Acute infectious diarrhoea is the leading cause of morbidity leading to dehydration, hospital admission and death in children. Viral causes (rotavirus) predominate as the pathogen. Initial management rely on assessment of severity of dehydration and fluid replacement. Early refeeding Antibiotic are needed only in some bacterial and parasitic infections. Probiotics, prebiotics and zinc reduce the duration and severity of symptoms. Honey, amazingly contain all these substances and extremely useful in diarrhoea

1. Dr Muhammad Barkaat Hussain
Assistant Professor Microbiology
Rabigh Medical College,
King Abdulaziz University, KSA
Diarrhea

3. About fourteen hundred years ago when scientific
knowledge regarding gastrointestinal diseases like
diarrhea did not exist, a person came to Prophet
Muhammad ‫ﷺ‬ and asked about his brother’s
abdominal illness. The Honorable Prophet ‫ﷺ‬
prescribed honey for his brother illness for four
consecutive days and his brother got cured (al
Bukhari).
History?

4. Learning outcomes
• At the end of the lecture you should be able to:
• Classify diarrhea on the basis of clinical presentations
• Enlist the most common microbiological causes of diarrhea
• Understand the difference between non-inflammatory and inflammatory
diarrhea
• Know how to distinguish or differentiate between medically important diarrhea
(that needs immediate treatment) from benign self-limited diarrhea.
• Discuss the lab investigations which are important in making correct
diagnosis.
• Understand the sequence in the treatment of acute diarrhea and its
prevention Explain the role of antibiotics, probiotics, prebiotics and zinc in the
management of diarrhea.

5. Definitions
• Gastroenteritis: is an inflammation of the stomach lining and the
intestine that is characterized by diarrhea and vomiting
• Diarrhea: three or more loose stools in a 24-hour period
(acute: the duration is 14 days or less; or persistent: longer than 14
days)
• GI infections may manifest with acute vomiting, acute watery
diarrhea, bloody diarrhea (dysentery), persistent diarrhea, or
enteric fever. Most pathogens may cause more than one syndrome.

6. Some facts about diarrhea
• Diarrhea is an important cause of morbidity and mortality
worldwide, particularly in children living in areas without
adequate access to safe water and sanitation
• The 9th leading cause of death globally in 2015 and was
responsible for 8.6% of deaths among children younger than 5
years
• Death rates from diarrhea have declined over the past decade
with improvements in sanitation, more widespread use of oral
rehydration solution, and the introduction of rotavirus
vaccination programs.

7. Clinical syndromes associated with GI infections
CLINICAL SYNDROME SIGNS AND SYMPTOMS PATHOGENIC MECHANISM EXAMPLE PATHOGENS
Acute watery diarrhea (90%)
Loose stools, often with mucus but
not blood
Occasional vomiting and anorexia
Low-grade fever, Malaise
Local infection in the gut
Norovirus genogroups I, II, and IV,
enteric adenovirus types 40 and 41,
rotavirus, enterotoxigenic Escherichia
coli, enteropathogenic E. coli,
Cryptosporidium, Clostridium
perfringens, Bacillus cereus
Dysentery (5 to 10%)
(acute bloody diarrhea)
Loose stools with gross blood and
mucus, Fever
Abdominal cramps and, in some
cases, tenesmus
May be clinically toxic
Local invasion of the gut
Shigella, enteroinvasive E. coli,
Campylobacter jejuni, Entamoeba
histolytica, nontyphoidal Salmonella,
Yersinia enterocolitica, Aeromonas,
Clostridioides difficile
Profuse purging (abrupt or
violent removal) 1%
Copious watery stools resembling
“rice water”
Low-grade fever
Overt signs of dehydration
Toxin mediated
Vibrio cholerae O1 and O139,
enterotoxigenic E. coli
Persistent diarrhea (3-4%)
Similar to acute diarrhea, but
symptoms persist for at least 14 days
or more
Local infection in the gut and/or
immune compromise of host
Giardia lamblia, Cryptosporidium
hominis/parvum, Cystoisospora belli,
Cyclospora
cayetanensis, enteropathogenic E.
coli, enteroaggregative E. coli
Acute vomiting
Sudden onset of nausea and vomiting
Little or no diarrhea
Local infection in the gut or
intoxication
Norovirus, food poisoning due
to Staphylococcus aureus, Bacillus
cereus
Enteric fever
Fever
Lymphadenopathy
Local invasion of the gut with
systemic spread
Salmonella enterica serovar Typhi, S.
enterica serovar Paratyphi A, B, or C

10. Non- inflammatory Diarrhoea
noninflammatory.
• The non-inflammatory diarrheal syndrome is characterized by watery stools
that may be of large volume (>1 L per day), without blood, pus, severe
abdominal pain, or fever.
• This type of diarrhoea is caused by bacteria, such as Vibrio cholerae,
enterotoxigenic Escherichia coli, and staphylococcal and clostridial food
poisoning; viruses, such as Rotavirus and Norwalk agent; and protozoa,
such as Cryptosporidium and Giardia.
• Infection with these agents can alter the normal absorptive and secretory
processes of the enterocyte, leading to watery diarrhoea.
• Many organisms cause these changes because they elaborate
enterotoxins. In this syndrome, the morphology of the mucosa remains
normal or is only minimally altered.
•
• Thus, stools do not have fecal leukocytes (or only a few) or occult blood.

11. Inflammatory Diarrhoea
noninflammatory.
• The acute inflammatory diarrhoea is characterized by frequent, small-volume,
mucoid or bloody stools (or both), and may be accompanied by tenesmus,
fever, or severe abdominal pain.
• The causative organisms induce an acute inflammatory reaction in the small or
large intestine, and the stools may have many leukocytes and, frequently, occult
or gross blood.
• Fecal polymorphonuclear leukocytes (or a positive stool lactoferrin test) indicate
the existence of an acute inflammatory process in the gastrointestinal tract.
• The greater the number of leukocytes, the lower in the gastrointestinal tract is the
inflammatory focus. When sheets of leukocytes are seen in stool specimens, the
disease is in the colon.

12. Inflammatory Diarrhoea
noninflammatory.
• Infectious causes of diarrhoea include Salmonella, Shigella, Campylobacter,
enterohemorrhagic E. coli, enteroinvasive E. coli, C. difficile, E. histolytica,
and Yersinia.
• The acute inflammatory diarrheal syndrome can also be of non-infectious
etiology, such as ulcerative colitis, Crohn’s disease, radiation or ischemic colitis,
or diverticulitis.
• An adequate medical history and a complete physical examination are essential
in determining the possible diagnoses, degree of severity, and complications, and
to suggest further investigations.

13. Bacteria
Aeromonas spp. Widely distributed in aquatic environments; may cause diarrhea or extraintestinal infection
Bacillus cereus
Vomiting illness; rare fatal cases with hepatic necrosis; testing for toxin available (preformed
toxin)
Campylobacter jejuni
Associated with poultry; common cause of traveler’s diarrhea in Asia; associated with
postinfectious arthritis and Guillain-Barré syndrome
Clostridioides difficile
Leading cause of mortality from gastrointestinal infection in United States (usually overuse of
antibiotics)
Clostridium botulinum
Vomiting illness due to preformed toxin ingestion; infant botulism due to germination of
spores presents with progressive weakness
Enteroaggregative Escherichia coli Persistent diarrhea in young children, associated with malnutrition
Enterohemorrhagic E. coli (STEC) Associated with dysentery and hemolytic-uremic syndrome in children
Enteroinvasive E. coli Associated with dysentery
Enteropathogenic E. coli Acute watery diarrhea
Enterotoxigenic E. coli Most common cause of traveler’s diarrhea
Listeria Associated with raw dairy products; pregnancy complications with systemic illness
Nontyphoidal Salmonella spp. Associated with dysentery, Intestinal carriage can be prolonged
Plesiomonas shigelloides May cause watery diarrhea, dysentery, or extraintestinal infection
Shigella spp. Most common global cause of dysentery
Staphylococcus aureus Vomiting due to preformed staphylococcal enterotoxin ingestion
Vibrio cholerae
Outbreaks of watery diarrhea associated with lack of sanitation and humanitarian crises (rice
water stool)
Vibrio parahaemolyticus Associated with shellfish consumption
Yersinia enterocolitica Zoonosis; able to grow in refrigerated food; associated with postinfectious polyarthritis
Yersinia pseudotuberculosis Appendicitis-like syndrome

14. Foodborne Syndromes
A-Nausea and Vomiting Lasting Less Than 24 Hours
1. Staphylococcus aureus (incubation period 1-8h)
2. Bacillus cereus (0.5-6h) (short-incubation emetic illness)
3. Noroviruses
B-Watery Diarrhea without Fever Lasting 1 to 2 Days
1. Enterotoxin-mediated syndrome: Clostridium perfringens type A (9-12h)
2. B. cereus (8-16h) (long-incubation diarrheal syndrome)
Highly heat resistant
Enterotoxins withstand
ordinary cooking

15. C- Watery Diarrhea and Abdominal Cramps Lasting More Than 2 Days:
1. Enterotoxigenic strains of E. coli (ETEC)
2. Vibrio parahaemolyticus
3. Vibrio cholerae strains O1 and O139
D- Dysentery, Abdominal Cramps, and Fever
Nontyphoidal Salmonella, Shigella, Campylobacter jejuni, enteroinvasive E.
coli, Entamoeba histolytica, and Yersinia enterocolitica
Foodborne Syndromes

16. E- Bloody Diarrhea with Minimal Fever:
Enterohemorrhagic E. coli (STEC), most often serogroup O157
F- Persistent Diarrhea Lasting 2 or More Weeks
Parasites including Cryptosporidium, Giardia, and Cyclospora.
Foodborne Syndromes

17. Investigations
• After an adequate medical history and physical examination, the clinician should
be able to classify the acute diarrheal illness and determine its severity and possible
complications.
• The clinician should also be able to determine whether any diagnostic tests are
needed. Because most episodes of acute diarrheal illness are self-limited,
diagnostic testing should be kept to a minimum.
• Investigations should be focused toward the diagnosis of specific pathogens as
suggested by the history. It is not appropriate to send the entire array of stool
cultures and stool examination for every patient. They should be performed only if
their results will influence management and outcome.
• Diagnostic testing should be reserved for patients with severe illness

18. Diagnostic tests for acute infectious diarrhoea
• Diagnostic tests for acute infectious diarrhoea in the normal host
include stool cultures for bacterial pathogens, stool examination for
ova and parasites, and stool testing for Clostridium difficile toxin and
for E. coli 0157:H7.
• In most microbiology laboratories, stool sent for culture of enteric
pathogens will be processed for Shigella, Salmonella, and
Campylobacter.
• Other enteric pathogens such as Yersinia, Vibrio, and E. coli 0157:H7
are not routinely sought.
• More invasive investigations, including flexible sigmoidoscopy with
biopsies and upper gastrointestinal endoscopy with duodenal
aspirate and biopsies, are reserved for special situations, such as an
immunocompromised patient in whom stool examination has not
yielded a diagnosis

19. Diagnosis

20. Treatment
• Rehydration – oral vs. IV
• Antiemetics and antimotility agents: in adults, not
recommended for children
• Bismuth subsalicylate (Pepto-Bismol) is safe and efficacious in
the treatment of infectious bacterial diarrhea. It stimulates
intestinal sodium and water reabsorption, binds enterotoxins,
and has a direct antibacterial effect.
• Antibiotics: Depends on pathogen (in severe illness , patients
older than 50, infants, immunocompromised patients):
Fluoroquinolone in adults
Third-generation cephalosporin in children

21. Treatment- Recent recommendations
NICE guidelines make a stronger recommendation for the use of
1. Probiotics (beneficial bacteria)
2. Prebiotics (undigested oligosaccharides)
3. Combination of probiotic and prebiotic is called symbiotic
4. Zinc supplementation
5. Antibiotics in case of some bacterial diarrhea

22. Natural sources of antibiotic, probiotics, prebiotics and
zinc
1. Probiotics (youghrut, honey)
2. Prebiotics (rice, bannana, honey)
3. Zinc supplementation (honey)
4. Natural, potent, broad spectrum and safe antimicrobial
substances (honey).
5. Amazingly, so for, antibacterial resistance to honey has been
reported.
6. Not only effective in GIT disorders, rather numerous human
illnesses like, infected wounds, burns, allergic disorders, cancer
etc.

23. Prevention

24. Summary
• Acute infectious diarrhoea is the leading cause of morbidity leading to
dehydration, hospital admission and death in children.
• Viral causes (rotavirus) predominate as the pathogen.
• Initial management rely on assessment of severity of dehydration and fluid
replacement.
• Early refeeding
• Antibiotic are needed only in some bacterial and parasitic infections.
• Probiotics, prebiotics and zinc reduce the duration and severity of
symptoms.
• Honey, amazingly contain all these substances.
• Yogurt, banana and boiled rice are also best natural therapy to treat acute
gastroenteritis.
• Hand washing has pivotal role in preventing gastroenteritis.
• Practicing golden teaching of Islam related to personal hygiene (Wudu) and
food (halal) can save us not only from gastroenteritis rather numerous
other diseases.

25. Acute rheumatic fever
(ARF)

26. Introduction
• Acute rheumatic fever (ARF) is a systemic illness
• Occurs 2-4 weeks after pharyngitis in some people
• Due to cross-reactivity to group A β-
haemolytic streptococcus (GAS), also called Streptococcus
pyogenes.

27. Epidemiology
• 4 million children affected worldwide
• 94% of cases are in developing countries
• Most common in tropical countries with no seasonal variation
• More common in females

28. Pathophysiology
• Streptococcus pyogenes is a gram-positive cocci and it produces
two cytolytic toxins: streptolysin O and S.
• Rheumatogenic strains of GAS contain M proteins in their cell wall
and are immunogenic.
• B cells are stimulated to produce anti-M protein antibodies against
the infection which also cross react with other tissues
• e.g. that of the heart (causing rheumatic heart
disease), brain, joints and skin leading to a constellation of
multiorgan signs and symptoms.
• This is also exacerbated by production of activated cross reactive T-
cells

29. Risk Factors
• Children and young people
• Poverty
• Overcrowded and poor hygiene places
• Family history of rheumatic fever
• D8/17 B cell antigen positivity

30. Clinical Features
• The Revised Jones Diagnostic Criteria describes the key
clinical features that may be present.
• In addition to this, you may elicit from the history that they had
a recent sore throat or scarlet fever.
• Also, in severe acute rheumatic failure, a heart murmur might
be heard on examination and it is most commonly the mitral
valve, which is affected.

31. Diagnostic Requirements
• Positive throat culture for Group A β-haemolytic streptococcus
or elevated anti-streptolysin O (ASO) or anti-
deoxyribonuclease B (anti-DNASE B) titre.
• AND
• 2 major criteria OR 1 major and 2 minor criteria present for
initial ARF. (Same criteria for recurrent ARF plus can also be
just 3 minor criteria)

32. Diagnostic Criteria
• Major Criteria (SPECS)
• Sydenham’s chorea
• Polyarthritis
• Erythema marginatum
• Carditis
• Subcutaneous nodules
• Minor Criteria (CAPE)
• CRP or ESR – Raised acute
phase reactant
• Arthralgia
• Pyrexia/Fever
• ECG – Prolonged PR interval

33. Erythema
marginatum
Erythema marginatum is an evanescent
(short lived), pink, nonpruritic,
nontender rash that involves the trunk
and sometimes the limbs but not the
face.
It is strongly associated with carditis. The
lesion is also known as “erythema
annulare” because its margins often
assume the form of a ring.

34. Investigations
• Bloods: ESR, CRP, FBC (WBC),
• Blood cultures to exclude sepsis
• Rapid Antigen Detection Test
• Throat culture: may be negative by the time rheumatic fever
symptoms occur
• Anti-streptococcal serology: ASO and anti-DNASE B titres
• ECG: prolonged PR interval
• CXR if carditis is suspected: congestive heart failure may be seen in
ARF due to valvular damage
• Echocardiography

35. Management
• Initial management in confirmed rheumatic fever
1.Antibiotics e.g. benzathine benzylpenicillin (1st choice due
to its long acting property, serving the purpose of GAS
eradication and secondary prophylaxis),
phenoxymethylpenicillin , amoxicillin. In confirmed penicillin
allergy, alternatives macrolides and clindamycin
2.Aspirin or NSAIDs e.g. naproxen or ibuprofen
3.Assess for emergency valve replacement
4.In severe carditis (e.g. congestive cardiac failure or 3rd degree
heart block) glucocorticoids and diuretics may be required

36. Definitive and Long‐term management
• Secondary prophylaxis with intramuscular Benzathine
benzylpenicillin every 3-4 weeks, oral Phenoxymethylpenicillin
twice daily, oral sulfadiazine daily, or oral azithromycin (in
penicillin allergy)

37. Complications and Prognosis
• 2% of the population can get permanent damage to heart
valves and chronic rheumatic heart disease
• With treatment ARF should resolve within 2 weeks but cardiac
inflammation may take months to resolve fully and thus, it is
common for patients to relapse within this time