Originally posted by Remy
"Anemones have nematocysts, a.k.a. stinging cells, and can be dangerous to the touch. These creatures can cause injury or death".
I'm not to worried ( should i Be ?), but i was wondering how often does death and injuries occur?
Its really very rare, but some people do have a problem with it, I have other articles along this line, but like I said its very rare.
BRIEF REPORT
Fulminant Hepatic Failure from a Sea Anemone Sting
Patricia J. Garcia; Roland M. H. Schein; and Joseph W. Burnett
15 April 1994 | Volume 120 Issue 8 | Pages 665-666
Coelenterate stings can produce various local and systemic reactions. We report the first known case of fulminant hepatic failure attributable to a sea anemone sting. The patient, who developed hepatic failure within 3 days of envenomation, had negative hepatitis serologic tests and no other potential hepatotoxin exposure. A biopsy of the liver showed massive hepatic necrosis. The patient's serum tested positive for IgG by enzyme-linked immunosorbent assay (ELISA) against Condylactis sp. antigen at a dilution of 1:450. We retrospectively tested serum from another man who had had transient elevations of liver function levels after a presumed coelenterate sting, and the titers to Condylactis sp. antigen were identically elevated.
A 28-year-old, previously healthy white man was transferred to Jackson Memorial Hospital in Miami, Florida, from St. Thomas, Virgin Islands, because of hepatic failure complicated by coma, severe coagulopathy, and acute renal failure. He had no history of alcohol or drug abuse or previous abnormal reaction to stings. The patient had sustained a sting from a sea anemone on the left scapula while free diving at 6 to 10 meters. Ten to 15 minutes after contact, he developed a vesicular eruption and severe pain in the back and arms. When he arrived at a local hospital approximately 30 minutes after the sting, he was alert and oriented and his vital signs were normal. Intravenous fluids and meperidine were administered during his 24-hour hospitalization. After discharge, he became progressively weak and lethargic and was rehospitalized 24 hours later with jaundice and elevated liver enzyme levels. Between hospitalizations he had remained in bed and taken no medications or alcohol. He was treated with piperacillin, aztreonam, dexamethasone, ranitidine, and bicarbonate. Because his neurologic status deteriorated further, 5 days after the sting he was endotracheally intubated and transferred to the intensive care unit at Jackson Memorial Hospital.
At arrival, he responded only to noxious stimuli. The remainder of the physical examination was normal except for jaundice and superficial ulcerations over the left scapular area Figure 1. Abnormal blood test results included prothrombin time, 75.2 s (normal range, 10.5 to 13.5 s); partial thromboplastin time, 74.5 s (normal range, 22.0 to 38.0 s); blood urea nitrogen, 15 mmol/L (42 mg/L); serum creatinine, 185 micromole/L (2.1 mg/dL); total bilirubin, 115 micromole/L (6.7 mg/dL); aspartate aminotransferase, 145 mu kat/L (8692 U/L); alanine aminotransferase, 155 mu kat/L (9313 U/L); and creatine kinase, 14.5 mu kat/L (872 U/L). A test for human immunodeficiency virus antibody (HIV) and hepatitis A, B, and C profiles were negative. Urine and blood toxicology studies were negative. During the next 3 days, the patient became progressively unresponsive. A computed tomographic scan showed a high-density area in the right temporal horn and posterior interhemispheric fissure and falx; the sulci were not visualized. The patient was treated for cerebral edema, although subarachnoid hemorrhage could not be excluded. In addition, he developed oliguric renal failure, with a serum creatinine of 813 micromole/L (9.2 mg/dL) and a urine sodium concentration of less than 10 mmol/L. The patient died after a liver and kidney were transplanted 4 days after he was transferred.
A biopsy of the explant liver showed massive necrosis with peripheral lobular regeneration throughout; the periportal area was clear. The kidneys showed mild tubular necrosis. Serum obtained 8 days after he was stung was positive by ELISA for IgG against Condylactis sp. antigen at a dilution of 1:450. The sea anemone identified by the patient's dive partners belonged to the group of Condylactis species Figure 2. Enzyme-linked immunosorbent assays for immunoglobulin G against other coelenterates were negative.
Contact with coelenterates accounts for most marine envenomations [1]. Coelenterates, a group of invertebrates, comprise more than 9000 species, of which approximately 100, belonging to the phylum Cnidaria, are recognized as venomous. The Cnidaria are subdivided into three classes: Hydrozoa, for example, Portuguese man-of-war; Schiphozoa, for example, jellyfish and sea nettle; and Anthozoa, for example, sea anemone and corals. Cnidaria inflict their stings with organelles, called nematocysts, located in their epithelial tissues [2]. These structures contain coiled polypeptide toxin-coated threads that can be expelled with a force of 2 to 5 psi and penetrate the nerve- and vascular-rich dermis [3].
Previously reported coelenterate envenomation syndromes include local reactions induced directly by the toxin; recurrent, delayed, or persistent reactions (fat atrophy, mononeuritis multiplex); and systemic sequelae of varying severity. Anaphylactic shock, acute renal failure, and sudden cardiac or respiratory arrest have reportedly caused death [4,5,6].
This patient's massive hepatic necrosis seems to have been caused by a toxin. The patient had no detectable antecedent liver disease, and his serologic tests for viral hepatitis A, B, and C were negative. The patient was not hypotensive after the sting, and no autopsy findings indicated other forms of ischemic liver injury. Although a MEDLINE search showed no previous reports linking coelenterate envenomation with acute hepatic failure, coelenterate-induced hepatic injury has been shown in rats challenged with intravenous sea nettle venom [7]. Mid-zonal liver necrosis and renal tubular damage were detected in the absence of alteration in central hemodynamic variables. The difference in histologic findings between this animal model and our patient may be related to species variability (mid-zonal necrosis is rare in humans) or to the short course of the animal experiments [8].
We are aware of only one report of hepatic injury after a presumed coelenterate sting in humans [9]. A Florida man experienced local pain, eruption, vomiting, and elevation of liver enzymes for more than 16 days. When we tested his serum retrospectively for titers against Condylactis sp. antigen, we found them to be identical to those of the patient whose case we report.
Specific anti-jellyfish IgG serum concentrations may appear a few days after envenomation and persist for many months. Significant titers have been defined as those positive after dilutions of 50-fold or greater. In a serologic study, each of 74 jellyfish-envenomated patients had clinically significant IgG titers, whereas 5 false-positive reactions occurred in 30 control patients [10]. When positive titers were present to several species, the antigen titer from the known offending species was the highest, thus supporting use of the ELISA as a diagnostic test.
Because coelenterate envenomation may produce acute hepatic injury, increased awareness may lead to better reporting of cases and stricter reinforcement of the use of protective diving clothing and early first-aid measures. Our experience emphasizes that care of the severely affected patient should take this clinical possibility into account.
Acknowledgments: The authors thank Dr. George Hensley for preparation of pathology specimens, Dr. Eugene Schiff for review of the manuscript, and Mrs. Jan Kampka and the Medical Media staff for technical assistance in the preparation of the manuscript.
From the University of Miami School of Medicine and the Department of Veterans Affairs Medical Center, Miami, Florida, and the University of Maryland School of Medicine, Baltimore, Maryland.
Requests for Reprints: Patricia J. Garcia, MD, Department of Veterans Affairs Medical Center, Medical Service RF 111, N.W. 16th Street, Miami, FL 33125.
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