Cryptococcus gattii

In Africa, South America, Southeast Asia and Australia, crytococcus gattii infects eucalyptus trees and bothers people with compromised immune systems, such as HIV/AIDS patients and organ transplant recipients, who inhale its spores. But the strain that was first documented on Vancouver Island, Canada, a decade ago and has now spread to Seattle and Portland causes chest pain, fever, shortness of breath and weight loss in otherwise healthy people and has killed at least six of them.

In February 2007, the first North Carolina case, an otherwise healthy man, was treated at Duke University Medical Center, the Duke researchers reported in PLoS One. In a paper they published a week ago in PLoS Pathogen, the researchers wrote that the cryptococcus gattii strain in the Pacific Northwest was new, much more virulent and favored mammals.

The second Duke paper followed on the heels of a report on human health and climate change that was authored by a group of researchers from several federal agencies. Lead author of the report was Christopher J. Portier, the head of the environmental systems biology group at the National Institute of Environmental Health Sciences in Research Triangle Park.

“The purpose of this paper is to identify research critical for understanding the impact of climate change on human health so that we can both mitigate and adapt to the environmental effects of climate change in the healthiest and most effective way,” the report from the Interagency Working Group on Climate Change and Health read.

Filling research gaps in new diseases and well-known diseases that are coming back because of altered growing seasons, more rain in some areas and droughts in others, more violent storms and rising temperatures has been on researchers’ minds for years.

In the past decades, they have identified 30 new diseases, including hepatitis C, avian flu, HIV/AIDS and severe acute respiratory syndrome, or SARS, according to a 2004 report in Nature Medicine. Environmental changes are among the reasons for the emerging diseases. But researchers have also tracked a resurgence of previously documented diseases in new geographic areas, among them tuberculosis and cholera.

The report from the federal interagency working group zeroed in on the following research areas:

• More mold, dust, pollen and air pollution are likely to increase the prevalence of airway diseases such as asthma and respiratory allergies, which already affect about 50 million Americans.
• More information is needed on how climate change affects exposure to toxins and chemicals that might boost cancers, with about 500,000 deaths per year the second leading cause of death in the U.S.
• Heat waves and rising global temperatures could increase the number of heat-related illness and death. The 2003 heat wave in Europe, for example, caused about 35,000 deaths.
• Some birth defects linked to environmental causes have been steadily increasing.
• Exposure to biotoxins from ever more frequent, harmful algal blooms and chemicals from new batteries and compact fluorescent light bulbs could boost neurological and waterborne diseases.
• By 2050, about 200 million people are expected to be displaced by the effects of climate change. The population relocation and the changes in temperatures could cause a resurgence of diseases caused by insects, such as malaria and yellow fever, which were once rampant in parts of the U.S.

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Malfunctioning mitochondria have been linked to cancer, immune defects, neurodegenerative diseases such as Parkinson’s and Alzheimer’s, sterility and deafness. North Carolina scientists have been among those on the forefront of mitochondrial research, including a group at the National Institute of Environmental Health Sciences in Research Triangle Park.

Gerald Shadel

On Tuesday, the NIEHS group hosted Gerald Shadel, a Yale University biochemist who is sort of a mitochondrion whisperer. His lab at Yale’s school of medicine tries to understand how mitochondria tell cells what to do and what happens when the communication breaks down.

“There’s a lot going on here,” Shadel said about the relationship between cells and mitochondria. “I’m going to tell you three stories.”

Mitochondria generate adenosine triphosphate, or ATP, from the food we eat and the air we breathe. ATP carries energy to, for example, power muscle cells to contract, nerve cells to generate electricity and immune cells to protect the body from disease-causing invaders.

To do its job inside of a cell, a mitochondrion is guided by its own genes. Mitochondrial DNA is passed down from mother to child and is separate from a cell’s DNA. In a way, mitochondria are cells within a cell, separate but inseparable. When the relationship goes well, enzymes inside the inner membrane make sure mitochondrial DNA is replicated correctly. When replication mistakes happen, they are repaired. The cell receives the right amount of ATP and clear signals what to do with it.

Aging is part of this cycle. It is brought on by oxidative stress. Byproducts from generating ATP, such as free radicals, cause the stress. Environmental factors can make a cell’s life a lot more stressful. Those factors include cigarette smoke, car emissions, asbestos, infections and excessive amounts of alcohol.

But when researchers in Shadel’s lab tinkered with one gene in the mitochondrial DNA, they were able to lower the oxidative stress and delay cellular aging.

Quieting down the gene’s signaling basically prompted mitochondria to burn cleaner, which damaged cells less, Shadel said. So far, researchers have successfully extended the life span of worm, yeast and mouse cells.

In another story Shadel told, things quickly go wrong in cells because of a mutation in the mitochondrial DNA that not only raises oxidative stress but also hampers mitochondria’s ability to repair replication mistakes in their genetic information.

About 400 mutations in mitochondrial DNA are known to lead to diseases. The onset of the disease appears to depend on which cells are affected. Ataxia telangiectasia is an immunodeficiency disease that affects several organs. It’s a rare disease but first signs appear in childhood. A-T is progressive and most sufferers die from recurrent infections by the time they are in their twenties.

A-T depletes the number of DNA copies in mitochondria, leading to mitochondrial dysfunction. Shadel suggested that after responding normally to initial infections, the immune system of A-T patients slowly breaks down as cells that remember immune responses to disease-causing intruders die because of the mitochondrial dysfunction.

Shadel’s lab also contributed to his third story, which dealt with maternally inherited deafness. The irreversible hearing loss is brought on by a mutation in mitochondrial DNA that affects hair cells in the inner ear. The hair cells are crucial to allow the auditory nerve to function.

But the mutation leads to a chemical signal that causes the hair cells to die, Shadel said.

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