Nontuberculosis Mycobacterium Flashcards
Nontuberculosis Mycobacterium (NTM)
NOT Transmitted person to person
Environmental organisms (live in biofilms, Commensal with amoebas)
NTM are divided into
Slow growing (>2 weeks on AFB) and Rapid growing (4-7 days on blood agar)
NTM Scotochromogens
Always pigmented
NTM photochromagens
Pigmented only when exposed to light
Non-chromogenic NTM
Not pigmented
Diseases caused by NTM
Pulmonary disease (MAC, M kansasii, M xenopi, M abscessus)
Skin and soft tissue infections (M chelonae, M abscessus, M fortuirum)
Lymph node (MAC)
Disseminated (MAC-HIV, M chelonae, M abscessus)
Line associated bacteremia
Slow growing Mycobacterium
M avium/intracellularae- most common
M kansasii
M marinum
M xenopi
M gordonae
Mostly cause pulmonary disease but can cause SSTI, lymphatic, and disseminated infections
M avium/intracellularae
Most common Mycobacterium
Present in water, soil, dust
Acquisition through inhalation
MAC pulmonary disease
Most common in immunocompetent
symptoms + microbiology + disease (cough, sputum production, fevers, weight loss)
Two patterns: older male smokers, older women (thin, pertussis, RML, bronchiectasis, Lady Windermere syndrome)
NTM in children
M avium most common
Manifests as chronic granulomatous lymphadenopathy in neck
Treatment involves surgical resection without antibiotics
M kansasii
Second most common mycobacterium
Almost always associated with disease
Photochromogenic colonies bright yellow/orange with exposed to light
Causes pulmonary disease
Treatment: Azithromycin, Ethambutol, Rifampin
Mycobacterium marinum
Fish tank granuloma
Infection after trauma or inoculation
Organisms produce membrane lipids to recruit macrophages to a site of infection
Transfer to more permissive host for growth and dissemination
Virulence factors seen in Tb
treatment: clarithromycin and ethambutol
Rapid growing Mycobacterium
M fortuitum
M chelonae
M abscessus
Skin and subcutaneous tissue infections (SSTI)
Affects immunocompetent people
M abscessus
Soil and water
Pulmonary and SSTI
Resistant to disinfectants (postsurgical and post-procedural infections)
Can grow in tattoo dyes
Treatment: difficult due to antibiotic resistance
Surgical debridement if SSTI
IV amikacin
M fortuitum and M chelonae
SSTI
Treat with 2-3 antibiotics
M leprae
Causes leprosy
Cannot grow in culture
Transmission not understood but thought to be person to person
Lesions 2 to 5 years after incubation
Presentation depends on immune response
3 cardinal signs: skin lesions, areas of cutaneous anesthesia, enlarged perephrial nerves
Two forms of leprosy
Tuberculoid- vigorous immune response, well formed granuloma, few AFB
Anesthetic macula’s or plaques
Lepromatous- minimal immune response, no granuloma, many AFB
Lesions on cooler parts of body
Organisms that look like Mycobacterium
Nocardia And actinomycetes (aerobic and anaerobic) filamentous gram - rods
How to determine what is what
Acid fast positive: Mycobacterium
Modified acid fast positive: Nocadia, aerobic actinomyces
Neither : actinomycetes
Aerobic actinomycetes
Gram +
Filamentous
Branched
Responsible for antibiotic production
Recovered in mycology or mycobacterium areas of lab
Sequencing is only adequate identification
Nocardia are most significant pathogen in this group
Nocardia
Gram + rod (beaded)
Modified acid fast stain
Slow growing, requires special culture
Aerobe, soil organism
Nocadia asteroides is most common
Nocadia infections
Immunocompetent (SSTI and pulmonary)
Inhalation for pulmonary infections
Immunocompromised (pulmonary disease- cough, fever, weight loss, cavitary lesions)
High risk for CNS disease
Treatment: sulfonamides
Anaerobic actinomyces
anaerobic branching
Gram + rod
Actinomyces Israeli most comin
Chronic granulomatous infection
Cervicofacial, pulmonary and abdominopelvic lesions
Treatment= PCN
