Welcome to Johne’s (“yo-knees”), the most important disease that you probably never heard of. It
is a serious, debilitating and sometimes fatal illness of cattle, goats, and sheep (among other animals), which the livestock and dairy industry is desperate to keep out of the public consciousness, despite the fact that it costs industrial agriculture many millions of dollars every year.
The reason for such industry reticence is that Johne’s disease in livestock is very similar – and possibly even identical – to Crohn’s disease in people, which currently afflicts an estimated 500,000 sufferers in North America alone, causing severe ulcerations of the gastrointestinal tract, immense pain, and loss of appetite and weight, often requiring surgical removal of the damaged bowel. And the big, dirty secret of today’s industrial dairy and meat producers is that animals suffering from flagrant Johne’s disease currently provide milk and meat directly to the American consumer.
In short, we eat lots of very, very sick cows, animals so ill that if you knew you were eating them, you wouldn’t.
As for the connection between Johne’s and Crohn’s, imagine that instead of trying their newly discovered antibiotic on bacteria, Alexander Fleming and his collaborators had injected it into people suffering from the flu. They would have concluded that penicillin wasn’t useful – a legitimate inference under these hypothetical circumstances, but tragically wrong. (Note to nonbiologists: antibiotics such as penicillin – for all their efficacy against certain bacteria – are useless against viruses.)
Now, fast-forward to the present. The received wisdom among physicians is that Crohn’s disease is caused by an “autoimmune” process, in which the body unaccountably turns against itself.
Asked about a possible bacterial cause of Crohn’s, the conventional medical response is a variant on our imagined attempt to cure a viral disease with penicillin: “Been there. Done that. Didn’t work.” Again, a seemingly legitimate inference, but in all likelihood, tragically wrong.
In fact, there is a bacterium strongly implicated in Crohn’s disease: Mycobacterium avium paratuberculosis (MAP). Closely related to the microbe that causes tuberculosis and leprosy, MAP is the critter that produces Johne’s disease – the livestock version of Crohn’s — in cattle and many other animals.
There is growing evidence that the connection between MAP and Crohn’s was ruled out prematurely and erroneously. Thus, early efforts to grow MAP in laboratories used the wrong culture medium (MAP, like the bugs that cause TB and leprosy, is notoriously slow-growing and fussy). Using the right materials, MAP has now been identified in Crohn’s patients and rarely in normal controls. Moreover, early attempts to cure Crohn’s with antibiotics likely failed for a very simple reason: they used the wrong antibiotics! Once again like TB and leprosy, MAP is very difficult to kill.
When it infects human beings, it has been claimed — but not confirmed — that MAP assumes a slightly different form than when it causes Johne’s in goats, sheep, or cattle. But there is no doubt whatever that MAP is the cause of Johne’s disease — and, moreover, MAP samples, taken from human beings with Crohn’s disease, induces Johne’s in goats. It nonetheless quickly became biomedical dogma that MAP did not cause Crohn’s in people, since human MAP could not be cultured in laboratories from Crohn’s sufferers.
In the last 15 years, however, things have changed dramatically.
As already noted, human MAP is a very slow-growing and finicky pathogen, as are most mycobacteria: another form, Mycobacterium leprae, which causes leprosy, even now cannot be grown in laboratory culture. But with suitable techniques, MAP can.
It is possible that Crohn’s is like “cancer,” “pneumonia,” or “heart disease,” which is to say, an amalgam of several different illnesses rather than a unitary phenomenon. Another possibility – much favored by medical and industry guardians of the conventional orthodoxy – is that MAP infection is a secondary, opportunistic consequence of Crohn’s rather than a cause. A similar claim, interestingly, was made 30 years ago by physicians rejecting any causative connection between gastric ulcers and Helicobacter pylori. No one has yet intentionally infected himself by eating a MAP-burger, analogous to Barry Marshall’s famous self-inoculation to demonstrate that H. pylori causes ulcers, but the parallels between MAP/Crohn’s and Helicobacter/gastric ulcers are numerous and instructive.
As to antibiotic treatment, it turns out that MAP is indeed very difficult to kill, just like its close relatives, the mycobacteria that cause leprosy and tuberculosis. But it can be done, when the right antibiotics are used; one successful combination, for example, includes clarithromycin, rifabutin, and clofazimine, and – as when treating leprosy and TB – must be continued for a long time.
Such treatments are long overdue, since Crohn’s disease shows all the hallmarks of a spreading zoonotic (animal-to-human) infection. Its incidence has sky-rocketed, closely paralleling the increase in factory farming and the frequency of Johne’s disease in domestic livestock. If Crohn’s were an “autoimmune” disease, as the old dogma has it, then such a rapid increase would be inexplicable, whereas the epidemiologic picture is consistent with that of a spreading pathogen. A large proportion of U.S. dairy herds appear to be infected with MAP, which is transmitted in milk and is not killed by pasteurization (ultra-pasteurization, on the other hand, with its higher temperature, might do the trick). Moreover, cattle suffering from Johne’s disease, and thus with fully disseminated MAP, are routinely slaughtered and their meat introduced into the food chain.
This is itself an extraordinary fact, worth repeating and emphasizing: Cattle suffering from a severe bacterial infection related to tuberculosis and leprosy, characterized by pussy, intestinal ulcers and overall body wasting, and which may be literally identical to a pathogen that causes a devastating illness in genetically susceptible people, are – right now, as you read this – routinely being slaughtered, and their infected meat introduced into the food stream.
Those who thrilled, in their youth, to the exploits of “The Microbe Hunters,” as portrayed by the likes of Paul de Kruif, might want to prepare themselves for a repeat performance: the glory days of Pasteur and Koch may well persist into the 21st century, involving illnesses not hitherto identified as infectious, and focused especially on zoonotic transmission. If so, genuine concern with homeland – not to mention, kitchen — security will require scientific alertness as well as political courage on the part of microbiologists, veterinarians, public health authorities, the Food and Drug Administration, and the Department of Agriculture, because there’s more going on here than meets the eye. Powerful economic interests have largely succeeded, thus far, in stifling serious consideration of the MAP/Crohn’s connection, and for their own “good” economic reasons. Drug companies as well as gastroenterologists currently treat Crohn’s with infusions of extremely profitable immunosuppressant drugs (whose side-effects are equally extreme), and – most critically – the meat and dairy industry stands to lose literally billions of dollars if forced to eradicate Johne’s or even to segregate sick animals. This is why the livestock industry desperately wants Johne’s to remain below the public’s radar.
Stay tuned, however: If public health authorities ever act responsibly on behalf of their ostensible mandate – public health – the resulting impact will make the recent furor over “mad cow disease” look like a whisper.