FOOD POISONING'S EFFECTS

Maryn McKenna does not mention controls for medical history in her article on evidence that foodborne pathogens cause lifelong consequences, “Food Poisoning's Hidden Legacy.” An elevated incidence of renal impairment and circulatory problems within six years after individuals suffered severe immediate symptoms of Escherichia coli ingestion, as compared with those suffering mild or no symptoms, does not prove their E. coli exposure was the cause. That conclusion assumes that there was no preexposure renal or circulatory dysfunction. For instance, a compromised excretory system could cause a more severe response to E. coli ingestion and, if not identified a priori, could later be perceived as a consequence of the exposure. Alternatively, those with a propensity for development of these medical conditions may have a heightened sensitivity to E. coli. Correlation alone does not prove causality.

Peter Irwin
via e-mail

Affected joints after infection with Salmonella bacteria, reported by McKenna, are an old, but apparently forgotten, problem. Those of us who have worked in developing countries have seen, treated and followed up on patients with typhoid fever, a severe infection caused by Salmonella typhi. Pain and swelling of the joints may continue long after discharge and apparent recovery. The different types of joint problems following typhoid infection listed by surgeon William W. Keen in 1898 included joint infection during the illness, rheumatic typhoid arthritis and septic typhoid arthritis. And Charles W. Wilson reported patients developing swollen joints after typhoid infections in the Journal of Bone and Joint Surgery in May 1899. We now see that other salmonellae can produce the same long-term problems.

Alan Dugdale
Brisbane, Australia

BREATH-DEFYING

On reading “The Limits of Breath Holding,” by Michael J. Parkes, I was reminded that in 1958 I decided to see how long I could hold my breath underwater. I found that if I floated face down and relaxed, I could flex my diaphragm muscles repeatedly to delay the urge to take a breath. Eventually I was able to do so for almost four minutes.

Jon Otterson
Madison, Wis.

There is a counterpart to holding one's breath: expelling air completely and seeing how long one can go before inhaling. There is a break point there, but the diaphragm is “held” in a state of complete relaxation instead of contraction. Does the same mechanism affect both sides of this coin?

Bryon Moyer
via e-mail

My foster mom claims that one late evening I was too quiet, and she found me unresponsive and turning blue. I was fortunate in not becoming another statistic of sudden infant death syndrome (SIDS). Could the role of a not so fully developed or underdeveloped diaphragm explain “involuntary breath holding” in infants and thus SIDS?

Bennett A. Wallace
Louisville, Ky.

PARKES REPLIES: The last two questions both highlight the need for more research on the diaphragm. Regarding Moyer's comments, we know that people can perform only very short breath holds with deflated lungs. Yet is the diaphragm “held” at its relaxed length with an isometric contraction or just completely relaxed? Further, these short breath holds neither confirm nor refute the hypothesized role of the diaphragm in the break point. Its chemoreceptors could still be stimulated by the rapid rise in carbon dioxide or the fall in oxygen. As for Wallace's question, many hypotheses attempt to explain SIDS. Experimentally testing the hypothesis of a “not so fully developed or underdeveloped diaphragm” in infants is not easy.

DEFECTIVE DINOS

“Time Traveler,” Richard Milner's short essay on artist Charles R. Knight, makes no mention of the many errors of reconstruction we now know to be in Knight's paintings of prehistoric creatures. It seems ironic to praise Knight for his illustrations of living creatures and to suggest that what he learned from these observations informed his dinosaur paintings and to then provide the reader with Knight's view of a T. rex and Triceratops with dragging tails.

John Byrne
via e-mail

MILNER REPLIES: Knight was keenly aware that a paleoartist's images are simply the best-informed guesses possible at the time, and his were made in collaboration with the top paleontologists of his day. Over the years he frequently updated his restorations as more complete fossils were discovered. In retrospect, his paintings have became valuable snapshots of the changing state of scientific knowledge.

The current obsession with tail dragging seems a trivial point on which to attack Knight's genius. In the image from Knight's mural at the Field Museum that Byrne refers to, one individual stands upright with its tail braced against the ground, while the other's torso is cantilevered forward, with tail held off the ground—thus hedging Knight's bets on its habitual posture. His achievements in creating the first scientifically sound and artistically beautiful restorations of prehistoric creatures remain unassailable.

POLIO PIONEER

An important piece of history on the development of oral polio vaccine is missing in “Birth of a Cold War Vaccine,” by William Swanson: neither Albert B. Sabin nor Jonas E. Salk received the Nobel Prize in Physiology or Medicine for their vaccines. Instead, in 1954, the Nobel committee awarded it to John Franklin Enders, then at Harvard Medical School, and his colleagues.

Prior to the work of the Enders group, it was not possible to produce a polio vaccine, because people thought that this virus, which affects nerve cells, could be grown only in nerve tissue. (Vaccine based on nerve tissue–grown viruses can cause allergic encephalomyelitis, inflammation of the brain and spinal cord.) Enders and his associates found that this virus could be grown in monkey kidney cells, and that is what made it possible to develop a polio vaccine.

Pinghui V. Liu
Boca Raton, Fla.

STRESS MASTER

It is a sad coincidence that “This Is Your Brain in Meltdown”—Amy Arnsten, Carolyn M. Mazure and Rajita Sinha's article describing how neural circuits for self-control shut down under stress—hit the newsstands the same week as the killing of 16 civilians in Afghanistan by a U.S. soldier. One can only hope that the authors' work and that of others will help reduce and perhaps prevent such tragedies and meltdowns in general. The current results do raise anew the fear, however, that every misbehavior, from murder on down to cheating at Scrabble, will eventually, and conveniently, be ascribed to a brain malfunction.

André Rocque
Department of Philosophy
Collège Montmorency, Laval, Quebec

I have observed that a small minority of people can “rise to the occasion”—their memories and minds do not go blank under stress—and that such people are more capable than most others in stressful situations. I wonder if the signaling pathways in their brain might differ from the typical person? It seems that champion players of the game show Jeopardy would be a ready sample of such individuals.

Tim Budell
Westford, Vt.

2 Comments

1. 1. jgrosay 04:13 PM 7/27/12

   Hi!: the Haemolytic-Uremic Sindrome -HUS- related to some E coli an Klebsiella infections is a proof of how many variations may exist inside the same bacteria species that affects the consequences of an individual strain infecting humans. The connection between the rods producing bloody diarrhea and cattle feces' contaminated water was empirically established long ago by country people, and many articles published about this not too frequent but serious disorder signaled a great variability in the effect of antibiotics on the production by bacteria of the verocytotoxin, the cause of HUS, but most point towards an increase in toxin production or release or both by the use of antibiotics for the gastrointestinal infections that end in HUS. There are enough studies as to say with certainty that an early use of intravenous fluid replacement, and an early medical care in an emergency room environment reduces the incidence of HUS and kidney failure in patients infected by toxin-producing strains of bacteria, and also that the use of products aimed to reduce intestinal movements and diarrhea, be them OTC or prescription drugs -Loperamide, Opiate seals...-, increases the incidence of HUS, so as a take home message, an early consultation with a doctor, an early intense, at least oral fluid replacement therapy for persons suffering a diarrhea, and refraining from any kind of therapeutic measures outside the two signaled -water and electrolyte replacement and visit to a doctor- may be of help in decreasing the incidence of this rare, but sometimes deadly complication of food poisoning.

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2. 2. CliffClark 07:52 PM 7/30/12

   Regarding Peter Irwin's e-mail on Shiga toxigenic E. coli and sequelae. Pretty decent control data do exist for some populations. Furthermore, the mechanism of damage caused by the Shiga-toxin is known, and involves damage to renal tubules in adults and further damage to glomeruli in children. The progression of disease has been followed, as has the partial or complete restoration of function in some patients. Subsequent to Shiga toxigenic E. coli infection and the hemolytic uremic syndrome some patients must remain on dialysis, surely a clear indication of permanent kidney damage from the initial infection. There are frequently neurological deficits both subtle and profound subsequent to Shiga toxigenic E. coli infection that definitely result from thrombi in small capillaries cutting off oxygen to the tissue behing the clot; everything behind the clot dies. Shiga toxin may also directly kill neurons. In the case of these bacteria, the evidence is pretty good for a direct causal link to long-term sequelae.

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