An Angina Drug Could Also Help Against This Dangerous Fungal Infection

Cryptococcal disease is among the most dangerous fungal infections. In 80% of the cases, it attacks people with a weak immune system. However, one out of five cases occurs in people who are healthy.

Current treatments for this fungal disease are very long and not that effective. But a team of Birmingham-based scientists may have found a way to make them more successful.

The Lowdown on Cryptococcal Disease

As a rule, cryptococcal disease first affects the lungs, thus causing respiratory problems. Two airborne fungi – C. gattii and C. neoformans – are the main causes of the disease. But the infection doesn’t have to remain located in the respiratory system.

When these fungi inhibit the white blood cells, they can easily move all over the body. In doing so, they can cause infections in the central nervous system, as well as the skin and bones.

This isn’t the only reason why this disease is one of the most dangerous fungal infections. It’s also much more difficult to treat than, say, a bacterial infection. That’s because fungi share many evolutionary similarities with humans. As such, they don’t have a primary metabolic pathway that a drug could target.

The Road to an Improved Drug

The researchers from the University of Birmingham have recently published their findings. They discovered that calcium-channel blockers (CCBs) could make the cryptococcal disease drugs more effective. Doctors prescribe these drugs to patients with chronic angina.

According to the researchers, these drugs can inhibit the white blood cells. Once they do, they can also destroy the harmful fungi before they can cause an infection.

Final Word

There is one minor problem with these findings. Namely, it would take an extremely high dose of CCBs to destroy the fungi. But the authors have no plans to abort their mission to beat one of the most dangerous fungal infections. They now want to see if other drugs that target calcium in the body could help against this disease.

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