Tuesday, June 26, 2007

summer safety tip #1

it's sweltering today.

i mean, hot and humid. the reason i can never live in the south.

i tried to run early this morning to avoid the humidity, but it was already almost unbearable. the only place with a breeze was by the river. seems like people might be tempted to go swimming today. in fact, i'm sure that a lot of folks will. i only hope they adhere to this very important summer safety tip:

DON'T SWIM IN FECULENT POOLS!

i am on PICU night float this month. already, we have had two cases of hemolytic uremic syndrome, or HUS, one of which was likely caused by a child swimming in a water source contaminated by Escherichia coli 0157:H7.
HUS is a syndrome that is typically characterized by a prodrome of diarrhea (90%) or an upper respiratory tract infection (the other 10%). the classic triad of HUS is hemolytic anemia, thrombocytopenia and acute renal failure. it usually occurs in kids <4 style="font-style: italic;">Yersinia, Salmonella, and Campylobacter species, Streptococcus pneumoniae and Clostridium difficile. 70% of HUS cases in children result from E. coli 0157:H7 or Shigella dysenteriae, both of which produce a toxin (shiga- or vero-toxin) that damages the lining of the blood vessels, or endothelium, throughout the body.

the effect of this toxin-mediated damage is profound. fibrin and platelets adhere to the damage on the vessel walls, resulting in low platelets (thrombocytopenia) and tiny little clots called microthrombi. red blood cells are either damaged by the toxin or chewed up as they try to flow past these thrombi (a process called microangiopathic hemolytic anemia).
(normal red blood cells above, damaged red cells below, called schistocytes.)

in HUS, these microthrombi occur primarily in the kidney, resulting in kidney failure. but, really, any organ can be involved. the picture below is of a portion of a kidney called the glomerulus, which is really just a tuft of small blood vessels. the light pink smudgy stuff at the end of the arrow is a microthrombus.

in a similar disease process seen more commonly in adults, thrombocytopenic thrombotic purpura (TTP), microthrombi occur in the brain, spleen, liver, pancreas, heart and kidney. TTP has a much poorer prognosis.

both kids in question had had several days of bloody diarrhea. we're not talking a few streaks here and there that you could explain with a fissure or hemorrhoid. we're talking lots of blood. both were dehydrated, anemic and thrombocytopenic. both had stool cultures that were positive for E. coli 0157:H7. both were in renal failure and are now at TBFCHITW (that's for you, flea, if you are reading this) on dialysis.

one of the most important questions from a public health standpoint is how did they get it? E. coli live among us. most are not harmful and are considered normal flora in our intestines. you might hear them referred to as coliform bacteria. we actually need these commensal organisms to digest our food. They actually make vitamin B12, amongst others, that we need to live. the 0157:H7 serotype is not so friendly or helpful.

0157:H7 is in contaminated meat, such as hamburger. if this doesn't make you want to be a vegetarian, nothing will. you are actually more likely to get 0157:H7 from hamburger than from a steak, as the bacteria are on the surface of the steak (and, hence, are killed in the cooking process) but get mixed up when the beef is ground up to make hamburger. raw or undercooked hamburger is often the culprit with outbreaks of 0157:H7.

another potential source is inadequately washed or unwashed produce. remember the spinach that was the source of the outbreak last fall? it's called fecal-oral contamination. enough said.

0157:H7 also lives in and on cows and other farm animals. some outbreaks have been tied to petting zoos.

contaminated water supplies are another concern, particularly in rural areas where there are a lot of cattle. pay attention to the coliform counts! this tells you how much poop has been in the water. the fish and wildlife service checks water supplies for coliform counts regularly and will close a pond or lake if the level is high enough.

the moral of this cautionary tale is to:
1) avoid contaminated water supplies (aka, the feculent pool)
2) take your child to the doctor when they have bloody diarrhea (please do this if nothing else!)
3) avoid raw/undercooked beef, unwashed vegetables/fruits, and unpasteurized milk or fruit juices

when it comes to E. coli 0157:H7, an ounce of prevention is worth everything.

2 comments:

daedalus2u said...

HUS involves nitric oxide, with Shiga toxin reducing NO production in human glomerular endothelial and mesangial cells. Many of the effects of hemolytic anemia are due to free hemoglobin destroying NO a lot faster than NO in erythrocytes. NO is protective of toxic effects of Shiga toxin in HUS. Externally administered NO (isosorbide) is helpful in HUS due to transplant (even though isosorbide is not a good NO donor). NO does inhibit coagulation through S-nitrosothiols, the reduction of NO by hemolysis would acutely affect NO levels, cause vasoconstriction and coagulation.

In mice, induction of kidney growth (by removing one), is protective of exposure to Shiga toxin.

Rapid IV volume expansion is somewhat protective. The dilution reduces hemoglobin concentration and so increases NO concentration (hemoglobin destruction of NO is first order with respect to both, so at fixed production, the product of Hct and NO is fixed). It also reduces the concentration of cells and reduces viscosity and presumably clotting kinetics. Interestingly, antibiotics are not recommended during the diarrhea stage. I suspect that it causes the bacteria to lyse, and that increases exposure to lipopolysaccharide.

It is very interesting to me that HUS increases plasma urea levels (and presumably excretion of urea and ammonia in sweat). The bacteria I am working with would convert that urea into NO and nitrite, some of which is absorbed into the skin. I suspect it might be a better NO donor than isosorbide. The increased excretion of urea, or even ammonia in sweat might be an evolved compensatory reaction to kidney damage.

daedalus2u said...

girl MD, I came across this abstract on how NO inhibits the production of Shiga toxin, and knowing your interest in mitigating the effects of feculent pools I thought I would pass it on.