Mycobacteria: TB, Leprosy, and Atypicals Flashcards

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1
Q

What is the most common infectious cause of mortality worldwide? How much of the population is infection? How was it treated when it was on the decline?

A

M. tuberculosis
four-drug regimens featuring isoniazid!!!!!
But now have multidrug resistant and extensively drug resistant strains - in immunosuppressed populations, infectious state continues

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2
Q

How do you stain M.tuberculosis? Why?

A

Acid fast; TB gram stains very poorly, mycolic acid is waxy and hard to stain.

Keep in mind that antibiotics prevent NEW peptidoglycan from being synthesized and that rapidly growing bacteria are easier to target. Slow growing bacteria are harder to kill.

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3
Q

What are the steps of the acid fast stain?

A
1- Cover smear w/carbolfuscian. Boil w/ extra stain for 10 minutes
2- decolorize with acid-alcohol
3- water
4- counterstain with methylene blue
5- rinse and blot dry

sputum sample lumpy places = cords, characteristic of TB

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4
Q
  1. What is unique about M. tuberculosis growth?
  2. What is the host and reservoir?
  3. Where can they grow in humans?
  4. Toxins?
  5. What is their mechanism of drug resistance?
A
  1. Grows in vitro, but slowly (even in human host!), requires special nutrients
  2. Humans
  3. Intra or extracellular
  4. NO
  5. Chromosomal
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5
Q
  1. What makes them environmentally hardy?
  2. What is their relationship with air?
  3. What are their three important structural components?
  4. Are they pathogenic in guinea pigs?
A
  1. Resistant to acid and alkali - they have to survive outside of the human body, they are transferred in the air
  2. Obligate aerobe - unusual for a pathogen, M. tuberculosis is restricted to oxygenated parts of the body
  3. 1- Mycolic acids (acid fastness), 2- Phosphatides (ceseation necrosis) 3- cord factor (trehalose dimycolate): virulence, microscopic serpentine appearance
  4. Yes
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6
Q
  1. How is M. tuberculosis transmitted?
  2. How many organisms do you need to initiate infection?
  3. What happens when the bacteria land on the lung?
  4. What happens with immunocompetent persons?
A
  1. inhalation of infected aerosols

2.

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7
Q

M. tuberculosis pathogenesis is a cell mediated immune response 2-3 weeks after initial infection. Name the two parts:

A
  1. CD4 helper T cells activate infected macrophages to kill intracellular bacteria
  2. CD8 suppressor T cells lyse other infected macrophages -> caseating granulomas (‘tubercules”) - gradular necrosis in the tissues - mycobacteria cannot continue to grow within these granulomas, so the infectious process pauses (latency)

TNF plays an important role in maintaining latency; Patients receiving TNF-alpha antagonists (Remicade) may reactivate TB

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8
Q

When TB infects the lungs, how does it spread to the bloodstream?

A

Bacilli proliferate locally and spread through the lymphatics to a hilar node, forming the Ghon complex (exudative lesion plus hilar node), launch from the Gohn complex to the bloodstream (bacteremia and hematogenous spread) -> miliary TB (loci of TB replication) -> potentially TB meningitis

TB granulomas are found there there is a high partial pressure of O2

With latency, you get calcified TB granulomas - can get reactivation of TB

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9
Q

What are some risk factors for infection?

What are some risk factors for poor outcome?

A
  1. crowded (prisons, hospitals, homeless shelters)
  2. HIV
  3. Uncontrolled HIV (inadquate highly active antiretroviral therapy)
  4. Steroids
  5. INF gamma deficiency
  6. TNF-alpha antagonist (Remicade)
  7. Age < 5 yrs
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10
Q

What does a classic active pulmonary TB present with?

A

cough, weight loss (consumption), fever, night sweats, hemoptysis (spitting up blood) and chest pain

Chest radiograph, cavity formation indicates advanced infection, associated with hgh bacterial load

noncalcified round infiltrated - may be confused with lung carcinoma

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11
Q
  1. What is TB scrofula?

2. What is the trend of mycobacterial cervical infections in adults v. peds?

A

1.Reactivation in lymph node
A painless enlarging persistent mass. Cervical lymph node is affected in 2/3. Systemic symptoms include fevel/chills, weight loss, or malaise
2. In adults caused by M. tuberculosis, in peds caused by atypical mycobacterium (contaminted objects in their mouths)

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12
Q
  1. What is the most common site for extrapulmonary infection?
A
  1. Genitourinary TB - TB almost always reaches the kidneys during the primary infection but does not present clinically; may be 20 yrs of latency before symptoms; usually secondary to renal tuberculosis
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13
Q

What are the main manifestations of skeletal TB?

A
  1. Arthritis of one joint

2. Pott disease (spinal infection); back pain, stiffness, paralysis of lower extremeties

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14
Q

What is the name of the hematogenous spread of TB throughout the body that looks like “millet seeds” in lungs on chest X ray?

A

Miliary Tb; more likely to develop right after primary infection, less likely as reactivation, highest risk in very young and old, fatal if untreated

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15
Q

What is something strange that manifests in TB meningitis in children?

A

Brudzinski Neck Sign
You see strange neurological signs i.e., you lift head and knees lift up
Develops in 5-10% of children younger than 2

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16
Q

What does the tuberculin skin test by purified protein derivative test?
What does the IGRA blood test indicate?
What are problems with both?

A

Exposure (get positive with vaccine)
Exposure, but not vaccine
May give false-negative if the patient is badly immunosuppressed or late in the course of TB

17
Q

What is the best way to prevent TB?

A

Good housing and nutrition
Live vaccine, BCG, is not, expensive and canot use on immunocompromised peoples, does not prevent initial infection, helps immune system drive into latent infection

18
Q

Why are atypical mycobacterium considered atypical?

A
  1. Cause neither TB nor leprosy
  2. Environmentally-acquired
  3. PPD TST usually negative
  4. Not lethal in guinea pigs
  5. Systemic diseases very rare without predisposing condition: HIV, cancer etc.
  6. Cutaneous infection most likely in immunocompetent adults, scrofula in children
19
Q

Is M. leprae culturable?

A
  1. NO, reservoirs are humans and armadillos, 14-day doubling time; slowest growing human pathogen; prefers 30C for growth, sticks to periphery; genetically appears to be a stripped-down version of M. tuberculosis
20
Q

What does M. leprae cause?
What are the symptoms derived from?
Method of transmission?

A
  1. leprosy, Hansen Disease
  2. Both infection and immune response
  3. Unclear, extremely long incubation period - only 5-10% of population is believed immunologically susceptible to symptoms
21
Q

What is characteristic of Paucibacillary leprosy?

A

aka tuberculoid form - vigorous CMI contains disease (CD4+, Th1) but causes immunogenic problems (body tries to clear out bacteria and fails)
- asymmetrical immunogenic peripheral nerve damage
-Lepromatin PPD (not diagnostic of exposure, used to determine patient’s ability to raise immune response) +
TREAT WITH DAPSONE - does not help with nerve damage

22
Q

What is characteristic of multibacillary leprosy?

A

aka lepromatous form - inadequate CMI response (useless Th2, nonprotectice antibodies); extensive skin involvement: >6 lesions, infiltrated nodules&plaques; symmetrical peripheral nerve damage from bacterial growth in Schwann cells
-lepromatin PPD (not diagnostic of exposure, used to determine patient’s ability to raise immune response -
TREAT WITH DAPSONE