what are the effects of e coli?

Answer 1

Extreme gastro-intestinal discomfort!!!

(Exit's both ends!)

More soberly:

E. coli can cause several intestinal and extra-intestinal infections such as urinary tract infections, meningitis, peritonitis, mastitis, septicemia and gram-negative pneumonia. The enteric E. coli are divided on the basis of virulence properties into enterotoxigenic (ETEC, causative agent of diarrhea in humans, pigs, sheep, goats, cattle, dogs and horses), enteropathogenic (EPEC, causative agent of diarrhea in humans, rabbits, dogs, cats and horses), enteroinvasive (EIEC, found only in humans), verotoxigenic (VTEC, found in pigs, cattle, dogs and cats), enterohaemorrhagic (EHEC, found in humans, cattle and goats), attaching porcine strains that colonize the gut in a manner similar to human EPEC strains) and enteroaggregative E. coli (EAggEC, found only in humans).

Answer 2

Phage development depends not only upon phage functions but also on the physiological state of the host,
characterized by levels and activities of host cellular functions. We established Escherichia coli at different
physiological states by continuous culture under different dilution rates and then measured its production of
phage T7 during a single cycle of infection. We found that the intracellular eclipse time decreased and the rise
rate increased as the growth rate of the host increased. To develop mechanistic insight, we extended a computer
simulation for the growth of phage T7 to account for the physiology of its host. Literature data were used to
establish mathematical correlations between host resources and the host growth rate; host resources included
the amount of genomic DNA, pool sizes and elongation rates of RNA polymerases and ribosomes, pool sizes of
amino acids and nucleoside triphosphates, and the cell volume. The in silico (simulated) dependence of the
phage intracellular rise rate on the host growth rate gave quantitatively good agreement with our in vivo
results, increasing fivefold for a 2.4-fold increase in host doublings per hour, and the simulated dependence of
eclipse time on growth rate agreed qualitatively, deviating by a fixed delay. When the simulation was used to
numerically uncouple host resources from the host growth rate, phage growth was found to be most sensitive
to the host translation machinery, specifically, the level and elongation rate of the ribosomes. Finally, the
simulation was used to follow how bottlenecks to phage growth shift in response to variations in host or phage
functions.