616 
Gorbacli 
an autoimmune disease. This mechanism implies 
translation of the specific substance by the mi- 
croorganism, as well as implantation of the mi- 
croorganism in the intestinal tract. 
These potential hazards can best be under- 
stood within the general framework of microbial 
pathogenesis. This involves specific mechanisms 
for causing disease, colonization of body sur- 
faces, and communicability within the environ- 
ment. 
E. coli in the Natural Environment 
The natural habitat of E. coli is the intestinal 
tract of humans and animals [1], The organ- 
isms can be found in soil and water under cir- 
cumstances of fecal contamination. The major 
locus within the body is the large intestine where 
populations are stabilized at 1 0 ,: — 1 0 s /g of in- 
testinal contents [2, 3]. The upper intestinal tract, 
including the stomach and small intestine, has a 
relatively sparse flora with only transient colon- 
ization by coliforms, usually in concentrations 
of <10 ;, /ml. The lower ileum is a transitional 
zone between the meager flora of the upper in- 
testine and the luxurious colilorm populations 
of the large bowel [4, 5]. 
The intestinal microflora is extremely complex, 
and E. coli occupies only a small portion of this 
ecological niche. Obligate anaerobic bacteria are 
the major components, with concentrations in 
the large intestine of 10 n -10 12 /g, nearly the 
number of bacteria which can be accommodated 
in that given mass [6, 7]. Thus, anaerobic organ- 
isms, of which there are over 500 species in the 
intestine of humans, outnumber facidtative or- 
ganisms, such as E. coli, by 1,000-fold. 
The indigenous microflora is confined to the 
intestinal lumen and the mucosal surface [8, 9]. 
Active penetration through the epithelium is an 
abnormal event. Microorganisms that possess in- 
vasive characteristics are pathogenic, i.e.. Shigel- 
la, Salmonella, and certain penetrating strains of 
E. coli. 
A number of control mechanisms protect the 
upper intestinal tract from contamination by coli- 
forms carried in food and drink [10]. Particu- 
larly important is gastric acid at the portal of 
entry [11], Most of the enteric bacilli that con- 
taminate food are destroyed in the stomach. Bile 
has antibacterial activity and is thought to have 
some impact on control of the upper intestinal 
flora. Propulsive motility or peristalsis moves mi- 
croorganisms progressively down the small bowel. 
There are also mucosal factors and immunoglob- 
ulins that protect the upper intestine from col- 
onization and invasion. The large intestine has 
additional control mechanisms which maintain 
coliform populations at relatively constant lev- 
els. Most important among these mechanisms is 
the metabolic activity of the normal indigenous 
microflora. An important point to emphasize is 
that these control mechanisms are overlapping 
and redundant so that a failure of one system 
may not affect the total microenvironment sig- 
nificantly. 
E. coli appears to be a lifelong companion, 
being acquired in the intestinal tract within one 
day of birth [3]. Among 163 known O serotypes 
of E. coli, only a relatively small number are 
found with any frequncy in the intestinal tract 
of humans [1]. An individual is likely to harbor 
between five and 10 serotypes at any one time 
[12, 13]. It should be recognized, however, that 
sampling for specific serotypes becomes a for- 
midable task so that the exact number of sero- 
types in the gut can nev er be determined. 
The stability of E. coli populations within the 
intestinal tract has been the subject of many in- 
vestigations. Certain strains may persist within 
the same indiv idual lot months [14]. On the oth- 
er hand, there are natural fluctuations in coli- 
form populations which cause new strains to be 
introduced. Hospitalized patients, for example, 
are known to acquire specific serotypes associat- 
ed with that institution within a few days of ad- 
mission [13]. In England, it has been found that 
serotypes of E. coli may cluster within patients 
on specific wards in the hospital [15]. The hos- 
pital food was found to be contaminated with 
E. coli, and it was postulated that the E. coli in 
the intestinal flora of patients were implanted by 
exposure to hospital food and medications [16]. 
Artificial attempts to implant E. coli in volun- 
teers have met with varying success, depending 
upon the strain employed and the size of the inoc- 
ulum. Using relatively small numbers ol organ- 
isms, Sears et al. [17, 18] found that the ingested 
strains either disappeared or were recov ered from 
the feces for only a few days. Even with larger 
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