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Flashcards in L22_Mycobacteria Deck (33):
1

What bacterium causes Tuberculosis?

Mycobacterium Tuberculosis

2

At one point eradication of M. tuberculosis seemed possible, what was this and what happened that stymied this hope?

It was thought possible because humans were the sole reservoir for the bug, and if you killed it in humans it would have nowhere to go. The AIDS epidemic fucked it all up

3

What particular strains are public nightmares?

MDR and XDR strains

4

How do mycobacteria stain?

They gram stain poorly, they are acid-fast (pink/red)

5

Describe the rate of growth of mycobacteria.

Very slow, this causes them to be inherently hard to treat with antibiotics

6

Describe the acid fast staining process

1 carbolfuschin stain
2 acid/alcohol decolorization
3 methylene blue counterstain
Acid fast bacteria retain carbolfuschin color during decolorization Acid fast (RED) Non- Acid Fast (BLUE)

7

Describe the transmission of M. tuberculosis and its spread throughout the body.

Transmission is almost always to lung by inhalation, then to lymph nodes, kidney, bones, CNS by hematogenous spread, to GI by swallowing infected sputum.

8

Describe the course of the disease and CMI response in most immunocompetent individuals.

Immunocompetent host raises strong CMI response, can hol dinfection latent for decades; immunosenescence or - suppression can reactivate and become infectious again if still in lung. Most immunocompetent hosts can clear the disease successfully and contain it.

9

Describe TNF-alpha role in M. Tuberculosis

TNF is important for retaining latency. If TNF antagonists are administered to a carrying host, they may reactivate a caseating granuloma.

10

Describe the ways in which M. tuberculosis can spread hematogenously.

Free bacteria can travel in the blood or some can use naive macrophages as trojan horses.

11

Describe the course of action once the body elicits an immunogenic response.

If patient is healthy after a few days active immunity will come online, infected macrophages (killed by CD8 cells) and free floating bacteria will be purged. What will remain are sites where the body could not completely eradicate the infection and will be walled off by granulomas, if there is a high pO2 the Tb can remain,
-if granulomas remain inactive they will gradually calcify and may remain quiescent for decades, however if at any point patient becomes immunocompromised these sites can be reactivated at any of these sites

12

What are the symptoms of classic pulmonary TB (75%)? What should you do if you witness these in a patient?

Cough, weight loss (consumption), fever, night sweats, hemoptysis, and chest pain. take chest X-ray and check sputum.

13

Extrapulmonary manifestations of M. tuberculosis are usually reactivations, name some of the common sites and any specific nomenclature.

Neck- Scrofula (in kids scrofulas are usually atypical mycobacteria)
genitourinary, CNS (meningitis or abscess), skeletal (long bone or spine[pott's disease]), miliary, GI(rare)

14

What two specific manifestations of tuberculosis should be watched for in immunosupressed individuals or children?

Miliary and meningitis

15

What tests are there for Tb and what do the tests tell you?

you can determine EXPOSURE only by TST and/or IGRA (not for current disease)

16

What is so difficult about the culture of M. Tuberculosis

It grows extremely slow. it takes 2 weeks for cultures and another 3 weeks for resistance tests

17

What therapies are there for Tb?

Begin Directly Observed Therapy with 4-plus drug course featuring Isoniazid; isolate patient for first two weeks.

18

Is there a vaccine for Tb?

BCG vaccine is a live attenuated M. bovis. it is not cost effect. It doesnt prevent infection but helps ramp up immune response and force latency earlier. will create a weak to moderate false positive TST

19

What are the most helpful factors in reducing incidence of Tb in a population?

good diet and housing: latent cases are not contagious.

20

How are atypical mycobacteria acquired? Do they cause Tb or Leprosy?

environmentally. they do not cause Tb or Leprosy

21

What is the typical infection route for atypical mycobacteria in an immunocompetent adult? children?

adult- cutaneous
children- scrofula

22

Immunosupressed host may have systemic symptoms from atypical mycobacteria particularly from which two species?

M. Kansasii and MAI/C (M. Avium/ M. intracellulare)

23

Describe the ease of treatment of atypical mycobacteria.

Infections may be difficult to treat once established; require multiple antibiotics

24

Describe growth of M. Leprae, culture system, speed, etc.

It has no in vitro growth system, slowest growing human pathogen, prefers 30C

25

What percentage of humans are susceptible to M. Leprae. How easily is it transmitted? What is its incubation period?

5-10%, doesn't transmit easily, extremely long incubation period

26

Leprosy is also known as?

Hansens Disease

27

Describe the range in which leprosy presents, what are the two extremes?

Tuberculoid (paucibacillary, vigorous CMI both contains infection and damages nerves PPD+)
Lepromatus (Multibacilary, weak CMI, extensive cutaneous symptoms, PPD-, nerve damage casue by overgrowth of bacteria)

28

What does the lepromin PPD test indicate?

It tests for anti-leprosy immunocompetence, NOT exposure

29

How do you treat leprosy?

2 yrs of dapsone+rifampin

30

What does M. Kansasii cause? what is it treated with?

Tb like symptoms treated with the same drugs

31

What does MAI/C cause?

pulmonary disease that is very difficult to distinguish from TB. They are highly drug resistant.

32

what does IGRA stand for?

Interferon gamma release assay

33

What is the correct immune response to M. Leprae?

TH1 response