Feco-Oral Transmitted Diseases: by Shegaw T

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Feco-oral transmitted Diseases
By Shegaw T 07/16/2022
Outline
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Definition
Etiology
Epidemiology
Occurrence
Reservoir
Mode of transmission
Incubation period
Period of communicability
Susceptibility and resistance
Life cycle
Clinical manifestation
Diagnosis
Treatment
Prevention and control
Objectives
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After the end of this session the student will be able to :

Identify the five important “Fs” in oral-fecal disease
transmission.
List diseases transmitted mainly in water , soil and
direct contact with feces.
Describe the clinical features of each diseases.
Describe the diagnosis and treatment of cases.
Implement preventive and control methods of oral-
fecal transmitted diseases
Introduction
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Infectious agents are excreted in the stool of infected

person and,
The portal of entry is mouth.
Fecal oral transmission occurs mostly through
unapparent fecal contamination of food, water and hands.
The 5 F’s plays an important role in the transmission of
these diseases.
 In feco - oral transmission of disease food takes a central
position b/c it can be directly or indirectly contaminated,
via polluted water, dirty hands, contaminated soil or flies.
W
ater
Feces Soil Food Mouth
Flies
Fomites
Finger
Fig. 2.1: The five “Fs” which play an important role in fecal oral diseases
transmission (finger, flies, food, fomites and fluid).
By Shegaw T 5 07/16/2022
A. Typhoid Fever
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 Definition: A systemic infectious disease

characterized by high continuous fever, malaise and
involvement of lymphoid tissues, spleen and other
reticulo endothelial tissue.
Typhoid Fever (continued)
7
Infectious agent
Salmonella Typhi
S. Paratyphi A, B and C - PTF
Salmonella enteridis (rare cause)
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Epidemiology
Annual incidence is estimated at about 22 million
cases with approximately 200,000 deaths
worldwide.
 However, its real impact is difficult to estimate
because the clinical picture is confused with those of
many other febrile infections.
Additionally, the disease is underestimated because
there are no bacteriology laboratories in most areas
of developing countries.
Cont…
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In Ethiopia, 43,727 cases were reported to MOH in

1993 and common from August –December.
Currently, it is observed at a great frequency in AIDS
pts than general population
Mostly Occurrence in poor socioeconomic ,school
age children (5-19)years.
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Reservoir
Humans the only
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Mode of transmission
Flies and cockroaches may infect foods in which the
organisms then multiply to achieve an infective dose.
Ingestion of contaminated food and water
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Incubation period
Varied based on inoculum size and host’s health and
immune status, but usually 1-3 weeks that can be
wide as 3- 60 days, and 1–10 days for Paratyphoid
fever.
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Period of communicability:
As long as the bacilli appear in excreta
Usually from the 1st week throughout convalescence.
About 10% of untreated pts will discharge bacilli for
3 months after onset of symptoms and
2%-5% become chronic carriers.
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Susceptibility and resistance

General
Decrease stomach acidity (Gastric achlorhydria)
Loss intestinal integrity ( IBDs)
HIV positive
Cont…
15
Pathogenesis
 Depends on a number of factors including the infecting species and
infectious dose.
 Ingested organisms survive exposure to gastric acid before gaining
access to the small bowel.
 The organism enters the gastrointestinal tract and invades the
mucosa of colon and ileum.
 After intracellular multiplication in the mucosal cells, bacteremia
will occur.
 Tissue invasion causes inflammation in the intestine and gall
bladder.
 Hematogenous dissemination occurs to spleen, liver and bone
marrow.
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Clinical manifestations
First week
The Severity of the illness may range from mild, brief illness to acute,
severe disease with central nervous system involvement and death.
Mild illness characterized by:
 Fever-daily increase in stepladder ways
 Anorexia
 Abdominal pain
 Lethargy
 Malaise and general aches
 Headache
 Epistaxis
 Diarrhea
 Constipation
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Clinical manifestation
Second week
Fever continuous
Severe illness with
 Weakness, confusion
 Mental dullness or delirium
 Abdominal discomfort and distention
 Diarrhea
 Feces may contain blood
 Splenomegaly
 Rose spots-pink papules on the upper abdomen and lower
chest -result of bacterial embolization .
Cont….
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“Rose spot”, the rash of enteric fever due to S. typhi or S. paratyphi

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Third week
Pt continues to be febrile & increasingly exhausted
The patient goes to a pattern of “typhoidal state"
characterized by extreme toxemia, disorientation,
and “pea-soup” diarrhea.
Intestinal perforation and hemorrhage.
If no complications occur:
 Begins to improve .
 Temperature decreases gradually.
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 Common manifestations suggestive of typhoid. F:

Headache
Joint pain
Back pain
Abdominal discomfort
Fever
Rose spots
Relative bradycardia
Leukopenia
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Complication
 It accounts 30% untreated case and accounts for 75% of all
death.
 GI perforation and hemorrhage
 Hepatitis
 Meningitis
 Arthritis, osteomyelitis
 Nephritis
 Myocarditis
 Bronchitis and pneumonia
 disseminated intravascular coagulation
T. Fever ……..
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Diagnosis
Based on clinical ground
Culture (blood, bone marrow ,Stool and urine)
Widal test O and H Ags – commonly use
Treatment
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Symptomatic treatment:
Use of antipyretics, e.g., paracetamol to control fever.
First line
 Ciprofloxacin, 500mg P.O., BID for 10-14 days Alternative
 Amoxicillin,1g, P.O.,QID., for children: 20 – 40mg/kg/day
P.O., in 3 divided doses for 14 days OR
 Chloramphenicol, 500mg P.O., QID, for 14 days: For children:
25mg/kg. OR
 Sulfamethoxazole+trimethoprim, 800mg/160mg P.O., BID
for 14 days. For children 6 weeks– 5 months, 100/20mg; 6
months – 5 yrs, 200/40mg; 6 – 12 yrs, 400/80mg BID……
Treatment
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For severe cases which are fluoroquinolone resistant:

 Ceftriaxone, 1g QD as a single dose OR in 2 divided
doses I.M. OR I.V. for 7-10 days. OR
 Chloramphenicol, 1g, IV bolus QID until 48 hrs after
fever has settled, followed by 500mg P.O., QID for a
total of 14 days. For children: 25mg/kg, IV bolus
QID, until 48 hrs after fever has settled, followed by
25mg/kg P.O., QID for a total of 14 days.
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Prevention and control

Treatment of patients and carriers
Education
Sanitary disposal of feces and control flies
Provision of safe and adequate water
Safe handling of food
Exclusion of typhoid carriers and patients.
Regular check-up of food handlers
Immunization.
- Live oral vaccine (TY21a) 3 doses can be given
- Purified Vi polysaccharide vaccine can be given SC or IM
in a single dose both should be given for >5yrs old.
Bacillary dysentery
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Definition
An acute bacterial infectious disease involving the
large and distal small intestine, caused by the

bacteria of genus shigella which invade and destroys
the intestinal epithelium..
Bacillary dysentery (continued)
27
Infectious agent
 Shigella -gram negative, non-motile bacteria
 Comprised of four species or serotypes
 Group A= Shigella dysentriae
 Group B= Shigella flexeneri
 Group C= Shigella boydii
 Group D= Shigella sonnei
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Epidemiology
 It occurs worldwide,
 prevalence is highest in tropical and subtropical world.
 Outbreaks commonly occur crowding and where personal hygiene
is poor, such , institutions for children, day care centers, mental
hospitals and refugee camps.
 It is estimated that the disease causes 600,000 deaths per year in
the world.
 Two- thirds of the cases, and most of the deaths, are in children
under 5 years of age.
 Ethiopia was frequently subjected to outbreaks of shigellosis as
recorded in Hararghe in 1978, Omo in 1979, Gondar in 1980 and
Illubabor in 1981.
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Reservoir
Humans the only
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Direct or indirect fecal-oral transmission
Transmission through water and milk may occur as a
result of direct fecal contamination.
Flies can transfer organisms from latrines to a non-
refrigerated food item in which organisms can
survive and multiply.
N.B. Only a very small dose is required less than 200
(even 10-100 bacteria) for infection to occur.
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Incubation period
12 hours to 4 days
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Period of communicability
During acute infection and until the infectious agent
is no longer present in feces, usually within four
weeks after illness
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Susceptibility is general
Age and nutritional status
The disease is more severe in young children,
elderly and malnourished
Breast feeding is protective
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Fever, vomiting and abdominal pain
Generalized abdominal tenderness
Diarrhea are bloody & of small quantity
Tenesmus (strain to defecation)
Dehydration
Tachycardia
B. Dysentery…..
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Complication
 Bacteremia
 rectal prolapse
 reactive arthritis
 hemolytic-uremic syndrome
 intestinal perforation
 death if not treated (20%)
 Dehydration is common and dangerous - it may
cause muscular cramp, oliguria and shock.
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Diagnosis
Sign and symptoms
Stool microscopy-common
Stool culture
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Treatment
Supportive treatment
Correct dehydration with ORS or IV fluids
Relieve pain and fever if necessary
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Drug treatment
First line
 Ciprofloxacin, 500 mg PO BID for 3 – 5 days. For children:7.5
– 15 mg /kg/day PO in 2 divided doses for only 3 days.
39
Treatment
Drug treatment
Alternatives
 Sulfamethoxazole+trimethoprim, 800 mg/160 mg PO BID for
5 – 7 days. For children: 6 weeks – 5 months; 100/20 mg; 6
months – 5 years, 200/40 mg; 6 – 12years, 400/80 mg BID
Or
 Ceftriaxone, 1-2g stat or 2 divided doses IM or slow IV. For
children: 20-50 mg/kg/day as a single dose or 2 divided doses
IM or slow IV.
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Detection of carriers and treatment of the sick
Hand washing
Proper excreta disposal
Adequate and safe water supply.
Control of flies.
Cleanliness in food handling and preparation.
Acute Watery Diarrhea
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What is cholera?
Acute Watery Diarrhea cont…
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Its global name is cholera

Cholera is an acute intestinal infectious diseases caused by
ingestion of food or water contaminated with the bacterium Vibrio
cholera unless treated promptly it quickly leads to severe
dehydration and death.
Cholera is -characterised by a sudden onset of profuse painless
watery diarrhoea or rice-water like diarrhoea, often
accompanied by vomiting.
Standard case definition: patients 5 years and above complains
s/s of dehydration like decrease skin turgor, sunken eye, thirsty, and
irritability and acute watery diarrheal with or with out vomiting.
Confirmed case: A suspected case in which Vibrio cholerae O1 or
O139 has been isolated from their stool.
AWD cont…
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Cholera is locally, nationally and internationally notifiable

disease .
All national governments are obliged to notify WHO within
24 hours.
If there is a sudden increase in the daily number of patients
with acute watery diarrhea, especially patients who pass ‘rice-
water’ stools typical of cholera.
In Ethiopia one confirmed case of cholera is enough to declare
an outbreak.
The case-fatality rate in untreated cases may 30-50%, but, if
treatment
By Shegaw T is applied appropriately, should keep case-fatality
07/16/2022
AWD (continued)
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Infectious agent
 There are over 100 different Vibrio species but only vibrio
cholerae causes cholera.
Vibrio cholerae 2 Sero groups:
Vibrio cholerae O1, subdivided into Classical and El Tor biotypes.
Vibrio cholerae O139 serogroup was first identified in 1992 in
India.
Vibrio cholerae which produces toxin = causes the severe diarrhea
Vibrio grows easily in saline water and alkaline media & survive at
low temperature but
 Do not survive in acid media; destroyed by gastric acid in the
stomach, by chlorine disinfectant solutions or by boiling during at
least one minute.
AWD
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AWD (continued)
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Epidemiology
It was Epidemic in Ethiopia
Adiss Ababa, Amhara , B/gumz in 2018
Pandemic
AWD (continued)
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Reservoir
Humans
AWD (continued)
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Ingestion of food or water directly or indirectly
contaminated with feces or vomitus of infected
person.
Contaminated food and/or water is the main mode of
transmission.
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Contaminated food and/or water is the main mode of transmission.
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Contamination of water can happen at51
the source, during transport and storage.
Corpses of cholera patients are highly infectious through their excreta.
Physical contact and food preparation during funerals can lead to ingestion of
contaminated food and beverages.
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AWD (continued)
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Incubation period
From few hours to 5 days, usually 2-3 days.
AWD (continued)
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For the duration of the stool positive stage, usually
only a few days after recovery.
Antibiotics shorten the period of communicability.
Cont…
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Varies.
Gastric achlorhydria increases risk of illness.
Breast-fed infants are protected.
AWD (continued)
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Risk factors for Cholera

 Overcrowding (internally displaced people, refugee,
camps, population gatherings, etc.)
 Inadequate quantity and/or quality of water
 Inadequate personal hygiene
Poor washing facilities
Inappropriate or poor sanitation
 Inadequate food safety
Risk factors…..
57
AWD (continued)
58
Abrupt painless watery diarrhea; the diarrhea looks
like rice water and nausea , vomiting.
In severe cases, several liters of liquid may be lost in
few hours leading to shock.
Severely ill patients have sunken eyes and cheeks,
scaphoid abdomen, poor skin turgor, and thready or
absent pulse.
But usually no fever.
C/feature……..
59
C/m of dehydration
60
AWD (continued)
61
Diagnosis
Based on clinical grounds.
Stool microscope
Culture (stool) confirmation.
AWD (continued)
62
Treatment
Oral or intravenous hydration is the primary treatment for
cholera.
In conjunction with hydration, treatment with antibiotics
is recommended for severely ill patients.
It is also recommended for patients who have severe or
some dehydration and continue to pass a large volume of
stool during rehydration treatment.
Antibiotic treatment is also recommended for all pregnant
women and patients with comorbidities (e.g., severe acute
malnutrition, HIV infection).
AWD (continued)
63
Treatment…
 Antibiotics are given as soon as the patient can tolerate oral
medication.
 None of the guidelines recommend antibiotics as prophylaxis for
cholera prevention, and all emphasize that antibiotics should be
used in conjunction with aggressive hydration.
 Education of healthcare workers, assurance of adequate supplies,
and monitoring of practices are all important for appropriate
dispensation of antibiotics.
Rx………..
64
AWD (continued)
65
Drug treatment
First line
 Doxycycline, 100mg, P.O., BID for 3 days. For children: 6mg/kg
daily for 3 days.
Alternatives
 Tetracycline, 500mg P.O., QID for 3-5 days. OR
 Sulfamethoxazole+trimethoprim, children 6 weeks – 5 months:
100/20mg children 6 months – 5 yrs: 200/40mg children 6 – 12
yrs: 400/80mg BID for 5 days adults: 800mg/160mg P.O., BID
for 5 days. OR
 Ciprofloxacin, 500mg P.O., BID, for 3-5 days
AWD (continued)
66

1. Case treatment
2. Safe disposal of human excreta and control of flies
3. Safe water supply
4. Hand washing and sanitary handling of food
5. Control and management of contact cases
6. Public education on boiling drinking water and preventive measures
7. Cooking of vegetables
8. Vaccine 2 doses 0.5 ml of killed vaccine is given in 4weeks interval
(not given for infants) protects for 3-6 months 50%
N.B. Single case of cholera is an epidemic and must be reported to
woreda, zone, regional bureau ,MOH and WHO.
Gastero enterities
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Definition:-is an inflammation of stomach and

intestine by bacteria, virus, parasites and poisons
manifested by acute gastro intestinal disorder.
Acute diarrheal disease is a clinical syndrome of
diarrhea, nausea and /or vomiting and often fever.
G. enteritis…
68
Infectious agents:
Viral, bacteria, protozoa, helminthiasis etc.
Viral gastroenteritis: presents in infants, children
and adults.
Several viruses (rotaviruses, enteric adenoviruses,
astroviruses and caliciviruses including Norwalk-like
viruses) infect children in their first years of life.
Acute bacterial gastroenteritis
69
 It is an acute inflammation of the large and small

intestine with diff. strains of E coli.
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Etiologies:
1. Entero toxigenic E-coli (ETEC): produces watery
diarrhea and abdominal pain by producing toxins which
increase intestinal fluid secretion.
2. Entero hemorrhagic E- coli (EHEC):- This lead to
initially watery then bloody diarrhea as a result of
production of a toxin that causes inflammation of the colon.
3. Enteroprolytic e-coli (EPEC) – This leads to mucoid
diarrhea by affecting the function of the microvilli of the
small intestine.
4. Enteroinvasive E. coli (EIEC): this leads to a shigellosis-
like condition by invading intestinal mucosa.
Cont…
71
Mode of transmission: -
Through contamination of H20, food etc
Clinical Manifestation: –
 Acute onset of watery diarrhea that is usually mild
and self limiting. Malaise, anorexia & abdominal
cramps , vomiting and fever may occur.
 Some strains can result in bloody diarrhea.
Cont…
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Diagnosis –
 Clinical Features
 Stool examination shows fecal leukocytes
Isolation of specific organism in stool specimen
(culture).
Cont…
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Treatment: -
 Rehydration (ORS)
 Rx based on the causative agent.
B. Amoebiasis
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Definition
An infection due to a protozoan parasite that causes
intestinal or extra-intestinal disease.
Amoebiasis (continued)
75
Infectious agent
There are three species of intestinal amoebae :
 E. histolytica,
 E. dispar, and
 E. moshkovskii.
E. dispar and E. moshkovskii are non-pathogenic and do not
cause clinical disease
All symptomatic disease is caused by E. histolytica.
 Trophozoite -large intestine, liver abscess, other extra
intestinal areas and degenerate within minutes outside the
body.
 Cyst-stools of chronic carriers and patients Cysts-viable for
weeks or months in appropriate moist environment.
76
Epidemiology
Worldwide
Most common in the tropics and sub-tropics.
WHO estimates 40-50 million cases of amoebic colitis and
amoebic liver abscess and up to 100,000 deaths annually.
Prevalent in areas with poor sanitation, in mental
institutions and homosexual.
Invasive amoebiasis is mostly a disease of young people
(adults).
Rare below 5 years of age especially below 2 years.
77
Reservoir
 Human
Amoebiasis……
78
 Mode of transmission – Fecal-oral transmission through
 Direct contact of person to person( fecal-oral)
 Venereal transmission among homosexual males( oral-
anal) .
 Food or drink contaminated with feces containing the cyst
 Use of human feces (night soil) for soil fertilizer
 Contamination of foodstuffs by flies, and possibly
cockroaches
 Fresh vegetables or fruit washed with contaminated water
79
Incubation period
Variable from few days to several months or years
Commonly 2-4 weeks
Extra -intestinal manifestations may take much
longer.
80
During the period of passing cysts of E. histolitica,
which may continue for years.
Amoebiasis cont….
81

General .
The intestinal amoebiasis is more frequent in male
children because they have more freedom to explore
their environment and they can be infected by E.
histolytica cysts.
TRANSMISSION
1. Cysts ingested in
food, water or from
hands contaminated
with feces.
ENVIRONMENT
HUMAN HOST 6. Feces containing infective
2. Cysts excyst, forming trophozoites cysts contaminate the
3. Multiply in intestine environment
4. Trophozoites encyst.
5. Infective cysts passed in feces.*
*trophozoites passed in feces
disintegrate.
Fig. 2.2 Transmission and life cycle of Entamoeba histolytica
By Shegaw T 82 07/16/2022
By Shegaw T 83 07/16/2022
84
 Approximately 90% are asymptomatic
 Diarrhea, flatulence, and lower abdominal pain are the most
frequent complaints.
Typically, stool consists watery, foul-smelling passages that contain
mucus and blood.
Diarrhea is intermittent alternating with episodes of normality or
constipation over a period of months to years.
With dysentery, feces are generally watery, containing mucus and
blood.
Abdominal pain localized in RUQ.
Approximately 5% of all pts with symptomatic amoebiasis present
with a liver abscess.
85
Diagnosis
Demonstration of entamoeba hystolytica cyst or
trophozoite in stool.
Ultrasound or CT scans can identify liver abscess &
other extra-intestinal sites of infection
Amoebiasis(continued)
86
Treatment
First line
 Metronidazole, 500 – 750 mg PO TID for 5 – 7 days. For
childerren: 7.5 mg/kg PO TID for 5 – 7 days
Alternative
 Tinidazole, 2g PO QD for 3 consecutive days. For children: 50
– 60 mg/kg daily for 3 days
87
Treatment
Eradication of cysts:
First line
Diloxanide Furoate, Adult 500mg 3 times daily P.O.,
for 10 days. Child over 25kg, 20mg/kg daily in 3
divided doses for 10 days; course may be repeated if
necessary.
Alternative
 Paromomycin, 25–35mg/kg/day P.O., divided in 3
daily doses for 7 days.
Amoebic Dysentery (continued)
88

Adequate treatment of cases
Provision of safe drinking water
Proper disposal of human excreta (feces) and hand
washing following defecation.
Cleaning and cooking of local foods
Giardiasis
89
Definition
A protozoan infection principally of the upper small
intestine associated with symptoms of chronic

diarrhea, steatorrhea (excess fat in the stool)
abdominal cramps, bloating, frequent loose and pale
greasy stools, fatigue and weight loss.
Giardiasis (continued)
90
Infectious agent
Giardia lamblia or G.duodenalis.
It has two morphological forms, trophozoite and cyst.
Trophozoite is actively motile and invading stage, and
lives on the villi of the small intestine.
 Cyst is inactive, non-motile and non-invading stage,
and responsible for the transmission of the disease.
91
Epidemiology
Worldwide distribution.
The prevalence 2-5% (developed countries) and
 20-30% (developing).
A cause of travelers' diarrhea up to 12% of travelers.
 In Ethiopia, ranges from 2.0% to 11.4%.
Children are more affected than adults.
Highly prevalent in areas of poor sanitation.
92
Reservoir
Humans
Animals also suspected.
93
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.
Ingestion of as few as 10 cysts is sufficient to
cause infection in humans.
It also suspected to be zoonotic since its major
reservoir hosts include dogs, cats, horses, humans,
cattle and birds.
94
Incubation period
 1 to 3 weeks; mostly after 7 to 10 days.
Entire period of infection, often months
95

Asymptomatic carrier rate is high.
Infection is frequently self limited.
Persons with AIDS may have more serious and
prolonged infection.
TRANSMISSION
1. Cysts ingested in food,
water or from hands
contaminated with
feces.
ENVIRONMENT
6. Feces containing infective
cysts contaminate the
environment
HUMAN HOST
2. Cysts excyst, forming
trophozoites
3. Multiply in intestine
4. Trophozoites encyst.
5. Infective cysts passed in feces.*
*trophozoites passed in feces
disintegrate
Fig. 2.3: Transmission and life cycle of Giardia Lamblia
By Shegaw T 96 07/16/2022
97
Ranges from asymptomatic infection to severe
failure to thrive and mal-absorption.
Young children usually have diarrhea but abdominal
distention and bloating are frequent.
Adults have abdominal cramps, diarrhea, anorexia,
nausea, rarely vomiting, malaise, bloating, many
patients complain of sulphour tasting (belching).
Foul-smelling greasy diarrhea or fatty stools
(steatorrhea) without blood or mucus .
98
Diagnosis
Macroscopically the stool is usually offensive, bulky,

fatty and non-bloody
Demonstration of Giardia lamblia cyst or trophozoite
in feces

99
Treatment
First line
Tinidazole, single oral dose of 2g
For children, 50-75mg/kg as a single dose (may be
repeated once if necessary)
Alternative
 Metronidazole, 250-500mg P.O., TID for five days
100

Good personal hygiene and hand washing before
food and following toilet use.
Sanitary disposal of feces.
Protection of public water supply from
contamination of feces.
Case treatment
Safe water supply
C. Feces Mainly in Soil
101
The diseases in this category are mainly transmitted

through fecal contamination of soil. These infections
are acquired through man’s exposure to fecal
contaminated soil.
Ascariasis
Hook warm
Trichriasis
Strongloidiasis
Etc
Ascariasis
102
Definition
A helminthic infection of the small intestine
generally associated with few or no symptoms.
Ascariasis (continued)
103
Infectious agent
Ascaris lumbricoides
 The largest and most common nematode to
infect the human intestine.
 Eggs viable for 10 years in moist, warm soil
 Within in two to four weeks, fertile eggs
embryonated and become infective.
104
Epidemiology
The most common parasite of humans where
sanitation is poor.
School children (5-10 years of age) are most affected.
Highly prevalent in most tropical countries.
In Ethiopia, around 37% of the population is
estimated to be infected.
105
Reservoir
Humans
Soil
106
Ingestion of infective eggs from soil contaminated
with human feces or uncooked product
contaminated with soil containing infective eggs.
Not directly from person to person or
Not directly from fresh feces
107
Incubation period
4-8 weeks.
As long as mature fertilized female worms live in the
intestine.
Susceptibility is general
TRANSMISSION
1. infective eggs ingested
in food or from
contaminated hands with ENVIRONMENT
feces. 6.Eggs become infective (embryonated)
in soil in 30-40 days.
7. Infective eggs contaminate the
environments.
HUMAN HOST
2. Larvae hatch. Migrate through
liver and lungs.
3.Pass up trachea and are
swallowed.
4.Become mature worm in small
intestine.
5. Eggs produced and passed in
feces.
Fig. 2.4 Transmission and life cycle of Ascaris Lumbricoids
By Shegaw T 108 07/16/2022

By Shegaw T 109 07/16/2022
110
Most infections go unnoticed until large worm is
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
(biliary, pancreatic) obstruction.
Serious complications include bowel obstruction due
to knotted/intertwined worms.
Cont…
111
Complications of ascariasis,
Intestinal obstruction,
Appendicitis ,
Biliary ascariasis,
Perforation of the intestine,
Cholecystitis ,
Pancreatitis and peritonitis, etc., may occur,
Biliary ascariasis is the most common complication.
Cont…
112
113
Diagnosis
Microscopic identification of eggs in a stool sample
Adult worms passed from anus, mouth or nose
114
Treatment
First line
 Albendazole, 400mg P.O. as a single dose, for
children: 1 – 2 years, 200mg as a single dose. Or
 Mebendazole, 100mg P.O.BID for 3 days or 500mg
once
Alternative (pregnant women)
 Pyrantel pamoate, 700mg P.O. as a single dose
115

Treatment of cases
Sanitary disposal of feces
Prevent soil contamination in areas where children
play.
Promote good personal hygiene
Trichuriasis (whipwarm infection)
116
Definition
A nematode infection of the large intestine especially
cecum, usually asymptomatic in nature.
Trichuriasis (continued)
117
Infectious agent
Trichuris Trichuria (whipworm)
118
Epidemiology
Worldwide, especially in warm moist regions.
Common in children 3-11 years of age.
119
Reservoir
Humans
120
Indirect particularly through ingestion of
contaminated vegetables.
Not immediately transmissible from person to
person.
121
Incubation period
Indefinite
122
Several years in untreated carriers.
123

Universal.
TRANSMISSION
1. Infective eggs ingested in
food or from contaminated
hands with feces ENVIRONMENT
6.Eggs become infective (embryonated) in soil after 3 weeks.
7. Infective eggs contaminate the environments
HUMAN HOST
2. Larvae hatch. Develop in small
intestine. Migrate to caecum.
3. Pass up trachea and are swallowed.
4. Become mature worms.
5. Eggs produced and passed in feces.
Fig. 2.5 Transmission and life cycle of Trichuris trichura
By Shegaw T 124 07/16/2022

By Shegaw T 125 07/16/2022
126
Severity is directly related to the number of infecting
worms.
Most infected people are asymptomatic.
Abdominal pain, tiredness, nausea and vomiting,
diarrhea or constipation are complaints by patients.
Rectal prolapse may occur in heavily infected very
young children
127
Diagnosis
Demonstration of eggs in feces
128
 Treatment
First line-options
 Mebendazole 500mg P.O single dose OR
 Albendazole 400mg P.O for three days
129

Maintaining good personal hygiene
Cutting nails especially in children.
Treatment of cases.
Entrobiasis( pinwarm infection)
130
Definition
A common intestinal helminthic infection that is
often asymptomatic.
Entrobiasis (continued)
131
Infectious agent
Entrobius vermicularis
132
Epidemiology
Worldwide
Prevalence is highest in school aged children,
followed by preschools and is lowest in adults except
for mothers of infected children.
Infection usually occurs in more than one family
member.
133
Reservoir
Human
5.Gravid females migrate through the anus
to the perianal skin and deposit eggs
4.Adult worms in (usually during the night).
caecum
6.Eggs become infective in a

few hours in perianal area
2.Larvae
3.Migrate hatch in
down 1.Ingestion of
duodenum eggs by man
to caecum
Fig. 2.6 Transmission and life cycle of Enterobius vermicularis
By Shegaw T 134 07/16/2022

By Shegaw T 135 07/16/2022
136
Direct transfer of infective eggs by hand from anus to
mouth of the same or another person , may be
patient self auto infection.
Indirectly through clothing, bedding, food or
other articles contaminated with eggs of the parasite.
137
Incubation period
2-6 weeks
138
As long as gravid females are discharging eggs on
perianal skin.
Eggs remain infective in an indoor environment for
about 2 weeks.
139

Universal.
140
Abdominal pain
Perianal itching
Disturbed sleep
Irritability
Secondary infection of the scratched skin
May invade the female genital tract, causing
vulvovaginits and pelvic granulomas.
141
Diagnosis
Stool microscopy for eggs or female worms
142
Treatment
First line-options
 Mebendazole 100mg P.O. BID for 3 days OR
 Albendazole 400mg P.O. as a single dose,
Alternative
 Piperazine 4g in a single dose
143

Educate the public
Treatment of cases
Reduce overcrowding in living accommodation.
Provide adequate toilets
Strongyloidosis
144
Definition
An often asymptomatic helmenthic infection of the
duodenum and upper jejunum.
Can complete its life cycle entirely within the human
host→unique among helminths
Strongyloidosis (continued)
145
Infectious agent
 Strongyloides stercolaris which is the smallest of the
intestinal nematodes
146
Epidemiology
In tropical and temperate areas.
More common in warm and wet regions.
147
Reservoir
Human
TRANSMISSION
1. Infective filariform
larvae penetrate skin, e.g.
feet. Autoinfection also
occurs.
ENVIRONMENT
6. In soil larvae become free living
produce more rhabditiform larvae.
7. Become infective filariform larvae in
the soil.
HUMAN HOST
2. Larvae migrate, pass up trachea and are
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
Fig. 2.7 Transmission and life cycle of Strongyloides stercoralis
By Shegaw T 148 07/16/2022

By Shegaw T 149 07/16/2022
150
Infective (filariform) larvae penetrate the skin and
enter the venous circulation.
151
Incubation period
2-4 weeks
152
As long as living worms remain in the intestine
up to 35 years in cases of autoinfection.
153

Universal.
Patients with AIDS or on immune-suppressive
medication
154
Pneumonia occurs during heavy larval migration
Mild peptic ulcer like epigastric discomfort to severe
watery diarrhea.
Heavy infection may result in malabsorption
syndrome.
Autoinfection leads hyperinfection or disseminated
strongyloidiasis (CNS, heart, liver and kidneys)
complication and septicemia in
immunocompromised pts=case-fatality rates 90%.
Strongyloidosis……
155
Complication
Pneumonia
Septicemia
Mal absorption syndrome
156
Diagnosis
Identification of larvae in stool specimen
157
Treatment
First line
Ivermectin 200mg/kg daily for 2 days.
For disseminated strongyloidiasis;
Ivermectin should be extended for at least 5–7 days or until
the parasites are eradicated.
Alternatives-options
 Albendazole 400mg P.O.BID for three consecutive days.
OR
 Thiabendazole 1500mg, P.O. BID, for children: 25mg/kg
p.o. for three consecutive days.
158

Proper disposal of human excreta (feces).
Personal hygiene including use of footwear.
Case treatment
Hookworm disease
159
Definition
A common parasitic infection with a variety of
symptoms usually in proportion the degree of
anemia.
Mixed infection is common.
Both of the species are found in Ethiopia, but
N. americanus is more common
Hookworm disease (continued)
160
Infectious agent
Ancylostoma duodenale (25,000-30,000eggs/day)
Necator americanus (9,000-10,000eggs/day)
161
Epidemiology
Widely endemic in tropical and subtropical countries
An estimated 900 million people are infected by
hookworm (both SPs), and 50,000-60,000 deaths
annually.
The soil moisture and temperature conditions favor
development of infective larvae
162
Reservoir
Humans
163
Penetration of the skin by the infective filariform
larvae (cutaneous route). Common sites of infection
are feet, buttocks, and hands, so barefooted
individuals are more prone to infection .
 Ingestion of the filariform larvae present in the soil
(oral route).
Breast milk from mothers to infants (transmammary
transmission) = rare
 Placenta (transplacental transmission) = very rare
164
Incubation period
Few weeks to many months depending on intensity
of infections and iron intake of the host.
165
Several years in the absence of treatment.
166

Universal.
No evidence that immunity develops with infection.
TRANSMISSION
1. Infective filariform larvae
penetrate the skin, e.g.
feet.
2. A. duodenale also
ENVIRONMENT
transmitted by ingestion
5. Eggs develop; rhabditiform larvae hatch.
of larvae. Feed in soil.
6. Develop in to infective filariform larvae in
about 1 week.
7. Filariform larvae contaminate soil
HUMAN HOST
2. Larvae migrate. Become mature
worms in small intestine (attach to
wall and suck blood).
3. Pass up trachea and are swallowed.
4. Eggs produced and passed in feces.
Fig. 2.8Transmission and life cycle of Hook worms
By Shegaw T 167 07/16/2022

By Shegaw T 168 07/16/2022
169
Majorities are asymptomatic in the endemic areas
1. Larval migration of the skin
 Edema, erythema, vesiculation, pustulation and rash with
intense itching called ground itch are common in N.americanus
infection.
2. Migration of larva to the lungs.
 Produces cough, wheezing and transient pneumonitis, asthma
and bronchitis.
 Light infection-no symptoms
 Heavy infection-result in symptoms of peptic ulcer disease like
epigastric pain and tenderness.
H.warm…..
170
3. Blood sucking
 Further loss of blood leads to anemia manifested by
exertional dyspenea, weakness and light-headedness.
 One A.duodenale is responsible for the loss of 0.15
to 0.26 ml (Av: 0.2ml) blood per day
 A single N.americanus worm causes blood loss of
0.03 ml per day
171
Diagnosis
Demonstration of eggs in stool specimen
172
Treatment
First line-options
 Mebendazole 100mg P.O. BID for 3 days or 500mg
stat OR
 Albendazole 400mg P.O. as a single dose
Alternatives:
 Pyrantel pamoate, 700mg P.O. as a single dose
173

Wearing of shoes
Case treatment
Taeniasis ( Tapewarm infection)
174
Definition
Taeniasis is an intestinal infection with the adult
stage of large tapeworms.
Cysticercosis is a tissue infection with the larval
stage.
Taeniasis cont…
175
Infectious agent
Taenia saginata (beef tapeworm)
Taenia solium (pork tapeworm)
Taeniasis cont…
176
Epidemiology
Worldwide
More frequent where beef or pork is eaten raw or
insufficiently cooked and where sanitary conditions
permit pigs and cattle to have access to human feces.
Prevalent in Latin America, Africa, South East Asia
and Eastern Europe.
Taeniasis cont…
177
Reservoir
Humans are definitive hosts of both species of
Taenia;
Cattle are the intermediate hosts for Taenia saginata
and pigs for Taenia solium.
Taeniasis cont…
178
Taenia Saginata:
• Ingestion of raw or under-cooked beef containing cysticerci;.
Taenia Solium
• Ingestion of eggs to mouth of oneself or to another person
or
• Ingestion of food or water infected with eggs
Taeniasis cont…
179
Incubation period
• 8-14 weeks, eggs appear in stool in both species.
Taeniasis cont…
180
T. Saginata is not directly transmitted from person to
person but T. solium may be.
Eggs of both species are disseminated into the
environment as long as the worm remains in the
intestine, sometimes more than 30 years.
Eggs may remain viable in the environment for
months.
Taeniasis cont…
181

General.
No apparent resistance follows infection but more
than one tapeworm in a person has rarely been
reported
Taeniasis cont…
182
TRANSMISSION ENVIRONMENT
1. Cysticerci ingested in 6. Segments and eggs

undercooked meat reach ground where
T.saginata in beef T.solium animals feed.
in pork. 7. Eggs ingested.
8. Embryos carried to
muscles. Develop into
infective cysticerci.
HUMAN HOST
2. Cysticerci attached to wall
of small intestine.
3. Become mature tapeworms.
4. Eggs released when gravid
segements become detached.
5.Eggs and gravid segments
passed in feces
183
Life cycle of Taenia solium
184
Taeniasis cont…
185
Clinical manifestation (for both species)

 Cysticercosis: Infection with T. solium larvae can occur by ingesting eggs
in food or from hands contaminated with feces.
 Eggs develop into cysticerci causing cysticercosis and neurocysticercosis.
Symptoms of cysticercosis may appear after some days and stay for 10
years after infection.
Passage of proglottidis (segmented adult worms) in the feces and peri anal
discomfort when proglottidis are discharged.
Minimal or mild abdominal pain or discomfort, nausea, change in appetite,
weakness and weight loss.
Symptoms of cysticercosis may appear after some days and vary with the
number of cysticerci and the tissues and organs like Subcutaneous ,
Ocular and Brain.
Subcutaneous type
186
The subcutaneous nodules are usually found in head,

limbs, neck, abdomen and back.
They are movable and painless.
Ocular type
187
Cysticercus is usually found in vitreous body or sub

retina.
Visual disturbance often occurs.
The died body of worm may provoke local
inflammation causing blindness.
Cont….
188
Brain type
189
The symptoms are related to the site of infection.

• The patients may manifest headache, N/V, epilepsy,
paralysis, weakness in limbs, diplopia, dizziness,
mental disorder.
• Epilepsy is the most frequent symptoms of brain
cysticercosis.
Cont….
190
Taeniasis cont…
191
Diagnosis
Identification of proglottidis (segments)
Eggs in feces or anal swab
Cysticercus – palpable subcutaneous cysticercus and
microscopic examination of an excised cysticercus
confirms the diagnosis.
Intracerebral and other tissues – CT scan, MRI or by
x-ray when the cysticerci are calcified.
Taenia spp….
192
Taeniasis cont…
193
Treatment
First line-Intestinal infestation
Praziquantel P.O 1200mg or 10mg/Kg single dose
Alternative
Niclosamide, 2g in a single dose P.O.
Treatment of neur ocysticercosis
 Albendazole P.O. 15mg/kg per day for 8–28 days or
Praziquantel 50–100mg/kg daily in three divided doses for
15–30 days.
Longer courses are often needed in patients with multiple
subarachnoid cysticerci.
Taeniasis cont…
194
T.Solium
 Treatment is the same as to T. saginata but praziqantel can
evoke an inflammatory response in the CNS if cryptic
cysticercosis is present.
 Cysticercosis management
Surgery and supportive medical treatment
 For symptomatic patients with neurocysticercosis, admission
is required.
 Combination of Praziquantel and Albendazole can be used.
 Besides, high dose of glucocorticoids can be used to decrease
inflammation.
Taeniasis cont…
195

Educate the public
Identification and immediate treatment of cases.
Freezing of pork/beef below -5C0 for more than 4
days kills the cystraci effectively or cooking to a
temperature of 56C0 for 5 minutes destroys cystcerci.
Deny swine access to latrines and human feces.
Guinea worm
196
Definition
An infection of the subcutaneous and deeper tissues
by large nematode.
Guinea worm cont….
197
Infectious agent
Dracunculus medinensis
 Vector
Cyclops species (crustacean copepods)
198
Epidemiology
The infection is endemic to Asia and Africa: India,
Nile Valley, central, western and equatorial Africa,
lowlands of Ethiopia and Eritrea.
In Africa (16 countries south of the Sahara)
199
Reservoir
Humans
200
Larvae discharged by the female worm into stagnant fresh
water are ingested by crustacean copepods (Cyclops
species).
In about 2 weeks, the larvae develop into the infective stage.
People swallow the infected copepods in drinking water
from infested step-wells and ponds.
The larvae are liberated in the stomach, cross the duodenal
wall, migrate through the viscera and become adults.
The female, after mating, grows and develops to full
maturity, then migrates to the subcutaneous tissues (most
frequently of the legs).
201
Incubation period
About 12 months
Guinea worm cont..
202
From rupture of vesicle until larvae have been
completely evacuated from the uterus of the gravid
worm, usually 2-3 weeks.
In water, the larvae are infective for the copepods for
about 5 days.
After ingestion by copepods, the larvae become
infective for people after 12-14 days at temperatures
>25oc and remain infective in the copepods for about
3 weeks.
203

Universal.
No acquired immunity; multiple and repeated
infections may occur in the same person.
204
205
Few or no clinical manifestations are evident until blister forms.
The female parasites in the subcutaneous tissue release toxic
byproducts of histamine-like nature, which cause systemic
allergic reactions, like fever, erythema, urticarial, pruritus,
fainting, asthma, dyspnea, etc and form local pain and swelling.
When the blister ruptures, the adult worm releases larva-rich
fluid and this is associated with a relief of symptoms
The worms migrate into other tissues and may cause arthritis,
pericarditis, abscesses etc
It occasionally penetrates the eyeball and causes loss of the eye..
206
Diagnosis
Clinical: Observation of blister, worm or larvae.
 Histologic features of subcutaneous sinus tract.
 Eosinophilia and radiographic evidence.
Epidemiological grounds
207
Treatment
Gradual extraction of the worm by winding of a few
centimeters on a stick each day that take weeks to
completely extract the warm remains the common
and effective practice.
Worms may be excised surgically.
Administration of thiabendazole or metronidazole
may relieve symptoms but has no proven activity
against the worm.
208
209
Adult Loa loa in the process of surgical removal after its subconjunctival
migration
210

Provide health education programs in endemic
communities to convey three messages:
❶The guinea-worm infection comes from their
drinking water.
❷Villagers with blisters or ulcers should not
enter any source of drinking water.
❸That drinking water should be filtered
through fine mesh cloth to remove cropepods.
Provision of safe drinking water
Read???
211
Hymenolepis nana (H.Nana)
Reading assignment
212
C. Direct Contact with Feces

poliomyelitis
Hydatid Disease (Echinococcosis)
CHAPTER EIGHT
FOOD-BORNE DISEASES
213
Group Assignment
Staphylococcal Food Poisoning -group 1
Botulism Food Poisoning- group 2
Salmonellosis Food Poisoning-group 3
Poliomyelitis-group 4
In terms of this outline
214
 Definition
 Etiology
 Epidemiology
 Occurrence
 Reservoir
 Mode of transmission
 Incubation period
 Period of communicability
 Susceptibility and resistance
 Life cycle
 Clinical manifestation
 Diagnosis
 Treatment
 Prevention
By Shegaw T and control 07/16/2022
215
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Feco-Oral Transmitted Diseases: by Shegaw T

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1

Feco-oral transmitted Diseases

After the end of this session the student will be able to :

Infectious agents are excreted in the stool of infected

Feces Soil Food Mouth

 Definition: A systemic infectious disease

In Ethiopia, 43,727 cases were reported to MOH in

Susceptibility and resistance

“Rose spot”, the rash of enteric fever due to S. typhi or S. paratyphi

 Common manifestations suggestive of typhoid. F:

For severe cases which are fluoroquinolone resistant:

Prevention and control

large and distal small intestine, caused by the

Susceptibility and resistance

Prevention and control

Its global name is cholera

Cholera is locally, nationally and internationally notifiable

Susceptibility and resistance

Risk factors for Cholera

Prevention and control

Definition:-is an inflammation of stomach and

 It is an acute inflammation of the large and small

Susceptibility and resistance

Fig. 2.2 Transmission and life cycle of Entamoeba histolytica

Prevention and control

intestine associated with symptoms of chronic

Susceptibility and resistance

Macroscopically the stool is usually offensive, bulky,

Prevention and control

The diseases in this category are mainly transmitted

Fig. 2.4 Transmission and life cycle of Ascaris Lumbricoids

By Shegaw T 108 07/16/2022

Prevention and control

Susceptibility and resistance

Fig. 2.5 Transmission and life cycle of Trichuris trichura

By Shegaw T 124 07/16/2022

Prevention and control

6.Eggs become infective in a

Fig. 2.6 Transmission and life cycle of Enterobius vermicularis

By Shegaw T 134 07/16/2022

Susceptibility and resistance

Prevention and control

Fig. 2.7 Transmission and life cycle of Strongyloides stercoralis

By Shegaw T 148 07/16/2022

Susceptibility and resistance

Prevention and control

Susceptibility and resistance

Fig. 2.8Transmission and life cycle of Hook worms

By Shegaw T 167 07/16/2022

Prevention and control

Susceptibility and resistance

1. Cysticerci ingested in 6. Segments and eggs

Clinical manifestation (for both species)

The subcutaneous nodules are usually found in head,

Cysticercus is usually found in vitreous body or sub

The symptoms are related to the site of infection.

Prevention and control

Susceptibility and resistance

Prevention and control

Hymenolepis nana (H.Nana)

C. Direct Contact with Feces

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