Poststreptococcal glomerulonephritis is caused by (bacteria type) .
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A 22-year-old woman comes to the student health center with pustules on her face, surrounding her nose and lips. The lesions appear honey-crusted, and are not painful. She has noticed no other symptoms, and denies fever, cough, or sore throat. Her past medical history is significant for a broken arm at age 8, but otherwise unremarkable. She is in her final year at college, and lives in a crowded residence hall. When the pustules are cultured, the results are catalase-negative cocci (pictured below). Which of the following sequelae would you be most worried about?
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Poststreptococcal glomerulonephritis or PSGN is where the kidneys’ glomeruli, which is the location where small molecules are first filtered out of blood and into the urine, become inflamed after an infection by streptococcal bacteria.
Most commonly, PSGN starts with an infection by strains of group A beta-hemolytic streptococci bacteria, and this particular group of streptococcus has a specific antigen on its surface that lumps it into a group called “group A”.
This group A streptococci also produces an enzyme called streptolysin, and when the bacteria is grown on a petri dish of blood, the enzyme completely lyses red blood cells that are near the bacterial colony—called beta-hemolysis.
Beta-hemolysis is where they’re completely destroyed—as opposed to alpha-hemolysis, where cells aren’t actually destroyed, but they’re just damaged or bruised.
Additionally, these strains are considered nephritogenic strains because they carry the M-protein virulence factor, a protein that essentially helps them get around host defenses.
An infection by a nephritogenic strain of group A beta-hemolytic streptococcus bacteria initiates a type III hypersensitivity reaction, where immune complexes are formed, composed of antigens and antibodies, often IgG or IgM, that end up being carried in the bloodstream to the glomerulus and become trapped.
Specifically these deposits end up in the glomerular basement membrane or GBM, and most of the time they’re subepithelial, meaning between the epithelial cells, or podocytes, and the basement membrane.
It’s also possible the antigens from the bacteria are first trapped in the glomeruli, and then antibodies bind in the glomerulus itself.
Either way, these complexes initiate an inflammatory reaction in the glomerulus, which involves activation and deposition of C3 complement, inflammatory cytokines, oxidants, and proteases that all damage the podocytes.
This damage ends up allowing larger molecules to filter into the urine, like red blood cells and proteins, which then get into the urine and cause hematuria and proteinuria.
Those red blood cells in the urine actually often make it darker or cola-colored; also there tends to be less urine produced than normal, called oliguria.