Hey All Y'all! I know I post infrequently, but would like to announce the Human Pathogens within the Dimorphic Onygenales meeting in conjunction with the GSA sponsored Fungal Genetics meeting at Asilomar, Pacific Grove, CA. #GSA #FGC2015 @DrValleyFever One month left to register!


Video from KVIE

A face to the disease.

Occupational exposure

Well, this just came across my desk today - Occupation exposure among cast and crew. It brings up several interesting aspects- number one being, I wish I knew who the actor was! Maybe we could have a spokesperson for VF! Other than that selfish response, I think it also highlights a great source of data that is only available in California. No other state considers coccidioidomycosis as a work related injury. I imagine these are not the only cases of cluster infections, but it seems that it would be really helpful to follow more of these exposures, and combine with our soil analysis. I'll be reporting more on soil work, as my lab just got funding to expand theses studies and my hope is that we will have a very robust and scalable application for environmental detection.


CSG 2014

Forgot to mention the annual Coccidioidomycosis meeting that happened weekend before last. It was very well attended, with some higher profile researchers giving talks. After the main meeting on Saturday, we had a gathering of folks interested in Cocci in the soil. Will post more info as it becomes available. For now, we are developing a linked in group. Comment or email to request joining.


More VF in the news

Another recent article on Daily Beast about Valley Fever. It goes on tho talk about the disease as a silent epidemic. It supports my previous post/update on why we need more basic research on this organism. It is undeniable that the disease burden has increased over the last 20 years- and we have no idea why. The recent drought, at its most extreme in the San Joaquin Valley (the "Valley" in VF) could increase conidia (aka spores) in the air/soil...or not. We don't have a good handle on the organism's biology or natural host. So, no idea if the CA drought will increase VF. We also don't understand why SOME people have such severe cases of VF. Is it fungal pathogenicity or human susceptibility? Or both? Or is it just dosage? Again, NIH willing, I hope to answer some of these questions! From another recent article, "Diseases that don't have a high profile also struggle for funding. Consider this: In the past 12 years, the National Institutes of Health has granted valley fever just 4 percent of the research funding it has directed toward . But valley fever has afflicted about four times more people than West Nile, with thousands more going undiagnosed. Valley fever has killed many more people, too." After getting a really crappy comment on our recent grant "only 4000 people have died form the disease" it makes me a bit irritated that the funding is so skewed...


Found this paper today. Not sure how I missed this one!

1982 research on Cocci epi Interesting 22 year study to determine conversion and dissemination for coccidiodomycosis. #fungi #coccidioides

Impact of coccidioidomycosis in California

New yorker article about Valley fever

oldie but goodie

This is a good article!

UPDATE 2014!

Yep. Been ages since posting. Updates include a new assistant professor position at NAU/TGEN-north in Flagstaff. Loving life! Coccidioides is now my main focus and we are working on a number of fronts. 1) Understanding innate immunity in early infection. Coccidioides plays this crazy game with ?resident aveolar macs? (we assume) wherein it seems to go completely undetected by the immune system in the first 4 days of infection. Meanwhile, it is growing and dividing within the cell wall, making a giant (80-120 microns!) spherule. Once it is mature (full of "mini-mees" aka endospores) it ruptures open. And then all hell breaks loose. Literally. The immune system goes CRA-CRA. Massive inflammation and tissue damage. Tons of neutrophil influx. But why nothing in the frst 4 days? Or is there something, we jsut don't see it? Perhaps the fungus actively supresses the host? All great questions, and we've submitted 2 grants to try to answer this question. 2) Understanding the effect of hybridization and introgression on pathogenicity. This is my bread and butter right now. This really cool finding from the genome work I did for my PhD has been gnawing at me, demanding further attention. This is the basis of my funded K22 grant from the NIH. We are just TODAY looking at RNA seq data from the first mouse infection and so far so good! We are finding some Coccidioides RNA in the lungs, and were able to do some real time PCR to detect some VERY INTERESTING patterns in the data that may help to explain observations in #1. 3) What the heck is going on in the soil? Another one of the main questions we have is "where the heck is this organism growing in the environment?" The disease is only acquired from the environment. There are weird cases of transmission from infected tissue in a transplant and contaminated dressings where the spherules in the body returned to being mycelia, but these are exceedingly rare. Basically everyone that gets sick inhales the spores from the soil. Despite a lot of work that has gone one, very little is know about where and when the organism is actively growing in the soil (never say dirt. I've learned this detail from USGS folks, lol). We have some ideas of course, but working on getting some funding to pursue this as well. Nothing like a great mystery to keep life interesting! OK! That's my update. I'll also post some links to recent articles about Cocci.