Toxoplasma gondii, a common parasite and one transmitted through cat feces, was seen to inflame the prostate in mice in a persistent and progressive manner, a study published in the journal The Prostate reports.

The study is titled “The common parasite Toxoplasma gondii induces prostatic inflammation and microglandular hyperplasia in a mouse model.”

Prostatic inflammation is a possible cause of diseases like benign prostatic hyperplasia (BPH) and prostate cancer, both common in older men.

Factors known to inflame the prostate include certain viruses, bacteria and steroids, as well as environmental and dietary factors. However, scientists aren’t sure of the particular role each factor plays in promoting prostatic inflammation. T. gondii, which infects most mammals, is present throughout the world; infection rates reach 80 percent in some countries.

Once people are first infected with T. gondii, the parasite rapidly divides in the body and causes toxoplasmosis, which leads to mild flu-like symptoms. Eventually, T. gondii becomes a lifelong infection as it stays silently in the body in the form of a tissue cyst called a bradyzoite. Since it causes its host no harm, T. gondii has not received widespread scientific attention.

In an effort to induce inflammation, researchers infected male mice with T. gondii and determined inflammation by analyzing two factors. First, they looked at the number and severity of infiltrating immune cells into the prostate, which is the main characteristic of inflammation. Second, they studied the proliferation of epithelial cells, which line the prostate and may lead to BPH and, possibly, prostate cancer.

Results showed that T. gondii infected the mouse prostate within the first 14 days of infection and established bradyzoite tissue cysts for at least 60 days. This infection caused a substantial inflammatory reaction in the prostate as well as reactive hyperplasia. This refers to the formation of multiple layers and the abnormal appearance of prostate epithelial cells, accompanied by the infiltrating inflammatory cells.

This study was the first to demonstrate that T. gondii can trigger prostatic inflammation in any species. As a result, researchers developed a new mouse model to study prostatic inflammation without the need to genetically manipulate the mice — lending greater credibility to the results.