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Gastrointestinal 2 > Bacterial and Viral Causes of GI Disease > Flashcards

Bacterial and Viral Causes of GI Disease Flashcards

1
Q

What are the 2 general types of diarrhea?

A
  1. inflammatory= hemorrhagic or dysenteric. Will have mucus, blood, or debris from an inflammatory response (leukocytes and fibrin).
  2. non-inflammatory= watery, osmotic, and often enterotoxin mediated.
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2
Q

If vomiting is a primary symptom with diarrhea, what should you consider?

A
  • enteric VIRUSES (rotaviruses; noroviruses)

- food poisoning due to preformed toxins (staphylococcus aureus enterotoxin, bacillus cereus heat-stable enterotoxin).

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3
Q

What pathogens are associated with a watery (non-inflammatory) diarrhea?

A
  • enteric viruses
  • ETEC (enterotoxin E. coli)
  • Vibrio cholerae
  • parasites (except Entamoeba histolytica)
  • food poisoning (Clostridium perfringens, Bacillus cereus enterotoxin).
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4
Q

What pathogenic cause should you consider if the diarrhea is persistent?

A

parasites

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5
Q

What fungus is associated with a watery diarrhea (non-inflammatory)?

A

Microsporidia

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6
Q

What are the 3 most common bacteria associated with inflammatory diarrhea?

A
  1. Campylobacter jejuni
  2. Salmonella
  3. Shigella
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7
Q

What are some other bacterial causes of inflammatory diarrhea?

A
  • Shiga toxin producing E. coli (STEC)
  • Clostridium difficile
  • Yersinia enterocolitica
  • Vibrio parahaemolyticus
  • Entamoeba histolytica (parasite)
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8
Q

How are these pathogens that cause diarrhea transmitted?

A

fecal-orally via crowding, food handlers (shedding when asymptomatic), ingestion of contaminated food or water, or poor hygiene especially in developing countries, nursing homes, day cares, and military barracks (often occuring via fomites).

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9
Q

How do you determine the etiology of a food-borne illness?

A
  • consider food consumption (raw or poorly cooked food, unpasteurized milk, or home canned food).
  • consider incubation period, duration of illness, predominant symptoms (vomiting, diarrhea, fever), and patient population.
  • consider social activities (pets or a petting farm, day care, travel, camping, group picnics).
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10
Q

If symptoms occur shortly after the ingestion of food, what should you consider?

A

preformed toxin

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11
Q

What are the most common disease agents associated with food-borne illness?

A
  • Campylobacter
  • E. coli
  • Listeria
  • Salmonella **(very common in U.S.)
  • Virbrio parahaemolyticus
  • Yersinia
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12
Q

What organisms are a result of food poisoning due to pre-formed toxins?

A
  • Staph aureus
  • Bacillus cereus
  • Clostridium
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13
Q

What is important to know about Staph aureus in regard to food poisoning?

A
  • food does not taste tainted
  • mean incubation period= 4 hours
  • diarrhea= watery but not bloody
  • severe vomiting, abdominal pain or nausea
  • NO fever
  • duration= 1 to 6 hours
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14
Q

What is the Staph aureus enterotoxin?

A
  • it is a superantigen= activates T cells
  • stimulates cytokine release
  • acts on neuronal receptors in upper GI tract (stimulating vomiting center in brain).
  • heat stable (ingestion of toxin is sufficient to cause illness).
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15
Q

What is important to know about Bacillus cereus?

A
  • spore forming gram positive bacillus

- makes heat stable toxin (unknown mechanism) and heat labile toxin (resembles E. coli and V. cholerae).

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16
Q

How does the heat LABILE toxin of Bacillus cereus cause pathogenesis?

A
  • stimulates cAMP= hyper-secretion of water and electrolytes

- associated with MEATS and VEGETABLES (causing diarrhea)

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17
Q

In what food is the heat STABLE toxin of bacillus cereus most common?

A

RICE (causing vomiting)

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18
Q

What is important to know about Clostridium?

A
  • anaerobic, gram positive, spore forming bacillus
  • C. difficile= antibiotic associated diarrhea
  • C. perfringens= food poisoning and gas gangrene
  • C. tetani= tetanus
  • C. botulinum= botulism
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19
Q

What does C. perfringens normally involve when causing food poisoning?

A
  • meat dishes
  • produces spores, which are heat resistant.
  • produces heat labile enterotoxin= released after ingestion of organism, altering membrane permeability causing fluid secretion.
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20
Q

How can you differentiate the symptoms of Staph aureus from C. perfringens?

A

C. perfringens will no not cause a fever or vomiting

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21
Q

What is the leading viral cause of gastroenteritis in children?

A

rotavirus

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22
Q

What is the leading viral cause of gastroenteritis of all ages?

A

norovirus

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23
Q

What happens to the villi with a viral gastroenteritis?

A

you get blunting and sloughing off of the villi with crypt hyperplasia leading to an osmotic (watery) diarrhea

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24
Q

What is the incubation period for rotavirus and norovirus?

A

around 1-4 days (little bit longer than toxins)

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25
Q

What is the duration of clinical disease for rotavirus and norovirus, respectively?

A
  • rotavirus= about a week

- norovirus= 1-3 days

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26
Q

How do you treat rotavirus and norovirus infections?

A

let it run its course and treat the dehydration and electrolyte balance only

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27
Q

*** What is important to know about the rotavirus itself?

A
  • ds RNA, 11 segments (aka segmented genome), and triple-shelled capsid
  • very stable virus
  • P (VP4) and G (VP7) outer shell proteins= components of the vaccine
  • only virus known to secrete an enterotoxin (NSP4) resulting in chloride secretion.
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28
Q

What rotavirus group makes up most human strains?

A
  • group A (VP6)
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29
Q

What vaccines are approved for rotavirus?

A
  • RotaTeq= live, oral, human-bovine reassortant

- Rotarix= live, oral, human monovalent attenuated vaccine

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30
Q

What is important to know about norovirus itself?

A
  • RNA, icosahedral, naked virus
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31
Q

What is a similar virus to norovirus, having the same family (caliciviridae), but milder symptoms?

A

sapovirus

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32
Q

What virus is the leading cause of sporadic cases and outbreaks of diarrheal illness?

A

Norovirus via contaminated food or water (cruise ships, nursing homes…)

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33
Q

Can norovirus spread easily?

A

YES because it has a low infectious dose (less than 100 particles) and pt is asymptomatic when shedding occurs.
- also resistant to disinfectants and has strain diversity

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34
Q

What do we need to know about the Vibrio species, itself?

A
  • gram negative, curved rods
  • highly motile
  • serogroups O1 and O139 produce cholera toxin (most sever cases).
  • requires high numbers of particles to infect, but it replicates rapidly, so you can reach infectious dose quickly.
35
Q

What are the most common species of Vibrio in the U.S.?

A
  • V. parahaemolyticus
  • V. vulnificus
  • nontoxigenic V. cholera
36
Q

Can vibrio survive in salt water?

A

YES so you can find it in raw oysters or shellfish (mostly V. parahaemolyticus).

37
Q

What happens with Vibrio parahaemolyticus clinically?

A

watery diarrhea (bloody in sever cases only).

38
Q

What will Vibrio vulnificus do clinically?

A

infects wounds and can cause systemic disease and sepsis (fever, chills, septic shock).

39
Q

What are enterobacteriaceae?

A
  • ubiquitous gram negative bacilli that ferment glucose; oxidase negative and a normal intestinal flora in humans
  • can cause sepsis, UTI, gastrointestinal tract infections and pulmonary infections.
40
Q

What 4 enterobacteriaceae are relevant for GI?

A
  • Escherichia coli
  • Shigella
  • Salmonella
  • Yersinia
41
Q

To what do the O, H, and K antigens refer in serological classification of enterobacteriaceae?

A
  • O= polysaccharide
  • H= flagella (aka you know it is motile)
  • K= capsule
42
Q

Does nonpathogenic E. coli exist in our gut as normal flora?

A

YES

43
Q

What is used to distinguish pathogenic E. coli?

A 
specific O (somatic) and H (flagellar) antigens 
*ex. O157:H7 associated with E. coli causing hemolytic uremic syndrome (HUS)
44
Q

What virulence factors are associated with E. coli?

A
  • adhesins (pili & fimbriae)

- enterotoxins= heat labile (LT), heat stable toxins (ST), or shiga toxin

45
Q

What are the 2 most common types of pathogenic E. coli in the states?

A
  1. Enterotoxigenic E. coli (ETEC)= watery diarrhea from LT or ST toxins.
  2. Shiga toxin-producing E. coli (STEC)= dysentery from shiga-like toxin; intimin
46
Q

What is the leading cause of traveler’s diarrhea?

A

Enterotoxigenic E. coli (ETEC)

*note: LT is the same pathogenesis as cholera

47
Q

*** What is the pathogenesis of ETEC (LT) and cholera?

A

CTx and LT bind to receptors on epithelial cells. They then activate a subunit that is transprted to adenylate cyclase. ADP ribose is transferred to a GTP-binding protein that regulates AC, increasing cAMP.

  • ST on the other hand binds guanylate cyclase, increasing cGMP.
    • Both increases in cAMP or cGMP cause decreases in Na+ absorption in the villi and increase Cl- and water secretion in crypt cells!
48
Q

What is traveler’s diarrhea?

A
  • watery non-inflammatory diarrhea with no blood or mucus. May have low-grade fever, nausea, and possible abdominal cramping.
  • lasts 2-5 days
49
Q

Where is the shiga toxin E. coli (STEC) commonly found?

A
  • livestock (beef contaminated during slaughter or petting zoo contact).
  • primary route of transmission is food-borne (ground beef, unpasteurized milk, or more recently spinach and lettuce)
50
Q

What are the 2 different forms of Shiga toxin?

A
  1. Stx-1
  2. Stx-2= more likely to cause HUS
    * Intimin is responsible for attachment/effacement (A/E lesions) that destroy the microvilli.
51
Q

What makes the O157 STEC strain unique from the non-O157 STEC strain?

A

O157 ferments lactose but NOT sorbitol, whereas non-O157 STEC ferments both.

52
Q

What is the mechanism of action for Shiga toxin?

A
  • has A (activating) and B (binding) subunits.
  • B subunit binds to globotriaosylceramide (Gb3), which is highly concentrated on intestinal villi and renal endothelial cells.
  • A subunit enters cells and prevents binding of tRNA to ribosome.
53
Q

What does STEC cause clinically?

A

hemorrhagic enteritis (bloody diarrhea), but starts out like ETEC since it begins as a watery diarrhea.

54
Q

What are the 3 characterstics of hemolytic uremic syndrome (HUS) from STEC?

A
  1. renal failure
  2. thrombocytopenia
  3. hemolytic anemia
    * only occurs in 5-10% of patients with STEC (especially children).
55
Q

What is EnteroINVASIVE E. coli?

A
  • resembles Shigella, but not common in the U.S.
  • transmitted via contaminated food and water
  • enters enterocytes causing cell death and inflammatory response, thus causing dysentery.
  • Will see a lot of fecal leukocytes like in Shigella
56
Q

What is EnteroPATHOGENIC E. coli?

A
  • causes infant diarrhea in developing countries
  • watery (non-inflammatory diarrhea).
  • uses laminin/laminin attachment
57
Q

What is EnteroAGGREGATIVE E. coli?

A
  • causes persistent watery or mucoid diarrhea (more than 2 weeks).
  • attaches via aggregative adherence fimbriae
  • forms biofilm
  • expresses Shigella enterotoxin (NOT SHIGA TOXIN)
  • antibiotic resistant
58
Q

Where was a huge outbreak of EnteroAGGREGATIVE E. coli?

A

Germany and France in 2011

59
Q

What do we have to know about Shigella species?

A
  • nonmotile, non-lactose fermenting
  • most common route of transmission in U.S. is person to person via low infectious dose (mostly children; think DAYCARES).
  • most common strain is S. sonnei= watery diarrhea.
  • most virulent strain is S.dysenteria (produces Shiga toxin)= dysentery
  • internalized by enterocytes causing abscesses, ulcers, and an inflammatory reaction.
60
Q

What is the most common cause of dysentery?

A
  • Shiga toxin producing Shigella (usually in children).
  • starts as a watery diarrhea, but in more severe cases you will see inflammatory colitis and bloody diarrhea with lots of fecal leukocytes.
  • can have a pseudomembrane= sloughed epithelial cells, bacteria, fibrin, and inflammatory cells.
61
Q

What are the 2 most common types of Salmonella subspecies in the U.S.?

A
  1. Enteritidis

2. Typhimurium

62
Q

What is the most common type of transmission for Salmonella?

A
  • undercooked chicken or eggs

- turtles and rodents

63
Q

How does Salmonella infect people?

A
  • enterotoxin activates cAMP (watery diarrhea).
  • adhesin induces “ruffling” of the membrane, causing endocytosis, to invade the lamina propria of the small intestine.
  • some serotypes can invade the bloodstream causing enteric (typhoid) fever.
64
Q

** What is the reservoir for enteric fever (typhoid) fever?

A

those with chronic infection of Salmonella Typhi in the gall bladder (mostly travelers to Latin America, and Asia).
* it survives within macrophages, replicating within phagolysosomes and gets into the reticular endothelial system (liver, spleen, bone marrow).

65
Q

What are the clinical symptoms of Enteric fever?

A
  • fever and headache with slow pulse and faint rash on abdomen and chest.
  • mild diarrhea also possible
66
Q

What is the most important complication of Enteric fever?

A

hemorrhage from perforations through wall of terminal ileum or proximal colon

67
Q

What are the 2 enteric Yersinia species?

A
  1. Yersinia enterocoltica

2. Yersinia pseudotuberculosis

68
Q

What is the pathogenesis of Yersinia?

A
  • invades M cells of Peyer’s patch and can replicate within the reticular endothelial system.
  • impairs PMN and macrophage activity
69
Q

** What can Yersinia mimic?

A
  • appendicitis (fever, abdominal pain, mesenteric lymphadenitis)
  • enterocolitis
  • polyarthritic syndrome (joint pain)
70
Q

What is important to know about Campylobacter?

A
  • curved, gram negative rods (resemble vibrios)
  • most common species= C. jejuni
  • causes dysenteric stools, fever, and lower abdominal pain lasting for 1 week.
71
Q

** With what disease is Campylobacter associated?

A

Guillain-Barre syndrome= acute demyelinating syndrome (autoimmune syndrome where antibody cross reacts with myelin).

72
Q

What is important to know about Clostridium difficile?

A
  • major cause of diarrhea in HOSPITALS
  • ingest spores
  • elimination of normal flora (due to antibiotic use) allows spores to germinate in the gut
  • pseudomembranes
73
Q

** What are the 2 toxins created by C. difficile?

A
  1. Toxin A= enterotoxin that disrupts intercellular junctions causing hyper-secretion of fluids.
  2. Toxin B= cytotoxin that depolymerizes actin causing loss of cellular cytoskeleton.
74
Q

What is a dangerous strain of C. difficile that has emerged?

A
  • NAPI, which expresses increased levels of toxins A and B, and has resistance to fluoroquinolones.
75
Q

What is important to know about Listeria monocytogenes?

A
  • gram positive rod
  • heat-resistant and can replicate at cold temps
  • elderly, pregnant women, and newborns are most at risk.
  • diarrhea, GI symptoms, or in the immunocompromised it can cause meningoencephalitis
76
Q

How do you diagnose inflammatory vs. non-inflammatory gastroenteritis?

A
  • fecal leukocyte test= methylene blue (need fresh stool sample).
  • test stool sample for lactoferrin (iron-binding glycoprotein present in PMNs).
77
Q

What pathogens are tested in a routine stool sample?

A

C. jejuni, Salmonella, Shigella, and Vibrio

78
Q

If you see blood in the stool, what other test should you order?

A

STEC culture or toxin

79
Q

What enzyme immuno assay is used to test for C. difficile?

A

glutamine dehydrogenase

80
Q

What do we have to know about Helicobacter pylori?

A
  • gram negative rods with polar flagella (resembles Campylobacter).
  • expresses Lewis antigens on LPS (molecular mimicry)
  • urease allows it to survive in acid pH bc it breaks up urea to produce ammonia (which neutralizes the microenvironment).
81
Q

What are some other virulence factors of H. pylori?

A
  • vacuolating cytotoxin (VacA)= induces vacuoles, apoptosis, and increases cell permeability.
  • Cag pathogenicity island= clusters of genes that contribute to type 4 secretion system.
  • BabA and SabA= adherence factors
82
Q

What can H. pylori cause?

A
  • most asymptomatic
  • gastric and duodenal ulcers (rare)
  • gastric adenocarcinoma MALT lymphoma and non-Hodgkin’s lymphoma of the stomach (rare)
83
Q

How do you diagnose H. pylori?

A
  • endoscopic biopsy (histological staining and urease test).
  • urea breath test
  • fecal antigen test

Gastrointestinal 2 (18 decks)

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