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Microbiology Exam 3 > 33 - Bacterial Infections of the GI Tract I > Flashcards

33 - Bacterial Infections of the GI Tract I Flashcards

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1
Q

What is diarrhea?

A

The passage of 3 or more loose or liquid stools per day

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2
Q

Can diarrhea be deadly?

A

Yes

It is the second leading cause of death in children under 5 worldwide

Leading cause of malnutrition in children under 5

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3
Q

How many cases of diarrhea do we see each year?

A
  1. 7 billion cases
    - Bad drinking water
    - Poor sanitation
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4
Q

What is a gastrointestinal tract infection?

A

Infections caused by bacteria, viruses and parasites

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5
Q

How are gastrointestinal tract infections transmitted?

A

Almost all through the fecal-oral route

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6
Q

What is the exception to the fecal-oral route of transmission?

A

Feces-contaminated water

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7
Q

Where must a GI infection enter the body?

A

Through the mouth

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8
Q

What characteristic must an infectious agent have in order to survive in the GI tract?

A

Able to survive in the low pH of the stomach

This typically takes care of most bacteria, but some are resistant

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9
Q

What are the 8 characteristics of the GI tract that contribute to the host defense?

A 
1 - Continuous epithelium
2 - Mucus
3 - Low pH (stomach)
4 - Gut motility
5 - Shedding of epithelium
6 - Bile
7 - Secretory IgA
8 - Normal microbiota
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10
Q

Which two of the host defenses actually trigger the expression of bacterial virulence factors in some infections?

A

Mucus and bile

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11
Q

What part of the GI tract has the most diverse natural flora?

A

Large intestine

The microbiota of the stomach and small intestine is much less dense and diverse than in the large intestine

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12
Q

What does competitive exclusion mean?

A

This is a feature of our normal microbiota that is beneficial by preventing pathogens from infecting the GI tract.

The “bad bacteria” has to compete with the “good bacteria,” preventing disease.

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13
Q

What does it mean that the normal microbiota can digest “undigestible” compounds?

A

The normal microbiota are able to digest certain things that we can’t… This can be good or bad.

They can digest certain carcinogens, which may be linked to GI cancer

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14
Q

Are the normal microbiota of the GI tract able to affect the innate and adaptive immune systems?

A

Yes

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15
Q

What is gastritis?

A

Inflammation of the stomach

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16
Q

What is gastroenteritis?

A

Inflammation of the stomach and intestines

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17
Q

What is dysentery?

A

Inflammatory disorder of the GI tract often associated with:

  • Diarrhea with blood and pus in the feces
  • Pain, fever, abdominal cramps
  • Usually resulting from disease of the large intestine
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18
Q

What is enteritis?

A

Inflammation of the intestines, especially the small intestine

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19
Q

What is enterocolitis?

A

Inflammation of the mucosa of the small and large intestine

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20
Q

What is colitis?

A

Inflammation of the large intestine (colon)

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21
Q

When a bacterial pathogen causes inflammation within the intestinal tract, what does this cause?

A

Damage to the intestines

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22
Q

What is fecal occult?

A

Microscopic blood in the feces

You can’t see it in the stool, so you will need to test for it

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23
Q

When there is inflammation in the intestines is it more or less likely that you will see fecal occult?

A

More likely

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24
Q

When there is inflammation in the intestines, are you more or less likely to see fecal leukocytes?

A

More likely

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25
Q

What are the common pathogens of the GI tract that cause inflammation?

A
  • Salmonella spp.
  • Campylobacter jejuni
  • C. difficile (severe cases)
  • EHEC
  • EIEC
  • Shigella spp.
  • Ibrio parahaemolyticus
  • Yersinia enterocolitica
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26
Q

What are non-inflammatory GI bacteria?

A

These are bacteria that are passing through the intestines or adhering to the intestinal epithelium, but they either do NOT contain a toxin or they produce a toxin that is NON-cytotoxic

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27
Q

What is a non-cytotoxic toxin?

A

It is a toxin that is able to increase electrolytes and water efflux in the GI tract, but does NOT kill cells (it affects them in some other way)

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28
Q

What are some examples of non-inflammatory GI bacteria?

A
  • EPEC
  • ETEC
  • Vibrio cholerae
  • Listeria monocytogenes
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29
Q

What types of bacteria produce watery diarrhea that is sometimes or often times bloody?

A
  • EHEC
  • Campylobacter jejuni
  • Shigella spp.
  • Yersinia enterocolitica
  • EIEC
  • Clostridium. Difficile
  • Vibrio parahaemolyticus
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30
Q

What types of bacteria produce watery diarrhea, but is rarely bloody?

A
  • EPEC
  • ETEC
  • food-poisoning
  • Clostridium perfringens
  • Bacillus cereus
  • Vibrio cholerae
  • Salmonella spp.
  • Listeria monocytogenes
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31
Q

Can GI pathogens cause disease outside of the GI tract?

A

Yes, many can

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32
Q

What is one very important factor to consider when diagnosing a GI tract infection?

A

Timing!

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33
Q

What are the generalized symptoms of bacterial GI tract infections?

A
  • Diarrhea
  • Vomiting
  • Fever
  • Abdominal discomfort
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34
Q

What assumptions can you make to help you with diagnosis if the symptoms begin 1-8 hours after ingestion?

A

The patient ingested a preformed toxin

This means that when they ate the food, the bacteria were already actively releasing the toxin - this accounts for the symptoms beginning right away

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35
Q

Which bacteria would cause symptoms to begin 1-8 hours after ingestion?

A
  • Staphylococcus aureus
  • Bacillus cereus (emetic)
  • Clostridium botulinum
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36
Q

What assumptions can you make to help you with diagnosis if the symptoms begin 8-16 hours after ingestion?

A

The patient ingested a bacteria that had not yet produced its toxin

This means that as the bacteria traveled through the patient’s GI tract, they began to actively release a toxin, so the symptoms took a little while to begin

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37
Q

Which bacteria would cause symptoms to begin 8-16 hours after ingestion?

A
  • Bacillus cereus (diarrheal)
  • Clostridium perfringens
  • Clostridium botulinum
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38
Q

What assumptions can you make to help you with diagnosis if the symptoms begin more than 16 hours after ingestion?

A

The bacteria did not release a toxin while they were simply passing though the GI tract, but instead they have adhered to the wall of the intestinal tract and are exhibiting a virulence factor while they are there

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39
Q

Which bacteria would cause symptoms to begin more than 16 hours after ingestion?

A
  • Shigella spp.
  • Salmonella spp.
  • Listeria monocytogenes
  • EHEC
  • EPEC
  • ETEC
  • EIEC
  • Campylobacter
  • Vibrio spp.
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40
Q

There are two types of bacterial food poisoning. What are they?

A

1 - Pre-formed toxins

2 - Spores ingested

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41
Q

What type of spores need to be ingested in order to cause bacterial food poisoning?

A

A large number of spores need to be ingested that germinate in the intestine and become vegetative bacteria

These vegetative bacteria produce toxins, but do not necessarily colonize or adhere to the GI tract, they are just passing through

While they are passing through, they produce toxins

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42
Q

What symptoms will you see from bacterial food poisoning?

A
  • QUICK onset diarrhea, vomiting or both

- NO fever

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43
Q

There are four bacterial causes of food poisoning. What are they?

A
  • Staphylococcus aureus
  • Clostridium botulinum
  • Clostridium perfringens
  • Bacillus cereus
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44
Q

Describe staphylococcus aureus

A
  • Gram-positive cocci in clusters

- Not spore forming

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45
Q

Describe the course of the disease from staphylococcus aureus

A
  • Ingestion of a preformed toxin
  • Severe vomiting, diarrhea and abdominal pain
  • Onset within 1-8 hours after consumption
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46
Q

What is the pathogenesis of staphylococcus aureus?

A
  • Heat-stable toxin

- Mechanism of action is not well understood

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47
Q

How do you treat staphylococcus aureus food poisoning?

A
  • Supportive therapy

- Hydration

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48
Q

What are the characteristics of colostridium botulinum?

A
  • Gram positive rod

- Spore forming

49
Q

What causes the symptoms in food poisoning from colostridium botulinum?

A

The botilism toxin

50
Q

What are the symptoms in the early onset of the disease?

A

Early: onset of vomiting, diarrhea, abdominal pain 1-8 h post ingestion of preformed toxin or 8-16 h post ingestion of spores

51
Q

What are the symptoms in the late onset of the disease?

A

Flaccid paralysis leading to progressive muscle weakness and respiratory arrest

52
Q

Can fatality occur from colostridium botulinum?

A

Yes, from the respiratory arrest

53
Q

What is the pathogenesis of colostridium botulinum?

A

Ingestion of…

  • Pre-formed toxin
  • Large number of spores that germinate in the intestine and produce toxins
54
Q

What does the major toxin do?

A

Botulism toxin

- Acts at a neuromuscular nerve junctions and interferes with signaling at synapses

55
Q

When is food poisoning from colostridium botulinum most commonly seen?

A

In cases of home-canning

56
Q

What complications arise?

A

If the patient survives, you see lingering weakness and dyspnea up to 1 year after the primary disease

57
Q

How do you treat food poisoning from colostridium botulinum?

A
  • Supportive therapy

- IV anti-toxin drug in severe cases

58
Q

What does the IV anti-toxin drug do?

A

Can possibly reverse the progression of the disease in severe cases

59
Q

Why are parents not advised to give their children honey as infants?

A

Because spores of colostridium botulinum can be found in honey and can affect infants up to 6-12 months

60
Q

What is this syndrome called?

A

Floppy baby syndrome

61
Q

What happens in floppy baby syndrome?

A

There is a germination of C. botulinum spores in the intestines which then grow and produce toxins

62
Q

Is C. botulinum poisoning more severe in infants or adults?

A

Adults

*Opposite case than normal

63
Q

What happens around 6 months of age that makes this no longer a concern?

A

The permeability of the intestinal mucosa changes

64
Q

What are the characteristics of Clostridium perfringens?

A
  • Gram-positive rod

- Spore forming

65
Q

What causes the symptoms of the disease?

A

C. perfringens enterotoxin

66
Q

What is the disease typically associated with?

A

Contaminated meat products or gravy that are stored below recommended temperatures

67
Q

When will you see an onset of symptoms?

A
  • Onset of diarrhea and abdominal cramps 8-16 hours after ingestion
  • Lasts approximately 24 hours
68
Q

What is the treatment for food poisoning by c. perfringens?

A

Supportive therapy

69
Q

What are the characteristics of Bacillus cereus?

A
  • Gram-positive

- Spore forming

70
Q

There are two forms of the disease. What are they?

A

1 - Emetic form

2 - Diarrheal form

71
Q

What will you see with the emetic form?

A
  • PRE-FORMED toxin

- Onset of vomiting, nausea and abdominal cramps 1-8 hours after ingestion

72
Q

Is the pre-formed enterotoxin heat stable or heat sensitive?

A

Heat stable

73
Q

What is the emetic form commonly associated with?

A

Improper storage of cooked rice

Spores can survive the cooking - bacteria can then multiply and produce heat-stable enterotoxin that is inactivated upon reheating

Mechanism of toxin is not known

74
Q

What will you see with in diarrheal form of bacillus cereus?

A
  • Onset of diarrhea, nausea and abdominal cramps 8-16 hours post-ingestion of contaminated food
  • Production of heat-liable enterotoxin in the intestines
75
Q

What does heat-liable mean?

A

They will breakdown when exposed to heat

76
Q

What is a main difference between the emetic form and the diarrheal form of bacillus cereus?

A

They both produce an enterotoxin

Emetic form = heat stable
Diarrheal form = heat liable

77
Q

What is the treatment for food poisoning from bacillus cereus?

A

Supportive therapy

78
Q

What does helicobacter pylori do once it gets into your system?

A

It gets into your system and stays there and continues to cause disease

79
Q

What are the characteristics of helicobacter pylori?

A
  • Gram negative curved rod

- Microaerophilic (5%)

80
Q

What diseases can be caused by helicobacter pylori?

A
  • Ulcers
  • Chronic gastritis
  • Stomach cancer in less than 1% of infections
81
Q

What is the pathogenesis of helicobacter pylori in the stomach?

A

Not completely understood

  • They have flagella
  • They secrete the enzyme urease, which catalyzes the conversion of urea to ammonia and carbon dioxide
  • They secrete cytotoxin VacA
  • They contain adhesins
82
Q

What is the first step in the formation of a stomach ulcer from helicobacter pylori?

A

H. pylori penetrates the mucous layer lining of the stomach’s epithelium

It is is attracted to the chemotactic substances, hemin and urea

83
Q

What is the second step in the formation of a stomach ulcer from h. pylori?

A

H. pylori recruits and activates inflammatory cells

It also releases urease that cleaves urea, producing NH3 that neutralizes stomach acid in its vicinity

84
Q

What is the third step in the formation of a stomach ulcer from h. pylori?

A

H. pylori cytotoxin and the ammonia produced by its urease, cause destruction of the mucus-producing cells, exposing the underlying connective tissue to stomach acid

85
Q

How do you diagnose a problem with helicobacter pylori in the stomach?

A
  • Urea breath test

- Biopsy

86
Q

When would you begin treatment for h. pylori?

A

Only after a positive test for H. pylori

87
Q

How do you treat h. pylori?

A
  • Antibiotics

- Proton pump inhibitor

88
Q

What would a proton pump inhibitor do?

A

Control acid to prevent further mucosal damage

89
Q

In the small intestine, what characteristics does listeria monocytogenes have?

A
  • Gram positive
  • Facultative anaerobic
  • Short rods
  • Sometimes occurs in pairs
  • Inracellular pathogen
90
Q

What are they key survival traits of listeria monocytogenes?

A
  • Wide growth range (1 degree-45 degrees C)
  • Can survive below refrigerator temperature
  • Resistant to high salt concentrations
  • Wide pH range
91
Q

How common is listeria monocytogenes?

A

Fairly rare

- 800 cases per year in the US

92
Q

Which animals can act as “reservoirs” for listeria monocytogenes?

A
  • Mammals
  • Birds
  • Fish
93
Q

What is the PRIMARY source of listeria monocytogenes?

A

Contaminated food

  • Ready to eat meals
  • Raw vegetables
94
Q

What types of patterns do we see with listeria monocytogenes

A

Both large outbreaks and sporadic cases

95
Q

Which population is at the highest risk of infection by listeria monocytogenes?

A
  • Young
  • Elderly
  • Immunocomprimised individuals like pregnant women
96
Q

Is there human to human transmission?

A

Yes

97
Q

Is there mother to baby transmission?

A

Yes, this is the primary human-to-human transmission type

98
Q

What is the typical presentation in healthy adults?

A
  • Usually asymptomatic

- May have a fever, nausea and/or diarrhea

99
Q

What is the typical presentation in immunocompromised?

A
  • Symptoms are NOT distinct

- Fever, persistent headache, stiff neck, vomiting and confusion

100
Q

What is the rate of mortality in listeria monocytogenes?

A

20-50%

101
Q

What are the lasting effects seen in survivors?

A

Significant neurologic sequelae in survivors

102
Q

What happens when a pregnant woman becomes infected with listeria monocytogenes?

A
  • May develop nausea, fever and/or diarrhea
  • Fever with no obvious infections in blood culture
  • Risk of disease transmission to the neonate
103
Q

What are the symptoms of neonatal infection with listeria monocytogenes?

A

Granulomatosis infantiseptica

  • Pyogenic granulomas that are distibuted over the whole body
  • All systems can be involved
  • Meningitis
  • Encephalitis
104
Q

What happens in early onset in utero transmission?

A
  • Can result in premature birth, abortion or still-birth

- Women health care workers need to be careful for this reason

105
Q

What is late onset neonatal infection of listeria monocytogenes?

A

An infection that begins 2-3 weeks after birth

106
Q

What is the first step in the pathogenesis of listeria monocytogenes?

A

Adherence and induced uptake is mediated by Internalin-A (IntA)

107
Q

What happens after IntA is at play?

A

Listeria monocytogenes is internalized into an endycytic vacuole in the small intestine

108
Q

After endocytosis occurs, what is next?

A

Acidification of the vacuole/phagosome by Listeriolysin O (LLO)

109
Q

What does this acidification process accomplish?

A

It disrupts the vacuole membrane in order to allow for escape to the cytosol

110
Q

This is a signal for the lysteria to release ________

A

Toxin

111
Q

Once the listeria monocytogenes has been released into the cytoplasm and secreted toxin, what is its pathogenesis?

A
  • Replication in host cell cytosol

- ActA mediated actin polymerization

112
Q

Where can the pathogen spread to?

A

Neighboring cells

Blood stream

113
Q

What is a disseminated infection?

A

An infection that gets into the blood and can spread to the liver, spleen and CNS***

114
Q

How do you diagnose listeria monocytogenes?

A

NOT microscopy

Culture of cerebral spinal fluid and blood

115
Q

Why can’t you use microscopy?

A

It is too insensitive

  • There are too few bacteria
  • Other gram positive bacteria cause bacteremia and infect the CNS
116
Q

What three ways can you test the sample in culture?

A
  • Cold enrichment selection
  • Weak beta-hemolysis on blood agar
  • Motility test
117
Q

How do you treat listeria monocytogenes?

A
  • Beta-lactams

- Trimethoprim-sulfamethoxazole

118
Q

How do you prevent listeria monocytogenes?

A
  • No vaccine is available
  • Properly cook animal products including ready-to-eat meats
  • Wash raw vegetables

Especially if the individual is immunocompromised or pregnant

For pregnant women, avoid sushi and other ready to eat meats all together

Microbiology Exam 3 (8 decks)

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