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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)
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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, syphliis, 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 200,1 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 a'nd viruses like boma 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 psychiatricpatients following treatment for parasites." In fact, .a review of 1300 human cases of trichinosis In Germany found CNS (central nervous system) invoivement in up to 24% of the cases (Mennlngeallnflamation or encephalitis). [Ref: Froscher]

Clinically, in cases likeneurocystlcercosls, 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 underreportlng (neurocysticercosis 'is not a reportable condition in most states and the incidence Qf trichinosis' is, we believe, vastly underestimated according to newly developed antibody assays only made available in 2003).

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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. gondli 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 transcrlptase 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 Director 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 colnfections before deciding on an appropriate course of treatment.

Finally, while toxoplasmosis gets a.lot of attent!on 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