The Role of Infections in Mental Illness

by Frank Strick, Clinical Research Director

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).

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