Transcript Etiology of Diarrhoea

Definition
In epidemiological studies diarrhoea is defined as:
Passage of three or more loose or watery stools in a 24-hour
period, a loose stool being one that would take the shape of a
container.
Definition
In Pediatrics,
Diarrhoea is an increase in the:
 Fluidity

Volume
Number
of stools relative to the usual
habits of each individual.

 Stool output > 10 g / kg / day,
> 200ml per m² BSA/d ,
>150-200 gr per m² BSA/d.
Importance of Diarrhoea
In under five children
Diarrhoea is a leading cause of:
Mortality
 Morbidity
 Severe malnutrition

High Childhood Morbidity
2.5 billion episodes/year
3.6 episodes/baby/year
In children under 5 years of age
High Childhood Mortality
3.2 million deaths/ year
5 million per year in 1980 to less than 2
million in 1999
In children under 5 years of age
‫‪‬اسها ل = ‪ %18‬مرگ ومیر کودکان‬
‫‪ ‬دومین علت مرگ ومیر کودکان‪.‬‬
‫‪ 1/5‬میلیون مرگ در سال‬
‫روتا ویروس‬
‫=‪(deaths=29%)527000‬‬
‫‪ETEC=300000-500000‬‬
Major Contributor to Malnutrition
DIARRHOEA
MALNUTRITION,
‫اختالالت روانی تکاملی و شناختی‬
Diarrhea attack rate / 100 child / year
Sev.PEM
Mod.PEM
Mild PEM
Normal
0
50
100
150
200
250
300
Guatemala ,1968
Acute Watery Diarrhoea
 Constitutes 80% of cases of diarrhoea
 Begins acutely, lasts less than 14 days (most episodes
last less than 7 days),
 Involves passage of frequent loose or watery stools
without visible blood.
 Vomiting may occur,Fever may be present
 Main sequelae:
 Dehydration that can be fatal
 Contributes to malnutrition
Dysentery (Bloody Diarrhoea)
 Constitutes 10% of cases of diarrhoea
 Diarrhoea with visible red blood in the stools
 Main sequelae:
 Anorexia
 Rapid weight loss
 Damage to the intestinal mucosa
Persistent Diarrhoea
 Constitutes 10% of cases of diarrhoea
 Diarrhoea that begins acutely as watery diarrhoea or as
dysentery and lasts for 14 days or more.
 Should not be confused with chronic diarrhoea which is
recurrent or long-lasting diarrhoea due to noninfectious
causes.
Etiology: Fecal-Oral Transmission
Infected animal
Infected
Person
Food
‫فقر – بهداشت نامناسب‬
Water
Etiology of Diarrhoea
 Identification of the etiology of diarrhoea on clinical grounds
alone is not usually possible except in epidemics or if there
is history of contact with a diagnosed case.
 With the availability of modern laboratory techniques,
causative pathogens could be identified in >75 % of cases of
diarrhoea.
Etiology of Diarrhoea
 The majority of diarrhoeas occur as a result of infection
with a few pathogens which tend to recur again and
again.
 The most important causes of acute diarrhoea in
developing countries are:





Rotavirus
Enterotoxigenic Escherichia coli
Shigella
Campylobacter jejuni
Cryptosporidium
Etiology of Acute Diarrhoea
Percent
20
18
15-25%
10-20%
16
10-15%
14
5-15%
12
5-15%
10
8
6
4
2
0
Rotavirus
E.E.Coli
Shigella
Camylobacter J.
Cryptosporidium
Enteropathogens that are infectious in
a small inoculum
(Shigella, enterohemorrhagic E. coli, Campylobacter
jejuni, noroviruses, rota virus, Giardia lamblia,
Cryptosporidium parvum, Entamoeba histolytica)
 can be transmitted by person-to-person contact,
others, such as cholera:
Are generally a consequence of contamination of food or
water supply .
Food-borne outbreaks of bacterial diarrhea in the United
States are most commonly due to:
 Salmonella,
 E. coli,
 Clostridium botulinum,
 Clostridium perfringens,
 Staphylococcus aureus

PATHOGENESIS OF INFECTIOUS DIARRHEA:
 organisms have preformed toxins (S. aureus, Bacillus
cereus),?
 produce secretory toxin(cholera, E. coli, Salmollella, Shigella)
 Adherence and/or translocation by bacteria.
 cytotoxic toxin (Shigella, S. aureus, Vibrio parahemolyticus,
C. difficile, E. coli, C. jejuni)
 invasive
 Multiple
(protein NSP4 acts as a viral enterotoxin)
Pathogenesis of Rotavirus Diarrhoea
Rotavirus invades the absorptive enterocytes of villi but spares crypt cells.
The viruses replicates and infected enterocytes are destroyed
Rotavirus
Rotavirus
Rotavirus inside enterocyte
Pathogenesis of Rotavirus Diarrhoea
11
2
1- Infected absorptive ente-rocytes are
killed causing patchy epithelial cell
destruc-tion and villous shortening
2- Destroyed absorptive cells are rapidly
replaced by cells that migrate from the
crypts. So, affected villi become
temporarily covered with immature
non-absorptive crypt-like secretory cells
having no brush border and no brush
border enzymes (e.g. lactase)
Effects of Rotavirus
Pathogenesis of Secretory Diarrhoea
1-Enterotoxigenic Bacteria secrete an
Enterotoxin that stimulates the
production of C-AMP (cyclic
adenosine mono-phosphate)
2-Increased C-AMP leads to:
Inhibition of absorption of Na+ & Clfrom the cells of villi
Stimulation of secretion of Cl- from crypt
cells
Entero-Adherent E. Coli
Entero-Adherent E. Coli adherent to
enterocyte of small intestine
(electron microscope X 20 000)
RISK FACTORS FOR GASTROENTERITIS:
 1- environmental contamination and increased exposure to
enteropathogens.
 2-young age,
 3-immunodeficiency,
 4- measles,
 5- malnutrition,
 6- lack of exclusive or predominant breast-feeding.
 7- nutritional deficiencies
‫‪ Zink deficiency‬‬
‫مرگ و میر ناشی از اسهال و پنومونی وماالریا را ‪%13-21‬افزایش میدهد‬
‫‪ Vitamin A deficiency‬‬
‫مرگ و میر ناشی از اسهال و سرخک وماالریا را ‪%20-24‬افزایش میدهد‬
clinical manifestations
Symptomatic, Asymptomatic C. jejuni Infections
clinical manifestations
 There is considerable overlap in the symptomatology.
 are related to the infecting pathogen and the dose or
inoculum
 development of complications (e.g., dehydration and
electrolyte imbalance)
 Usually the ingestion of preformed toxins (e.g., those
of S. aureus) is associated with:
 the rapid onset of nausea and vomiting within 6 hr,
with possible fever, abdominal cramps, and diarrhea
within 8-72 hr.
 Watery diarrhea and abdominal cramps after an 8-16
hr incubation period are associated with enterotoxinproducing e. perfringens and B. cereus.
 Abdominal cramps and watery diarrhea after a 16-48
hr incubation period can be associated with
noroviruses, several enterotoxin-producing
bacteria, Cryptosporidium, and Cyclospora and
have also been a notable feature of influenza virus
HINI infections.
 Several organisms, including Salmonella, Shigella,
c. jejuni, Yersinia enterocolitica, enteroinvasive or
hemorrhagic (Shigatoxin-producing) E. coli, and
V.parahaemo/yticus, produce diarrhea that can contain
blood as well as fecal leukocytes in association with
abdominal cramps, tenesmus, and fever;
COMPLICATIONS:
 Most of the complications associated with gastroententIs are
related to delays in diagnosis and delays in the institution
of appropriate therapy.
 1-dehydration
 2- prolongation of the diarrheal episodes
 3-malnutrition
 4- secondary infections
 5-In developing countries and HIV-infected populations,
associated bacteremias are well-recognized complications
in malnourished children with diarrhea.
 6-micronutrient deficiencies (iron, zinc).
Extra-intestinal complications
 Specific pathogens are associated with extra intestinal
manifestations and complications
 These are not pathognomonic of the infection,
 nor do they always occur in close temporal association
with the diarrheal episode