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GI Week 4 - WLB > Microbiology of the Lower GI - Zimmer > Flashcards

Microbiology of the Lower GI - Zimmer Flashcards

1
Q

What are the GI system defenses of the intestines?

A
  • Normal flora
  • Peyer’s Patches
    • M cell: conduit to PP, capable of transporting large antigens
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2
Q

What is the normal flora of the large intestines?

A
  • Microbe rich, “microbiome” studied here
  • Anaerobes
  • Gram-negative rods
  • Enterococcus – can survive wide range of stressors and environmental conditions
  • Spirochetes
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3
Q

What are the first colonizers of breast-fed infants?

A
  • facultative anaerobic bacterial groups such as:
    • streptococci
    • staphylococci
    • enterococci
    • lactobacilli
    • enterobacteria
    • together with some strictly anaerobic ones
      • especially bifidobacteria
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4
Q

What are the first colonizers of formula-fed infants?

A
  • microbiota → more diverse and prone to changes
  • contains higher counts of:
    • Bacteroides
    • Clostridium
    • Enterobacteriaceae
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5
Q

Why is the normal flora of the lower GI tract beneficial?

A
  • Generate vitamins, help in digestion
  • Stimulate the development of immunological tissues
  • Prevent establishment and infection of alien microbes
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6
Q

What are the four mechanisms that microorganisms cause disease?

A
  1. Toxin production – bacteria release toxin that causes illness.
  2. Host immune response – response of host to microbe that causes illness.
  3. Microbial proliferation and invasion – growth and spread of microbes that causes damage that is significant in illness.
  4. Cancer – Microbe promotes uncontrolled proliferation of cells of host organism
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7
Q

When does true “food poisoning” occur?

A
  • True food poisoning occurs after consumption of food containing toxins
    • Symptoms begin almost immediately after ingesting the food with toxin in it
      • 30 min to 6 hr incubation period
    • Toxin is pre-formed
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8
Q

How are food-associated infections different from food poisoning?

A
  • Symptoms begin with a longer incubation period
  • Organisms produce toxin in the GI tract or invade mucosal epithelium
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9
Q

What is a bacterial exotoxin when it targests the intestines?

A

Enterotoxin

(something bacteria excretes)

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10
Q

What three bacteria cause food poisoning by generating pre-formed toxins in food?

A
  1. Staphylococcus aureus
  2. Bacillus cereus
  3. Clostridium botulinum
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11
Q

What are the symptoms when S. aureus causes food poisoning?

A
  • Nausea, vomiting, stomach cramps, and diarrhea for 1-3 days
  • Appear 1-7 hrs following ingestion of food
  • Self-limiting, once toxin is gone, illness is gone
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12
Q

How do you get a positive diagnosis of S. aureus causing food poisoning?

A
  • Toxin-producing S. aureus can be identified in stool or vomit
  • Most conclusive test is the linking of an illness with a specific food, or in cases in which multiple vehicles exist, detection of pre-formed enterotoxin in food sample(s).
    • Only necessary when tracking outbreaks
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13
Q

How does S. aureus cause food poisoning?

A
  • Can generate 7 different toxins
  • Ingestion of toxin, not the bacterium, is what causes the illness
  • Toxin can survive high temperatures, although S. aureus cannot.
    • However it is one of the most resistant non-spore forming human pathogens, survives in dry state for extended periods.
  • S. aureus temperature range of 15°-45°C and NaCl concentrations as high as 15 percent for growth
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14
Q

Is antibiotic treatment a good option for S. aureus food poisoning?

A

No, antibiotics don’t target the toxin.

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15
Q

Bacillus cereus

Gm +/-

Spore forming?

Aerobe/Anaerobe

Hemolysis?

A
  • Gram +
  • Large Bacilli
  • endospore-forming
  • Facultative anaerobe
  • Mostly motile
  • Β hemolytic
  • Box-car shaped gram positive rods
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16
Q

What is the Bacillus cereus reservoir?

A

Spores can survive rice cooking process

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17
Q

Where are Bacillus cereus spores commonly found?

A

B. Cereus spores are commonly found in the soil and sometimes in plant foods that are grown close to the ground – such legumes, cereals, spices etc..

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18
Q

What are the two forms of Bacillus cereus Food Poisoning?

A
  • Emetic (vomiting):
    • 1 to 6 hours incubation
    • Nausea and vomiting
    • resembles the vomiting illness caused by Staphylococcus aureus enterotoxins
  • Diarrheal:
    • 6-15 hours incubation
    • Watery diarrhea and abdominal cramps
    • clinically similar to the symptoms of Clostridium perfringens infection
  • Duration for both only about 24 hrs
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19
Q

What is the mechanism of Bacillus cereus Food Poisoning Emetic (vomiting) type?

A
  • Mechanism:
    • Caused by preformed enterotoxin that forms holes in membranes:
      • Cereulide = an ionophoric low molecular-weight peptide that is pH-stable and heat- and protease- resistant
    • Self limiting
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20
Q

What is the mechanism of Bacillus cereus Food Poisoning Diarrheal type?

A
  • Mechanism:
    • Caused by large molecular weight enterotoxin that causes intestinal fluid secretion, probably by several mechanisms
    • This toxin is not likely pre-formed!
  • Ingestion of large amounts of bacteria cause it to generate the toxin in the small intestine
  • Vulnerable populations might get sicker and require antibiotics
  • Poor outcomes for systemic infection
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21
Q

How do you positively diagnose Bacillus cereus?

A
  • Because of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen.
  • B. cereus in food and vomitus or feces of same serotype
  • Large numbers of B. cereus of serotype known to produce endotoxin
  • Only necessary when tracking outbreaks
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22
Q

Clostridium botulinum

Gm +/-

Shape

Aerobe/Anaerobe

A
  • Gram +
  • Bacilli (Rods with terminal spores)
  • Spore-forming
  • Obligate anaerobe
  • Motile
  • Clostridium
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23
Q

What are the three illnesses associated with C. botulinum?

A
  • Foodborne botulism
    • ingesting toxin in food
  • Wound botulism
    • generating toxic in wound
  • Infant botulism
    • ingesting spores

Not really a GI illness, diarrhea not prominent

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24
Q

How do you diagnose C. botulinum infection?

A
  • Symptoms and history, results of physical exam indicate botulism
  • Tests to exclude other causes of the illness
  • Organism or toxin in stool sample only indirect evidence
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25
Q

What is the treatment for foodbourne C. botulinum infection?

A
  • Ventilator if respiratory failure and paralysis
  • Antitoxin if paralysis is not yet complete
  • Remove contaminated food if still likely in gut
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26
Q

What kind of toxin does C. botulinum produce?

A
  • Neurotoxin
    • irreversibly blocks the release of acetylcholine from the motoric end plate which results in muscle weakness and paralysis
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27
Q

What are the symptoms of Botulism?

A
  • Toxin is absorbed from GI tract to bloodstream
  • Symptoms
    • Toxin already produced, symptoms can begin when toxin hits GI tract
    • double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness
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28
Q

What are the symptoms of infant botulism?

A
  • Incubation period, spores have to produce toxin-forming bacteria
  • Sx:
    • lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone
    • Can lead to paralysis of respiratory system and other muscles
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29
Q

What foods reservoirs contain C. botulinum?

A
  • Canned foods that have not been properly heat treated
  • Honey
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30
Q

What are the five bacterias that cause food borne bacterial illness?

A
  1. Clostridium perfringens
  2. Salmonella enterica ssp.
  3. Campylobacter jejuni
  4. Listeria monocytogenes
  5. Vibrio parahaemolyticus
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31
Q

What are the mechanisms that food borne illness pathogens cause disease?

A
  • Toxin production – bacteria release toxin that causes illness.
    • Secretion of exotoxin
  • Host immune response – response of host to microbe that causes illness.
  • Microbial proliferation and invasion – growth and spread of microbes that causes damage that is significant in illness.
    • Direct cellular invasion
      • Sometimes replicate in cells, sometimes not
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32
Q

What are the big 3 (for the US) Bacterial sources of food borne illness?

A
  • Campylobacter jejuni
    • Intestinal cell invasion
  • Salmonella enterica
    • Intestinal cell invasion
  • Clostridium perfringens
    • Enterotoxin
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33
Q

Clostridium perfringens

Gm +/-

Shape

Aerobe/Anaerobe

Motility

Toxin

A
  • Gram +
  • Bacilli
  • Spore-forming
  • Obligate anaerobe
  • Non-motile
  • Enterotoxin binds to receptors in endothelial cell junctions, then generates pores in host mucosa cells.
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34
Q

What are the symptoms of Clostridium perfringens Food Associated Illness?

A
  • Diarrhea and abdominal cramps
  • Incubation 6 to 24 hours (typically 8-12)
  • Symptoms last for less than 24 hours
  • Usually NO fever or vomiting
  • The illness is not passed from one person to another
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35
Q

How do you positively diagnose Clostridium perfringens Food Associated Illness?

A
  • Detection of toxin or high amounts of bacteria in feces
  • C. perfringens normally present in the GI tract, the problem is when you ingest a C. perfringens load high enough to produce enough toxin to generate symptoms
  • Commonly acquired in CAFETERIAS
    • often occurs when foods are prepared in large quantities and kept warm for a long time before serving
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36
Q

Campylobacter jejuni

Gm +/-

Shape

Aerobe/Anaerobe

Motility

A
  • Gram -
  • Bacilli (Spirilli)
  • microaerophilic
  • Motile
  • Cold sensitive
  • Sensitive, sometimes killed before it can be cultured!
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37
Q

What agar is used to grow Campylobacter jejuni?

A
  • Karmali agar is a selective medium:
    • Charcoal-based.
    • Because it is difficult to grow → must eliminate competing microorganisms
    • Contains vancomycin active against the gram-positive organisms, cefoperazone active against many normal flora, cycloheximide active against yeasts
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38
Q

What are the symptoms in Campylobacteriosis caused by Campylobacter jejuni?

A
  • Diarrhea, cramping, abdominal pain, and fever
  • 2-5 day incubation
  • Symptoms can last a week
  • Can have vomiting
  • Diarrhea can be bloody!
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39
Q

What is the mechanism of Campylobacter jejuni causing Campylobacteriosis?

A

Symptoms are an inflammatory response to cell invasion

40
Q

How do you positively diagnose Campylobacteriosis?

A

stool culture

41
Q

What is a possible complication of Campylobacteriosis?

A

Guillain-Barré syndrome

42
Q

Salmonella

Gm +/-

Shape

Spore formation

Motility

A
  • Gram -
  • Bacilli
  • Non spore forming
  • H2S positive
  • Lactose negative
  • Motile, flagellated
43
Q

What are the subspecies of Salmonella that cause food borne illnesses/gastroenteritis?

A
  • S. Enteritidis
  • S. Typhimurium
44
Q

What agar is used to identify Salmonella?

A
  • Salmonella Shigella (SS) agar:
    • has bile salts that inhibit gram-positive and coliform organisms
    • contains indicator
      • lactose fermenting organisms would appear red from the acid produced
    • Ferric citrate added for indication of H2S production
      • black color is the produced iron sulfide precipitate
45
Q

What are the symptoms of Salmonellosis?

A
  • Symptoms caused by invasion mechanism!
    • replicates in host cells as well as invades
  • Diarrhea, fever, and abdominal cramps
  • 12 hr to 3 day incubation
  • Symptoms typically last 4 to 7 days
  • Most persons recover without treatment
  • Remember: reactive arthritis as a possible complication
46
Q

What are the food reservoirs for Salmonella?

A
  • Eggs
  • Dairy
    • Ice cream
  • Human transmission
47
Q

How is Salmonellosis positively diagnosed?

A

Stool culture

48
Q

What is the treatment for Salmonellosis?

A

Hydration.

Antibiotics only necessary if infection spreads beyond gut.

49
Q

Vibrio spp.

Gm +/-

Shape

Aerobe/Anaerobe

Motility

A
  • Gram (-)
  • Vibrio (curved rod)
  • facultative anaerobes
  • Flagellated, motile
  • Oxidase +
  • Gram-negative rod with single flagellum, water loving
50
Q

What type of culture is used to diagnose Vibrio spp.?

A
  • Mixed culture of oxidase-negative Escherichia coli (colorless) and oxidase-positive Vibrio cholerae (purple) showing how the direct oxidase test differentiates between the two organisms.
  • Kovács oxidase reagent was added directly to the plate.
51
Q

What are the symptoms of Vibrio parahaemolyticus infection?

A
  • Fairly mild bloody diarrhea, stomach cramps, fever, nausea, and/or vomiting,
  • Symptoms last less than a week.
  • In the immunocompromised, it can spread to the blood and cause serious or deadly infections in other parts of the body
52
Q

How is Vibrio infection diagnosed?

A

Vibrio may be isolated from cultures of stool, wound, or blood.

53
Q

What is the disease causing mechanism in Vibrio parahaemolyticus infection?

A
  • Likely through enterotoxins:
    • hemolysins TDH (thermostable direct hemolysin) and/or TRH
    • V. parahaemolyticus lacking these toxins is not pathogenic
  • Form pores in red blood cells but also in epithelial cells, disrupting gut homeostasis
54
Q

What is the food reservoir of Vibrio parahaemolyticus?

A

Shellfish

55
Q

Listeria monocytogenes

Gm +/-

Shape

Aerobe/Anaerobe

Motility

Hemolysis

Oxidase +/-

A
  • Gram positive rod-shaped bacteria
  • Gram (+)
  • Bacillus
  • Non-fastidious!!!
    • able to grow without special nutrition/agar
  • Flagellated, motile
  • Non spore forming
  • Oxidase -
  • β-hemolytic but zone of discoloration is really only directly under the colonies
56
Q

What are the symptoms of Listeriosis?

A
  • Mild GI infection for most
  • Fever and muscle aches or stiff neck
  • More vulnerable are older adults, pregnant women, newborns, and adults with weakened immune systems OPPORTUNISTIC
    • If you develop while pregnant: fever and chills
    • Meningitis and sepsis in vulnerable populations
57
Q

How do you diagnose Listeriosis?

A
  • Stool sample ID inappropriate
  • Positive ID is the bacterium found in a normally sterile site
58
Q

What is the disease causing mechanism of Listeria monocytogenes?

A
  • Invasive mechanism
    • If you have the classic clinical symptoms, the disease has already reached the invasive stage
  • Immune cells spread Listeria to other organs
    • Trojan horse
    • Liver is a major target
59
Q

What are the food reservoirs for Listeria monocytogenes?

A
  • Foods you don’t cook:
    • sprouts
    • deli meats
    • smoked seafood
    • soft cheeses
    • raw milk
  • Hardy bacterium can hang a long time at food processing facilities
60
Q

How do Shigella spp. cause infection?

A
  • Very closely related to E. coli.
  • Invasive and produces a toxin
  • Transmission: Mostly bacterium passing from stools or soiled fingers of one person to the mouth of another person.
61
Q

What are the symptoms of infection with Shigella sonnei?

A
  • diarrhea (often bloody)
  • fever
  • stomach cramps
  • Symptoms start 1-2 days following exposure
  • Usually resolves in 5 to 7 days
62
Q

What are the three types of Shigella species that can cause GI illnesses and diarrhea?

A
  1. Shigella sonnei: most Shigella-caused GI illnesses
  2. Shigella flexnori: causes bacillary dysentery
  3. Shigella dysenteriae: rarest but most severe dysentery
63
Q

What is dysentery?

A
  • Frequent, small bowel movements with blood and mucus, accompanied by rectal pain and spasms (tenesmus)
  • Not a synonym for bad diarrhea!
64
Q

What is the difference between Amoebic and Bacillary Dysentery?

A
  • Bacillary → GI illness caused by bacteria
    • sudden onset fever, chills, pus-containing diarrhea
    • more prostration (exhaustion)
    • acute course
  • Amoebic → GI illness caused by amoeba/protozoa
    • gradual onset of bloody diarrhea
    • less prostration (exhaustion)
    • chronic course
65
Q

Shigella spp.

Gm +/-

Shape

Aerobe/Anaerobe

Motility

A
  • Gram (-)
  • Bacillus
  • Facultative anaerobe
  • Nonmotile
  • Non spore forming
  • Mainly lactose negative, H2S (-)
  • “Shigella have no flagella”
66
Q

What is the mechanism of disease Shigella spp.?

A
  • Bacteria gain entry to M-cells in gut
    • entry mediated by type III secretory system and other effector proteins, and cytoskeletal rearrangements
  • Macrophages phagocytose bacteria
  • Macrophage apoptosis occurs
  • Bacteria survive
  • Infection of neighboring cell
    • Shigella actin rockets to move around
  • Initiation of inflamation
67
Q

What is the treatment for infections caused by Shigella spp.?

A
  • Since Shigella is invasive, if not treated it can spread beyond the GI tract and cause complications
  • Antibiotics for more severe cases, most usually resolve without antibiotics
68
Q

What is a potential complication of Shigella spp.?

A
  • Possible complication: hemolytic uremic syndrome (HUS)
  • S. flexnori also a cause of reactive arthritis
69
Q

What is so scary about Shigella dysenteriae?

A
  • Invasive, plus has a phage-borne toxin
    • Shiga toxin, also called the verotoxin
    • Toxin acts on vascular endothelial cells
      • inactivates ribosome => dead cell
  • Most severe dysentery!
70
Q

What are the diseases caused by E.coli?

A
  • Diarrhea
  • Urinary tract infection
  • Neonatal sepsis
  • Gram-negative sepsis
71
Q

What makes E.coli pathogenic?

A
  • They acquire a toxin!
    • Shiga toxin-producing E. coli (STEC)—Also known as VTEC or enterohemorrhagic E. coli (EHEC)
      • Outbreaks in U.S. O157:H7
    • Enterotoxigenic E. coli (ETEC)
      • Traveler’s Diarrhea, diarrhea in children
72
Q

What is the difference between toxin delivery in ETEC and STEC E.coli strains?

A
  • ETEC
    • delivery of enterotoxin from lumen
  • STEC
    • intimate attachment of bacteria
    • actin condensation
    • microvillous effacement
    • delivery of shiga toxin
73
Q

What are the symptoms of E.coli ETEC and STEC strains?

A
  • Profuse watery diarrhea and abdominal cramping
    • Can progress to bloody diarrhea for STEC
  • Fever, chills, nausea with or without vomiting, loss of appetite
  • Less common: headache, muscle aches and bloating
  • Incubation → 1-3 days ETEC, 3-8 for STEC
  • Illness typically lasts 3-4 days, less than 10.
74
Q

What is a potential complication of E.coli STEC strain infections?

A

STEC: hemorrhagic colitis (HC) and/or HUS can result as a complication; children more vulnerable

75
Q

What is the treatment for E.coli ETEC and STEC strains?

A

Treatment: antibiotics generally not recommended

76
Q

Why is it generally not recommended to treat infections caused by E. Ecoli TEC and STEC strains?

A

Antibiotics → kill bacteria

Decaying bacteria release more toxin

77
Q

What are the food reservoirs for E.coli STEC and ETEC strains?

A
  • STEC => gut of cattle
    • BEEF
  • Unwashed fruits or vegetables
78
Q

What are E. coli STEC AB5 toxins?

A
  • Each toxin’s genetic locus must have two open reading frames, encoding an A and B component, encoded on the Open Reading Frame
    • Genes are stxA. stxB on a lambda bacteriaphage
  • The E. coli toxins themselves are called Stx1 and Stx2.
    • Stx1 differs from Shigella dysenteriae verotoxin by a single amino acid
    • Both can be expressed by a single strain of E. coli
79
Q

What is the proposed model for pathological coagulation response leading to HUS in E.coli STEC strains?

A
  • Shiga toxin injures endothelial cells during the first few days of infection
    • possibly even before bloody diarrhoea occurs
  • Endothelial injury generates thrombin
  • Fibrin is deposited in the microvasculature
  • Concentrations of PAI-1 rise.
    • PAI-1 blocks fibrinolysis, further accelerating the accumulation of fibrin in vessels, and exacerbating the thrombotic injury.
80
Q

What does the future detection of E.coli STEC strains involve?

A
  • Rapid whole-genome sequencing for near-real-time analysis of an emerging pathogenic E. coli strain
  • Next-gen sequencing: strains completely sequenced within 1 week of receipt (in 2011)
81
Q

What are the supportive care treatments that are upcoming in the future treatment of E.coli STEC strains?

A
  • Renal function protection:
    • intravenous volume expansion
  • Monitor for the development of microangiopathic complications
  • Anti-Stx antibodies and Mn2+ possibly combined with antibiotics less likely to induce toxin production in in vitro and animal models
    • not available yet
  • NO antiperistaltic agents! (Increased risk of HUS)
82
Q

What is the primary reservoir for Vibrio cholerae?

A

Water

83
Q

What is the mechanism of Vibrio cholerae infections causing cholera?

A
  • Typically only serogroups O1 and O139 produce cholera toxin and thus cause cholera
    • Activates adenylate cyclase
    • cAMP → decrease Na+ absorption, ­increase Cl- excretion
    • Water moves into lumen
84
Q

What are the symptoms of cholera?

A
  • An acute illness:
    • profuse watery diarrhea, sometimes described as “rice-water stools”
    • vomiting
    • rapid heart rate
    • loss of skin elasticity
    • dry mucous membranes
    • low blood pressure
    • thirst
    • muscle cramps
    • restlessness or irritability
85
Q

How is cholera diagnosed?

A
  • Confirmed only by isolation of the causative organism from the diarrheic stools of infected people.
  • Less reliable methods are available for poor areas where laboratories may not be available.
86
Q

What is the treatment for cholera?

A
  • Antibiotic therapy may help for severe cases
  • Rehydration therapy is really the biggest factor in treatment
87
Q

What is the source of S. Typhi?

A

Untreated water is the source.

(Humans are the only carriers)

88
Q

What is Typhoid fever? Sx?

A
  • Infection caused by S. Typhi
  • Life-threatening illness
    • In GI tract and then to bloodstream
  • Sx:
    • High fevers (103-104 °F)
    • Weakness and headache
    • Stomach pains, loss of appetite, diarrhea or constipation
    • Sometimes, a rash of flat, rose-colored spots
  • After symptoms clear, person could become a carrier
  • Antibiotic treatment is recommended
89
Q

What are low inoculum organisms?

A
  • Tens to hundreds of virions/cysts/bacteria will cause disease
    • Examples: Shigella, Giardia, Entamoeba, Norovirus
    • STEC E. coli, only 100 organisms
90
Q

What are high inoculum organisms?

A
  • Tens of thousands or more needed
    • Examples: Vibrio cholerae, C. perfringens
91
Q

How are low incoculum organisms acquired?

A
  • Medium of infection does not need to be grossly infected, transmission through bodily contact or almost-clean water possible
    • Secondary cases common.
  • Can be spread in cay-care centers, families
    • Example: Toddler contracts Cryptosporidosis in wading pool
92
Q

How are high incoculum organisms acquired?

A
  • Medium of infection is highly contaminated:
    • food that is contaminated then held at permissive temps
    • grossly contaminated water
  • Secondary cases rare
    • Example: traveler gets cholera from seafood carried to U.S. from Ecuador in luggage
93
Q

Clostridium difficile

Gm +/-

Shape?

Spore?

Motility?

Toxins?

A
  • Gram +
    • Gram positive but sometimes staining is “gram variable”
  • Bacilli
  • Spore-forming
  • Obligate anaerobe
  • Motile
  • Makes exotoxins
94
Q

What damage is caused in Clostridium difficile Antibiotic Associated Diarrhea?

A
  • Exotoxins cause cell death, shallow ulcers, pseudomembranes
  • Early lesions superficial
  • May eventually invade
  • Pseudomembranous colitis
95
Q

How do you diagnose Clostridium difficile Antibiotic Associated Diarrhea?

A
  • Stool smear
  • Difficult to culture
  • Obligate anaerobe
  • Toxin detection (2 tests available)
  • Scope dangerous
96
Q

What is the treatment for Clostridium difficile Antibiotic Associated Diarrhea?

A
  • Antibiotics (metronidazole, vancomycin)
  • Severe disease: bowel resection
  • New therapy: fecal transplant

GI Week 4 - WLB (8 decks)

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