DP - 2003 Mar
TI - Oral treatment of organophosphate poisoning in mice.
PG - 286-8
AB - OBJECTIVE: Organophosphates are used as pesticides, herbicides, and
chemical warfare agents. Treatment of organophosphate poisoning is with
intravenous atropine and pralidoxime in addition to supportive care. This
study determined the efficacy of oral agents in preventing death from
organophosphate poisoning. METHODS: The organophosphate paraoxon (8 mg/kg)
was used in a murine model with lethality at four and 24 hours as an end
point. For oral treatment, 15 male Balbc mice were given either atropine
sulfate (4 mg/kg), or a combination of atropine sulfate (4 mg/kg) with
pralidoxime (100 mg/kg), by oral gavage. A control group of 22 mice
received water by oral gavage. Chi-square analysis was used to compare
results in the different groups. RESULTS: Of the control group, six of 22
survived to four hours after paraoxon exposure. Of the exposed animals
treated with oral atropine, eight of 15 survived to four hours. Of the
exposed animals treated with a combination of atropine and pralidoxime, 13
of 15 survived to four hours. All animals surviving to four hours survived
to 24 hours. The increased survival of animals in the atropine group
relative to the control group was not significant (p = 0.09). Survival was
significant in the group treated with atropine and pralidoxime relative to
atropine alone (p = 0.02) and to the control group (p = 0.0002). All
treated mice surviving at four hours were alive at 24 hours. CONCLUSIONS:
Both oral atropine and a combination of oral atropine and pralidoxime
improved survival, and combination therapy achieved statistical
significance. Generalization of this result to other organophosphate
pesticides, other doses of paraoxon, and other species cannot be made
without further investigations.
AD - Department of Emergency Medicine, Brody Medical School at East Carolina
University (BJB, JMF, JAL, WJM), Greenville, NC.
SO - Acad Emerg Med 2003 Mar;10(3):286-8.

DP - 2003 Feb
TI - Electrolyte-balanced sports drink for polydipsia-hyponatremia in
schizophrenia.
SO - Am J Psychiatry 2003 Feb;160(2):385-6.

DP - 2003 Feb 15
TI - Short and long term mortality associated with foodborne bacterial
gastrointestinal infections: registry based study.
PG - 357
AB - OBJECTIVES: To determine the excess mortality associated with infections
with Salmonella, Campylobacter, Yersinia enterocolitica, and Shigella and
to examine the effect of pre-existing illness. DESIGN: Registry based,
matched cohort study. SETTING: Denmark. PARTICIPANTS: 48 857 people with
gastrointestinal infections plus 487 138 controls from the general
population. MAIN OUTCOME MEASURE: One year mortality among patients with
gastrointestinal infections compared with controls after adjustment for
comorbidity. RESULTS: 1071 (2.2%) people with gastrointestinal infections
died within one year after infection compared with 3636 (0.7%) controls.
The relative mortality within one year was 3.1 times higher in patients
than in controls. The relative mortality within 30 days of infection was
high in all four bacterial groups. Furthermore, there was excess mortality
one to six months after infection with Yersinia enterocolitica (relative
risk 2.53, 95% confidence interval 1.38 to 4.62) and from six months to
one year after infection with Campylobacter (1.35, 1.02 to 1.80) and
Salmonella (1.53, 1.31 to 1.79). CONCLUSIONS: Infections with all these
bacteria were associated with an increased short term risk of death, even
after pre-existing illnesses were taken into account. Salmonella,
Campylobacter, and Yersinia enterocolitica infections were also associated
with increased long term mortality.
AD - Department of Epidemiology Research, Danish Epidemiology Science Centre,
Statens Serum Institut, DK-2300 Copenhagen S, Denmark.
SO - BMJ 2003 Feb 15;326(7385):357.

DP - 2003 Feb 1
TI - Consumption of arsenic through cooked rice.
SO - Lancet 2003 Feb 1;361(9355):435-6.

DP - 2003 Jan 17
TI - Outbreak of botulism type E associated with eating a beached
whale--Western Alaska, July 2002.
PG - 24-6
AB - 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 (Figure). 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.
SO - MMWR Morb Mortal Wkly Rep 2003 Jan 17;52(2):24-6.

DP - 2003 Jan 17
TI - Infant botulism--New York City, 2001-2002.
PG - 21-4
AB - Infant botulism results from germination of swallowed spores of botulinum
toxin-producing clostridia that colonize the large intestine temporarily.
Four cases of type B infant botulism in one New York City (NYC) borough
were diagnosed within a 12-month period during 2001-2002. All four
patients resided in Staten Island (2000 population: 443,728). The annual
incidence of infant botulism in the United States is two cases per 100,000
live births; incidence in NYC is four cases per 100,000 live births.
Staten Island recorded 5,899 live births in 2000; incidence of infant
botulism during this 12-month period was 68 cases per 100,000 live births.
This report summarizes the investigation of these four cases; as expected
with infant botulism, a common source of exposure was not identified. All
four patients recovered after treatment and were discharged from local
hospitals. State and local health departments should be notified promptly
when infant botulism is suspected to arrange diagnostic testing.
SO - MMWR Morb Mortal Wkly Rep 2003 Jan 17;52(2):21-4.

DP - 2003 Jan 6
TI - Severity of Irukandji syndrome and nematocyst identification from skin
scrapings.
PG - 38-41
AB - OBJECTIVES: (1) To identify the causative jellyfish species by examining
skin scrapings in patients presenting to Cairns Base Hospital with marine
stings, and (2) to describe clinical outcomes of those with Irukandji
syndrome and those in whom nematocysts were identified from skin
scrapings. DESIGN AND SETTING: (1) A retrospective case series of 128
patients, identified from Cairns Base Hospital emergency department
records with discharge diagnoses of marine stings between 1 July 2001 and
30 June 2002. (2) A prospective study of skin scrapings from 50 patients
presenting with marine stings from the same period. MAIN OUTCOME MEASURES:
Number of patients with Irukandji syndrome, their opioid requirements and
cardiac findings (where available); identification of causative species
from nematocysts isolated from skin scrapings. RESULTS: 116 patients
retrospectively identified with marine stings had Irukandji syndrome. Of
50 patients who had skin scrapings, 39 had nematocysts consistent with
Carukia barnesi. Symptoms experienced ranged from local pain alone to
severe Irukandji syndrome with elevated troponin I levels, changes on
electrocardiogram, cardiac dysfunction on echocardiography, and high
opioid dose requirements. One patient had an unidentified cnidome on his
skin scraping. He developed severe Irukandji syndrome and subsequently
died from its complications. CONCLUSION: This is the first published
report of Carukia barnesi being successfully identified from skin
scrapings. Most patients with identifiable cnidomes experiencing Irukandji
syndrome were stung by Carukia barnesi, which we show causes a wide range
of illness, including cardiac dysfunction. Our finding of a cnidome not
consistent with Carukia barnesi in the setting of Irukandji syndrome makes
it possible that other species of jellyfish may also cause this syndrome.
AD - Emergency Department, Cairns Base Hospital, Cairns, Queensland 4870,
Australia.
SO - Med J Aust 2003 Jan 6;178(1):38-41.

DP - 2003 Jan 6
TI - Jellyfish envenoming syndromes: unknown toxic mechanisms and unproven
therapies.
PG - 34-7
AB - Interest in envenoming syndromes caused by Australian jellyfish has been
intense since the deaths in early 2002 of two tourists in Queensland,
attributed to the Irukandji syndrome. We review current knowledge of these
envenoming syndromes, mechanisms of venom action and therapy, focusing on
the deadly box jellyfish, Chironex fleckeri, and the array of jellyfish
thought to cause the Irukandji syndrome. Current understanding of
jellyfish venom activity is very limited, and many treatments are unproven
and based on anecdote.
AD - Department of Biochemistry, University of Western Australia, 35 Stirling
Highway, Crawley, WA 6009, Australia. pbailey@iinet.net.au
SO - Med J Aust 2003 Jan 6;178(1):34-7.