May 2009

I. THE OUTBREAK

On October 2, 2008, the California Department of Public Health (CDPH) issued a report linking an outbreak of Campylobacter illnesses to unpasteurized milk from Alexandre Eco Farms Dairy. The report was the result of an investigation commenced on July 14, 2008, when Dr. Thomas Martinelli, the County Health Officer for Del Norte County, California reported four cases of laboratory confirmed Campylobacter infections and five additional cases of diarrhea in Del Norte County residents. Eight of the original nine sick individuals were members of the Alexandre Eco Farms “cow-leasing” program. Eight of these individuals had consumed milk produced on the farm. The ninth sick individual worked with cattle on the Alexandre Eco Farms Dairy. One of the eight individuals who were sick, Mari Tardiff, had already been hospitalized with GBS, following the onset of acute gastroenteritis after consumption of the milk.

As part of the investigation, health department officials retrieved a refrigerated carton of partially consumed Alexandre Eco Farms milk from Mari Tardiff’s home. Mari had consumed a portion of the milk before her illness. The specimen tested positive for Campylobacter jejuni DNA using a test called polymerase chain reaction (PCR). Testing indicated that multiple strains of Campylobacter jejuni were present in the milk. Del Norte County officials eventually identified 16 cases of Campylobacter jejuni associated with the outbreak. Fifteen of those were persons who consumed milk from Alexandre Eco Farms Dairy. The 16th case was the farm employee. CDPH and Del Norte county officials concluded that “the available epidemiologic and laboratory data support the conclusion that this cluster of acute diarrheal illness in Del Norte County was an outbreak of C. jejuni infections caused by consumption of unpasteurized milk from [Alexandre Eco Farms Dairy.]”

The causal link between Alexandre Eco Farms Dairy and Mari’s illness was so clear, and her injuries so remarkable, that the physicians that treated her published a report on her case in the medical journal. “Investigation of the First Case of Guillain-Barre Syndrome Associated with Consumption of Unpasteurized Milk – California, 2008.” Amy K. Earon, T. Martinelli, W. Miller, C. Parker, R. Mandrell, D. Vugia. The authors explained the laboratory methods used in investigating Mari’s illness:

We reviewed the patient’s medical record and interviewed her husband to assess her symptoms and exposures. We used polymerase chain reaction (PCR) and multilocus sequence typing (MLST) to test a six-week old unpasteurized milk sample, obtained from the cow leasing-program and partially consumed by the patient, for genes encoding the bacterial membrane component lipooligosaccharide (LOS) in GBS-associated Campylobacter jenuni.

In addition to the DNA testing, the authors also tested Mari’s blood for anti-bodies to GBS. The authors then explained that the PCR and MLST testing of the milk detected Campylobacter jejuni gene. In addition, the blood test was positive for anti-bodies that indicated the presence of GBS. The authors concluded, “Combined laboratory and epidemiologic evidence established the first reported association between GBS and unpasteurized milk consumption.”

II. MARI TARDIFF’S ILLNESS

On the weekend after Mari drank raw milk, she developed flu-like symptoms, including diarrhea and vomiting. By Thursday, June 12, the food poisoning was overwhelming her body with an amazingly swift force. First her vision blurred. Then her hands went numb. Mari went to an emergency room, and there lab work was done and abdominal X-rays were taken. But doctors could not determine what was wrong. On Friday, Peter took Mari to a neurologist. An MRI was normal but the doctor and radiologist mentioned a frightening possibility – Guillain-Barré syndrome, or GBS, a potentially fatal inflammatory disorder.

Hours later Mari’s legs were on fire, searing with pain that, ironically, only hot water helped to soothe. Her legs hurt so much that she soon retreated to bed, wrapping her legs in warm towels and a heating blanket. During that night, Mari awoke and realized she could not move. Peter bear-hugged her to lift her to the toilet and then carried her back to bed. In the early hours of the morning, he called for help, which led to an ambulance ride to the small Sutter Coast Hospital, and then a medivac flight to the Intensive Care Unit at the larger, better-equipped Rogue Valley Medical Center (RVMC) in Medford, Oregon. She remained hospitalized for two and one-half months.

Mari was moved to Redding Rehabilitation Hospital and was finally able to come home on November 1, 2008. Today, Mari lives in her family room, which now is equipped with a hospital bed, portable toilet, a Hoyer lift and a stand-up frame, all purchased by the Tardiffs. Using their own resources, they also renovated a downstairs half-bath and laundry room into a handicapped-accessible bathroom and shower. The Tardiffs pay two nurses $10.50 an hour to care for Mari from 7:30 A.M. until 7:00 P.M. five days a week while Peter is at work. Home health physical and occupational therapists also come to the house five days a week.

Mari works very hard at therapy but it is a slow, painful process. Peter has found it so upsetting that he no longer can watch. Every improvement is celebrated, but he knows how much discomfort and frustration goes into each minute, regained movement. Mari may never walk again. She lost her job, she lost her dreams and plans that she held dear. The illness has been a long, arduous journey for Mari, her family and friends, and while she has made progress, there remains a long way to go.

Raw Milk Risks: Mari Tardiff Campylobacter Illness from Marlerclark on Vimeo.

READ MORE ON CAMPYLOBACTER AND GULLAIN BARRE SYNDROME
Continue Reading The Alexandre Eco Farms Dairy Raw Milk Campylobacter Outbreak

The E. coli O157:H7 Bacteria

E. coli O157:H7 is one of hundreds of strains of the bacterium Escherichia coli. Most strains of E. coli are harmless and live as normal flora in the intestines of healthy humans and animal. The E. coli bacterium is among the most extensively studied microorganism. The combination of letters and numbers in the name of the E. coli O157:H7 refers to the specific markers found on its surface and distinguishes it from other types of E. coli. The testing done to distinguish E. coli O157:H7 from its other E. coli counterparts is called serotyping. Pulsed-field gel electrophoresis (“PFGE”), sometimes also referred to as genetic fingerprinting, is used to compare E. coli O157:H7 isolates to determine if the strains are distinguishable.

E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis associated with consumption of hamburgers from a fast food chain restaurant. Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one isolation with serotype O157:H7, and that was a case in 1975. In the ten years that followed there were approximately thirty outbreaks recorded in the United States. This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987 when Washington became the first state to mandate its reporting. As a result, only the most geographically concentrated outbreak would have garnered enough notice to prompt further investigation.

The virulence of E. coli O157:H7 is a result of its ability to produce Shiga-like toxins. It has been theorized that generic E. coli picked up this deadly ability through horizontal transfer of virulence genes from the Shigella bacteria. Genome sequencing of E. coli O157:H7 has since confirmed that gene transfer did in fact occur, and that the evolution of ever more virulent forms of bacteria will likely continue to occur. The CDC has emphasized the prospect of emerging pathogens as a significant public health threat for some time.

Foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections. Surveys performed on feedlots have demonstrated that cattle can be infected with E. coli O157:H7 through close contact, and under muddy conditions. The prevalence of E. coli O157:H7 among cattle in these feed lots can reach 63-100%, especially during the summer. The prevalence of E. coli O157:H7 in the summer, which is when outdoor grilling of hamburgers becomes most common, is a significant public safety risk.

According to a recent study, an “estimated 73,480 illnesses due to E. coli O157:H7 infections occur each year in the United States, leading to an estimated 2,168 hospitalizations and sixty-one deaths annually.” The hemorrhagic colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within twenty-four hours, and sometimes fevers. The typical incubation period—which is to say the time from exposure to the onset of symptoms—in outbreaks is usually reported as three to eight days. Infection can occur in people of all ages but is most common in children. The duration of an uncomplicated illness can range from one to twelve days. In reported outbreaks, the rate of death is 0-2%, with rates running as high as 16-35% in outbreaks involving the elderly, like those at nursing homes.

What makes E. coli O157:H7 truly and decidedly dangerous is its very low infectious dose, and how relatively difficult it is to kill these bacteria. Unlike Salmonella, for example, which usually requires something approximating an “egregious food handling error, E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection.” As few as twenty organisms have been said to be sufficient to infect a person and, as a result, possibly kill them. And unlike generic E. coli, the O157:H7 serotype multiplies at temperatures up to 44 degrees Fahrenheit, survives freezing and thawing, is heat resistant, grows at temperatures up to 111 degrees Fahrenheit, resists drying, and can survive exposure to acidic environments.

And, finally, to make it even more of a dangerous threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact. There is also the serious risk of cross-contamination between raw meat and other food items intended to be eaten without cooking. Indeed, a principle and consistent criticism of the USDA E. coli O157:H7 policy is the fact that it has failed to focus on the risks of cross-contamination versus that posed by so-called improper cooking. With this pathogen, there is ultimately no real margin of error, and the cost of error can be death. It is for this precise reason that the USDA has repeatedly rejected calls from the meat industry to hold consumers responsible for E. coli O157:H7 surviving after cooking.

Hemolytic Uremic Syndrome (HUS)

E. coli O157:H7 infections can lead to a severe, life-threatening complication called hemolytic uremic syndrome (“HUS”). HUS accounts for the majority of the acute and chronic illness and death caused by the bacteria. HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins. It is the most common cause of renal failure in children. Approximately half of the children who suffer HUS require dialysis, and at least 5% of those who survive have long-term renal impairment. The same number suffers severe brain damage. While somewhat rare, serious injury to the pancreas, resulting in death or the development of diabetes can also occur. There is no cure or effective treatment for HUS. And, tragically, as too many parents can attest, children with HUS too often die.

HUS develops when the toxin from the bacteria, known as Shiga-like toxin (“SLT”), enters the circulation through the inflamed bowel wall. SLT, and most likely other chemical mediators, attach to receptors on the inside surface of blood vessel cells (endothelial cells) and initiate a chemical cascade that results in the formation of tiny thrombi (blood clots) within these vessels. Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors, and include the kidney, pancreas, and brain. By definition, when fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and acute renal failure (loss of kidney function).

As already noted, there is no known therapy to halt the progression of HUS. HUS is a frightening complication that even in the best American centers has a notable mortality rate. Among survivors, at least five percent will suffer end stage renal disease (“ESRD”) with the resultant need for dialysis or transplantation. But, “[b] ecause renal failure can progress slowly over decades, the eventual incidence of ESRD cannot yet be determined.” Other long-term problems include the risk for hypertension, proteinuria (abnormal amounts of protein in the urine that can portend a decline in renal function), and reduced kidney filtration rate. Since the longest available follow-up studies of HUS victims are 25 years, an accurate lifetime prognosis is not really available and remains controversial. All that can be said for certain is that HUS causes permanent injury, and it requires a lifetime of close medical monitoring.

ReferencesContinue Reading The E. coli O157:H7 Bacteria and Hemolytic Uremic Syndrome (HUS)

Since the Jack in the Box E. coli Outbreak of 1993, I have been involved in every E. coli Outbreak and have represented the most seriously injured cases.  There have been far too many deaths.

* AFG / Supervalu E. coli Outbreak – Minnesota
* AgVenture Farms Petting Zoo E. coli O157:H7 Outbreak Litigation –…