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IAHI Block 2 > Bacteriology of the Colon > Flashcards

Bacteriology of the Colon Flashcards

1
Q

Gut bacteria that can cause systemic disease

A

Listeria

Salmonella Typhi/non typhoidal salmonella serotypes

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2
Q

Pathogens that invade cells/ cause inflammation/intoxicate

A

Shigella
Enterohemorrhagic E. Coli
Campylobacter/Helicobacter

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3
Q

Bacteria whose pathology and symptoms are due to exotoxin production

A

Vibrio Cholerae

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4
Q

What are the sites of terminal digestion and absorption of nutrients

A

The mucosal villi and crypts lined by a single layer of columnar epithelial cells

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5
Q

What absorbs most of the water from chyme

A

The large intestine (90%)

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6
Q

Differences in absorption between small and large intestine

A

In large intestine, villi are absent, and the colonic mucosa is full of Crypts of Lieberkhun

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7
Q

Fluid Balance
How many Liters of fluid enter the upper gastrointestinal tract each day?
What is the the average daily fecal excretion?

A

8.5 L

150mL

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8
Q

Infections alter normal intestinal physiology in one of three ways:

A
  • Penetration through an intact mucosa
  • Inflammatory or cytotoxic destruction of the ileal or colonic mucosa
  • Shift in bidirectional water and electrolyte fluxes in the upper small bowel by intraluminal toxins or minimally invasive organisms
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9
Q

Barriers to invading pathogens (6)

A
  1. Epithelial barrier and intestinal motility (epithelium continuously regenerating)
  2. Structural barrier (Tight cell junctions)
  3. Chemical barrier (Gastric acidity)
  4. Paneth cells (Secrete antimicrobial peptides)
  5. Adaptive immunity (Mucosal associated lymphatic tissue)
  6. Microbial recognition (Pattern Recognition Receptors)
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10
Q

5 Take home points about normal microbiota

A
  • Neonates are colonized following delivery
  • Colonization drives the maturation of the mucosal immune system
  • Intact microbiota monopolizes physical and nutritional niches at the mucosal surface
  • Normal microbiota contributes to nutrient acquisition by fermenting non-digestible dietary components, contributing to normal growth and differentiation
  • Normal microbiota provide powerful host defense mechanism to limit the ability of pathogens to take up residence and invade the human body
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11
Q

Listeriosis

A

Aerobic non spore forming Gram positive rod

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12
Q

Listeriosis
Human Pathogen:
Growth range:
How it enters the body:

A

Human Pathogen: L. monocytogenes
Growth range: 1-45° and high salt concentrations
How it enters the body: Penetration through an intact mucosa to the reticuloendothelial system

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13
Q

Listeriosis is restricted to well defined populations:

A
  1. Neonates
  2. Elderly
  3. Pregnant Women
  4. Persons with defects in cellular immunity
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14
Q

Listeria pathogenesis

A
  1. Ingest contaminated food
  2. L. monocytogenes are able to survive in stomach acid and bile salts
  3. Adherence to host cells
  4. Entry into enterocytes or M cells in Peyer patches
  5. Phagosome is initially intact
  6. pH drop in the phagosome activates listeriolysin O and 2 different phospholipase C enzymes
  7. Bacteria replicate free in cytoplasm
  8. ActA located on one pole of the bacterium polymerizes host actin allowing intracellular movement to membrane
  9. Actin polymerization pushes the bacterium to uninfected cells and the cycle begins again
  10. Systemic infection - passage through the intestinal lining, entry into macrophage and spread
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15
Q

Listeria - Epidemiology

A

Human listeriosis is sporadic
Undercooked processed meats, unpasteurized milk, contaminated cheese…
Can be isolated from the feces of animals
Can grow inside of wide range of temperatures

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16
Q

Human to human transmission of Listeria occurs from _____ to ____ in _____

A

mother; child; utero

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17
Q

Lysteria Clinical Diseases
Neonatal:
Pregnant Women:
Adults:

A
  • Neonatal disease
    Early onset disease acquired in utero - abortion, stillborn or premature birth
    Granulomatosis infantiseptica = granuloma formation in multiple organs
    Late onset disease -2-3 weeks after birth - characterized by meningitis
  • Pregnant women (third trimester - influenza-like)
  • Adults
    Healthy - mild influenza like illness
    Immunocompromised - meningitis
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18
Q

Listeria - Laboratory Diagnosis

A

Gram stain of CSF for meningitis patients
Culture - 1 to 2 days - cold enrichment
Biochemical Tests
Serologic tests - 13 serotypes

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19
Q

Listeria - treatment, prevention, control

A

Ubiquitous in environment so control is difficult
No vaccine
Combination treatment = gentamicin with penicillin
Naturally cephalosporin resistant

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20
Q

Salmonella:

Method of Entry:

A
  • Gram negative rods, found in soil ,water, normal intestinal flora
  • Method of Entry: Penetration through an intact mucosa
  • Inflammatory or cytotoxic destruction of the ileal or colonic mucosa
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21
Q

Serotyping schemes to identify individual salmonella isolates

A

H antigen = flagellar proteins
K or Vi = capsular antigens for E. coli and S. typhi, respectively
O antigens = Lipopolysaccaride

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22
Q

Salmonella does not ferment _________

A

lactose

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23
Q

Salmonella Pathogenesis

A
  • Broad host range EXCEPT for Typhi and Paratyphi
  • Salmonella can resist stomach acid; attach to the mucosa of the small intestine and invade into M cells and enterocytes
  • Replicates within endocytic vacuoles
  • Endocytic vacuoles are modified and stabilized by the injection of bacterial proteins through two type III systems = spacious vacuole
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24
Q

Pathogenicity Island 1 genes = ______

Pathogenicity Island 2 genes = ______

A

invasion; evasion of immune response

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25
Q

Gastroenteritis due to Salmonella

A
  • Infection and replication induces an inflammatory response
  • Disruption of the enterocytes and malabsorption
  • Release of prostoglandins, stimulation of CAMP and fluid secretion
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26
Q

Pathogenesis of Enteric or Typhoid Fever

A
  • Bacteria invade cells and replicate as in gastroenteritis
  • Typhi also replicates in macrophages and spreads through the reticuloendotheilal system to liver, spleen, blood and bone marrow
  • Bacteremia causes the fever and may lead to localized suppurative infections or in rare cases perforation of the intestine
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27
Q

Gastroenteritis to salmonella Epidemiology (6)

A
  1. Ingestion
  2. Incidence is greatest in children (under 5) and adults (older than 60)
  3. Occurs most frequently during the summer months
  4. Common food sources include poultry, eggs, dairy products, ground beef
  5. Nontyphoidal US infections > 1.4 million with 600 deaths/year
  6. Infectious dose is high (10^6 - 10^8 bacteria)
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28
Q

Typhoid or Enteric Fever Epidemiology

A
  • Relative to strains causing gastroenteritis, the inoculum for Typhi is low
  • Transmission person to person and through fecal contamination
  • Enteric fever is endemic to India, South/Central America, Africa
  • Travelers should be vaccinated when going to endemic areas
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29
Q

Salmonella outbreaks in children can occur with the introduction of _____

A

PET TURTLES!

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30
Q

Salmonella clinical diseases:
S. Gastroenteritis:
S. Septicemia:
Enteric Fever:

A
  • S. Gastroenteritis: Symptoms - 6 - 48 hours after consumption of contaminated food (fever, cramps, headache, nausea, vomiting) - persists for 7 days but self limiting
  • S. Septicemia: ALL SALMONELLA SPECIES CAN CAUSE A BACTEREMIA
  • Immunocompromised patients at risk for septicemia
  • Enteric Fever:
    10-14 days after ingestion - gradual fever, headache, myalgias, anorexia, rose spots
  • After bacteremic phase gastrointestinal symptoms occur: colonization of gall bladder and reinfection of the intestines
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31
Q

Mary Mallon - Typhoid Mary

A
  • First person identified in US as asymptomatic carrier of S. Typhi
  • She was a cook - infected 51 people, three of whom died
  • Typhoid fever was traced to the places where she worked
  • Arrested and quarantined
    She died of pneumonia and complications of a stroke
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32
Q

Salmonella - Laboratory Diagnosis

A
  • Stool culture - must use selective medium to recover salmonella versus normal flora
  • Lactose negative, motile, makes H2S, other differential biochemical tests
  • Epidemiological investigations use pulsed-field electrophoresis
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33
Q

Salmonella - Treatment, Prevention, Control

A
  • Symptomatic relief but no antibiotics for Salmonella gastritis
  • Careful food preparation and storage, hand washing
  • Ampicillin, trimethoprim-sulfamethoxazole for systemic infections
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34
Q

Traveler vaccinations for Salmonella

A

Live attenuated vaccine Ty21a: good for 5yrs, 6 capsules every other day, booster at 4 yrs, not recommended for children

Typhim - Vi polysaccharide capsular vaccine, not recommended for children under 2 years of age

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35
Q

Shigella Characteristics

A
  • Family member of the Enterobacteriaceae (Gram negative)
  • Non motile (no flagella), does not ferment lactose, no capsule
  • Infectious dose is low, easily spread person to person by the fecal oral route
  • 4 recognized biogroups - dysenteriae, flexneri, boydii, sonei
36
Q

Shigella -

4 recognized biogroups

A

dysenteriae, flexneri, boydii, sonei

37
Q

Shigella - Pathogenesis

A
  1. Shigella replicate intracellularly in the colon
  2. They invade M cells in Peyer patches and initially colonize the small intestine
  3. Bacteria inject type III “effectors” into cells to instruct the cytoskeleton to engulf them
  4. The effectors are called Invasion Protein Antigens or IpaA, IpaB, IpaC and IpaD
  5. Once inside of host cells the bacterium lyses the vacuole and replicates free in the cytoplasm
  6. Similar to Listeria, Shigella polymerize host actin to move to the membrane to penetrate uninfected cells
  7. Shigella induce apoptosis in phagocytic cells which leads to a release of IL-1β resulting in intense inflammatory response
38
Q

Shigella - Toxins

A

Ipa proteins - induce bacterial uptake - injected by the type III secretory system
Shigella secrete Shiga toxin
- Exported by a type II secretory pathway
- Shiga toxin is a typical A:5B toxin
*B = recognizes the host glycolipid GB3
*A = enzymatic activity of the toxin; cleaves 28S ribosomal RNA disrupts protein synthesis and colonic epithelium dies and cells and mucous are lost from the large intestine

39
Q

____ are the only reservoir for Shigella

______ is a pediatric disease (60% of cases in children under 10

A

Humans

Shigellosis

40
Q

Shigella Transmission

A

Infectious dose is low (100-200 bacteria) so person to person transmission is easy through fecal-oral route

41
Q

Shigella - Clinical Disease

A 
Incubation period after ingestion 1-3 days
Symptoms
- Abdominal cramps
- Tenesmus or straining to defecate
- Diarrhea
- Pus and blood in stools
- Neutrophils and mucous in stool
42
Q

Dysentery

A

Term coined by Hippocrates to describe the frequent passage of stool containing blood and mucous

43
Q

Shigella laboratory Diagnosis

A
  • Lactose negative colonies on selective medium (colorless as opposed to pink colonies on MacConkey agar)
  • Shigella is NOT motile while salmonella is flagellated and motile and Shigella does not produce H2S
44
Q

Shigella - Treatment, Control and Prevention

A
  • Mild infections are usually self limiting
  • Antibiotic treatment may shorten illness but are only used for severe illness
  • Antidiarrheal agents such as loperamide or diphenoxylate with atropine can make illness worse
  • In presence of antidiarrheal agents, Shiga toxin is not flushed from the system, leading to more extensive cell death and inflammation
45
Q

Enterohemorrhagic E. Coli (EHEC) - Characteristics

A

Family member of the Enterobacteriaceae (Gram Negative)
Infectious dose is low (100-200 bacteria) - spread person to person by fecal oral route
Member of the family of pathogenic E. coli

46
Q

EHEC pathogenisis

A

Culture filtrates from these bacteria were cytotoxic to Vero cells
Toxic activity could be neutralized with antibodies to Shiga toxin
Produce a distinct histopathology called attaching and effacing lesions
EPEC = EHEC that do not synthesize Shiga toxins
Alterations in the cellular cytoskeleton due to bacterial type III secretion
EHEC also injects a protein called Tir
Bacteria grow in place and release shiga toxin

47
Q

Tir

A

EHEC protein that integrates into the mammalian cellular membrane and binds tightly to a bacterial outer membrane protein called intimin

48
Q

Shiga toxins are encoded on lysogenic bacteriophage in E. Coli (2 types)

A 
Stx-1 = Shiga toxin
Stx-2 = 60% homology to Shiga toxin (A:5B)
49
Q

Shiga toxin

A

Stops host protein synthesis by cleaving host ribosomal RNA
Binds to cell with GB3 receptor
Strains expressing both toxins are more virulent
Stimulate the expression of inflammatory cytokines

50
Q

EHEC epidemiology

A

EHEC associated with certain H and C serotypes
Certain serotypes may be selected for in the intestinal tract of cattle
Undercooked beef, meat, cattle feces

51
Q

EHEC clinical diseases
Hemorrhagic colitis:
Hemolytic uremic syndrome (HUS):

A

Hemorrhagic colitis: Characterized by severe abdominal pain and bloody diarrhea that occurs 3-4 days after ingestion of contaminated food
Hemolytic uremic syndrome (HUS): Occurs in children under 10 years of age - acute renal failure; thrombocytopenia; microangiopathic hemolytic anemia
*vomiting in about 50% of patients

52
Q

EHEC laboratory diagnosis

A

Culture - differential identification based on the inability to ferment sorbitol
EHEC is colorless and normal
Look for certain serotypes associated with HC or HUS
Immunoassays to detect the presence of Stx-1 or Stx-2

53
Q

EHEC treatment, prevention and control

A

Treatment consists of supportive care
Monitoring of the development of microangiopathic complications (HUS)
Antiperistaltic agents increase the risk of systemic complications
Antibiotic therapy is generally not beneficial - may increase shiga toxin production and release
Careful cooking of food

54
Q

Campylobacter: Physiology and Structure

A

Gram negative curved rod
Microaerophilic, can grow at 42°
Non-fermentative
Motile with single flagellum at one or both poles

55
Q

Major isolates of Campylobacter associated with human disease

A

C. jejuni
C. upsalensis
C. coli
C. fetus

56
Q

Campylobacter pathogenisis

A
  1. Inflammation - gastrointestinal infections produce histologic damage to the mucosal surfaces of the jejunum, ileum and colon
  2. Infection is associated with the development of autoimmune disorders (Guillan-Barre syndrome; reactive arthritis)
  3. Other than LPS and antigenic cross-reactivity, one toxin has been discovered that stops cell division - cytolethal distending toxin (cdt)
57
Q

Campylobacter Epidemiology

A

Infections are associated with the consumption of contaminated food, particularly chicken
Not a reportable disease - difficult to grow and identify bacteria

58
Q

Highest isolation rates of Campylobacter are in ______ and ______ _____

A

Summer and early fall

59
Q

Campylobacter clinical diseases
Acute enteritis:
Extraintestinal infections:

A

Acute enteritis: Gastrointestinal infection characterized by bloody stools, inflammation, ulcerated mucosa, diarrhea
Extraintestinal infections: C. fetus in compromised patients - resistant to serum antibody and complement killing

60
Q

Campylobacter - laboratory diagnosis

A

Microscopy - darting motility in fresh fecal samples
- S shaped organism in stool
- Presence of RBCs and WBCs in stool
Antigenic detection
Culture - difficult - slow growth; microaerophilic

61
Q

Campylobacter - Treatment, Prevention and Control

A

Treatment recommendations - Fluid replacement as long as diarrhea lasts
Severe cases are treated with azithromycin or erythromycin
Severe infections include: high fever; bloody stool; symptoms lasting over 1 week

62
Q

Helicobacter - Physiology and Structure

A 
Gram negative curved rods
Multiple polar flagella, highly motile
Microaerophilic
Produce a powerful urease enzyme that converts urea to NH3 and CO2
Difficult to culture and isolate
63
Q

Helicobacter - pathogenesis

A

Gastric colonization can be lifelong so part of the pathogenesis involves survival in this extreme environment

  1. Urease expression allows the bacterium to survive in acidic gastric juice
  2. They swim through the mucus using flagella
  3. They adhere to the gastric epithelium via specific receptors that include the Lewis blood-group Ags and laminin
  4. pH at the epithelial surface is 7.0
64
Q

Helicobacter - pathogenesis

The production of ______ ______ in humans in strongly correlated with the possession of ___ genetic loci

A

Peptic ulcers; two

65
Q

VacA (Helicobacter)

A

A multifunctional toxin

  • Forms anion specific channels
  • forms large vacuoles in cultured cells
  • alters tight junctions
  • induces gastric epithelial erosion in animal models
66
Q

Second locus associated with peptic ulcers (Helicobacter)

A

Second locus encodes many genes including:
Specialized secretion system called a type IV secretory system
This secretion system injects CagA which induces IL-8 release - also induces pedestal formation
Other products also enhance IL-8 transcription in epithelial cells

67
Q

Helicobacter pathogenesis
Urease:
Flagella:
Adhesins:

A

Urease: secretion to survive in gastric juice
Flagella: allows them to propel into mucus layer and to reach the gastric epithelial cells
Adhesins: allow bacterium to stick to the apical region of epithelial cell

68
Q 
Heliobacter - Epidemiology
Reservoir:
Transmission:
Highest Incidence:
Asymptomatic:
Increased risk:
Associated diseases:
A

Reservoir: Humans only
Transmission: fecal-oral route
Highest Incidence: Developing countries
Asymptomatic: 70-80% of infected individuals
Increased risk: Persons with gastritis, gastric ulcer or duodenal ulcers
Associated diseases: infection is also associated with gastric adenocarcinoma and gastric B-cell lymphomas

69
Q

Helicobacter - Clinical diseases
Gastric Helicobacters:
Enterohepatic Helicobacters:

A

Clinical outcome depends on site of colonization
Gastric Helicobacters: H. pylori; gastritis, peptic ulcer, gastric adenocarcinoma, gastric mucosa-associated lymphoid tissue (MALT) B-cell lymphomas
Enterohepatic Helicobacters: Isolates from homosexual men with procititis, proctocolitis, or enteritis

70
Q

A chronic inflammatory response to Helicobacter may contribute to the development of ______

A

cancer

71
Q

Helicobacter - Laboratory Diagnosis

A
  1. Urea breathing test
  2. Histologic examination of gastric biopsy
  3. Biochemical detection of urease activity from gastric biopsy
  4. Detection of H. pylori antigens from stool samples
72
Q

Helicobacter - Treatment, Prevention and Control

A

Recommended treatment: Proton pump inhibitor + macrolide + β-lactam
NO vaccine - not sure whether eradication is good

73
Q

Vibrio
Structure:
Important human pathogens:

A

Structure: Gram negative curved rods
Important human pathogens:
- Vibrio cholerae serogroups 01 and 0139 - produce cholera toxin
- Vibrio vilnificus - associated with wound infections and septicemia
- Vibrio parahaemolyticus - gastroenteritis, wound infection, septicemia

74
Q

Vibrio - Physiology and structure

A 
Curved rods with single polar flagella
Require NaCl for growth
Oxidase positive
Toxin co-regulated pili
Serogroups are based on LPS
75
Q

Vibrio serotypes

A

Serotypes O1 and O139 produce cholera toxin and are associated with epidemic disease
Serotype O1 is subdivided into Classical and El Tor biotypes
- Current pandemic is due to El Tor

76
Q

Vibrio pathogenisis (Cholera toxin)

A

Cholera Toxin is an A:5B protein
Cholera toxin and Labile toxin (ETEC) are structurally and functionally similar
Toxins bind ganglioside receptors on intestinal epithelial cells = GM1
The A subunit ADP-ribosylates the G protein and induces cAMP production
Camp stimulates the CFTR inducing Cl- secretion, inhibiting NaCl absorption and causing water efflux - tremendous loss of water

77
Q

Other factors encoded on Vibrio phage

A

TCP = Toxin coregulated pilus; used by bactera to adhere to the mucosal epithelium and used by the phage to infect the bacteria
Chemotaxis proteins - also used for adherence to host epithelial cells
Zona Occludens toxin (ZOT) - disrupts tight junctions
Accessory cholera enterotoxin (Ace) - increases fluid secretion

78
Q

Why is Vibrio pathogenesis hard to prevent?

A

The expression of toxins prevents the development of live attenuated vaccines

79
Q

Vibrio epidemiology

A

Vibrio grows in nature in estuarine and marine environments
Pathogenic vibrios infect shellfish
Asymptomatic individuals can shed the organism
Cholera is transmitted by contaminated water and food
Infectious dose = approximately 10^8 with normal stomach acid levels

80
Q

Vibrio clinical diseases:
V. Parahaemolyticus:
V. Vulnificus:

A

2-3 days after ingestion, abrupt onset of watery diarrhea and vomiting
DIarrhea becomes colorless and odorless and contains small specks of mucous = rice water stool
Dehydration, cramps, metabolic acidosis
Mortality rate can be 60% if untreated
V. Parahaemolyticus: gastritis ranging from mild to severe
V. Vulnificus: wound infection/septicemia

81
Q

Vibrio laboratory diagnosis

A

Microscopy - curved gram-negative rods in large numbers in stool material from wound infections
Culture - Relatively easy to isolate in the laboratory; confirmation by a relatively small number of biochemical tests

82
Q

Vibrio treatment, prevention and control

A
  1. Fluid electrolyte replacement
  2. Antibiotics can reduce toxin production and decrease transmission
  3. Improvements in sanitation
  4. Vaccines
    - Formalin inactivated whole cell vaccine (IM)
    - Dukoral given PO - also given for travelers diarrhea due to ETEC
83
Q

Dukoral

A

Heat and formalin killed O1 classical and El Tor strains - IgA response prevents colonization
Non-toxic B subunits - IgA response prevents toxin binding

84
Q

Klebsiella Pneumonia Resistant to Carbapenems (CRKP) and Carbapenem resistant Enterobacteriaceae (CRE)

A

Cephalosporins and Carbapenems are antibiotics usually reserved to treat the sickest patients
Difficult to control, can be fatal in up to 40% of cases

85
Q

Family of Pathogenic E.Coli (5):

A
  1. Enterotoxigenic E. coli (ETEC) - Labile toxin (LT‐1) and stable toxin (STa)
  2. Enteropathogenic E. coli (EPEC) - attaching and effacing lesion
  3. Enteroinvasive E. coli (EIEC) - like Shigella, invasive, inflammatory
  4. Enteroaggregative E. coli (EAEC) - adherence, colonization
  5. Uropathogenic E. coli (UPEC) - fimbrial adherence, UTI

IAHI Block 2 (12 decks)

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