DESTRUCTION OF NORMAL RESIDENT MICROFLORA AS THE MAIN CAUSE OF AIDS
By Vladimir L. Koliadin
The main clinical manifestation of AIDS is ultra-high vulnerability
of the patients to opportunistic infections (OI) as well as severe and
recurrent course of these diseases. These infections are caused by microorganisms
which are normally present in organism of healthy individuals and environment,
but harmless to otherwise healthy hosts. That is why, almost in the very
beginning of AIDS epidemic, this syndrome was unanimously attributed to
deficiency of the immune system of AIDS patients. Since then, the "AIDS
= immunodeficiency" postulate has never been seriously doubted. Even
though mainstream AIDS researchers and AIDS- dissidents disagree violently
on what causes this deficiency of the immune system, both sides tacitly
agree that just immunodeficiency is responsible for the severe and frequently
incurable OI in AIDS patients. A hypothesis presented in this paper (in
short -- "destroyed-microflora" hypothesis) challenges this totally
shared postulate, and provides quite a different view on both nature of
AIDS and its causal factors.
The main points of the "destroyed-microflora" hypothesis
1. Contrary to a widely shared belief, the immune system (T- cell mediated
immunity) plays no any significant role in protection from the bacterial
and parasitic OI observed in AIDS patients. The main factor which prevents
these infections in healthy individuals is normal resident (friendly) microflora
-- the harmless and frequently useful microorganisms which populate various
body compartments: mucous membranes of inner tract (guts, lungs, respiratory
tract, etc.) as well as skin. These microflora occupy ecological niches
in organism and prevent these areas from colonization by other species
of microorganisms, including species pathogenic for the host macroorganism.
2. The main factor which triggers bacterial and parasitic OI in HIV-positives
and AIDS patients is destruction of their normal microflora -- the natural
protection against OI. Microflora in AIDS patients is destroyed by unusually
prolonged exposure to broad- spectrum antibacterial and antiparasitic antibiotics,
and, probably, by exposure to drugs with cytostatic effect (AZT, ddI, etc.).
Destruction or severe depletion of the normal microflora makes the ecological
niches vacant, and they are being easily colonized by pathogenic species
of microorganisms which are normally present in harmless quantities in
organism and environment. Otherwise, these microorganisms cannot proliferate
effectively because they lose ecological competition with normal resident
microflora. Moreover, many species forming the normal microflora are incorporated
in vital functions: digestion and utilization of food, production of vitamins.
Depletion of the microflora results in depression of these functions and
leads to worsening general health and decline of non-specific resistance
of the organism.
3. CD4 lymphocytopenia observed in many HIV-positives and almost all
AIDS patients as well as concomitant viral infections are of secondary
nature: they are caused by severe and permanent psychological stress (caused
by intensive propaganda of the "HIV = AIDS = Death" postulate),
worsening general health due to bacterial and parasitic OI and toxic medication.
Neither CD4-lymphocytopenia itself nor viral infections pose any direct
threat to life -- they are only indicators and consequences of worsening
general health and concomitant depression of the non-specific resistance
of the organism.
4. Epidemic of severe OI named AIDS started in highly promiscuous groups
(the gay community and severe drug abusers) in late 1970's because of the
popular fashion to use broad-spectrum antibiotics as a permanent prophylaxis
against sexually transmissible diseases (STD) frequent in these groups,
and partially by frequent treatment of recurrent STD by broad-spectrum
antibiotics. Then, with the acceptance of the wrong "AIDS = immunodeficiency"
and, later, "HIV = AIDS" postulates, the dubious practice to
administer broad-spectrum antibiotics (as permanent prohylaxis against
allegedly possible OI) became normal for individuals with non-specific
symptoms named pre-AIDS (CD4- lymphocytopenia, lymphoadenopathy, severe
diarrhea, weight loss, and CD4-lymphocytopenia), with AIDS diagnosis, or
with a positive test for HIV-antibodies. This increased dramatically the
number of individuals exposed for unusually long time to broad-spectrum
antibiotics, and resulted in rapid growth of incidence of severe and incurable
OI due to destruction of normal resident microflora - - the natural defense
5. The course of events typical to most cases of AIDS -- HIV- seroconversion
-> CD4-lymphocytopenia -> severe and recurrent OI (AIDS) -- is not
a result of the "HIV = immunodeficiency = OI" mechanism specified
by the official viral theory, but a direct consequence of the general belief
in the "HIV=AIDS=Death" and "AIDS=immunodeficiency"
postulates and clinical strategy based on these postulates. A positive
test for HIV-antibodies causes severe and permanent psychological stress
and, frequently, is followed by permanent prophylaxis by broad-spectrum
antibiotics and toxic medication by drugs with clearcut cytostatic effect
(AZT, ddI, ddC, etc.). The permanent severe stress and cytostatic drugs
lead to CD4- lymphocytopenia; broad-spectrum antibiotics and, partially,
cytostatic drugs destroy normal resident microflora -- the natural protection
against OI. Progression of CD4-lymphocytopenia and first signs of OI, in
turn, force physicians to intensify therapy by broad-spectrum antibiotics
and, frequently, by antiretrovirals. This leads to further destruction
of the normal resident microflora and facilitates OI. Thus, a vicious circle
takes place: medication normally prescribed with intention to cure complications
of AIDS in reality has an opposite effect -- it facilitates further progression
of the disease. Naturally, AIDS demonstrates very high mortality -- simply
because the individuals are being treated by just the same sort of drugs
as those which have caused this condition.
The above described hypothesis seems to explain the basic peculiarities
of AIDS: (i) HIV-AIDS correlation, (ii) susceptibility of the patients
to OI, (iii) severe course of the disease and extremely high mortality,
(iv) emergence and concentration of AIDS in highly promiscuous groups --
male homosexuals and severe drug abusers, (v) rapid and synchronous growth
of incidence of AIDS in different high-risk groups, (vi) relatively low
progression of health decline in HIV-positives, but rapid progression after
detecting CD4-lymphocytopenia or diagnosis of AIDS.
The role of normal resident microflora in health and disease
Even though the role of normal resident microflora in organism is grossly
underestimated by mainstream biomedical schools of thought, it is well
understood by many authors [1-9]. Various species of microorganisms normally
populating human organism form a complex ecological system which is far
from being fairly understood yet. To a great extent this lack of understanding
is caused by little interest of the mainstream biomedical science to this
subject. In brief, the role of microflora may be summarized as follows
1. Partially normal resident microflora is formed by various species
of microorganisms which are harmless passengers and play no any significant
role in body functions directly. On the other hand, these species occupy
ecological niches in various areas of the organism (mucous membranes, lungs,
gut, skin) and prevent them from colonization by other species of microorganisms,
including potentially pathogenic species, due to successful ecological
competition with the latter.
2. Another part of normal microflora is formed by microorganisms which
are obviously useful for the host macroorganism and directly incorporated
in its vital functions. First of all, it is friendly microflora of gut
which play immediate role in digestion and utilization of food as well
as in production of vitamins.
This symbiosis (mutually useful coexistence) of the host human macroorganism
and its normal microflora is a natural result of thousands years of coevolution
of homo sapience and microorganisms. It is a direct consequence of the
benefits from this symbiosis for the host macroorganism -- harmless nature
of these species, their successful competition with other microorganisms
pathogenic for the host organism, and their direct incorporation in biochemical
functions of the host.
According to the "destroyed-microflora" hypothesis, normal
resident microflora (not the immune system as it is totally believed) is
the main factor preventing AIDS-associated and other opportunistic bacterial
and fungal infections in healthy individuals. Just destruction of the normal
resident microflora (not deficiency of the T-lymphocytes) is the factors
which makes the individuals highly susceptible to bacterial and parasitic
Is it just the immune system what normally protect from OI?
In the very beginning of the epidemic of AIDS, it was noticed that AIDS
patients were extremely susceptible to infections caused by low-grade pathogens
that were earlier known to cause OI only in compromised hosts -- mainly
in individuals subjected to therapy by drugs with immunosuppressive effect:
cancer patients (treated by cytostatic drugs), recipients of transplantants
(treated by immunosuppressive drugs). On the other hand, these microorganisms
are normally present in small quantities in healthy individuals and environment,
but do not cause infection in healthy individuals. This observation, along
with depletion of T-lymphocytes in individuals with OI, was explained by
protective role of the immune system in otherwise healthy individuals,
and susceptibility to OI was attributed to deficiency of the immune system.
Since that time, the postulate "AIDS = immunodeficiency" became
totally accepted as the ultimate truth.
According to the "destroyed microflora" hypothesis, the above
described observation has quite different explanation which does not rest
on the "AIDS = .immunodeficiency" postulate. The central point
of the hypothesis is that the main factor normally protecting from bacterial
and parasitic OI is the normal resident microflora, not the immune system
as it is widely believed. In individuals with OI, these microflora are
being seriously depleted or destroyed by prolonged exposure to broad-spectrum
antibiotics and, probably, to other drugs -- mainly those with clearcut
cytostatic effect. Do all the categories of individuals susceptible to
OI (cancer patients, recipients of transplants, and first patients with
AIDS) had been subjected to some factors which might destroy their resident
microflora? There at least two such factors.
First, it is extremely prolonged use of broad-spectrum antibiotics.
Individuals treated by drugs with immunosuppressive effect (cancer patients,
recipients of transplantants, etc.) as well as patients with other forms
of immunodeficiency are normally subjected to permanent prophylaxis by
broad-spectrum antibiotics (which are well known to destroy normal microflora).
As for first AIDS patients, they were mainly highly promiscuous male homosexuals
and severe drug abusers who admittedly used broad- spectrum antibiotics
as a permanent prophylaxis against sexually transmissible diseases (STD)
-- extremely frequent in these groups because of high promiscuity, and
many of them had been frequently exposed to broad-spectrum antibiotics
while treatment of recurrent STD.
Second factor depleting microflora is drugs with cytostatic effect normally
used for anti-cancer therapy, and for deliberate suppression of the immune
system in recipients of transplantants. After 1984, with the advent of
the "HIV = AIDS" formula, many patients with a positive test
for HIV, pre-AIDS symptoms, or AIDS diagnosis became also subjected to
exposure to drugs with cytostatic effect (AZT, ddI, ddC, etc.).
Thus, besides compromised T-cells, all the categories of individuals
which demonstrate high susceptibility to bacterial and parasitic OI have
another common trait -- unusually long-term exposure to factors depleting
normal resident microflora (broad- spectrum antibiotics and, partially,
drugs with cytostatic effect). As for the deficiency of T-lymphocytes itself,
there are no any tangible evidence that T-cells can protect from OI, and
that deficiency of T-cells mediated immunity is the prime factor which
triggers infections. To the same extent, the observed association between
T-cell deficiency and OI is explainable by simultaneous exposure of the
individuals to immunosuppressive factors (drugs with cytostatic effect,
stress, compromised general health, etc.) and factors which destroy normal
microflora (broad-spectrum antibiotics, cytostatic drugs). Moreover, the
very detection of immunodeficiency with a great probability results in
prescription of long-term prophylaxis by broad-spectrum antibiotics (leading
to further destruction of the normal resident microflora and its replacement
by conditionally pathogenic flora which cause OI).
Another plausible explanation of the observed association between deficiency
of T-cells and high susceptibility to bacterial and parasitic OI is that
this immunodeficiency is of secondary nature -- i.e. infections themselves
cause reduction of T- lymphocytes counts in peripheral circulation. This
assumption fits current biomedical dogmas. For example, T-cell population
is known to be depressed in persons with lepromatous leprosy, and degree
of this depression is correlated directly with the bacillary load .
This correlation cannot be explained by the primary nature of T-cell deficiency
-- simply because infection develops first. The primary role of bacterial
infection in depletion of T-cells is the most plausible explanation .
There are also some other reasons to doubt the direct causal link between
immunodeficiency and OI.
1. Bacterial and parasitic opportunistic infections associated with
AIDS normally develop in the body compartments which are beyond any direct
reach of the immune system: mucous membranes of the gut, lungs, respiratory
tract, etc. as well as surface of the skin.
2. AIDS patients demonstrate no any significant increase in susceptibility
to usual (non-opportunistic) infections from which the immune system protects,
even though pathogenic microorganisms are present in small quantities in
environment and organism. It is a sign that the immune system of AIDS patients
is still competent enough to tackle with infections.
3. Microorganisms usually proliferate very rapidly unless some factors
stifle and limit this process. If just the CD4-lymphocytes were the factor
which controls proliferation of the microorganism casing OI, any significant
drop in CD4+ cell counts would have resulted in rapid development of OI
(provided the microorganisms are normally present in small quantities in
the organisms). Nevertheless, many individuals live with low counts of
CD4- lymphocytes for long time without any signs of OI. This supports the
view that it is not the immune system, but some other factors what control
proliferation of these microorganisms.
Prolonged prophylaxis by antibiotics main cause of AIDS
Most HIV-positives and almost all AIDS patients, irrespective to the
risk-group they belong to, are subjected to long-term prophylactic treatment
by broad spectrum antibacterial and antiparasitary drugs (antibiotics).
Because of the total belief in the dubious "AIDS = immunodeficiency"
and "HIV = AIDS = Death" formulas, either a positive test for
HIV or some symptoms which are considered as pre-AIDS are frequently followed
by unprecedented in its intensity and longevity prophylaxis by broad spectrum
antibiotics, including cocktails of these drugs. At the same time, just
longevity of administering and broad-spectrum of antibiotics are the main
factors which determine degree of destruction of normal microflora [3,4,11]
There are at least three biological mechanisms which explain the link between
prolonged broad-spectrum antibacterial prophylaxis and the main clinical
manifestations of AIDS -- severe and incurable OI and rapid decline of
1. Normal resident microflora prevents the ecological niches they populate
from colonization by other species of microorganisms. Destruction or severe
depletion of the microflora results in otherwise impossible colonization
of the freed ecological niches by other species of microorganisms, including
conditionally pathogenic ones. This explains the ultra-high susceptibility
of AIDS patients to bacterial and parasitic opportunistic infections. A
classical and well known model of such a process is the fungal infections,
mainly that caused by Candida ( ubiquitous fungi, not sensitive to antibacterial
drugs), which frequently follow even relatively short courses of broad-spectrum
antibacterial therapy due to depletion of normal resident microflora (sensitive
to antibiotics) [11,12].
2. Many species forming normal resident microflora take an active part
in vital functions of the host macroorganism -- digestion and utilization
of food, production of vitamins [1,3,4]. Long term depletion or destruction
of these species by antibiotics naturally result in malfunctions of the
subsystems of the organism these microorganisms are involved in, and worsening
the general health status. This partially explains the "non-specific
illness" observed in AIDS patients.
3. Prolonged use of antibiotics frequently results in emergence of drug-resistant
strains of microorganisms -- simply due do classical natural selection
of drug resistant mutants under the selective pressure of antibiotics [3,4,13-15].
In organisms whose normal microflora -- the main natural protection against
OI -- has been destroyed by antibacterial therapy, these drugs are the
only factor which stifles proliferation of conditionally pathogenic microorganisms.
Therefore, emergence of drug-resistant strains makes further drug therapy
ineffective and leads to incurable and progressive course of infection
with frequent lethal outcome.
Natural questions arising in the context of "destroyed- microflora"
hypothesis are: Why AIDS is new while antibiotics had been in use at least
for three decades before AIDS epidemic had started? Why AIDS-like syndrome
has not been observed in multiple clinical studies of antibiotics?
Antibiotics were designed for short-term therapy of conditions caused
by proliferation of pathogenic microorganisms. Classical scheme of treatment
implies isolation of pathogenic microorganisms which cause the disease,
determining to what antibiotics they are sensitive, and administering just
these narrow spectrum drugs for therapy. Duration of a traditional course
of antibiotics does not normally exceed several weeks; and just such a
scheme of treatment by antibiotics is normally tested in clinical trials
of these drugs. It is worth noting here that even such short- term therapy
relatively frequently results in noticeable destruction of the resident
microflora with its typical manifestation -- fungal infections [3,4,11,12].
In contrast with most other categories of individuals treated by antibiotics,
AIDS patients and HIV-positives are subjected to unprecedented in its intensity
and longevity prophylaxis by antibiotics -- for many months and years.
Moreover, powerful broad- spectrum drugs (many of them are relatively new)
are normally used, and frequently in combination of several drugs. Wide
use of broad- spectrum antibiotics and administering combinations of these
drugs for long-term prophylaxis is a relatively new practice; and it became
extremely popular only in the AIDS era. The only categories of patients
subjected to similar prohylaxis by antibiotics before AIDS epidemic were
individuals subjected to therapy by immunosuppressive drugs (e.g. patients
with cancer, recipients of organs and tissues) or those with immunodeficiency
of other nature. And only these categories demonstrate high incidence of
OI (even though these OI are normally attributed to deficiency of their
Due to total uncritical acceptance of a wrong "HIV = immunodeficiency
= AIDS" view, AIDS patients and HIV-positives virtually became subjects
of a large-scale experiment on unprecedented long-term administering of
broad-spectrum antibiotics. The epidemic of severe OI misleadingly named
AIDS is a natural outcome of this "experiment". 6. Some additional
arguments in support of the "destroyed- microflora" hypothesis:
- unprecedented long-term prophylaxis by broad-spectrum antibiotics
is a factor common to all AIDS patients and many HIV- positives (irrespective
to the risk-group); on the other hand such prophylaxis is extremely rare
in other categories of patients;
- a positive test for HIV or otherwise nonspecific symptoms called pre-AIDS
are frequently, if not always, followed by unprecedented long-term prophylaxis
by broad-spectrum antibiotics; this explains why AIDS is highly correlated
with and normally preceded by a positive test for HIV or non-specific symptoms
named pre-AIDS (lymphoadenopathy, thrush, diarrhea, weight loss);
- the official HIV=AIDS hypothesis fails to explain why male homosexuals
are the main targets of AIDS; the attempts to explain this essential epidemiological
peculiarity of AIDS via presumably drastic difference in rates of transmission
of HIV during anal and vaginal intercourse have no any factual underpinning;
at the same time, in 1970's broad-spectrum antibiotics became popular in
promiscuous segment of gay community as a long-term prophylactic measure
against otherwise frequent sexually transmissible diseases ; specific
spectrum of sexually transmissible diseases (not treatable well by penicillin
or other narrow-spectrum antibiotics) in gays as well as growing availability
of broad-spectrum antibiotics are responsible for arising this "fashion"
mainly in the gay community, and admittedly, in other groups with extremely
high promiscuity (marked also by severe abuse of recreational drugs);
- the official HIV-causes-AIDS hypothesis fails to explain why AIDS
is distributed very unevenly over the globe: for example AIDS is extremely
rare on the territory of the former Soviet Union (even though incidence
of sexually transmissible diseases there is at the same order of rate as
in the USA), but AIDS is reported frequent in Africa and Latin America;
on the other hand, in the former Soviet Union neither HIV-testing nor prolonged
prophylactic use of powerful broad spectrum antibiotics are popular to
a noticeable extent; at the same time, according to [3, p.195], "in
countries within Africa, Asia, Latin America and elsewhere ... the overuse
and abuse of antibiotics ... amounts to a truly frightening crisis";
- among symptoms normally preceding full-blown AIDS, various forms of
candidiasis, including thrush, are widely met; on the other hand, infections
caused by Candida are frequent in patients subjected even to short-term
broad-spectrum antibacterial therapy, and such infections is a reliable
sign that normal microflora have been destroyed [1-4,11,12];
- most patients with AIDS suffer from severe diarrhea and weight loss;
there is no any visible link between immunodeficiency and diarrhea; at
the same time, severe diarrhea is frequent in patients whose normal microflora
of the gut have been destroyed by antibiotics ;
- drug-resistant strains of microorganisms are frequently detected in
AIDS patients, and just this drug-resistance is partially responsible for
the frequent lethal outcome of opportunistic infection incurable by antibiotics;
there is no any visible link between deficiency of the immune system and
drug- resistance of microorganisms; on the other hand, drug-resistance
is a natural consequence of natural selection of drug-resistant mutants
during long-term use of antibiotics [3,4,13-15];
- during the years 1983-1990, when incidence of AIDS was growing rapidly
in the USA, this growth was strikingly synchronous in different risk-groups;
such epidemiological feature is hardly compatible with infectious nature
of AIDS as well as with "multicausal" hypotheses (explaining
AIDS in various risk-groups by different non-infectious factors); at least
these views need quite an artificial additional postulates: either that
rate of individual- to-individual infection is almost equal in various
risk groups (infectious hypothesis) or that exposure to various non-infectious
causal factors in different risk groups was growing synchronously ("multicausal"
theories); in contrast, "destroyed-microflora" hypothesis do
not need such artificial assumptions -- because the causal factor (long-term
prophylaxis by broad spectrum antibiotics) is common to almost all HIV-positives
and AIDS patients irrespective to the risk group they belong to.
Social history of AIDS in the light of the "destroyed- microflora"
In late 1970's, long-term (self)administering of broad- spectrum antibiotics
became a popular fashion in the gay community (as a prophylactic measure
against sexually transmissible diseases), especially in its most promiscuous
segment, as well as in some groups of heterosexual population with specific
lifestyle marked by high level of promiscuity, heavy abuse of recreational
drugs, etc. Availability of new powerful antibiotics contributed much to
emergence and growing popularity of such a "fashion". The "fashion"
to use broad-spectrum antibiotics for a long time resulted in gradual depletion
of the normal resident microflora -- natural defense against bacterial
and parasitic OI. In individuals prone to more intensive "prophylaxis"
by antibiotics (mainly those with extremely high promiscuity), this process
was progressing more rapidly. Naturally, the first cases of severe OI emerged
among just these individuals (what made researchers think that an infectious
agent causes AIDS). Later, OI became to emerge in other adherents of the
The first cases of severe OI were spotted by the CDC in 1979- 1981 and
erroneously attributed to immunodeficiency as the primary biological cause.
This error had a tragic consequences: the individuals were put under long-term
prophylaxis by broad spectrum antibiotics -- just the substances by which
their condition had been caused. Naturally, such "prophylaxis"
and treatment resulted in further destruction of their normal microflora
with concomitant severe and incurable OI and frequent lethal outcome. The
wrong "AIDS = death" view was widely accepted. This caused rapid
expansion of the dubious practice to administer broad-spectrum antibiotics
as a permanent prophylaxis or treatment for individuals with some signs
of OI, CD4-lymphocytopenia, or nonspecific symptoms named pre-AIDS --thrush,
lymphoadenopathy, diarrhea, weight loss. The growing number of severe and
incurable OI, which occurred after some period of such treatment due to
destruction of normal microflora, were explained by progression of immunodeficiency
and seemed to confirm "AIDS = Death" formula.
With the promulgation of the "HIV=AIDS" formula in 1984 as
the ultimately proven scientific fact and expanding the practice of testing
for HIV-antibodies, the number of potential victims of the deadly practice
to administer broad-spectrum antibiotics as a permanent prophylaxis skyrocketed.
Any individual who demonstrated a positive test for HIV antibodies, became
a potential target for such prophylaxis. Permanent and severe psychological
stress, caused by intensive propaganda of the "HIV=AIDS = death"
formula, and toxic medication led to gradual decline of CD4-lymphocytes
in individuals with a positive test for HIV. This apparent progression
of immunodeficiency forced physicians to intensify prophylaxis by broad
spectrum antibiotics, what, in turn, led to further destruction of normal
resident microflora and made the individuals devoid of their natural defense
against OI. The rapid growth of AIDS incidence in second half of 1980s
was a natural consequence of this self-accelerating process. Unfortunately,
for most researchers, the visible link between HIV-positiveness and AIDS,
rapid growth of incidence of AIDS, and extremely high mortality seems to
be an ultimate proof that the officially accepted "HIV = AIDS = Death"
postulate is the ultimate truth.*
This work was supported by private donations from Dr. Ingeborg
Heinrich (UK). To some extent, some parts of this work were spin-offs of
a research on mathematical ecology supported by grant UAD000 from the International
Science Foundation. I thank the editorial board of "Continuum"
for permanent supply me with issues of the magazine -- the unique information
I found there had played an esential role in the birth of the "destroyed
This article is dedicated to memory of Jody Wells -- the
man who contributed much more to victory over the plague of AIDS than thousands
and thousands mainstream AIDS researchers
1. Hentges, D. (ed.), Human Intestinal Flora in Health
and Disease (New York: Academic Press, 1983)
2. Grubb, R., Midtvedt, T., Norin, E. (eds), The Regulatory
and Protective Role of the Normal Microflora (New York: Macmillan, 1989)
3. Cannon, G. Superbug: Nature's revenge. Why antibiotics
can breed disease (Virgin Publishing Ltd., 1995)
4. Lappe, M., When antibiotics fail. Restoring the ecology
of the body. (Berkeley, California: North Atlantic Books, 1986)
5. Van der Waaji, D., de Vries-Hospers, H., Colonization
resistance of the digestive tract; mechanisms and clinical consequences.
Ann Ist Super Sanita, 1986, vol.22, No 3, pp. 875-882
6. Van der Waaji, D., Mechanisms involved in the development
of the intestinal microflora in relation to the host organism: consequences
for colonization resistance. Symposia of the Society for General Microbiology,
1992, vol.49, pp.1-12
7. Wilson, K.H. and Perini, F., Role of competition for
nutrients in suppression of Clostridium difficile by colonic microflora.
Infection and Immunity, 1988, vol.56, pp. 2610-2614
8. Freter, R. Mechanisms of bacterial colonization of
the mucosal surface of the gut. In Virulence Mechanisms of Bacterial Pathogens
(ed. J.A.Roth) pp. 45-60 (American Society for Microbiology, Washington
9. Smith, H. The revival of interest in mechanisms of
bacterial pathogenicity. Biological Reviews of the Cambridge Philosophical
Society, 1995, vol.70, No 2, pp.277-316
10. Barret, J.T. Textbook of immunology. An introduction
to immunochemistry and immunobiology. Fifth edition. (The C.V. Mosby Company,
St.Louis - Washington, D.C. - Toronto, 1988)
11. Huppert, M., Cazin, J., Smith, H., Pathogenesis of
Candida albicans infection following antibiotic therapy. J. Bacteriol.,1955,
12. Odds, F., Candida and Candidosis (London: Balliere
13. Neu, H., The crisis in antibiotic resistance. Science,
1992, v.257, pp. 1064-1072
14. World Health Organization, Antimicrobial resistance.
Report of scientific working group (Geneva: WHO, 1982)
15. Cohen, M., Epidemiology of drug resistance: implications
for post-antimicrobial era. Science, 1992, v.257, pp.1050-1055
16. Urs, M., The gay community's need for "HIV".
Continuum, 1996, vol. 4, No 1, pp.16-19 (May/June 1996)
17. George, W., Sutter, V., Finegold, S., Antimicrobial
agent- induced diarrhea - a bacterial disease. J. Infect. Dis., 1977; v.136(6),