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SARS exam 2 > Tuberculosis and E. coli > Flashcards

Tuberculosis and E. coli Flashcards

1
Q

What are the 3 causative agents of tuberculosis?

A
  • Mycobacterium tuberculosis (major cause)
  • Mycobacterium bovis (minor cause)
  • Mycobacterium avium (minor cause)
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2
Q

During what time period was TB a common cause of death?

A

from the middle ages through the 1800s

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3
Q

When did rates of TB sharply decline?

A

1940s- coincides with beginning of antibiotic use

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4
Q

Why have rates of TB begun to increase again?

A

HIV pandemic, general public health failures around the world, drug resistance

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5
Q

What were some causes of TB decline before the 1940s?

A

improved sanitation, increased general health, increased SES

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6
Q

What percent of the world is infected with TB? Of those infections, how many are active?

A

1/3 of the world’s population is infected, 10% of infections are active

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7
Q

What is the second leading cause of death due to a single infectious agent?

A

Tuberculosis

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8
Q

How many people die each year due to TB?

A

Greater than 1 million

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9
Q

What percentage of TB cases are in low/middle income countries?

A

95% (think of it as a disease of the poor)

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10
Q

What are the two modes of transmission for TB?

A

inhalation and ingestion

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11
Q

What is the infectious dose for TB that is inhaled?

A

1 bacterium

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12
Q

How is TB typically ingested? How can this be prevented?

A

highly contaminated milk; pasteurization

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13
Q

Does ingestion of TB require a large infectious dose?

A

Yes- much higher than inhalation; probably due to pH of GI tract

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14
Q

Describe the process of TB infection.

A
  • TB enters alveoli and is taken up by alveolar macrophage (phagocytosis), phagasome has TB bacteria in it which blocks it from binding with lysosome
  • TB replicates in phagasome until macrophage bursts
  • TB from burst cell is able to infect surrounding macrophages
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15
Q

What is a granuloma?

A

Healthy macrophages, lymphocytes, and other immune cells surround infected macrophages and wall it off from the rest of the body

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16
Q

What is caseation? (TB)

A

Center of granuloma breaks down leaving cell parts and TB bacteria, resembles cheese like structure

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17
Q

What is calcification? (TB)

A
  • happens to most caseous lesions in latent infections; calcium deposits inside of the granuloma
  • the longer it takes to calcify the more likely it is to liquify
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18
Q

What is activation of lesions? (TB)

A
  • liquefaction of caseous lesions; allows for rapid replication of bacteria; liquid may drain into airways
  • this is how TB can spread to other people or cause more lesions
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19
Q

What is cavitation? (TB)

A

‘airfield granuloma,’ because TB likes oxygen it is able to replicate rapidly and spread to other areas of lungs/other people

20
Q

What is the standard treatment for uncomplicated TB?

A

4 drugs for 2 months, followed by 2 drugs for 4 months (total of 6 months)

21
Q

What are the factors of drug resistance in TB?

A

poor compliance, inappropriate treatment, poor quality drugs

22
Q

What populations are at risk for developing drug resistant TB?

A

people w/ poor compliance, people that relapse after treatment, people visiting areas w/ high drug resistance

23
Q

What does DOT stand for? What is it?

A

Directly observed therapy; treatment of people with TB is observed by professional either at home or in clinic

24
Q

What is the purpose of DOT?

A

ensures compliance, can check for side-effects; combat development of drug resistance

25
Q

What does MDR-TB stand for?

A

multi-drug resistant tuberculosis

26
Q

What drugs is MDR-TB resistant to?

A

rifampin and isoniazid (first line drugs)

27
Q

Where do the majority of cases of MDR-TB occur?

A

China, India, and Russia

28
Q

How many cases of MDR-TB occurred in 2012? How much did this increase from 2011?

A

450,000 cases in 2012, almost twice what was seen in 2011

29
Q

What is the mortality rate of MDR-TB?

A

About 40 percent (38)

30
Q

What does XDR-TB stand for?

A

Extremely drug resistant tuberculosis

31
Q

What drugs is XDR-TB resistant to?

A

rifampin & isoniazid plus a quinolone and a injectable second line drug

32
Q

How many countries has XDR-TB been reported in?

A

92

33
Q

What percent of MDR-TB are XDR?

A

about ten percent

34
Q

What type of bacteria is E. coli O157:H7 classified as?

A

Enterohemorrhagic E. coli (EHEC)

35
Q

What are three of the traits that EHEC gets from the 1,600 genes it has that commensal E. coli does not?

A

shiga toxin, enterohemolysin and proteases

36
Q

When, where, and how did E. coli O157:H7 emerge?

A

Jack-in-the-Box fast food restaurants in the western US; due to undercooked hamburger meat
1982

37
Q

What is the route of infection for E. coli?

A

Ingestion; 95% of bacteria thought to survive the stomach

38
Q

Does E. coli survive refrigeration?

A

yes

39
Q

What are ways in which E. coli can be spread?

A

meat, vegetables (spinach, lettuce, things eaten raw), contaminated water (either swimming or drinking), unpasteurized juice, daycare centers

40
Q

What is the primary reservoir for E. coli?

A

cattle (no clinical signs of infection)

41
Q

In what ways does E. coli persist in the environment?

A
  • persists on grass for months
  • stress response lets in survive in aquatic environments
  • some strains form biofilms that are resistant to ameboids
  • can survive within environmental protozoas
42
Q

What are the symptoms of disease caused by O157?

A
  • diarrhea (often bloody= probably from shiga toxin)
  • Hemorrhagic colitis
  • vomiting
  • nausea
  • cramps
  • neurological symptoms (seizures, blindness)
43
Q

Describe hemolytic uremic syndrome (HUS)?

A
  • occurs in rare cases
  • early symptoms similar to hem. colitis
  • later symptoms= hemolytic anemia, thrombocytopenia, decreased urine output , can lead to kidney failure
  • more common in young and elderly
  • child mortality= ~5%
44
Q

How is O157 treated?

A

Mainly electrolyte balance, antibiotic treatment can actually be detrimental due to release of shiga toxin
(HUS may require dialysis)

45
Q

List preventative measures for O157.

A

cook food thoroughly, wash hands/food/surfaces/countertops, use a separate cutting board for meat/veggies, pasteurize milk and juice, avoid drinking pool water/contaminated water, trying to decrease prevalence in cattle

46
Q

What factors led to the emergence of O157?

A

mutation, recognition of a new disease

SARS exam 2 (5 decks)

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