Path Bact

Front 1

Give the causative agent for the following clinical course:
Abrupt onset, fever, chills, cough (purulent, rust colored), dyspnea, pleuritic pain, prostration

Back 1

S. pneumonia

Front 2

S. pneumonia
1. gram + or -?
2. encapsulated y/n?

Associated with otitis media, sinusitis, meningitis if bacteremia, colonization of nasopharynx

Back 2

1. Gram +
2. Y

Front 3

1. How does S. pneumonia present on CXR?
2. What does the CBC look like?
3. What type of Ab does the body generate that are effective?

Back 3

1. Lobar pneumonia that came from smaller bronchopneumonia
2. Leukocytosis with a left shift (increase in # of immature cells)
3. anticapsular

Front 4

S. Pneumonia: clinical course: if untreated, high fever, chills, tachypnea for 7-10 days, followed by resolution of fever w/ dramatic clinical recovery coinciding with development of anti-capsular antibodies

Back 4

Resolution of the chest film lags

Front 5

1. What are protective mechanisms against S. pneumonia infection?
2. What are important factors in colonization?

Back 5

1. Mucociliary elevator (sweep stuff out), PMN, sIgAs
2. Adhesins, pneumlysin (creates pores in host membrane, damage ciliated epithelium, and the mucociliary elevator), smoking, sIgA protease

Front 6

1. What is the CbpA choline binding protein A imp. for in S. pneumonia infection?

Acute inflammation is the hallmark of infection

Back 6

1. Transcytosis, allows invasion, Aspiration and compromise of the mucociliary barrier also aid in migration

Front 7

Pathogenesis of S. pneumonia:
-Release of N-formyl methionine containing particles
-Complement activation (pneumolysin, teichoic acid, peptidoglycan fragments)

Back 7

-Activation of macrophages -> release proinflammatory cytokines IL-1 and TNF alpha
-bronchiolar epith. and alveolar lining cells release chemokines IL-8

Front 8

1. What is acute congestion described as?
2. What is Red hepatization?
3. What is gray hepatization?
4. How is it resolved?
5. Complications?

Back 8

1. Vascular congestion, proteinaceous fluid in EC spaces, some PMNs, many organisms
2. acute inflammatory infiltrate of PMNs, RBCs and fibrin
3. Occurs when RBCs are lysed, fibrin and PMNs remain
4. Fibrin exudate is lysed and reabsorbed or coughed up (expectorated)
5. org. with obliteration of alveoli, abscess formation

Front 9

Abscess formation- very intense inflammatory response, Pneumocytes are destroyed by pneumolysin, ROS are released by inflammatory cells and by bactera

Back 9

Susceptible to S. pneumoniae if immunocompromised, splenectomy, diabetes, sicle cell disease

Front 10

1. How is S. pneumoniae cleared?
2. Is Diptheria gram + or -?
3. Cocci or rod?
4. Is the exotoxin in the genome or a phage?

Back 10

1. Antibody mostly by opsonization
2. Gram +
3. Rod
4. Phage

Front 11

Infection presents with pharyngitis, low grade fever, erythema of posterior pharynx which evolves with white/gray spots, grayish membrane, extends to soft palate and uvula-causes aysphixation in children

Back 11

Diptheria

Toxin is binary, has A and B fragments linked by a disulfide bond

Front 12

Infection- cervical lymph node enlargement, soft tissue edema -bull neck appearance, extend into laryns and trachea, hoarseness & dyspnea, respiratory obstruction in children

Back 12

Diptheria

can lead to polyneuritis- demyelination due to scwann cell injury

Myocarditis

Front 13

Diptheria Fragment A or B:
1. BInds glycoproteins on cell surface
2. inhibits protein synthesis by ADP-ribosylating EF-2
3. Inserts in endosomal membrane translocating and releasing fragment A in the cytosol

Back 13

1. B
2. A
3. B

Front 14

1. What are the clinical effects of diptheria due to?

Myco TB- slow growing, non-spore forming intracellular aerobe, has high lipid content which forms basis for acid fast stain, need 10^6 bacteria to see Mx

Back 14

1. Toxin, Ab to toxin prevents the disease

Front 15

1. What is the portal of entry for TB?
2. How many organisms for infection?
3. Intracellular or extracellular?
4. Primary target cell for TB?
5. What is the major route of infection in non-opsonized bacteria?

Back 15

1. Respiratory via fine droplets
2. 1-3 upper lower lobe or lower upper lobe
3. Intracellular
4. Macrophages
5. Mannose receptor on macrophage

Front 16

1. How does TB survive uptake my macrophages?

During 3 weeks following infection it proliferates in MO and airspaces, spreads to draining nodes, bacteremia seeding to multiple sites. Most ppl are asymptomatic

Back 16

1. Surfactant protein A, and manipulation of endosome (decrease acidification, maturation arrest)

Front 17

TB: prior to immune response, bacteria causes the MO to secrete TNF-alpha and decrease the macrophage respiratory burst resulting in decreased killing of bac.

Back 17

M. TB secretes proteins that recruit uninfected macrophages to early granulomas

Has hilar adenopathy, resembles bacterial bronchopneumonia

Front 18

1. What are the 5 key molecules in forming a granuloma for TB?
2. What happens if there are defects in the molecules?

Back 18

1. TLR-2, IL-12, IFN gamma, TNF, and NO (used to kill org.)
2. Difficulty forming a good granuloma, progressive disease

Front 19

1. presentation of primary TB?
2. What is miliary TB?

Coughing up TB with blood in it helps spread it

Back 19

1. infection is subpleural either in upper lower lobe or lower upper lobe, Ghon complex formation (lesion)
2. Disseminated TB, ka milliary b/c it looks like millet seeds. Can occur in spleen, bone marrow, liver

Front 20

1. What are some reasons for 2ndary TB?
2. HIV patients get secondary TB at what %/yr?
3. Where is 2ndary TB prominent?

Back 20

1. Re-infection, Reactivation of latent viable bacteria, waning immunological response, 5% of patients with primary TB get 2ndary TB
2. 10%
3. Upper lobes of the lung b/c it is aerobic bacteria

Front 21

1. Is miliary TB from primary or secondary TB?
2. What type of necrosis is common in TB?
3. Main dif. between primary and secondary TB?

Back 21

1. Both
2. Caseation
3. Location. 2- upper lobe, 1 is middle of lung

Front 22

1. Portal of entry for M. Leprae?
2. What is the cellular target?
3. Where does it grow best?

*Disseminates in blood

Back 22

1. Via aerosols from lesions in the respiratory tract
2. Macrophages
3. Cool tissues of skin and extremities

Front 23

Tuberculoid leprosy- localized lesions which are flat and red, develop indurated hyperpigmented margins with depressed pale centers, granulomas with few organisms, loss of sensation in entrapped nerves- major reason for disfiguration

Back 23

Lepromatous Leprosy (defect in Th1 response)
- macular, papular, or nodular skin lesion
- skin, peripheral nerves, upper airways, eyes, testes, hands and feet
-Decreased sensation in lesions
- lymph nodes, spleen, contain organisms

Front 24

Tuberculoid vs lepromatous leprosy:
1. High granulomas
2. High TH1 cytokines
3. High bacteria
4. High DTH response
5. High TH2 Cytokines

Back 24

1. Tuberculoid
2. Tuberculoid
3. Lepromatous
4. Tuberculoid
5. Lepormatous

Front 25

Tuberculoid leprosy if healthy, form granulomas with TH1 cells surrounding it, increase TLR 1/2, few bacteria

Back 25

Lepromatous leprosy:
T cell anergy to the lepromin Ag, macrophages are stuffed with bacilli, contain CD8+ suppressor cells in lesion, Decreased TLR 1/2 responses