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42 Cards in this Set
- Front
- Back
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Acid fastness
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a. Determined by C-chain length of mycolic acid
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Aerobic, non acid-fast
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a. <50C
b. Corrynebacgerium diphtheriae |
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Anaerobic, non acid-fast
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a. <50C
b. Actinomyces isrealii |
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Aerobic, weakly acid fast
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a. 50-60C
b. Nocardia |
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Aerobic acid-fast
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a. 70-90C
b. Myobacterium |
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Atinomyces
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a. Considered fungi
b. Branching filamentous appearance c. True bacteria→ no mitochondria or nucleus d. Sensitive to penicillin but resistant to antifungals |
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Actinomyces characteristics
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i. Gram+
ii. Anaerobic iii. Non-acid fast iv. Rod |
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Actinomyces epidemiology
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i. Colonize mouth, colon, and vagina
ii. Worldwide iii. No person-to-person spread iv. Endogenous infection |
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Actinomyces virulence
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i. Low virulence
ii. Infection when mucosal barrier is disrupted |
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Actinomycosis
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1. 3x more common in men
2. Acute or chronic pyogenic infection 3. Multiple abscesses and interconnecting sinus tract 4. INFECTED TISSUES CONTAINS SULFUR GRANULES-- PATHOGNOMIC |
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Cervicofacial actinomycosis
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1. Occurs as soft tissue swelling, abscess, or mass lesion
2. Often mistaken for neoplasm 3. Consider any mass or relapsing lesion in the head and neck 4. Contiguous spread to cranium, spine, or thorax a possibility |
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Radiograph of actinomyces
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1. Mass lesion
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Abdominopelvic actinomycosis
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1. Difficult dx
2. Takes mo/yr to develop 3. Appendicitis, diverticulitis, IUCD 4. Any abdominal organ or region may be involved 5. Presentation→ abscess or mass lesion |
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Identification of A. israeli
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1. Look for sulfur granules in clinical samples
2. Gram + anaerobe 3. Filamentous branching rods 4. Difficult to culture, molar tooth appearance after 1 week |
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Nocardia characteristics
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i. Gram +
ii. Filamentous rods iii. Short chain mycolic acid (weak acid-fast) |
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Nocardia epidemiology
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i. No person-to person transmission
ii. Normal soil microflora iii. Mostly in AIDS and other IC patients |
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Nocardia pathogenesis
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i. Acquired by inhalation→ abscess with PMN infiltration
ii. Produces catalase and SOD→ neutralize ROS iii. Cord factor prevents acidification of phagosome |
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PMNs and nocardia
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1. PMNs phagocytose nocardia but can’t kill
2. CMI needed for cure |
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Bronchopulmonary nocardiosis
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1. Sub-acute presentation
2. Patients seek help after days to weeks 3. Cavitaiton and dissemination to CNS or SC tissues |
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Symptoms of bronchopulmonary nocardiosis
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a. Cough
b. Dyspnea c. Fever present but not diagnostic |
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Identification of nocardia
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i. Filamentous
ii. Weak acid-fastness iii. Aerial hyphae |
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Mycobacterium tuberculosis characteristics
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1. Aerobic
2. Acid-fast 3. Complex lipid coat 4. Bacilli 5. Very slow growth |
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M. tuberculosis epidemiology
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1. Sub-saharan Africa, Asia, Eastern Europe
2. Multidrug Restistant Tuberculosis 3. Extensively-drug resistan tuberculosis |
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Exposure to m. tuberculosis infection
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1. Patients with pulmonary TB release droplet nuclei
2. Nuclei aerosolized by coughing, sneezing 3. Reach terminal air passages if inhaled 4. Risk of disease depends on innate and cell mediated immunity |
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M. tuberculosis virulence
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1. CMI either kills the MTB bacilli or keeps the bacilli dormant in walled-off locations
2. Dormant bacilli represent a latent infection 3. Can reactivate to cause TB if immunity weakens→ 2° TB |
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Primary tuberculosis
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1. Symptoms in months after 1st exposure
2. Immune control of AFB may result in calcified lesions (ghon focus) 3. MTB best grows in regions with high O2 |
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Clinical presentation of primary tuberculosis
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a. Fever, cough, night sweats, weight loss
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Screening of m. tuberculosis
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1. I/D injection of 5 PPD units→ result in 48-72 hours
2. >10 mm induration→ positive for immigrants, MTB lab workers 3. 5 mm induration is positive in HIV individuals 4. BCG vaccination yields a positive result |
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Acid-fast stain of m. tuberculosis
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a. Early-morning sputum after mild alkali treatment
b. Examine for three consecutive days |
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Growth of m. tuberculosis
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a. On Lowenstein-Jensen or Middlebrook 7H10/7H11 agar
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Nucleic acid-based assays of m. tuberculosis
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a. DNA probes
b. PCR c. Real-time RT-PCR |
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QuaniFERON-TB gold test
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a. Blood is mixed with MTB antigens
b. In MTB+ sample, measurable IFN in 16-24 hr incubation c. Clinical exam and extra tests needed (CXR, sputum test, culture) |
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Mycobacterium leprae characteristics
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1. Slow grower
2. Acid-fast intracellular parasite 3. Limited ability to propagate outside of host 4. Impacts only dermis 5. 5 yr incubation |
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M. leprae epidemiology
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1. Early stages→ most infectious
2. Transmitted through skin/mucus lining of nose/throat 3. Children are more susceptible 4. CMI very important |
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M. leprae diseases
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1. Very slow progression
2. Involves superficial tissues 3. Bacillus attacks the dermis and spreads up the nerve sheath 4. May cause loss of sensation (demyelination) |
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Tuberculoid leprosy
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1. CMI present→ limited disease
2. Relatively few bacteria in skin and nerves 3. Few flat or slightly raised skin lesions 4. Pale or slightly red, dry and numb to touch |
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Lepromatous leprosy
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1. Reduced or absent CMI
2. Widespread disease and large numbers of bacteria 3. A much more and diffuse involvement of the skin 4. Thickening of many peripheral nerve |
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identification of m. leprae
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1. Clinical picture is a 99% dx
2. Slow grower→ culture not effective dx 3. Usual dx through biopsy specimens and acid-fast staining |
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Paucibacillary leprosy
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1. PB
2. Indeterminate, tuberculoid, and borderline tuberculoid |
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Multibacillary leprosy
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1. MB
2. Borderline lepromatous and lepromatous leprosy |
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MOTT
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1. Mycobacterium other than tuberculosis
2. M. marinum, M. ulcerans can cause skin infections 3. Aquarium pathogen |
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Mycobacterium avium complex
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1. MAC
2. M. avium and M. intracellulare 3. Causes disseminated infection in IC 4. Most common non-MTB infection in AIDS patients 5. Up to 50% with AIDS may develop MAC infection 6. Fever, swollen lymph nodes, diarrhea fatigue, weight loss |
