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Toxicology Case: The poison in the pond: Blue-green algae toxicosis in a young dog
A look at the presenting signs, diagnosis and treatment of blue-green algae toxicosis in a 9-month-old German shepherd mix.
A 9-month-old 60.5-lb (27.5-kg) spayed female German shepherd mix was presented to a veterinary clinic nonambulatory and recumbent.
(GETTY IMAGES/KAREN HERMANN)
Before the clinic visit, the owner had taken the dog for a walk and noted no abnormalities. After the walk, the dog was left in the backyard unsupervised for about 30 minutes and then let inside the house. The owner noticed the dog's eyes were rolling back and its gait was uncoordinated. The dog also defecated in the house.
At presentation, the dog was ataxic, panting, and drooling excessively. Its body temperature was 103.4 F (39.7 C). No other abnormalities were noted during the physical examination. The dog began seizing in the examination room and vomited multiple times. The vomitus contained a plastic bag and large amounts of pond water with filamentous green slimy algae. The owner confirmed she had removed algae from the backyard pond and placed it in a plastic bag earlier that day.
Based on the large amounts of algae present in the vomitus and the rapid onset of severe neurologic signs, blue-green algae poisoning was suspected.
The dog was treated with diazepam (0.5 mg/kg intravenously) and intravenous fluids (0.9% saline solution at a rate of 60 ml/kg/day). It was also given one dose of activated charcoal (2 g/kg orally) through a stomach tube. The results of an electrocardiographic examination, complete blood count (CBC), and serum chemistry profile were all normal at this time.
Initially, the dog responded well to the diazepam; however, it started seizing again 30 minutes later. This time the diazepam had little effect in controlling the seizures. During the seizures, the dog stopped breathing. An endotracheal tube was placed immediately, and cardiopulmonary resuscitation was started. An electrocardiographic examination showed ventricular premature contractions that progressed to a flat line.
Atropine (0.02 mg/kg) was administered intravenously along with 2.9 mg/kg of doxapram to stimulate respiration, followed by another dose of doxapram (1.45 mg/kg) to further improve respiration. The dog improved rapidly. Pulse oximetry showed oxygen saturation at 94% to 98%. The dog's electrocardiogram (ECG) and blood pressure returned to normal. After receiving manual ventilation (12 breaths/min) for about 90 minutes, the dog started breathing on its own.
About three hours after presentation, before the dog was sent to a critical care facility, the dog seized again. Diazepam (0.5 to 1 mg/kg intravenously to effect) and then propofol (3 mg/kg intravenously) were administered, and the dog was transported while sedated.
Fifteen minutes after arriving at the critical care facility, the dog started seizing again and went into respiratory failure. The dog was intubated with a cuffed endotracheal tube and immediately began receiving positive pressure ventilation (8 to 20 breaths/min). Diazepam (0.5 to 1 mg/kg intravenously to effect) and then phenobarbital (2 mg/kg intravenous bolus) were administered for the seizures. The dog was kept sedated with fentanyl (5 μg/kg bolus and then 5 to 7 μg/kg/hour constant-rate infusion [CRI]) and propofol (0.1 to 0.6 mg/kg/min CRI) while receiving mechanical respiration.
A thoracic radiographic examination showed evidence of mild aspiratory pneumonia (about 5% of anterior lung lobe was involved). The dog continued to receive intravenous fluids (Normosol-R—Hospira), and antibiotics (ampicillin 250 mg/ml and sulbactam 125 mg/ml [Unasyn—Pfizer]; 20 mg/kg intravenously every eight hours for three days then orally for seven more days) were given.
After receiving mechanical respiration for about 18 hours, the dog started breathing on its own and was taken off the ventilator. During this time, the dog's blood pressure, heart rate, and ECG all remained normal. The only blood work changes noted 24 hours after presentation were slight increases in alanine transaminase (197 IU/L; normal = 20 to 100 IU/L) and alkaline phosphatase (236 μmol/L; normal = 0 to 212 μmol/L) activities.
The dog continued to improve and was discharged from the hospital three days after the exposure. Five days later, the owner reported that the dog was acting completely normal.
Blue-green algae are members of the phylum Cyanobacteria. Some species of cyanobacteria can produce toxins. They are microscopic organisms that form visible colonies in water under favorable conditions (stagnant water, fertilizer runoff) mostly during hot-weather months. The case discussed here occurred in July.
Blue-green algae blooms—large accumulations of algae—can occur in lakes, ponds, or rivers. These blooms are usually dark green or sometimes reddish brown. The wind propels the toxic algae to the shoreline where animals are exposed when they drink blue-green algae-contaminated water. Dogs are affected when they swim and drink contaminated water or when they eat toxin-producing algae.1
Common toxin-producing genera of cyanobacteria include Microcystis, Anabaena, Oscillatoria, Aphanizomenon, Nodularia, and Nostoc species. Four types of toxins are known to be produced by cyanobacteria, but the two main types are hepatotoxins and neurotoxins.
Hepatotoxin peptides (heptapeptides or pentapeptides) are the most common cause of blue-green algae poisoning in animals.1 Hepatotoxicosis from hepatotoxic peptides is characterized by signs of vomiting, diarrhea, anorexia, lethargy, hepatopathy, and acute hepatic failure as well as death.
The most common neurotoxins that cyanobacteria produce are alkaloids anatoxin-a and anatoxin-a(s). Anatoxin-a is the most common neurotoxin. It is a strong postsynaptic depolarizing neuromuscular blocking agent that affects nicotinic and muscarinic acetylcholine receptors. Anatoxin-a(s) inhibits peripheral cholinesterase irreversibly. Blue-green algae neurotoxins interfere with neurotransmission across neurons or neuromuscular junctions, causing central nervous system (CNS) signs and death due to respiratory failure.1-3
Neurotoxicosis due to blue-green algae is potentially lethal, although few cases of this poisoning in dogs have been reported in North America.2 The lethal oral dose in dogs is not known. In mice, the approximate oral LD50 of anatoxin-a is 5 mg/kg. In dogs, anatoxin-a ingestion is known to cause muscle fasciculations, seizures, collapse, weakness, respiratory failure, and death within 10 minutes to a few hours of exposure.2,3
The slight increase in alkaline phosphatase activity noted in this case may have been due to muscular activity or anoxia during seizures, whereas the slight increase in alanine transaminase activity could be due to phenobarbital administration.
In cases similar to this one, possible differential diagnoses should include mushroom, metaldehyde, or strychnine poisoning; water intoxication; pesticide poisoning (organophosphates, carbamates or organochlorines, pyrethrins or pyrethroids); metabolic or infectious disease; and head trauma.
A tentative diagnosis is based on a history of exposure (swimming in or drinking lake or pond water, algae on the fur or muzzle or in the vomitus) and the rapid onset of neurologic signs (vomiting, ataxia, seizures, respiratory failure) or death.1
Initial clinical signs of blue-green algae poisoning in dogs due to either hepatotoxicosis or neurotoxicosis may be similar. However, with hepatotoxicosis, within hours of exposure, there are signs of liver failure accompanied by many-fold increases in liver-specific enzyme activities such as alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and coagulopathy (increased prothrombin time, activated partial thromboplastin time). With neurotoxicosis, marked increases in liver enzyme activities are not seen during the course of illness.
Unfortunately, there are no widely available, rapid, inexpensive tests available to confirm blue-green algae toxicosis.4 To definitively diagnose blue-green algae poisoning—after providing treatment—submit pond water and stomach contents for microscopic identification of toxigenic algae. Specimens (1 to 2 L of algae obtained by straining through cheese cloth) can be sent to a veterinary diagnostic laboratory for identification, purification, and quantification of algal toxins or mouse bioassay or for enzyme-linked immunosorbent assay.1
In a recently published case report, anatoxin-a was detected in the urine and bile of a dog that had been euthanized because of neurotoxic blue-green algae exposure.2 In the case reported here, the presence of neurotoxic blue-green algae toxins was not confirmed.
Suspected poisoning cases must be treated aggressively and quickly before a definitive diagnosis is established. The main goals of treatment are decontamination, seizure control, respiratory support, and supportive care.
Because of the rapid onset of clinical signs, inducing emesis may not be feasible or practical. However, in asymptomatic dogs, emesis can be induced with hydrogen peroxide (2.2 ml/kg orally, repeat once if emesis is unsuccessful the first time) or apomorphine (0.04 mg/kg intravenously, or dissolve part of a pill and instill subconjunctivally and rinse after emesis has occurred) followed by activated charcoal (2 to 4 g/kg).
Give diazepam (0.5 to 2 mg/kg intravenously), propofol (3 to 6 mg/kg intravenously or 0.1 to 0.6 mg/kg/min CRI), or phenobarbital (2 to 5 mg/kg intravenously) to control seizures. However, if the patient's respiratory system is compromised, avoid giving phenobarbital or propofol. Place a cuffed endotracheal tube and provide assisted respiration if needed, such as in this case.
Give atropine sulfate (0.04 to 0.1 mg/kg intravenously) to control muscarinic signs such as hypersalivation, bradycardia, and increased bronchial secretions. Antiemetics (maropitant 1 mg/kg subcutaneously once a day) and broad-spectrum antibiotics can be given as needed.
Perform a CBC and serum chemistry profile at presentation and every 24 hours for two or three days or as long as needed. Monitor blood glucose concentrations, hematocrit, and blood gases in symptomatic cases.
After ingesting neurotoxic blue-green algae, dogs can develop life-threatening clinical signs quickly. Providing ventilator support to these dogs for extended periods may be critical for successful treatment outcomes.
Safdar A. Khan, DVM, MS, PhD, DABVT
ASPCA Animal Poison Control Center
1717 S. Philo Road, Suite 36
Urbana, IL 61802
To view the references for this article, visit dvm360.com/AlgaeToxRefs.