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Microbiology Virology > MAC > Flashcards

MAC Flashcards

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1
Q

MAC

A

Mycobacterium avium complex
2 related organisms:
1. M. avium
2. M. Intracellulare

Cultured in solid + liquid media

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2
Q

Virulent or avirulent to normal host??
BUT CAN CAUSE ……… in …. pts.

A

Relatively avirulent to normal host BUT can cause disseminated disease in AIDS patients

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3
Q

Where is MAC found?

A

Found: soil, water (natural water sources, pools, spas, hot tabs) & animals – acquired, ingestion or inhalation - No person-person transmission

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4
Q

—3 major disease syndromes
Associated with/ caused by :
MAC

A
  1. Pulmonary disease, usually adults with intact immune system
  2. Disseminated disease in patients with AIDS
  3. Cervical lymphadenitis
    • Disease rises from primary acquisition, NOT from latency reactivation
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5
Q

Most common source
. (MAC

A

Most common source = exposure to recirculating hot water systems
(Jacuzzi?)

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6
Q

Mycobacterium avium complex (MAC) – pulmonary disease

Risk factors

A

COPD (chronic obstructive pulmonary disease), chronic bronchiectasis, prior hospitalization for pneumonia, use of steroids

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7
Q

Pulmonary disease
MoT

A

Inhalation, disease may not manifest for months or yrs, smoking & COPD is risk factor

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8
Q

Pulmonary disease
Signs symptoms

A

CHRONIC illness, middle aged man + heavy smoking, COPD, bronchiectasis, cancer—
Chronic productive cough, weight loss, fever, night sweats

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9
Q

Rate of cavitation
TB vs MAC (pulmonary disease)

A

Rate of cavitation may be higher than TBC

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10
Q

(MAC) – disseminated disease

Associated with

A

Associated with AIDS & CD4 count <100 (in most cases, CD4 are <50)

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11
Q

-(MAC) – disseminated disease
MoT

A

Ingestion (most cases) or inhalation – dissemination after localized lung or gut infection

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12
Q

(MAC) – disseminated disease
What happens?

A

Bacteraemia & dissemination to liver, spleen, nodes & bone marrow

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13
Q

(MAC) – disseminated disease
(( not highlighted)) symptoms

A

(‘Fever, weight loss, severe anemia, night sweats, abdominal pain, hepatosplenomegaly, intra-
abdominal lymphadenopathy)
.

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14
Q

Mycobacterium avium complex (MAC) – lymphadenitis
MoT

A

Cervical or abdominal lymphadenitis if ingested, thoracic lymphadenitis if inhaled

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15
Q

-(MAC) – lymphadenitis
Appearance

A

Usually granulomas w/o caseation (forms a firm, dry mass like cheese in appearance), may ulcerate & form fistulas

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16
Q

Cervicofacial lymphadenitis

A

((Cervicofacial lymphadenitis is mostly seen in children between 1-5y/o (>80% of cases) ))

17
Q

(MAC) – diagnosis

A

• Culture PLUS compatible symptoms & signs
• Patients with COPD or CF may have (+) sputum culture w/o disease (colonized)
• Culture: 21d for solid & 14d for liquid media, samples: sputum, BAL, lymph node biopsy, liver
• Disseminated disease: blood or bone marrow cultures (+) in >90%

18
Q

‘Mycobacterium leprae

Causative agent of?

A

Causative agent of “Leprosy” or “Hansen’s disease”. Before antibiotics, leprosy patients were isolated in leprosaria (hospital for people with it) & left to die
Leprosy is NOT a highly contagious disease, it is curable

19
Q

Mycobacterium leprae

Tx

A

: Clofazimine & Rifampin in 1970s. Dapsone in 1980s – curable disease.

20
Q

Mycobacterium leprae - epidemiology
Patients under Tx …
Countries

A

‘Patients under Tx no longer transmit,

21
Q

Mycobacterium leprae
Can it be grown

A

M. leprae cannot be cultivate

22
Q

Mycobacterium leprae
MoT

A

Transmission poorly understood - probably respiratory & nasal secretions

Skin to skin contact cannot be excluded as mode of transmission, nor documented – shaking hands, hugs – NOT RISK FACTOR
• Prolonged close contact over months or years with a patient with untreated leprosy is needed

23
Q

‘Natural reservoir:

Mycobacterium leprae

A

. !armadillos!, chimpanzees & monkeys

24
Q

.–Mycobacterium leprae
Diagnosis

A

Microbiology
• Aerobic intracellular, acid-fast bacillus

Staining
• Stains with gram stain (positive) & acid-fast stain

Culture
• Cannot be cultured in laboratory media – in vitro
Immunology
• !Adaptive cellular immunity! is the cornerstone for controlling infection
• Leprosy = prototype of clinical manifestations associated with level of immunity
• !Clinical findings correlate with the spectrum of immunological response

25
Q

Leprosy classification system
WHO classification system - 2 subtypes

A
  1. Paucibacillary: <5 skin lesions AND -ve skin slit smears for Acid fast bacilli
  2. Multibacillary: >5 skin lesions + positive skin slit smears for AFB
26
Q

Ridley-Jopling classification system – 5 types

A

Ridley-Jopling classification system – 5 types
change over time
1. Tuberculoid (TT) 2. Borderline tuberculoid (BT) 3. Mid-borderline (BB) 4. Borderline lepromatous (BL) 5. Lepromatous leprosy (LL)
• Patients with TT or LL have stable cell-mediated immunity – clinical manifestations do not change over time
• Patients with borderline disease, unstable cellular immunity – clinical manifestations change over time – upgrade to TT if immunity becomes stronger, or downgrade to LL if immunity wanes/ declines

27
Q

M. leprae histology
Tuberculoid leprosy (TT)
. Lepromatous leprosy (LL)

A

TT: Strong cellular immunity - well formed granulomas -abundant lymphocytes- few bacilli

LL: Defects in cellular immunity – w/o well formed granulomas – less lymphocytes – many bacilli

28
Q

M. leprae Pathology

A

• !! Peripheral sensory nerve damage = leading cause of functional morbidity in pts with leprosy!!
• Damage directly by M. leprae or the immune response
. • Main findings: hypopigmented, erythematous or infiltrative skin lesions, with or w/o neurologic signs/symptoms (hypoesthesia, weakness, autonomic dysfunction, peripheral nerve thickening)
• These vary significantly between the subtypes of disease

.’

29
Q

M. leprae – manifestations
Tuberculoid leprosy (TT) & stable BT

A

strong cellular immunity, few bacilli • Macules or plaques, well defined borders, significant sensory loss
. • As immunity moves towards BB – ! lesions becomes irregular, increase in number, have decreased sensation ! but not fully like TT

30
Q

Lepromatous leprosy & stable BL
Manifestations

A

‘Lepromatous leprosy & stable BL – ! non efficacious immunity !, high bacilli load
• Innumerable macules or plaques, become infiltrated & nodular - Lepromatous Leprosy = most severe form, lesions usually have intact sensation
,
• Infiltrative dermopathy, mostly in cool sites (earlobes, central portion of face) – LEONINE FACES, hair loss of eyelashes, eyebrows

• Involvement of eye, nasal mucosa (septal perforation), larynx, kidney, liver
• Bone involvement; bone resorption, ! loss of digits !
• Marked peripheral nerve thickening, esp. ulnar, median & posterior tibial

31
Q

M. leprae - diagnosis

A

Skin slit smears • Small incision through epidermis, scraping dermal surface, smear scrapings on glass slide, stain with
Ziehl-Nielsen or Fite stain
Skin or nerve biopsy
• Demonstration of bacilli (for TT spectrum, non caseating granulomas, for Lepromatous, foamy
macrophages filled with bacilli & no granulomas)

32
Q

‘Leprosy reactions
Type 1

A

Leprosy type 1 reactions – reversal reactions

• Leading cause of neurologic impairment in leprosy – with all stages except TT
• Development of acute, new, painful & tender erythematous subcutaneous nodules
• Increased in erythema, warmth & occasional ulceration of pre-existing plaques & nodules
• Increased swelling & tenderness of peripheral nerves, systemic symptoms & signs rare

33
Q

Leprosy type 2 reactions

A

Leprosy type 2 reactions – Erythema Nodosum Leprosum
-• Deposition of antigen-antibody complexes to skin, mostly BL & LL patients within first 2yrs after Tx
• Development of acute, new, painful & tender erythematous subcutaneous nodules
• Also may involve internal organs: arthritis, neuritis, iridocyclitis, orchitis etc.
• Systemic symptoms are common: high fever, malaise, can be fatal in severe cases

Microbiology Virology (7 decks)

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