Nosocomial infections are those infections which develop more
readily in a hospital environment. Such infections are those which
are not present in the patient at the time of admission but develop
during the time in hospital, and are found at the time or soon
after discharge from the hospital. Such infections include bacterial
and fungal infections, aggravated by conditions which favour cross-contamination,
and by resistant strains of bacteria. The term includes infections
developed or carried by hospital staff.
The most prevalent type of nosocomial infection in England, where
the rate of infection is high at 9 per cent, is MRSA, Methicillin
(or Multiple) Resistant Staphylococcus Aureus. In England these
infections affect over 100,000 hospital patients per year and
kill over 5000 of them. Some medical commentators have put the
true figures at up to four times greater than this.
These hospital acquired infections arise through the urinary
tract (23 per cent), the lungs (22 per cent), wounds (9 per cent)
and blood (6 per cent). The surprising fact is that the infections
are not mainly surgical site infections, but arise from person-to-person
contact and procedures in the ward.
In the general population outside the hospital setting Staphlococcus
Aureus, whether resistant to antibiotics or not, is a very common
bacteria, present on human skin and in the nose, which does us
no harm. So we simply need to analyse why this bacteria, which
has been with us throughout human history, has recently become
an easily transmitted killer in our hospitals.
Many reports and initiatives have concentrated on greater hospital
cleanliness, barrier nursing and the development of new antibiotics
and bacteriophages. These are important, but none of the reports
have looked at the most likely reason for an otherwise harmless
bacteria becoming a deadly person-to-person transmitted killer.
The most likely reason is the loss of innate immunity.
We know that the miliaria class diseases described elsewhere
on this website are very prevalent in the population in general,
and particularly in older people. It follows that miliaria class
diseases will be very prevalent in persons admitted to hospitals.
Many of the hospital staff may also have miliaria class diseases
such as hypertension, cellulite, eczema, asthma, diabetes, and
obesity. With all of the current treatments for these diseases
aimed at the symptoms only, in hospitals we may have an enclosed
community of untreated miliaria sufferers.
Miliaria in patients is further exacerbated by their being fairly
immobile in warm beds and eating a high carbohydrate diet.
If we take a typical case of a person over fifty with diabetes,
or even slightly raised blood glucose, the person will undoubtedly
have miliaria of the lower legs. There will be an absence of skin
insensible perspiration as the sweat gland ducts are blocked by
miliaria disease. In the absence of sweat of the correct salinity
the normal skin anti-microbial peptides do not function.
We should therefore assume that in such a case the skin of the
lower legs has completely lost its protective function. In infective
terms, it is as if the person is lying in the hospital bed with
raw exposed flesh. Would any doctor or nurse handle the legs of
this patient if they knew there was no innate immunity?
We can see how easily person-to person infection occurs. It is
not only any part of the skin that is involved. The interior of
the nose, the mouth, the intestinal tract, the lungs, and any
other mucosal surfaces are subject to miliaria. Infections are
just as likely to be carried between persons with miliaria class
diseases through the air, via food or during physical examinations.
Miliaria arises from the action of the ducts in the body in conserving
excess sodium and chloride when they are habituated to do so.
This starts when the flow of sweat or mucus or other liquid solution
through ducts is faster than usual. If the faster flow continues
for a time, the excess conservation becomes fixed at a higher
level by adverse habituation. This adverse habituation is more prevalent in the lower legs as these are seldom exercised enough to keep the sweat ducts in condition.
The sodium content of the fluid
is lowered and normal anti-microbial peptides become ineffective.
The immune reaction to the presence of microbes blocks the duct.
This adverse habitutaion can be changed back to original habituation
by the use of ActiveSignalTM Sodium. This signals the
presence of sodium and so switches off the over conservation by
the duct.
ActivSignalTM therapeutic products are not absorbed into the
body and so have a predictable action without side effects.
The first commercial ActivSignal product is now under development.
In order to provide the best possible protection against nosocomial
infections, it is highly desirable that both patients and staff
take simple precautions against miliaria class conditions.
As we have seen, if there is even slight hyperglycaemia and therefore
hyponatremia, then the apparent lack of sodium in the body prevents
the resetting of the ducts to normal original habituation. Glycaemia
can be lowered to normal by a low carbohydrate diet and exercise.
In addition anti-diabetes drugs may be used to
lower glycaemia.
Precautions against over conservation of sodium and to restore
euglycaemia have such huge benefits for the health of people,
particularly those living in advanced societies, that it must
be hoped that they will undertake treatment against miliaria class
conditions well before the need to enter hospital arises.