Interferon gamma-activated monocytes limit the availability of iron by down-regulating transferrin receptors, iron uptake and intracellular ferritin concentrations. This inhibits the multiplication of Legionella. (Remember, it needed iron added to its agar.)
Once L. pneumophila enters a macrophage by coiling phagocytosis, it remains in the phagosome. Ribosomes, smooth vesicles, and mitochondria surround the Legionella containing phagosome. The organism inhibits phagolysosomal fusion and acidification of the phagosome.
Cell mediated immunity is the primary host defense against Legionella. Lymphocytes become sensitive to the organism and secrete cytokines that activate macrophages. Activated macrophages then down regulate the complement receptor so they phagocytize fewer Legionella. Interferon gamma-activated monocytes limit the availability of iron by down-regulating transferrin receptors, iron uptake and intracellular ferritin concentrations. This inhibits the multiplication of Legionella. PMNs also help. They can't kill L. pneumophila (at least not in vitro), but they release apolactoferrin. Apolactoferrin is endocytosed by monocytes and further helps the monocytes limit the availability of iron to Legionella. Humoral immunity is not effective. Legionella resists killing by antibody and complement. In fact, antibody promotes uptake of L. pneumophila by macrophages.
Shared virulence property of Neisseria meningitidis and Neisseria gonorrhoeae:
- N. meningitidis and N. gonorrhoeae adhere to receptors on the surface of mucous secreting epithelial cells, are endocytosed, transverse the cell and are egested from the cell.
- REM: N. meningitidis metabolises glucose and maltose, while N. gonorrhoeae only metabolises glucose.
- Both are oxidase positive.
- 80-95% C. perfringens
- 10-40% C. novyi
- 5-20% C. septicum
Campylobacter jejuni does not invade blood vessels. It is Campylobacter fetus that exhibits vascular tropism, as does Pseudomonas aeruginosa.
What is vascular tropism?
Campylobacter fetus has vascular tropism. Once in the bloodstream, Campylobacter fetus attaches to the vascular endothelium, and can cause endocarditis, mycotic aneurysms, cellulitis and septic thrombophlebitis. Patients with vascular disease are at increased risk.