Pharmacotherapy for gastroenteritis typically focuses on managing symptoms, preventing dehydration, and treating the underlying cause if it's bacterial or parasitic in nature.

1. GASTROENTERITIS
BY
SRIRAM THIRUNAVUKKARASU,
PHARM.D,

2. INTRODUCTION:
• The primary manifestation is diarrhea, but it may be accompanied by nausea, vomiting,
and abdominal pain.
• Diarrhea associated with nausea and vomiting is referred to as gastroenteritis.
Epidemiology
• Occurs worldwide
• Oral to fecal route of transmission
• Water common reservoir
• Overcrowding & poor sanitation are risk factors
• Animals may be source of infection
Diarrheal illnesses may be classified as follows:
1. Osmotic, due to an increase in the osmotic load presented to the intestinal lumen,
either through excessive intake or diminished absorption
2. Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed
3. Secretory, when increased secretory activity occurs

3. SIGNS & SYMPTOMS
• General features: diarrhea, loss of appetite, abdominal cramps, nausea, vomiting and possibly
fever
• Dysentery
• Peristaltic abdominal pain are typical. Other findings include headache, myalgia, and
hyperactive bowel sounds.
• Rotavirus gastroenteritis. This disorder commonly starts with a fever, nausea, and vomiting,
followed by diarrhea. The illness can be mild to severe and last from 3 to 9 days. Diarrhea
and vomiting may result in dehydration.
• Diarrhea secondary to gastroenteritis is the most common cause of dehydration in children,
especially up to age 2
• Enteric fevers
• Systemic with severe headache, high fever, abscesses, intestinal rupture, shock and death

4. PATHOLOGY
• The most common form of acute gastrointestinal infection is gastroenteritis, causing diarrhoea with or without
vomiting.
• Bacteria can cause diarrhoea in three different ways.
Mucosal adherence
• Most bacteria causing diarrhoea must first adhere to specific receptors on the gut mucosa.
• A number of different molecular adhesion mechanisms have been elaborated; for example, adhesions at the tip of the
pili or fimbriae which protrude from the bacterial surface aid adhesion.
• For some pathogens this is merely the prelude to invasion or toxin production but others such as enteropathogenic.
• Escherichia coli (EPEC) cause attachment-effacement mucosal lesions on electron microscopy (EM) and produce a
secretory diarrhoea directly as a result of adherence.
• Adhere in an aggregative pattern with the bacteria clumping on the cell surface and its toxin causes persistent
diarrhoea.
• Diffusely adhering E. coli (DAEC) adheres in a uniform manner and may also cause diarrhoea seen in children.

5. Mucosal invasion:
• Invasive pathogens such as Shigella spp., enteroinvasive E. coli (EIEC) and Campylobacter spp. penetrate into
the intes- tinal mucosa.
• Initial entry into the mucosal cells is facilitated by the production of ‘invasins’, which disrupt the host cell
cytoskeleton.
• Subsequent destruction of the epithelial cells allows further bacterial entry, which also causes the typical
symptoms of dysentery: low-volume bloody diarrhoea, with abdominal pain.
Toxin production :
Gastroenteritis can be caused by different types of bacterial toxins:
• Enterotoxins, produced by the bacteria adhering to the intestinal epithelium, induce excessive fluid secretion
into the bowel lumen, leading to watery diarrhoea, without physically damaging the mucosa, e.g. cholera,
enterotoxigenic E. coli (ETEC).
• Some enterotoxins preformed in the food primarily cause vomiting, e.g. Staph. aureus and Bacillus cereus.
• A typical example of this is ‘fried rice poisoning’, in which B. cereus toxin is present in cooked rice left
standing overnight at room temperature.
• Cytotoxins damage the intestinal mucosa and, in some cases, vascular endothelium as well (e.g. E. coli)

6. TOXIN PRODUCTION

8. Table 4.27 Pathogenic mechanisms of bacterial gastroenteritis
Pathogenesis mode of action clinical presentation Examples
mucosal adherence Effacement of intestinal Moderate watery diarrhoea Enteropathogenic E. coli (EPEC)
mucosa Enteroaggregative E. coli (EAggEC)
Diffusely adhering E. coli (DAEC)
mucosal invasion Penetration and Dysentery Shigella spp.
destruction of mucosa Campylobacter spp.
Enteroinvasive E. coli (EIEC)
Toxin production
Enterotoxin Fluid secretion without Profuse watery diarrhoea Vibrio cholerae
mucosal damage Salmonella spp.
Campylobacter spp.
Enterotoxigenic E. coli (ETEC)
Bacillus cereus
Staphylococcus aureus producing enterotoxin B
Clostridium perfringens type A
Cytotoxin Damage to mucosa Dysentery Salmonella spp.
Campylobacter spp.
Enterohaemorrhagic E. coli 0157 (EHEC)

9. LAB ANALYSIS:
• Markers of fecal leukocytes (lactoferrin), or occult blood suggest inflammatory
diarrhea caused by invasive pathogens.
• Pathogens commonly cultured in these patients include Shigella, Salmonella,
Campylobacter, Aeromonas, Yersinia, noncholera Vibrio, and C. difficile.
• However, the absence of leukocytes in a stool specimen does not rule out
inflammatory diarrhea.
• The mean sensitivity of fecal leukocytes for the prototypical inflammatory diarrhea
disease agent Shigella averages 73% (range, 49% to 100%).14 The absence of fecal
WBCs suggests a noninflammatory diarrhea.
• A definitive diagnosis of infectious diarrhea is often made by culture of the pathogen
or isolation of the toxin (e.g., C. difficile) from a stool sample.
• severe diarrhea; oral temperature ≥101.3°F; bloody stools; or stools containing
leukocytes, lactoferrin, or occult blood.
• More sensitive tests to diagnose parasitic infections include direct
immunofluorescence staining (DFA) to detect G. lamblia and Cryptosporidium, and
enzyme immunoassay (EIA) to detect G. lamblia and Cryptosporidium antigen.

10. TREATMENT -REHYDRATION.
• The treatment of cholera and other dehydrating diarrheal diseases was revolutionized by the promotion of oral
rehydration solutions.
• The efficacy of which depends on the fact that glucose-facilitated absorption of sodium and water in the small intestine
remains intact in the presence of cholera toxin.
• The World Health Organization recommends a solution containing 3.5 g sodium chloride, 2.5 g sodium bicarbonate, 1.5
g potassium chloride, and 20 g glucose (or 40 g sucrose) per liter of water.
• Oral rehydration solutions containing rice or cereal as the carbohydrate source may be even more effective than
glucose-based solutions, and the addition of L-histidine may reduce the frequency and volume of stool output.
• Patients who are severely dehydrated or in whom vomiting precludes the use of oral therapy should receive IV solutions
such as Ringer's lactate.
• Although most secretory forms of traveler's diarrhea—usually due to enterotoxigenic and enteroaggregative E. coli—can
be treated effectively with rehydration, bismuth subsalicylate, or antiperistaltic agents, antimicrobial agents can shorten
the duration of illness from 3–4 days to 24–36 h.
• Antibiotic treatment for children who present with bloody diarrhea raises special concerns. Laboratory studies of
enterohemorrhagic E. coli strains have demonstrated that a number of antibiotics induce replication of Shiga toxin–
producing lambdoid bacteriophages, significantly increasing toxin production by these strains.
• Clinical studies have supported these laboratory results, and antibiotics are not recommended for the treatment of
enterohemorrhagic E. coli infections in children.

12. • Loperamide should not be used by patients with fever or dysentery; its
use may prolong diarrhea in patients with infection due to Shigella or
other invasive organisms.
The recommended antibacterial drugs are as follows:
• Adults: (1) A fluoroquinolone such as ciprofloxacin, 750 mg as a single
dose or 500 mg bid for 3 days; levofloxacin, 500 mg as a single dose or
500 mg qd for 3 days; or norfloxacin, 800 mg as a single dose or 400
mg bid for 3 days. (2) Azithromycin, 1000 mg as a single dose or 500
mg qd for 3 days. (3) Rifaximin, 200 mg tid or 400 mg bid for 3 days
(not recommended for use in dysentery).
• Children: Azithromycin, 10 mg/kg on day 1, 5 mg/kg on days 2 and 3 if
diarrhea persists. Alternative agent: furazolidone, 7.5 mg/kg per day in
four divided doses for 5 days.
• All patients should take oral fluids (Pedialyte, Lytren, or flavored mineral
water) plus saltine crackers. If diarrhea becomes moderate or severe, if

13. PATIENT EDUCATION
• Patients should be educated on the importance and proper methods of oral rehydration and
early appropriate feeding.
• All patients, especially the parents of infants and young children, must be extensively educated
about the signs and symptoms of dehydration.
• Patients with food-borne exposures should be educated on deterrence.
• Immunocompromised patients and individuals with liver disease should be educated not to
consume raw shellfish, especially oysters.
• Travelers to underdeveloped areas should be made aware of proper avoidance measures,
appropriate treatment, and current endemic illnesses.
• Take enteric precautions to avoid spread to family members, especially by washing hands
before eating and after each stool or diaper change. Avoid cross-contamination of foods
during preparation (eg, cutting boards).
• Avoid raw or undercooked eggs or poultry.
• Consume acidic foods, such as citrus. Consume dry foods, such as bread and nuts and Drink
carbonated beverages.

14. THANK
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