At the same time when the use of antibiotics and antifungals intensified, a parallel increase in surveilling infections and infection outcomes, and equally pest control measures, can arguably result in a higher probability of resistance detection. If this were true, it might well be sufficient to explain the pattern of accelerating resistance. In fact, if this was the sole explanation, it would be reassuring. It would mean that the older the data, the higher the probability that resistance was not detected when it evolved. In support of this notion, the number of publications on antibiotic resistance is increasing year to year [13].

Many newer antibiotics and antifungals are variations on older substances. Moreover, almost all of the antibiotics are derived from natural antibiotics. Therefore, resistance evolution might become faster, because growing reservoirs of resistance genes and resistant microorganisms in the environment can cause cross-resistance [14,15]. Also, some mutations conferring resistance reduce the fitness costs of genes providing resistance against other antibiotics [16]. Moreover, antibiotic resistance, despite often being costly, can persist in the environment in the absence of the selective agents [17,18]. This applies both to the persistence of resistant bacteria as well as the persistence of antibiotic resistance genes and can be caused by several mechanisms that mitigate the costs [17] or concurrent selection, for example, by heavy metals [14] or by pesticides [19]. Finally, as resistance mechanisms against different antibiotics might be under co-selection mediated by genetic linkage [20], the increase in resistance genes, resistant microbes, and antibiotic residues will facilitate faster resistance evolution. Many of the mechanisms mentioned for antibiotics and possibly others such as increase in mutagenesis or evolution of bet-hedging almost certainly apply to antifungals as well and can be seen as combining to reduce the available genomic resistance space. The risk of emergence of resistant nontarget species of agricultural fungicides is illustrated by potential cross-resistance of Cryptococcus gattii against agriculturally used benomyl and clinically used azoles [21].

We think that each of these hypotheses, especially (2) and (3), warrants further investigation. Resistance evolution is an important challenge to healthcare and food security alike. The pattern of accelerating resistance evolution we identified here for antifungals is certainly of enough significance to motivate studies to investigate how this pattern arises and should inform ways of reversing the trend. For antibiotics, the question of whether resistance evolution is accelerating needs to be urgently addressed. Even though the original data used in several references [4–7] could not be identified for antibiotics, it is possible that the trend observed in antifungals also applies to antibiotics. We have to assume that the estimates are based on expert knowledge. And almost certainly, data must exist and await being collated to investigate this pattern. The fact that antifungals show a pattern of accelerating resistance is of high importance itself because of their critical role in food production but should also serve as a sentinel for the study of antibiotic resistance evolution.