In January of last year, I was exposed via inhalation to Palytoxin Poisoning from our salt water tank. Zoanthids are coral that contain this lethal poison. We were attempting to boil live rock which had green algae on it. We had done this many times before so thought nothing of it until we discovered 3 stalks of Zoas on the rocks. Within 30 minutes neither one of us could breathe and were experiencing severe chest pain and dizziness. We then went to the hospital. The fact that palytoxin poisoning is possible by disrupting this type of coral is not commonly known and you are not warned when purchasing at a salt water store. This is a very dangerous situation as there is no known anti-toxin and 3 out of 4 people die from exposure.
Picture of zoanthids above. As you can see they are very beautiful. A stalk is about the size of the end of a pencil eraser. Medical Journal insertion is below.
Aquarist be warned: Palytoxin-induced acute respiratory distress syndrome
Abstract:
Palytoxin is a potent poison released from a variety of marine organisms. It has an intravenous
median lethal dose(LD50) of 150ng/kg in mice, making it one of the most potent naturally
occurring toxins. Toxicity is commonly seen following ingestion and less frequently from
exposure through the transdermal, inhalational or ocular route. The toxin inhibits the sodiumpotassium
ATPase pump disrupting transmembrane ion fluxes culminating in cell death; since
the ATPase pump is ubiquitous, many organ systems can be affected. Palytoxin inhalation is a
rare cause of acute respiratory distress syndrome. Here we report a family that was affected by
this toxin as they were cleaning their saltwater aquarium.
Introduction
Many aquarists attempt to simulate the natural living environments of their pets with corrals,
algae, sea anemones and other aquatic organisms. Unfortunately, aquarists may be unaware of
the toxins released by the organisms in their artificial aquatic biomes. Palytoxin is one of the
many marine toxins known to man. Human poisoning after consumption of postulated palytoxin
contaminated food is thought to be the commonest presentation. The inability to detect the toxin
in serum or other body fluids hampers a convincing diagnosis of palytoxin toxicity. Acute
respiratory distress syndrome is a rare presentation following palytoxin exposure.
Case presentation
Patient 1
A 46-year-old woman with history of type 1 diabetes mellitus and anxiety disorder presented to
the emergency department due to complaints of acute dyspnea, cough and burning sensation in
the chest. These complaints started several seconds after she and her spouse were exposed to
fumes from boiling aquarium rocks covered in green coral algae in their salt water fish tank.
Upon presentation in the emergency department, she was afebrile, pulse rate was 130/minute,
respiratory rate 32/minute, oxyhemoglobin saturation was 88 percent on ambient air. Physical
examination was remarkable for increased work of breathing and diminished breath sounds throughout the lungs. A frontal chest x-ray showed no acute process (Figure1). Her laboratory
investigations were remarkable for leukocytosis of 18 x10(9)/L with left shift (normal white count
3.4 – 9.6 x10(9)/L) , lactate of 5.4 mmol/L (normal range 0.6 – 2.3 mmol/L) an anion gap of 16
(normal: less than12). Her urine drug screen was negative.
She was admitted to the intensive care unit for close monitoring and initiated on normal saline
infusion, intravenous glucocorticoids, bronchodilators and empiric antibiotic coverage. Despite
all these, she developed hyperthermia as high as 40.3 centigrade later in the day. The next day
her respiratory status worsened requiring Venturi mask. ABG showed hypoxemia with a
PaO2/FiO2 ratio of 140. Repeat Chest x-ray and chest computer tomography (CT) showed
diffuse bilateral pulmonary opacities suggestive of adult respiratory distress syndrome (Figure 2
– 4). She was treated supportively with separation from the offending inhalational insult, highflow
supplemental oxygen, rehabilitation, and DVT prophylaxis. She was successfully weaned
to nasal cannula oxygen on the 4th day of hospitalization and discharged from the hospital on
the 5th day.
Patient 2
The 49-year-old husband of the patient 1 above also presented to the ED with a persistent
cough and shortness of breath after accidental exposure to the vapors. He had been standing
behind his wife as she was boiling the coral rocks. He also developed cough, wheezing, and
shortness of breath immediately after the exposure. At the time of admission, his pulse rate was
110/minute, respiratory rate 24/minute, oxyhemoglobin saturation normal. Physical examination
revealed rhonchi at the lung bases. His laboratory workup revealed WBC 25 x10(9)/L with left
shift (normal white count 3.4 – 9.6 x10(9)/L), anion gap 16 (normal 12) and lactate 3.8 mmol/L
(normal range 0.6 – 2.3 mmol/L). His urine drug screen was negative. A plain-film frontal chest
radiograph was normal. A high-resolution CT chest demonstrated ground-glass infiltrate at the
lower lungs posteriorly. The patient was managed with supplemental oxygen, bronchodilator
therapy, intravenous rehydration, empiric IV levofloxacin, and IV hydrocortisone. The patient’s
condition improved after 48 hours of management. He was weaned off oxygen and discharged
home on a bronchodilator, oral prednisone and the remainder of the levofloxacin course.
The complex non-polymeric chemical structure of this naturally occurring poison was elucidated
in 1981. It is not inactivated by boiling and is stable in neutral aqueous solutions for prolonged
periods. Acidic or alkaline conditions promote rapid decompensation, thus loss of its toxicity
when sources are treated with disruptions in pH.(10) The inhalational median lethal dose (LD50)
of palytoxin in rats is 0.36g/kg; it is more lethal than sarin(LD50 154g/kg) and VX nerve
gas(LD50 110.7g/kg). The sodium-potassium ATPase pump is the primary binding site of the
toxin, converting these ion-specific pumps into non-selective cationic pores.(13) The disrupted
ion pumps result in cell death due to Ca2+ overloading. Palytoxin and its congeners alter the
ion homeostasis in excitable (muscles and nerves) and non-excitable(GI tract, lung) tissues.
Clinical effects of inhaled palytoxin poisoning
In 2005, approximately 200 people near Genoa, Italy experienced symptoms of rhinorrhea,
cough, mild dyspnea, bronchoconstriction, and fever in summer when an unusual bloom of
Ostreopsis ovata was noted on the coast. The symptoms peaked and resolved in association
with the bloom climax and dissipation, respectively. The putative Palytoxin was identified in the
seawater samples using light chromatography with mass spectrometry.(14) In the large study
population by Murphy, the most common clinical effects reported were fever (61.4%), dyspnea
(54.5%), cough (34.1%), tachycardia (20.5%), muscle weakness (18.2%) and vomiting
(18.2%).(9) Patients developing chest pain, fever, dyspnea, and tachycardia were more
commonly admitted in the ICU.(9)
Tubaro et al. noted a scarcity of information regarding confirmed poisonings due to the
methodological difficulties for toxin detection in human biological samples.(15) Hence, a case
definition of inhalational exposure to palytoxin was proposed which constitute the following –
1. Stay at the seaside(<90m from the shore-line) in concomitance with an algal bloom, or in
laboratories dealing with algae/algal toxins, inhalation of steam from cleaning aquaria
2. Seeking medical care
3. Presence of at least two of the following signs/symptoms – local dermatitis, systemic
cutaneous rash, numbness or weakness of the extremities, dizziness, myalgia, chest
pain, breathing difficulties, fever, neurological disorder.(15)
Both our patients satisfy the case definition of palytoxin poisoning as mentioned above. Patient
1, who was in immediate contact with the toxin, developed acute respiratory distress syndrome.
Patient 2, who was in the vicinity but farther from the coral rocks, developed less severe
symptoms/signs consistent with palytoxin poisoning. The severity of symptoms/signs following
transient exposure to its fumes is noteworthy.
Management of palytoxin exposure
There is no specific antidote to palytoxin, so management of palytoxin poisoning is supportive
and focused on treating the clinical sequelae, such as respiratory failure, ARDS, and shock.
Oxygen, bronchodilators, intravenous fluids, antihistaminics, and steroids (inhalational and/or
systemic) are commonly employed, although controlled efficacy data is lacking. No definitive guidelines for the management of patients exposed to this toxin have been developed due to its
rarity.
Conclusion
Palytoxin poisoning is a potential complication of exposure to aquarium-related flora. Diagnosis
of palytoxin poisoning is hampered due to the absence of tests which can detect the toxin in
human tissue and is therefore a clinical diagnosis. Major symptoms develop following a few
seconds of exposure to this potentially lethal toxin due to its potent nature. There is no antidote
to palytoxin poisoning, and management is supportive. It is imperative that physicians be aware
of this toxin’s lethal nature for prompt management.
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