John Robson’s interesting article below reminded me of a biology class at UCFV. One day my biology instructor, Donna, was telling us about a new strain of late blight of tomatoes (and potatoes)  Phytophthora infestans.  She said with intense excitement, “Class!  We are seeing evolution in action, right before our eyes!” She went on to talk about the alarm being expressed at the BC Ministry of Agriculture because we had a vibrant and world-class tomato greenhouse industry that we fought to protect from the virus.  And now a Mexican was threatening to mate with a BC virus and destroy our very lucrative export product.

 I loved this woman’s classes.  She brought a bright, energy and enthusiasm into every lecture she gave.  After class I posed this question to her, “If Madonna should go to Australia and marry an aboriginal pygmie,  they could have a wonderful baby, who, given a good education and upbringing, could become an Oxford lecturer,……..right?”  Donna thought about that for all of half a second and said, “Yes, that is right.”  We talked about the mixing/mating of ‘late blight’ genes a bit more and she agreed that there was no evolution happening there, in the sense it is so easily used.  The bacteria were producing bacteria that were producing bacteria……..No change at all from one kind of life form to another kind of life,…. able to reproduce itself.

Human beings mate and exchange genes and produce their new offspring, (baby) but the offspring remains fully human, and can live to reproductive age and keep mixing up the gene pool.  But they will never give birth to a more complex child that adds a brand new feature to pass on to subsequent generations.  What we see a steady stream of is, THE LOSS of information, and the transference of DEFECTIVE information.  We never see in an increase in beneficial, more complex information.

I can hear folk say that scientists of the future will be able to do any number of things to human life, in the lab.  If so, will you dare call that unguided, natural processes, NO INTELLIGENCE REQUIRED?  –   Gerda

Late blight of potatoes and tomatoes, the disease that was responsible for the Irish potato famine in the mid-nineteenth century, is caused by the fungus-like oomycete pathogen Phytophthora infestans. It can infect and destroy the leaves, stems, fruits, and tubers of potato and tomato plants. Before the disease appeared in Ireland it caused a devastating epidemic in the early 1840s in the northeastern United States.

P. infestans was probably introduced to the United States from central Mexico, which is its center of origin. After appearing in North America and Europe during the 1840s, the disease spread throughout most of the rest of the world during subsequent decades and had a worldwide distribution by the beginning of the twentieth century.

Severe late blight epidemics occur when P. infestans grows and reproduces rapidly on the host crop. Reproduction occurs via sporangia that are produced from infected plant tissues (Fig. 1) and is most rapid during conditions of high moisture and moderate temperatures (60°-80°F). Sporangia disperse to healthy tissues via rain splash or on wind currents. Reproduction is asexual; each sporangium is an exact copy of the one that initiated the parent lesion, and each can initiate a new lesion.

Late Blight Collage1

Phytophthora infestans affects several different plant species and has the potential to cause devastating disease almost everywhere potatoes are grown. It is also a serious pathogen on tomatoes in cool, wet climates. In central Mexico it is a parasite or pathogen of many different wild Solarium species. In Canada and the United States P infestans has been reported to infect hairy nightshade (Solanum sarachioides), bittersweet (S. dulcamara) and Petunia (Petunia hybride) in addition to potatoes and tomatoes. In South America it has been reported as an important pathogen of pear melon (Smuticatum).

Recent Introductions of Exotic Strains

During the early 1990s several exotic strains of P. infestans were introduced from Mexico. These strains have increased the severity of late blight on potato and tomato because they are more aggressive than earlier ones in the United States and Canada. They initiate infections more quickly and reproduce more profusely, causing epidemics to occur rapidly. To combat these strains it is necessary to use more resistant potato and tomato cultivars or to use fungicides more intensively. Unfortunately, resistance of potato foliage and stems is not necessarily related to tuber resistance. For example, though the foliage of the cultivars Allegany and Elba is moderately resistant, the tubers are quite susceptible.

Late Blight Photo Collage #4

Figure 8. Green tomato fruits infected with P. infestans. The pathogen is sporulating from the infected fruits. (photo: T. A. Zitter)

Figure 9. Potato stem infected with P. infestans.

Figure 10. Infected tomato plants with lesions on stems and foliage. (photo: T. A. Zitter)

Disease development (growth and reproduction of the pathogen) is favored by moderate temperatures (60°-80°F) and wet conditions. It can develop in very warm daytime temperatures (ca. 95°F) if conditions are extremely wet and night temperatures are moderate (60°-75°F). Epidemics can be rapid and devastating because of the high reproductive potential of this pathogen. Individual lesions can produce 100,000 to 300,000 sporangia per day. Each sporangium is capable of initiating a new infection that will become visible within three to four days and produce sporangia within another day or two under optimal conditions. Thus rapid reproduction of the pathogen and destruction of leaflets can defoliate potatoes or tomatoes and completely destroy healthy fields in a short time (Figs. 11-13). Such epidemics result from many sequential cycles of infections: every lesion produces many sporangia, each of which can be dispersed to a new leaflet to initiate a new infection, which in turn can produce many sporangia, and so on.

Tubers may be infected by P. infestans whenever sporangia and tubers come into contact, from early in the tuberization process until harvest. Infections most commonly occur when sporangia are washed from lesions on stems and foliage to the soil and then through the soil to tubers. Infections can occur on developing or mature tubers, but contact between tubers and sporangia is more likely when the tubers are enlarging; tuber enlargement creates cracks in the soil and gives sporangia ready access. Tubers become infected most often when soils are cool and wet (near field capacity); soil temperatures higher than 65°F seem to suppress infections. Because sporangia can survive days or weeks in soil, tubers can become infected for a period of time after infections in the foliage are no longer producing sporangia.

Tubers infected by late blight are especially susceptible to soft rot. If some tubers in a crop are infected, store the crop in cool, dry conditions. If infected potatoes are stored at high relative humidity and moderate temperatures, soft rot can be severe, destroying infected tubers first but subsequently destroying previously healthy ones (Fig. 14).

Infections can probably also occur during harvest and subsequent handling. Although late blight inoculations during storage were previously considered highly unlikely, such occurrences have been documented recently.

Late blight in the United States may need to be managed very differently in the future than in the past. Before exotic strains were introduced in the early 1990s, the late blight pathogen could only reproduce asexually via sporangia. Sexual reproduction requires two individuals of different mating type (Al and A2), and before the 1990s all strains were of the same mating type. Both mating types of P. infestans (A1 and A2) are now present in the United States and Canada, however, and have sometimes come into contact. Thus sexual reproduction is now theoretically possible.

Sexual reproduction will also yield recombinant individuals, thus providing a supply of “new” genotypes among the progeny. Whereas the majority of recombinant progeny are expected to be less problematic than parental strains, it is possible that some progeny could be more problematic.


2 Billion Years Unchanged, Bacteria Pose an Evolutionary Puzzle

by Tanya Lewis, Staff Writer   |   February 03, 2015

Nonevolving bacteria

These sulfur bacteria haven’t evolved for billions of years.
Credit: UCLA Center for the Study of Evolution and the Origin of Life

View full size image

Wedged inside rocks in the deep sea off the coast of Western Australia lurks an organism that hasn’t evolved in more than 2 billion years, scientists say.

From this deep-sea location, a team of researchers collected fossilized sulfur bacteria that was 1.8 billion years old and compared it to bacteria that lived in the same region 2.3 billion years ago. Both sets of microbes were indistinguishable from modern sulfur bacteria found off the coast of Chile.

But do the findings contradict Darwin’s theory of evolution? [Evolution vs. Creationism: 6 Big Battles]

“It seems astounding that [this] life has not evolved for more than 2 billion years — nearly half the history of the Earth,” the study’s leader, J. William Schopf, a paleobiologist at UCLA, said in a statement. “Given that evolution is a fact, this lack of evolution needs to be explained.”

Darwin’s theory of evolution by natural selection states that all species develop from heritable genetic changes that make an individual better able to survive in its environment and reproduce.

So how can Darwin’s theory account for these apparently nonchanging bacteria? The answer comes in looking at the bacteria’s similarly stable surroundings. True, the deep-sea bacteria in this study haven’t changed for eons, but neither has their environment, Schopf said. Darwin’s theory doesn’t call for organisms to evolve unless their environment changes, so the microbes’ lack of evolution is consistent with the theory, Schopf added.

To compare the fossils, Schopf and his colleagues used a method known as Raman spectroscopy to measure the composition and chemistry of the rocks. Then, using confocal laser scanning microscopy, they produced 3D images of the fossils and compared these visualizations with the modern bacteria. The ancient microbes looked identical to the present-day ones, the team found.

The fossils studied date back to a period known as the Great Oxidation Event, which occurred when oxygen levels surged on Earth between 2.2 billion and 2.4 billion years ago. During this time, there was also a large rise in sulfate and nitrate levels, which provided all the nutrition the sulfur bacteria needed to survive and reproduce. The environment inside these deep-sea rocks hasn’t changed since then, so there has been no need for the organisms to adapt, the researchers said.

The findings were published yesterday (Feb. 2) in the journal Proceedings of the National Academy of Sciences.


SUPER BUGS, not Super After All: by   Creation ministries International.

After over 12 years as a medical practitioner, I suddenly found myself an avid consumer, rather than a provider, of medical care. Involved in a serious road accident in 1986, I spent many months in hospital, including weeks in an intensive care unit.

While in intensive care, I became infected with one of the varieties of so-called ‘supergerms’, which are the scourge of modern hospitals. These are strains of bacteria which are resistant to almost every (and in some cases every) type of antibiotic known to man.

Several others in the same unit with me died as a result of infection by the same bacterial strain. The germs overwhelmed their immune systems and invaded their bloodstream, untouched by the most expensive and sophisticated antibiotics available.

This ‘supergerm’ problem1 is an increasingly serious concern in Western countries. It strikes precisely those hospitals which are more ‘high-tech’, and handle more serious illnesses. Applying more disinfectant is not the answer; some strains of germs have actually been found thriving in bottles of hospital disinfectant! The more antibacterial chemical ‘weapons’ are being used, the more bacteria are becoming resistant to them.

The reality of increasing bacterial resistance seems at first to be an obvious example of onwards and upwards evolution. But the facts, when carefully examined, show otherwise.

Natural selection, but not evolution

Evolution is basically the belief that everything has made itself—that natural processes (over millions of years, without miraculous, divine input of intelligence) have created an increasingly complex array of creatures. According to evolution, there was once a time when none of the creatures in the world had lungs. This means that there was no genetic information (the ‘blueprint’ for living things, carried on the molecule DNA) for lungs—anywhere. Then, at a later time, ‘lung information’ arose and was added to the world, but no ‘feather information’ as yet—feathers evolved later.

In other words, for every feature which arises by evolution, there would need to be new genetic information added to the total information in the biosphere (i.e., all the information in all creatures on earth). Some features could be lost subsequently, of course, so there will not always be a gain, but if microbes turned into magpies, maple trees and musicians, there must have been a massive net increase in information. This is not just any jumble of chemical sequences, but meaningful information, since it codes for complex structures which have purposeful functions.

So if new information, new functional complexity, can be shown to be arising by itself where previously there was none, this would give some credibility to the idea of molecules-to-man evolution, although it would not strictly prove that it had occurred. However, it can be shown that in every situation where populations of living things change, they do so without increase (and often with a decrease) of information. Thus, it is completely illegitimate for anyone to claim that such changes show ‘evolution happening’. Let’s look at what is known about how the ‘superbugs’ became resistant, and ask—did any new structures or functions arise in the process (which is another way of asking whether there was any evidence of evolution)?

The body’s natural defences will often ‘mop up such a small population before it can multiply and cause harm.

There are a number of different ways in which germs can become resistant to these poisons. A ‘superbug’ is, by definition, resistant to many different antibiotics. It may have become resistant to antibiotic A in one way, to antibiotic B in a completely different way, and to antibiotic C in another way again. So if we look at all the known ways of resistance arising in a population of germs, we will see if any of them are uphill, information-adding processes.

1. Some germs already had the resistance.

If out of a million bacteria, five already have a feature which makes them resistant (however that arose) to, say, penicillin, then soaking them in penicillin will kill all of them except for the five. Now the body’s natural defences will often ‘mop up’ such a small population before it can multiply and cause harm, so resistance will not become a problem. However, if that doesn’t happen, then those five germs can multiply, and their offspring will obviously also be resistant. So within a short time, there will be millions of germs resistant to penicillin. Notice that:

(i) This is why multiple resistance to major antibiotics is more common in hospitals which treat more serious conditions—these are the hospitals which will frequently be using the sophisticated, expensive ‘heavy artillery’ antibiotics, so this sort of ‘natural selection’ will happen more often.

(ii) In this kind of instance, the information to resist the antibiotic was already there in the bacterial population—it did not arise by itself, or in response to the antibiotic. That some germs were already resistant to man-made antibiotics before these were invented is common knowledge to microbiologists. Soil samples from villages where modern antibiotics had never been used show that some of the germs are already resistant to drugs like methicillin which have never existed in nature. Bacteria revived from the frozen intestines of explorers who died in polar expeditions carried resistance to several modern antibiotics, which had not been invented when the explorers died.2

2. Some germs directly transfer their resistance to others.

In an amazing process, the closest thing to sex in bacteria, one germ inserts a tiny tube into another, and a little loop of DNA called a ‘plasmid’ transfers from one to another. This sort of gene transfer, which can obviously pass on information for resistance to a drug, can even happen between different species of bacteria.

Notice, again, that the information for the resistance must already exist in nature before it can be passed on. There is no evidence of anything totally new arising which was not there before. This is information transfer, not information creation.

So far, we have dealt with situations in which resistance was obviously already there. Evolutionists would claim, of course, that such resistance evolved originally in the (unobservable) past. However, if observed changes in the present do not show us new information, what support is there for the idea that such information arose in the past? The mechanism that is put forward for this past evolution is invariably mutation—a copying mistake, an accidental change in the DNA code passed on to the offspring. So that brings us to the final way in which bacteria can become resistant.

3. Some germs become resistant through mutation.

Interestingly, where this happens, there is no clearcut evidence of information arising. All such mutations appear to be losses of information, degenerative changes. For example, loss of a control gene may enhance resistance to penicillin.3

These bacteria are not more aggressive than their colleagues, it is only that doctors have less power to stop them.

Some antibiotics need to be taken into the bacterium to do their work. There are sophisticated chemical pumps in bacteria which can actively pump nutrients from the outside through the cell wall into the germ’s interior. Those germs which do this efficiently, when in the presence of one of these antibiotics, will therefore efficiently pump into themselves their own executioner.

However, what if one of these bacteria inherits a defective gene, by way of a DNA copying mistake (mutation) which will interfere with the efficiency of this chemical pumping mechanism? Although this bacterium will not be as good at surviving in normal circumstances, this defect actually gives it a survival advantage in the presence of the man-made poison.4 Once again, we see that information has been lost/corrupted, not gained.


It is precisely because the mutations which give rise to resistance are in some form or another defects, that so-called supergerms are not really ‘super’ at all—they are actually rather ‘wimpy’ compared to their close cousins. When I was finally discharged from hospital, I still had a strain of supergerm colonizing my body. Nothing had been able to get rid of it, after months in hospital. However, I was told that all I had to do on going home was to ‘get outdoors a lot, occasionally even roll in the dirt, and wait.’ In less than two weeks of this advice, the supergerms were gone. Why? The reason is that supergerms are actually defective in other ways, as explained. Therefore, when they are forced to compete with the ordinary bacteria which normally thrive on our skin, they do not have a chance. They thrive in hospital because all the antibiotics and antiseptics being used there keep wiping out the ordinary bacteria which would normally outcompete, wipe out and otherwise keep in check these ‘superwimps’.5

If they are ‘weaker’, then why do they cause so much death and misery in hospitals? These bacteria are not more aggressive than their colleagues, it is only that doctors have less power to stop them. Also, those environments which will tend to ‘select’ such resistant germs, like intensive care units, are precisely the places where there will be critically injured people, physically weakened and often with open wounds.

This is why more than one microbiologist concerned about these super-infections has mused (only partly tongue in cheek) that the best thing to happen in major hospitals might be to dump truckloads of germ-laden dirt into the corridors, rather than keep on applying more and more chemicals in a never-ending ‘arms race’ against the bacteria. In other words, stop using the antibiotics (which of course is hardly feasible), and all this ‘evolution’ will reverse itself, as the bacterial populations shift back again to favour the more hardy, less resistant varieties.

Summary and Conclusion

1. ‘Supergerms’ are actually not ‘super’ at all. They are generally less hardy, and less fit to survive outside of the special conditions in hospitals.

2. There are many instances in which germs become resistant by simple selection of resistance which already existed (including that ‘imported’ from other bacteria).

Supergerms are actually defective in other ways.

3. Where a mutational defect causes resistance, the survival advantage is almost always caused by a loss of information. In no case is there any evidence of an information-adding, ‘uphill’ change.

4. ‘Supergerms’ give no evidence to sustain the claim that living things evolved from simple to complex, by adding information progressively over millions of years.


Death, suffering and disease (including infection) are part of the curse which came upon a once-perfect world through the rebellion of our original ancestor, Adam, against his Maker.

Bacteria actually provide evidence against evolution. Bacterial populations multiply at incredibly high rates. In only a matter of a few years, bacteria can go through a massive number of generations, equivalent to millions of years in human terms. Therefore, since we see mutation and natural selection in bacterial populations happening all the time, we should see tremendous amounts of real evolution happening. However, the bacteria we have with us today are essentially the same as those described by Robert Koch a century ago. In fact, there are bacteria found fossilised in rock layers, claimed by evolutionists to be millions of years old, which as far as one can tell are the same as bacteria living today.

The famous French biologist Pièrre Grassé, who held the chair of evolution at the Sorbonne for many years, admitted that mutations in bacteria simply showed shifts back and forth around a mean, but no net effect. Overall, he said, ‘mutations do not produce any kind of evolution.’6

When next you read about ‘supergerms’, remember that everything known about them is consistent with the Genesis creation of an originally good, complex world ruined by sin.


John Robson | January 4, 2016 11:18 AM ET   – The antibiotic window is slamming shut – National Post
Here’s an “end of the world news” item: super-gonorrhea is overwhelming the last antibiotic defences in Britain, so apparently we need new antibiotics. Anything but chastity.

Such stories clearly threaten the infamous TEOTWAWKI (“The End Of The World As We Know It”), not just an inconvenience. Yet they get brief space on the back pages while A1 goes to some politician’s latest fatuity that wouldn’t matter even if it were true and relevant.

Gonorrhea may soon be an ‘untreatable disease,’ Britain’s chief medical officer warns

LONDON – Sally Davies, Britain’s chief medical officer, has sounded the alarm on the spread of antibiotic resistant gonorrhea.

The sexually transmitted infection is increasingly caused by strains of Neisseria gonorrhoeae that resist antibiotic treatment. “Gonorrhoea is at risk of becoming an untreatable disease due to the continuing emergence of antimicrobial resistance,” Davies wrote to doctors and pharmacies. The Guardian reports that a recent outbreak of a superbug strain of the disease – one that doesn’t respond to the antibiotic azithromycin – has put Britain on high alert.

Davies urged doctors to use proper treatment protocols. A recent study found that many doctors in Britain still prescribe ciprofloxacin, which hasn’t been recommended for a decade now.

Two things are ominously true and relevant about this particular gonorrhea story. First is the emergence of antibiotic resistance in any number of diseases that attack you in any number of places. Since the Second World War, we have enjoyed blessed immunity from sudden death by bacterial infection that haunted humans since we first saw the city lights.

We have forgotten what it was like when the president’s son got a blister playing lawn tennis … and died. (Calvin Coolidge Jr., age 16.) And it has contributed to our false sense, not just of security, but of omnipotence and impunity, as well.

It is not immediately obvious why people who embraced the theory of evolution so eagerly expected bacteria not to evolve. But we did.

Hence, second, when people can’t ignore the emerging evidence, they call for more of the same: better drugs, more careful prescriptions, less routine agricultural overuse. Science will find a way so we don’t have to change our ways.

When this newspaper reported briefly that Britain’s on “high alert” because the newest strain of “the clap” (a.k.a., Neisseria gonorrhoeae) doesn’t respond to azithromycin, it cited the country’s chief medical officer warning doctors and pharmacies not to prescribe older antibiotics it is also resistant to. Meanwhile, a longer Washington Post story said that in 2013, the U.S. Centers for Disease Control and Prevention called antibiotic-resistant gonorrhea an “urgent threat,” with about a third of cases resisting at least one antibiotic, so doctors should use ceftriaxone with azithromycin.

Fine … if you want to breed gonorrhea resistant to both. As the Post noted, “Bacteria are fast-evolving creatures” with a creepy capacity to share genes. So “it’s our use of antibiotics that really has to evolve.”

We cannot stop bacterial evolution or even delay it much

Well, sure. But the main point is, when the party’s over, you have to stop partying.

We cannot stop bacterial evolution or even delay it much. It’s an unstoppable tragedy of the commons where the most desperate, least careful and least scrupulous medical conduct sets the pace. A blistering pace, from tens of thousands of Indian newborns succumbing to untreatable infections, malaria resisting artemisinins, viral-drug-proof HIV, to flesh-eating bugs, VRE and MRSA. You name it, it’s coming. Head lice shrug off chemicals. Even Arctic birds show traces of drug-resistant E. coli. It’s everywhere, and the antibiotic window is slamming shut.

So what can we do, if ignoring it won’t work?

We should restore pre-antibiotic infection control protocols. But doing so would require moving away from big, centralized, bureaucratic government hospitals, which is unthinkable because … Because we don’t want to start thinking differently. We’ve bet the future on experts and life without consequences, including financial ones. So we cling to the hope of a a new class of antibiotics to which bacteria can’t adjust, sterilizing wipes, antibacterial soaps, creams, body washes and even pens and mattresses, as though germs will now kindly stop evolving at the touch of a button.

The illusion of technique convinces us there’s nothing nature can throw at us that the lab can’t throw back. But insanity is doing the same thing over and over and expecting a different result. Particularly turning our genitalia into Petrie dishes.

Wikipedia cites the CDC on gonorrhea that, “Testing all women who are sexually active and less than 25 years of age each year is recommended.” But “sexually active” does not mean what they think it means. A woman under 25 can swing naked from the chandelier without fear, provided only her husband is present and he’s faithful.

Oh but we can’t do that. We’re liberated. Well, over 20 years ago, P.J. O’Rourke wrote, “The sexual revolution is over and the microbes won.” And that’s not all they won. But while I have no solution to the grim issue of untreatable pneumonia or malaria, I know what protects you from drug-resistant gonorrhea: monogamy.

I also know what doesn’t: believing science has made us as gods, or at least godlets, who through political will can guarantee ourselves long, healthy pleasure quests with painless planned exits. It is not so, any more than happy pills can fix a wretched life.

Death still comes like a thief in the night, wielding accidents, cancers, lunatics, terrorists and more. But that’s no reason to invite him (or her, or them) into your bed.

If that’s the end of the world as you know it, it’s probably high time anyway.

National Post