Gastroenteritis and Peritonitis Flashcards

1
Q

Gastroenteritis

A
  • Gastrointestinal illness is one of the most common problems seen in outpatients and is also one of the most common reasons for hospitalization of children and adults. Worldwide, gastrointestinal illness causes a major portion of morbidity and mortality and could be considered one of the big four infectious killers (along with malaria, tuberculosis, and HIV). It is common in developed countries and even more common in the developing countries.
  • Gastroenteritis can be episodic or widespread.
  • All the common agents of gastroenteritis are spread by the fecal-oral route. The pathogen replicates in the intestine and is passed in the feces. The next host then becomes infected by inadvertently ingesting contaminated material
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2
Q

Gstroenteritis - Clinical Syndromes and Mechanisms of Disease

A
  • One of the biggest distinctions between different gastrointestinal pathogens involves whether they infect the small or large intestine.
  • None of the pathogens we will be discussing infects primarily the stomach. (Helicobacter pylori causes ulceration in the stomach or duodenum).
  • Other important factors include the type of toxin, if present, and whether tissue invasion occurs.
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3
Q

Gastroenteritis - Nausea and Vomiting

A
  • Nausea with or without vomiting is extremely common and is not always the result of GI illness.
  • Other precipitating factors include medications, systemic illness, Migraine headache, etc..
  • The most common infectious agent associated with vomiting (apart from food poisoning) is Norovirus.
  • Vomiting begins within 1-2 days after exposure and continues for 2-3 days. Fever and diarrhea may be present. (Other etiologic agents of this syndrome give similar manifestations).
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4
Q

Gastroenteritis - Watery Diarrhea

A
  • Watery diarrhea implies infection of the small intestine and at least for certain pathogens is mediated through a toxin.
  • The most common pathogen causing this syndrome is rotavirus, which probably causes disease by a combination of an enterotoxin and a direct pathogenic effect on the intestinal wall, so that malabsorption can occur after infection.
  • Vibrio cholerae, the agent of cholera is a classic example of causing watery diarrhea by a toxin, which increases cAMP and increases secretion of chloride with water. With cholera, many liters of water can be lost within hours and when death occurs, it is due to hypovolemic shock from volume loss.
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5
Q

Gastroenteritis - Malabsorption

A
  • Small intestinal pathogens can also cause diarrhea accompanied by malabsorption of nutrients.
  • In this case, there is little fluid loss and the diarrhea is relatively low volume. However, patients may have prolonged diarrhea with significant weight loss.
  • Giardiasis is one of the infectious illnesses presenting in this fashion.
  • Though the specific mechanism of diarrhea is not known, it may involve the immune response to the organism.
  • There are also important noninfectious etiologies of diarrhea that must be considered.
  • Lactose intolerance is quite common, especially in non-European populations. However, weight loss usually does not occur because nutrients other than milk products are absorbed normally.
  • Gluten enteropathy is an immune disorder in which a small intestinal inflammatory process occurs after exposure to gluten (found in wheat and certain other grains) and is being increasingly recognized in the US.
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6
Q

Gastroenteritis - Dysentary and Other Inflammatory Diseases of the Colon

A
  • infectious colitis
  • Dysentery refers to a clinical illness with fever, lower abdominal pain, and bloody diarrhea resulting from certain pathogens that infect the colon.
  • Shigellosis (Shigella dysenteriae) and amebiasis (Entamoeba histolytica) are among the classic examples of this syndrome.
  • In clinical practice, dysentery must be differentiated from routine diarrhea with hemorrhoidal bleeding (a combination of two common entities) and from inflammatory bowel disease (Crohn’s or ulcerative colitis).
  • Other common causes of dysentery include E. coli and Campylobacter spp.
  • The most common serious cause of infectious colitis in the US is Clostridium difficile colitis, which results from the production of a cytolytic toxin by the microorganism.
  • Human intestine is frequently colonized with C. difficile, but people remain asymptomatic until their bacterial flora is changed by antibiotic administration. (Cases are quite rare in the absence of antibiotic treatment).
  • The microorganism proliferates and can produce enough toxins to cause serious disease.
  • Within the last five years, the frequency and severity has markedly increased, and now the newer quinolones are among the most important risk factors.

•It is important to try to make an etiologic diagnosis of infectious colitis, since the treatments of the different entities are so different, and the morbidity and mortality can be high.

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7
Q

Gastroenteritis - Syndrome of Food Poisoning

A
  • Food poisoning results from ingestion of infectious agents accompanied by their preformed toxins (food poisoning).
  • Food poisoning is also frequently used to describe illness produced by pathogens transmitted by food that then cause disease after replication in the host intestine.
  • vomiting
  • paralysis
  • histamine release
  • paresthesias
  • diarrhea with or without vomiting
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8
Q

Gastroenteritis - Syndrome of Food Poisoning - Vomiting

A
  • Vomiting (with or without diarrhea) that occurs within two to six hours of ingestion of contaminated food.
  • This vomiting is generally due to a heat-stable neurotoxin (although called an enterotoxin) produced by Staphylococcus aureus.
  • Because the toxin is heat stable, cooking the food before ingestion does not prevent illness.
  • As a general rule, infectious illnesses require at least 24 hours of incubation (allowing time for replication) in the host before causing disease, so symptoms occurring earlier than 24 hours suggest preformed toxins.
  • Bacillus cereus (be serious) can produce a toxin similar to that of S. aureus and causes a similar clinical syndrome.
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9
Q

Gastroenteritis - Syndrome of Food Poisoning - Paralysis

A
  • One of the most notable forms of food poisoning is botulism in which a preformed neurotoxin is ingested, followed by paralysis because of its effect on the neuromuscular junction.
  • This results when foods are contaminated by Clostridium botulinum prior to ingestion (a notable problem of foods with improper canning).
  • The toxin is killed by boiling, but the spore is heat stable, so cooking does not eliminate the risk because toxin can be produced by the surviving spores.
  • Botulism can also occur in infants when foods (e.g. honey) are ingested that are contaminated with C. botulinum but before toxin has been produced. The toxin is then produced in the intestine causing a more delayed onset of symptoms.
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10
Q

Gastroenteritis - Syndrome of Food Poisoning - Histamine Release (Scombroid)

A
  • Histamine release (scombroid) can occur within hours after ingestion of shellfish that contain histamine as well as histamine degradation produced by marine bacteria.
  • Thus, this is an anaphylactoid reaction (mediated by histamine, but without an allergic antibodyantigen reaction).
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11
Q

Gastroenteritis - Syndrome of Food Poisoning - Paresthesias

A

•A variety of toxins can be ingested with fish and shellfish, resulting in paresthesias and other neurologic syndromes.

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12
Q

Gastroenteritis - Syndrome of Food Poisoning - Diarrhea with or without Vomiting

A
  • These syndromes are often called food poisoning, but they depend on replication and/or toxin production after ingestion of the offending pathogen.
  • About 12-24 hours after ingestion of Clostridium perfringens, sufficient toxin has been produced in the intestine that diarrhea results. The manifestations are relatively short.
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13
Q

Laboratory Evaluation of Intestinal Infections

A
  • routine non specific tests
  • blood cultures
  • fecal specimens
  • serologic (antibody detection)
  • endoscopy
  • imaging
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14
Q

Laboratory Evaluation of Intestinal Infections - Blood Cultures

A

•Blood cultures are frequently positive in cases of enteric fever (typhoid or paratyphoid), but are rarely positive in other forms of gastroenteritis.

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15
Q

Laboratory Evaluation of Intestinal Infections - Fecal Specimens

A

Clostridium difficile testing

– This is by far the most useful fecal test in hospitalized patients in the US.

  • The testing can be done by culturing the organism, by detecting the toxin, or by a PCR test that will detect organisms with the toxin genes.
  • The toxin assay is limited by poor sensitivity, so the best test is the PCR.
  • Ova and parasite (O&P) examination (performed on three consecutive days)
  • Antigen detection (Giardia and Cryptosporidium)
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16
Q

Laboratory Evaluation of Intestinal Infections - Serologic

A

•Serologic (antibody detection) test (Entamoeba histolytica)

  • This test has a sensitivity of about 95% in patients with invasive amebiasis.
17
Q

Laboratory Evaluation of Intestinal Infections - Endoscopy

A
  • Upper endoscopy (EGD) with small bowel biopsy is useful in diagnosing the causes of malabsorption with weight loss, including giardiasis and gluten enteropathy.
  • Lower endoscopy (colonoscopy or sigmoidoscopy) with biopsy can be useful in identifying infectious causes of colitis (e.g. amebic colitis, C. difficile colitis) and distinguishing them from noninfectious etiologies such as inflammatory bowel disease.
18
Q

Laboratory Evaluation of Intestinal Infections - Imaging

A

•CT scan of the abdomen frequently identifies a thickened colon wall in patients with colitis and can point to that diagnosis when the initial diagnosis is not obvious.

19
Q

Peritonitis

A
  • The peritoneum is normally sterile, but encloses the colon, which contains about 1011 bacteria, 99.9% of which are anaerobic.
  • Bacteria are constantly escaping through the intestinal wall (translocation) but are efficiently killed by the immune response within the peritoneum.
  • Peritonitis results when there is a breach in the normal protection system, from the gross spillage of large numbers of bacteria (perforation), growth in ascites (primary peritonitis), or the presence of a foreign device (CAPD peritonitis).
20
Q

Secondary Peritonitis

A
  • Most peritonitis is secondary and results when there is a rupture of a hollow viscous allowing the release of massive numbers of bacteria into the peritoneum along with fecal contents (colon), bile (gallbladder), etc.
  • This overwhelms the protective mechanisms and results in systemic sepsis as well as local scarring and abscess formation.
  • The microbiology generally reflects the microbiology of the perforated viscus with a mixture of aerobic gram negative and anaerobic organisms (gram negative and gram positive) as well as enterococci and streptococci.
  • Some of the common entities resulting in rupture and peritonitis are perforated gastric or duodenal ulcer, perforated gallbladder, perforated appendicitis or diverticulitis.
  • These are uniformly surgical diseases and require repair of the defect, drainage of infected material, and antimicrobial therapy.
21
Q

Primary Peritonitis

A
  • Primary peritonitis (spontaneous bacterial peritonitis; SBP) occurs when ascites (buildup of transudative fluid) is present in the peritoneum.
  • This is most often due to chronic liver failure.
  • In this case, bacteria arrive through the bloodstream (bacteremia) or by translocation through the intestinal wall in the absence of perforation.
  • This is almost always caused by a single bacterial species. The most common is E. coli, but Streptococcus pneumoniae is also common (particularly if the fluid is due to the nephrotic syndrome), which emphasizes that the pathogenesis of this infection is very different from secondary peritonitis, since S. pneumoniae, the most common bacterial cause of pneumonia does not colonize the GI tract; rather, it reaches the peritoneum through the bloodstream.
  • The ascites then makes a good culture medium, allowing the bacteria to grow.
  • The diagnosis of primary peritonitis can be made by using a needle to aspirate peritoneal fluid through the abdominal wall (not a difficult procedure when ascites is present).
  • It is suspected when the fluid has >250 neutrophils/ml and confirmed by a positive gram stain or culture.
  • Treatment is medical with antibiotics chosen for their activity against the proven or most likely pathogen.
  • Peritonitis can also result from organisms causing granulomatous infection, such as Mycobacterium tuberculosis.
22
Q

Peritonitis and CAPD

A
  • Peritonitis is also a major complication of CAPD (continuous ambulatory peritoneal dialysis).
  • About half of chronic renal failure patients are treated by hemodialysis and the other half are treated with peritoneal dialysis.
  • Recurrent peritonitis is the most common cause for failure, requiring a switch to hemodialysis.
  • The offending organisms are introduced through the dialysis catheter into the peritoneum and are similar in spectrum to those causing other device-related infections.
  • In general, device-related infections are difficult to clear because bacteria adhere to the device, but some of these infections can be cleared without device removal by diving antibiotics into the peritoneum with the dialysate fluid.
23
Q

Vibrio Cholerae

A

a) non-invasive (PMNs enter lamina propria)
b) cholera toxin (A and B subunits)
c) upregulates cAMP leading to secretion of chloride from CFTR and reduction in sodium absorption
d) epidemic cholera from only a few serotypes
e) resident in coastal waters of the Gulf of Mexico

24
Q

Cholera

A

a) Gram-negative curved rods on gram stain of stool
b) Volume repletion: 4-5 days 100% of body weight
c) Antibiotics
d) Fecal Oral spread

  • About 10 cases in the US/year; half returning from out of country; half from seafood
  • During an epidemic, infection leads to clinical disease in 1/30-100 person
  • 2010 Haiti earthquake (8,231 dead from disease since earthquake; spread to Dominican Republic and Cuba)
  • Rice water stools (containing bits of mucus)
  • Two whole cell killed vaccines
25
Q

Norovirus

A
  • Acute gastroenteritis effects ~12% of population/year
  • Majority caused by viruses
  • Calcivirus species cause 23 million cases/per year in the US; Norovirus is a calcivirus
  • single strand RNA
  • no lipid envelope– impervious to alcohol
  • as few as 18 virions may cause disease
  • detected by PCR
  • Person to person: fecal-oral
  • Foodborne-shell fish
  • Waterborne
  • Droplet nuclei
  • Cause of travelers’ diarrhea; coinfection
  • Secondary attack rate high
  • incubation period: 24-48 hours
  • duration of illness: 12-60 hours
  • vomiting in half the cases
  • disinfect with dilute Chlorox
26
Q

Villus Atrophy in Norovirus

A
27
Q

Giardia duodenalis

A
  • cysts
  • trophozoites ~12 microns
  • small intestine (not invasive)
  • encystment
  • Humoral immunity: secretory IgA antibody
  • Worldwide pathogen : children, travelers (15,223 cases reported in 2012 in US) immunocompromised, hypochlorhydria
  • St. Petersburg, Russia
  • Aspen, Colorado
  • Water is the major source: cyst survives cold water, chlorination, person to person
  • Humans and animals; maybe dog to man
28
Q

Diagnosis of Giardiasis

A
  • Stool microscopy: 60%;
  • with 3 specimens, 90%
  • String test
  • PCR: Biofire::Salmonella, Campylobacter, Plesiomonas shigelloides, Vibrio, Yersinia enterocolitica, diarrheagenic E. coli/Shigella, Cryptosporidium, Cyclospora cayetanensis, Entamoeba histolytica, Giardia, Adenovirus, Astrovirus, Norovirus, Rotavirus and Saprovirus
29
Q

Acute Giardiasis

A
  • Diarrhea (may initially be watery)
  • Malaise: 85%
  • Foul smelling fatty stools: 70%
  • Cramps and bloating: 70%
  • Weight loss: 65%
  • Vomiting: 30%
  • Fever : 10-15%
30
Q

Traveller’s Diarrhea

A
  • ETEC (Enterotoxigenic Escherichia coli ) found in developing countries, responsible for traveller’s diarrhea and childhood diarrhea
  • Heat stable toxin may suppress colon ca (rare in developing countries)
31
Q

Causes of Traveller’s Diarrhea

A
  • Visitors from resource-rich to resource-poor regions of the world
  • Self-limiting; duration ~11 hours
  • >90% of cases caused by bacteria
  • Majority of cases due to ETEC or EAEC (Enteroaggregative Escherichia coli)
  • Usually occur within 4-14 days of visiting
  • Low risk: Northern Europe, Australia, NZ, US, Canada, Japan
  • Moderate risk: Caribbean and countries bordering Mediterranean
  • High risk: Asia, Africa, South and Central America and Mexico
32
Q

EHEC

A
  • Enterohemorrhagic Escherichia coli
  • EHEC is a strain of E. coli that produces a toxin called Shiga toxin.
  • The toxin causes damage to the lining of the intestinal wall.
  • Asymptomatic in cattle in GI tract
  • Shiga binds to glycolipid receptor Gb3 found on kidney epithelial cells in humans leading to HUS– in cattle the receptor is in the gut.
33
Q

Vibrio vulnificus

A
  • Halophilic vibrio
  • Found in coastal waters
  • Can be found in shellfish, water
  • May cause severe local infection if enters a scratch or fish hook injury
  • Disseminates in patients with liver disease