Gastroenteritis, Cholera

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  Acute

diarrhea  Sudden onset

 Usually

self limited [within 3-5 days] unless child dies from dehydration.

 Persistent

diarrhea  May be sudden or insidious but stool [frequency & characteristics] vary from day to day.  May lead to permanently impaired growth or even death.

Acute diarrhea versus persistent diarrhea  Most

often caused by pathogenic organisms.

 Children

1 to 30 months are more susceptible.

 May

initially be related to a specific organism but, intestinal damage, malabsorption and other bacteria keep it going.  Malnourished children are more susceptible.

Acute diarrhea versus persistent diarrhea  Fever

and/ or vomiting may or may not be accompany.  May result in rapid dehydration.

 Neither

fever nor vomiting is common.

 Dehydration

is usually mild but enough to suppress appetite.

Causative agents of gastroenteritis

Protozoal

Bacterial

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 General: well alert. Eyes: normal Mouth & tongue: moist. Thirst: not thirsty. Skin pinch: go back quickly. Status: no signs of dehydration.

-: some dehydration. -:Restless, irritable*. -: sunken. -: Dry. -:Thirsty, drink eagerly*. -:go back slowly*. -: if the patient has 2 or more signs including at least one sign *, there is some dehydration

Assessment of diarrhea patients for dehydration Condition: Severe dehydration. General: Lethargic, unconscious, floppy *. Eyes: very sunken & dry. Mouth &tongue: very dry. Thirst: drinks poorly or not able to drink *. Skin pinch: go back very slowly*. Status: if the patient has 2 or >, including at least one sign*, there is severe dehydration

N.B. In children >5 ys, & adults, other signs for severe dehydration are: 1- Absent radial pulse. 2- Low blood pressure.

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 Complaints: Thirst Seizures due to hyper-natremia.

osmotic P.

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

 1-

give anti-motility drugs. Why?

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  It

is 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 oral vaccines in some countries:  (A)- First one  Nature: live attenuated vaccine (O1 strain).  Dose: a single dose  New

 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,  C-Third

WHO informations

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.

A

live 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.