#Super strain chlamydia europe skin#

attaches to sialoglycoproteins or sialoglycolipid receptors on tracheal/bronchial epitheliumĢ. Mycoplasm with the following characteristics:Ī. Classically thought of as surface parasites of the mucosa, but subset can gain access to intracellular compartment, which would help to explain its viability despite its susceptibility to lysis or phagocytosis Those with a tip structure tend to cause diseaseį. 'Fried egg-like' colonies on agar, but slow-growing so clinically uselessĮ.

Clinically, morphology is irrelevant because not visible via light microscopy (unless colored red by PAS stain)ĭ. Mechanisms for cellular plasticity and organelle developmentģ. Most common shape = Erlenmeyer flask-shapedĢ. Highly pleomorphic: Mollicutes characterized based on reproducible shapes and sizes despite lack of cell wall ġ. Studded with many proteins, giving the outer membrane some strength to compensate for the lack of a cell wallĬ. Very susceptible to the environment - even a little bit of osmotic pressure will cause cell lysisĢ. Resistance to penicillin/lactams - peptidoglycan synthesis inhibitorsġ.

No cell wall: only group of bacteria without cell walls, lack mechanism to keep rigid, more sensitive to growth inhibition or lysis via complement or Abġ. Reversible with antibiotic therapy get secondary infections from this occasionaįamily of bacteria with the following characteristics:Ī.

#Super strain chlamydia europe skin#

Scalded (peeling) skin syndrome involving Exfoliatin toxin: destroys the tight junctions between cells typically Erythematous membranes of toxic shock syndrome: 'strawberry tongue'Ĥ. Rash Associated with TSST- looks like a sunburnģ. Concurrently: fever (resolves quickly), pain (extends duration of the 60 days), hypotension (resolves after aĬouple days), confusion, headache (resolves quickly), diarrhea (gradually decreases over one week)Ģ. Progression over 60 day period: Erythroderma -> erythematous membranes desquamation -> hair & nail lossĪ. Common symptoms of Staphylococcus toxic shockġ. Non-menstrual: ~50% TSST other superantigens, 50-70% women, mostly in the setting of infection, up to 20% Menstrual: almost all TSST, all women, all younger, colonization not infection, low mortalityĤ. Massive increase in the 1980's - investigation into Rely tampons - super absorbentģ. Most are menstrual related, some aren'tĢ. Toxin-mediated Staph disease with the following characteristics:ġ. For an entire page of theory and counter-arguments about PSGN pathogenesis see page 19 of noteset. (by consumption of alternate pathway components).į. C3b deposition and, in early cases, activation of the alternate complement pathway is almost always observed Depending upon when biopsy is analyzed, deposition of immunoglobulin may be observed (not in early stage) Ģ.

Histologically, glomeruli exhibit extracapillary proliferation with marked condensation and lobulation.ġ. Hypertension, headache, depression of complement factors, reduction of glomerular filtration rate.Į. Characterized by abrupt onset of hematuria, proteinuria, often accompanied by a fever, edema, oliguria, In GAS, it's associated with certain M types (1-4, 12, 15, 49, 55-57, 59, 60) and usually occurs only once per personĭ. If damage is sufficient, dialysis or transplantation may be needed.Ĭ. May be a major cause of primary glomerular injury that can possibly cause other issues, such as hypertension.ġ. PSGN is not the result of genetic predisposition.ī. This suggests that the older individuals have protective antibodies from previous strep infections that haveĬross-reactivity with the PSGN causing strain.Ģ. Often, young children will develop PSGN, but their older siblings and parents will not develop the disease. Tends to appear in epidemic situations.ġ. More common in children and young adults & males > females. Infection and is associated with Groups A, C (S.