Kaelbel Wholesale, Inc. v. Soderstrom

Decision Date21 February 2001
Docket NumberNo. 4D99-406.,4D99-406.
Citation785 So.2d 539
PartiesKAELBEL WHOLESALE, INC., a Florida corporation, Appellant, v. Pamela SODERSTROM, Appellee.
CourtFlorida District Court of Appeals

Gilbert E. Theissen of Heinrich Gordon Hargrove Weihe & James, P.A., Fort Lauderdale, for appellant.

Arnold R. Ginsberg of Ginsberg & Schwartz, Robert J. Bryan, P.A., and Lance R. Stelzer, Miami, for appellee.

WARNER, C.J.

We are confronted in this appeal with the question of whether the trial court erred in allowing expert evidence under the standard of Frye v. United States, 293 F. 1013 (App.D.C.1923). Appellant contends that the evidence did not meet the Frye test requirement that it be generally accepted in the relevant scientific community. Particularly, the experts' testimony linked appellee's ciguatera poisoning, which she contracted from fish supplied to a restaurant by appellant, to her development of Guillain-Barré Syndrome ("GBS"), a neurological disorder. We conclude that the testimony did not meet the Frye test and reverse the final judgment.

I. Biological Explanation of Ciguatera and Guillain-Barré Syndrome

Appellee, Pam Soderstrom, had dinner at a restaurant in Fort Lauderdale, consuming snapper for her main course. Shortly after dinner, she noticed a tingling sensation in her left hand. She continued her evening activities and then went to bed. During the night, her sleep was interrupted by an upset stomach and some mild diarrhea. The next day the "pins and needles" sensation continued, now in both hands, but the intestinal problems subsided. By late the next day, with the symptom still persisting, she became alarmed, as the tingling was in both arms and both legs. She visited a hospital emergency room, where a doctor suspected that she had suffered ciguatera poisoning, based upon her symptoms and her history of consuming fish two days before. Appellant's brief explains:1

Ciguatera is the name given to as many as twenty different naturally occurring marine toxins produced by tropical algae. Although it has been known since the early sixteenth century, it first acquired a name in the late eighteenth century when a Portuguese biologist in Cuba first recorded intoxication following the consumption of a "cigua" or turban shellfish. These toxins can be found in hundreds of different species of fish and are thought to bioaccumulate up the food chain as small marine organisms ingest the algae and are, in turn, eaten by larger and larger fish. The toxins are tasteless, odorless and unaffected by cooking or freezing.
Since ciguatoxin is acquired by ingestion, gastrointestinal disturbances, such as vomiting, abdominal cramping and diarrhea are usually the earliest symptoms to appear. These symptoms generally last a day or two and are commonly followed by disturbances to the sensory nervous system. These disturbances consist of paresthesias (numbness and tingling) in the extremities, dyesthesias (reversal of hot and cold sensation) and gustatory paraesthesias (food tasting metallic). Ciguatera causes these sensory disturbances by interfering with structures in the nerve cell called sodium (Na+) channels.
Nerve cells have a fibrous covering called myelin which, in some respects[,] is similar to the insulation around an electrical wire. However, unlike an electrical wire, the myelin covering is not continuous. Instead, at regular intervals, there are gaps in the myelin where structures called Nodes of Ranvier are located. These Nodes act like relay stations and continually reamplify the neural impulse as it travels along the nerve. They accomplish this by means of a controlled influx of sodium (Na+) ions coupled with a corresponding outflux of potassium (K+) ions through microscopic channels in the cellular membrane. These sodium (Na+) and potassium (K+) channels are, for the most part, located at the Nodes of Ranvier and, through a controlled opening and closing of these channels, the nerve impulse, which would otherwise continue to weaken, is reamplified and then sent along the nerve to the next Node. There the process is repeated and, in this fashion, the impulse is transmitted along the entire length of the nerve.
Ciguatera causes sensory disturbances when the molecules of the toxin attach themselves to the sodium (Na+) channels at the Nodes of Ranvier. When the ciguatoxin molecules bind to the sodium (Na+) channels, they have the effect of locking these channels open and this, in turn, places the nerve in a constant state of activation. Because of the continual stimulation, the nerve discharges repeatedly, giving rise to numbness, tingling, and a variety of other abnormal sensations.

In appellee's case, her symptoms were mild, and the doctor did not admit her to the hospital. The next day she saw another doctor, who prescribed an IV infusion of Mannitol, which usually is effective in reducing the symptoms of ciguatera. However, the drug had no effect on appellee's symptoms, and in fact they began to worsen, experiencing weakness in both of her legs. As the symptoms increased, even after a second Mannitol treatment, she realized that she was losing all strength and needed hospitalization. By the time she was admitted, she was paralyzed from the waist down. At that point, the doctors diagnosed her as suffering from GBS.

As appellant observes in its brief:

Guillain-Barré Syndrome ("GBS") is a neurological disorder which usually attacks motor nerves and is currently the most common cause of acute generalized paralysis. GBS was first described more than one hundred years ago and was initially called Landry's Ascending Paralysis because of a characteristic pattern of weakness and paralysis starting in the lower extremities and, over a matter of days, ascending up the body. In severe cases, it may affect respiration and even eye movement. In Plaintiffs case, she was in Intensive Care for almost three weeks, paralyzed from the waist down and unable to even control her eyelids. It [the paralysis] was unquestionably "the most disabling part of her problem."
GBS affects a different part of the nerve than ciguatera. Instead of disrupting the flow of sodium (Na+) ions through the sodium channels, GBS attacks the myelin sheath and is therefore referred to as one of many "demyelinating" neuropathies. Like the insulation around a wire, the myelin helps to preserve the strength of the nerve impulse as it travels along the nerve. When the myelin sheath of a motor nerve becomes damaged, the impulse is no longer conducted normally. This, in turn causes weakness, and when the damage is severe —paralysis.
Although our knowledge of this disease is still evolving, the current view is that GBS is the result of an aberrant auto-immune response to certain events, usually bacterial or viral infections, which precede the onset of this disease by one to four weeks. It has long been known that the body defends itself against bacterial and viral invasions by producing antibodies which target and attack these invaders, and, it is now believed by some, that the destruction of the myelin (demyelinization) seen in GBS is the result of an aberrant antibody response to these infections or other stimuli which provoke an immunologic response.
Since GBS has been recognized for more than a hundred years, the list of known or suspected antecedent events to GBS is quite extensive. Even so, the cause of GBS is not always known, and even today, roughly one-third of GBS cases are considered idiopathic. Although ciguatera has never been suspected as a cause of GBS, a diarrhea causing bacteria called campylobacter jejuni, and a viral infection known as cytomegalovirus ("CMV") have both long been known as precursors to this disease. Interestingly enough, aside from plaintiff's previously mentioned bout with diarrhea, hospital tests performed after her admission for GBS revealed the presence of an earlier CMV infection.

After appellee made some level of recovery, she filed suit against appellant alleging that it had supplied the fish to the restaurant, that the fish was defective, having contained the ciguatera toxin, and that the ciguatera toxin had caused the GBS. Prior to trial, appellant moved to exclude appellee's expert testimony as to the causal link between ciguatera and GBS, alleging that this was a novel theory and not generally accepted within the relevant scientific community, thus inadmissible under Frye. Although the motion was initially denied, appellant renewed it prior to trial. Rather than interrupt the trial with a series of Frye hearings, the court decided to listen to the expert evidence as it was presented to the jury and make its ruling at the close of the evidence. Ultimately, the court reserved ruling and submitted all issues to the jury. The jury returned a verdict in appellee's favor, and, post-trial, the court denied the motions for judgment notwithstanding the verdict, prompting this appeal in which appellant claims that appellee's experts' testimony did not meet the Frye test.

II. Expert Testimony

Appellee presented two experts, the first of whom was Dr. Robert Lange, an internist specializing in the field of epidemiology, which is the study of diseases in populations rather than individuals. He considered himself an expert on ciguatera but not on GBS, with which he had no clinical experience. While he conceded that ciguatera has never been associated with GBS in any medical or scientific literature, Dr. Lange still opined that ciguatera poisoning caused appellee's GBS based upon his explanation of how such causation might occur in the body. He first explained how ciguatera affected the nerves of the body, which explanation was consistent with what has been previously set forth in this opinion. He postulated that after prolonged activation of the sodium channels by the ciguatera toxin, the sodium channel is "probably" distorted, and its shape is affected. (Emphasis added). The sodium...

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