The Role of Infections in Mental Illness

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The Role of Infections in Mental Illness

 

by Frank Strick, Clinical Research Director

THE RESEARCH INSTITUTE FOR INFECTIOUS MENTAL ILLNESS (RIIMI)

Call 1800 6992466 then press pound (#) 8314255555

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San Francisco, USA

Other Notes: They serve clients world-wide via phone consultations.

 

In considering an infectious etiology to any chronic mental illness

there are at least four categories to consider. First are those

infections already recognized to induce psychiatric symptoms. These

include pneumonia, urinary tract infection, sepsis, malaria,

Legionnaire's disease, syphilis, typhoid, diphtheria, HIV, rheumatic

fever and herpes. (Ref: Chuang)

 

While the psychiatric effects of these infections are known to the

medical field, they are rarely screened for if the initial

presentation is made to a mental health professional. Moreover, the

significance of some of these infections may date back to prenatal

development. Research done at the John Hopkins Children's Center and

published in the Archives of General Psychiatry in 2001 found that

mothers with evidence of Herpes Simplex Type 2 infection at the time

of pregnancy had children almost six times more likely to later

develop schizophrenia. And in the US, Europe and Japan, birth clusters

of individuals who develop schizophrenia later in life closely mirror

the seasonal distribution of Ixodes ticks at the time of conception

(Lyme disease).

 

Second are those parasitic infections such as neurocysticercosis where

the brain is directly invaded by the infective agent through a

well-established, imageable (visible on brain scan) mechanism (cysts,

lesions, cerebral swelling etc.) Signs of psychiatric disease

(depression and psychosis) were found in over 65% of

neurocysticercosis cases (caused by a tapeworm whose incidence in the

US is rising due to demographic increases in foreign immigrant

populations.) [Ref: Forlenza] While the mechanisms for psychiatric

manifestations are easy to demonstrate when brain tissue is directly

affected, there are also multiple documented reports in the literature

of psychiatric symptoms associated with other parasites like

giardiasis, ascaris (roundworm), trichinae (cause of trichinosis), and

Lyme borrelia and viruses like borna virus. Documentation also exists

of these psychiatric symptoms resolving when the underlying hidden

infection is treated.

 

Dr. J. Packman of Yale University wrote over ten years ago that

" Patients with parasitic loads are more likely to exhibit mental

status changes and there is an improvement in mental status of a

subset of psychiatric patients following treatment for parasites. " In

fact, a review of 1300 human cases of trichinosis in Germany found CNS

(central nervous system) involvement in up to 24% of the cases

(Menningeal inflamation or encephalitis). [Ref: Froscher]

 

Clinically, in cases like neurocysticercosis, the problem is not the

lack of a well-defined mechanism but the lack of mental health

practitioners qualified to make such a diagnosis or even suspect it.

Even infectious disease specialists tend to underestimate the scope of

the problem, in part due to underreporting (neurocysticercosis is not

a reportable condition in most states and the incidence of trichinosis

is, we believe, vastly underestimated according to newly developed

antibody assays only made available in 2003).

 

Next are those parasitic, bacterial and viral infections like

toxoplasmosis and strep where a strong statistical link to mental

illness has been demonstrated but research is underway to establish a

causal connection. In humans acute infection with toxoplasmosis gondii

can cause brain lesions, changes in personality and symptoms of

psychosis including delusions and auditory hallucinations. Researchers

at Rockefeller University and NIMH have suggested that after

streptococcal infection some children may be at increased risk for

Obsessive Compulsive Disorder. Toxoplasma gondii can alter behavior

and neurotransmitter function. Since 1953, eighteen out of nineteen

studies of T. gondii antibodies in persons with schizophrenia and

other severe psychiatric disorders have reported a higher percentage

of T. gondii antibodies in the affected persons. (For example, in one

large study toxoplasmosis infection was twice as common in mentally

handicapped patients as in healthy controls and in a recent German

study of " individuals with first episode schizophrenia compared to

matched controls, 42% of the former compared to just 11% of the latter

had antibodies to toxoplasma " ).

 

Two other studies found that exposure to cats (the primary carrier for

toxoplasmosis transmission) in childhood is a risk factor for the

development of schizophrenia. Furthermore, certain antipsychotic and

mood-stabilizer drugs such as Halperidol and Valproic acid inhibited

this parasite in vitro at a concentration below that found in the

cerebrospinal fluid and blood of individuals being treated with this

medication, suggesting that some medications used to treat

schizophrenia and bipolar disorder may actually work by inhibiting the

replication of toxoplasmosis gondii. (Ref: Jones-Brando, Torrey, Yolken)

 

Other studies have shown that antipsychotic drugs like Thorazine,

Haldol and Clozapine inhibit viral replication and that the

cerebrospinal fluid of patients with recent-onset schizophrenia shows

a significant increase in reverse transcriptase (an enzyme) activity -

which is an important component of infectious retroviruses (a type of

virus). Furthermore, when the CSF (cerebral spinal fluid) from these

patients was used to inoculate a New World monkey cell line there was

a tenfold increase in reverse transcriptase activity which suggests

the presence of a replicating virus. Malhotra has demonstrated the

absence of CCR5-32 homozygotes (specific matching genetic codes) in

over 200 schizophrenic patients - which dramatically increases

susceptibility to retroviral infection. (Ref: F.Yee).

 

It is research like this that has led Johns Hopkins virologist Robert

Yolken and psychiatry professor and former special assistant to the of the National Institute for Mental Health Dr. E. Fuller

Torrey to believe that toxoplasmosis is one of several infectious

agents that causes most cases of schizophrenia and bipolar disorder.

The idea is not new. In fact, as far back as 1922 the famous

psychiatrist Karl Menninger hypothesized that schizophrenia was " in

most instances the byproduct of viral encephalitis. " Torrey notes that

in the late nineteenth century schizophrenia and bipolar disorder went

from being rare diseases to relatively common ones at the same time

that cat ownership became popular. And Yolken designed a retrospective

study of twenty-five hundred families showing that mothers of children

who later developed psychoses were 4.5 times more likely to have

antibodies to toxoplasmosis than the mothers of healthy controls. Due

to the frequency of cat ownership, a large percentage of the US

population (up to 50%) has been exposed to toxoplasmosis but most

immunocompetent carriers remain asymptomatic until another

immunological burden such as HIV or a separate parasite weakens the

host defenses and precipitates pathogenic expression. That is what

makes interpretation of the chronic state so tricky and at the

Research Institute for Infectious Mental Illness we make sure to try

to identify any parasitic coinfections before deciding on an

appropriate course of treatment.

 

Finally, while toxoplasmosis gets a lot of attention due to Torrey's

and Yolken's pioneering studies and the known mechanism of brain

lesions, there are many other infective agents that may not target the

brain specifically but can severely affect mental function through the

cumulative downstream consequences of chronic infection. While the

importance of this link in the etiopathogenesis of mental illness is

rarely recognized, these focal and systemic infections are very common

and their psychiatric effects often severe. (Parasites are the most

common causes of mortality and morbidity in the world.) In this

nonspecific category are scores of parasites, protozoa, helminths,

bacteria, fungi and viruses which, if not directly invading and

disabling brain tissue and neurotransmitter function, do so indirectly

by depleting the host of essential nutrients, interfering with enzyme

functions, and releasing a massive load of waste products - enteric

poisons and toxins which disrupt brain metabolism. (A single mature

adult tapeworm can lay a million eggs a day and roundworms, which

infect about twenty-five per cent of the world's population, lay

200,000 daily).

 

Remember, the brain is your body's most energy-intensive organ. It

represents only three percent of your body weight but utilizes

twenty-five percent of your body's oxygen, nutrients and circulating

glucose. Therefore any significant metabolic disruptions can impact

brain function first. This link is borne out statistically. Mental

patients have much higher rates of parasitic infection than the

general population. Between 1995 and 1996 researchers at the

University of Ancona did stool tests on 238 residents of four Italian

psychiatric institutions and found parasites in 53.8 percent of the

residents including all of those residents with behavioral

aberrations(Ref: Giacometti). In our experience parasites are often

implicated in cognitive dysfunction and chronic emotional stress

disorders and, to the untrained eye, classic symptoms like apathy,

exhaustion, confusion, appetite and memory loss, " nervous stomach, "

social withdrawal, lethargy and loss of sex drive and motivation are

frequently assumed to signal a depressive disorder without an adequate

differential diagnosis being made or even attempted. Adding to the

confusion, classic indicators of acute infection such as fever or

elevated antibodies often reverse themselves in chronic cases due to

secondary hypothyroidism and immunodepression. Unfortunately, until

Western psychiatry further recognizes that the mind/body connection

goes in both directions patients will continue to suffer from a de

facto lack of differential diagnostic criteria in clinically identical

syndromes.

 

Even for those clinicians who recognize the devastating psychological

effects that chronic intestinal, focal and even dental infections can

have on normal brain function, accurate diagnosis presents formidable

challenges. In fact some standard parasite stool test procedures

identify less than ten percent of active infections and even the

" politically correct " holistic specialty labs miss many infections

that are nondetectable in fecal specimens, have inconsistent shedding

patterns, are extra intestinal or otherwise hard to identify. For

example, according to the World Health Organization, over two billion

people are infected with worms, yet rarely will they show up in stool

assays.

 

(These numbers are not surprising once you realize that the exposure

vectors are potentially everything you eat, drink, breathe and touch.

If you think you have to leave the country to be exposed to exotic

parasites, think again. In fact, try walking into the kitchen of your

favorite restaurant and see if the cook speaks English.)

 

At the Research Institute for Infectious Mental Illness we use

multiple labs with complementary strengths and a combination of

advanced scientific diagnostic procedures including O & P microscopy,

multifluid antigen and antibody detection, stool cultures, enzyme

immunoassay, mucosal markers, inflammation assays, imaging techniques

and other indirect laboratory indicators combined with extensive

historical and clinical evaluations to identify chronic infectious

stressors. (Patients previously diagnosed with " Chronic Candidiasis "

often find that Candida was merely a cofactor or consequence of more

significant infections and infestations which created obstacles to

long-term cure.) " Mental " symptoms often improve dramatically when

hidden neuroimmune infections are treated successfully and normal

brain metabolism resumes, especially in " sudden-onset " syndromes.

After identifying and treating the primary infections we focus on

rebuilding the host's immunological defenses and mucosal integrity to

prevent relapse. Premature nutritional supplementation, even in frank

anemia, can be counterproductive since some vitamins and minerals

(e.g., iron) can be growth factors for microorganisms which the body

intentionally downregulates the uptake of during active infection. But

individually formulated subsequent nutritional supplementation is

usually essential for full recovery. We also screen patients for heavy

metals, environmental chemicals, molds and electromagnetic stressors,

" Brain allergies, " food sensitivities, hormone disorders, diet and

numerous other variables which can influence cognitive and affective

function. To speed recovery, our evidence-based Integral Medicine

approach may include appropriate treatments from consulting

nutritionists, homeopaths, acupuncturists, herbalists and bodyworkers.

 

The erosion or loss of brain function is arguably the most frightening

and disabling experience a person can have. Almost by definition,

standard psychological or psychiatric intervention postulates a

dichotomy between disorders of the body and those of the mind and has

a long way to go in recognizing the importance of infectious

etiologies in mental health care. The Research Institute for

Infectious Mental Illness provides testing, clinical and consulting

services to clients from all over the world and educates professionals

in this critical area. Long distance phone consultations are also

available.

 

This article may be reprinted by anyone if the RIIMI clinic contact

info is listed.