Gastroenteritis

 One of the primary concerns related to
gastrointestinal (GI)infection, regardless of the cause,
is dehydration, which is the second leading cause of
worldwide morbidity and mortality.
 Worldwide, dehydration is especially problematic for
children younger than age 5.
 However, the highest rate of death occurs among the
elderly.
 Rehydration is the foundation of therapy for GI
infections, and oral rehydration therapy (ORT) is
usually preferred.

 Gastroenteritis, also known as infectious
diarrhea and gastro, is inflammation of
the gastrointestinal tract—the stomach and intestine.
 Diarrhea is defined as the production of stool of
abnormally loose consistency, usually associated with
excessive frequency of defecation and excessive stool
output.
 Acute Diarrhea lasts 14 days or less.
 Persistent Diarrhea lasts more than 14 days.
 Chronic Diarrhea lasts more than 1 month.

 Dysentery is defined as frequent, small bowel movements
accompanied by blood and mucus with tenesmus or pain
on defecation.
 Antibiotic-associated diarrhea is defined as unexplained
diarrhea that occurs in association with the administration
of antibotic.
 The antimicrobials most frequently implicated include
CLINDAMYCIN, PENICILLINS, AND
CEPHALOSPORINS, although almost all antibiotic classes
have been reported to cause diarrhea.
 Clostridium Difficile associated diarrhea(CDAD) is caused
by spore forming, gram positive bacillus C.difficile.

 Gastroenteritis is usually caused by viruses.
 However, bacteria, parasites, and fungus can also cause
gastroenteritis.
 In children, rotavirus is the most common cause of severe disease.
 In adults, norovirus and Campylobacter are common causes.
 Eating improperly prepared food, drinking contaminated water or
close contact with a person who is infected can spread the disease.
 Diarrheal disease or Gastroenteritis is the 4th leading cause of death
worldwide, with more than 3 millions deaths per year.
 For children less than 5 years old, diarrheal disease accounts for 21%
of all deaths.
 In hospitalized patients, Clostridium difficile is an important comial
pathogen associated with antibiotic-related diarrhea.

 CAUSATIVE ORGANISMS OF INFECTIOUS DIARRHEA
VIRUS(COMMON) BACTERIA(COMMON)
Adenovirus Campylobacter
Astrovirus Escherichia Coli
Calcivirus Salmonella
Rotavirus Shigella

 CAUSATIVE ORGANISMS OF INFECTIOUS DIARRHEA
VIRUS(UNCOMMON) BACTERIA(UNCOMMON)
Aichivirus Aeromonas
Coronavirus Chlamydia
HIV Clostridium difficile, Staphylococcus
aureus
Torovirus Vibrio

 Viruses that cause gastro include astrovirus, rotavirus, enteric
adenovirus, and calicivirus.
 Calicivirus are generally categorized into 2 genera: “Norwalk -like
viruses”(NLV) or small round structured virus and “Sapporo –
like virus”(SLV) or typical calicivirus.
 Viruses are most common causes of gastroenteritis.
 32-42% of all are caused by viral infection.
 Calicivirus is most common virus that cause gastroenteritis.
 Rotavirus is main cause of severe diarrhea in children under 5
years of age.
 20-60% of rotavirus diarrhea requires hospitalization.
 In adults, calicivirus are the main cause of viral gastroenteritis.

 The most common bacteria responsible for food-borne
illness was Salmonella followed by Campylobacter,
Shigella, and E-Coli.
 In hospitalized patients, C.difficile accounts for
approximately 30-40% of all cases of Infectious
Diarrhea.

 Salmonella species are gram negative bacilli.
 The most common serotypes are S.Enteritidis and
S.typhimurium.
 S.enteritidis causes an estimated 2.5 million cases of
food poisoning every year.
 Chicken eggs are implicated in 82% cases.
 Alfalfa sprouts are recognized source of Salmonella
poisoning.
 S.typhi , the causative organism of typhoid fever, is
also a significant cause of infectious diarrhea.

 Shigella, nonmotile, gram negative bacilli, are classified
into 4 major subgroups, S.dystenteriae, S.flexneri, S.boydii,
and S.sonnei.
 S.dysenteriae and S.flexneri are the predominant species
worldwide.
 Infection due to Shigella are highly contagious due to low
inoculum required for infection.
 All shigella species are capable of producing a potent Shiga
Toxin with enterotoxic, cytotoxic, and neurotoxic
properties.
 Person to person spread is the most common source of
infection.

 Campylobacter species are motile, gram-negative rods.
 C.jejuni accounts for majority of cases of infectious
diarrhea.
 Cases generally arise due to outbreaks in contaminated
eggs or poultry or other meats.
 88% of chickens in retail markets are culture-positive for
Campylobacter.
 Exposure to sick pets, especially puppies, has been reported
in outbreaks.
 Due to the use of quinolones in chicken, fluoroquinolone-
resistant Campylobacter has emerged as a significant
pathogen.

 A number of cases of E.coli food poisoning have increased in the recent
years.
 Six types of E.coli have specific characteristics that enable them to
cause diarrhea in susceptible host.
 These include enterotoxigenic E.coli(ETEC), enteroinvasive E.coli
(EIEC), enterihemmorrhagic E.coli(EHEC), enteropathogenic
E.coli(EPEC), diffusely adherent E.coli(DAEC), and enteroaggregative
E.coli(EAEC).
 ETEC, the most common cause of traveler’s diarrhea, is characterized
by adherence to the gastric mucosa and production of toxins.
 EHEC is characterized by bloody diarrhea that may be complicated by
the hemolytic-uremic syndrome(HUS) or thrombotic
thrombocytopenic purpura.
 EAEC has emerged as a significant eneteric pathogen; it may be
responsible for 9-36% cases of adult traveler’s diarrhea and 20% -30%
of cases of persistent diarrhea.

 Giardia, a flagellated enteric protozoan , and
Cryptosporidium , an intracellular protozoan
parasite, are common causes of endemic and epidemic
diarrheal diseases throughout the world.
 Infection is caused by ingestion of cysts or oocytes
from infected patients.

 Infectious diarrhea involves a net fluid balance
derangement in the GI tract.
 With a normal daily fluid intake of 1.5 L along with salivary,
gastric, biliary, and pancreatic secretion, approximately 8.5
L of fluid enters the upper GI tract each day.
 In addition, a bidirectional flux of fluids occurs in the
small intestine, generally exceeding 50 L each day.
 Daily fecal fluid is normally less than 150 ml per day, which
indicates that the majority of fluids are reabsorbed, usually
in the small intestine.
 Thus, even a small derangement in fluid reabsorption can
overload the large intestine’s ability to reabsorb fluids.

 Enteric microbes can alter normal fluid reabsorption physiology
in one of the 3 ways.
 1st , noninflammatory diarrhea is characterized by a shift in the
flux of bidirectional water and electrolytes and is generally
caused by intraluminal – toxins or minimally invasive bacteria.
 2nd , inflammatory diarrhea is characterized by destruction of
the ileus or colon, usually due to cytotoxin production or direct
microbial invasion.
 Production of lipo-oxygenase or other host factors may also
contribute to the diarrhea.
 3rd, penetrating diarrhea is caused by organisms that penetrate
intact mucosa, usually in the distal small intestine, to multiply in
reticuloendothelial cells or the lymphatic system.

 A number of host and microbial properties increase the
risk for infectious diarrhea.
 Age-related susceptibility to certain pathogens is one
reason.
 For example, rotavirus generally infects young children,
whereas calicivirus is more commonly isolated from adults.
 Age –related differences are likely due to differences in
intestinal immunity as well as pathogen exposure.
 Other host factors include gastric acidity, intestinal
motility, and normal enteric flora that limits the
overgrowth of pathogenic organisms.

 Microbial factors that increase the risk of diarrhea include a
variety of toxins including neurotoxins, enterotoxins, and
cytotoxins.
 Neurotoxins, produced by S.aureus and Bacillus cereus, are
exotoxins that affects the CNS and do not directly affect fluid
secretion in the intestine.
 Enterotoxins have a direct effect on intestinal mucosa to increase
fluid secretion and cause voluminous watery diarrhea.
 Vibrio cholerae, E.coli, Salmonella, shigella, and clostridium
perfringes all produce a variety of enterotoxins.
 Cytotoxins are responsible for mucosal destruction , resulting in
inflammatory colitis.
 Entohemorrhagic E.coli(EHEC) or E.coli O157: H7 produces one
or two cytotoxins that causes hemorrhagic colitis or HUS.

 Infectious diarrhea is generally classified into non-
inflammatory or inflammatory diarrhea.
 Inflammatory diarrhea is characterized by bloody,
purulent, mucoid stools and is often accompanied by
tenesmus, fever, and abdominal pain.
 Non-inflammatory diarrhea is generally less severe; typical
signs and symptoms include watery diarrhea without fever,
abdominal pain, fecal WBC, or occult blood.
 S.aureus, B.cereus, or C.perfringes generally causes non-
inflammatory diarrhea.
 Inflammatory diarrhea is generally caused by Vibrio,
shigella, E.coli, Campylobacter, Chlamydia, and C.difficile.

 Most cases of watery, non-inflammatory diarrhea are
self-limited and last less than 1 day.
 Typical signs and symptoms of infectious diarrhea are
based on specific pathogens.

 Human typhoid fever is a severe systemic illness caused by
Salmonella typhi.
 In the pre-antibiotic era, typhoid fever associated with a 15%-
20% mortality rate and in antibiotic resistant strains mortality
can range from 15%-30%.
 Hospitalization most often occurs in children or young adults.
 After an incubation period of 7-14 days, patients present with
fever, malaise, and influenza – like symptoms.
 Bradycardia is often reported.
 Blanching, erythematous, maculopapular lesions approximately
2-4 mm in diameter are reported in 5%-30% cases.
 Complications of typhoid fever include GI bleeding, CNS
manifestation , and death.

 HUS is defined as the presence if microangiopathic
hemolytic anemia, acute renal failure, and
thrombocytopenia.
 The most common cause of HUS is shiga-toxin
producing E.coli(STEC) serotype O157:H7.
 Cattle have been recognized as the main source of
E.Coli O157:H7, although other animals, including
sheep, pigs, and deer , are also recognized.

 Clinical evaluation (MHx, Physical Examination)
 Finding suggestive of gastroenteritis include:
 Copious, watery diarrhea.
 Ingestion of potentially contaminated food.
 Untreated water.
 Recent travel.
 Contact with similarly ill people.

 If a rectal examination shows occult blood or if watery
diarrhea persist for more than 48 hours, stool examination
(fecal WBC, ova, parasites) and culture are indicated.
 However , for the diagnosis of giardiasis or
cryptosporidiosis, stool antigen detection using an ELISA
has a higher sensitivity.
 Rotavirus and enteric adenovirus infections can be
diagnosed using commercially available rapid assays that
detect viral antigen in the stool, but these are usually done
only to document the outbreak.
 Patients with recent antibiotic use should have a stool assay
for C.difficile toxin.

 Serum electrolytes.
 BUN
 Creatinine should be obtained to evaluate hydration
and acid-base status in patients who appear seriously
ill.
 CBC is nonspecific, although eosinophilia may
indicate parasitic infection.

 The greatest danger presented by gastroenteritis is
dehydration.
 The loss of fluids through diarrhea and vomiting can
upset the body’s electrolyte balance, leading to
potentially life-threatening problems such as
arrhythmia.
 The risk of dehydration increases as symptoms are
prolonged.
 Dehydration should be suspected if a dry mouth,
increased or excessive thirst, or scanty urination is
experienced.

 If symptoms do not resolve within a week, more
serious gastroenteritis may be involved.
 Symptoms of great concern include a high fever(102 F
or 39 c or above) , blood or mucus in diarrhea, blood in
the vomit, and severe abdominal pain or swelling.

 Treatment depends on the cause but may include:
 Plenty of fluids and Right Diet.
 Oral Rehydration drinks.
 Admission to hospital and intravenous fluid
replacement in severe cases.
 Antibiotics, if bacteria are the cause.
 Drugs to kill parasites, if parasites are the cause.
 Avoiding anti-vomiting and anti-diarrhea drugs unless
prescribed or recommended by your doctors, because
these medications will keep the infection inside your
body.

 Initial assessment should consist of an evaluation for
dehydration, duration of illness, and inflammatory
versus non-inflammatory diarrhea.
 Symptomatic therapy should be initiated, with further
management dictated by key clinical and
epidemiologic findings.
 Fecal specimens should be obtained if a patient is
experiencing severe, bloody, inflammatory, or
persistent diarrhea or if an outbreak is suspected.

 ORAL REHYDRATION THERAPY
 The most common risks associated with diarrheal
diseases are dehydration and malnutrition.
 Non-cola beverages, Gatorade, fruit juices , and soup
are generally sufficient for patients with mild or
moderate diarrhea.
 For severe diarrhea, rehydration with glucose
containing oral rehydration solution(ORS) should be
instituted.

 In patients with diarrhea, nutrient-independent sodium
absorption across the intestinal epithelial cells is impaired;
however the coupled transport of glucose and sodium is
preserved.
 The original ORS contained 90 mEq/L of sodium.
 This amount was chosen as a compromise between normal
sodium loss due to infectious diarrhea in
adults(approximately 120-140 mEq/L of stool).
 The original ORS solution was estimated to have saved
millions of lives since its introduction but associated with
Hypernatremia in patients.

 Due to this concern, a new ORS formulation was
introduced in 2002.
 This solution preserves 1:1 M ratio of sodium to glucose
that is necessary for efficient transport.
 The reduced-osmolarity ORS has been shown to
decrease stool output, reduce vomiting, and reduce the
need for supplemental intravenous therapy.
 Initial treatment for severe dehydration must include
administration of a rehydration solution.

PATHOGEN 1st LINE AGENTS ALTERNATIVE AGENTS
ENTEROTOXIGENIC
DIARRHEA
VIBRIO CHOLERA
DOXYCYCLINE 300 mg single dose;
Tetracycline 500 mg orally 4 times
daily * 3 days ; or Trimethoprim-
sulfamethoxazole DS tablet twice
daily * 3 days;
Norfloxacin 400 mg orally twice
daily* 3 days or
Ciprofloxacin 500 mg orally twice
daily * 3 days or 1 g orally single dose.
Chloramphenicol 50 mg/kg IV
every 6 hours, Erythromycin
250-500 mg orally every 6-8
hours, and furazolidone.
Enterotoxigenic E.coli Norfloxacin 400 mg or
Ciprofloxacin 500 mg orally twice
daily for 3 days.
Trimethoprim-
sulfamethoxazole DS tablet
every 12 hours.
Clostridium Difficile Metronidazole 250 mg 4 times daily
to 500 mg 3 times daily for 10 days
Vancomycin 125 mg orally 4
times daily for 10 days.
Bacitracin 20,000-25,0000
units 4 times daily for 10 days.

PATHOGEN 1st LINE AGENTS ALTERNATIVE
AGENTS
INVASIVE (DYSENTERY
LIKE) Diarrhea
Shigella Species.
Trimethoprim-
every 12 hours for 3-5 days.
Ofloxacin 300 mg,
norfloxacin 400 mg or
ciprofloxacin 500 mg twice
daily for 3 days.
Salmonella Nontyphoidal Trimethoprim-
every 12 hours for 3-5 days.
OR
Ofloxacin 300 mg, norfloxacin
400 mg or ciprofloxacin 500 mg
twice daily for 3 days.
Azithromycin 1g orally 1 day,
followed by 500 mg orally once
daily for 6 days.
Enteric Fever(Typhoid) Ciprofloxacin 500 mg twice daily
for 5 days or
Ceftriaxone 2g IV daily for 5 days
or
Cefotaxime 2g IV 3 times daily for
5 days
Azithromycin 1g orally 1 day,
followed by 500 mg orally once
daily for 6 days.
Cefixime, cefotaxime, and
cefuroxime or
chloramphenicol 500 mg 4
times daily orally or IV for 14
days.

PATHOGEN 1st LINE AGENTS ALTERNATIVE
AGENTS
CAMPYLOBACTER Erythromycin 500 mg orally twice
daily for 5 days.
Azithromycin 1 g orally 1 day ,
followed by 500 mg daily for 6 days.
Norfloxacin 400 mg or
Ciprofloxacin 500 mg twice
daily for 5 days.
Traveler’s Diarrhea
Prophylaxis
Ciprofloxacin 500 mg daily for 3
days.
Rifaximin 200 mg 1-3 times a
day or 400 mg twice a day for 3
days.
Traveler’s Diarrhea
Treatment
Ciprofloxacin 500 mg twice daily
for 3 days.
Or
Trimethoprim-
orally twice daily for 3 days.
Azithromycin 500 mg orally
once daily for 3 days.
Rifaximin 200 mg 1-3 times a
day or 400 mg twice a day for 3
days.

 Shigella causes bacillary dysentery, which refers to a
diarrheal stool containing pus and blood.
 Worldwide, there are an estimated 165 million cases of
shigellosis annually with 1 million associated deaths.
 Shigellosis is a disease that mostly affects children 6
months to 10 years of age.
 Shigellosis is a serious problem in day-care centers and
areas with crowded living conditions such as urban centers.
 Most cases of shigellosis are a result of person-to-person
transmission.
 Shigella transmission from contaminated food and water,
although less common, is associated with large outbreaks.

 Shigella are nonmotile, gram-negative rods and are
members of the family Enterobacteriaceae.
 Infection with Shigella occurs after ingestion of as few as 10
to 100 organisms.
 This low dose of organisms probably explains the person-
to-person spread and the high secondary attack rate when
an index case is introduced into a family.
 Shigella strains invade intestinal epithelial cells with
subsequent multiplication, inflammation, and destruction.
 The organism infects the superficial layer of the gut, rarely
penetrates beyond the mucosa, and seldom invades the
bloodstream.
 However, bacteremia can occur in malnourished children
and immunocompromised patients.

 Biphasic illness
 Early—high fever, watery diarrhea without blood
 Later—after approximately 48 hours, colitis develops
with urgency, tenesmus, and dysentery.
 Low-grade fever
 More frequent small-volume stools (“fractional stools”)
 Abdominal cramping

 Major complications of shigellosis include:
 Proctitis or rectal prolapse (infants and young children)
 Toxic mega colon (primarily in the setting of S. dysenteriae1
infection)
 Intestinal obstruction
 Colonic perforation
 Bacteremia (more common in children)
 Metabolic disturbances
 Leukemoid reaction
 Neurologic disease
 Reactive arthritis or Reiter’s syndrome
 Hemolytic-uremic syndrome (HUS)

 Although infection with Shigella generally is self-limited
and responds to supportive care, antibiotic therapy is
indicated because it shortens the duration of illness and
shedding and consequently reduces the risk of
transmission.
 Antibiotic resistance is a worldwide concern and growing
problem for enteric bacterial pathogens.
 Currently, the treatment of choice is a fluoroquinolone
when the antibiotic susceptibility of the organism is
unknown.
 Cephalosporins or azithromycin can be used in the
management of pediatric shigellosis.

 Salmonella typhi and Salmonella paratyphi, which cause typhoid fever, have
high host specificity for humans.
 Nontyphoidal Salmonella are important causes of reportable food-borne
infection.
 There are an estimated 1.4million cases of nontyphoid Salmonella illness
annually in the United States.
 The highest incidence is in those younger than 1 year of age and older than 65
years of age or in those withHIV/AIDS.
 Outbreaks of intestinal salmonellosis have been reported owing to
unpasteurized orange juice, tomatoes, cantaloupe, alfalfa sprouts, and cilantro.
 Exotic pets, especially reptiles (e.g., snakes, turtles, and iguanas), are an
increasing source of human salmonellosis, accounting for an estimated 3% to
5% of all cases.
 Risk factors for salmonellosis include extremes of age, alteration of the
endogenous bowel flora of the intestine (e.g., as a result of antimicrobial
therapy or surgery), diabetes, malignancy, rheumatologic disorders, human
immunodeficiency virus (HIV) infection, and therapeutic immunosuppression
of all types.

 Salmonella are motile, gram-negative bacilli.
 In salmonellosis, the organisms penetrate the
epithelial lining to the lamina propia with production
of diffuse inflammation.
 The distal ileum and colon are sites of infection.

 Gastroenteritis
 Onset 8 to 48 hours after ingestion of contaminated food.
 Fever, diarrhea, and cramping
 Stools are loose, of moderate volume, and without blood.
 Headache, myalgia, and other systemic symptoms can
occur.
 Diagnosis relies on isolation of the organism from stool or
ingested food.
 Certain underlying conditions (e.g., AIDS, inflammatory
bowel disease, and prior gastric surgery) predispose the
patient to more severe disease.

 Enteric Fever
 Febrile illness 5 to 21 days after ingestion of contaminated
food or water.
 Chills, diaphoresis, headache, anorexia, cough, weakness,
sore throat, dizziness, and muscle pains are frequently
present before the onset of fever.
 Diarrhea is an early symptom and occurs only in 50% of
cases.
 Intestinal hemorrhage or perforation, leucopenia, anemia,
and subclinical disseminated intravascular coagulopathy
may be seen.
 Culture of stool, blood, or bone marrow for Salmonella
species is helpful.

 Gastroenteritis
 Salmonella gastroenteritis is usually self-limited, and
antibiotics have no proven value.
 Patients respond well to ORT.
 Symptoms typically diminish in 3 to 7 days without
sequelae.
 Antibiotic use may result in a higher rate of chronic
carriage and relapse.
 Antimicrobial use should be limited to preemptive therapy
among patients at higher risk for extra-intestinal spread or
invasive disease.
 Antimotility agents should not be used.

 Enteric Fever(Typhoid)
 The current drug of choice for typhoid fever is a fluoro-quinolone, such
as ciprofloxacin.
 The recommended dose of ciprofloxacin for uncomplicated typhoid is
500 mg orally twice daily for 5 to 7 days.
 Drug resistance is a recognized problem in the Indian subcontinent,
Southeast Asia, Mexico, the Arabian Gulf, and Africa.
 All S. typhi isolates should be screened for nalidixic acid and
fluoroquinolone resistance.
 If nalidixic acid resistance is present, the patient should be given
higher doses of ciprofloxacin or ofloxacin (10 mg/kg twice daily) for 10
to 14 days.
 A third-generation cephalosporin and azithromycin (1000 mg once on
day 1 followed by 5 days of 500 mg daily) are alternative agents for S.
typhi strains.

 Patients with complicated typhoid fever (i.e., metastatic
foci, ileal perforation, etc.) should receive parenteral
therapy with ciprofloxacin 400 mg twice daily or
ceftriaxone 2000 mg once daily.
 Antimicrobial therapy can be completed with an oral agent
after initial control of the symptoms of typhoid fever.
 In persons with AIDS and a first episode of Salmonella
bacteremia, a longer duration of antibiotic therapy (1–2
weeks of parenteral therapy followed by 4 weeks of oral
fluoroquinolone) is recommended to prevent relapse of
bacteremia.

 Three typhoid vaccines are available currently for use: (1)
an oral live-attenuated vaccine (VivotifBerna-TM vaccine,
Swiss Serum and Vaccine Institute),
 (2) aparenteral heat-phenol-inactivated vaccine (Typhoid
Vaccine,Wyeth-Ayerst), and
 (3) a parenteral capsular polysaccharide vaccine (Typhim
Vi, Pasteur Merieux).
 Immunization is recommended only for travelers going to
endemic areas such as Latin America, Asia, and Africa;
household contacts of a chronic carrier; and laboratory
personnel who frequently work with S. typhi.

 Campylobacter jejuniis the most commonly identified bacterial cause
of diarrhea worldwide.
 Risk factors for Campylobacter infection include consumption of
chicken, sausage, red meat, and contaminated water; foreign travel;
receipt of an antimicrobial agent; household exposure to chickens; and
contact with pets (especially birds and cats).
 Between 25% and 50% of C. jejuni infections appear to be related to
chicken exposure or consumption.
 The age and sex distributions of Campylobacter infections are unique
among bacterial enteric pathogens.
 In developed countries, there are two age peaks: younger than 1 year of
age and 15 to 44 years of age.
 There is a mild male predominance among infected persons. The
reason for this distinct age and sex distribution remains unknown.
 Campylobacter diarrhea is primarily a pediatric disease in developing
countries.

 Campylobacter spp. are gram-negative bacilli that have
a curved or spiral shape.
 Campylobacter are sensitive to stomach acidity; as a
result, diseases or medications that buffer gastric
acidity may increase the risk of infection.
 Data suggest that the infectious dose for C. jejuniis
similar to that for Salmonella spp.
 After an incubation period, infection is established in
the jejunum, ileum, colon, and rectum.

 Incubation period of 1 to 7 days
 Abdominal cramps, fever, and diarrhea
 Dysentery is seen in approximately 50% of cases.
 Diarrhea is either loose and watery or grossly bloody.•
 Some patients present mainly with abdominal cramps
and pain and minimal diarrhea.
 Fecal leukocytes and red blood cells (RBCs) are
detected in the stools of 75% of infected individuals.
 Diagnosis of Campylobacter is established by stool
culture.

 Extra-intestinal C. jejuni infection, including septic arthritis,
cholecystitis, pancreatitis, meningitis, endocarditis,
osteomyelitis, and neonatal sepsis, can present in three different
ways:
 1.Transient bacteremia with acute Campylobacter enteritis in a
normal host with benign course
 2. Sustained bacteremia or deep focus of infection in a previously
normal host that responds to antimicrobial therapy
 3. Sustained bacteremia or deep infection in a compromised host
 The most important post-infectious complication of C. jejuniis
Guillain-Barré syndrome (GBS).
 The risk of developing GBS is very small (less than one case of
GBS per 1000 C. jejuni).
 GBS typically occurs 1 to 3 weeks after diarrhea.

 Hydration and electrolyte balance, often with ORT, are the cornerstone of treatment.
 The specific circumstances that antibiotics should be considered include high fevers,
bloody stools, symptoms longer than 1 week, pregnancy, infection with HIV, and other
immunocompromised hosts.
 Until a few years ago, fluoroquinolones were the drug of choice for campylobacteriosis.
 However, a major problem among Campylobacter strains is growing resistance,
occurring world-wide.
 Fluoroquinolone resistance in human isolates of C. jejuniin occurs at a rate of 18%, and
resistance levels in southeast ASIA is 80%.
 Fluoroquinolones should not be used unless susceptibility is confirmed.
 Erythromycin is considered the optimal drug for treatment of Campylobacter infections.
 The rate of resistance of Campylobacterto erythromycin remains low.
 Other advantages of this drug include ease of administration, low cost, lack of major
toxicity, and narrow spectrum of activity.
 The recommended dosage for adults is 250 mg orally four times daily or 500 mg orally
twice daily for 5 to 7 days.
 For very ill patients, treatment with gentamicin, imipenem, cefotaxime, or
chloramphenicol is indicated, but susceptibility tests should be performed.

 EHEC are the pathogenic subgroup of Shiga toxin-
producing E. coli(STEC).
 Acute hemorrhagic colitis has been associated mainly with
the O157:H7 serotype.
 This serotype has been responsible for larger outbreaks of
infection, has higher rates of complications, and appears to
be more pathogenic than non-EHECSTEC strains.
 The spectrum of disease associated with E. coli O157:H7
includes bloody diarrhea, which is seen in as many as 95%
of patients, non-bloody diarrhea, hemolytic-uremic
syndrome(HUS), and thrombotic thrombocytopenic
purpura.

 The highest incidence is in patients aged 5 to 9 years and 50 to 59 years.
 Outbreaks of diarrhea due to O157:H7 E. coli and other STECs have
occurred from contaminated beef, classically hamburgers served at
fast-food chains, raw milk and other dairy products, vegetables (e.g.,
alfalfasprouts, coleslaw, and lettuce), and apple juice.
 The most important reservoir for E. coli O157:H7 is the gastrointestinal
tract of cattle.
 Person-to-person transmission is also possible because of the low
infectious dose.
 Swimming in infant pools or contaminated lakes or drinking municipal
water also appears to be a risk factor.
 The incidence of diagnosed E. coli O157:H7 infections is greater among
rural than urban populations, and E coli O157:H7 infections occur in
summer and autumn.

 The infectious dose of EHEC is very low, between 1 and 100 colony-
forming units (CFUs).
 The two major virulence factors for EHEC are the production of two
Shiga like cytotoxins (Stx I and II) and adhesion-causing attachment-
effacement (A/E)lesions.
 These Stx cytotoxins are responsible for vascular damage and systemic
effects such as HUS.
 Adhesion mediates initial attachment of EHEC to intestinal epithelial
cells.
 Following attachment, these organisms produce A/E lesions on
individual intestinal epithelial cells.
 A/E lesions infect the small or large intestine and cause diarrhea.

 Incubation period of 3 to 5 days
 Bloody stools
 Fever usually absent
 Leukocytosis.
 Abdominal tenderness
 HUS in 2% to 10% of patients (especially children
1–5years of age and the elderly in nursing
homes).Develops on average 1 week after the onset
of diarrhea.

 The only current treatment of EHEC infection is supportive, including
fluid and electrolyte replacement, often in the form of ORT.
 Most illnesses resolve in 5 to 7 days.
 Patients should be monitored for the development of HUS.
 Antibiotics are currently contraindicated because they can induce the
expression and release of toxin.
 Anti-motility agents should be avoided because they may delay
clearance of the pathogen and toxin.
 This, in turn, may increase the risk of systemic complications.
 Proper cooking of foods is essential.
 Supervision of hand washing by children in day-care centers and
exclusion of symptomatic children may reduce person-to-person
spread.

 Cholera, the first reportable disease, is endemic in South
Asia,particularly in the Ganges delta region.
 The biotypes of Vibrio cholerae responsible for pandemics are
serogroup O1 (El Tor)and serogroup O139.
 Cholera can be transmitted by water or by food contaminated with
contaminated water, particularly undercooked seafood.
 V. cholerae grows well in warm temperatures, causing marked
seasonality in the incidence of cholera.
 People of blood type O are more susceptible to El Tor vibrios than
people of other blood types.
 Inoculum size affects the likelihood and severity of cholera infection.
 The infectious dose is lower in patients who are taking antacids owing
to the neutralization of gastric acid.

 V. c holerae is a gram-negative bacillus.
 Vibrios pass through the stomach to colonize the upper small intestine.
 Vibrios have filamentous protein extensions that attach to receptors on the
intestinal mucosa, and their motility assists with penetration of the mucus
layer.
 The cholera enterotoxin consists of two sub-units, one of which (subunit A) is
transported into the cells and causes an increase in cyclic AMP, which leads to
a deluge of fluid into the small intestine.
 This large volume of fluid results in the watery diarrhea that is characteristic of
cholera.
 The stools are an electrolyte-rich isotonic fluid, the loss of which results in
blood volume depletion followed by low blood pressure and shock.
 Of note, the diarrheal fluid is highly infectious.

 Incubation period of 18 hours to 5 days
 Abrupt onset of watery diarrhea and vomiting
 Large volumes of rice-water stools
 Dehydration, may be severe.
 Patients suffering from severe dehydration owing to rapid
fluid loss are at risk for death within several hours of
disease onset.•
 Severe muscle cramps in extremities owing to the
electrolyte imbalance caused by the fluid loss.
 These cramps should resolve with treatment.
 Metabolic acidosis

 The cornerstone of cholera treatment is fluid replacement.
 Without treatment, the case-fatality rate for severe cholera is approximately
50%.
 For cholera, rice-based ORT is better than glucose-based ORT because it
reduces the number of stools.
 Patients with significant disease should receive a short antibiotic course, 1 to 3
days, to shorten the duration of illness and decrease the number of stools.
 Doxycycline 300 mg once daily is the drug of choice.
 Other antibiotics shown to be effective include erythromycin, azithromycin,
trimethoprim-sulfamethoxazole, and ciprofloxacin.
 The main prevention strategies include ensuring a safe water supply and safe
food preparation, improving sanitation, and patient education.
 Several oral vaccines are in development, and two are available.
 However, these vaccines do not provide protection against all cases of cholera
because the immunity may be over-come by high inocula.

 Travelers’ diarrhea occurs commonly when visitors from developed countries
travel to developing countries.
 Over 50 million people are at risk for travelers’ diarrhea each year.
 Travelers’ diarrhea can occur following the consumption of food or water
contaminated with bacteria, viruses, or parasites.
 Bacteria such as Shigella, Salmonella, Campylobacter, and E. coli are
responsible for 60% to 85% of the travelers’ diarrhea cases.
 Noroviruses are being recognized increasingly as a significant cause of
travelers’ diarrhea as well.
 Risky foods include tap water; uncooked foods, including seafood, fruits, and
vegetables; and foods that are stored inadequately, particularly buffet-style
meals.
 Additionally,alcohol consumption of more than five drinks per day has been
demonstrated to be a risk factor, especially in males.
 Education about the types of foods to avoid during travel canbe an effective
method of prevention.

 The goal of treatment is to maintain hydration and functional status to prevent
disruption of travel plans.
 For travelers with mild cases of diarrhea, ORT is often all that is needed.
 However, antibiotics are very effective at reducing the duration of illness.
 The use of trimethoprim-sulfamethoxazole has fallen out of favor because of the
development of resistance in many regions.
 In general, fluoroquinolones, specifically levofloxacin (500 mg once daily) and
ciprofloxacin (500 mg twice daily), are the drugs of choice for travelers’ diarrhea.
 A 24-hour regimen can be used unless the traveler has a fever or bloody stools, in which
case a 3-day regimen is necessary.
 Alternatives to fluoroquinolones should be used in Asia, where resistance is high among
Campylobacter.
 Azithromycin, as a single 1000-mg dose, represents an alternative to the fluoroquinolone
class.
 Additionally, the Food and Drug Administration (FDA) recently approved rifaximin for
the treatment of travelers’ diarrhea at a dose of 200 mg three times daily for 3 days.
 Rifaximin is not effective against C. jejuni,and efficacy has not been documented against
Salmonella or Shigella.

 C. difficile is the leading cause of nosocomial enteric infection.
 C. difficile toxins can be found in the stool of 15% to 25% of patients with
antibiotic-associated diarrhea (AAD) and more than 95% of patients with
pseudomembranous colitis.
 More than 90% of health care–associated CDAD occurs after or during
antimicrobial therapy.❺
 Clindamycin, cephalosporins, and penicillins are the antibiotics most
associated with CDAD, but almost all antimicrobial agents except
aminoglycosides have been associated with CDAD.
 Recent studies have shown fluoroquinolones to be strongly associated with
CDAD.
 Other risk factors for CDAD include increasing age, severe underlying disease,
surgical GI procedures, presence of a nasogastric tube, receipt of antiulcer
medications, stay on an intensive-care unit, long duration of hospital stay, long
duration of antibiotic, and receiving multiple antibiotics.

 The incidence of community-associated C. difficile
infection (defined as occurring in patients not
hospitalized in the year prior to diagnosis) is
increasing.
 In addition to antibiotic use, community-
associated C. difficile cases are associated with the
use of gastric acid suppressive agents (e.g., proton
pump inhibitors and H2-receptor antagonists).
 C. difficile is spread by the fecal-oral route, and
patient-to-patient transmission has been
documented.

 C. difficile is a gram-positive, spore-forming anaerobe.
 The organism is ingested either as the vegetative form or spores,which can
survive for long periods in the environment and can transverse the acidic
stomach.
 In the small intestine, spores germinate into the vegetative form.
 In the large intestine, CDAD can develop if the normal flora is disrupted by
antibiotic therapy.
 Toxin production is essential for disease to occur.
 The main virulence factor for disease related to C. difficile is the production of
toxins A and B.
 These toxins are responsible for inflammation, fluid and mucus secretion, and
mucosal damage, which lead to diarrhea or colitis.

 Symptoms can start as early as the first day of antimicrobial therapy or several
weeks after antibiotic therapy is completed.
 Diarrhea
 Acute watery diarrhea with lower abdominal pain, low-grade fever, and mild or
absent leukocytosis
 Mild, with only three or four loose watery stools per day
 C. difficile toxins are present in stool, but sigmoidoscopic examination is
normal.
 Colitis
 Profuse, watery diarrhea with 5 to 15 bowel movements per day, abdominal
pain, abdominal distention, nausea, and anorexia
 Left or right lower quadrant abdominal pain and cramps that are relieved by
passage of diarrhea
 Dehydration and low-grade fever
 Sigmoidoscopic examination may reveal a nonspecific diffuse or patchy
erythematous colitis without pseudomembranes.

 Stopping the inciting antibiotic is the most important step in the initial
treatment of CDAD.
 If stopping antibiotic therapy is not effective or not practical, antimicrobial
therapy directed specifically against C. difficile should be given for 10 days.
 Oral metronidazole (500 mg three times daily or 250 mg four times daily) and
oral vancomycin (125 mg four times daily) have similar rates of efficacy, but
metronidazole is considered the drug of choice for most cases because of cost
and concerns regarding the emergence of vancomycin-resistant enterococcus
(VRE).
 Severe disease is defined as the presence of complications of colitis, such as
sepsis, volume depletion, electrolyte imbalance, hypotension, paralytic ileus,
and toxic megacolon.
 Patients with signs of severe disease should receive oral vancomycin as initial
therapy.
 Surgical intervention may be indicated and lifesaving, particularly in cases
complicated by toxic megacolon or colonic perforation.

 In circumstances where oral therapy cannot be given, intravenous
metronidazole (500 mg every 6–8 hours), vancomycin retention enemas (500
mg every 4–8 hours).
 Antiperistaltic agents should not be given because the use of these agents is
associated with the development of toxic megacolon.
 Therapeutic response should be based on clinical signs and symptoms.
 Relapse is suggested by the returning of symptoms 3 to21 days after stopping
metronidazole or vancomycin.
 Since antibiotic resistance is not a factor in relapse, most relapses usually
respond to another course of either metronidazole or vancomycin.
 Vigilant hand washing and isolation precautions are keys to controlling C.
difficile.

 Persistent diarrhea are caused by protozoal pathogens
such as Giardia and Cryptosporidium.
 The diarrhea lasts for more than 7 days.
 Giardia infections generally respond to metronidazole.
 Cryptosporidium commonly affects
immunocompromised patients(especially AIDs
patient) and can be difficult to eradicate without
immune reconstitution.
 Nitazoxanide, a broad spectrum antiparasitic agent
has been shown to reduce oocyte shedding and hasten
resolution of shedding.

 Viruses are the most common cause of diarrheal
illness inthe world, resulting in about 4,50,000 and
16,00,000 hospitalizations for adults and children,
respectively, and over 4000 deaths.
 A number of viruses may cause gastroenteritis,
including rotaviruses, noroviruses, astroviruses,
enteric adenoviruses, and coronoviruses.

 Incubation period of 2 days
 2- to 3-day prodrome of fever and vomiting
 Profuse diarrhea without blood or leukocytes (up to
10–20 stools per day)
 Severe dehydration
 Anorexia
 Fever may be present
 Presentation in adults may vary from asymptomatic to
nonspecific symptoms of headache, malaise, and chills
to severe diarrhea, nausea, and vomiting.
 Diagnosis can be made by PCR of the stool.

 Rotavirus causes between 6,00,000 and 875,000 deaths
each year, with the highest rates in the very young and in
developingcountries.
 Rotavirus is the leading cause of childhood gastroenteritis
and death worldwide.
 Most infections occur in children between 6 months and 2
years old, typically during the winter season, but adults
may be infected as well.
 Rotavirus causes over 2 million hospitalizations and
600,000 deaths per year in children younger than 5 years of
age.
 Person-to-person transmission occurs through the fecal-
oral route

 The cornerstone of rotavirus treatment is supportive care
and rehydration with ORT or intravenous fluids if
necessary.
 Antimotility and antisecretory agents should not be used
owing to their potential side effects in children and the
self-limited nature of the disease.
 A new live oral rotavirus vaccine was approved recently by
the FDA for use in infants aged 6 weeks to 32 weeks and
provides protection against rotavirus infection for at least
24 months.
 The CDC Advisory Committee on Immunization Practices
recommends vaccination at 2, 4, and 6 months.

 Each year in the United States, approximately 76 million
food-borne illnesses occur, leading to 325,000
hospitalizations and over 5000 deaths.
 A number of bacterial and viral pathogens (e.g.,Salmonella,
Shigella, Campylobacter, E. coli, and noroviruses) can
cause food poisoning.
 Other bacteria that can cause foodborne illness include
Staphylococcus aureus, C. perfringens, C. botulinum,and
Bacillus cereus.
 Food poisoning should be suspected if at least two
individuals present with similar symptoms after the
ingestion of a common food in the prior 72 hours.

 Wash hand thoroughly with soap and water after going to
the toilet or changing nappies, after smoking, after using a
handkerchief or tissue, or after handling animals.
 Wash your hands thoroughly with soap and water before
preparing food or eating.
 Use disposable paper towels to dry your hands rather than
cloth towels, since the bacteria can survive for some time
on objects.
 Keep cold food cold(below 5 c) and hot food hot (above 60
C) to discourage growth of bacteria.
 Make sure foods are thoroughly cooked.

 Clean the toilet and bathroom regularly, especially the
toilet seat, door handles and taps.
 When travelling overseas to countries where sanitation
is suspected, only drink bottled water.
 Avoid food buffet, uncooked foods or peeled fruits and
vegetables , and ice in drinks.
 Gastroenteritis is usually resolved within 2-3 days and
there are no long-term effects.
 If dehydration occurs, recovery is extended by a few
days.

Gastroenteritis

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