Lung infections Flashcards

Question

Whats the difference between Legionnaires disease and Pontac fever?

Answer 1

Legionnaires disease * Acute fulminating pneumonia * low attack rate Pontac fever * mild, non-pneumonic febrile infection * High attack rate

Answer 2

* Man made water distribution systems * >warm storage tanks, pipes, AC cooling towers, shower heads * even potting compost (Austrailia) * bacteria multiple * released as water droplets (aerosols)

Answer 3

* chlorinate water

Answer 4

* Infects lung macrophages

Answer 5

* Colonises within Biofilms * Access to nutrients from other biofilm species for its growth

Answer 6

* Legionella pneumophila found inside ameobal cyst * evolved to survive within in * Using the same strategy it has adopted to survive within macrophages * Intefering with host immune clearance

Answer 7

* L.pneumophila enters macrophage * Via phagocytosis using ICM/DOT proteins * Resides within permissuble vacuole resistant to lysosymal activity - prevents lysome and phagosome from fusing * No enzymatic activity, free-radical release * Thus, establishes replication within phagosome * Averts macrophage function

Answer 8

* Controlled **ICM/DOT genes** * Encodes for **secretion apparatus** related to **Type IV conjugation system** * Pump effector proteins -> host vacuole

Answer 9

1. Flagella expression >fla mutants less infective for macrophages/amoebae 2. Pillin genes >attachment to host cells (+biofilm) >intracellular growth (inside host vacuoles) 3. Type IV secretion Dot/Icm complex 4. Macrophage infectivity protein (Mip protein) 5. Kat A (periplasm) and Kat B (cytosol)

Answer 10

* Complex of Dot/Icm proteins * Span across bacterial and host membrane * To translocate effector molecules ->host cell * Required ATP energy provided by Dot B protein * Changes in Dot A/B does not affect invasion in amoeba - A.castellani (Host organism)

Answer 11

* produces catalase/peroxidase activity -> detoxifies it * why> maintain criticallu low H2O2 levels * To prevent host from mounting oxidativr burst defense * Compatible w/phagosome trafficking mediated by typr IV secretion apparatus

Answer 12

* Ingested by phagocyte->phagosome * >isolated from endosomal pathway * Bacteria->replicative form * >resistant to acidic environment and fusion block remobed * Fuses with lysosome - privide niche environment for replication * Nutrients deplete (amino acids) , and second messenger molecule ppGpp triggers cascade of regulatory events * Enters stationary phase and recruit proteins * >Let A, Let S, Let E, Rpos, FliA * These proteins coordinate transition of bacteria to exit of host cell membrane * Express motilty * Produce IcmT proteins meduate exit by forming pores in membrane * Zinc metalloprotease (Msp) - degrades host vacuole and outmembrane, explored and mutlplied bacteria swims out * Starts infection cycle again

Answer 13

* Weakly gram-negative * Strongly acid fast aerobic rod * Multi-lobed appearance * 24-30 hoour doubling time

Answer 14

Unusual cell wall

Answer 15

Spreads person to person by infectious aerosol

Answer 16

* **CMN groups ** * Lipid rich cell wall of **mycolic acids** * Resistant to biocides, detergents and antibiotics ## Footnote Structure: cytoplasm >cytoplasmic membranes>peptidoglycan layer> CMN groups. lipid rich cell wall

Answer 17

Bacilliary growth= growth of rod-like bacteria Prevention of dissemination= stop spread of disease Hematogenous dissemination= spread into bloodstream Primary acute infection= aggressive form

Answer 18

Granuloma is formed to protect bacteria from spreading. Surrounded by necrotic tissue. > organises aggregates > surrounds areas of tissues infected by mycobacterium tubercolosis > act as a barrier that contains the infection > preventing the bacteria from spreading to other parts of the body > containment limit the infection's progression. Recruitment of * epitheliod cells (type of immune cell) * multinucleated giant cells -***specialized cells that form when multiple individual cells fuse together, resulting in a single cell with multiple nuclei***. * activated macrophages * CD4+ T lymphocytes * CD8+ T lymphocytes

Answer 19

* Bacterium= Tubercle bacilli * inhale implants on to bronchioles/alveoli * engulfed by macrophage/neutrophils -> phagocytosis * multplies intracellulary * >spreads to lymph nodes, bloodstream and distant organs After 2 weeks * Granuloma forms * Lymphocystes surround it =**Ghon Tubercle** * Central portion of Ghon tubercle undergoes necrosis "cheesy appearance" * Necrotic tissue breaks down - fluid-like subsance * sloughs into bronchus * forming cavity * entry into tracheal broncheal system * infectious - spread to other areas via coughing and sneezing (airborne transmission) * Macrophages try to contain and clear infection = **Healing by resolution** * Some cases cannot be completely cleared -> scar tissue/fibrosis calcification * >created distinctive structure = **Ghon complex**

Answer 20

* Evades destruction from pahgocytosis * Dusrupts phagosome maturation * So no bacterial degredation by lysosome * Persist and survive in host * Contributes to the complexisity of infection and influence course of disease

Answer 21

* Priority of treatment (active/latent) * active->non infectious within 2 weeks of treatment * >Isoniazid,rifampin, ethambutol: Directly observed treatment shortcourse (DOTS)