Microbes And Mental Illness

Microbes and Mental Illness

By Robert C. Bransfield, M.D.


Microbes are the greatest predator of man. As medical
technology improves, there is increasing recognition that infectious
disease contributes not only to acute, but also chronic relapsing
illness and mental illness. The evidence to support this is a
combination of insights from theoretical biology (particularly
Darwinian medicine), research, and direct clinical observations.

We lead our entire lives surrounded by microbes. In a
state of health, there is a balance, a reasonable resistance to
infectious disease, and a peaceful co-existence. In contrast, with

infectious disease, there is an imbalance between the threat posed by
microbes and host defenses. This balance is affected by environmental
factors (including exposure to pathogens) and a number of host factors
such as genetics and/or increased vulnerability as a result of a state
of chronic stress. Although the stress response is adaptive in a short
time frame to allocate resources during a crisis, if the stress
response is persistent, rather than cyclic, it further increases
vulnerability to disease.

The most common sequence of disease begins with a
vulnerability and an exposure to one or more stressors. The
vulnerability may commonly include genetic and/or increased
vulnerability as a result of chronic stress. As a result of these and
other vulnerabilities, the microbe more easily penetrates the host's
defenses and an initial infection may then occur.

Although infection may occur from microbes that are always
present in the environment, a greater number of organisms or more
virulent organisms further increase risk. Acute infections are most
noteworthy in general medicine. However, the course of the infection
most relevant to psychiatry includes injury from a prior infection;
chronic, low-grade, persistent relapsing infections; or the
persistence of the infectious agent in the inactive state. When
persistent, relapsing infection occurs, there may be extended period
of latency followed by some triggering event(s) (i.e.: chronic stress,
injury, surgery, or other infectious agents), which may then cause the
activation of the infectious agent(s) and the progression of the
pathological process.

Some injury in infectious disease is a result of toxic
products or direct cell injury, but a significant amount of injury is
a result of host defenses gone awry in response to the infection.
Neural injury may occur by a variety of mechanisms, which include
vasculitis, direct cell injury, toxins, inflammation, cytokines,
autoimmune mechanisms, incorporation of parasite DNA into host DNA,
and excitotoxicity. This injury leads to a vicious cycle of disease,
resulting in dysfunction of associative and/or modulating centers of
the brain. Injury to associative centers more commonly causes
cognitive symptoms, while injury to modulating centers more commonly
causes emotional and allocation of attention disorders.

Psychiatric syndromes caused by infectious disease most
commonly include depression, OCD, panic disorder, social phobias,
variants of ADD, episodic impulsive hostility, bipolar disorders,
eating disorders, dementia, various cognitive impairments, psychosis,
and a few cases of dissociative episodes.

In clinical experience, the link between infectious
disease and psychopathology has been

an issue with Lyme disease, syphilis, babesiosis, ehrlichiosis,
mycoplasma pneumonia, toxoplasmosis; stealth virus, borna virus, AIDS,
CMV; herpes, strep and other unknown infectious agents. In the
collective database of patients demonstrating psychiatric symptoms in
response to infectious disease, the majority of the cases has been
infected by ticks. Aristotle referred to ticks as "filthy disgusting
animals" (1). They spend their lives living in dirt, feeding on the
blood of mice, rats, and other wild animals (2). When they bite
humans, they pose a risk of injecting an infectious cocktail of
pathogens into the host.

Patients with psychiatric symptoms from tick-borne
diseases are most commonly infected by Borrelia burgdorferi, (Bb) the
causative agent of Lyme disease and quite often other coinfections-
infections. There is an increasing recognition that many chronic
relapsing infections are complex interactive infections in which
microbes interact with each other in a manner that contributes to the
disease process. The models most commonly discussed are coinfections
associated with HIV and tick-borne coinfections. For example,
coinfections associated with Lyme disease may be acquired at the same
time, before or after the Bb infection. Interactive infections,
however, is a more accurate term than coinfections, since these
infections invariably cause an interaction that changes the disease
process.

To understand coinfections, we need to begin by defining
each disease separately. This,

of course, is an area of much controversy in regard to late stage
chronic relapsing Lyme disease. A similar controversy exists in regard
to other chronic infections. It is difficult to explain how
interaction occurs when there is such disagreement defining the
clinical syndrome and pathophysiology associated with each infection
separately.

A couple of years ago, other tick-borne diseases were not
considered to be very significant in contributing to chronic,
relapsing Lyme disease. Once there was a greater focus upon these
organisms, it became clear that coinfections were a significant issue.
We can better understand chronic, relapsing diseases such as Lyme
disease by taking a closer look at interactive coinfections, host
vulnerability, and host response that contributes to the disease
process.

Some very interesting work is being done to better
understand the role of interactive coinfections between Bb and stealth
virus, Candida, Babesia, and Ehrlichia. For example, stealth virus
facilitates lipid production which facilitates Bb growth (3), Bb is
protected from host defenses inside Candida cells (4), Babesia causes
immunosupression, and Ehrlichia causes bone marrow suppression.

In summary, the complexities of these issues teach us
humility. To better understand the

clinical syndrome associated with these infections, internists need to
recognize the significance of mental symptoms in chronic interactive
infections and psychiatrists need to better appreciate the role of
microbes in causing mental illness.



(1) Adapted from Burrascano, J., The New Lyme Disease
Diagnostic Hints and Treatment Guidelines for Tick-Borne Illness, l2th
Edition, copyright 10/98.

(2) Burgdorfer, W.B., Increased Evidence of Mosquito/
Spirochete Associations; 11th International Scientific Conference on
Lyme Disease and other Spirochetal & Tick-Borne Disorders.

(3) Discussion with Dr. John Martin

(4) Discussion with Dr. Linda Mattman


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