One figure, one table omitted
Botulism is a neuroparalytic illness caused by toxins produced by the
bacterium Clostridium botulinum, an obligate anaerobe
found commonly in the environment. Intoxication with toxin type E is associated
exclusively with eating animal foods of marine (salt or fresh water) origin.
Persons who eat raw or fermented marine fish and mammals are at high risk
for botulism from type E toxin. On July 17, 2002, the Alaska Division of Public
Health investigated a cluster of suspected botulism cases among residents
of a fishing village in Alaska. This report summarizes the findings of the
outbreak investigation, which linked disease to eating raw muktuk (skin and
a pink blubber layer) from a beached whale. To avoid delays in treatment,
health-care providers evaluating patients suspected of having botulism should
base treatment decisions on clinical findings. Public health authorities should
be notified immediately about any suspected botulism case.
During July 13-15, residents of a western Alaska village on the Bering
Sea shore shared a meal consisting of muktuk harvested from a beached adult
beluga whale found near their village. The villagers estimated that the whale
had been dead for at least several weeks. They cut the whale fluke (tail)
into pieces and stored them in zipper-sealed plastic bags in a refrigerator
until they were eaten 1 or 2 days later. On July 17, after a physician from
western Alaska reported three suspected cases of botulism among patients who
had eaten the muktuk, the Alaska Section of Epidemiology began an investigation.
A case of foodborne botulism was defined as illness in a person who
had eaten the muktuk and subsequently had symmetric descending flaccid paralysis
of motor and autonomic nerves. Persons who ate muktuk were interviewed and
examined, and their hospital records were reviewed. Serum, stool, and gastric
contents from patients and leftover blubber were tested for botulinum toxin.
Of 14 persons identified who ate the muktuk, eight (57%) had an illness
that met the case definition. Five of the eight patients were female; the
median age was 73 years (range: 13-83 years). Symptom onset after ingestion
of muktuk occurred within 36 hours in all patients. Five patients were hospitalized,
four received antitoxin, and two required mechanical ventilation. Three stool,
three gastric fluid, and seven serum samples from the eight patients and seven
samples of muktuk were tested for botulinum toxin at CDC's National Botulism
Surveillance and Reference Laboratory. The diagnostic laboratory received
all laboratory specimens on July 26, and results were reported on August 1.
Type E toxin was detected in stool from one patient. All seven samples of
muktuk were positive for type E botulinum toxin.
Reported by:
J Middaugh, MD, T Lynn, DVM, B Funk, MD, B Jilly, PhD, Div of Public
Health, Alaska Dept of Health and Social Svcs. Div of Bacterial and Mycotic
Diseases, National Center for Infectious Diseases; S Maslanka, PhD, Div of
Applied Public Health Training, Epidemiology Program Office; J McLaughlin,
MD, EIS Officer, CDC.
CDC Editorial Note:
This report summarizes a foodborne outbreak of botulism in a western
Alaska village that resulted from residents eating muktuk contaminated with
type E botulinum toxin. During 1973-1998, a total of 814 cases and an annual
median of 24 cases (range: 14-94 cases) of foodborne botulism were reported
to CDC1; 236 (29%) of these cases occurred
in Alaska (CDC, unpublished data, 2003). Although botulism is a rare disease,
its presentation is distinctive (Box). Because of the epidemic potential of
foodborne botulism, every case should be reported and investigated immediately.
CDC Editorial Note:
All patients suspected of having foodborne botulism should be placed
in an intensive care setting, monitored regularly for respiratory function
deterioration, and provided mechanical ventilation if necessary. Prompt administration
of polyvalent equine-source antitoxin can decrease the progression of paralysis
and severity of illness but will not reverse existing paralysis. Botulinum
antitoxin is available in the United States only through the public health
system. Therefore, rapid clinical diagnosis, notification of public health
authorities, and timely administration of antitoxin are imperative.2 Laboratory confirmation of botulinum intoxication
cannot be relied on in making treatment decisions because the standard test,
the mouse bioassay, requires approximately 4 days for final results.2 In addition, the sensitivity of laboratory testing
of clinical samples is low.3- 4 In
this outbreak, typed toxin was detected in only 8% of samples from patients
who had definitive exposure to contaminated muktuk.
CDC Editorial Note:
The probable mode of contamination of the whale in this outbreak was
either growth and toxin secretion by C. botulinum present
in the intestinal tract of the whale or traumatic introduction of C. botulinum spores into the beached whale tissue from contact with
sand, rocks, and driftwood, and subsequent germination and toxin production. C. botulinum type E has been found in Alaska coastline
soil,5 and outbreaks of botulism associated
with eating beached marine mammals are documented (Alaska Section of Epidemiology,
unpublished data, 2003). A previous report on the accumulation of C. botulinum toxins in the North Sea coastal food chain associated
with beached whales suggested the disposal of the carcasses as a preventive
measure.6 However, because of the impracticality
of frequent scanning of the vast Alaska shoreline and high costs associated
with disposal, the U.S. Fish and Wildlife Service does not remove beached
mammal carcasses regularly.
CDC Editorial Note:
Because of the epidemic potential of foodborne botulism and the status
of botulinum toxins as a category A agent of terrorism, health-care providers
should be familiar with the presentation of botulism. Treatment is based on
clinical diagnosis, and rapid recognition and reporting of cases are the cornerstones
of successful public health interventions to prevent additional illnesses.
Persons should avoid eating beached marine mammal carcasses and boil raw or
fermented Alaska Native dishes ≥10 minutes before eating to inactivate
botulinum toxin. Additional information on botulism prevention is available
at
http://www.phppo.cdc.gov/phtn/botulism/alaska/alaska.asp and
http://www.epi.hss.state.ak.us/pubs/botulism/bot_01.htm.
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
• Caused by eating foods contaminated with preformed toxins of Clostridium botulinum
Home-canned foods and raw or fermented Alaska Native dishes commonly
associated with illness
During 1973–1998, a total of 814 cases and an annual median
of 24 cases (range: 14–94 cases) of foodborne botulism reported in the
United States; 236 (29%) in Alaska
Humans affected by toxin types A, B, E, and rarely F; type E
intoxication associated exclusively with eating marine animals
Classified as a category A terrorism agent
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
• Cranial nerve palsies
Symmetrically descending flaccid voluntary muscle weakness possibly progressing to respiratory compromise
Normal body temperature
Normal sensory nerve examination findings
Intact mental status despite groggy appearance
Differential diagnosis includes Guillain-Barré syndrome,
myasthenia gravis, stroke, drug overdose, and other entities
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
Normal cerebrospinal fluid values • Specific electromyography
(EMG) findings including — normal motor conduction velocities —
normal sensory nerve amplitudes and latencies — decreased evoked muscle
action potential — facilitation following rapid repetitive nerve stimulation
Standard mouse bioassay positive for toxin from clinical specimens
and/or suspect food; requires up to 4 days for final results
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
Prompt administration of polyvalent equine-source antitoxin —
can decrease the progression of paralysis and severity of illness —
will not reverse existing paralysis — available in the United States
only through the public health system
Place suspect cases in an intensive care setting
Monitor for respiratory function deterioration every 4 hours
using forced vital capacity testing
Provide mechanical ventilation if necessary
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
BOX. Epidemiology, diagnosis, treatment, and prevention of foodborne botulism
Boil raw or fermented Alaska Native dishes and homecanned foods
>10 minutes before eating
Follow recommended home-canning procedures
Notify state health department immediately of suspected cases
References
Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidemiologic review. Ann Intern Med.1998;129:221-8.
Woodruff BA, Griffin PM, McCroskey LM.
et al. Clinical and laboratory comparison of botulism from toxin types A,
B, and E in the United States, 1975-1988. J Infect Dis.1992;166:1281-6.
Dowell Jr VR, McCroskey LM, Hatheway CL.
et al. Coproexamination for botulinal toxin and clostridium botulinum: a new
procedure for laboratory diagnosis of botulism. JAMA.1977;238:1829-32.
Miller LG. Observations on the distribution and ecology of Clostridium botulinum type E in Alaska. Can J Microbiol.1975;21:920-6.
Stede M. Problems of disposal of dead marine mammals. Dtsch Tierarztl Wochenschr 1997;104:245-7.