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MSII Microbiology > Unit 4 - Mycobacteria > Flashcards

Unit 4 - Mycobacteria Flashcards

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1
Q

what is the bacteriology of Mycobacterium tuberculosis?

A
  • Gram stains poorly, but almost uniquely acid-fast
  • grows slowly in vitro, requires special nutrients
  • obligate aerobe
  • multi-drug resistant and extensively drug resistant strains are public health emergency in US and abroad
  • resistant to acid and alkali (environmentally hardy) and resistance is Xmal (no known plasmids)
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2
Q

what are important structural components of Mycobacterium tuberculosis?

A
  • mycolic acids (acid fastness)
  • wax D (adjuvant used in Freund’s)
  • phosphatides (caseation necrosis)
  • cord factor/trehalose dimycolate (virulence, microscopic serpentine appearance)
  • phtiocerol dimycocerosate (lung pathogenesis)
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3
Q

is TB or atypical mycobacteria pathogenic in guinea pigs?

A

TB is pathogenic in guinea pigs

atypicals are not

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4
Q

what is the reservoir for TB? how is it transmitted?

A

humans; human-to-human transmission is typical via respiratory droplets (infected aerosols)
-rarely transdermal or GI infection

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5
Q

explain TB pathology

A

resides in MP, prevents fusion of phagosome with lysosome –> bacteria proliferate w/in MP as Trojan horses

  • exudative lesions: in lungs at initial site of infection (acute inflammatory response); large numbers of bacilli are present, and host defences are week
  • -loose aggregates of immature MP, neutrophils, fibrin, and caseation necrosis are sites of growth
  • granulomatous lesions: central area of infected Langerhan’s giant cells surrounded by zone of epithelioid cells
  • proliferating lesion: develop where bacillary load is small and host CMI responses dominate
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6
Q

what is a Ghon complex?

A

exudative lesions + draining lymph nodes

-usually in lower lobe, and launches into blood stream

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7
Q

what is a tubercule? tuberculoma?

A

older caseating granuloma surrounded by fibrous tissue, central caseation necrosis (old infection, rather than active)

  • heals by fibrosis and calcification
  • may erode and empty its contents:
  • -directly: infects more of lung
  • -coughed up: swallowed to infect GI, inhaled to infect more lung
  • -hematogenously: infect organs in early infection before CMI, and later on if patient immunocompromised
  • tuberculoma = tubercule that is enlarging like a tumor
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8
Q

where can reactivation fo TB occur? in who is it seen?

A

lesions may be in apices, kidneys, brain, bone, and lower lung
-seen in immunocompromised, debilitated

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9
Q

how do you stop quiescent TB?

A

vaccinate for measles, varicella, and pertussis

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10
Q

describe the CMI response to TB?

A

terminates unimpeded growth of TB 2-3 weeks after initial infection in 2 phases:
`1. CD4 helper T cells activate some infected MP to kill intracellular bacteria
2. CD8 suppressor T cells lyse other infected macrophages –> caseating granulomas (tubercules)

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11
Q

what does TNF have to do with TB?

A

plays important role in maintaining latency

-patients getting TNF-alpha antagonists (like Remicade) may reactivate

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12
Q

what MP protein is critical for TB clearance?

A

NRAMP

-mutations may lead to more frequent and serious clinical disease

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13
Q

what makes TB organisms hard to clear completely?

A
  • can be intracellular (not obligate)
  • caseous material is hard to penetrate
  • bacteria multiply slowly
  • -persisters have periods of metabolic inactivity
  • -both protect from drugs that kill rapidly growing cells
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14
Q

are TB carriers contagious if they have a negative sputum test?

A

they still might be contagious

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15
Q

where do most cases of TB result from in US?

A
  • poverty
  • poor health and diet (elderly men, Native Americans, African Americans)
  • crowded, at-risk environments
  • HIV
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16
Q

what are immunosuppression-related risk factors for TB?

A
  • uncontrolled HIV (inadequate HAART)
  • steroids
  • IFN-gamma deficiency
  • TNF=alpha antagonists (remicade)
  • age <5 yrs
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17
Q

what is classic active pulmonary TB? symptoms? radiograph?

A

75% of patients

  • cough, weight loss (consumption), fever, night sweats, hemoptysis, chest pain
  • cavity formation - indicates advanced infection, associated with high bacterial load
  • noncalcified round infiltrates - may be confused with lung carcinoma
  • tuberculomas
  • HIV+ X-ray may look normal despite symptoms and +sputum
  • fiberoptic bronchoscopy is most effective procedure for obtaining cultures (bronchoalveolar lavage)
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18
Q

what is extrapulmonary involvement of TB?

A

in 20% of patients

  • 60% of them are sputum negative with normal chest radiograph
  • nonpulmonary symptoms mimic wide variety of diseases
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19
Q

what is TB scrofula? tests?

A

reactivation in LN (2/3 are cervical)

  • painless, enlarging, or persistent mass
  • 95% of mycobacterial cervical infection in adults are TB reactivation; in peds, it’s atypical mycobacterium (not old enough)
  • PPD and fine needle aspiration for culture are best tests
  • surgery considered only after antibiotic treatment underway
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20
Q

what is genitourinary TB?

A

most common site for extrapulmonary infection

  • TB almost always reaches kidney during primary infection, but doesn’t present clinically; may be 20 years of latency before symptoms
  • genital TB is secondary to renal TB
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21
Q

go into more detail about genital TB?

A
  • aseptic UTI or even infertility
  • females: infertility, menstrual disorders, pain (infected fallopian tube)
  • -pregnancy unusual if TB present; spontaneous abortion or ectopic pregnancy occurs
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22
Q

go into more detail about renal TB? tests?

A
  • both infection and healing can block tubes
  • dysuria, hematuria, flank pain, “sterile pyuria”
  • IV urography is best option for identification of renal, ureteric, and bladder TB
  • also use US, CT, MRI
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23
Q

describe CNS TB

A
  • visualize by MRI with gadolinium enhancement
  • MRI is most sensitive test for detecting extent of leptomeningeal disease
  • -superior to CT to find parenchymal abnormalities (tuberculomas, abscesses, infarctions)
  • CSF analysis: detect decreased glucose, increased PRO, pleocytosis
  • -PCR assay may be diagnostic
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24
Q

describe skeletal TB?

A

two main manifestations

  1. arthritis of one joint
  2. Pott disease (spinal infection) as vertebral osteomyelitis
    - back pain, stiffness, paralysis of lower extremities, meningitis
    - do CT/MRI, but don’t delay treatment as paralysis could be permanent
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25
Q

describe GI TB? tests?

A
  • rare
  • abdominal pain, diarrhea, weight loss, anemia, fever with night sweats
  • obstruction (palpable) or hemorrhage in ileocecal region (either TB of M. bovis from unpasteurized milk)
  • radiograph for calcified granulomas
  • CT scan shows mesenteric lymphadenopathy with hypoattenuating center (necrosis)
  • exploratory surgery is required
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26
Q

describe miliary TB? symptoms? treatment?

A
  1. 5% of cases; more likely to develop right after primary infection (less likely reactivation)
    - hematogenous spread of TB thru body
    - many noncalcified foci of infection appear (like millet seeds) in lung on CXR
    - highest risk in very young/old
    - fatal if untreated even a week; treat on first suspicion
    - history of cough and respiratory distress
    - lymphadenopathy, hepatosplenomegaly, tachypnea, cyanosis
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27
Q

what is subtle miliary TB? what is seen on imaging?

A

papular, necrotic or purpuric lesions on skin or choroidal tubercles in retina
-tiny nodules best seen by CXR w/ bright spotlight, lateral Xray, chest CT

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28
Q

what is TB meningitis?

A

in 5-10% of children younger than 2 years

  • nuchal rigidity
  • altered DTR
  • lethargy
  • CN palsies
  • Brudzinski’s neck sign
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29
Q

what are special considerations in pediatric TB?

A

indicates recent transmission

  • track contacts and index case
  • unusual sites are middle ear, skin, and ocular structures
  • gastric aspirates are used instead of sputum if <6 yo (cannot bring up sputum)
  • start treatment as soon as samples are taken, as can be lethal before TST is positive
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30
Q

when can you rule out TB in pediatrics?

A

present w/ pneumonia, pleural effusion, cavitary/mass lesion in lung, failure to thrive, significant weight loss, unexplained lymphadenopathy

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31
Q

how is erythema nodosum related to TB?

A 
primary infection (tender nodules on leg)
-immunogenic from strong CMI response
32
Q

what is oropharyngeal TB?

A

painless ulcer w/ local adenopathy

33
Q

what is Remicade-activated TB?

A

patients getting Remicade for RA, Crohn’s, etc. may reactivate latent infections (TNF-alpha inhibitors)

34
Q

how is AIDS+TB different from normal TB?

A

many symptoms and more rapid decline

35
Q

explain what the PPD/TST is

A

positivity develops 2-10 weeks post-infection

  • diameter of erythema and induration from delayed hypersensitivity to tuberculin is measured
  • may be false negative (<5 mm) if patient is badly immunosuppressed or late in course of TB
  • must be sure not to inject to bloodstream (hematogenous spread)
36
Q

what do results of PPD/TST mean?

A

15 mm: +
10 mm: + if also has risk factors
5 mm: + if has deficient CMI
-misleading weak (<5 wks) or coinfected with measles)

37
Q

what is the IFN-gamma release assay

A

(IGRA) uses TB peptides in blood test

-doesn’t require 2nd visit, and is specific for TB, not the vaccine

38
Q

explain the steps to acid fast staining?

A
  1. cover smear with carbofuschin; steam over boiling water for 8 minutes; add more stain if it boils off
  2. after slide has cooled, decolorize with acid-alcohol for 15-20 seconds
  3. stop decolorization action of acid by rinsing with water
  4. counterstain with methylene blue for 30 seconds
  5. rinse briefly with water to remove excess methylene blue
  6. blot paper with bibulous paper; examine directly under oil immersion
39
Q

what is the acid fast status of TB VS E. coli? specificity/sensitivity?

A

TB is acid fast (pink carbolfuschin stain), while E. coli is not (methylene blue counterstain)
-however, “smear negative” ones may still be infectious while all “smear positive” patients are positive (very specific, but not sensitive)

40
Q

when should urinalysis and urine culture be taken in TB?

A

for patients with GU complaints

41
Q

explain TB and culture

A

liquid media is preferred,b ut it takes about 2 weeks

  • needed for antibiotic resistance testing
  • molecular (rRNA probe and PCR tests) are available and faster, but not as sensitive
  • TB bacteremia can be detected from blood cultures, esp. if immunosuppressed, but need special media
42
Q

how long do traditional antibiotic tests take? what is a better alternative?

A

ART: 3-4 weeks b/c of TB’s slow doubling time
DNA sequencing or microscopic-observation methods are faster depending on reagents and personnel
-luciferase assay is faster

43
Q

what should you do to infectious TB patients?

A

isolate in private room with negative rpessure

-all contacts must wear high-efficiency masks for first 2 weeks of treatment

44
Q

what is the initial emperic treatment of TB?

A

4-drug regimen: isoniazid, rifampin, pyrazinamide, and ethambutol/streptomycin
-once TB isolate is fully susceptible, the fourth drug can be discontinued

45
Q

what do you do for multi-drug resistant TB?

A

use a minimum of 1 susceptible injectable and at least 3 additional drugs to prevent development of additional resistance

  • treat with consultation of an expert
  • perform susceptibility tests
46
Q

how long is treatment in susceptible TB (asymptomatic/latent), CNS involvement, pulmonary involvement, or pediatrics

A

sus: 3-6 mo
CNS: 9-12 mo
pulm: 6 mo
peds: 6 mo

47
Q

what should pregnant TB patients get for treatment?

A

since at increased risk for isoniazid-induced hepatotoxicity, should undergo monthly ALT monitoring while on treatment

48
Q

what happens if TB “persisters” survive treatment?

A

reactivates later

49
Q

why is directly observed therapy used?

A

due to noncompliance (patients rebel after a few months)

50
Q

what is the BCG (bacillus Calmette-Guerin) vaccine?

A

live attenuated M. bovis

  • prevents up to 70% of symptomatic infections
  • blood-based immunity that drives TB into latent phase, but doesn’t prevent latent infection
  • seldom used in US
  • watch for 3-6 mm PPD+ if vaccinated abroad or in military
  • -can differentiate with IGRA
  • not for immunocompromised
51
Q

is latent TB still contagious?

A

no, it’s no longer contagious

-a strong CMI will make it latent

52
Q

why are atypical mycobacteria “atypical”?

A
  • cause neither TB nor leprosy
  • environmentally acquired (don’t need to trace past contacts)
  • PPD and TST are usually negative
  • less aggressive infections
  • systemic disease is very rare without a predisposing condition
53
Q

what type of atypical disease is seen in adults VS children?

A

immunocompetent adults: cutaneous infection

children: scrofula

54
Q

what are group 1 atypicals? examples? diseases?

A

Photochromogens

  • produce pigment when grown in light
  • M. kansasii is environmental (unknown reservoir) in midwest, Texas, England
  • -pulmonary/systemic disease like TB, and killed by same antibiotics
  • M. marinum in fresh/salt water
  • -forms fish tank granulomas (ulcerating lesions on abrasions exposed to swimming water or aquariums)
  • -treat with tetracycline
  • -most common atypical mycobacteria infection
55
Q

what are group 2 atypicals? examples? diseases?

A

Scotochromogens

  • produce pigment when grown in dark or light
  • M. scrofulaceum produes scrofula (mostly in children)
  • reservoir is water, and harmless in respiratory tract
  • fix by surgically removing affected notes
56
Q

what are group 3 atypicals? examples? disease?

A

Nonchromogens

  • doesn’t produce pigment
  • M. avium and M. intracellulare are hard to distinguish (so called MAI or MAC)
  • cause pulmonary disease indistinguisable from TB in only severely immunocompromised patients
  • environmentally widespread, found in soil and water
  • highly drug resistant, so use clarithromycin + ethambutol or rifabutin or cipro (diff than TB)
57
Q

what are group 4 atypicals? examples? disease?

A

Rapidly growing mycobacteria (culturable in <1 week)

  • M. fortuitum/chelonei (hard to distinguish)
  • -found in soil and water
  • -cause problems in immunocompromised, prosthetic hips, indwelling catheters, puncture wounds
  • -treat with amikacin and doxycyclin + surgical excision of site
  • M. abscessus (environmental)
  • -chronic lung infections, skin, bone joints
  • -highly antibiotic resistant
  • M. smegmatis (normal flora under foreskin)
58
Q

explain the bacteriology of leprosy (Hansen’s disease)

-reservoirs? growing time?

A

M. leprae (genetically stripped down version of TB)

  • no in vitro culture system
  • reservoirs are humans (major) and armadillos (minor)
  • 14-day doubling time (slowest growing human pathogen)
  • prefers 30 C for growth, sticks to periphery of humans
59
Q

what is the pathogenesis of Hansen’s disease? how does it spread? where does it infect?

A

infection requires prolonged contact w/ infectious patient (but exact mech of transmission unclear)

  • spread by nasal secretions and skin lesions
  • found world-wide, but 90%+ of those exposed never develop disease (months to 50 yr incubation)
  • -5-10% have unknown predisposition to symptomatic infection
  • intracellular replication in skin histiocytes, endothelial cells, Schwann nerve cells
60
Q

what is responsible for the nerve damage in Hansen’s disease?

A

both bacterium and CMI

61
Q

what are the two extremes of Hansen disease symptoms?

A
  1. tuberculoid leprosy (paucibacillary)

2. lepromatous leprosy (multibacillary)

62
Q

explain the symptoms of tuberculoid leprosy

A

strong CMI response (CD4, Th1, IFN-gamma, IL-2/12) causes immunogenic problems

  • few bacilli seen (<5 dry skin lesions, but repetitive injury/healing can cause shortening of fingers)
  • granulomas with giant cells form
  • immunogenic nerve damage (CMIs kill)
  • lepromatin skin test positive
63
Q

explain the symptoms of lepromatous leprosy

A

poor CMI response (useless Th2, nonprotecctive Ab, anergy)

  • large numbers of bacilli in skin, mucous membranes
  • foamy histiocytes form
  • nerves damaged by bacteria
  • lepromatin skin test negative (no CMI)
  • extensive skin involvement (>6 lesions, infiltrated nodules and plaques, bacilli visible on smears from lesion fluid)
  • symmetric peripheral nerve damage from bacterial growth in Schwann cells
  • infection destroys nasal cartilage, reaches eye
64
Q

what are constitutional symptoms seen in both forms of leprosy? nerve problems?

A
  • wasting and muscle weekness
  • peripheral nerve involvement –> loss of sensory and motor function, subsequent injury
  • -ulnar/median nerves –> claw hand
  • -posterior tibial –> plantar insensitivity, clawed toes
  • -common peroneal –> foot droip
  • -radial cutaneous, facial, greater articular nerves
65
Q

what does leprosy show on exam for both forms of leprosy?

A
  • hypoesthesia
  • skin lesions (first physical signs usually cutaneous)
  • peripheral neuropathy
66
Q

what does tuberculoid leprosy show on exam?

A
  • few sharply demarcated, hypopigmented macules on buttocks, face, exterior surfaces of limbs
  • superficial nerves near lesions may enlarge and be palpable
  • neuropathic pain, muscle atrophy
  • lepromatin PPD+
67
Q

what does lepromatous leprosy show on exam?

A
  • extensive bilaterally symmetric cutaneous macules, nodules, plaques, papules
  • lesions have poorly defined borders and raised centers
  • eye infection
  • loss of nasal cartilage
  • leonine facies (thickened and corrugated facial skin)
  • lepromatin PPD-
68
Q

what is the lepromin skin test?

A

extract of M. leprae is injected intradermally

  • induration measured 48 hrs later
  • test is used in symptomatic patients to determine where they fall in the spectrum; it’s NOT diagnostic of exposure
  • if more positive, more tuberculoid; if more negative, more lepromatous
69
Q

what does skin smear show in leprosy?

A

swab and full-thickness biopsy from leading edge of lesions for acid-fast staining and histology
-PCR effective but not standard

70
Q

what does tuberculoid leprosy labs show?

A

granulomatous changes with epithelial cells and lymphocytes

-tests will be otherwise negative, so diagnose on exam

71
Q

what does lepromatous leprosy labs show?

A

bacilli visible and lipid-laden MP “foam cells”

  • acid fast stain of skin lesions or nasal scrapings
  • VDRL and RPR positive
72
Q

what is leprosy treatment?

A

tuberculoid: dapsone + rifampin for 2 years (b/c slow growing)
lepromatous: dapsone + rifampin + clofazimine for 2 years+ (until lesions free of organisms)

73
Q

how do you treat pediatric patients/

A

prophylaxis with dapsone if exposed

74
Q

how is thalidomide involved with leprosy?

A

can treat severe erythyma nodosum that arises due to dapsone

75
Q

how do you prevent leprosy?

A

isolate infected patients

MSII Microbiology (23 decks)

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