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Dermatology Board Prep > DERM (11) Infections, Infestations, and Bites > Mycobacterial disease > Flashcards

Mycobacterial disease Flashcards

1
Q

What is the treatment for a type-1 reversal reaction with upgrading in leprosy?

A

Prednisone

high-yield question

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2
Q

What is the treatment for a type-2 vasculitis type reactionary state in leprosy?

A

Thalidomide

High-yield, tx is most commonly tested of the reactionary states in leprosy

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3
Q

What is the immunity status of somebody who gets the tuberculous chancre?

A

No immunity, it is like syphilis, they have never had tuberculosis before, hence no immunity to it.

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4
Q

What is the immunity status of somebody who gets the tuberculosis verruca cutis?

A

These are those who have had tuberculosis, so there have moderate to high immunity.

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5
Q

What cells does mycobacterium leprae parasitize?

A

Macrophages and Schwann cells

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6
Q

Is Mycobacterium leprae intra or extracellular?

A

Obligate intracellular, weakly acid-fast bacillus

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7
Q

What temperatures are required for the growth of Mycobacterium leprae?

A

Cool temperatures (30-35 degrees C)

This is why there is a predilection for lesions on areas that are cooler like the nose, testes, and ear lobes as well as peripheral nerves that are close to the skin surface.

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8
Q

How is Mycobacterium leprae transmitted?

A

Nasal/oral droplets; also 9-banded armadillos in the southeast of the US

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9
Q

What is the risk of acquiring leprosy from a household contact?

A

25%

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10
Q

Can Mycobacterium leprae be cultured in vitro?

A

No! Must be cultured in mouse footpads or in armadillos

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11
Q

What is the incubation period for Leprosy?

A

Prolonged, average 4-10 years but can go up to 30 years

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12
Q

Sex differences in Leprosy epidemiology?

A

Males get it more often, lepromatous form is 2x more common in men

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13
Q

What are the primary skin lesions in Leprosy?

A

Erythematous or hypopigmented, annular plaque w/ mild scaling

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14
Q

What are the most common nerves to be affected by leprosy?

A

Peripheral nerves enlarged in all forms of leprosy. Most common nerves: CN-5, CN-7, median, radial, ulnar, greater auricular, posterior tibial and common peroneal nerves

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15
Q

What type of neural symptoms are noted from leprosy?

A

Claw hand and papal hand (median and ulnar nerve neuropathies). stocking-glove anesthesia, neuropathic ulcers of plantar surfaces, foot drop, atrophy of interosseous muscles, and ocular damage (from CN-7) dysfunction

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16
Q

What is the Ridley-Jopling scale?

A

This is a scale that separates leprosy into the two polar forms with cell-mediated immunity and antibody response and then the spectrum of intermediary presentations.

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17
Q

What are the two major forms of leprosy and the type of immune response these correlate with?

A

Lepromatous = Th2 response (lepromatous)

Tuberculoid = Th1 response (Tuberculo1d)

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18
Q

What are the three borderline forms of leprosy?

A

Borderline tuberculoid leprosy, mid-borderline leprosy, borderline lepromatous leprosy

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19
Q

What cytokines are important in the cell-mediated tuberculoid reaction to leprosy?

A

IL-2 and IFN-gamma

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20
Q

What cytokines are important in the antibody-mediated lepromatous reaction to leprosy?

A

IL-4, IL-10

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21
Q

In what type of reaction (lepromatous vs tuberculoid) are there more M. leprae bacteria?

A

The lepromatous or antibody-mediated reaction pattern

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22
Q

What is “upgrading” of leprosy reactions?

A

This is when the reaction pattern moves towards being cell-mediated more

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23
Q

Describe what the lepromin test is?

A

Immunologic test indicative of host resistance to M. leprae. Sample of mycobacterium that is not enough to cause infection is injected subcutaneously.

  • In tuberculoid leprosy: the immune system recognizes the test and produces allergic reaction = positive test
  • In lepromatous leprosy the system does not recognize the test bacteria and it remains negative
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24
Q

What is the pathogenesis of leprosy?

A

Macrophages: Produce IL-1, TNF-a, and IL-12 when the organism is encountered

Th1 response: IL-2, Interferon-gamma, TNF-beta are generated and inflammation is maintained

Th2 response: IL-4, IL-5, IL-10, and IL-13, are released which suppress macrophage activity

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25
Q

What type of lesions in leprosy are clinically stable vs unstable?

A

Polar forms = stable, borderline forms = unstable

Patients with either lepromatous or tuberculoid leprosy (polar forms) remain in this state through disease course. Borderline forms of leprosy are unstable however and their clinical or pathologic features are somewhere between the two polar forms and can change.

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26
Q

What is the difference clinically between lepromatous and tuberculoid leprosy?

A

Lepromatous = Macules, papules, nodules, diffuse infiltration

*​Numerous lesions a symmetric distribution

Tuberculoid = Macules, often hypo pigmented

*One or few lesions in a localized or asymmetric distribution

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27
Q

What is the difference in sensation between lepromatous lesions and tuberculoid lesions in leprosy?

A

Lepromatous = Sensation not affected

Tuberculoid = Sensation is absent

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28
Q

Difference between lepromatous and tuberculoid leprosy in regards to the number of bacilli in lesions?

A

Lepromatous = Many bacilli in the skin (globi)

Tuberculoid = None dected

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29
Q

What are some important physical exam findings associated with leprosy?

A
  • Anesthesia or hypesthesia of individual cutaneous lesions.
  • Check for changes in sensation to touch, temperature and neuropathic changes including atrophy, flexion contractions, vasomotor alterations and secretory disturbances

The nerves can become enlarged and palpable themselves and these should be palpated during exam

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30
Q

What are the most common sites for lepromatous leprosy?

A

Face, buttocks, lower extremities

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31
Q

What is histoid leprosy?

A

A clinically distinct variant of lepromatous leprosy where there is dermatofibroma like papules and nodules making up the primary cutaneous findings.

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32
Q

What is a differential diagnosis for leonine facies?

A

A Lion PALLLLMMSS you

Paget’s disease of bone

Amyloidosis

Leishmaniasis/Lipoid proteinosis/Leprosy/Lymphoma

Mastocytosis/MF

Sarcoid/Scleromyxedema

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33
Q

What are some common sequelae of leprosy?

A

Leonine facies, madarosis, lagophthalmos (corneal anesthesia, keratitis, episcleritis, blindness), saddle nose deformities, elongated soft ear lobs, orchitis and gynecomastia in males, claw hand deformity (median and ulnar nerve damage) and palpal hand deformity (ulnar nerve damage), shortening of digits from bone resorption, foot drop, hammertoes, acquired ichthyosis of lower extremities, and neurotrophic ulcers.

34
Q

Describe lesions of borderline leprosy

A

Asymmetric lesions, with the severity being dependent on what pole (tuberculous or lepromatous) the pt is leaning towards. These are usually poorly defined erythematous arcuate plaques with a well-defined central clearing. Usually the hair is absent over the lesion

35
Q

What is the clinical description of tuberculoid leprosy and where would you want to biopsy?

A

Few to solitary well-demarcated plaques. They can have slightly elevated borders which is the preferred site for bx.

36
Q

What are the two major types of leprosy reactional states?

A

Type 1 = reversal reaction with “upgrading”

Type 2 = vasculitis (most commonly erythema nodosum leprosum)

37
Q

What is the pathogenic process for type 1 leprosy reactional state, and what are the clinical manifestations?

A
  • Delayed-type hypersensitivity reaction
  • Increased inflammation at sites of established skin lesions and the emergence of “new” skin lesions. Acute nerve pain or tenderness and loss of function can occur or recent (<6 month hx) or progressive neurologic impairment in the absence of painful nerves
38
Q

What is the pathogenic process for type 2 leprosy reactional state, and what are the clinical manifestations?

A

Pathogenesis: excessive humoral immunity w/ a Th2 cytokine pattern and formation of immune complexes. This leads to a systemic and cutaneous small-vessel vasculitis

Clinical signs: Nodular skin lesions, fever/myalgias/malaise, severe joint pain/swelling, iridocyclitis, hepatosplenomegaly, orchitis, glomerulonephritis

39
Q

How do you treat type 1 reversal reaction with “upgrading” in leprosy?

A

Prednisone (think increased inflammatory response)

40
Q

How do you treat type 2 leprosy reactional state/vasculitis?

A

Thalidomide

41
Q

What is the Lucio phenomenon in leprosy and what is its treatment?

A

Severe necrotizing vasculitis w/ thrombosis; only occurs in patients from western Mexico with diffuse lepromatous leprosy.

  • Clinically looks like purpuric macules and ulcerative bullous lesions below the knees; treat with prednisone
42
Q

What is the histology of a lepromatous leprosy lesion?

A

Diffuse dermal infiltrate of foamy histocytes with globi (clumping of mycobacteria). Fite stain highlights these

  • Virchow cells: macrophages w/ numerous bacilli as well as lipid droplets in their cytoplasm
43
Q

What is the histology of tuberculoid leprosy?

A

Granulomatous nodular infiltrates with the dermis. There can be sparse perineural infiltrate w/ lymphocytes, histiocytes, and plasma cells.

  • These are arranged as epithelioid granulomas running east-west in the dermis (lavender sausages)

*Fite stain usually negative

44
Q

What histo stains can detect bacilli in leprosy?

A

Gram, Ziehl-Neelsen, or Fite (most common, bacilli are bright red)

Methenamine silver: detects fragmented acid-fast bacilli

Sudan III: stains bacilli black

Sudan IV: known as scarlet red, stains the bacilli red

45
Q

What common test can be falsely positive in leprosy?

A

The VDRL or FTA-ABS for syphilis can be false positive in pts with lepromatous or borderline lepromatous leprosy

46
Q

How is diagnosis of leprosy confirmed?

A

Dx can be confirmed by finding bacilli in cutaneous scrapings, lymph nodes, or nasal secretions

  • PCR: amplification of genes encoding antigenic proteins (e.g. 36 kDa proline-rich antigen, Ag85B) and/or M. leprae-specific repetitive repeat sequences (RLEP region)
  • Serologic assays for anti-PGL IgM/IgG antibodies are only sensitive for the diagnosis of leprosy in the setting of multibacillary disease
  • Serum levels of anti-PGL-1 IgG and IgM antibodies are highest in those with lepromatous disease and lowest (or absent) in those with BT or tuberculous disease, therefore representing a marker of mycobacterial “load”.

Old school testing: histamine, pilocarpine, and lepromin (Mitsuda)

47
Q

What treatment is needed for leprosy?

A

Multidrug therapy is extremely effective. After the first dose, the patient is no longer contagious (though still requires a long course of tx).

Rifampin, clofazimine, dapsone, ofloxacin, minocycline are different options used. Recommendations depend on disease type and age.

48
Q

What are risk factors for cutaneous tuberculosis?

A

Low-income countries, impoverished populations, HIV (+), immunosuppressive therapies (especially TNF inhibitors), and innate defects of the IL-12/IFN-γ axis

49
Q

If you are thinking cutaneous tuberculosis in a child what is the best diagnostic test? How about in those who have had the BCG?

A
  • Diagnosis made with tuberculin skin test vs interferon-γ release assays (QuantiFERON® Gold)
  • Skin test better in children; interferon-γ test better for patients who have had BCG (live, attenuated M. bovis) vaccination (false (+) with skin test)
50
Q

What is the immunity status of those with tuberculous chancre?

A

This occurs in those who have not previously been exposed/have no prior immunity

51
Q

What is the clinical description of tuberculous chancre?

A

2 to 4-week inoculation period; painless, red, and indurated papule that ulcerates – heals after 3 to 12 months leaving an atrophic scar and calcified regional lymph nodes; may spread to lymph nodes

52
Q

What is the immunity status of someone to tuberculosis who gets tuberculosis verruca cutis?

A

Occurs in patients w/ previous infection w/ moderate-to-high immunity

53
Q

Clinical of tuberculosis verruca cutis?

A

Occurs via re-infection via inoculation, in patients w/ previous infection w/ moderate-to-high immunity; #1 form of cutaneous TB; warty/verrucous, growing papule may heal over years

54
Q

What is scrofuloderma?

A

This is the result of contiguous spread of tuberculosis infection to the skin from underlying disease (usually cervical lymph nodes and bones)

Clinical this presents as fluctuant nodules that develop sinus tracts, draining to skin, with a tethered appearance (almost like hidradenitis suppurativa). This occurs in low immunity states

55
Q

What is orificial tuberculosis?

A

Occurs in patients with advanced TB and poor cell-mediated immunity; autoinoculation of mucosa/skin close to anatomic orifice draining active systemic TB infection → ulceration/drainage; does NOT heal spontaneously

56
Q

What is lupus vulgaris?

A

This is the contiguous spread (hematogenous/lymphatic) of TB to the skin. Clinically appears as red-brown, sometimes annular, papules/plaques (with “apple jelly” color on diascopy) There is central scarring of the lesions

-Head/neck #1 site (esp.the nose, cheeks and ear lobes)

-Occurs in a moderate-to high immunity state (previously sensitized individuals)

57
Q

What is acute miliary tuberculosis and what are the skin findings that can occur?

A

Hematogenous dissemination from the lung that spreads everywhere, most often in immunosuppressed pts; pinpoint blue-red papules capped by minute vesicles that lead to small scars

58
Q

What is a tuberculous gumma?

A

Hematogenous dissemination leads to a deep nodule that ulcerates/drains.

  • Most common on the extremities; immunosuppressed pts
59
Q

What are tuberculids?

A

Immune reactions within the skin due to hematogenous dissemination of M. tuberculosis or its antigens from a primary source.

  • occurs in an individual with strong anti-tuberculous cell-mediated immunity
60
Q

What is papulonecrotic tuberculid, and what would be a DDx for it?

A

Dusky red papules or papulopustules that are widely distributed in a somewhat symmetric pattern and favor the extensor aspects of the extremities and buttocks +/- pruritus

  • DDx: PLEVA vs. small vessel vasculitis
61
Q

What is lichen scrofulosorum?

A

Firm, typically perifollicular, pink or yellow-brown, tiny flat-topped papules with variable scale, usually on the trunk.

  • Most common in kids with nodal or skeletal TB
62
Q

What is erythema induratum (nodular vasculitis)?

A

Lobular panniculitis that is associated with M. tuberculosis, most common on bilateral calves. It heals with atrophic hyperpigmented scars

63
Q

What complications can arise as a result of the BCG inoculation?

A

This is an inoculation of attenuated mycobacterium bovis

  • Can cause: Local/generalized tuberculids, lupus vulgaris, scrofuloderma, and fever, local inflammation, SQ abscesses w or w/o ulcer, severe regional LAD, osteitis, and tuberculous foci in distant organs
64
Q

What are the most common mycobacteriosis infections of the skin that occur in immunocompetent hosts?

A

Leprosy>Tuberculosis>Buruli Ulcers

65
Q

What are Buruli ulcers?

A

These are caused by mycobacterium ulcerans. This is a slow-growing acid-fast bacillus that produces indolent ulcers.

  • It is endemic in wetlands of tropical and subtropical countries and enters the skin via minor trauma
  • Nodule forms which goes to ulcer on extremities; can become >15cm and extend to bones.
66
Q

What are the main treatments for buruli ulcer?

A

Excision (tx of choice, continuous local heating to 40*C, hyperbaric O2, oral rifampin plus intramuscular streptomycin daily for 8 weeks.

67
Q

Can Mycobacterium marinum be picked up from a swimming pool?

A

Yes, the bacteria are resistant to chlorine

68
Q

What skin lesions are caused by Mycobacterium marinum?

A

Erythematous/blue ulcerating nodules in a sporotrichoid pattern (most common atypical mycobacterium to show sporotrichoid spread)

  • Rarely infections can go deeper than the skin infecting tendons, joints, etc.
69
Q

How is the diagnosis of mycobacterium marinum made?

A

Diagnosis is confirmed with culture (+ in 70-80% of cases): M. marinum grows best at 31 degrees Celsius (~3 weeks required for growth), as opposed to the usual 37 degrees for most other mycobacteria; PCR is quicker

70
Q

What is the treatment for mycobacterium marinum?

A

Clarithromycin +/− rifampin/ethambutol, minocycline, and TMP-SMX

71
Q

What is Mycobacterium kansasii and what cutaneous disease does it cause?

A

Closely related to M. tuberculosis (infxn w/ kansasii can increase immunity against tuberculosis).

  • “Yellow bacillus” because of beta-carotene crystal depositions that can be seen after exposure to light
  • Most common in temperate climates like US, UK, northern France and Belgium
  • Can come from cattle and swine but natural reservoir is water
  • Skin disease includes: verrucous plaques, ulcers, and nodules which may be arranged in a lymphocutaneous (sporotrichoid) pattern
72
Q

What is the source of most infections with Mycobacterium fortuitum, M. chelonae, and M. Abscessus?

A

This group is a rapid growing mycobacteria that usually occur after trauma/surgery or medical treatments (like implant placement, liposuction, and botox). Also tattoo’s, nail salon, and footbaths.

73
Q

What is the treatment for M. Fortuitum, M. chelonae, and M abscessus?

A

Clarithromycin

74
Q

What are the most common skin findings for MAC (M. avium and M. intracellulare)?

A

Pulmonary infection is the most common overall. But on the skin, it can cause lesions from local inoculation or dissemination which include: pustules, ulcers on the legs, and nodules

75
Q

What lab abnormality can be seen in MAC infection (disseminated)?

A

Elevated alkaline phosphatase

76
Q

Describe the organism causing leprosy?

A

Mycobacterium leprae -Obligate intracellular, weakly acid-fast bacillus that parasitizes macrophages and Schwann cells

77
Q

Why does leprosy tend to have a distribution in cooler skin areas (nose, testes, ear lopes, superficial nerves, etc)?

A

Requires cool temperatures (30-35*C)

78
Q

How is leprosy spread?

A

Mostly nasal/oral droplets; also 9-banded armadillos in southeast US

79
Q

What is the incubation period for leprosy?

A

Prolonged, average 4-10 years but up to 30 years)

80
Q

Important epidemiology of leprosy?

A

bimodal age range (10-15 y/o and 30-60 y/o); M>F; lepromatous form 2x more common in men

81
Q

Primary skin lesions of leprosy?

A

erythematous, or hypopigmented, annular plaque w/ mild scaling

DERM (11) Infections, Infestations, and Bites (13 decks)

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