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Microbio Exam 1 > Mycobacteria > Flashcards

Mycobacteria Flashcards

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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
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

Microbio Exam 1 (13 decks)

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