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Flashcards in Mycobacteria Deck (61):
1

Mycobacterium are neither gram positive or gram negative; __________ are used instead/

-Acid fast stains

2

3 groups of mycobacteria

1. M. tuberculosis complex
2. nontuberculosis mycobacteria
3. M. leprae

3

Physiology and structure of mycobacteria

-slow rate of replication
-lipid-rich outer layer of mycolic acids
-resistant to desiccation
-acid-fast stains, not gram stains
-nonspore forming, non-motile bacilli
-obligate aerobes

4

3 several important properties due to myobacteria's outer layer of mycolic acids

-resistance to gram staining
-resistance against dessication which is important in airborne transmission
-myocolic acid biosynthesis is target for INH drug

5

Mycobacteria are facultative _______ pathogens

-intracellular

6

M. tuberculosis niche and mechanism for survival

-replication within macrophages
-stays within vesicle and prevents its fusion with lysosomes

7

Because M. tuberculosis is spread by an airborne route, it usually first encounters ________ and then is carried to a __________.

-alveolar macrophage
-regional lymph node

8

At the level of histopathology, the immune response to mycobacterial infections is dominated by __________.

-granulomas
-inflammatory aggregates of macrophages and T cells
-may contain multinucleated giant cells

9

Caseous necrosis often develops at the centers of _______ granulomas.

-tuberculosis

10

What type of immune response is required to combat tuberculosis?

-cell-mediated rather than humoral response, as expected in an intracellular pathogen
-Th1 response is most effective

11

While M. tuberculosis replicated well in resting macrophages, it can be killed by _______.

-activated macrophages

12

Why do HIV patients suffer from a high rate of tuberculosis?

-they lack their CD4+ T cell responses which are crucial in the cell mediated response necessary to combat TB

13

CD4+ T cells which recognize M. TB and become activated produce ________. What does this do?

-interferon-gamma
-this in turn activates macrophages to produce TNF-alpha and to kill bacteria within their phagosomes

14

TB is one of the leading infectious causes of death worldwide. About ______ of the world's population are infected. Most of these infections are asymptomatic and fall into the category of LTBI. These people however have about a _______ lifetime risk of developing active TB.

-1/3 (2 billion)
-10%

15

T/F: TB is a relatively new disease of humanity.

-false; been with humans from the beginning

16

TB was also known as _____ in Europe.

-consumption

17

Rates of TB continued to fall until the mid 1980s when the _______ spurred a rise in the incidence again.

-AIDS epidemic

18

Blocks/defects in what 3 things increase susceptibility to mycobacteria

-CD4+ T cell responses
-TNF blockage
-IFN-gamma receptor defects

19

Current problems with TB

-still many latent infections
-increasing drug resistance
-global levels of disease remain high, partly due to HIV

20

Risk factors for TB

-homelessness, urban poverty, malnutrition, crowding, alcoholism
-increases in inmates, healthcare workers, and immigrants from regions with high endemic TB

21

Transmission of TB

-airborne transmission by aerosol droplet nuclei
-can remain suspended in air for hours

22

Protection from TB requires what kind of mask?

-N95 respiratory mask

23

T/F: Having HIV doesnt increase risk of getting TB

-true, just makes it worse

24

Clinical diseas of primary TB infection

-aerosol deposition of bacilli into alveoli
-replication in macrophages and migration to regional LN
-control of infection with development of cellular immunity
-often no evidence of primary infection beyond position TST
-Lymphohematogenous seeding of lungs and extrapulmonary sites

25

Latent TB infection (LTBI)

-controlled primary infection without clinical disease
-no evidence of active TB on chest x-ray
-chest x-ray may show calcification at pulmonary site of initial infection (Ghon focus) or in mediastinal nodes (Ranke complex)
-NOT CONTAGIOUS

26

Reactivation of TB

-may occur after initial control of infection by immune system
-risk of reactivation if issue developed in cell-mediated immunity

27

In pulmonary TB, reactivation is most common where?

-apex of lung

28

Histologic Characteristics of pulmonary TB

-caseous necrosis and formation of cavities
-rupture of cavities into bronchi and spread to other areas of lung
-

29

Symptoms of Pulmonary TB

-local symptoms: cough and sputum production, shortness of breath
-Prominent systemic symptoms: fever, chills, night sweats, fatigue, weight loss
-highly contagious

30

3 other forms of TB outside of pulmonary TB

-primary progressive TB pneumonia
-Miliary TB
-extrapulmonary TB

31

Primary progressive TB pneumonia

-local disease following initial infection

32

Miliary TB

-progressive, disseminated hematogenous tuberculosis
-when M. tb overwhelms the immune system

33

Extrapulmonary TB

-direct spread along mucosal surfaces: GI tb, laryngeal TB
-direct extension form lungs to pleural space
-lymphohematogenous spread

34

What can extrapulmonary TB via lymphohematogenous spread cause?

-meningitis
-lymphadenitis (scrofula)
-renal TB
-Skeletal TB "pott's disease"

35

Lab diagnosis of TB

-Tuberculin skin test (TST or Mantoux test): intracutaneous injection of purified protein derivative (PPD)
-interferon-gamma release assays

36

Limits to Tuberculin skin test

-false positive TST reactions: other mycobacterium in environment, recent BCG vaccination
-false negative TST reactions: weakened cellular immune response, malnutrition or chronic disease, AIDS patients
-criteria for interpretation of TST reflect patient risk factors

37

T/F: it is the redness of a TST, not the induration that is diagnostic of TB

-false; it is the induration
-15 mm in everyone, lower if in higher risk population

38

How does a IGRA work?

-stimulates patient T cells with 2 peptides secreted by M. tb
-tests production of INF-gamma by patient T cells
-not affected by vaccination with BCG because uses 2 peptides not included in that vaccine

39

Culture and staining of M. tb

-smear and culture of sputum: culture may take 2-3 weeks or more to grow, DNA probes often used to rapidly ID isolate
-Acid-fast staining
-Fluorochrome stains

40

Molecular detection of TB

-PCR assays
-Xpert MTB/RIF assay: automated, rapid detection of Mtb, heminested real-time PCR of rpoB, detection of rifampin resistance

41

First line drugs for active TB

-Isoniazid (INH)
-Rifampin
-Pyrazinamide
-Ethambutol
**Add Streptomycin for TB meningitis

42

Isoniazid (INH)

-inhibits mycolic acid synthesis
-strong, early bactericidal activity againt replication M. tb
-toxicity issues

43

Toxicity and Isoniazid

-hepatitis
-peripheral neuropathy: competitively inhibits activity of pyridoxine as cofactor, so give P supplement for patients with nutritional deficiencies and chronic diseases

44

Rifampin and side effects

-inhibits RNA polymerase
-Side effects: orange body fluids, hepatitis, interactions with other drugs

45

Pyrazinamide function and toxicity

-targets 30S ribosomal protein RpsA
-inhibits trans-translation and recycling of stall ribosomes
-may act against semi-dormant organisms
-toxicity: hepatitis and polyarthralgia

46

Ethambutol

-inhibits synthesis of cell wall arabinogalactan
-toxicity: retrobulbar neuritis: decreased red-green color discrimination or decreased visual acuity

47

Treatment of active TB

-use at least 3, usually 4, first line drugs
-treat for 6 months at least: 2 months on all 4, followed by 4 months of INH and RIF
-directly observe therapy to monitor adherence

48

How does one monitor TB while on medication?

-obtain sputum at least monthly
-90-95% should be negative sputum by 3 months-
-considered not contagious if 3 consecutive AFB smears are negative

49

Treatment of LTBI

-9 months of INH or 6 months of rifampin
-hepatic toxicity from INH increases over age 35

50

What type of vaccine is BCG vaccine?

-live, attenuated
-limited efficacy
-can cause disease in immunocompromised

51

What are the NTM?

-mycobacteria except M. tuberculosis and M. leprae
-divided into slow and rapid growers
-also classified by pigment production

52

Epidemiology of NTM

-frequently found in the environment

53

Clinical diseases from NTM

-Pulmonary diseases: chronic cough, fatigue, weight loss, NO fever
-Disseminated MAC: in HIV patients with Cd4+ <50, fever, weight loss, anemia, diarrhea, hepatosplenomegaly, no respiratory symptoms
-hypersensitivity pneumonitis: hot tub lung
-cervical lymphadenitis: in young children, usually from MAC, swollen but limited signs of inflammation
-Skin and soft tissue infections: rapid growers

54

Testing and laboratory diagnosis of NTM

-usually need culture of organism
-may be found as non-pathogens in cultures from non-sterile sites

55

Treatment of NTM

-multiple drug regimens
-prolonged courses of treatment
-antibiotic prophylaxis for HIV patients to prevent disseminated MAC

56

Leprosy is also called ________.

-Hansen's disease

57

T/F: Leprosy is easy to culture in vitro

-false; still cannot be
-infects wild armadillos and can be cultured in mouse footpads

58

How is leprosy spread?

-contact with nasal secretions or droplet spread
-perhaps biting insects?

59

Clinical manifestations of leprosy

-grows as lower temperatures found within skin and extremities
-peripheral sensory nerve damage
-infiltrative skin lesions
-2 categories of disease: multibacillary or paucibacillary

60

How is Leprosy diagnosed?

-history, exam, and biopsy
-NO CULTURE bc it cannot be grown in vitro

61

Treatment of leprosy

-multidrug regimens
-rifampin, dapsone, clofazimine
-5 years of treatment