Gram Positive Bacteria Flashcard
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Unlock answers| aerobic weakly acid-fast genera: |
actinomycetes (nocardia) 50-60 C length of beta chain |
| aerobic, true acid-fast genera: |
all Mycobacterium species 70-90 C length of beta chain |
| general characteristics of Actinomyces israelii |
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 |
| disease caused by Acintomyces israelii |
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 |
| types of actinomycosis (4) |
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) |
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identifying features of A. israelii
culture: difficult; molar tooth appearance after 1 wk clinical specimen: sulfur granules gram+ anaerobe filamentous rod |
| anaerobic non acid fast species: |
Actinomyces israelii < 50 C in beta chain |
| three important Actinomycetes w/ mycolic acid: |
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 |
| how is Nocardia usually acquired? pathogenesis? |
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) |
| name the 2 clinical outcomes of Nocardia disease |
1. bronchopulmonary nocardiosis 2. cutaneous nocardiosis: Primary (mycetoma, lymphocutaneous infection, cellulitis) Secondary (spread of organism from pulmonary diseases) |
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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 |
| organisms most commonly causing primary & secondary cutaneous nocardiosis: |
1* N. brasillensis 2* N. asteroides |
| identifying features of Nocardia |
aerial hyphae clinical specimen: sputum or pus weakly acid-fast growth improves w/ C02 |
| most virulent species of Mycabacterium tuberculosis Complex |
| Mycobacterium tuberculosis |
| Mycobacterium tuberculosis produces many genes for... |
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 |
| leading cause of death due to a single infectious agent (worldwide) & contributing factors: |
tuberculosis
HIV epidemic poorly managed TB programs incr mvmt of ppl & overcrowding |
| transmission of Mycobacterium tuberculosis: |
| droplet nuclei from pts w/ pulmonary TB (coughing, sneezing, or speaking) |
| primary tuberculosis |
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) |
| secondary tuberculosis |
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+ |
| what happens after M. tuberculosis is trapped in upper airways: |
-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
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| how does the host respond to M. tuberculosis? |
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) |
| clinical forms of TB |
1. pulmonary TB *most common 2. extrapulmonary TB |
| identifying M. tuberculosis |
| this is one of the few mycobacteria that can reduce nitrate |
| explain the quantiFERON-TB Gold Test (QFT-G) |
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 |
| leprosy (Hansen's disease) |
cause: Mycobacterium leprae (7xs slower growth than M. tuberculosis) affects: skin ; peripheral nerves |
| rate of leprosy contracted after exposure |
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 |
| types of Mycobacterium leprae diseases (2) |
1. Tuberculoid TB (paucibacillary PB) 2. lepromatous TB (multibacillary MB) |
| Mycobacterium avium complex (MAC) |
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 |
