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29 Cards in this Set

  • Front
  • Back

Hansen's Disease (leprosy)

caused by Mycobacterium leprae


most cases in India, SE Asia, Brazil & Africa


>75% of US cases from foreign-born immigrants (Mexico, SE Asia, India)


states on Western gulf of Mexico (TX, LA)

M. leprae microbiology

acid-alcohol-fast


slightly curved bacillus


can't culture on artificial media


slow growth!

M. leprae transmission

person-to-person via contact with nasal secretions, inhalation of bacilli onto nasal mucosa, skin contact (less important)




armadillo-to-human spread




incubates 9 mo- 20 years after infection

M. leprae pathogenesis

intracellular pathogen: keratinocytes, histiocytes, Schwann cells, monocytes & macrophages




releases phenolic glycolipid = antioxidant in macrophages; scavenges oxygen-derived metabolites




Lipoarabinomannan on surface inhibits T cell proliferation

Leprosy risk factors

close contact with patient


disease type in index pt. (esp. lepromatous)


armadillo exposure


age (older)


PARK2/PACRG gene


immunosuppression

Ridley-Jopling classification

based on skin, neurologic & biopsy


reflects range of clinical & pathologic features


-immune response & AFB load in tissue bx

Ridley-Jopling classes

I: very early lesions w/ very rare AFB


TT (tuberculoid): robust immune response with few AFB


LL (lepromatous): weaker immune response w/ many AFB


borderline = B (most pts)

Clinical Hansen's disease

indeterminate leprosy (IL)


-few hypopigmented areas of skin


-low AFB number in dermis & nerves


-75% recover spontaneously

Tuberculoid leprosy (TL)

paucibacillary


localized w/ few well-defined lesions


lesions are flat, blanched, few AFB


TH1 induced, inflammatory response


local nerves involved (anesthesia & motor loss)


skin test to M. leprae and other antigens positive



Lepromatous leprosy (LL)

multibacillary leprosy


most disfiguring (lack of immunity)


decreased skin response to M. leprae


TH2 induced = helper T cells stimulate Ab production (ineffective vs. intracellular organism)

Lepromatous leprosy (LL) lesions

diffuse to nodular (lepromas)


esp. on cooler body parts - nasal mucosa, anterior 1/3 of eye, peripheral nerve trunks at elbow, wrist, ankle




many AFB in macrophages


nerve involvement => sensory loss

Diagnosis - physical

hypopigmented or reddish skin patches

decr. or loss of sensation w/in skin patches


paresthesias


painless wounds/burns on hands or feet


lumps or swelling on earlobes or face


tender, enlarged peripheral nerves



Diagnosis - Lab

AFB stains - nasal secretions, skin scrapings, nerve biopsy


PCR for M. leprae DNA in tissue

Treatment

Dapsone, Rifampin, Clofazimine, Minocycline

Therapy complications

Type 1 reaction (reversal) = incr. infl. of lesions, neuritis


Type 2 reaction (erythema nodosum leprosum) = lepromatous cases, painful papules, neuritis, fever, uveitis, nephritis




Rx: corticosteroids, thalidomide

Non-tuberculous mycobacteria (NTM) phenotyping

slow growers = take 2+ weeks to grow on culture


rapid growers appear in cultures in a few days



Photochromogens

yellow or orange colony after exposure to light


slow growers

Scotochromogens

yellow or orange colony in dark or light


slow growers

nonchromogens

lack pigment


slow growers

non-tuberculous mycobacteria genotyping

molecular probes:


-DNA probes (acridium ester-labeled)


- PRA (polymerase restriction endonuclease assay)


-DNA sequence analysis (of 16S rRNA gene)

NTM epidemiology

cases increasing


can be found in water, soil, domestic/wild animals & birds




most inf. from inhalation or direct inoculation from environmental source




not considered contagious

NTM pathogenesis

less virulent than M. tb (usually)


may colonize w/o disease


slowly progressive disease

M. avium-intracellulare (MAI, MAC)

non-pigmented strains


worldwide


lung infection!


slow progression


mimics TB clinically & on chest X ray

MAI

extrapulmonary or disseminated disease occurs in immunosuppressed pts, AIDS with CD4<50




fever, weight loss >20lbs, anorexia, abd. pain, diarrhea, hepatosplenomegaly & lymphadenopathy




Rx: multiple drugs; macrolides most active (clarithromycin, azithromycin)

M. kansasii

photochromogen


midwest & southern U.S.


lung infection resembles TB/MAI


extrapulmonary disease can spread to any organ system (high risk = AIDS, organ transplant, hairy cell leukemia)




Rx: Isoniazid, rifampin, ethambutol for 18 mo

Rapidly growing mycobacteria

resemble diphtheroids on Gram stain


rapid growth on subculture


grow well on routine lab media


most common: M. abscessus, M. fortuitum, M. chelonae




cutaneous/subQ involvement most common


acquired by trauma, surgery

Rapid grower Rx

possible susceptible to traditional ABs: amikacin, ciprofloxacin, sulfonamides, cefoxitin, imipenem, doxycycline, linezolid, clarithromycin, tigecycline




surgical debridement, removal of infected foreign bodies

M. marinum

photochromogen


free-living in fresh & salt water


can cause skin infections after mild trauma: "swimming pool" or "fish tank granuloma"




Rx: excision or clarithromycin

M. gordonae

Scotochromogen - "tap water bacillus"


pseudo-outbreaks


saprophyte


variety of infections in immunocompromised hosts - pulm., cutaneous, disseminated