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Abbey MSII Unit 4 > Micro TB/Non-TB > Flashcards

Micro TB/Non-TB Flashcards

1
Q

mycobacterium tuberculosis bacteriology

A

acid-fast
grows SLOWLY in vitro with special nutrients
obligate aerobe
no toxins
resistance is chromosomals - non known plasmids

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2
Q

virulence factors for mycobacterium tuberculosis

A
  1. mycolic acids (acid fastness)
  2. wax D (adjuvant)
  3. phosphatides (caseation necrosis)
  4. cord factor (trehalose dimycolate)
  5. phtiocerol dimycocerosate (lung pathogenesis)
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3
Q

what is the reservoir for mycobacterium tuberculosis and how are they spread

A

humans (human-human transmission)

respiratory droplets

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4
Q

where does mycobacterium tuberculosis reside in the body? how?

A

in macrophages - prevents fusion of phagosome wit lysosome and bacteria proliferate

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5
Q

ghon complex

A

exudative lesions plus draining lymph nodes

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6
Q

exudative lesions

A

mycobacterium tuberculosis initial site of infection in lungs - cause acute inflammatory response

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7
Q

granulomatous lesions

A

central area of infected langhans’ giant cells surrounded by zone of epithlioid cells

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8
Q

tubercule

A

older granuloma surrounded by fibrous tissue, central caseation necrosis, heals by fibrosis and calcification

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9
Q

what happens to tubercules?

A

may erode and empty its contents directly into lung, coughed up where it can be swallowed to infect GI or inhaled to infect new parts of lung, or can go into bloodstream to infect organs

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10
Q

where do reactivation lesions of TB occur?

A

kidneys, brain, bone, lower lung - seen in immunocompromised, debilitation

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11
Q

what is TB controlled by?

A

CMI: CD4+ Th-1 cells, macrophages, gamma-interferon (IFNγ is an important activator of macrophages and inducer of Class II major histocompatibility complex (MHC) molecule expression)

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12
Q

NRAMP

A

macrophage protein critical in TB - mutations lead to more frequent and serious clinical disease

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13
Q

why is TB hard to clear completely?

A
  1. intracellular (not obligate)
  2. caseous material is hard to penetrate
  3. multiply slowly - “persisters” have periods of metabolic inactivity, both protect from drugs that kill rapidly-growing cells
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14
Q

what is seen on exam of TB?

A

fever, fatigue, night sweats, weight loss

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15
Q

pulmonary TB symptoms

A

cough and hemoptysis

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16
Q

scrofula

A

cerbical adenitis (lymph nodes), usually unilateral

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17
Q

what is scrofula usually caused by in adults? in children?

A

in adults: TB

in children: m. scrofulaceum

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18
Q

what is a common symptom of primary infection of TB?

A

erythema nodosum (indicative of strong CMI response)

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19
Q

miliary TB symptoms

A

multiple disseminated lesions like millet seeds with high mortality - seen in the very young and very old

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20
Q

disseminated TB symptoms

A

meningitis (brudinski sign), osteomyelitis (esp vertebral) = pott’s disease

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21
Q

GI TB symptoms - what has similar symptoms?

A

abdominal pain and diarrhea, obstruction or hemorrhage in ileocecal region (may be TB or M. bocis from unpasteurized milk)

22
Q

oropharyngeal TB symptoms

A

painless ulcer with local adenopathy

23
Q

renal TB symptoms

A

dysuria, hematuria, flank pain, “sterile pyuria” (symptoms of UTI but nothing in culture)

24
Q

remicade-activated TB symptoms

A

patients receiving remicade for rheumatoid arthritis, crohn’s, etc may reactivate latent infections

25
Q

PPD skin test

A

PPD injected, diamter of erythem and induration from delayed hypersensitivity to tuberculin is measured

26
Q

why is a diagnosis of TB in children difficult?

A
  • sputum smear won’t work (can’t cough up sputum)
  • may develop serious disease before PPD is +
  • never latent PD (no time for reactivation)
  • less common
27
Q

labs for TB

A
  • acid-fast staining of sputum or other specimens (smear positive patients are positive but smear negative may still be infectious)
  • sputum smears
  • culture (2 weeks)
  • PCR-based for rRNA, DNA (not very sensitive)
28
Q

quantiferon

A

TB blood test detects latent infections and is specific for TB, not vaccine

29
Q

drug used to treat TB

A

isoniazid

30
Q

what is used in a isoniazid resistant strain of TB?

A

rifampin

31
Q

similarities between TB and histoplasmosis. difference?

A

similarities: 1. granulomas 2. trojan horse macrophage 3. months-years treatment 4. airborne
difference: different drugs used to treat

32
Q

TB vaccine

A

BCG (bacillus calmette-guerin) - live attenuated M. bovis - prevents up to 70% of symptomatic infections but NOT latent

33
Q

atypical mycobacteria

A
  • acid fast like TB
  • opportunistic from environment
  • less aggressive
  • cutaneous in adults and scrofula in children
34
Q

photochromogens

A
  • atypical mycobacteria
  • produces pigment in light
  • does not kill geinea pigs (unlike TB)
  • m. kansasii (environmental in MW and Texas)
  • m. marinum (fresh and salt water) - from swimming and aquariums
35
Q

difference between m. kansasii and m. marinum

A

m. kansasii (environmental, resembles TB) - killed by same antibiotics as TB
M. marinum - treated with tetracycline instead and has ulceratin lesions on abrasions

36
Q

scotochromogenes

A
  • atypical mycobacteria
  • produces pigment in dark
  • does not kill guinea pigs
  • m. scrofulaceum produces scrofula (more common in children presenting with scrofula)
  • reservoir is in water
  • fixed surgically removing nodes
37
Q

nonchromogens

A
  • atypical mycobacteria
  • no pigment
  • does not kill guinea pigs
  • M. avium and M. intracellulare (MAI, MAC(
  • cause pulmonary disease indistinguishable from TB
  • environmentally spread
  • highly drug resistant - use clarithromycin to treat
38
Q

rapidly growing mycobacteria

A
  • atypical mycobacteria
  • no pigment, doesn’t kill guinea pigs
  • culturable in less than a week
  • m. fortuitum/m. chelonei (soil and water, different drugs)
  • m. abscessus (environmental, highly antibiotic resistant)
  • m. smegmatis (normal flora under foreskin)
39
Q

m. leprae bacteriology

A
  • no in vitro culture system
  • reservoirs are humans and armadillos
  • 14 day doubling time (VERY slow growing)
  • prefers 30C for growth (periphery)
40
Q

pathogenesis of m. leprae

A
  • prolonged contact with infectious patient
  • nasal secretions and skin lesion spread
  • 90% never develop disease
  • nerve damage by bacterium and CMI
41
Q

where does replication of m. leprae occur?

A

schwann nerve cells, also skin histiocytes and endothelial cells

42
Q

what are the two extremes of symptoms in m. leprae?

A

tuberculoid and lepromatous

43
Q

tuberculoid leprosy

A

STRONG CMI response (CD4, Rh1)

  • few bacilli seen
  • granulomas containing giant cells form
  • IMMUNOGENIC NERVE DAMAGE
  • LEPROMATIN skin test +
44
Q

lepromatous leprosy

A
  • POOR CMI response (useless Th2 - non protective antibodies)
  • large numbers of bacilli in skin and mucus membranes
  • foamy histocytes form
  • nerves damaged by bacteria
  • LEPROMATIN skin test - (because no CMI)
45
Q

what is leprosy also called?

A

hansen’s disease

46
Q

tuberculoid symptoms

A

hypopigmented macular or plaque-like skin lesions, thickened superficial nerves, anesthesia of skin lesions

47
Q

lepromatous symptoms

A

multiple nodular skin lesions, “leonine facies”, early in therapy

48
Q

lepromin skin test

A

extract of m. leprae is injected intradermally, induration is measured 48h later - used in symptomatic pateitns to determine where they fall in spectrum

49
Q

labs for tuberculoid and lepromatous

A
  • tests negative for tuberculoid (exam)

- acid fast for lepromatous, VDRL and RPR positive

50
Q

treatment of leprosy

A

DAPSONE

Abbey MSII Unit 4 (7 decks)

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