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Infectious Diarrhea by Dr Arun Aggarwal Gastroenterologist

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Diarrhea: noninflammatory and inflammatory. Enteropathogens elicit noninflammatory diarrhea through enterotoxin production by some bacteria, destruction of villus (surface) cells by viruses, adherence by parasites, and adherence and/or translocation by bacteria. – PowerPoint PPT presentation

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Title: Infectious Diarrhea by Dr Arun Aggarwal Gastroenterologist


1
Infectious Diarrhea
  • Dr. Arun Aggarwal Gastroenterologist

2
Etiology
  • Diarrhea noninflammatory and inflammatory.
  • Enteropathogens elicit noninflammatory diarrhea
    through enterotoxin production by some bacteria,
    destruction of villus (surface) cells by viruses,
    adherence by parasites, and adherence and/or
    translocation by bacteria.
  • Inflammatory diarrhea caused by bacteria that
    invade the intestine directly or produce
    cytotoxins.

By Dr Arun Aggarwal Gastroenterologist
3
Causative Agents of Gastroenteritis
  • BACTERIA   
  • Aeromonas
  • Bacillus cereus   
  • Campylobacter jejuni   
  • Clostridium perfringens   
  • Clostridium difficile   
  • Escherichia coli   
  • Plesiomonas
  • shigelloides   
  • Salmonella   
  • Shigella   
  • Staphylococcus aureus   
  • Vibrio cholerae 01 and 0139   
  • Vibrio parahaemolyticus   
  • Yersinia enterocolitica
  • VIRUSES
  • Astroviruses  
  • Caliciviruses  
  • Norovirus   
  • Enteric adenoviruses 
  • Rotavirus  
  • Cytomegalovirus   
  • Herpes simplex viruses
  •  Balantidium coli   
  • Blastocystis hominis   
  • Cryptosporidium parvum   
  • Cyclospora cayetanensis   
  • Encephalitozoon intestinalis   
  • Entamoeba histolytica   
  • Enterocytozoon b bieneusi   
  • Giardia lamblia   
  • Isospora belli   
  • Strongyloides stercoralis   
  • Trichuris trichiura

PARASITES
By Dr Arun Aggarwal Gastroenterologist
4
  • Chronic or persistent diarrhea lasting 14 days or
    more may be due to
  • an infectious agent such as Giardia lamblia,
    Cryptosporidium parvum, and enteroaggregative or
    enteropathogenic E. coli
  • any enteropathogen that infects an
    immunocompromised host
  • residual symptoms due to damage to the intestine
    by an enteropathogen after an acute infection.

By Dr Arun Aggarwal Gastroenterologist
5
Indications for stool examination for O P
  • Pt have a history of recent travel to an endemic
    area, stool cultures are negative for other
    enteropathogens, and diarrhea persists for more
    than 1 wk
  • part of an outbreak of diarrhea
  • immunocompromised.

By Dr Arun Aggarwal Gastroenterologist
6
Epidemiology
Agent
Salmonella Poultry, egg, peanut butter, reptiles
Campylobacter Raw poultry
E. Coli Beef, spinach, milk
Yersinia Pork, iron overload (thallasemia)
V. Cholerae Iron overload ( thallassemia)
By Dr Arun Aggarwal Gastroenterologist
7
Factors that increase susceptibility to infection
with enteropathogens include
  • Young age
  • Immune deficiency
  • Measles
  • Malnutrition
  • Travel to an endemic area
  • Lack of breast-feeding
  • Exposure to unsanitary conditions
  • Ingestion of contaminated food or water
  • Level of maternal education
  • Attendance at a childcare center.

By Dr Arun Aggarwal Gastroenterologist
8
Immune-Mediated Extraintestinal Manifestations of
Enteric Pathogens
Manifestation Related Enteric Pathogen(s)
Reactive arthritis Salmonella, Shigella, Yersinia, Campylobacter, Cryptosporidium, Clostridium difficile
Guillain-Barré syndrome Campylobacter
Glomerulonephritis Shigella, Campylobacter, Yersinia
IgA nephropathy Campylobacter
Erythema nodosum Yersinia, Campylobacter, Salmonella
Hemolytic anemia Campylobacter, Yersinia
HUS S. dysenteriae , E. coli
9
Specific Pathogens
By Dr Arun Aggarwal Gastroenterologist
10
Cholera
  • Gram negative, slightly curved rod.
  • V. cholera O1 and O139 are responsible for
    causing disease.
  • The two biogroups (or biotypes) of V. cholerae O1
    are differentiated as classic and El Tor
  • V. cholerae O1 has two major O antigenic types
    (Ogawa and Inaba) and an unstable intermediate
    type (Hikojima).
  • V. cholerae O139 is closely related to the El Tor
    biotype

By Dr Arun Aggarwal Gastroenterologist
11
Epidemiology
  • Transmission is usually by fecal-oral spread with
    contaminated water.
  • Humans are the only known reservoirs of V.
    cholerae.
  • Colonization usually requires the ingestion of a
    large number of viable vibrios (gt108 viable
    units), in part, because the organisms are killed
    by acid environments including the normal
    stomach.
  • The primary mechanism of fluid loss is activation
    of adenylyl cyclase at the cytoplasmic surface of
    the basolateral membrane by the enterotoxin,
    cholera toxin.

By Dr Arun Aggarwal Gastroenterologist
12
Clinical Features
  • Profuse, painless, watery diarrhea with a
    rice-water consistency and a fishy odor,
    sometimes with flecks of mucus but no blood.
  • Fecal leukocytes are not present because V.
    cholera does not invade the mucosa.
  • Diagnosis is primarily clinical.
  • The gold standard for cholera diagnosis remains
    stool culture on TCBS medium.

By Dr Arun Aggarwal Gastroenterologist
13
Treatment
  • Rehydration is the most important treatment.
  • Antibiotics are useful in shortening the duration
    of illness, reducing the period of excretion of
    the organisms, and decreasing the requirements
    for fluid replacement.
  • Doxycycline is drug of choice, Bactrim can be
    used for lt8 yrs, quinolones are effective.

By Dr Arun Aggarwal Gastroenterologist
14
Complications
  • Lethargy, seizures, altered consciousness, fever,
    hypoglycemia, hyperglycemia, and death.
  • Inadequate fluid and electrolyte replacement may
    lead to acute tubular necrosis.
  • Hypokalemic arrhythmia can cause sudden death.
  • Children with low potassium levels can develop
    paralytic ileus and abdominal distention that can
    make oral rehydration impossible.
  • Pulmonary edema occurs in some children, probably
    because of fluid overload during rehydration.

By Dr Arun Aggarwal Gastroenterologist
15
Vaccine
  • Phenol-killed organisms administered parenterally
    as a two-dose primary series followed by boosters
    every 6 mo to maintain immunity.
  • Vaccine has about 50 efficacy by 36 mo after
    vaccination, does not protect against O139
    vibrios, and is highly reactogenic (i.e., pain,
    erythema, local induration, fever, headaches).
  • Vaccine should be used only in very high-risk
    persons (e.g., those with achlorhydria) with a
    very high probability of exposure.
  • It is not recommended for children lt6 mo of age.

By Dr Arun Aggarwal Gastroenterologist
16
Salmonella
By Dr Arun Aggarwal Gastroenterologist
17
  • Gram negative rod, dont ferment lactose, grow
    aerobically.
  • Poultry and poultry products (mainly eggs) cause
    about half of the common-source outbreaks.
  • Meats, especially beef and pork, cause about 13
    of the outbreaks, and raw or powdered milk and
    dairy products are the source of about 5 of the
    outbreaks.
  • The estimated number of bacteria that must be
    ingested to cause disease is 106108 organisms.
  • Ingested Salmonella organisms reach the stomach,
    where acid is the first protective barrier.
  • Achlorhydria, buffering medications, rapid
    gastric emptying after gastrectomy or
    gastroenterostomy, and a large inoculum enable
    viable organisms to reach the small intestine.

By Dr Arun Aggarwal Gastroenterologist
18
  • In the small and large intestines, salmonellae
    have to compete with normal bacterial flora to
    multiply and cause disease prior antibiotic
    therapy disrupts this competitive relationship.
  • After multiplication within the lumen, the
    organisms penetrate through the Peyer patches,
    typically at the distal part of the ileum and the
    proximal part of the colon.
  • Children with sickle cell disease are prone to
    Salmonella septicemia and osteomyelitis.

By Dr Arun Aggarwal Gastroenterologist
19
Clinical manifestations
  • The most common clinical presentation is acute
    enteritis.
  • After an incubation period of 672?hr (mean,
    24?hr), there is an abrupt onset of nausea,
    vomiting, and crampy abdominal pain primarily in
    the periumbilical area and right lower quadrant,
    followed by mild to severe watery diarrhea and
    sometimes by diarrhea containing blood and mucus.
  • Fever (temperature of 101102F 38.539C).
  • The stool typically contains a moderate number of
    polymorphonuclear leukocytes and occult blood.
  • Symptoms subside within 27 days in healthy
    children.

By Dr Arun Aggarwal Gastroenterologist
20
Conditions That Increase the Risk of Salmonella
Bacteremia During Salmonella Gastroenteritis
  • Neonates and young infants (3 mo of age)
  • AIDS, chronic granulomatous disease, and other
    immuno deficiencies
  • Malignancies, especially leukemia and lymphoma
  • Immunosuppressive and corticosteroid therapy
  • Hemolytic anemia, including sickle cell disease,
    malaria, and bartonellosis
  • Collagen vascular disease
  • Inflammatory bowel disease
  • Gastrectomy or gastroenterostomy
  • Achlorhydria or antacid medication use
  • Impaired intestinal motility
  • Schistosomiasis
  • Malnutrition

By Dr Arun Aggarwal Gastroenterologist
21
  • Diagnosis stool culture, rectal swab, latex
    agglutination, serological assays
  • Treatment correction of dehydration and
    electrolyte disturbances.
  • Antibiotics ampicillin, bactrim, cefotaxime,
    ceftriaxone, quinolones

By Dr Arun Aggarwal Gastroenterologist
22
  • In patients with gastroenteritis, antimicrobial
    agents do not shorten the clinical course, nor do
    they eliminate fecal excretion of Salmonella.
  • By suppressing normal intestinal flora,
    antimicrobial agents may prolong the excretion of
    Salmonella and increase the risk of creating the
    chronic carrier state.
  • Antibiotics therefore are not indicated routinely
    in treating Salmonella gastroenteritis.
  • They should be used in infants (3 mo of age) and
    other children who are at increased risk of a
    disseminated disease . (previous table)

By Dr Arun Aggarwal Gastroenterologist
23
Shigella
By Dr Arun Aggarwal Gastroenterologist
24
  • Four species of Shigella are responsible for
    shigellosis S. dysenteriae (serogroup A), S.
    flexneri (serogroup B), S. boydii (serogroup C),
    and S. sonnei (serogroup D).
  • Contaminated food (often a salad or other item
    requiring extensive handling of the ingredients)
    and water are important vectors.
  • Person-to-person transmission is probably the
    major mechanism of infection.
  • Shigellae require very low inocula to cause
    illness. Ingestion of as few as 10 S. dysenteriae
    serotype 1 organisms can cause dysentery.

By Dr Arun Aggarwal Gastroenterologist
25
  • The basic virulence trait shared by all shigellae
    is the ability to invade intestine.
  • The pathologic changes of shigellosis take place
    primarily in the colon.
  • Secretory IgA and serum antibodies develop within
    days to weeks after infection with Shigella.
    (protection is serotype specific).

By Dr Arun Aggarwal Gastroenterologist
26
  • Incubation period 12?hr to several days.
  • Severe abdominal pain, high fever, emesis,
    anorexia, generalized toxicity, urgency, and
    painful defecation characteristically occur.
  • Physical examination may show abdominal
    distention and tenderness, hyperactive bowel
    sounds, and a tender rectum on digital
    examination.
  • The diarrhea may be watery and of large volume
    initially, evolving into frequent small-volume,
    bloody mucoid stools.

By Dr Arun Aggarwal Gastroenterologist
27
  • Neurologic findings occur in as many as 40 of
    hospitalized infected children.
  • Convulsions, headache, lethargy, confusion,
    nuchal rigidity, or hallucinations may be present
    before or after the onset of diarrhea.
  • The most common complication of shigellosis is
    dehydration.
  • S. dysenteriae serotype 1 infection is commonly
    complicated by hemolytic-uremic syndrome.
  • This syndrome is caused by Shiga toxinmediated
    endothelial injury.

By Dr Arun Aggarwal Gastroenterologist
28
  • Diagnosis clinical picture, stool examination,
    rectal swab, blood cultures
  • Treatment fluid and electrolytes
  • Antibiotics azithromycin, ampicillin, bactrim,
    cefixime, nalidixic acid, quinolones.

By Dr Arun Aggarwal Gastroenterologist
29
E. coli
By Dr Arun Aggarwal Gastroenterologist
30
ETEC EIEC EPEC STEC/ EHEC EAggEC
Population at risk gt1 Yr travellers gt1 yr lt2 yr 6mo- 10 yr lt1 yr travellers
Watery diarrhea
Bloody diarrhea --- --- (HUS) ---
Duration Acute Acute Acute/ persistent Acute Acute/ persistent
By Dr Arun Aggarwal Gastroenterologist
31
Camplylobacter
By Dr Arun Aggarwal Gastroenterologist
32
  • Human campylobacterioses most commonly result
    from ingestion of contaminated food or water,
    from direct contact with environmental sources
    (i.e., a pet), or from person-to-person
    transmission.

By Dr Arun Aggarwal Gastroenterologist
33
  • Patients may have loose, watery stools or bloody
    and mucus-containing stools (dysentery).
  • Fever, vomiting, malaise, and myalgia are common.
  • The abdominal pain is periumbilical.
  • Abdominal pain may mimic appendicitis or
    intussusception.
  • Persistent infection may mimic chronic IBD.

By Dr Arun Aggarwal Gastroenterologist
34
  • Diagnosis stool culture, rectal swab,
    serological studies.
  • The optimum incubation temperature for C. jejuni
    and C. coli is 42 to 43ºC as a result, the term
    "thermophilic" campylobacters is sometimes
    applied to these species.
  • Treatment
  • Fluid replacement
  • Correction of electrolytes
  • Antibiotics azithromycin, aminoglycosides,
    doxycycline, trimethoprim
  • Antibiotics are recommended for patients with the
    dysenteric form of the disease, high fever, or a
    severe course and for children who are
    immunosuppressed or have underlying diseases.

By Dr Arun Aggarwal Gastroenterologist
35
Yersinia
By Dr Arun Aggarwal Gastroenterologist
36
  • Y. enterocolitica is transmitted to humans
    through food, water, animal contact, and
    contaminated blood products.
  • The organisms most often enter by the alimentary
    tract and cause mucosal ulcerations in the ileum.
    Necrotic lesions of Peyer patches and mesenteric
    lymphadenitis occur.
  • Presentation enterocolitis with diarrhea, fever,
    and abdominal pain.
  • Acute enteritis is more common among younger
    children, and mesenteric lymphadenitis that may
    mimic appendicitis.

By Dr Arun Aggarwal Gastroenterologist
37
  • Diagnosis stool culture, rectal swab.
  • Treatment self-limiting disease and no benefit
    of antibiotic therapy is established.
  • Patients with systemic infection and very young
    children in whom septicemia is common should be
    treated.
  • Yersinia strains are sensitive to
    trimethoprim-sulfamethoxazole, aminoglycosides,
    third-generation cephalosporins, and quinolones.

By Dr Arun Aggarwal Gastroenterologist
38
  • Patients on deferoxamine should discontinue iron
    chelation therapy during treatment for Y.
    enterocolitica, especially if they have
    complicated gastrointestinal infection or
    extraintestinal infection.

By Dr Arun Aggarwal Gastroenterologist
39
C. difficile
By Dr Arun Aggarwal Gastroenterologist
40
  • C difficileassociated diarrhea, also known as
    pseudomembranous colitis or antibiotic-associated
    diarrhea, is a major cause of nosocomial
    diarrhea.
  • C. difficile is a ubiquitous spore-forming
    gram-positive anaerobic bacillus.
  • The organism produces two toxins toxin A
    (enterotoxin) acts on the intestinal mucosa to
    produce diarrhea toxin B (cytotoxin) increases
    vascular permeability in low doses and is lethal
    to experimental animals in high doses.

By Dr Arun Aggarwal Gastroenterologist
41
  • Virtually all known antibiotics have been
    implicated penicillins, broad-spectrum
    cephalosporins, and clindamycin are the most
    frequent offenders.
  • Newborns are often colonized with C. difficile
    during the first weeks of life. Carriage
    decreases to the adult rate of 13 by 2 yr of
    age.
  • Illness is unusual in neonates and infants the
    basis for this remains unknown.

By Dr Arun Aggarwal Gastroenterologist
42
  • The classic picture of pseudomembranous colitis
    is diarrhea with blood and mucus accompanied by
    fever, cramps, abdominal pain, nausea, and
    vomiting. Disease occurs during and as long as
    weeks after antibiotic therapy.
  • The diagnosis is confirmed by detecting C.
    difficile or its toxin in the stool.
  • Findings at sigmoidoscopy or colonoscopy include
    pseudomembranous nodules and plaques
    characteristic of toxin-related colitis. Fecal
    leukocytes are present in approximately one half
    of cases occult or frank blood is common.

By Dr Arun Aggarwal Gastroenterologist
43
  • The first and essential step in treatment is the
    discontinuation of the current antibiotics, if
    possible.
  • If symptoms persist, antibiotics cannot be
    discontinued, or the illness is severe, then oral
    metronidazole (2040?mg/kg/24?hr divided q 68?hr
    PO) or vancomycin (2540?mg/kg/24?hr divided q
    6?hr PO) should be given for a 710 day course.

By Dr Arun Aggarwal Gastroenterologist
44
  • The initial response rate is gt95, but 530 of
    patients have clinical relapse, usually within
    12 wk of treatment.
  • These patients should be re-evaluated and treated
    again most will respond to a second course of
    the original treatment.
  • A few patients develop multiple recurrences, with
    short-lived responses to repeated treatment.
  • Treatment strategies for these patients include
    oral cholestyramine, oral bacitracin, oral
    immunoglobulin, reconstitution of bowel flora
    with oral lactobacilli or baker's yeast, or
    instillation of fecal flora by tube feeding or
    enemas (faeces transplant).

By Dr Arun Aggarwal Gastroenterologist
45
Rota Virus
By Dr Arun Aggarwal Gastroenterologist
46
  • Rotavirus causes 3 million cases of diarrhea,
    50,000 hospitalizations, and 2040 deaths
    annually in the United States.
  • Disease tends to be most severe in patients 3-24
    months of age.
  • Infants younger than 3 mo of age are relatively
    protected by transplacental antibody and possibly
    breast-feeding.

By Dr Arun Aggarwal Gastroenterologist
47
  • The virus is shed in stool at very high
    concentration before and for days after the
    clinical illness.
  • Very few infectious virions are needed to cause
    disease in a susceptible host.
  • The gastric mucosa is not affected despite the
    commonly used term gastroenteritis.
  • Selective viral infection of intestinal villus
    tip cells thus leads to
  • an imbalance in the ratio of intestinal fluid
    absorption to secretion
  • malabsorption of complex carbohydrates,
    particularly lactose.

By Dr Arun Aggarwal Gastroenterologist
48
  • Clinical manifestations incubation period lt48
    hrs
  • mild to moderate fever and vomiting followed by
    the onset of frequent, watery stools.
  • Diagnosis Enzyme immunoassays, which offer
    approximately 90 specificity and sensitivity,
    are available for detection of group A rotavirus
    and enteric adenovirus in stool samples.
  • Laboratory findings Isotonic dehydration with
    acidosis.

By Dr Arun Aggarwal Gastroenterologist
49
Treatment
  • Avoiding and treating dehydration are the main
    goals in treatment of viral enteritis.
  • A secondary goal is maintenance of the
    nutritional status of the patient.
  • Controlled studies have shown no benefit from
    antiemetics or antidiarrheal drugs.
  • Therapy with probiotic organisms such as
    Lactobacillus species has been shown to reduce
    somewhat the intensity and duration of illness.
  • Vaccine

By Dr Arun Aggarwal Gastroenterologist
50
Amebiasis
By Dr Arun Aggarwal Gastroenterologist
51
  • Infection is established by ingestion of parasite
    cysts.
  • Cysts are resistant to environmental conditions
    such as low temperature and the concentrations of
    chlorine commonly used in water purification the
    parasite can be killed by heating to 55C.
  • Infection is not transmitted by trophozoites
    because of their rapid degeneration outside the
    body or in the low pH environment of normal
    gastric contents.
  • Food or drink contaminated with Entamoeba cysts
    and direct fecal-oral contact are the most common
    means of infection.

By Dr Arun Aggarwal Gastroenterologist
52
  • Once E. histolytica trophozoites invade the
    intestinal mucosa, they produce tissue
    destruction (ulcers).
  • The organisms multiply and spread laterally
    underneath the intestinal epithelium to produce
    characteristic flask-shaped ulcers.
  • These lesions are commonly seen in the cecum,
    transverse colon, and sigmoid colon.
  • Amebae may produce similar lytic lesions if they
    reach the liver these lesions are commonly
    called abscesses.

By Dr Arun Aggarwal Gastroenterologist
53
  • Clinical presentations range from asymptomatic
    cyst passage to amebic colitis, amebic dysentery,
    ameboma, and extraintestinal disease.
  • colicky abdominal pains and frequent bowel
    movements (68/day).
  • Stools are blood stained and contain a fair
    amount of mucus.

By Dr Arun Aggarwal Gastroenterologist
54
Hepatic Amebiasis
  • Fever is the hallmark of amebic liver abscess.
  • abdominal pain
  • distention, and enlargement and tenderness of the
    liver.
  • Changes at the base of the right lung, such as
    elevation of the diaphragm and atelectasis or
    effusion, may also occur.
  • Laboratory examination findings are a slight
    leukocytosis, moderate anemia, high ESR and
    nonspecific elevations of hepatic enzyme
    (particularly alkaline phosphatase).
  • Stool examination for amebae yields negative
    results.

By Dr Arun Aggarwal Gastroenterologist
55
  • Diagnosis is based on detecting the organisms in
    stool samples, sigmoidoscopically obtained
    smears, tissue biopsy samples, or, rarely,
    aspirates of a liver abscess.
  • The most sensitive serologic test, indirect
    hemagglutination, yields a positive result years
    after invasive infection.

By Dr Arun Aggarwal Gastroenterologist
56
  • Two types of drugs are used to treat infection
    with E. histolytica.
  • The luminal amebicides, such as iodoquinol,
    paromomycin, and diloxanide furoate, are
    primarily effective in the gut lumen.
  • Metronidazole or other nitroimidazoles,
    chloroquine, and dehydroemetine are effective in
    the treatment of invasive amebiasis.
  • All individuals with E. histolytica trophozoites
    or cysts in their stools, whether symptomatic or
    not, should be treated.
  • Invasive amebiasis of the intestine, liver, or
    other organs requires the use of metronidazole
    (3050?mg/kg/24?hr divided tid PO for 10 days.

By Dr Arun Aggarwal Gastroenterologist
57
Giardia
By Dr Arun Aggarwal Gastroenterologist
58
  • Giardia lamblia (also referred to as G.
    intestinalis and G. duodenalis) is a flagellated
    protozoan that infects the duodenum and small
    intestine.
  • Clinical manifestations range from asymptomatic
    colonization to acute or chronic diarrhea and
    malabsorption.
  • Giardia is a particularly significant pathogen in
    people with malnutrition, certain
    immunodeficiencies, and cystic fibrosis.

By Dr Arun Aggarwal Gastroenterologist
59
  • The life cycle of Giardia is composed of two
    stages trophozoites and cysts.
  • Giardia infects humans after ingestion of as few
    as 10100 cysts.
  • Cysts are passed in stools of infected
    individuals and may remain viable in water for as
    long as 2 mo.
  • Giardia cysts are relatively resistant to
    chlorination and to ultraviolet light
    irradiation. Boiling is effective for
    inactivating cysts.

By Dr Arun Aggarwal Gastroenterologist
60
Clinical Signs and Symptoms of Giardiasis
  • Symptoms
  • Frequency
  • Diarrhea
  • Malaise, weakness
  • Abdominal distention
  • Flatulence
  • Abdominal cramps
  • Nausea
  • Foul-smelling, greasy stools
  • Anorexia
  • Weight loss
  • Vomiting
  • Fever
  • Constipation
  • 64100
  • 7297
  • 4297
  • 3597
  • 4481
  • 1479
  • 1579
  • 4173
  • 5373
  • 1435
  • 028
  • 027

By Dr Arun Aggarwal Gastroenterologist
61
  • A definitive diagnosis of giardiasis is
    established by documentation of trophozoites,
    cysts, or Giardia antigens in stool specimens or
    duodenal fluid.
  • Diagnostic testing include the use of polyclonal
    antisera or monoclonal antibodies against Giardia
    organismspecific antigens in EIA or
    immunofluorescent assays.
  • PCR and gene probebased detection systems
    specific for Giardia have been used in
    environmental monitoring.

By Dr Arun Aggarwal Gastroenterologist
62
  • Asymptomatic excreters generally are not treated
    except in specific instances such as in
  • outbreak control
  • for prevention of household transmission by
    toddlers to pregnant women
  • patients with hypogammaglobulinemia or cystic
    fibrosis
  • in situations requiring oral antibiotic treatment
    where Giardia may have produced malabsorption of
    the antibiotic.

By Dr Arun Aggarwal Gastroenterologist
63
  • Metronidazole is the treatment most often
    prescribed in the United States for adults.
  • Furazolidone is less effective than metronidazole
    but is often prescribed in children because it is
    available in liquid form.
  • Paromomycin, a nonabsorbable aminoglycoside, is
    less effective than other agents but is
    recommended for treatment of pregnant women with
    giardiasis because of potential teratogenic
    effects of other agents.

By Dr Arun Aggarwal Gastroenterologist
64
Approach to diarrhea
By Dr Arun Aggarwal Gastroenterologist
65
  • Assess the degree of dehydration and provide
    fluid and electrolyte replacement,
  • Prevent spread of the enteropathogen
  • In select episodes determine the etiologic agent
    and provide specific therapy if indicated.
  • Information about oral intake, frequency and
    volume of stool output, general appearance and
    activity of the child, and frequency of urination
    must be obtained.

By Dr Arun Aggarwal Gastroenterologist
66
  • Data should be obtained about
  • childcare center attendance
  • recent travel to a diarrhea endemic area
  • use of antimicrobial agents
  • exposure to contacts with similar symptoms
  • intake of seafood, unwashed vegetables,
    unpasteurized milk, contaminated water, or
    uncooked meats.
  • Duration and severity of diarrhea
  • stool consistency
  • presence of mucus and blood
  • other associated symptomatology, such as fever,
    vomiting, and seizures.

By Dr Arun Aggarwal Gastroenterologist
67
EXAMINATION OF STOOL
  • Stool cultures should be obtained as early in the
    course of disease as possible from patients in
    whom
  • HUS is suspected,
  • in patients with bloody diarrhea,
  • if stools contain fecal leukocytes,
  • during outbreaks of diarrhea
  • in persons who have diarrhea and are
    immunosuppressed.

By Dr Arun Aggarwal Gastroenterologist
68
Adjusting Fluid Therapy in Diarrhea
  • AVERAGE COMPOSITION OF DIARRHEA
  • Sodium 55mEq/L
  • Potassium 25mEq/L
  • Bicarbonate 15mEq/L
  • APPROACH TO REPLACEMENT OF ONGOING LOSSES
  • Solution D5 1/4 NS 15mEq/L bicarbonate
    25mEq/LKCl
  •  Replace stool mL/mL every 16hr

By Dr Arun Aggarwal Gastroenterologist
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Adjusting Fluid Therapy for Emesis or Nasogastric
Losses
  • AVERAGE COMPOSITION OF GASTRIC FLUID
  • Na 60mEq/L
  • K 10mEq/L
  • Cl 90mEq/L
  • APPROACH TO REPLACEMENT OF ONGOING LOSSES
  • Solution D5 1/2 NS 10mEq/LKCl  
  •  Replace output mL/mL every 16hr

By Dr Arun Aggarwal Gastroenterologist
70
Fluid Management of Dehydration
  • Restore intravascular volume
  • Normal saline 20mL/kg over 20min (Repeat until
    intravascular volume restored)
  • Calculate 24-hr water needs
  • Calculate maintenance water
  • Calculate deficit water
  • Calculate 24-hr electrolyte needs
  • Calculate maintenance sodium and potassium
  • Calculate deficit sodium and potassium
  • Select an appropriate fluid (based on total water
    and electrolyte needs)  
  • Administer half the calculated fluid during the
    first 8hr, first subtracting any boluses from
    this amount
  • Administer the remainder over the next 16hr
  • Replace ongoing losses as they occur

By Dr Arun Aggarwal Gastroenterologist
71
Treatment of Hypernatremic Dehydration
  • Restore intravascular volume
  • Normal saline 20mL/kg over 20min (Repeat until
    intravascular volume restored)
  • Determine the time for correction based on the
    initial sodium concentration
  • Na 145157mEq/L 24hr
  • Na 158170mEq/L 48hr
  • Na 171183mEq/L 72hr 
  • Na 184196mEq/L 84hr
  • Administer fluid at a constant rate over the time
    for correction
  • Typical fluids D5 1/4 NS or D5 1/2 NS (both with
    20mEq/L KCl unless contraindicated)
  • Typical rate 1.251.5 times maintenance

By Dr Arun Aggarwal Gastroenterologist
72
Solution Glucose (mmol/L) Na (mEq/L) K (mEq/L) Cl (mEq/L) Base (mEq/L) Osmolality (mOsm/kg)
WHO solution 111 90 20 80 30 311
Rehydralyte 140 75 20 65 30 310
Pedialyte 140 45 20 35 30 250
Pediatric Electrolyte 140 45 20 35 48 250
Infalyte 70 50 25 45 34 200
Naturalyte 140 45 20 35 48 238
By Dr Arun Aggarwal Gastroenterologist
73
Prevention.
  • Patients who are hospitalized should be placed
    under contact precautions, including handwashing
    before and after patient contact, gowns when
    soiling is likely, and gloves when touching
    contaminated material.
  • Patients and their families should be educated
    about the mode of acquisition of enteropathogens
    and methods to decrease transmission.
  • Patients who attend childcare centers should be
    excluded from the center or cared for in a
    separate area until diarrhea has subsided.

By Dr Arun Aggarwal Gastroenterologist
74
Isolation
STANDARD PRECAUTIONS
  • Standard precautions, formerly known as universal
    precautions, are intended to protect health care
    workers from blood and body fluids and should be
    used whenever providing care.
  • Standard precautions involve the use of
    barriersgloves, gowns, masks, goggles, and face
    shieldsas needed to prevent transmission of
    microbes associated with contact with blood or
    body fluids.

By Dr Arun Aggarwal Gastroenterologist
75
  • Contact precautions include gowns and gloves and
    single room isolation.
  • Droplet precautions include masks for close
    contact (lt3?ft) and single room isolation.
  • Cohorting of children infected with the same
    pathogen is acceptable.
  • Airborne precautions include masks and single
    room isolation with negative-pressure
    ventilation.
  • Transmission-based precautions are continued for
    as long as a patient is considered to be
    contagious.

By Dr Arun Aggarwal Gastroenterologist
76
Questions
By Dr Arun Aggarwal Gastroenterologist
77
  • A 2-year-old child who attends day care presents
    with abdominal cramps and severe bloody diarrhea,
    which has been present for 2 days. He has no
    fever. Which infection is most consistent with
    this clinical picture
  • a. Rotavirus
  • b. Giardia lamblia
  • c. E. coli O157H7
  • d. Norvovirus infection
  • e. Shigellosis

By Dr Arun Aggarwal Gastroenterologist
78
  • A three year old has just returned from Central
    America. You see him after five days of fever
    diarrhea which is described as green, bloody,
    foul-smelling, mucosy. He has pain on
    defecation. The preliminary report on the stool
    culture is non-lactose fermenters You suspect
  • Pseudomonas
  • E. coli
  • Salmonella
  • Proteus
  • Aeromonas

By Dr Arun Aggarwal Gastroenterologist
79
  • A 10 week old afebrile infant has bloody
    diarrhea. The stool culture grows Salmonella. You
    would
  • Perform an LP
  • Treat with appropriate antibiotic
  • Obtain a bone scan to rule/out osteomyelitis
  • Treat only if child has significant toxicity or
    severe gastroenteritis
  • Rule out HIV infection

By Dr Arun Aggarwal Gastroenterologist
80
  • Which of the following is LEAST frequent with
    rotavirus infection?
  • Fever
  • Vomiting
  • Coryza preceding the diarrhea
  • Blood and mucus in the stool
  • Diarrhea lasting more than 48 hours

By Dr Arun Aggarwal Gastroenterologist
81
  • A 1 yr old boy is brought to you with vomiting
    and loose stools for the past 4 days. Initially,
    mother gave pedialyte, but for the last 24 hrs,
    the baby has been vomiting all feeds. Mother
    doesnt know when he last urinated. O/E child is
    sleepy and responds only when blood was
    withdrawn.
  • Pulse 142/min, RR 32/min, wt 10 kg
  • Skin turgor is decreased with obvious
    tenting. Nail beds were pink with prompt
    capillary refill.
  • Which of the following would represent the
    best choice for initial fluid orders?
  • D5W/ 0.2 NS _at_100cc/hr. Add 20 meq KCl after
    urination.
  • D5W/ 0.45 NS to run at 150 cc/hr for the next 8
    hrs
  • D5W/ 0.45 NS _at_100cc/hr for the next 8 hrs. Add
    20 meq KCl after urination
  • NS _at_ 150 cc/hr for the next 8 hrs

By Dr Arun Aggarwal Gastroenterologist
82
  • During teaching rounds you come across a patient
    with Rota virus diarrhea. Patient continues to
    have diarrhea day 10 after onset. You tell the
    residents that the diarrhea is secondary to
    malabsorption due to loss of cells lining the
    villi. One smart resident asks you how long it
    would take for intestinal cells to turn over.
  • 1 day
  • 2-3 weeks
  • 3-5 days
  • 1-2 months
  • 8-10 days

By Dr Arun Aggarwal Gastroenterologist
83
  • Results of a stool culture from a 2 yr old boy
    who has been hospitalized with bloody diarrhea
    indicate that the causative agent is Shigella sp.
    The boy is allergic to trimethoprim-
    sulfamethoxazole.
  • Of the following the most appropriate
    antimicrobial agent to use for this patient is
  • amoxicillin
  • azithromycin
  • cefdinir
  • ciprofloxacin
  • linezolid

By Dr Arun Aggarwal Gastroenterologist
84
  • Medication that can safely be used in case of
    acute diarrhea
  • Loperamide
  • Octreotide
  • Racecadotril
  • All of the above
  • None of the above

By Dr Arun Aggarwal Gastroenterologist
85
  • Racecadotril enkephalinase inhibitor
  • Enkephalins are endogenous pro- absorptive agents
    that directly inhibit the activity of adenylate
    cyclase on the enterocyte baselateral membrane.
  • Racecadotril is a synthetic, potent inhibitor of
    enkephalinase, devoid of any effect on intestinal
    motility, thus without the potential to induce
    the bloating that can be associated with
    enteropooling.

By Dr Arun Aggarwal Gastroenterologist
86
Things to remember..
  • New WHO ORS
  • Super ORS
  • SGLT 1
  • Feeding (BRAT)
  • Medications
  • Probiotics
  • Antibiotics (for Shigella, cholera, Giardia,
    Yersinia)
  • Zinc

By Dr Arun Aggarwal Gastroenterologist
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