actinomycetes (nocardia)

50-60 C length of beta chain

all Mycobacterium species

70-90 C length of beta chain

gram+

filamentous branching

anaerobic

non-acid fast

disease more common: men & w/ poor oral hygiene

virulence: low, infection w/ mucosal disruption

(endogenous)

usually present in oral cavities, colon, & vagina

Actinomycosis (acute/chronic pyogenic infec, both suppurative AND granulomatous)

char: multiple abscesses & interconn sinus tracts

*infected tissues show sulfur granules (pathognomonic)

usually: polymicrobial

several types

1. cervicofacial: soft tissue swelling/abscess/mass lesion; often mistaken for neoplasm; potential spread

2. thoracic: involves pulm parenchyma/pleural space, may cross fissures/pleura; spread to mediastinum, contiguous bone, or chest wall

3. abdomen/pelvis: diff to dx; present as abscess or mass lesion (long time to develop)

4. cerebral (single brain abscess)

Actinomyces israelii

< 50 C in beta chain

1. Corynebacterium

2. Nocardia

3. Mycobacterium

1. most common Nocardia in the US

2. Condition of patients most commonly infected by Nocardia

1. Nocardia asteroides

2. AIDS and other immuno-deficiencies 

inhalation of fragmented bacterial mycelia and usually => abscess w/ extensive PMN infiltration & necrosis

-toxins observed, no clear role

-produces catalase & SOD

-cord factor inhib acidification of phagosome (PMNs can phagocytose but not efficiently kill => CMI needed to eliminate infection)

1. bronchopulmonary nocardiosis 

2. cutaneous nocardiosis:

Primary (mycetoma, lymphocutaneous infection, cellulitis)

Secondary (spread of organism from pulmonary diseases)

bronchopulmonary nocardiosis (Nocardia asteroides most commonly)

presentation: sub-acute; more acute w/ immunocompromised; nodules, abscess, empyema, prominent cough; purulent sputum NOT malodorous

*cavitation & dissemination to CNS or S/C tiss

1* N. brasillensis

2* N. asteroides

aerial hyphae

clinical specimen: sputum or pus

weakly acid-fast

growth improves w/ C02

lipid synthesis, these lipids are cross-linked to fatty acids & arabinogalactan (impor for host interaction & survival in macrophage) & peptidoglycan layer => AFB & low permeability of cell wall

-complex cell wall => very slow growth

tuberculosis

HIV epidemic

poorly managed TB programs

incr mvmt of ppl & overcrowding

clinical illness during 1st year after 1* exposure: caseous center enlarges --> tissue destruction --> releases bacilli from un-activ macroph

not assoc w/ high transmissibility

10%

presentation: flu-like illness; fever, cough, night sweats, weight loss, "snow storm" on Chest rad

characteristic: Ghon focus (CMI control of MTB => calcified lung lesions)

AFB contained in granulomas of activated macroph (not eradicated) = latent infection

if released (liquefaction allows bact growth) can cause disease years later (bacillary antigens => tissue dmg: bronchi erosion, spreading along bronchial tree)

little tissue dmg

PPD rxn+

-most AFB are expelled by ciliated cells, <10% reach alveoli (endocytosed by alveolar macroph; LAM inhib phag/lys fusion; AFB replication --> ruptures macroph & releases AFB)

-caseous necrotic center (cheese-like) develops

monocytes present AFB-antigens to T cells => start CMI/HMI

@ 2-4 wks: 1. macrophage activating CMI (activated macroph kill AFBs)

2. tissue damaging response (kill un-activated macrophages w/ AFBs)

how is AFB growth inhibited (as seen w/in granulomas)?

where does MTB grow best? why?

low 02 & pH

kidneys/vertebral bodies (areas w/ high 02)

1. pulmonary TB *most common

2. extrapulmonary TB

M. tuberculosis

dx: latent & active TB (cannot differentiate bt/w the two)

process: blood samples mixed w/ 2 MTB-specific antigens

results: w/ MTB+ sample, WBCs release measurable IFN-gamma

cause: Mycobacterium leprae (7xs slower growth than M. tuberculosis)

affects: skin & peripheral nerves

3-5% ("due to CMI, not readily contagious"?)

early stages - most infectious

transmission: skin/mucus lining (nose & throat)

higher risk: children

progression: infection begins attack on dermis --> spreads up nerve sheath

1. Tuberculoid TB (paucibacillary PB)

2. lepromatous TB (multibacillary MB)

1. M. avium

2. M intracellulare

causes: disseminated infect in immunocompromised (esp HIV+)

most common: non-TB mycobacterial infection (AIDS pts - 50% will develop MAC infec)

presentation: fever, swollen lymph nodes, diarrhea, fatigue, & wt loss