lecture 16 Flashcards

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1
Q
  1. What are three causative agents of pneumonia discussed in class?
A

.Streptococcus pneumoniae
Klebsiella pneumoniae
Polymicrobial infections

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2
Q

How are Streptococcus and Legionella able to evade phagocytosis in the lungs?

A

.

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3
Q
  1. What are the natural defenses of the gastrointestinal tract?
A

.All intestinal surfaces are coated with a layer of mucus
Immune system cells in GALT (gut-associated lymphoid tissue)
Secreted antibodies can be found on most GI tract surfaces
Muscular walls of the GI tract keep food and microorganisms moving through peristalsis
Saliva contains lysozyme and lactoferrin
Stomach fluid is antimicrobial due to its high acidity (pH ~2)
Bile (produced by the liver) is also antimicrobial
Commensal microbiota provide the protection of microbial antagonism

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4
Q

How does the abundance and diversity of the normal GI microbiota compare with microbiota in other regions of the body?

A

more diverse and abundant
Includes bacteria as well as archaea, fungi and protozoa
Mouth has >500 species of microbes
Stomach has relatively few
Small, large intestines have the highest concentrations (up to 100 billion cells/mL), with 1000 or more different species

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5
Q
  1. What are some functions of the normal microbiota of the gastrointestinal tract?
A

Allow for degradation of some foods, e.g. dietary fiber, that human digestive enzymes alone do not act on
Provide nutrients that we can’t provide ourselves such as vitamins; e.g. E. coli synthesizes vitamin K
Presence of normal biota is important for proper functioning of epithelial cell structure
Plays an important role in “teaching” the immune system to react to microbial antigens

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6
Q
  1. What are some characteristics of Clostridium difficile and its pathogenesis/virulence factors associated with acute diarrhea?
A

Charateristics:
Mild cases have some abdominal pain, malaise
Severe cases exhibit fever and leukocytosis (increase in number of white blood cells)
Colon is inflamed (colitis) and gradually sloughs off loose, membrane-like patches called pseudomembranes
If the condition is not stopped, perforation of the cecum and death can result

Pathogenesis and Virulence Factors
Able to superinfect the large intestine when antibiotic treatment has disrupted the normal biota
Spore formation allows it to resist subsequent treatments with antimicrobial drugs
Produces A and B enterotoxins
Cause areas of necrosis in the large intestine

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7
Q

Why is it known as “antibiotic-associated diarrhea”?

A

C. difficile

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8
Q
  1. How many people are affected by C. difficile each year?
A

250,000 infections per year, resulting in ~14,000 deaths

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9
Q

What are some of the risk factors and methods of prevention and treatment this pathogen? What is probiotic treatment?

A

Uncomplicated cases respond to withdrawal of antibiotics and replacement therapy for lost fluids and electrolytes
More severe infections are treated with certain antibiotics for several weeks until the intestinal biota returns to normal
Vancomycin is often used, but C. difficile spores are not affected
Treatment techniques being developed
Treatment with a prophylactic drug that specifically inhibits C. difficile along with initial antibiotic treatment
Restoration of normal biota by ingestion of a mixed culture of lactobacilli and yeasts (i.e. PROBIOTIC treatment: administering “healthy” microbes to compete with pathogenic microbes)
Fecal transplants (oral or enema) from a healthy person with normal microbiota have been very effective; more tests are being done

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10
Q
  1. What is a fecal transplant, and how can this be used in treatment of C. difficile infection?
A

(oral or enema) from a healthy person with normal microbiota have been very effective; more tests are being done

is the transfer of stool from a healthy donor into the gastrointestinal tract for the purpose of treating recurrent C. difficile colitis.

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11
Q
  1. What are some characteristics of Vibrio cholerae, the causative agent of cholera?
A

Vibrio cholerae are curved rods, motile with a single polar flagellum

causative agent: Phylum Proteobacteria; Gram negative, facultative anaerobes

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12
Q

What are important symptoms and a key treatment/therapy for this disease?

A

Incubation period of a few hours to a few days
Abrupt symptoms of vomiting followed by copious, watery feces called secretory diarrhea or “rice-water stools”
Fluid losses of up to 1 liter per hour
In severe cases, untreated patients can lose up to 50% of body weight

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13
Q
  1. Does Vibrio cholerae have a low or high infectious dose, and what does this imply about its virulence?
A

High infectious dose: 108 cells
Cells penetrate the mucus barrier using their flagella
Adhere to microvilli of epithelia and multiply
Never enter host cells or invade mucosa
Virulence of V. cholerae due entirely to the cholera toxin (CT)

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14
Q

What role does the cholera toxin play in pathogenesis, and where are genes for this toxin encoded?

A

Toxin causes intestinal cells shed large amounts of electrolytes into the intestine accompanied by profuse water loss
Cholera toxin genes are encoded by a temperate bacteriophage
Virulent strains of V. cholerae contain this prophage
Virulence can be transferred to non-virulent strains by infection with this bacteriophage

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15
Q
  1. What role do microbial biofilms play in tooth decay and periodontal disease?
A

Periodontal disease is mediated by communities of microorganisms rather than a single organism, i.e. it is an example of a polymicrobial disease
Polymicrobial biofilms containing the right combination of bacteria begin the periodontal destruction process

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16
Q

How are anaerobic conditions established and maintained in these biofilms?

A

Causative agents tend to be strict anaerobes, so anaerobic conditions in biofilms contribute to the disease (just as in dental caries)

17
Q
  1. What are two roles that Streptococcus mutans plays in tooth decay (associated with its virulence factors)? How does the presence of sucrose play a role?
A

.In the presence of sucrose, S. mutans produces sticky polymers called fructans and glucans
These adhesives help bind them to the smooth enamel surfaces
Contribute to the sticky bulk of the plaque biofilm

18
Q

What are some methods of prevention and treatment of tooth decay?

A

In the presence of sucrose, S. mutans produces sticky polymers called fructans and glucans
The best way to prevent dental caries is through dietary restriction of sucrose and refined carbohydrates

19
Q
  1. What is periodontal disease? What is the name of one of the microorganisms associated with this polymicrobial disease?
A

due to bacterial colonization and varying degrees of inflammation that occur in response to gingival damageOccurs if gingivitis persists
Increases the size of the pockets in the gum
Can cause bone resorption severe enough to loosen the tooth in its socket

Periodontal disease is mediated by communities of microorganisms rather than a single organism, i.e. it is an example of a polymicrobial disease
Polymicrobial biofilms containing the right combination of bacteria begin the periodontal destruction process

20
Q
  1. What are some of the defenses of the urinary tract and some examples of the normal microbiota?
A

Flushing action of urine flowing out of the system
Desquamation (shedding) of epithelial cells lining the urinary tract
Normal biota are the most common microbial threat to the urinary tract
Cells lining the urinary tract have different chemicals on their surface than those lining the GI tract
Bacteria that are adapted to adhere to the GI tract cannot easily attach to the urinary epithelium
Defenses in the urine
Defenses in the vagina

*In both genders, the outer region of the urethra harbors some normal biota
Kidneys, ureters, bladder, and upper urethra are presumably kept sterile by urine flow and regular bladder emptying

21
Q
  1. What are some of the defenses of the female genital tract? Which regions have a normal microbiota?
A

Mucus and antibody secretions
After puberty and before menopause: Secretion of glycogen, which is fermented by normal microbiota resulting in decrease in pH

Only the vagina is colonized, no known microbiota beyond the cervix

22
Q
  1. What role do Lactobacillus spp. play in preventing colonization by other organisms, and how do Lactobacillus populations change over the course of a woman’s life?
A

Lactobacillus species thrive in the acidic environment and contribute to it by converting glycogen and sugars to acid
The predominance of Lactobacillus, combined with the acidic environment, discourages the growth of many microorganisms
The estrogen-glycogen effect continues with minor disruptions through childbearing years until menopause

23
Q
  1. What are urinary tract infections (UTIs), cystitis, and pyelonephritis? How common are UTIs among healthcare-associated infections?
A

Urinary tract infections (UTIs): Result from the invasion of the urinary system by bacteria or other microorganisms

24
Q
  1. Which microbe is the cause of most of the majority of UTIs? Where does it come from, and what are some of its virulence factors?
A

Uropathogenic Escherichia coli (UPEC) accounts for 80% of UTIs

UPEC are normal GI tract biota, and are not strains of E. coli that cause diarrhea and other digestive tract diseases

UPEC virulence factors
Fimbriae that allow tight attachment during urine flow
Flagella allow for further colonization in absence of flow

25
Q
  1. What are some characteristics of Candida albicans, the most common causative agent of vaginitis? Is this fungus normally associated with humans? Under what conditions does it act as an opportunistic pathogen?
A

Dimorphic fungus
Normal biota in 50 – 100% of humans
Live in low numbers on mucosal surfaces of the mouth, gastrointestinal tract, vagina, etc.

Can become an opportunistic pathogen if normal microbiota is disturbed, or in immunocompromised hosts

26
Q
  1. What are urinary tract infections (UTIs), cystitis, and pyelonephritis?
A

Cystitis: Infection of the urinary bladder

27
Q
  1. What are urinary tract infections (UTIs), cystitis, and pyelonephritis?
A

Pyelonephritis: Infection of the kidneys

More serious disease, resulting from further colonization from bladder