Kaplan Microbiology A7

Front 1

Mycobacteria:

1) What's so special about them?
2) What 3 diseases are they responsible for?

Back 1

1) Acid-fast bacilli, have high-lipid content (mycolic acid) in cell wall
2) Tuberculosis (Mycobacterium tuberculosis), disseminated disease in AIDS patients (M. avium intracellulare), leprosy (M. leprae)

Front 2

Actinomycetes:

1) Gram? Characteristic growth pattern?
2) Where are these organisms often found?
3) 2 genera of actinomycetes that are clinically relevant?

Back 2

1) Gram +, branching filament growth pattern (visually resembles fungi)
2) Soil
3) Actinomyces, Nocardia

Front 3

Mycobacterium tuberculosis:

1) Respiration? Staining? Shape?
2) Why does it stain the way it does? What property gives it this ability

Back 3

1) Obligate aerobe, ACID FAST bacilli
2) After stained, resists decolorization by acidic alcohol rinse, because of WAXY LIPID CELL WALL WITH MYCOLIC ACIDS

Front 4

Mycobacterium tuberculosis:

1) What 2 things does the cell wall have that are essential for tuberculin ability?
2) What kind of reactions do these factors induce?

Back 4

1) Lipoproteins, glycolipoproteins
2) Induces type 4 hypersensitivity reactions (delayed type hypersensitivity)

Front 5

Mycobacterium tuberculosis:

1) How quickly does it grow? How many days does it require to grow before it's visualized?
2) Doubling time?

Back 5

1) Slow growing, 20-60 days before visualized
2) 18 hours

Front 6

Mycobacterium tuberculosis:

1) How do you test for it?
2) What factor does it have that's associated with virulence? What does it do?
3) What grouping pattern is seen in virulent strains?

Back 6

1) Purified protein derivative (PPD) of cell wall for skin testing
2) CORD factor - inhibits PMN migration, causes granulomas formation, attacks mitochondrial membranes
3) Serpentine, because of the cord factor

Front 7

M. tuberculosis:

1) Where is it only found?
2) Who is it more common in?
3) What are the incidence rates like?

Back 7

1) In humans
2) Low socioeconomic groups
3) Rapid, recent rise b/c of AIDS epidemic and immigration

Front 8

M. tuberculosis:

1) Mode of transmission?
2) Who is the most infectious person?
3) What is greater, the risk of infection or risk of disease? Why?

Back 8

1) Droplet nuclei inhalation
2) One w/ untreated cavitary pulmonary TB, actively expelling bacilli
3) Risk of infection - disease is dependent on weakened immune response

Front 9

1) What is the first response after infection with M. tuberculosis? When does it occur?
2) What does infection correlate with?
3) Which immunity is associated with resistance or protection from M. tuberculosis?

Back 9

1) DTH, 3-4 weeks after infection
2) + tuberculin reaction
3) Acquired cellular immunity

Front 10

M. tuberculosis:

1) When does a primary exudative type infection occur?
2) Signs of infection with primary exudative type?

Back 10

1) When organism is inhaled, spread through alveolar macrophages to hilar lymph nodes. May have hematogenous dissemination.
2) Minimal, immune competent hosts will limit organism to lungs.

Front 11

M. tuberculosis:

1) What is primary productive type infection characterized by?
2) What does this depend on?

Back 11

1) Tubercle that forms (with or without caseation)
2) Host's immune response

Front 12

M. tuberculosis:

1. What does the primary site of infection form?
2) What kind of hypersensitivity develop?
3) Where does the infection become quiescent?
4) What is the PPD test like after infection?
5) What may happen in immunocompromised or debilitated patients?

Back 12

1) Calcified lesions (*GHON COMPLEXES*
2) Delayed-type
3) Pulmonary and metastatic sites
4) Positive
5) Have progressive primary disease from local sites, or more distant sites w/out disease becoming quiescent

Front 13

M. tuberculosis:

1) Where does secondary infection, or reactivation usually occur and why?
2) What 3 things are associated with tubercle formation?
3) Why does secondary infection happen?

Back 13

1) Localized, esp. in LUNG APICES because of higher oxygen (it's an obligate aerobe)
2) Caseation, necrosis, fibrosis
3) Breakdown of quiescent foci or new infection, despite acquisition of T cell immunity

Front 14

1) Clinical presentation of TB?
2) 85% of cases are what type of TB? What does this type present with?
3) Where can miliary TB appear in the body?

Back 14

1) Nonspecific constitutional - fatigue, weight loss, anorexia, weakness, fever, night sweats
2) Pulmonary - cough, hemoptysis, pneumonitis
3) Anywhere, but favors bone/joints (osteomyelitis), meninges (meningitis), kidneys, peritoneum, lymph nodes, + high oxygen level areas

Front 15

M. tuberculosis:

1) Where are primary lung infections usually found?
2) What are 80% of pulmonary TB cases in adults due to?
3) What methods do you use to diagnose TB?

Back 15

1) Subadjacent to pleura in lower part of upper lobe, or upper part of lower lobe - places that receive most air
2) Reactivation of an infection acquired years or decades earlier
3) Abnormal chest x-ray, acid-fast bacteria in sputum, culture of M. tuberculosis.

Front 16

1) What is the skin test for tuberculosis? When do you read it?
2) What is interpretation based on? What is +? What is -?
3) Reaction to PPD is what type of hypersensitivity?

Back 16

1) PPD - 2 to 3 days
2) Diameter of induration. 10+ positive, 5-10 doubtful
3) Type 4

Front 17

Treatment for tuberculosis:

1) How long?
2) How many drugs should be used?
3) How long should you tx if the patient is HIV positive?
4) What are the 1st line drugs used against drug resistant strains?
5) What are the additional drugs used to combat resistance?

Back 17

1) 6-9 months
2) At least 3
3) 9-12 months
4) RIPE - rifampin, isoniazid, pyrazinamid, ethambutol
5) Streptomycin, ethionamide, ciprofloxicin

Front 18

1) What kind of prophy do you use w/ people who've had contact with recently converted or newly diagnosed active disease?
2) What kind of immunization is available - where is it used and what kind of immunity does it establish? Downside?
3) What strain is the BCG strain dervied from?

Back 18

1) INH prophy
2) BCG - areas w/ high TB incidence. Cell-mediated immunity. Test + for PPD skin test
3) Attenuated M. bovis strain

Front 19

Mycobacterium bovis:

1) This is responsible for tuberculosis in who?
2) How do you get it?
3) Will M. bovis result in a positive PPD skin test?

Back 19

1) Cattle and humans
2) Drinking unpasteurized milk, or pulmonary TB by inhaling infected droplets (dairy farmers)
3) Yes

Front 20

What are the 5 most important strains in nontuberculous mycobacteria (atypical)?

Back 20

1. **M. avium intracellulare
2. M kansasii
3. M. marinum
4. M. scrofulaceum
5. M. fortuitum-chelonei

Front 21

1) Is mycobacteriosis spread human to human?
2) What disease M. kansasii, M. avium-intracellulare, and M. fortuitum-cheloni usually cause? In who?
3) What does M. scrofulaceum cause? In who?
4) What does M. marinum cause? When?
5) What do M. kansasii and M. avium-intracellulare cause in AIDS patients?

Back 21

1) No - usually environmental agents (soil)
2) Pulmonary disease - older white white men w/ chronic bronchitis and emphysema
3) Lymphadenitis, children.
4) Cutaneous lesions, when organism contaminates open wound - "swimming pool" granuloma
5) Disseminated disease

Front 22

1) Treatment of mycobacteria?
2) What drug is especially effective against M. kansasii?
3) What drug is especially effective against M. avium intracellulare?
4) What is occasionally recommended in addition to drugs?

Back 22

1) Usually resistant to anti-TB drugs - 6 drugs
2) Rifampin
3) Clarithromycin
4) Surgical resection

Front 23

M. leprae:

1) Where can it NOT grow?
2) What is special about its staining?
3) What kind of hypersensitivity does it induce in patients?
4) What disease does it cause?

Back 23

1) On any in vitro culture medium
2) Acid fast
3) Delayed-type
4) Leprosy (Hansen disease)

Front 24

1) Where is leprosy endemic?
2) How is it transmitted?
3) Where are lesions classically found?

Back 24

1) Africa, Asia, South America
2) Nasal secretions, ulcer exudates
3) Cooler regions of body - skin of nasopharynx, larynx, cartilage, eyes, testicles

Front 25

1) What are the 2 forms of leprosy?
2) Is tuberculoid leprosy progressive? What do clinical findings show?
3) Is lepromatous leprosy invasive? What does pathologic examination show?

Back 25

1) Tuberculoid, lepromatous
2) Indolent, non-progressive. Mature granulomas in the dermis
3) Progressive + invasive. Foamy histiocytes w/ no epithelioid and giant cells.

Front 26

1) Immunity to M. leprare is mediated by wha tcells?
2) How infectious is it?
3) Tx?

Back 26

1) CD4+ T cells
2) Low infectivity
3) Long term (3-5 years) antibiotic tx

Front 27

Actinomycetes (Actinomyces, Nocardia, Streptomyces)

1) What are they characterized by?
2) What 2 important species cause actinomycosis?
3) What is characteristic of an Actinomyces infection after extraction of an abscessed tooth? What is diagnostic?

Back 27

1) Filamentous form
2) A. israelii, A. naeslundii
3) Sulfur granules - multiple sinus tracts open to the outer surface of skin, w/ diagnostic yellow material

Front 28

1) A. israelii:respiration? staining? Gram? Shape?
2) Where is A. israelii found? When it is usually pathogenic?

Back 28

1) Anaerobic, nonacid-fast Gram + bacilli
2) Normal oral flora (not found in soil), only pathogenic after oral trauma

Front 29

Cervicofacial actinomycosis:

1) When does this happen? What part of the body does it affect?
2) What are the 3 symptoms?

Back 29

1) After development of dental caries or after dental work. Lower jaw.
2) Pyogenic abscesses, sulfur granules (with gram + mycelial filaments surrounded by eosinophils and leukocytes), osteomyelitis (bone infection)

Front 30

1) What is thoracic actinomycosis caused by?
2) What is abdominal actinomycosis due to?
3) What does pelvic actinomycosis arise in?

Back 30

1) Extension from cervicofacial infection in 20% of cases
2) Traumatic perforation of intestinal mucosa (ruptured appendix, perforated ulcer)
3) Women with IUDs

Front 31

1) What are the two most common isolates found in soil and aquatic environments?
2) Nocardia: respiration, gram, staining, shape?
3) Who usually gets nocardiosis?
4) What does nocardiosis infection begin with?
5) What is the most common site of metastatic infection, and how does it get there? What is the most common pathologic finding?
6) Tx?

Back 31

1) Nocardia, N. asteroides
2) Aerobic, gram + partially acid fast filamentous
3) It's opportunistic, most pts have underlying disease like hematologic malignancies
4) Chronic lobar pneumonia
5) CNS, through blood. Abscess formation.
6) Sulfonamides, surgical drainage of abscesses

Front 32

What are the two main differences between Nocardia and Actinomyces?

Back 32

Actinomyces = anaerobic and non acid fast

Nocardia = aerobic, partially acid fast