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Most of us who live with and love dogs have quite a list of things to make us prematurely gray: vaccinating vs. over-vaccinating, Lyme-disease–carrying ticks, providing safe food (with an ever-changing lineup of antioxidants, tocopherols, omegas and probiotics) for our furry companions. With all these day-to-day concerns, canine health problems caused by a fungus may not come immediately to mind. Especially if you live in the Southwest, though, it’s definitely something to keep on your radar screen.
Though we rarely think about it, we are surrounded by fungi. They decompose our dead organisms, brew our beer and help produce antibiotics. But some are not so helpful—for example, Coccidioides immitis, the fungus that found its way into our dog Hunter.
Coccidiodomycosis is the medical term for the systemic infection caused by this fungus; the more common name is valley fever, or desert rheumatism. The southwestern United States—from California to central Texas and into Mexico, particularly in the ecological niche known as the Lower Sonoran life zone—provides the fungus with the conditions it needs to survive. It grows several inches deep in the soil and spreads with the help of burrowing rodents. Add some wet weather, wind and dust storms, and this filamentous mold can travel great distances, right into some unsuspecting vertebrate’s lungs or open wound.
In fact, fewer than 10 inhaled arthrospores (fragments of the original fungus) are sufficient to cause the disease in susceptible animals, according to the authors of The 5-Minute Veterinary Consult. Many dogs who are exposed (up to about 60 percent) will be asymptomatic or develop self-limiting upper respiratory tract infections; in about 40 percent, the infection will develop in the lower respiratory tract. Rarely, in susceptible individuals, it may spread (disseminate) from the lungs to other organs. Diagnosis of the disseminate form can be tricky, as the symptoms range from bone swelling and joint enlargement to neurological dysfunction and ocular disease.
Hunter was in that small percentage of susceptible individuals. When we found him in the middle of traffic in the Mexican town of Rosarito, he had a large head wound and, as it turned out, would need more than a few bowls of healthy food and a bath to get back on his feet. He dragged his back legs, was obviously in pain and didn’t have much of an appetite. When our veterinarian suggested that he might be suffering from valley fever and showed me the radiographs, I was appalled: His bones were being consumed little by little—osteolytic lesions are typical of disseminate valley fever in dogs.
Hunter was helped by fluconazole, which we gave him for more than a year. Little by little, he regained function in his back legs. As he began to feel better, he also learned to swim in the glorious dog beaches of San Diego and eventually even learned to tolerate (well, most of the time) his canine “siblings.” Today, Hunter is a relatively happy, strong dog who is probably somewhere around five years old. He takes supplements daily to aid with pain and arthritis, loves to lie in the sunshine and adores people. He eats well and was declared at least temporarily fungus-free on our last trip to the vet. Of course, this is no guarantee that the fungus is gone; much of the literature on the disease warns that a negative test result may only mean a temporary abatement of the problem.
Certain breeds seem to be more susceptible than others to the disseminated form, and male dogs are more prone to it than females. Research into a vaccine that will protect both humans and animals from valley fever  is in progress, and at the Valley Fever Center for Excellence  in Tucson, Ariz., scientists are attempting to determine the natural incidence of the disease among dogs in that region. It appears hopeful that we will be able to control just how much this fungus remains among us. And then we can all get back to worrying about which tocopherols to sprinkle on our dogs’ food in the morning.
Illustration by Ken Orvidas