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HDID - Bacteriology > Mycobacterium Characteristics and Clinical Characteristics > Flashcards

Mycobacterium Characteristics and Clinical Characteristics Flashcards

1
Q

Mycobacterium Species: What are the major human pathogens?

A

M. tuberculosis
Tuberculosis (TB)

  • M. leprae
    Leprosy
  • M. avium-intracellulare complex (MAC)
    Common infection in AIDS patients
  • M. bovis
    Primarily an animal pathogen
    Human disease caused by consumption of unpasteurized milk
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2
Q 
General Characteristics about Mycobacterium:
- Morphology 
- stain protocol? 
- unique feature of the genome? 
 Unique features of its cell wall?
A
  • Morphology: aerobic bacilli
  • Staining: Acid Fast Positive - Mycobacterium resist de-colorization by acid alcohol
  • Genome: G+C rich
  • Cell Wall: Lipid Rich; Mycolic Acids; PPD; Cord factor

Other: slow growth; non motile

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3
Q

Characteristics attributable to the cell wall?

A
  1. Acid-fastness
  2. Clumping - when growing in liquid media
  3. Antibiotic resistance
  4. Antigenicity
  5. Slow growth
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4
Q

Classification of Pathogenic Mycobacteria Species

A

1) M. TB Complex: M TB, M. bovis, M. africanum
2) M. Laprae

3) Other: Non TB Mycobacteria (NTM)
divided into:
 slow growing (>7 day), 
fast growing (<7 days)
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5
Q

Unique Biochemical Rxns of M. tb vs M. bovis

A 
• M. Tuberculosis 
		○ Niacin Positive ---unique to M. Tb 
		○ Nitrate Reductase positive 
	• M. bovis 
		○ Niacin Negative 
		○ Nitrate Reductase positive
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6
Q

What lab tests can be done for Mycobacterium species indentification:

A

• Ribotyping:
○ A species specific molecular probe
○ Amplification of hypervariable regions of the 16S rRNA genes

• BACTEC Culture system 
	○ Use of Radioactive carbon 
	○ But very expensive

Microscopic Observation Drug Susceptibility (MODS) assay
○ M. Tb grows faster in liquid medium
○ Cord formation can be visualized in liquid with auramine rhodamine fluoroescent stain
○ Can also test drug susceptibility

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7
Q

Describe the normal host immune response to M. Tb –

  • what MHC is important?
  • what cells are important?
  • what cytokines and receptors are important ?
A
  • Phagocytosis of the mycobacteria (now intracellular)
  • lysosome and phagosome fusion and acidification
  • Presentaiton of antigen on MHC II to CD4
  • macrophage secretion of IL-12
  • Differentiation of TH1 cells
  • Cytokines: TNF alpha, and IFN gamma
  • activation of the macrophage -
  • Cells and cytokines lead to formation of granuloma (Type IV hypersensitivity reaction aka DTH) to contain the mycobacterium
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8
Q

How does the mycobaterium hinder some of the host immune response ?

A
  • Prevents acidification of the lysosome
  • Prevents fusion of the lysosome/phagosome
  • Slow growth – can hide in granulomas and remain latent
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9
Q

Describe the early pathogenesis of TB?

  • how is TB transmitted - where does it multiply?
  • what’s unique about this process ?
A
  • Week 1 - inhalation of droplet;
  • week 2 - bacilli multiple within macrophages
  • Week 3 - CD4 cells infiltrate, cytokine release macrophage activation
  • week 4 - Granulomas
  • the progression of the disease is over the course of weeks; the bacteria divide very slowly
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10
Q

What are some diagnositc tests for TB?

A
  • PPD (Tb Skin Test = TST) —- will elicit DTH reaction to previous exposure to PPD.
    False positive if patient has had BCG vaccine
  • Interferon gamma Release Assay (IGRA); Quantiferon TB Gold Assay:
    Measure the amount of INF secreted in response to M. TB specific antigens
    able to differentiate from BCG
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11
Q

By what mechanism does M. Tb display drug resistance?

A

M. Tb only displays drug resistance by point muations

not inherited via plasmids or transposons

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12
Q

Name 3 Anti-TB drugs and their mechanism of action

A

Isoniazid – inhibition of mycolic acid synthesis

Rifampin – Bind to and inhibit RNA polymerase.

Streptomycin (an aminoglycoside) – bind 30s rRNA; disrupting protein synthesis

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13
Q

M. leprae - lab features?

  • Stain
  • morphology
  • unique molecular and defensive feature
  • other unique quality in the lab …
A
  • Stain: Acid fast
  • Morphology - Bacilli; obligate intracellular
  • PGL -1 (phenolic glycolipid specific to M. leprae) - protects bacilli within macrophages by scavenging for radicals and super-oxide anions
  • cannot be cultured in vitro in the lab
    in vivo cultures in mice and armadillos
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14
Q

How does host immune response to M. leprosy determine the outcome?

A

TH1 dominant response – Tuberculoid leprosy; good granulomas contain the bacteria

TH2 Dominant response – Lepromatous leprosy; diffuse disease

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15
Q

Diagnostic Tests for M. leprae

A
  • Lepromin Skin Test: Tuberculoid patients form DTH reaction
  • Antibodies: can be used for diagnosis, but offer no protective measures
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16
Q

What is another name for Leprosy?

A

Hansen’s Disease

17
Q

How is leprosy transmitted?

What is an indeterminate lesion?

A

Transmitted: droplets from the nose and mouth; during close and frequent contacts with untreated persons

only 5% of persons exposed will develop an indeterminate lesion
75% of these persons will heal spontaneously
25% of the 5% will have tubuerculoid or lepromatous symptoms

18
Q

What is the Hallmark presentation of leprosy?

What are the unique clinical features of tuberculoid leprosy vs lepromatous leprosy?

What are the classic facial features?

A

Hallmark: Anesthetic skin lesions + thickened peripheral nerve

Tuberculoid: few lesions; single but progressive nerve involvement

Lepromatous: many symmetrical lesions; can be erythematous, papulosquamous
several nerves involved. Slow progression

The Neuritis can lead to deformity

Facial Features: cold facials regions are attacked
- loss of eye brows; saddle nose deformity; ear lobe nodules

19
Q

Diagnosis of Leprosy

A
  • Physical Examination: skin and nerves

- Skin Bx: acid fast bacilli

20
Q

Treatment of Leprosy (3 drugs)

A

Multi Drug Therapy: Dapsone, Rifampicin, Clofazimin

21
Q

Prevention of Leprosy

A

Rifampicin to those in close contact

BCG immunizations

22
Q

TB Epidemiology:

  • Transmission
  • Risk factors
A

Transmission: Inhalation of droplets from infectious adults with pulmonary or pulmonary TB

Risk Factors:

  • The degree of illness of the patient (lungs with cavitations have more bacteria)
  • The contact: frequency of exposure, over crowding, poor ventilation, occupational setting
23
Q

Describe the Natural Course of TB

  • what is a characteristic feature of primary TB
  • What are the risk factors for TB disease (either primary progressive vs reactivation)
A
  • 70% of persons exposed to TB will not get sick -
  • 30% will develop primary TB
  • 90% of primary TB cases will be properly contained in granulomatous reaction – Latent TBI
    of these: reactive risk depends on immune state of the person with LTBI
  • 10% will continue as TB disease
  • Characteristic feature of primary TB: Ghon Focus (lesion in the lung); Ghon Complex (lung + infected LN)

Risk Factors: Recent Acquisition/exposure risks;
Immunocompromised: HIV, old or young, DM, ESRD, malignancy
Genetic immunodeficiency: INF gamma, IL-12, IL-23

24
Q

Upon Clinical Presentation: Differentiate between LTBI and Active Pulmonary TB disease

A

LTBI: Asymptomatic; normal Physical Exam
CXR may be normal, or show old granuloma
TST/IGRA - Positive
Sputum Culture - Negative

Active TB Disease: 
pulmonary and Systemic Symptoms 
Abnormal pulmonary findings 
CXR: Consolidation; Cavity or Pleural effusion 
TST/IGRA - Positive or Negative 
Sputum culture: Positive
25
Q

Treatment Of Latent TBI

A 
§ Preferred: 
				□ Isoniazid daily x 9 month
			§ Alternative: 
				□ Isoniazid daily x 6 month
				□ Rifampin daily x 4 months
				□ Isoniazid and Rifapentine weekly x 3 months
26
Q

Active Pulmonary TB:

  • primary TB imaging
  • progressive primary TB imaging
  • post - primary TB imaging
A

Primary: Hilar LAD; Lower lung infiltrates; CXR normal in 15% of patients

Progressive Primary: Confluent, well defined consolidation; always LAD;

Reactivation: Consolidation with Cavitation; CXR abnormal; some lung destruction may be present

27
Q

What are the two forms of CNS Extra-pulmonary TB?

A
  • Basilar Meningitis:
    CSF - lymphocytes; high protein; low glucose
    Subacute course of fever, HA, AMS (meningococcal meningitis – acute onset)
  • Tuberculoma – granuloma in the brain
28
Q

Extra-Pulmonary TB:

  • TB of Spine (what’s the other name, what are the manifestations)
  • Miliary TB (why is it called this? what is it?)
A

TB of the Spine = Pott’s Disease

  • anterior vertebral column disease
  • Vertebral column collapse (Gibbus formation)

Miliary TB — widspread hematogenous disease; most severe form of TB;
organs: lung, liver, spleen, bone marrow, CNS
Radiology Hallmark: millet seed like lesions

29
Q

What are the first line treatments for TB:

A 
- 		• Isoniazid (INH)
		• Rifampin (RIF)
		• Pyrazinamide (PZA)
		• Ethambutol (EMB)
		• Streptomycin 
		   (special indications only)
30
Q

what are the second line treatments of TB?

A
  • Fluoroquinolones (Levofloxacin, Moxifloxacin)

* Injectables (Capreomycin, Kanamycin, Amikacin)

31
Q

Describe the Treatment regimen of TB?

what vitamin is always given during this therapy?

A
  • Department of health will get involved
  • 6 months of Multi Drug therapy for pulmonary, pan-sensitive TB
    (Do i have to know this?
    Intensive 2 months: Isoniazid, Rifampin, Pyrazinamide, Ethambutol
    Continuation 4 months: Isoniazid, Rifampin

• Vitamin B 6 always given with INH to prevent nerve damage

32
Q

Describe the 2 forms of drug resistance in TB

A

• Multi-Drug Resistance (MDR):
Resistance to isoniazid and rifampin

• Extensive Drug Resistance (XDR): 
	MDR + resistance to 2nd line drugs
	(Fluoroquinolones + ³ 1 injectable )
33
Q

Non TB Mycobacteria:
- where are they found?
what is unique about transmission?

A

Not transmitted person to person

found ubiquitously in water, soil and plants

34
Q

Clinical Manifestations of NTM

-

A

○ Pulmonary - – most common
§ M. avium/intracellulare (MAC), M. kansasii, M. abscessus

	○ Lymphadenitis 
	○ Skin and soft tissue --- 
	○ Health Care Associated 
		- Associated with surgery, injections or cosmetic procedures, catheters 
		   - Rapid growers (M. abscessus, M. fortuitum) 
	○ Disseminated disease 
		§ Predominantly M. avium and M. intracellulare (MAC)
		§ Occurs in HIV-infected patients with CD4 < 50 cells/mm3
35
Q

Treatment of NTM

A 
• Treatment of NTM 
		○ Combination therapy 
			§ Macrolides (azithromycin or clarithromycin)
			§ Ethambutol
			§ Rifampin 
			§ Aminoglycosides
		○ Difficult
		○ Go by sensitivities

HDID - Bacteriology (21 decks)

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