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Microbiology > CH 24 - Digestive System Infections > Flashcards

CH 24 - Digestive System Infections Flashcards

1
Q

Cirrhosis
(definition)

A

Scarring of liver that interferes with normal liver function

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2
Q

Dental caries
(definition)

A

Biofilm-mediated process that damages tooth enamel

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3
Q

Dysbiosis
(definition)

A

Imbalance in normal microbiota

May be caused by taking antimicrobial medications

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4
Q

Dysentery
(definiton)

A

Serious form of diarrhea characterized by blood, pus, & mucus in feces

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5
Q

Gastroenteritis
(definition)

A

Acute inflammation of stomach & intestines

Syndrome of nausea, vomiting, diarrhea, abdominal pain

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6
Q

Gingivitis
(definition)

A

Inflammation of gums

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7
Q

Hemolytic Uremic Syndrome (HUS)
(definition)

A

Serious condition characterized by RBC breakdown & kidney failure

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8
Q

Hepatitis
(definition)

A

Inflammation of the liver

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9
Q

Microvilli
(defintion)

A

Tiny extensions from surfaces of cells such as those lining the intestinal villi

Increase surface area of mucosa

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10
Q

Oral Rehydration Therapy (ORT)
(definition)

A

Treatment used to replace fluid & electrolytes lost due to diarrhea

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11
Q

Potential Dangers in Thanksgiving Dinner

A
  1. Taenia solium (tapeworm)
  2. Clostridium botulinum
  3. Salmonella enterica (Campylobacter)
  4. Staphylococcus aureus
  5. Escherica coi
  6. Dental caries (Streptococcus mutans)
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12
Q

Normal Microbiota of the Digestive System:

Esophagus/stomach/duodenum, oral cavity (tongue/teeth), lower small intestine/colon

A

Esophagus/stomach/duodenum:
- Few resident microbes

Oral cavity (tongue/teeth):
- Viridans streptococci

Lower small intestine & colon:
- Tremendous amount of microbes
- Act as microbial antagonists against transient microbes

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13
Q

Antibiotic-Associated Diarrhea

A

Microbiota prevent colonization of some pathogenic bacteria

Use of antibiotics disrupts normal microbiota (mild to severe diarrhea)

Toxin-producing bacteria can colonize newly uninhabited intestine
- Damage epithelial cells
- Ex: Clostridium difficile

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14
Q

Dental Caries:
Causative Agent

A

Streptococcus mutans
- G+ facultative anaerobe
- 10,000 CFU/mL in mouth

Other bacteria participate as well

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15
Q

Streptococcus mutans Virulence Factors:

A
  1. Extracellular matrix of glucans from sucrose
  2. Tolerant to acidic environment
  3. Produce lactic acid when metabolizing sugars
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16
Q

Dental Caries:
Symptoms

A
  • Toothache
  • Discoloration
  • Roughening of enamel
  • Tooth breakage
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17
Q

Dental Caries:
Pathogenesis

A
  1. Attachment of bacteria to enamel & formation of cariogenic plaque
  2. Addition of sugars (sucrose) to environment causes drop in pH (~5)
    - Due to fermentation
    - Dissolves calcium phosphate of enamel
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18
Q

Dental Caries:
Prevention

A
  1. Good oral hygiene
    - Reduce/eliminate sugary foods
  2. Fluoride
    - Protects teeth from demineralization caused by acid
    - Promotes remineralization
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19
Q

Dental Caries:
Treatment

A

Drilling of diseased region & filling defect to restore contour of tooth
- Filling of composite or amalgam

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20
Q

Peptic Ulcers:
Causative Agent

A

Helicobacter pylori
- G-
- Multiflagellated
- Microaerophile

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21
Q

Peptic Ulcers:
Symptoms

A
  • Stomach ache
  • Abdominal pain
  • Acid reflux
  • Regurgitation
  • Vomiting
  • Belching
  • Flatulence
  • Nausea
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22
Q

Untreated Helicobacter pylori Infection Can Cause:

A
  1. Peptic ulcers (duodenal or gastric)
  2. Gastroesophageal reflux (GERD)
  3. Cancers of esophagus & stomach
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23
Q

Peptic Ulcers:
Pathogenesis

A
  1. Bacteria invade mucus & attach to gastric epithelial cells
  2. Helicobacter, its toxins, & inflammation cause layer of mucus to become thin
  3. Gastric acid destroys epithelial cells & underlying disease
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24
Q

Peptic Ulcers:
Epidemiology (Urease Test)

A

Conversion of urea into CO2 can be detected in breath

Breakdown of urea by urease enzyme
- Releases ammonia & CO2

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25
Q

Peptic Ulcers:
Treatment

A
  1. Proton pump inhibitors (PPIs)
    - Reduce acid (heal stomach)
  2. Antibiotics (kill bacteria)
    - Clarithromycin
    - Amoxicillin
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26
Q

Peptic Ulcers:
Barry Marshall

A

Drank H. pylori & developed ulcer

Marshall & Warren won Nobel Prize in 2005

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27
Q

Cholera:
Causative Agent

A

Vibrio cholerae
- G-
- Polar flagellum

Found naturally in aquatic environments (salt & fresh water)

Infects humans upon consumption of contaminated food & water

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28
Q

Cholera:
Symptoms

A
  • Watery diarrhea in large volumes (1-6 L/hr; “rice-water” stool)
  • Vomiting
  • Muscle cramps
  • Organ failure
  • Cholera toxin (causes primary symptom)
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29
Q

Cholera:
Epidemiology

A

1.3-4 million cases/year
- 21-143,000 deaths/year (WHO)

1849 cholera epidemic
- 600 deaths/5000 population (12%)

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30
Q

Cholera:
Dr. John Snow

A

“Father” of modern epidemiology

Worked to determine source of cholera epidemic in London 1854
- Traced to single water source (water pump)

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31
Q

Cholera:
Pathogenesis

A
  1. Bacteria ingested
  2. Colonize small intestine
  3. Express cholera toxin (CT)
    - Encoded by lysogenic bacteriophage
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32
Q

Cholera:
Cholera Toxin (CT)

A

B subunit = binding
- Binds to gangliosides on epithelial cell surfaces

A subunit = active
1. Translocated
2. Catalyses ADP-ribosylation of Gs protein
3. Gs activates adenylate cyclase
4. Overproduction of cAMP
5. AMP causes ion channels to open
6. Massive secretion of ions & water into lumen

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33
Q

Cholera:
Treatment

A

Oral rehydration therapy (ORT)
- Electrolytes to successfully rehydrate pts

IV rehydration (non-responsive pts)

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34
Q

Cholera:
Prevention

A

Whole cell killed vaccine
- Somewhat protective but short-lived
- Doesn’t work well in small children

Continued search for live vaccine

35
Q

Shigellosis:
Causative Agent

A

Shigella
- G-
- Non-flagellated

Fecal-oral contact (primarily young children)

All species cause dysentery

36
Q

Shigellosis:
Shigella species

A
  1. S. flexneri
  2. S. boydii
  3. S. sonnei
  4. S. dysenteriae
37
Q

Shigellosis:
Pathogenesis

A

Invades cells in large intestine

  1. Attaches to epithelial cell of colon
    - Triggers endocytosis
    - Multiplies in cytosol
  2. Invades neighboring epithelial cells
    - Avoids immune defenses
    - Abscess forms as epithelial cells killed
  3. Shigella that enters blood = quickly phagocytized & destroyed
38
Q

Shigellosis:
Shiga Toxin (ST)

A

A-B toxin
- Carried on lysogenic bacterophage

Inhibits protein synthesis

Can cause hemolytic uremia syndrome (HUS)
- Associated with Enterohemorrhagic Escherichia coli (EHEC) which also carry ST NOT Shigella

39
Q

Shigellosis:
Epidemiology

A

Human source of transmission (fecal-oral)
- Transmission occurs most often as result of overcrowding (common in day care)

NOT easily killed by stomach acid

Low infectious dose (as few as 10 organisms)

40
Q

Shigellosis:
Prevention

A

Controlled by sanitary measures

NO vaccine

41
Q

Shigellosis:
Treatment

A

Fluid & electrolyte replacement

Antibiotics
- Ampicillin & cotrimoxazole (shorten duration)
- 20% of Shigella species resistant

42
Q

Escherichia coli Gastroenteritis:
Most diarrhea-causing E. coli fall into 4 groups

A
  1. Enterotoxigenic E. coli (ETEC)
  2. Enteroinvasive E. coli (EIEC)
  3. Enteropathogenic E. coli (EPEC)
  4. Enterohemorrhagic E. coli (EHEC)
43
Q

Escherichia coli Gastroenteritis:
Enterotoxigenic E. coli (ETEC)

A

Most common cause of “traveler’s diarrhea”

44
Q

Escherichia coli Gastroenteritis:
Enteroinvasive E. coli (EIEC)

A

Disease closely resembles Shigella species

45
Q

Escherichia coli Gastroenteritis:
Enteropathogenic E. coli (EPEC)

A

Causes outbreaks in hospital nurseries in developing countries

46
Q

Escherichia coli Gastroenteritis:
Enterohemorrhagic E. coli

A

Often produces severe illness
- Production of Shiga toxin

Shiga toxin encoded on lysogenic bacteriophage

Many infected individuals develop hemolytic uremia syndrome (HUS)

Most common strain = O157:H7

47
Q

Escherichia coli Gastroenteritis:
Symptoms

A

Infection depends on virulence of strain

Symptoms range from:
- Vomiting & loose stools
- Profuse diarrhea
- Severe cramps & bloody diarrhea

Recovery usually within 10 days

48
Q

Escherichia coli Gastroenteritis:
Virulence factors

A

Depends on type of E. coli

  1. Capsule
  2. LPS
  3. Pili
  4. Toxins
49
Q

Salmonellosis:
Causative Agent

A

Salmonella species
- G-
- Motile

Live in GI tract of animals
- Infect humans through contamination of water & food

50
Q

Salmonellosis:
Types of Salmonella Associated with Human Diseases

A
  1. S. enterica
  2. S. typhi

Infect humans through contamination of water & food

51
Q

Salmonellosis:
Symptoms

A

Gastroenteritis
- Nausea, vom, non-bloody stools

Vary depending on virulence of strain

Typically short-lived& milkd

52
Q

Salmonellosis:
Pathogenesis

A
  1. Ingested in contaminated food/water (chicken eggs)
  2. Adhere to epithelial cells of small intestine
    - Taken up by phagocytsosis (T3SS triggers)
  3. Multiplies within phagosome
    - Eventually kills host cells
  4. Inflammatory response increases fluid secretion
    - Diarrhea, fever, abdominal cramps
  5. Salmonella shed in feces
53
Q

Salmonellosis:
Serotype Typhi

A

Causes typhoid fever

Fecal-oral route

Can enter blood
- Phagocytized but NOT digested
- Phagocytes carry Salmonella to liver, spleen, bone marrow, & gallbladder

Can establish semipermanent in gallbladder
- Carriers can remain infected for years (even with treatment)

54
Q

Salmonellosis:
Epidemiology

A

Bacteria survive long periods in environment

Chickens naturally carry (undercooked food source)

Household pets (turtles, iguanas, etc._

55
Q

Salmonellosis:
Prevention

A

Cooking kills bacteria

Live attenuated vaccine
- Prevents typhoid fever
- 50-70% effective

56
Q

Salmonellosis:
Treatment

A

Antibiotic therapy

Rehydration

57
Q

Campylobacter jejuni

A

Pathogen
- G-
- Microaerophilic

Leading bacterial cause of diarrhea in US!!

58
Q

Campylobacter jejuni:
Symptoms

A

Watery/foul-smelling diarrhea

Followed by:
- Bloody stools
- Fever
- Severe abdominal pain

59
Q

Campylobacter jejuni:
Virulence Factors

A
  1. Adhesins
  2. Cytotoxins
  3. Endotoxin
60
Q

Campylobacter jejuni:
Major Source/Transmission

A

Major source = chickens
- 24% of raw chicken contains Campylobacter
- Commensal part of microbiome of chicken (no disease)

Transmitted fecal-oral route

61
Q

Campylobacter jejuni:
Diagnosis

A

Based on S/S

62
Q

Campylobacter jejuni:
Prevention

A

Proper hygiene after handling raw poultry

63
Q

Campylobacter jejuni:
Treatment

A

Most cases resolve without treatment

64
Q

Campylobacter jejuni:
Guillan-Barre Syndrome

A

Sequelae

~40% of cases due to Campylobacter

65
Q

Viral Gastroenteritis:
Causative Agents

A
  1. Cailciviruses
  2. Astroviruses
  3. Rotaviruses
    - Most common cause in small children
    - dsDNA
66
Q

Viral Gastroenteritis:
Symptoms

A
  • Abdominal pain
  • Cramping
  • Diarrhea
  • Nausea
  • Vomiting
67
Q

Viral Gastroenteritis:
Pathogenesis

A

Rotaviruses infect epithelial cells of small intestine

Damaged lining fails to absorb fluids
- Watery diarrhea

68
Q

Viral Gastroenteritis:
Epidemiology

A

More cases occur in winter

Transmitted fecal-oral route

69
Q

Viral Gastroenteritis:
Treatment

A

Fluid & electrolyte replacement

70
Q

Viral Gastroenteritis:
Prevention

A

Vaccine for rotavirus

71
Q

Norovirus

A

ssRNA virus
- Small
- Non-enveloped
- Calicivirus family

Originally caused Norwalk Virus

72
Q

Norovirus:
Symptoms

A
  • Nausea
  • Vomiting
  • Watery diarrhea

Symptoms subside in 12-60 hrs

73
Q

Norovirus:
Pathogenesis

A

Infects epithelium of upper small intestine
- Epithelial cell death
- Decreases production of digestive enzymes

Epithelium recovers in ~2 weeks

74
Q

Norovirus:
Epidemiology

A

23 million cases in US annually

Transmission = fecal-oral route

Outbreaks often occur in institutions, cruise ships, etc.
- Contaminated food/water

75
Q

Norovirus:
Prevention

A

Hand washing & disinfectants

NO vaccine

76
Q

Norovirus:
Treatment

A

NO proven antiviral med

77
Q

Viral Hepatitis:
Symptoms

A
  • Jaundice
  • Abdominal pain
  • Fatigue
  • Nausea
  • Vomiting
  • Appetite loss

Symptoms may occur years after infection

78
Q

Viral Hepatitis:
Pathogenesis

A

Hepatitis A virus (HAV)
- Fecal-oral route

Other Hepatitis viruses (HBV, HCV)
- Sexual contact or blood-borne

Host immune system responses = responsible for liver damage`

79
Q

Viral Hepatitis:
Diagnosis

A
  • Jaundice
  • Enlarged liver
  • Fluid in abdomen

Most individuals with HAV will be sick for several weeks but recover completely

80
Q

Viral Hepatitis:
Prevention

A

Good hygiene

Vaccine against HAV

81
Q

Giardia Infections:
Causative Agent

A

Giardia lamblia
- Diarrhea-causing protozoan

1 of most frequent causes of human waterborne disease in US

82
Q

Giardia Infections:
Transmission (& pathogenesis)

A
  1. Ingestion of cyst
    - Fecal contaminated food/water, streams
    - Chlorination doesn’t kill (boiling & filtration works)
  2. Trophozoite adheres to small intestine via sucking disk
    - Interferes with fat absorption
83
Q

Giardia Infections:
Symptoms

A
  • Non-bloody, foul-smelling diarrhea
  • Abdominal cramps
84
Q

Entamoeba histolytic
(general overview)

A

Diarrhea
- Ranging from mild asymptomatic to severe dysentery

May invade intestinal mucosa
- Causes erosions

May penetrate portal blood circulation
- Forms abscesses in liver & lung

100,000 deaths worldwide

Microbiology (15 decks)

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