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Microbio Exam 1 > Mycobacteria > Flashcards

Mycobacteria Flashcards

1
Q

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

A

-Acid fast stains

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2
Q

3 groups of mycobacteria

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

Physiology and structure of mycobacteria

A
  • 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
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4
Q

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

A
  • resistance to gram staining
  • resistance against dessication which is important in airborne transmission
  • myocolic acid biosynthesis is target for INH drug
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5
Q

Mycobacteria are facultative _______ pathogens

A

-intracellular

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6
Q

M. tuberculosis niche and mechanism for survival

A
  • replication within macrophages

- stays within vesicle and prevents its fusion with lysosomes

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7
Q

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

A
  • alveolar macrophage

- regional lymph node

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8
Q

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

A
  • granulomas
  • inflammatory aggregates of macrophages and T cells
  • may contain multinucleated giant cells
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9
Q

Caseous necrosis often develops at the centers of _______ granulomas.

A

-tuberculosis

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10
Q

What type of immune response is required to combat tuberculosis?

A
  • cell-mediated rather than humoral response, as expected in an intracellular pathogen
  • Th1 response is most effective
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11
Q

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

A

-activated macrophages

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12
Q

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

A

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

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13
Q

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

A
  • interferon-gamma

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

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14
Q

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.

A
  • 1/3 (2 billion)

- 10%

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15
Q

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

A

-false; been with humans from the beginning

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16
Q

TB was also known as _____ in Europe.

A

-consumption

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17
Q

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

A

-AIDS epidemic

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18
Q

Blocks/defects in what 3 things increase susceptibility to mycobacteria

A
  • CD4+ T cell responses
  • TNF blockage
  • IFN-gamma receptor defects
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19
Q

Current problems with TB

A
  • still many latent infections
  • increasing drug resistance
  • global levels of disease remain high, partly due to HIV
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20
Q

Risk factors for TB

A
  • homelessness, urban poverty, malnutrition, crowding, alcoholism
  • increases in inmates, healthcare workers, and immigrants from regions with high endemic TB
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21
Q

Transmission of TB

A
  • airborne transmission by aerosol droplet nuclei

- can remain suspended in air for hours

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22
Q

Protection from TB requires what kind of mask?

A

-N95 respiratory mask

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23
Q

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

A

-true, just makes it worse

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24
Q

Clinical diseas of primary TB infection

A
  • 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
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25
Q

Latent TB infection (LTBI)

A
  • 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
Q

Reactivation of TB

A
  • may occur after initial control of infection by immune system
  • risk of reactivation if issue developed in cell-mediated immunity
27
Q

In pulmonary TB, reactivation is most common where?

A

-apex of lung

28
Q

Histologic Characteristics of pulmonary TB

A

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

29
Q

Symptoms of Pulmonary TB

A
  • local symptoms: cough and sputum production, shortness of breath
  • Prominent systemic symptoms: fever, chills, night sweats, fatigue, weight loss
  • highly contagious
30
Q

3 other forms of TB outside of pulmonary TB

A
  • primary progressive TB pneumonia
  • Miliary TB
  • extrapulmonary TB
31
Q

Primary progressive TB pneumonia

A

-local disease following initial infection

32
Q

Miliary TB

A
  • progressive, disseminated hematogenous tuberculosis

- when M. tb overwhelms the immune system

33
Q

Extrapulmonary TB

A
  • direct spread along mucosal surfaces: GI tb, laryngeal TB
  • direct extension form lungs to pleural space
  • lymphohematogenous spread
34
Q

What can extrapulmonary TB via lymphohematogenous spread cause?

A
  • meningitis
  • lymphadenitis (scrofula)
  • renal TB
  • Skeletal TB “pott’s disease”
35
Q

Lab diagnosis of TB

A
  • Tuberculin skin test (TST or Mantoux test): intracutaneous injection of purified protein derivative (PPD)
  • interferon-gamma release assays
36
Q

Limits to Tuberculin skin test

A
  • 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
Q

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

A
  • false; it is the induration

- 15 mm in everyone, lower if in higher risk population

38
Q

How does a IGRA work?

A
  • 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
Q

Culture and staining of M. tb

A
  • 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
Q

Molecular detection of TB

A
  • PCR assays
  • Xpert MTB/RIF assay: automated, rapid detection of Mtb, heminested real-time PCR of rpoB, detection of rifampin resistance
41
Q

First line drugs for active TB

A
  • Isoniazid (INH)
  • Rifampin
  • Pyrazinamide
  • Ethambutol
  • *Add Streptomycin for TB meningitis
42
Q

Isoniazid (INH)

A
  • inhibits mycolic acid synthesis
  • strong, early bactericidal activity againt replication M. tb
  • toxicity issues
43
Q

Toxicity and Isoniazid

A
  • hepatitis
  • peripheral neuropathy: competitively inhibits activity of pyridoxine as cofactor, so give P supplement for patients with nutritional deficiencies and chronic diseases
44
Q

Rifampin and side effects

A
  • inhibits RNA polymerase

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

45
Q

Pyrazinamide function and toxicity

A
  • targets 30S ribosomal protein RpsA
  • inhibits trans-translation and recycling of stall ribosomes
  • may act against semi-dormant organisms
  • toxicity: hepatitis and polyarthralgia
46
Q

Ethambutol

A
  • inhibits synthesis of cell wall arabinogalactan

- toxicity: retrobulbar neuritis: decreased red-green color discrimination or decreased visual acuity

47
Q

Treatment of active TB

A
  • 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
Q

How does one monitor TB while on medication?

A
  • 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
Q

Treatment of LTBI

A
  • 9 months of INH or 6 months of rifampin

- hepatic toxicity from INH increases over age 35

50
Q

What type of vaccine is BCG vaccine?

A
  • live, attenuated
  • limited efficacy
  • can cause disease in immunocompromised
51
Q

What are the NTM?

A
  • mycobacteria except M. tuberculosis and M. leprae
  • divided into slow and rapid growers
  • also classified by pigment production
52
Q

Epidemiology of NTM

A

-frequently found in the environment

53
Q

Clinical diseases from NTM

A
  • 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
Q

Testing and laboratory diagnosis of NTM

A
  • usually need culture of organism

- may be found as non-pathogens in cultures from non-sterile sites

55
Q

Treatment of NTM

A
  • multiple drug regimens
  • prolonged courses of treatment
  • antibiotic prophylaxis for HIV patients to prevent disseminated MAC
56
Q

Leprosy is also called ________.

A

-Hansen’s disease

57
Q

T/F: Leprosy is easy to culture in vitro

A
  • false; still cannot be

- infects wild armadillos and can be cultured in mouse footpads

58
Q

How is leprosy spread?

A
  • contact with nasal secretions or droplet spread

- perhaps biting insects?

59
Q

Clinical manifestations of leprosy

A
  • grows as lower temperatures found within skin and extremities
  • peripheral sensory nerve damage
  • infiltrative skin lesions
  • 2 categories of disease: multibacillary or paucibacillary
60
Q

How is Leprosy diagnosed?

A
  • history, exam, and biopsy

- NO CULTURE bc it cannot be grown in vitro

61
Q

Treatment of leprosy

A
  • multidrug regimens
  • rifampin, dapsone, clofazimine
  • 5 years of treatment

Microbio Exam 1 (13 decks)

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