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