Allah

Gastroenteritis
Definition of Gastroenteritis

 It is a clinical syndrome caused by a

variety of pathogenes.
 It is Diarrheal disease of children.
Commonly affecting children under five
years of age, with a peak of incidence in
those under 2 years.(maximum
incidence from 6 months- 12 m.).
WHO classification of diarrhea
according to its onset
A- Acute [ < 14 days as in
gastroentritis]
Persistent > or= 14 days
Chronic : if recurrent or long
lasting .
Characteristics of acute diarrhea
versus persistent diarrhea
 Acutediarrhea  Persistent diarrhea
 Sudden onset  May be sudden or
insidious but stool
[frequency &
characteristics] vary
from day to day.
 Usually self limited  May lead to
[within 3-5 days] permanently
unless child dies impaired growth or
from dehydration. even death.
Acute diarrhea versus persistent
diarrhea
 Most often caused  May initially be
by pathogenic related to a specific
organisms. organism but,
intestinal damage,
malabsorption and
other bacteria keep it
going.
 Children 1 to 30  Malnourished
months are more children are more
susceptible. susceptible.
Acute diarrhea versus persistent
diarrhea
 Fever and/ or  Neither fever nor
vomiting may or may vomiting is common.
not be accompany.
 May result in rapid  Dehydration is
dehydration. usually mild but
enough to suppress
appetite.
Causative agents of gastroenteritis

Bacterial Protozoal

Viral
 Bacterial:
 A- E.Coli:
 Enterohemorrhagic [most serious]
 Enteroinvasive [dysentry]
 Enteropathogenic [common in hospital
infection (among neonates) ]
 Enterotoxigenic [ watery diarrhea]
 Others as, shigella, salmonella, cholera,
staph., campylobacter jejuni, clostridium
perfringes.
 Viral:
 Rota virus [the commonest in 25-40%]
 Enteroviruses [Coxsackie, ECHO
[enteric cytopathogenic human orphan],
polio, norwalk, adenoviruses
 Virus A hepatitis (anicteric
gastroenteritis)
 Measles virus and other viruses
especially with low body immunity.
continue
 Protozoal:
 Giardia lamblia, in the first part of small
intestine.[recurrent, bulky, pale, foul smelling
stool].
 E.hystolytica: dysentry by invasion of mucosal
cells. Children causing persistent diarrhea.
 Balantidium coli.
 Cryptosporidium: common in malnourished
and immuno-compromised
Reservoirs:
Man (cases & carriers) &
Animals.
Modes of infection:
ingestion of contaminated water,
food, milk or meat.
Predisposing factors
 1- Environmental factors:
 unsanitary environment.
 2- Host factors:
For the child:
 Age: <5 ys (more common under 2 ys),
maximum incidence from 6-12 months.
 Malnutrition
 Severe infection as after measles, tonsilitis,
otitis media.
 Immuno-suppression or immuno-deficiency.
Continue predisposing factors

 3- Agent factors:
 Bacterial agents more in summer and
viral agents more in winter.
 Diarrhea & mal/ or under
nourishment relationship
 Diarrhea causes damage of the mucosal
lining of the intestine Malabsorption.
 The malabsorption loss of nutrients
with subsequent malnutrition.
 Appetite with diarrhea more
malnutrition, also malnutrition may depress
appetite especially with protein deficiency.
 Malnutrition will lowered body immunity
especially with the current anorexia.
 Also with abuse of antimicrobials,
immune system is depressed.
 All these will repeated infections
either upper respiratory and or
gastroentestinal.
 These infections more anorexia,
more malnutrition and more diarrhea.
Clinical picture
 Mild: self limited, no fever + diarrhea<5
times/ day.
 Severe: Fever, vomiting, diarrhea up to
20 times /day with subsequent
dehydration.
 Dehydration: sunken eyes– dry mouth—
oliguria—acidosis—depressed anterior
fontanel---apathy—mental confusion.
skin elasticity
Assessment of diarrhea patients for
dehydration
Condition: No dehydration -: some dehydration.
General: well alert. -:Restless, irritable*.
Eyes: normal -: sunken.
Mouth & tongue: moist. -: Dry.
Thirst: not thirsty. -:Thirsty, drink eagerly*.
Skin pinch: go back -:go back slowly*.
quickly.
Status: no signs of -: if the patient has 2 or
dehydration. more signs including at
least one sign *, there is
some dehydration
Assessment of diarrhea patients for
dehydration
Condition: Severe N.B.
dehydration. In children >5 ys, &
General: Lethargic, adults, other signs
unconscious, floppy *. for severe
Eyes: very sunken & dry. dehydration are:
Mouth &tongue: very dry.
Thirst: drinks poorly or not able 1- Absent radial
to drink *. pulse.
Skin pinch: go back very
slowly*. 2- Low blood
Status: if the patient has 2 or pressure.
>, including at least one
sign*, there is severe
dehydration
Type of dehydration [it depends on
sodium level]
 Isotonic dehydration:
 There is a loss of both water +sodium.
 Sodium serum concentration normal.
 Osmolality is normal.
 Complaints:
 There are signs of dehydration with
thirst.
Types of dehydration
 Hypertonic (hyper-natremic) dehydration:
 Causes: Increase osmotic pressure in the intestinal
lumen by intake of fluids with high concentration
of Na and /or glucose.
 [ex. Drinking conc. fruit Juices ]

 Serum Na water loss osmotic P.

 Complaints:
 Thirst
 Seizures due to hyper-natremia.
Type of dehydration
 Hypotonic [hypo-natremic ] dehydration:
 Causes:
 Intake of fluids with very low concentration of
sodium. Ex., intravenous 5% glucose solution.
 There will be sodium loss with reabsorption of
water so this will lead to:
 Serum conc. of Na osmolality of serum
 Complaints:
 Lethargy with seldom seizures.
Acidosis in diarrhea

 Caused by:
 1-Loss of bicarbonate ions, can't be
replaced by the kidney, because of the
poor renal blood flow (hypovolemia).
 2-Lactic acid concentration because of
the hypovolemic shock [stress increase
glucose burning].
Signs of acidosis

 1-deep rapid respiration [ to

compensate for by respiratory alkalosis].

 2- vomiting.

 3- Appetite.
Hypokalaemia with diarrhea

 Potassium lost in stool.

 When both K &bicarbonates lost
together, hypokalemia doesn’t develop.
 Why?
 Because the acidosis that develop
causes K to move from intracellular to
extracellular fluids in exchange for
hydrogen ions.
When hypokalemia occur?

 When acidosis is corrected without

correction of K.
 Signs:
 Muscle weakness
 Cardiac arrythmia
 Paralytic ileus especially when
associated with antiemetic drugs.
Diagnosis
 1- clinically: from the clinical picture.
 2- Laboratory investigations:
 * Stool examination for detection of
parasitic infestations.
 * Stool culture for isolation of bacterial
agents.
 * Eliza or PCR for viral detection.
 * Serological testing for the antibody
titre.
Prevention [ General prevention ]

 1- Sanitary environment
 2- Health education to mothers about:
 A- Adequate nutrition:
 Exclusive breast feeding—proper
weaning—dietary supplementation.
Prevention [ general P.]

 B- Prevention of infection:
 Water supply—animal milk—bottles&
teats (boiling)
 Hand washing—clean articles &
utensils.
 Discarding any feed remains.
Prevention [ general P.]

 C- Medical care:
 Schedule of immunization
 Medical check up and utilization of
health services.
 3- Prevention and control of any
systemic infections.
Prevention [ Specific prevention]

 Specific prevention: vaccinations are

available against some organisms as
cholera, rota virus, virus A hepatitis,
E.Coli.
 These are especially indicated for
travellers from non-endemic to endemic
areas.
Control
 1- Early case finding:
 By health awareness+ efficient health services.
 2- Management of cases:
 at home if mild or at hospital if severe.
 A-Rehydration therapy:
 It replace water & electrolytes.
 ORS in packets, 5.5gm [ Na Cl---Na bicarbonate
{ acidosis}–K Cl [hypokalemia}—glucose
{nutrient} ].
continue

 ORS for mild and moderate cases.

 Nasogastric tube is indicated with
vomiting.
 Intravenous fluids in severe cases.
 B-Chemotherapy:
 Only in certain cases.
 Why?
Why antibiotics are not recommended as a
first line therapy

 1-most childhood diarrhea are caused by viral

agents [25-40% of cases in Egypt are due to
rota virus].
 2-Many other cases are caused by parasites
like Giardia and amoeba [not affected by
antibiotics]
 3-the use of many antibiotics may lead to
secondary enteritis and persistent diarrhea
because they destroy the flora of the intestine.
continue

 4- Sensitivity studies show that most

other cases are caused by bacteria
which are resistant to the most
frequently used antibiotics.
 5-Using antibiotics when not
indicated may reduce its effectiveness
when needed [due to resistance].
Continue control
 C-Diet therapy:
 If no dehydration continue feeding with fluid
intake.
 Cases with mild dehydration ORS+ milk.
 Moderate cases initially give rehydration S.
then fasting few hours (only fluids) until
dehydration improves, then give milk and mashed
starchy food [ Keep away of conc. Sweety fluids].
 Severe cases are hospitalized until general
condition improved and all signs of dehydration,
acidosis are corrected then give milk +starchy food.
continue
 D-Symptomatic treatment:
 For fever.
 Don’t give anti-emetics. Why?

 1-Because correction of acidosis can

stop vomiting.
 2-It causes sedation and or precipitate
paralytic ilieus.
Continue symptomatic tt

 Don’t give anti-motility drugs. Why?

 1- it keeps the toxins and pathogens

inside the intestine.
 2- It can cause ilius or respiratory failure.
Continue control

 E-treatment of underlying diseases:

 Malnutrition
 Systemic infection
 Parasitic infestation
Web sites

 At www.yahoo.com, yahoo groups,

 Dr.nihalsalah, files, ……
 -----------------------------------------
 www.esnips.com/user/drnehal
Sobhan Allah
Cholera
Causative agent
 1- Vibrio cholera serogroup O1 including two
biotypes:
 Classical V. & El-Tor V.
 It live off the surface of intestinal mucosa and produce a
potent endotoxin damaging the cells.
 2-A new serogroup O139 which have the same
cholera toxin, &It causes the same clinical
picture of vibrio cholera O1.But differ from O1
in:
 Lipopolysaccharide capsule structure
 Producing capsular antigen.
 Virulence

 Cholera produce a potent endotoxin

which inhibits Na Cl absorption by
intestinal villi.
 It causes increase in bicarbonate with
chloride secretion. All those factors
cause change of osmolality
extensive secretion of fluid &
electrolytes.
 Resistance

A delicate organism, sensitive to

sunlight, heat, acidity, dryness and
chlorine.
 In most contaminated articles it live [ 1-3
days].
 May live in water for 3-4 weeks & in
vegetables and fruits.
)case )2007 2315
Occurrence
 Many cholera pandemics have been reported ,
ex. The epidemic in Egypt in 1947.
 El-Tor vibrio spread in pandemics, in 1977,
1978, in 1993.
 In 1994, The O139 vibrio was isolated in 7
countries[Pakistan, bangaladish, nepal,
Malysia, China, serilanka, India].
 Also, cholera outbreaks occurred among the
refugees in Zaire in July.
Incubation period

 I.P:
 From few hours to 5 days [2-3 days].
Clinical picture
 Itis an acute infection of the small
intestine. It is characterized by :
 Acute, profuse, painless watery diarrhea
[ Rice water stool ] with mucous and
electrolytes.
 Occasionally vomiting,
 Anxiety, dehydration and acidosis,
ending by circulatory collapse + renal
failure.
 Reservoirs

 1- Human R.: cases Carriers [all types

of carriers including chronic]
 2- Environmental R.
 Recently observed in association with
zooplankton in brackish water or
estuaries.
 Susceptibility
 1- Risk increase with achlorohydria
 2- People with blood group O are exposed
more to el-Tor +O139.
 3-Infection with V.Cholera O1 give protection
against O1[ classical+ El-Tor].
 4- Infection with El-Tor give protection against
El-Tor only.
 5-In endemic areas young ages but in newly
infected areas usually adults more.
Modes of transmission

 By ingestion:
 1- Direct: person to person mainly in
children [in sporadic cases].
 2- Indirect: water borne cause
epidemics and outbreaks. Also, in
Food:by flies, soiled hands and utensils.
 Diagnosis

 1- Clinical picture
 2- Laboratory:
 Stool examination + rectal swab, vibrio
appear in the dark ground illumination
microscopy.
 Stool culture
 Prevention

 1- Environmental sanitation
 2- Health education
 3-Specific prevention:

Chemoprophylaxis Vaccination
Chemoprophylaxis

 By tetracycline 500mg 4 times/day.

 By furoxone 100mg 4 times/ day.
 Indications:
 For travelers to endemic areas.
 For carriers
 For contacts
 For pilgrims on their coming back.
 Vaccination
 By a parenteral vaccine (old vaccine)
 Preparation: a whole cell, heat killed, phenol
preserved.
 Dose: twice with1-4weaks apart, ½ ml 1st dose
then 1 ml 2nd dose.
 Booster dose/ 6months.
 Route: I.m or S.C
 Effect: 50%
 Protective 6 days after vaccination up to 6
months.
Continue vaccination

 Indications:
 To travelers to& from endemic areas
 Contacts
 To residents of endemic areas dring
outbreaks.
continue vaccination

 New oral vaccines in some countries:

 (A)- First one
 Nature: live attenuated vaccine (O1 strain).
 Dose: a single dose
 Route: Oral.
 Effectiveness: about 80-85% protection
 (About 85% protection against classic vibrios
and about 60-70% in El-Tor vibrios.
Continue vaccination
 (B)-Second one
 Nature: Inactivated O1 strain plus B-subunit
of cholera toxin.
 Dose: 3 doses Given one day apart.
 Route: oral vaccine
 Effectivenes: From 58% to 85% protection
 They give protection up to 6 months.
 Indications:
 For travelers to and from endemic areas
 For contacts
Recently, WHO informations
 In 2006, WHO published official
recommendations for Oral
Cholera Vaccine use in complex
emergencies.
The use of the parenteral
cholera vaccine has never been
recommended by WHO due to
its low protective efficacy and
the high occurrence of severe
adverse reactions.
 Recently, WHO informations

 C-Third One
 An internationally licensed oral cholera vaccine
(OCV) is currently available on the market and is
suitable for travellers.
 Effectiveness: It was proven safe and effective
(85–90%) after six months in all age groups,
declining to 62% at one year among adults) and is
available for individuals aged two years and above.
 Dose:It is administered in two doses 10-15 days
apart and given in 150 ml of safe water.
 Its public health use is relatively recent. Within the
past few years several immunization campaigns
were carried out with WHO support.
Alive attenuated vaccine for
cholera O139 are being tested
International measures
 In the past a vaccination certificate for
travelers from & to endemic areas was asked.
It was valid 6 days after 2nd dose of parenteral
vaccine up to 6 months. Otherwise quarantine
measures were done for 5 days in a special
place.
 Chemoprophylaxis were given instead of
parenteral vaccinefor travellers, especially for
pilgrims on coming back.
 Now oral vaccaines are indicated and given
for international travelers by some countries as
they are more effective than the old parenteral
one.
Control

 1- for cases: notification, isolation at

home or in hospital , disinfection,
treatment [antibiotics, rehydration
therapy], release after 3 negative slool
examinations.
 The dead bodies are soaked in formalin
first.
Conltrol
 2- for contacts:
 Segregation {no school, no work} and stool
examination .
 If +ve for vibrio, give chemotherapy.
 If –ve, then release after 3 negative
examinations
 Chemoprophylaxis
 New oral vaccines are indicated if they are
available.
Continue control
 General epidemic measures:
 Declaration and notification of the disease to
WHO.
 Health education for the public
 Investigate water and food sources, channels
of infection
 Environmental sanitation:
 Closure of swimming pools, superchlorination
of water.