microbe of the month: Williopsis mrakii
A beast of a yeast could banish thrush and other fungal growths, writes Bernard Dixon
Tuesday 15 August 1995
Never mind. There's news - good news - of killer yeasts instead. It comes from the University of Abertay Dundee, where Graeme Walker, Valerie Hodgson and David Button are playing a remarkable variation on the biblical theme of swords into ploughshares. They have been studying a yeast called Williopsis mrakii and have found that it produces a toxin which may prove useful in treating human infections caused by another yeast - Candida albicans. Yet this toxin is of the very type that can be a nuisance when it interferes with industrial processes such as brewing.
Killer yeasts first came to light more than 30 years ago, when researchers found that some strains of brewer's yeast, cultivated in the laboratory, secreted toxic proteins. The yeasts were immune to the poisons, which were, however, lethal to other, sensitive strains. Subsequent research showed that "wild" strains of brewer's yeast, living in the environment, were even more likely to produce the deadly proteins. Several yeasts unrelated to brewer's yeast turned out to be killers, too.
From an industrial standpoint, killer yeasts are often unwelcome, though their ill-effects are offset by good. On the one hand, the arrival of a deadly wild yeast in a brewery can signal disaster if it destroys the pedigree yeasts conducting the fermentation. Killer yeasts were a major nuisance more than a decade ago when several British companies were experimenting with continuous processes for making beer, in contrast to conventional brewing in batches. One of the problems which virtually terminated the experiment was that the carefully controlled conditions used for continuous brewing also favoured the multiplication of wild, killer yeasts if they accidentally contaminated the brew.
Killer toxins can also be beneficial to industrialists. Yeasts used to make wine in some countries produce them, thereby preventing wild yeasts, sensitive to the poisons, from taking over. Recently, the advantages of this arrangement have encouraged genetic engineers to transfer the genes responsible for toxin production into pedigree yeasts lacking them. On the other hand again, simultaneous use of both killer and toxin-sensitive yeasts in the same premises carries obvious risks.
The interest of the Dundee team in killer toxins stems in part from the fact that there is ample room for improvement in methods of dealing with disease-causing yeasts and other fungi. Speaking at a symposium in Bath earlier this year by the Society for General Microbiology (SGM), consultant microbiologist Pamela Hunter contrasted the limited range of antifungal drugs with the rise in infections of this sort over the past 20 years. Paradoxically, changes in medicine itself have caused this increase: patients have been made more vulnerable to fungal invasion as a result of cancer treatment, organ transplantation and other life-saving procedures.
Graeme Walker and his colleagues describe their own approach to the problem in this month's issue of Microbiology, the SGM's journal. They were aware of suggestions that the sensitivity of yeasts to particular killer toxins might be exploited as a means of identifying strains in the laboratory. This prompted them to go one stage further and explore the possibility that the same proteins could be valuable for treatment. So they screened 24 different yeasts, all putative killers, by exposing them to other, potentially sensitive yeasts, including samples of Candida isolated from vaginal, nasal and other swabs from patients at Ninewells Hospital, Dundee.
No less than 21 of the 24 yeasts proved to be producers of lethal toxins. The proteins varied considerably in their range and intensity of action against the sensitive yeasts. However, one particular strain of W. mrakii was highly effective against the clinical specimens of Candida and the researchers singled it out for further investigation. They found that at low concentrations, the toxin produced by W. mrakii simply prevented Candida from growing, whereas at higher concentrations, it killed the yeast, probably by damaging the membrane surrounding the cells. They believe it could, with further development, be a novel and useful agent to deploy not only against Candida but other fungi, too.
Such an innovation is certainly needed. Even the least complicated infections caused by Candida are sometimes very unpleasant. Oral thrush, for example, can cover the tongue, soft palate and inside of the mouth with a white- ish "pseudomembrane", while vaginal thrush produces a similar condition accompanied by yellow-white discharge.
Worse again, chronic mucocutaneous candidiasis may affect skin and mucous membranes throughout the body, with horn-like projections growing out of the skin. In addition, Candida can invade internal tissues, damaging the heart, kidney, lungs and other organs. This type of infection is, in principle, treatable with flucytosine, though in many cases, the fungus becomes resistant to the drug.
Candida is a great opportunist. It is invariably present on our skin and mucous membranes, and in our intestinal tract. But it is ever ready to cause disease if our normal defences are impaired, whether by some other illness or by medical intervention. It would be ironic if the key to controlling Candida were to come from killer yeasts that have themselves been notorious as destructive opportunists in industry.
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