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7.gastrointestinal Infections

Acute gastrointestinal infections, particularly diarrhea, are prevalent worldwide, especially among children under five, who face higher mortality risks from dehydrating diarrhea. The document distinguishes between watery and inflammatory diarrhea, detailing their causes, symptoms, and treatments, including specific pathogens like Shigella, Salmonella, and E. coli. It also covers the pathophysiology, clinical presentation, and management strategies for various gastrointestinal infections, emphasizing the importance of fluid replacement and appropriate antibiotic use in severe cases.

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0% found this document useful (0 votes)
15 views53 pages

7.gastrointestinal Infections

Acute gastrointestinal infections, particularly diarrhea, are prevalent worldwide, especially among children under five, who face higher mortality risks from dehydrating diarrhea. The document distinguishes between watery and inflammatory diarrhea, detailing their causes, symptoms, and treatments, including specific pathogens like Shigella, Salmonella, and E. coli. It also covers the pathophysiology, clinical presentation, and management strategies for various gastrointestinal infections, emphasizing the importance of fluid replacement and appropriate antibiotic use in severe cases.

Uploaded by

addadda48
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Gastrointestinal infections

1
2 Introduction
 Acute gastrointestinal illnesses rank second only to acute
upper respiratory illnesses as the most common diseases
worldwide

 The incidence of diarrhea for all children under 5 years is


estimated to be 2.9 episodes per child per year

 Younger children also have a higher risk of death from


acute dehydrating diarrhea, and diarrheal disease
3
Cont.
 Gastroenteritis is an illness characterized by diarrhea which may
be accompanied by nausea, vomiting, fever, and abdominal pain.

 Diarrhea is usually defined as a decrease in consistency of bowel


movements (i.e., unformed stool) and an increase of stools to ≥3
per day.

 For best diagnosis and management, it is important to distinguish


secretory diarrhea that produces watery diarrhea from
inflammatory diarrhea.

 inflammatory diarrhea caused by invasive pathogens, often


presents as fever, tenesmus, or bloody stool.
Watery vs. Inflammatory diarrhea

Watery Inflammatory
Percentage of patients 90 5–10
Stools
Appearance Watery Bloody
Volume Increased: ++/+++ Increased: +/++
Number per day <10 >10
pH 5.0–7.5 6.0–7.5
Occult blood Negative Positive
Fecal PMN cells Absent or few Many
Watery vs. Inflammatory

Watery Inflammatory

Mechanisms Production of toxins Mucosal invasion

Complications

Dehydration Could be severe Mild

Others Acidosis, shock, Tenesmus, rectal pro-


electrolyte imbalance lapse, seizures
Watery Inflammatory
Etiology Vibrio cholerae Shigella
Enterotoxigenic Escherichia coli Salmonella
(ETEC)
Enteropathogenic E. coli (EPEC) Campylobacter

Rotaviruses Yersinia
Noroviruses Enterohemorrhagic E. coli
(EHEC)
Enteroinvasive E. coli (EIEC)
Enteroaggregative E. coli (EAEC)

Cytotoxigenic C. difficile
7 Bacillary Dysentery (Shigellosis)

 The shigellae are gram-negative bacilli belonging to the


family Enterobacteriaceae.

 usually affects children 6 months to 10 yrs of age.

 more common in daycare centers and in areas with crowded


living conditions or poor sanitation

 transmitted through the fecal–oral route

 the bacteria multiply and spread within the submucosa of


the small bowel
8 Pathogenesis
 Infection with Shigella occurs after ingestion of as few as 10 to 100
organisms

 Shigella strains invade intestinal epithelial cells, with subsequent


multiplication, inflammation, and destruction.

 This organism only rarely invades the bloodstream;


 But bacteremia may occur in malnourished children and in
immunocompromised patient

 Symptoms develop in about 3 days (range, 1–7) after contracting the


bacteria.
9 Clinical presentation and Diagnosis

 Early—high fever, bloody diarrhea

 Later— colitis develops with urgency, tenesmus, and


dysentery, low-grade fever, vomiting

 Diagnosis

Stool examination (show leukocytosis, RBC)


10
Cont.
v Complication

proctitis (infant and young children)

intestinal obstruction

colonic perforation

bacteremia

metabolic disturbance
11 Treatment
 Infection with shigella is generally self-limited but
antibiotic therapy is indicated to shorten duration of illness
and to reduces the risk of transmission

 First-line drug: is ciprofloxacin

 Children : Ceftriaxone/Azithromycin

 Duration of treatment: five days


12 Salmonellosis

 Salmonella enterica are gram-negative bacilli belonging


to the family Enterobacteriaceae

 Non-typhoidal Salmonella (NTS) are important causes


of food-borne infection.
13 Cont.
 Risk factors

P extremes of age

P alteration of endogenous GI flora due to ab use

P acid suppressive therapy

P diabetes , malignancy, HIV

P immune suppressive therapy


14 Pathogenesis

 The inoculum necessary for clinical illness is estimated to be


106 organisms

 Once ingested and successfully beyond host defense


mechanisms organisms can attach and invade the distal
ileum and proximal colon.

 Gastroenteritis often is characterized by massive neutrophil


infiltration followed by lymphocytes and macrophages
15 Cont.

 Release of toxic substances by neutrophils may contribute


to inflammation and result in:

Ø tissue damage,

Ø fluid secretion, or

Ø leakage across the intestinal mucosa


16 Clinical presentation
 Most patients experience symptoms within 48 hours of ingestion of
contaminated food or water.

 Patients often complain of nausea and vomiting followed by


abdominal cramps, headache, fever, and diarrhea

 bacteremia is the most common complication of gastroenteritis.

 High-risk patients include

 Infants,

 Elderly, and

 Patients with immunosuppression


17 Treatment

 Salmonella gastroenteritis is usually self-limited,

fluid and electrolyte replacement is the primary


mode of treatment

most patients respond well to ORT


18
Cont.
 Antibiotic therapy

used in high-risk patients

neonates or infants

persons older than age 50 years

immunodeficiency

Ciprofloxacin for 5–7 days is recommended.

Alternatives: azithromycin, Cotrimoxazole


19
Campylobacteriosis

 Campylobacter jejuni is the most commonly identified


cause of bacterial diarrhea worldwide.

 is primarily a pediatric disease


20
Cont.
Risk factors

P contaminated foods of animal origin

P unpasteurized milk

P contaminated water

P contact with farm animals and pets

P use of antimicrobial therapy

P foreign travel

P poor sanitation
21 Pathophysiology

P Campylobacter spp. are gram-negative bacilli

P are sensitive to stomach acidity; as a result, diseases or


medications that buffer gastric acidity may increase the
risk of infection

P after an incubation period, infection is established in the


jejunum, ileum, colon, and rectum
22
Clinical presentation
 Incubation period of 1 to 7 days.

 fever, headache, and myalgias is followed by crampy


abdominal pain, and several bowel movements

 Abdominal pain is more prevalent in Campylobacter


infection than shigella/salmonella

 Tenesmus occurs in approximately 25% of patients.

 Diagnosis of Campylobacter is established by stool culture.


23 Treatment

 Fluid replacement is the cornerstone of therapy

 Antibiotic therapy should be considered in patients with

 high fevers, bloody stools, symptoms lasting longer


than 1 week, pregnancy,

Immunocompromising conditions
24
Cont.
 First line: Macrolides

 Alternative: fluoroquinolone

 N:B antimotility agents should be avoided

Prolong the duration of symptoms and associated with


worse outcomes
25 Escherichia Coli
 Diarrheagenic E. coli is differentiated into several distinct
categories based on pathogenic features of diarrheal disease:

Enterotoxigenic E. coli (ETEC)

Enteropathogenic E. coli (EPEC)

Enteroinvasive E. coli (EIEC)

Enteroaggregative E. coli (EAEC)

Enterohemorrhagic E. coli (EHEC)


26 Cont.

 The most common diarrheagenic E. coli infection is


caused by ETEC manifested by watery (enterotoxigenic)
diarrhea.

 Dysentery is caused by EHEC.

 Infections with EIEC and EPEC are primarily a disease of


children in developing countries.

 EAEC strains are implicated in persistent diarrhea ( ≥14


days) in HIV-infected patients.
27
Pathogenesis

 Enterotoxigenic E. coli are capable of producing


enterotoxins

 luminal accumulation of electrolytes that draws water into


the intestine, and production of a cholera-like secretory
diarrhea

 EHEC is able to produce shiga-like toxins

 the cytotoxic effect of shiga-like toxins disrupts the mucosal


integrity of the large intestine, causing diarrhea
28 Clinical presentation
 ETEC:

 watery stools, nausea and abdominal cramp

 abrupt in onset and resolves within 24 to 48 hours without complication

 EHEC:

 as many as 12 bloody stools per day

 cramping abdominal pain, abdominal distension

 nausea occurs in about two-thirds of patients, and vomiting occurs in


less than half.

 the white blood cell count is elevated and accompanied by a left shift
29 Cont.
 EPEC

Acute onset of profuse watery diarrhea, vomiting, and


low-grade fever.
 EAEC

Persistent, watery, mucoid, secretory diarrhea with low-


grade fever
 EIEC
Presents most commonly as watery diarrhea
30 Treatment

 Prevent dehydration by correcting fluid and electrolyte


imbalances.

 ETEC: antibiotics are rarely needed except in severe cases.


Recommended antibiotics include TMP-SMX and
quinolones
31 Cont.

 EHEC: the only recommended treatment is supportive,


including fluid and electrolyte replacement

antibiotics are CI because they can induce the


expression and release of toxin.

antimotility agents should be avoided because they


delay clearance of the pathogen and toxin,
32 Cholera (Vibrio Cholerae)

 is caused by the bacterium vibrio cholerae that leads to a


massive loss of fluid loss

results in life-threatening dehydration

 cholera can be transmitted by contaminated water or food

 A relatively large inoculum of 10 3 to 10 6 organisms is


required for infection if water is the vehicle, and 102 to 104
if the vehicle is food.
33 Pathophysiology

 vibrios cholerae is a gram-negative bacillus

 pathology of cholera results from an enterotoxin (cholera


toxin) produced by the bacteria

 vibrios pass through the stomach to colonize the upper small


intestine.

They possess filamentous protein extensions that attach to


receptors on the intestinal mucosa, and

their motility assists with penetration of the mucus layer


34 Cont.
 The enterotoxin causes an increase in cyclic adenosine
monophosphate (cAMP), and results in inhibition of sodium
and chloride absorption by microvilli

 The net effect of the cholera toxin is isotonic fluid secretion


by SI that exceeds the absorptive capacity of duodenum

 This results in the production of watery diarrhea with


electrolyte concentrations similar to that of plasma.
35 Clinical presentation
Diarrhea:

 patients may lose up to 1 L of isotonic fluid


every hour

the onset of diarrhea is abrupt

is followed rapidly or sometimes preceded by


vomiting
36 Cont.
 Fever: < 5% of patients

 Abdominal distension and ileus

 Laboratory abnormalities: increased RBC volume and


total protein, magnesium, and calcium levels
37 Complication

 Hypoglycemia

 Seizures

 Fever

 Mental alterations

 Metabolic acidosis

 Prerenal azotemia

 Aspiration pneumonia
38 Treatment

 Goals of therapy

rapid restoration of fluid losses,

correction of metabolic acidosis, and

replacement of potassium deficiency


39
Cont.

 Rehydration

Mild cases:

ORS; for children: < 2yrs: 50 – 100ml; 2-10yrs: 100


– 200ml after each loose stool.

For severe cases: Ringer lactate/NS 50-100ml/min until


shock is reversed;
40 Cont.
 Antibiotics are not necessary in most cholera cases

 However, in severe cases, antibiotics shorten the duration of diarrhea,


decrease fluid loss, and shorten the duration of the carrier state.

 A single dose of

 Doxycycline

 Ciprofloxacin

 Erythromycin/azithromycin

 Cotrimoxazole
41 Prevention
 ensuring a safe water supply

 safe food preparation,

 improving sanitation, and

 patient education

 Vaccination

In high-risk groups, such as children and patients


infected with HIV, in countries where the disease is
endemic.
42 Clostridium difficile infection

 C. difficile is the primary cause of hospital-acquired


infectious diarrhea in hospitalized patients, including
children

 C. difficile, a gram-positive, spore-forming anaerobe, is


spread by the fecal–oral route
43 Pathophysiology

 the organism is ingested either as the vegetative form or


spores, which can survive for long periods

 once the GI tract is colonized with spores, disruption of the


gut flora, which occurs with antibiotic therapy, allows C.
difficile to proliferate.

 toxin production is responsible for the inflammation, fluid


and mucus secretion and mucosal damage
44
Risk factors
Common risk factors include

increasing age

severe underlying illness

ICU admission

gastric acid suppression

exposure to broad spectrum antimicrobials


45
Clinical presentation
 Symptoms can start as first day of antibiotic therapy or
several weeks after antibiotic therapy is completed

 Colitis

p r o f u s e , w a t e r y d i a r r h e a , a b d o m i n a l p a i n ,
abdominal distention, nausea, and anorexia

left or right lower quadrant abdominal pain


46
Cont.
 toxic megacolon: suggested by acute dilation of the
colon to a diameter greater than 6 cm

 fulminant colitis: Acute abdomen and systemic


symptoms such as fever, tachycardia, dehydration, and
hypotension
47 Treatment

 Patients who develop CDI while receiving an antibiotic


should have the antibiotic discontinued, if possible or
switch to an agent with a lower risk of CDI.
48
Cont.
First line

mild- moderate disease

 Metronidazole(500 mg orally TID 7–14 days; or,30 mg/kg/day


divided q 6 hr for children)

Severe disease (WBC greater than 15,000 cells/mm3)

 oral vancomycin (125 mg qid for 7-14 days or, 40-50


mg/kg/day divided q 6hr for children)

 use of antimotility agents should be avoided since they may


precipitate toxic megacolon.
49
Viral gastroenteritis
 Viruses are the most common cause of diarrheal illness in
the world

 Many viruses may cause gastroenteritis, including


rotaviruses, noroviruses, astroviruses, enteric adenoviruses,
and coronaviruses
50

Agents Responsible for Acute Viral Gastroenteritis and Diarrhea


Virus Peak age Transmission Symptoms

Rotavirus 6month -2 Fecal–oral, water, Diarrhea, vomiting, fever,


years food abdominal pain

Adenovirus <2 years Fecal–oral Diarrhea, respiratory symptoms,


vomiting, fever

Astrovirus < 7 years Fecal–oral, water Vomiting, diarrhea, fever,


abdominal pain

Noroviruses > 5 years Fecal–oral, food Nausea, vomiting, diarrhea,


abdominal cramps, headache,
fever, chills, myalgia
51
Cont.
Rotavirus

 is a double-stranded, RNA virus accounts for the most


common cause of infectious diarrhea in children

 The cornerstone of rotavirus treatment is supportive


care and rehydration with ORT or IV fluids.

IV hydration in case of shock, severe emesis, and


high stool output (>10 mL/kg/hr).
52
Cont.

 antimotility agents should be avoided

 zinc supplementation: shorten the duration and


frequency of diarrhea

Dose: ≤6 month 10mg/d for 10 days

> 6 month 20mg/d for 10 days


53 Prevention

 Promotion of exclusive breast-feeding (prevent through


promotion of passive immunity)

 Improved complementary feeding practices

malnutrition is an independent risk for the frequency and


severity of diarrheal illness

 Improved water and sanitary facilities

 Promotion of personal and domestic hygiene

 Rotavirus immunization

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