Lecture 2 Shigella produce shiga toxin, damage to intestine and blood vessels giving bloody diarheea EHEC E.Coli also known as Verotoxin give bloody diarheea similar to Shiga toxin Vibrio cholera cholera toxin producing watery, nonbloody diarheea by incresing cAMP in the intestinal cells leading to fluid loss in the intestinal lumen ETEC E.Coli - enterotoxin produce the same effect as the Vibrio cholerae enterotoxin Bacillus anthracis - causes tissue edema by increasing cAMP concentration in cells Clostridium botulinum anaerobic moostly in soil and oily food producing a toxin inhibiting acetylcholine release leading to muscle paralysis (most potent toxin known), type A.B and E Clostridium tetani anaerobic, wounds, toxin named tetanospasmin blocking glycine at the neuron synapses resulting in inhibition of muscle relaxation Clostridium difficile exotoxin A (enterotoxin-watery diarheea), exotoxin B (cytotoxin colonic mucosa and produce pseudomembranes) Clostridium perfringens found in necrotic tissue, toxin produces necrosis of tissue, tissue digestion = gas gangrene Bordetella pertussis - similar to a cold but 1 or 2 weeks violent coughs and mucus hyperproduction, affecting the cilia, produce inflammation and tissue damage RI tract Cytolytic enzymes membrane disrupting by pore forming or by damaging phospholipase

Lecture 3 Exotoxins proteins/enzymes produced by gram + bacterias, are good antigens, antitoxins = protective antibodies against toxin, most toxic substances known, produce specific diseases. Toxoid inactivated exotoxins, no longer producing disease, used as vaccine since they retain their antigenicity Endotoxins produced by gram bacterias, no vaccine available only antibiotics, low toxicity compared to exotoxins, all produce same effects fever/shock etc. Also it leads to production of vasoactive mediators and inflammatory cytokines (can mediate septic shock) DPT vaccine Diphteria, Pertussis, Tetanus A-B toxins polypeptides consisting of B-subunit (binding) and A-subunit (delivered in cytoplasm having toxic activity by inactivating host cell target protein by ADP-ribosylation). Examples: diphteria, cholera, botulinum, pertussis toxins Cytolytic toxins damage the cellular membranes Cytotoxins inhibition of protein synthesis like shiga toxins: examples of bacterias producing exotoxins: P. aeruginosa, E.Coli, Vibrio cholerae, B. Pertussis Enterotoxin activate secondary messenger pathways

Lecture 4 Streptococci gram + diplicocci, anaerobs, nonmotile, have a carbohydrate C in the cells walls used for classification, also Lancefield groups to classify it (A to T), penicillin treatment Pyogenic (pus-forming) group A,B,C and G (pyogenes, agalactiae etc.) Non pyogenic (non-pus forming) S.mutans, bovis, mitis, salivarius etc. S. pneumoniae distinct group S.Pyogenes b-haemolysis, most virulent, normally found in pharynx (most frequent cause of acute pharyngitis) and on the skin (scarlet fever, impetigo, folliculitis), attaches to pharyngeal mucosa by protein F, lipoteichoic acid and M protein (it is the major virulence factor which induces antibodies) Pyrogenic exotoxins leads to release and buildup of cytokines leading to toxic shock Extracellular factor helping with spreading hyaluronidase (breaking down connective tissue), stretokinase (enzyme that facilitates the spread by resulting in fibrin digestion), C5 peptidase (inactivates C5a which has activity of attracting white cells namely neutrophils), cytolitic toxins (SLO being a cell poison lysing RBC, leukocytes, tissue cells, platelets, and antibodies agains it called ASLO which are produced during infection) Rheumatic fever and acute glomerulonephritis produced postinfectios both being immunologic mechanisms through the reaction of the immune system

Lecture 5.A Pneumonia S. pneumoniae, Staphylococcus aureus in children, Hamophilus influenzae, also gram bacterias like klebsiella pneumoniae, pseudomonas aeruginosa, E.coli, Proteus etc. S.Pneumoniae a-haemolytic, gram + diplococci, can be eliminated by phagocytosis, IgA or cilia, capsule which is the major pathogenity factor combating phagocytosis Autolysin-LytA normally inactive responsible for release of pneumolysin a cytotoxin inserting to plasma membrane producing pores leading to lysis being most potent hemolysis S. Viridans produce dental abcesses and/or gingival infections, also endocarditis if they are introduced in blood S.Mutans produce dental caries by attacking enamel of teeth Enterococci resistant to B-lactamase antibiotics, penicillins and cephalosporins

Lecture 5.B Staphylococci gram + cocci in clusters, normally found in skin and mucous membranes being part of normal flora, its capsule contains protein A inhibiting phagocytosis S.aureus responsible for most human infections, pus-forming, pyogenic skin infections like folliculitis, impetigo, cellulitis, eye infection, glandular and RT infections like pneumonia. SSSS and TSS Toxic shock syndrome both being caused by staphylococcus, resistant to penicillin and methicillin S.epidermidis opportunistic, can produce cystitis, septicemia, endocarditis, meningitis S. saphrophyticus opportunistic, can produce urinary tract infections in young women