Atypical Mycobacteria Flashcards
Why are atypical called atypical?
Cause neither TB nor Leprosy
Environmentally-acquired
PPD (purified protein derivative) TST (tuberculin skin test) usually negative
Less aggressive infections, not lethal in guinea pigs
Systemic disease very rare without predisposing condition: HIV, cancer, Other Immunosuppression, Old age, Infected surgical site, Diabetes, Lung Disease
Cutaneous infection most likely in immunocompetent adults, scrofula in children
Group 1:
Photochromogens (produce pigment when grown in light)
M. kansasii is environmental (unknown reservoir) in Midwest, Texas, and England, produces pulmonary/systemic disease most closely resembling TB, killed by same antibiotics
M. marinum found in fresh and salt water, forms “fish tank” granulomatous, ulcerating lesions on abrasions exposed to swimming water or aquariums, treat w/ tetracycline. The most common atypical mycobacterial infection.
Group 2: Scotochromogens (produce pigment when grown in dark or light)
M. scrofulaceum produces scrofula
Reservoir is in water, can be harmless in respiratory tract
Fix by surgically removing affected nodes
Group 3: Nonchromogens
M. avium / M. intracellulare are very difficult to distinguish, jointly called MAI, MAC
Cause pulmonary disease indistinguishable from TB in severely immunocompromised patients
Environmentally widespread, found in soil and water
Highly drug resistant, use clarithromycin in combination with ethambutol, rifabutin, or cipro
Group 4: Rapidly growing mycobacteria
Culturable in <1wk
M. fortuitum / M. chelonei (very difficult to distinguish)
Found in soil and water
Cause problems in immunocompromised, prosthetic hips, indwelling catheters, puncture wounds
Treat with amikacin+doxycyclin plus surgical excision of site
M. abscessus
Environmental
Chronic lung infections, skin, bone joints
Highly antibiotic resistant
M. smegmatis: normal flora under foreskin
M. leprae
Not culturable
Reservoirs are humans (major) and armadillos (minor)
14-day doubling time; slowest growing human pathogen
Prefers 30C for growth, sticks to periphery of humans (the low temperature keeps it in the periphery)
Genetically, appears to be a stripped-down version of M. tuberculosis
Causes leprosy, aka Hansen Disease
Symptoms from both infection and immune response
Worldwide incidence is at historic lows, but Leprosy is still deemed a public health problem in 9 countries; they account for 84% of reported cases.
~150 cases/yr in US
M. leprae pathogenesis
Exact mechanism of transmission is unclear
Requires prolonged contact w/ infectious case
Rare zoonosis from armadillos
Extremely long incubation period: months to 50yrs
Most common sequel of exposure is asymptomatic seroconversion: only 5-10% of population is believed immunologically susceptible to symptoms
M. leprae pathogenesis
Paucipacillary leprosy
- characteristic of immune response?
-PPD?
Paucibacillary leprosy = tuberculoid form:
vigorous CMI contains disease (CD4+, Th1) but causes immunogenic problems
<5 dry skin lesions containing few bacteria
Asymmetric immunogenic peripheral nerve damage
Lepromatin PPD(+)
M. leprae pathogenesis
multibacillary leprosy
PPD?
multibacillary leprosy = lepromatous form
Inadequate CMI response (useless Th2, nonprotective antibodies)
Extensive skin involvement: >6 lesions, infiltrated nodules & plaques, bacilli may be visible on smears from lesion fluid
Symmetric peripheral nerve damage from bacterial growth in Schwann cells
Lepromatin PPD(-)
M. leprae pathogenesis
Wasting and muscle weakness are constitutional symptoms
Peripheral nerve involvement leads to loss of sensory and motor function, subsequent injury:
Ulnar and median nerves - Clawed hand
Posterior tibial - Plantar insensitivity and clawed toes
Common peroneal -Foot drop
Radial cutaneous, facial, and greater auricular nerves
In lepramatous form, infection also destroys nasal cartilige and reaches eye
M. leprae diagnosis
Tuberculoid exam
Hypoesthesia, skin lesions, and peripheral neuropathy. The first physical signs of leprosy are usually cutaneous.
Tuberculoid:
- 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(+)
M. leprae diagnosis exam lepromatous
Lepromatous:
Extensive bilaterally symmetric cutaneous macules, nodules, plaques, papules
Lesions have poorly-defined borders and raised centers
Eye infection
loss of nasal cartilage
“leonine facies”: facial skin becomes thickened and corrugated
Lepromatin PPD(-)
What is the lepromin skin test used for?
Lepromin skin test is not diagnostic of exposure; used to determine patient’s ability to raise immune response
M. leprae diagnosis lab
What will lepromatous look like?
What will tuberculoid look like?
Skin smear: swab and full-thickness biopsy from leading edge of lesions for acid-fast staining and histology.
Lepromatous will have bacilli visible and lipid-laden macrophages “foam cells”
Tuberculoid will have granulomatous changes with epithelial cells and lymphocytes.
PCR testing is effective but not yet standardized
What is the treatment for M. leprae?
Tuberculoid: dapsone+rifampin, 2yrs
Lepromatous: dapsone+rifampin+clofazimine, 2yrs+ (until lesions are free of organism)
Peds: prophylaxis with dapsone if exposed
Prevention: Isolate infectious patients
Lepromatous patients may develop painful immunogenic symptoms on treatment, called erythema nodosum leprosum (ENL). Severe cases may be treated with thalidomide, but every precaution must be taken to keep it away from pregnant women; it is a potent teratogen.
