Mycobacteria

Question 1

Mycobacterium tuberculosis features

Answer 1

1/3 world pop infected
Multidrug resistance
Almost uniquely acid fast, can see cords in the stain
Slow in vitro growth
Obligate aerobe–only colonizes in oxygen rich parts of the body
No toxins produced
Drug resistance is chromosomal, no known plasmids

Question 2

Pathogenesis of mycobacterium tuberculosis

Answer 2

Humans are the reservoir
Transmitted primarily by inhalation of infected aerosols; rarely transdermal or GI infection
Extremely infectious (low ID…<10 bacteria)
Alveolar macrophages phagocytose the inhaled bacilli.
Naïve macrophages are unable to kill the intracellular mycobacteria
M. tuberculosis proliferates within mononuclear phagocytes, traveling to extrapulmonary sites, where it can establish latent (immunocompetent) or active (peds, HIV+, immunosenescence) extrapulmonary infection:
Lymph nodes
Kidney
Bones
Meninges
A cell-mediated immune (CMI) response terminates the unimpeded growth of theM. tuberculosis2-3 weeks after initial infection.
M. tuberculosis persists in the body, but is enclosed in granulomas
Mycobacteria cannot continue to grow within these granulomas, so the infectious process pauses (latency).

Question 3

M. Tuberculosis diagnosis

Answer 3

Exam- fever, fatigue, night sweats, weight loss
Pulmonary TB- cough, hemoptysis
Scrofula- cervical adenitis
Miliary TB- multiple disseminated lesions
Meningitis- high inflammation, brudzinski’s signs
Osteomyelitls (Pott’s disease)
GI TB- abdominal pain and diarrhea
Renal TB- dysuia, hematuria, flank pain

Remicade (Rheumatoid arthritis, crohn’s medication) may reactivate latent infections

Diagnose with acid fast (cords must be present) or a culture (slow)

Question 4

TB treatment

Answer 4

At least six months of multidrug courses featuring isoniazid

Directly observed therapy (nurses watch them take their pills)

Question 5

TB prevention

Answer 5

Good housing and nutrition- TB won’t likely come out of latency
Semi-effective vaccine may protect against active infection, but not latent infection

Question 6

Atypical mycobacteria

Answer 6

Cause neither TB nor leprosy
Environmentally-aquired
PPD negative usually
Less aggressive infections
Usually infect predisposed individuals

Question 7

Photochromagens

Answer 7

Atypical mycobacteria
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.

Question 8

Scotochromagens

Answer 8

Atypical mycobacteria
Produce pigment when grown in light or dark
M. scrofulaceum produces scrofula
Reservoir is in water, can be harmless in respiratory tract
Fix by surgically removing affected nodes

Question 9

Nonchromagens

Answer 9

Atypical mycobacteria
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

Question 10

Rapidly growing mycobacteria

Answer 10

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

Question 11

Mycobacteria Leprae Features

Answer 11

Leprosy (Hansen’s disease)
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
Genetically, appears to be a stripped-down version of M. tuberculosis

Question 12

Pathogenesis of M. Leprae

Answer 12

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

Spread by nasal secretions and skin lesions

Question 13

Exposure to leprosy potential outcomes (3)

Answer 13

1. Asymptomatic seroconversion (proper immune response)
2. Clearance failure with vigorous CMI (Immunogenic symptoms, granulomas, tuberculoid leprosy)
3. Clearance failure with weak CMI (Pathogenic symptoms, foamy histocytes form, extensive skin involvement)