week), feces or urine culture (2nd and 3rd
week), bone marrow culture (most sensitive)
 Differential dx
 Malaria, typhus , shigellosis etc

Treatment
 CAF or ciprofloxacin or ceftriaxone for seriously ill patients

 Ampicillin or co-trimoxazole for carriers (Rx is usually for 4
weeks)
 If Sever cases parenteral drug
 Prognosis - Untreated 10% die
- Treated 0.1% die

Preventation
1. Treatment of case
2. Education on hand washing, particularly food handlers, patients and
child care givers.
3. Sanitary disposal of feces and control of flies
4. Provision of safe and adequate water and Safe handling of food
6.Exclusion of typhoid carriers and patients from handling of food
7.Immunization for people at special risk e.g. Travelers to endemic
areas.
Complications
 Perforation, GI Hemorrhage
 Myocarditis
 Meningitis
 Arthritis
 Leucopenia
 Thrombocytopenia

2. Amoebic dysentery ( Ameabiasis)
 Definition:- an infection due to a protozoa parasite that cause

intestinal or extra–intestinal disease.

it is a gastrointestinal disease of human.

Cont.…

Cont..
 Etiology: - E- histolytica
 EpI:- world wide but most common in the tropics and
subtropics
 Prevalent in area with poor sanitation, in mental institutions
and homosexuals.
 Invasive Amebiasis is mostly a disease of young people
(adults).

People with the greatest risk for ameabiasis include:
 people who have traveled to tropical locations where there’s

underdeveloped sanitation
 immigrants from tropical countries with underdeveloped
sanitary conditions
 people who live in institutions with underdeveloped sanitary
conditions, such as prisons

Mode of transmission
 Feco-oral - ingestion of food or water contaminated by feces

containing the cyst
 Incubation period: - variable from few days to several months
or years; commonly 2-4 weeks.
 Period of communicability: through out the period of passing
cysts of E. histolytica, which may continue for years.
 Susceptibility and resistance:
 Susceptibility is general.
Life cycle

Clinical Manifestations
 Starts with a prodromal episode of diarrhea

 abdominal cramps, nausea
 vomiting and tenesmus.
 Dysentery- containing mucus and blood
 bloody diarrhea and tissue destruction.

Diagnosis
 Demonstration of entamoeba histolytica cyst or trophozoite in

stool
 Amoebiasis may be diagnosed when E. histolytica is seen in
your stools (faces) after a stool sample is sent to the
laboratory and examined under a microscope.
 finally, a colonoscopy may be necessary to check for the
presence of the parasite in your large intestine (colon).

Treatment
 Metronidazole or Tinidazole
 Antiemetic for sever vomiting
 Surgery may be necessary if the colon or peritoneal tissues
have perforations.

Prevention and control of Amebiasis
1. Adequate Rx of cases
2. Provision of safe drinking water
3. Proper disposal of human excreta and hand washing

after toilet
4. Clearing and cooking of local foods (e.g.Raw vegetables)
to avoid eating food contaminated with feces.

3. Bacillary Dysentery (shigellosis)
 Definition:- An acute bacterial disease involving the large and distal

part of small intestine, caused by the bacteria of the genus shigella.
 Etiology:- Four species or serotypes of shigella
1. Group A - shigella dysentriae (most common cause)
2. Group B - shigella flexneri
3. Group C - shigella boydi
4. Group D - shigella sonnei

 Enteroinvassive E-coli cause bacillary dysentery

Cont.…
 EPI:- It occurs world wide, and is endemic in both tropical and

temperate climates.
 Reservoir:- Human
 Mode of transmission:- Mainly by direct or indirect fecal-oral
transmission from a patient or carrier
 Incubation period:- 12 hrs – 4 days (usually 1-3 days)
 Period of communicability:- Until the infectious agent is no
longer present in feces, usually four weeks after illness
Susceptibility and Resistance
 Susceptibility is general.
 The disease is more severe in young children
 the elderly
 malnourished
 Breast-feeding is protective for infants and young children .

Clinical manifestation
 Fever, vomiting, rapid pulse and abdominal cramp are prominent.

 Diarrhea usually appears after 48 hrs with dysentery supervening
two days later.
 Generalized abdominal tenderness.
 Tenesmus is present and feces are bloody, mucoid and of small
quantity.
 Dehydration is common and dangerous- it may cause , oliguria
and shock.
Diagnosis
 Based on clinical grounds

 Stool microscopy (presence of pus cells)
 Stool culture confirms the diagnosis
Treatment:-
 Fluid and electrolyte replacement
 Cotrimoxazole in sever cases or Naldixic acid in the case of
resistance.
Prevention and control
1. Detection and Rx of case

2. Hand washing after toilet and before handling or eating food.
3. Proper excreta disposal especially from patients, convalescents
and carriers
4. Adequate and safe water supply
5. Control of flies
6. Cleanliness in food handling and preparation.
4. Cholera
Definition:-An acute illness caused by an enterotoxin elaborated

by vibrio cholera.
Etiology:- Vibrio cholera
EPI : periodic out breaks in different parts of the world and
given rise to pandemics.
 Endemic predominantly in children
Reservoir- Human
Mode of transmission:- by ingestion of food or water directly
or indirectly contaminated with feces or vomitus of infected
person.
Incubation period:- few hours to 5 days usually 2-3 days
Period of communicability:- As long as stools are positive,
usually only a few days after recovery.
 Antibiotics shorten the period of communicability.
Susceptibility and Resistance:

 Variable
 Gastric achlorhydria increases risk of illness
 Breast fed infants are protected

Clinical Manifestation
 Abrupt painless watery diarrhea; the diarrhea looks like rice
water.
 In severe cases, several liters of liquid may be lost in few
hours leading to shock
 Severely ill patients are cyanotic, have sunken eyes and
checks, scaphoid abdomen, poor skin turgor, and week ,rapid
or absent pulse.
 Loss of fluid continues for 1-7 days
Diagnosis
 Based on clinical grounds

 Culture (stool) confirmation
Treatment:
1. prompt replacement of fluids and electrolytes
-Rapid IV infusions of large volumes.
-Isotonic saline solution alternating with isotonic sodium bicarbonate

or sodium lactate
2. Antibiotics like TTC dramatically reduce the duration and volume of

diarrhea resulting in early eradication of V. cholerae.
Prevention and control of cholera
1.Case Rx
2.Safe disposal of human excreta and control of flies
3.Safe public water supply
4.Hand washing and sanitary handling of food
5.Control and management of contact cases.

5. Gastroenteritis

 an inflammation of stomach and intestine by bacteria, virus

and poisons.
 Acute diarrheal disease: is a clinical syndrome of diarrhea,
nausea and /or vomiting and often fever.
 Dehydration occurs rapidly in children and is a common
cause of death.

Occurrence
 Low birth weight and premature children easily get E.coli
infection.
 In the weaning period new type of foods are introduced to
children.
 They are then exposed to a variety of micro-organisms
(pathogenic and non pathogenic).
 Malnutrition is common during this period, and
malnourished children have a lower resistance to infection.
 Traveler's diarrhea occurs in people who are exposed to a
new environment.
 It is thought to be the guts response to new intestinal flora
acquired through feco oral contact, but other factors like
changes in food may also contribute.
N.B. Many organisms can cause diarrhea but it is difficult to

prove the particular organism that is responsible even with
sophisticated techniques.

Acute bacterial gastroenteritis
 It is an acute inflammation of the large and small intestine with

different strains of E coli.
I/P: typically l0 hrs to 6 days for most strains.
Mode of transmission:- through contamination of water, food etc
Clinical Manifestation:- Acute onset of watery diarrhea that is

usually mild and self limiting.
 Malaise, anorexia & abdominal cramps may occur.
 Some strains can result in bloody diarrhea.
Diagnosis
 Clinical Features
 Stool examination shows fecal leukocytes
 Isolation of specific organism in stool specimen
Treatment:- Rehydration (ORS)

 Cotrimoxazole,
 Ciprofloxacin for resistant strains.

6. Giardiasis
Definition:- a protozoan infection principally of the upper small intestine.

 It is associated with symptoms of chronic diarrhea, steatorrhea,
abdominal cramps, bloating, frequent loose and pale greasy stools,
fatigue and weight loss.
Infectious agent : Giardia lamblia
EPI:- Occurrence – world wide distribution. Children are more affected

than adults.
 The disease is highly prevalent in areas of poor sanitation

Reservoir: Human
Mode of transmission:- Person to person transmission occurs by

hand to mouth transfer of cysts from feces of an infected
individual especially in institutions and day care centers.
Period of communicability:-entire period of infection, often for

months.

 Susceptibility and resistance:-
Asymptomatic carrier rate is high.

 Infection is frequently self-limited.
 Persons with AIDS may have more serious and prolonged
infection.
Life cycle:- Similar to E. histolytica.

Life cycle
Transmission Environment
1. Cysts ingested in food, 6 .Feces containing infective
water or from hands cysts contaminate the
contaminated with feces environment
Human host
2. Cysts excyst, forming trophozoites
3. Multiply in intestine
4. Trophozoites encyst
5. Infective cysts passes in feces
* Trophozoites passed in feces disintegrate

 Ranges from asymptomatic infection to severe failure to thrive

and malabsorption
 Young children usually have diarrhea but abdominal distension
is frequent
 Adults have abdominal cramps, diarrhea, anorexia, nausea,
malaise, bloating
 many patient complain of sulphur tasting (belching)

Diagnosis
 Demonstration of G. lambia cyst or trophozoite in feces.
Treatment
 Metronidazole or tinidazole.

1.Good personal hygiene and hand washing before food and

following toilet use
2.Sanitary disposal of feces
3.Protection of public water supply from contamination of feces
4.Case Rx
5.Safe water supply

7. Ascariasis
Definition:- A helminthic infection of the small intestine generally

associated with few or no symptoms
Etiology:- Ascaris lumbricoids
EPI:-The most common parasite of humans where sanitation is poor.

 School children (5-10 yrs) are most affected.
 Highly prevalent in moist tropical countries
Reservoir:- Human, soil

Mode of transmission:
 Ingestion of food or drink contaminated with infective ascaris eggs

from soil contaminated with human feces
 do not directly pass from person to person or from fresh feces.
Incubation period:- 4-8 weeks
Period of communicability:- As long as mature fertilized female worms

live in the intestine.
 Usual life span of adult worms is12 months
Susceptibility and resistance:- susceptibility is general

Life cycle
Transmission Env’t
1.Infective eggs ingested in 7.Eggs become infective (embryonated)
food or from contaminated in soil in 30-40 days.
hands 8. Infective eggs contaminate the
environment
Human host
2. Larvae hatch.
3. Migrate through liver and lungs
4. Pass up trachea and are swallowed
5. Become mature worm in small
intestine
6. Eggs produced and passed in feces

 Most infections go unnoticed until large worms passed in feces
and occasionally the mouth and nose.
 Migrant larvae may cause itching, wheezing and dyspnea,
fever, cough productive of bloody sputum may occur
 Abdominal pain may arise from intestinal or duct (billiary,
pancreatic) obstruction.
 Serious complications include bowel obstruction due to
knotted or intertwined worms.
Diagnosis
 Microscopic identification of eggs in stool sample
 Adult worms pass from anus, mouth or nose.
Treatment:- Albendazole, Mebendazole, Piperazine,Levamisole
Prevention and Control
1. Rx of cases
2. Sanitary disposal of feces
3. Prevent soil contamination in areas where children play
4. promote good personal hygiene (hand washing)

9. Trichuriasis
Definition:- it is a nematode infection of the large

intestine caused by T. trichuria. (Caecum & upper colon).
Etiology:- Trichuris trichuria (whip worm)
EPI:- it occurs world wide especially in warm moist

regions common in children 3-11 years of age
Reservoir- Human,soil

Whip worm

Mode of transmission:- indirect, particularly through ingestion
of contaminated vegetables.
 Not immediately transmitted from person to person
I/p:- indefinite
Period of communicability:- several years in untreated

carriers.
Susceptibility & Resistance:- susceptibility is universal

Life cycle
Transmission Enviroment
1. Infective eggs 5. Eggs become infective
ingested in food or from (embryonated) in soil after 3
contaminated hands. weeks
6. Infective eggs contaminate
the environment
Human host
2. Larvae hatch & develop in small
intestine migrate to caecum.
3. Become mature worms
4. Eggs produced and passed in feces.

 Most infected people are asymptomatic

 Abdominal pain, fatigue, nausea and vomiting diarrhea or
constipation
 Rectal prolepses may occur in heavily infected very young
children
 severity is directly related to the number of infecting worms.
Diagnosis: demonstration of eggs in feces
Treatment: Albendazole or mebendazole

1.Sanitary disposal of feces
2.Maintaining good personal hygiene (i.e. washing hands and

vegetables and other soil contaminated foods).
3.Cutting nails especially-in children
4.Rx of cases.

10. Enterobiasis (oxyuriasis, pin worm infects)
Definition:- A common intestinal (caecum) helminthes

infection caused by Enterobius vermicularis
EPI- it occurs world wide affecting all socioeconomic classes.

 Prevalence is highest in school-aged (5-10 yrs) children
followed by preschools but lower in adults except for
mothers of infected children
 Infection usually occurs in more than one family member

Reservoir- Human
Mode of transmission:- direct transfer of infective eggs by

hands from anus to mouth of the same or another person or
indirectly through clothing, bedding, food or other articles
contaminated with eggs of the parasite.
I/p- 2-6 weeks.

Cont.…
Period of communicability:- As long as gravid females are

discharging eggs on perianal skin.
 Eggs remain infective in an indoor environment for about 2
weeks
Susceptibility and resistance:- susceptibility is universal.

Life cycle
1. Ingestion of eggs by man
2. Larvae hatch in duodenum and migrate down to caecum
3. Adult worms in caecum
4. Gravid females migrate through the anus to the perianal

skin and deposit eggs (usually during the night)
5. Eggs become infective in a few hrs in perianal area.

Clinical Manifestation:-
 perianal itching
 disturbed sleep
 irritability and some times secondary infection of the
scratched skin
Diagnosis: Stool microscopy for eggs or female worms
Treatment: Mebendazole 100mg po stat or
Albendazole-400mg po stat
1. Educate the public about hygiene (i.e. hand washing, before

eating or preparing food, keeping nails short and discourage nail
biting)
2. Reduce over crowding in living accommodations
3. Provide adequate toilets
4. Rx of cases
11. Stronglodiosis
Definition:- An often asymptomatic helminthic infection of the

duodenum and upper jejunum (can affect all portion of the small
intestine)
Infectious Agent:- Strongloides stercoralis
EPI- It occurs in tropical and temperate areas more common in

warm and wet regions.
Reservoir:- Human, soil

Mode of transmission:- Infective (filariform) larvae penetrate
the skin and enter venous circulation
IP: 2-4 weeks (from skin penetration to when rhabiditiform

larvae( It is the initial developmental larval stage) appear in the
feces)
Period of communicability: as long as living worms remain in

the intestine: up to 35 years in cases of autoinfection

Cont..
 Susceptibility and resistance: susceptibility is universal.
 Patients with AIDS or an immune - suppressive medications
are at risk of dissemination.

stronglodiosis

Life cycle
1. Infective filariform larvae penetrate skin e.g. feet.

Autoinfection also occurs
2. larvae migrate, pass up trachea and swallowed
3. Become mature worms in small intestine
4. Eggs laid. Hatch rhabditiform larvae in intestine

5. Rhabditiform larvae
- passed in feces or
- become filariform larvae in intestine, causing

autoinfection
6. In soil larvae become free living worms produce more

rhabditiform larvae
7. Become infective filariform larvae in the soil

 Clinical Manifestation:
 pneumonia occurs during heavy larval migration.
 Mild peptic ulcer like epigastric discomfort to severe watery
diarrhea.
 Heavy infection may result in malabsorption syndrome.

Diagnosis:- Identification of larvae in stool specimen
Treatment:-
 Albendazole (400mg po per day for 03 days or
 Thiabendazole – 500 mg PO BID for 03 days.
1. Proper disposal of human excreta
2. personal hygiene including use of foot wear
3. Case Rx
12. Hook worm/Ancyclostomosis/
Definition: A common chronic parasitic infection with a

variety of symptoms usually in proportion of the degree of
anemia.
 It affects small intestine.
Agents:- Ancylostomiasis duodenal and Necatoriasis

Americanus

EPI- Widely endemic in tropical and subtropical countries
where sanitary disposal of human feces is not practiced and the
soil moisture and temperature conditions favor environment of
infective larvae.
Reservoir-Human
Mode of transmission:- through skin penetration by the

infective larvae.

I/P:- Symptoms may develop after a few weeks to many months
depending on intensity of infection
Period of communicable:
 Infected people can contaminate the soil for several years in
the absence of Rx.
Susceptibility & Resistance: susceptibility is universal.

 No evidence that immunity develops with infection

Life cycle
1. Infective filariform larvae penetrate the skin
2. Larvae migrate- pass up trachea and are swallowed
3. Become mature worms in small intestine (attach to wall and suck

blood)
4. Eggs produced and passed in feces
5. Eggs develop- Rhabditiform larvae hatch-Feed in soil
6. Develop in to infective filariform larvae in about 1 week
7. Filariform larvae contaminate soil

The clinical Manifestation is related to
1. Larval migration to the skin

 Produces short lasting localized maculopapular rash
associated with itching called ground itch
2.Larval migration to lungs

 Produces cough, wheezing and transient pneumonitis

Cont.…
3.Blood sucking
 Light infection – no symptom
 Heavy infection – result in symptoms of PUD like epigastric
pain and tenderness.
 Further loss of blood leads to anemia manifested by exertional
dyspnea, weakness and light headedness.

Diagnosis
Demonstration of eggs in stool specimen
Treatment:-
 mebendazole 200 mg POBID for 03 dys
 Albendazole 400mg p.o stat
Prevention & control
1. sanitary disposal of feces
2. wearing of shoes
3. Case Rx
13. Poliomyelitis
Definition: A viral infection most often recognized by the acute

onset of flaccid paralysis.
Etiology: Polioviruses (type I II and III)
EPI: Occurs world wide prior to the advent of immunization.

 Primarily a disease of infants and young children
 more than 90% of infections are unapparent and flaccid
paralysis occurs in less than 1 % of infections

Reservoir: human, especially children
Mode of transmission: primarily person to person, spread

principally through the fecal oral route.
 In rare instances milk, food stuffs and other materials
contaminated with feces have been incriminated as vehicles.
I/P:- Commonly 7-14 days
By, Tsehaye G.
Cont..
Period of communicability:- As long as the virus is excreted (<

60dys)
Susceptibility and resistance:- susceptibility is common in

children but paralysis rarely occurs.
 Infection confers permanent immunity

 Usually asymptomatic or non – specific fever is manifested in

90% of cases
 If it progresses to major illness, severe muscular pain, stiff neck
and back with or without flaccid paralysis
 Paralysis is asymptomatic and occurs with in 3 to 4 days of illness
 The legs are more affected than other parts of the body
 Paralysis of respiratory and swallowing muscle is life threatening
Clinical course of the disease
1. Asymptomatic (unapparent infection) –90-95%

 Show no signs and symptoms
2. Abortive infection (cells that have been infected with a virus

but did not produce any progeny virus )– occurs in 4-8 % of cases
 S/S of URTI – fever, sore throat, myalgia
 S/S of GI – anorexia, nausea, vomiting, loose stool, stomach
aches

3. None – paralytic poliomyelitis
 There is involvement of CNS without signs of paralysis & subsides
without sequelae
 Signs of meningeal irritation, headache, fever, neck rigidity
4. Paralytic poliomyelitis
 When non – paralytic poliomyelitis progresses to paralytic
poliomyelitis
 Flaccid paralysis of a group of muscles associated with fever,
myalgia, neck rigidity,
Diagnosis
 Based on clinical and epidemiological grounds
Treatment: symptomatic
Prevention and control:
1. Educate public about the advantage of immunization in early

child hood
2. Safe disposal of human excreta

14. Echinococus granulosus (echinococcosis or Dog tape
worm)
Definition:- caused by the larval stages of cestodes

(tapeworms) of the genus Echinococcus
 Cysts usually develop in the liver, but are also found in the
lungs, kidneys, spleen, nervous tissue or bone.
Infectious agent:- Echinococcus granulosis, A small tape worm

of dog

EPI:- World wide
 The prevalence of this parasite depends on the close association
of human and infected dogs.
Reservoir:-The domestic dog is definitive host

 They may harbor thousands of adult tapeworms in their
intestines with out signs of infections
 Herbivores, primarily sheep, act as intermediate hosts
 Mode of transmission:- hand to mouth transfer of eggs from
infected dogs or indirectly through contaminated food, water, soil
or fomites.
 Incubation Period:- Variable, from 12 months to many years depending
on the number, location of cysts & how rapidly they grow.

 Period of communicability:- Infected dog begins to pass eggs
approximately 7 weeks after infection
 Susceptibility and resistance;- Children are more likely to be exposed to
infection because they are more likely to have close contact with infected
dogs and are less likely to have adequate hygienic habits.

Life cycle
 Tapeworm eggs are passed in the feces of an infected dog

 Ingesting tapeworm eggs
 They hatch into embryos in the intestine, penetrate the
intestinal lining, and carried by blood throughout the body to
major filtering organs (mainly liver and/or lungs).
 They transform and develop into larval echinococcal cysts in
which numerous tiny tapeworm heads (called protoscolices)

Clinical feature
 usually asymptomatic
 Depends on
 involved organs
 Size of cysts
 Cough ,dyspnea, Abdominal pain ,jaundice

Lab investigation
 Ultrasound
 Serologic testing
Treatment
 Albendazole
 Mebendazole (Vermox)

 Prevention and control:-
 Educate the public about avoiding exposure to dog feces
 Interrupt transmission from intermediate to definitive hosts
 by preventing dogs access to uncooked viscera

Cont.…
 supervision of live stock slaughtering and safe disposal of

infected viscera, by incinerating or deep-burying of
infected organs from dead intermediate hosts.
 Periodically treat high risk dogs; reduce dog population
 Case Rx

15. Dracunculiasis (Guinea - Worm)
 An infection of the subcutaneous and deeper tissues by a large

nematode
Etiology- Dracunculus medinensis
Reservoir - Human
Occurrence
 Common in regions with dry climates
 Incidence has declined dramatically because of global eradication
efforts.
 There are only 78,000 cases worldwide, the majority in Sudan
Dracunculiasis…
 Larva discharged by parent worm- fresh water
-Crustacean infected with Cyclops
-Develop in to infective stage.

 Man swallows the infected Cyclops in drinking water
Incubation period- 12 months
Period of communicability- 2-3 wks

Clinical manifestation
 Few or no clinical manifestation until the blister forms

 Fever, generalized allergic symptoms, including periorbital
edema, wheezing and urticaria
 Local pain & swelling, emergence of the worm
 Blister ruptures as a result of immersion in water.
 The adult worm release larva rich fluid
 Ulcers may complicate with 2o infection, local inflammation,
abscess formation or rarely tetanus.
Dracunculiasis…
DX
 Based on the finding develop with the emergence of the adult worm.
RX
 Gradual extraction of the worm by winding of a few cm on a stick each day
 Surgical excision of the worm
 Thiabendazole (25 mg/kg bid for 03 days)
or
 Metronidazole (250 mg tid for 10 days)

Dracunculiasis…
Prevention and Control

 Provision of safe drinking water
 Boil drinking water or filter through fine nylon to remove
Cyclops.
 Chemically treating infected water
 Health education.

Shistosomiasis/Bilarhziasis/
 Chronic disease caused by the reaction of the body to

the eggs of the worm.
Etiology
 S. mansoni
 S. japonicum - affect intestine
 S. haematobium - affects urinary bladder.

Shistosomiasis…
Reservoir- Man
Occurrence
 S. Mansoni & S. Haematobium are found in Africa.
 S. Japonicium is found in Japan, China, Philippines.
 Infection is acquired from water containing- free swimming larval form
(cercariae) developed in snails.
 The egg of S. Haematobium leave the mammalian body in the urine.
Incubation Period- 2-6 wks

Cont..
Period of Communicability
 Not communicable from person to person.
 Infected person spread the infection by discharging eggs in
urine (S. Heamatobium) and in feces for (S. Mansoni)

 Schistosomiasis has several stages

 Invasion
 Maturation
 Established infection and
 Late stage

Cont..
 Invasion
 Cercariae penetrate the skin
 Itching papules & local edema
 The Cercariae enter the circulation & reach the liver via the
right side of the heart & the lung.

Cont..
 Maturation
 Schistosoma mature in the liver
 Associated with fever, abdominal pain &
generalized urticaria
 It is known as katayama syndrome

Shistosomiasis…
 Established infection
 The stage of egg production
 The eggs w/c do not reach the lumen provoke an
inflammatory reaction
 Signs of colitis, blood diarrhea and cramp in S.Mansoni
infection
 Terminal hematuria & dysuria in S. Haematobium infection

Shistosomiasis…
 Late Stage
 Fibrosis & calcification due to many eggs in the tissues.
 Around the bladder -Obstruction & dilatation of the ureters
(hydro ureter) & kidney (hydronephrosis)
 Pyelonephritis
 Calcification of the bladder
 Ca of the bladder.

Shistosomiasis…
 Portal hypertension - in the liver - leads to hypersplenism &

anemia, esophageal variasis & massive bleeding
 Pulmonary hypertension - in the lung-leads to CHF.
DX
 Finding eggs in stool or urine
 Biopsy (rectal snip, bladder biopsy)
RX
 Praziquantel 40 mg/kg stat.
Shistosomiasis…

 Snails control
 copper sulphate
 Environmental sanitation
 Preventing snail breeding is more important than killing snails
 Health education the most important controlling method
 Prevent exposure to contaminated water.
THANK YOU ALL

Part 2-Cdc Feco Oral Disease

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Part 2-Cdc Feco Oral Disease

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Mizan tepi university

College of Medicine and Health Science Department of

Prevention and control of feco - orally transmitted

 At the end of this lesson students will able to;

By, Tsehaye G. 05/31/2024

1.The agent are excreted in the stools

2.The portal of entry - mouth

3. Fecal oral transmission- occurs mostly through unapparent

fecal contamination of food, water and hands.

By, Tsehaye G. 05/31/2024

By, Tsehaye G. 05/31/2024

1. Early case detection and appropriate Rx of cases

2. Safe human excreta disposal

4. Safe water supply

5. Hand washing and sanitary handling of food and utensils(kits)

6. Control and check up of food handlers

7. Avoid eating of uncooked foods

1.As a result of fecally contaminated water and food

 These infections are acquired through exposure to fecally

By, Tsehaye G. 05/31/2024

 Diseases transmitted mainly through direct contact with

2. Hydatid disease or Echinococus

By, Tsehaye G. 05/31/2024

 Definition: It is a systemic infectious disease characterized by

By, Tsehaye G. 05/31/2024

By, Tsehaye G. 05/31/2024

 Epidemiology:- common in world wide, poor socioeconomic

By, Tsehaye G. 05/31/2024

 Susceptibility and resistance:-

By, Tsehaye G. 05/31/2024

 First Week:- mild illness x-zed by fever rising stepwise (ladder

 Second week:- sustained fever, weakness, mental dullness or

By, Tsehaye G. 05/31/2024

 Third week:- patients continue to be febrile and extremely

By, Tsehaye G. 05/31/2024

1. Fever:- sustained fever (ladder fashion)

2. Rose spots:- small pallor, blanching, slightly raised macules

3. Relative bradycardia:- slower than expected from the level

4. Leucopenia:- WBC count is less than 4000/mm3 of blood

By, Tsehaye G. 05/31/2024

 Based on clinical manifestation

By, Tsehaye G. 05/31/2024

 CAF or ciprofloxacin or ceftriaxone for seriously ill patients

- Treated 0.1% die

By, Tsehaye G. 05/31/2024

By, Tsehaye G. 05/31/2024

 Definition:- an infection due to a protozoa parasite that cause

By, Tsehaye G. 05/31/2024

By, Tsehaye G. 05/31/2024

By, Tsehaye G. 05/31/2024

 people who have traveled to tropical locations where there’s

By, Tsehaye G. 05/31/2024

 Feco-oral - ingestion of food or water contaminated by feces

By, Tsehaye G. 05/31/2024

 Starts with a prodromal episode of diarrhea

By, Tsehaye G. 05/31/2024

 Demonstration of entamoeba histolytica cyst or trophozoite in

By, Tsehaye G. 05/31/2024

By, Tsehaye G. 05/31/2024

2. Provision of safe drinking water

3. Proper disposal of human excreta and hand washing

4. Clearing and cooking of local foods (e.g.Raw vegetables)

to avoid eating food contaminated with feces.

By, Tsehaye G. 05/31/2024