Transcript 1c4f3102-5d1c-45bb-a233

WAFA SAMA’N
Pediatrics MD.
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Incidence: The second most common cause of death in children
<5 years.
 Account for 1.5 million death of children/year
globally.(13% of all deaths).
 Every child <5 years has 3.6 episode of diarrhea/year.
 Mortality due to diarrhea has declined cause of
Rotavirus vaccine, improved nutritional status, better
management of disease.
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Etiology: Feco-oral route transmission.
 Ingestion of contaminated food or water.
 Person to person transmission occur in pathogens
infectious in small inoculum ,like
Shigella,campylobacter,EHEC,Norovirus,
 Rotavirus, E.histolyticum and Giardia.
 Most common cause is viral like
Rota,norovirus(Norwalk) then adenovirus and enteric
viruses.
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 Bacterial causes like salmonella,Shigella and E.Coli.
 Waterborne outbreaks of diarrhea caused by
cryptosporidium commonly and others like:-Shigella, E.coli,
Norovirus and Giardia.
 Antibiotics associated pseudomembranous colitis is due to
Clostridium defficile.
 Usually all children acquired Rotavirus, enterovirus and
Giardia lamblia in the first 5 years of life.
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Diarrhea Classification
 Pathophysiology
 Osmotic
 Secretory
 Exudation
 Abnormal motility
 Duration
 Acute (< 2 weeks)
 Chronic (> 2 weeks)
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Mechanism of Diarrhea:Mechanism
Non-inflammatory
Enterotoxin/Adherence
Inflammatory
Invasion/cytotoxin
Penetration
Location
Proximal Small Bowel
Colon
Distal Small Bowel
Illness
Watery Diarrhea
Dysentery
Enteric Fever
Stool
Examination
No fecal leukocytes
Mild or no lactoferrin
Fecal Neutrophil
lactoferrin
Fecal mononuclear
leukocyte
V.cholera,E.coli
(ETEC,EPEC,EAEC)
,Norwalk,Giardia,Staphaur
eus,Cl.perfringes.
Shigella,E.coli(EIEC,
EHEC) Salmonella
enteritidis,Cl.defficil
e,E.histolytica.
Salmonella typhi
Yersina
Enterocolitica
Example
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Osmotic diarrhea
 Def: Increased amounts of poorly absorped,
osmotically active solutes in gut lumen
 Interferes with reabsorption of water
 Solutes are ingested
 magnesium
 sorbitol
 malabsorption of food (mucosal injury, lactase
deficiency)
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Secretory diarrhea
 Excess secretion of electrolytes, fluid across mucosa
 Usually coupled with decrease in absorption
 Watery, high-volume diarrhea with dehydration
 Enterotoxins: Cholera, E. coli, food poisoning,
Rotavirus (?), Norwalk virus (?)
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Osmotic/Secretory
VOLUME OF STOOL
<200ml/24 hrs
>200ml/24 hrs
Response to fasting
Diharrea stops
Diharrea continues
Stool Na
<70 mEq/l
>70 mEqu/l
Reducing substances
Positive
Negative
Stool pH
<5
>6
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 In secretory Diharrea enterotoxin produced by microorganism
cause inhibition of Na-Cl pump but not(glucose-Na) pump.
 In inflammatory diharrea extensive histological damage,release
of cytokines leads to increase crypt secretion of Chloride ion by
increasing c-AMP.Uncoupling of both Na-H,Hco3-CL –and NaGlucose uptake.
 In Shigellosis superficial invasion of colonic mucosa and
phagocytic activation with apoptosis and inflammatory
interleukins release leading to neutrophilic degranulation.
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Risk Factors: Environmental contamination of water and food.
 Young age.
 Immunedefficiency.
 Measles.
 Malnutrition.
 Lack of exclusive breast feeding.
 Vitamin A defficiency.
 Zink defficiency is known also to increase mortality in
pneumonea,measles and diharrea.
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Complications: Dehydration.
 Prolongation of diharrea with resultant malnutrition
 Secondary infections.
 Micronutrient defficiency(Zinc,Iron).
 Extraintestinal manifestations like reactive
arthritis,GuillianBarre(C.jejeuni),glomerulonephritis,
HUS and erythema
nodosum(salmonella,campylobacter).
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Treatment: ORS is considered the cornerstone in treatment
because it has appropriate osmolality about 310
mos/Kg.
 ORS can’t be given in shock,ileus,vomiting,high stool
output>10cclKG
 Home made remedies like carbonated
beverages(soda),fruit juice are not suitable for
rehydration or maintainance because of high
osmolality and low Na concentration.
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•Enteral feeding should be continued during recovery from episode of diarrhea.
•Although brush border of intestine is affected ,still satisfactory absorption of
CHO,protiens and fats can occur.
•Once rehydration is complete food should be reintroduced to replace ongoing
losses by emesis or diharrea.
Breast feeding or non diluted formula should be given.
Food like rice soup,vegetables,fruits and yogurt can be given in the recovery period.
Fatty food or food high in simple sugars should be avoided.
Energy given should be 100 Cal/Kg/d and proteins 2-3glKg/d.
Acute lactose intolerance is seen in some patients ,so they should be given
Lactose free formula like replacing some of milk requirements with yogurt or milk
free diet like comminuted chicken or elemental milk.
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Oral rehydration solutions
Components
WHO
Ricelyte
Pedialyte
Na (mEq/L)
90
50
45
K (mEq/L)
20
25
20
Cl (mEq/L)
80
45
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Citrate (mEq/L)
30
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Glucose (g/L)
20
30
25
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Additional therapy: Zinc supplement reduce duration ,severity and prevent
recurring diharrea.
 Probiotics like non-pathological bacteria,can restore
beneficial intestinal flora,decrease proinflammatory
cytokines and increase anti-inflammatory factors
 Lactobacillus bifidobacterium and lactobacillus
rhamenosus reduced duration in Rota.
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Additional therapy: Anti-motility(Loperamide) NO Role.
 Anti-emetics like phenothiazine, no role.
 Ondansetron is a selective anti 5HT receptors and a
safe anti-emetic can be given as a single dose before
ORS if there is vomiting.
 Antibiotics should not be given routinely because
indiscriminate use lead to bacterial resistance and may
prolong bacterial shedding
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Prevention: Promotion of exclusive breast feeding so no other fluid
or food should be given in 1st 6 months.
 Improved complementary feeding preparation with
hygenic practice.
 Vit-A supplement.
 Rota virus immunization.oral live attenuated
pentavalent vaccine.
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Viral causes of gastroenteritis
 Rotavirus
 Calcivirus(Norwalk)
 Enteric Adenovirus
 Astrovirus
 Others Torovirus,Coronavirus and Pesivirus
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Rotavirus
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Mostly in infants between3-24 months.
Low infection inoculum size so personperson spread is common.
All children exposed by age 4-5 years
Double stranded RNA virus
Several groups (A-E )
Most common cause of viral diarrhea
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Rotavirus
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Pathogenesis
 Selectively infects &destroys villous tip cells in small
intestine ,gastric mucosa is not affected.
 Villi have absorptive &digestive functions so both are
affected in Rota viral infection.
 Viral enteritis enhance mucosal permeability to macro
molecules leading to increase incidence of food
allergy.
 Infants are more prone to infection because of
decrease intestinal reserve , gastric acidity and lack of
specific immunity.
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Transmission
 Fecal-oral
 Contaminated water supplies
 Poor hygiene
 Food
 Fomites
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Clinical manifestations: Incubation period <48 hrs.
 Low grade fever,vomiting followed by diharrea
lasting<one week,usually watery,no blood or white
cells.
 Infants commonly develop dehydration.
 Malnourished children develop severe &prolonged
illness.
 Newborns usually are asymptomatic some may
develop NEC outbreaks in nurseries.
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Diagnosis of rotavirus
 Electron microscopy
 Small intestine
 Stool
 Antigen in stool
 commercial ELISA
 PCR, nucleic acid probes
 No RBC or WBC in stool
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Rotavirus Clinical Syndromes
 Asymptomatic carriers
 Diarrheal illness
 2-3 day incubation
period
 diarrhea, vomiting
fever 3-7 days
 high infectivity
 Complications
 dehydration
 chronic diarrhea
 dissemination
 NEC
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Prevention of Rotavirus
 Natural immunity 93% protective (sIgA)
 Good hand washing&isolation .
 Vaccine
Was licensed in 1998 for infants 2,4,6 mo. offered
80% protection.
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Norwalk virus
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Norwalk virus
 “winter vomiting disease” 1968, Norwalk
 Cause 40% of nonbacterial epidemics
 Explosive epidemics
 camps, cruise ships, nursing homes
 Food borne illness
 raw shellfish
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Norwalk virus: Clinical Features
 24-48 hour incubation period
 vomiting prominent
 diarrhea 1-3 days
 less severe than rotavirus
 Small 27-35-nm single stranded RNA virus
 Most common cause of GE outbreaks in older
children &adults
 Similar to staph food poisoning
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How does Norwalk virus
cause diarrhea?
 Infection affects proximal small bowel
 Patchy mucosal injury
 Malabsorption
 ? Excess secretion
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Other viruses causing
gastroenteritis
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Adenovirus
Enteric serotypes 40,41
80-nm single stranded DNA
Do not cause respiratory symptoms
Common cause of GE in children and adults
Prolonged course 10-14 days
 Astrovirus
 Second common cause of viral GE
 Single stranded RNA 30-nm diameter
 Similar to Rota infection but milder
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Bacterial Etiology: Salmonella
 Two main species with many different
serotypes(S.Enterica S.bongori)Serotypes are divided
according to somatic O antigen and flagella H antigen.
 G-ve flagellated rods killed by heat.
 Transmitted by raw poultry,eggs,vegetables
contaminated water.
 Person-person spread uncommon because of large
inoculum size.
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Presentation
 Salmonellosis(acute enteritis):
 Incubation period 6-72 hrs.
 Nausea,vomiting,abdominal pain ,fever
diharrhea,usually watery but st bloody.
 Rarely septicimia and septic shock.
 Extraintestinal manifestations like osteomyelitis,septic
arthritis,meningitis
 Usually self limiting disease like food poisoning.
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Treatment: Correct dehydration
 Antimotility drugs are contraindicated because they
increase incidence of perforation
 Antibiotics are not used in simple enteritis because
they increase resistance prolonged bacterial shedding
&carrier state.
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Treatment: Antibiotics are indicated in infants <3 months
 In patients with immune deficiency
 In patients with typhoid fever
 In septicimia and localized infection
 In chronic carrier before cholycystectomy
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Shigella: There are 4 species (S.dysenteriae S.sonnei S.flexneri
S.bodyii)
 Aerobic non-motile G-ve rods
 Transmitted by contaminated water and food
 Person-person is common ,because the inoculum size
is only 100 bacteria
 Invasion of colonic mucosa with production of
enterotoxin
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Complications: Acute bloody diarrhea( tenesmus,crampy pain with
fever)
 Hemolytic uremic syndrome(acute renal
failure,hemolytic anemie,thrombocytopenia)
 Neurological complications (lethargy,coma and
convulsions)
 Reiter syndrome(conjunctivitis urethritis and arthritis)
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Treatment: Fluid and electrolyte correction
 Antibiotics treatment in all children with shigellosis.
 Antibiotics are given to shorten duration of illness so
the child will not be infectious
 Prolonged course if untreated with resultant
malnutrition
 Ceftriaxone is drug of choice
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Pseudomembranous Colitis : Clostridium difficile is the causative bacteria
 It is found in colon as inactive spore form
 Antibiotics disrupt normal flora in intestine so
dormant spores are activated
 They produce toxin that damage the colonic mucosa
with production of membrane
 Antibiotics implicated mostly
Clindamycin,Ampicillin,amxycillin
 Oral metronidazole or Vancomycin is drug of choice
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Amebiasis
 Two species that are genetically identical
E.histolyticum and E.dispar
 E.dispar usually asymptomatic carrier
 E.histolytica in 90% of cases are asymptomatic cyst
passer
 Infection transmission is by cyst because they are
resistant to cold and chlorination
 Trophozoites are not infectious
 Person-person transmission can occur
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Symptoms
 Amebic dysentery with colicky abdominal pain
frequent bowel motions,bloody diarrhea and tenesmus
 No general signs and symptoms
 Low grade fever
 May invade intestinal mucosa to cause abscess in liver
and rarely in brain
 Chronic amebic colitis indistinguishable from IBD
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Treatment
 All individuals with cyst or trophozoites in their stool
whether symptomatic or not should be treated
 Metronidazole is the drug of choice for invasive
amebiasis
 Iodoquinol and paromomycin is the treatment of
choice for amebic cyst
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Giardia lamblia
 Flagellated protozoan infects the duodenum and
proximal jejunum
 It is found as cyst and trophozoites form
 10-100 cysts are enough to cause infection
 Water and food borne infection
 Person-person infection is common
 Most common intestinal parasite
 Cysts are resistant to chlorination but killed by boiling
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Symptoms
 Acute infectious diarrhea no mucus or blood in stool
 Chronic diarrhea leading to malabsorption and failure
to thrive with fats and sugar in stool
 Most infections are asymptomatic
 No extra intestinal spread
 Diagnosed by stool analysis or duodenal aspirate and
biopsy
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Treatment
 Asymptomatic carriers are not treated
 Albendazole treatment for 5 days
 Others like metronidazole,furazolidone and
paromomycin are effective treatment
 Infections in pts who have agammaglobulinemia
should be treated
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Antimicrobial Therapy:Organism
Antimicrobial Agent
Indications for Rx
Campylobacter
Erythromycin/Quinolones
Early in the course of disease
Clostridium difficile
Metronidazole/Vancomycin
Moderate to severe disease
E.coli
TMP/SMZ
Severe or prolonged illness
Nursery epidemics
Salmonella
Cefotaxime/Ceftriaxone
Ampicillin/TMP/SMX
Bacteremia,suppuration
Infants<3mon,typhoid fever
All cases +ve stool
Shigella
Ampicillin,Ceftriaxone
Ciprofloxacin
Giardia lamblia
Metronidazol/albendazol
Entamoeba hisolyticum
Metronidazol/iodoquinol
Trophozytes/cyst
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The End.
Thank You For Listening.
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