Blue-green Algae (Cyanobacteria)
Blue-green algae, technically known as cyanobacteria, are not true algae but bacteria capable of photosynthesis. The chlorophyll and characteristic phycocyanin they contain give them their typical blue-green color. These microorganisms are among the oldest living beings on our planet and have adapted to various environmental conditions over billions of years.
In warm summer months, cyanobacteria can multiply explosively under favorable conditions, forming so-called “algal blooms”. This massive proliferation leads to the formation of toxins that can be highly dangerous to humans and animals. The toxicity is classified as very strong (+++). Dogs, in particular, are at increased risk due to their tendency to drink from or swim in stagnant waters.
There are over 2000 different species of cyanobacteria worldwide, not all of which are toxic. The most dangerous representatives belong to the genera Microcystis, Anabaena, Oscillatoria, and Nodularia. Their toxins can be divided into three main groups: hepatotoxins (liver-damaging), neurotoxins (nerve-damaging), and dermatotoxins (skin-irritating). The concentration of these toxins in affected waters can be so high that even small ingested amounts can lead to life-threatening poisoning.
The most important facts at a glance
Poisoning by blue-green algae (cyanobacteria) poses a serious threat to dogs and cats, especially during warm summer months. These microorganisms produce various toxins with hepatotoxic, neurotoxic, and dermatotoxic effects, which can cause life-threatening poisoning even in small amounts.
Symptoms usually develop rapidly and include gastrointestinal complaints, neurological deficits, or skin reactions, depending on the toxin type. The hepatotoxic variants are particularly dangerous, as they can lead to acute liver failure. Diagnosis is based on anamnesis with exposure evidence, the characteristic clinical picture, and laboratory diagnostic changes, mainly elevated liver enzymes and coagulation disorders.
Treatment must be initiated immediately and includes decontamination, intensive medical care, and symptomatic measures. Silymarin has proven to be a helpful therapeutic agent to inhibit toxin uptake into liver cells. The prognosis largely depends on the timing of treatment initiation and significantly worsens if clinical symptoms have already appeared.
Follow-up care includes regular check-ups and, if necessary, an adjusted diet and hepatoprotective medication. Long-term sequelae are possible and require individualized care.
Preventive measures are crucial and include avoiding stagnant waters with visible algal blooms and heeding warning signs near public waters. With increasing global warming, an increase in the frequency of blue-green algal blooms is to be expected, which underscores the importance of educating pet owners about this danger.
Causes, development and progression
There are many types of blue-green algae. Not all are equally toxic.
Some blue-green algae produce cyanotoxins. These are classified as neurotoxins, hepatotoxins, and lipopolysaccharides (LPS).
The toxins have high acute toxicity and can lead to life-threatening poisoning as early as 1 hour (neurotoxins) or approximately 24 hours (hepatotoxins).
The toxins nodularin and microcystin are presumably responsible for the hepatotoxic effect of blue-green algae.
Supplement
The mass proliferation of cyanobacteria is favored by several environmental factors. Primarily, persistently high temperatures (above 25°C) in combination with an increased nutrient supply are responsible. Especially phosphate and nitrogen compounds, which enter water bodies through agricultural fertilization, municipal wastewater, or surface runoff, significantly promote the growth of these microorganisms.
Climate change is increasingly exacerbating this problem. The increasingly warmer summers in Central Europe extend the potential bloom period of cyanobacteria and increase the likelihood of toxic algal blooms. Scientific studies show a significant increase in the frequency and intensity of blue-green algae blooms in recent decades.
Toxin formation itself is a complex biochemical process that depends on various environmental factors. Not all strains of the same cyanobacteria species produce toxins, and even toxin-producing strains do not do so under all circumstances. Toxin production is influenced by factors such as light intensity, temperature, pH value, and nutrient availability.
The most common toxins are:
- Microcystins and Nodularins: These cyclic peptides are primarily hepatotoxic and can cause severe liver damage.
- Anatoxins and Saxitoxins: As neurotoxins, they block signal transmission in nerve cells and lead to neurological symptoms.
- Lipopolysaccharides (LPS): These endotoxins can cause skin irritations and allergic reactions.
Poisoning in pets primarily occurs through oral intake when drinking contaminated water or by licking their fur after bathing in affected waters. Direct skin contact can also be a route of exposure.
Mechanism of action
After oral intake, the toxins nodularin and microcystin enter liver cells and accumulate there. Liver damage is particularly pronounced due to the accumulation of toxins.
They inhibit certain enzymes (protein phosphatases), thereby impairing the structure and a variety of metabolic processes in liver cells. This is followed by degeneration and focal necrosis of liver cells, followed by hemorrhages.
Liver function is impaired. This also affects the synthesis of clotting factors.
Liver enzymes are released. The blood clotting time is prolonged. The hemorrhages lead to an increase in bilirubin.
These effects are used for laboratory diagnostics.
Supplement
Blue-green algae produce different toxins, each with specific mechanisms of action:
- Microcystins – highly potent liver toxins (hepatotoxins)
These toxins specifically damage the liver. After absorption, they enter liver cells via special transport molecules and block certain enzymes necessary for cell metabolism. The result is massive destruction of liver cells within a very short time. This manifests clinically as:
Vomiting, diarrhea
Yellowing of Mucous Membranes (Jaundice)
Blood clotting disorders
Severe circulatory problems up to liver failure
Microcystins are among the most dangerous cyanotoxins and can be fatal to dogs even in small amounts.
- Anatoxin-a – acute nerve poison (neurotoxin)
Anatoxin-a acts at the junctions between nerves and muscles. It mimics the body’s own neurotransmitter acetylcholine, but unlike acetylcholine, it is not broken down by the body. This leads to continuous muscle stimulation without the possibility of recovery. Symptoms appear rapidly, sometimes within minutes:
Muscle tremors, salivation
Restlessness, shortness of breath
Seizures
Respiratory paralysis and death due to respiratory muscle exhaustion
This effect can lead to death within a short time without immediate veterinary care.
- Saxitoxins – Blockade of nerve conduction
Saxitoxins attack signal transmission in the nervous system by blocking sodium channels, which are necessary for signal transmission along the nerves. The result is flaccid paralysis:
Weakness, ataxia (gait instability)
Muscle flaccidity
Respiratory paralysis
These toxins act particularly quickly and their effect is similar to the poison of the pufferfish (tetrodotoxin).
- Cylindrospermopsin – Slower-acting cytotoxin
Cylindrospermopsin inhibits protein synthesis in liver and kidney cells. This leads to oxidative stress, resulting in cell damage in multiple organs.
Symptoms of intoxication
Poisoning symptoms depend on the type of blue-green algae. Initial symptoms usually affect the gastrointestinal tract in addition to skin irritations.
- Skin, conjunctival, and mucous membrane irritations
- Dermatitis, sometimes allergic in nature
- Drooling
- Vomiting, sometimes bloody
- abdominal cramps
- Diarrhea, sometimes bloody
- Fever
With the ingestion of large quantities, pronounced neurotoxic damage and liver damage occur.
- Tremor
- Decrease in heart rate
- Increase in respiratory rate
- Ataxia
- Seizures
- Paralysis
- Drop in blood pressure
- Coagulation disorder
- Difficulty breathing
- Coma
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The clinical signs of blue-green algae poisoning vary depending on the toxin type ingested, the amount of toxin, and the individual sensitivity of the animal. Generally, the first symptoms appear very rapidly – within 30–60 minutes for neurotoxins, and within 24 hours for hepatotoxins after exposure.
Upon contact with dermatotoxic cyanobacteria, local skin reactions initially appear. Affected animals suffer from:
- Intense itching and redness of the skin
- Swelling, especially on sparsely haired body areas
- Conjunctival irritation with increased tear production
- Mucous membrane irritations in the mouth and nasal area
With oral ingestion of neurotoxic cyanobacteria, neurological symptoms dominate:
- Muscle tremors and muscle stiffness
- Coordination disorders and ataxia
- Increased salivation
- Respiratory paralysis with cyanosis
- Seizures up to status epilepticus
- Impaired consciousness up to coma
The hepatotoxic variants initially cause gastrointestinal complaints, followed by signs of liver damage:
- Acute vomiting, often with blood present
- Severe abdominal pain and diarrhea
- Increasing apathy and weakness
- Yellowing of mucous membranes (jaundice)
- Bleeding tendency due to coagulation disorders
- Photosensitization with increased skin reactions to sunlight
In cats, poisoning often progresses more subtly than in dogs. They often show less pronounced gastrointestinal symptoms, but earlier signs of liver damage. Due to their selective drinking habits, cats are generally less frequently affected than dogs.
Symptom progression can be extraordinarily rapid. Especially with neurotoxins, the period between the first signs and a life-threatening condition can be less than an hour, which underscores the urgency of veterinary emergency measures.
Diagnosis
Diagnosing blue-green algae poisoning is challenging and relies on several pillars. The initial crucial step is the anamnesis, with evidence of possible exposure. Pet owners should therefore always inform the veterinarian if the animal had access to stagnant waters, especially during warm summer months.
The clinical examination provides important clues through the characteristic symptom pattern. If blue-green algae intoxication is suspected, the following diagnostic steps are initiated:
Laboratory diagnostic examination includes a comprehensive blood count with a special focus on liver enzymes (ALT, AST, AP, GLDH), kidney values (urea, creatinine), electrolytes, and coagulation parameters. In hepatotoxic poisonings, typically highly elevated liver enzyme levels are observed as early as 12–24 hours after exposure. Coagulation time is prolonged due to impaired synthesis of coagulation factors in the liver, which can be detected by prothrombin time (PT) and activated partial thromboplastin time (aPTT).
Imaging techniques such as ultrasound can reveal changes in liver structure. Characteristic findings include hepatomegaly with increased echogenicity and, if applicable, ascites as a sign of liver dysfunction. In severe cases, liver hemorrhages may also be visualized.
Direct toxin detection is complex and not universally available. In specialized laboratories, cyanotoxins can be detected in water samples, vomit, or stomach contents using ELISA or HPLC methods. Microscopic detection of cyanobacteria in water samples can also support the diagnosis.
Differential diagnoses must exclude other acute poisonings (e.g., rat poison, heavy metals), infectious hepatitis, acute pancreatitis, and primary neurological diseases. The combination of a suitable anamnesis, a characteristic clinical picture, and corresponding laboratory changes usually allows for a reliable diagnosis.
Therapeutic principles
The antidote silymarin (silibinin) is intended to prevent the uptake of nodularin and microcystin into liver cells and mitigate the toxic effects. It is initially infused and then infused every 24 hours until the elevated liver enzymes in the blood normalize.
External (skin) and internal (gastrointestinal tract) decontamination should be performed as quickly as possible.
This means carefully rinsing the eyes with open eyelids, thoroughly washing the fur with a mild soap and lukewarm water.
The therapy is symptomatic.
Water and electrolyte balance must be monitored and stabilized. Sufficient fluid replacement can be supported by administering glucose infusions.
Liver and kidney function must be monitored.
If necessary, further symptomatic medications such as anticonvulsants and atropine may be required in cases of severe blood pressure drop.
Supplement
The treatment of blue-green algae poisoning requires rapid action and follows a multi-stage approach. Since no specific antidote exists for all cyanotoxins, symptomatic therapy is paramount.
First aid begins with immediate decontamination. In cases of recent exposure and no poisoning symptoms yet, controlled induction of vomiting may be considered. However, this is only advisable if ingestion occurred less than 1–2 hours ago and no neurological symptoms are present. Alternatively, gastric lavage can be performed under general anesthesia. The administration of activated charcoal (1–4 g/kg body weight) binds unabsorbed toxins in the gastrointestinal tract and prevents their absorption.
In case of external contact, a thorough washing of the fur with mild shampoos is urgently necessary to remove adhering toxins. Special care should be taken to clean paws, belly, and mouth, as animals frequently lick these areas.
Intensive medical care includes:
For hepatotoxic poisonings, silymarin (silibinin) has proven helpful. It is initially administered as an infusion and then continued every 24 hours until liver enzymes normalize. Silymarin acts by inhibiting toxin uptake into liver cells and also possesses antioxidant properties.
Fluid therapy with crystalloid solutions (e.g., Ringer’s lactate) is fundamental to stabilize circulatory function and promote renal excretion of toxins. In cases of severe liver damage with hypoalbuminemia, colloidal solutions or plasma transfusions may also be necessary.
For neurological symptoms, anticonvulsants such as diazepam (0.5-2 mg/kg i.v.) or, in cases of therapy-resistant seizures, phenobarbital (2–4 mg/kg i.v.) are used. In cases of respiratory insufficiency, oxygen therapy or, in severe cases, even mechanical ventilation may be required.
Hepatoprotectants such as S-Adenosylmethionine (SAMe), Vitamin E, and N-Acetylcysteine are used as supportive measures to reduce oxidative stress and promote liver regeneration. In cases of coagulation disorders, Vitamin K1 administration and, in severe cases, fresh plasma transfusions may become necessary.
Continuous monitoring of vital parameters, acid-base balance, and organ functions is essential throughout the entire treatment period to detect complications early and respond accordingly.
Prognosis & follow-up care
The prognosis for blue-green algae poisoning is highly dependent on the timing of treatment initiation, the type and amount of toxins ingested, and the individual health status of the animal. Generally: The earlier therapy begins, the better the chances of survival.
With early decontamination within the first hour after exposure and before the onset of clinical symptoms, the prognosis is considered favorable. If clear signs of poisoning are already present, especially neurological symptoms or signs of acute liver failure, the prognosis significantly worsens. The mortality rate in severe cases can be 50–80% despite intensive medical care.
Animals that survive the acute phase require careful aftercare. This includes regular follow-up examinations with blood counts to monitor liver and kidney function. In the first weeks after poisoning, these check-ups should be weekly, later at longer intervals. Complete liver regeneration can take several weeks to months, depending on the severity of the damage.
The diet of convalescent animals should be easily digestible and high-quality, with moderate protein content, so as not to overload the liver. Special diets for liver diseases can be helpful. Additionally, hepatoprotectants such as silymarin, SAMe, or phosphatidylcholine can be administered over a longer period to support liver regeneration.
Long-term sequelae are possible and depend on the extent of the initial organ damage. Chronic liver insufficiency with impaired detoxification function, increased sensitivity to medications, or chronic neurological deficits can persist as residuals. In some animals, secondary photosensitization develops, which requires special precautions when exposed to sunlight.
Pet owners should be educated about preventive measures after surviving blue-green algae poisoning to avoid future exposures. This particularly includes avoiding stagnant waters during warm summer months or when visible algal blooms are present.
Research outlook
Research into cyanobacteria and their toxins has gained significant momentum in recent years, not least due to the increasing problems caused by climate change. Current studies focus on several promising approaches that could improve both understanding and treatment options.
In the field of early warning systems, molecular biological methods are currently being developed that can identify toxin-producing cyanobacterial strains more quickly and precisely. PCR-based methods enable the detection of genes responsible for toxin production before the toxins themselves are present in detectable concentrations. This could enable earlier warnings of dangerous algal blooms in the future.
Innovative treatment approaches focus on specific antidotes against cyanotoxins. Monoclonal antibodies that specifically bind to microcystins or anatoxins and neutralize their effect are promising here. Initial in vitro studies show positive results, but clinical applications are still pending.
The development of adsorbents with high specificity for cyanotoxins could revolutionize decontamination therapy. Modified activated carbon compounds and synthetic polymers show significantly higher binding capacity for cyanotoxins in experimental studies than conventional activated carbon.
In the area of prevention, research is being conducted on biological control methods for cyanobacteria. Certain bacteriophages and competing microorganisms could be used in the future to control the excessive growth of toxic cyanobacteria in waters without disturbing the ecological balance.
Research into genetic factors that influence individual susceptibility to cyanotoxins could enable personalized risk assessment and treatment in the future. Initial studies indicate breed-specific differences in the metabolism of microcystins in dogs.
Long-term studies on the chronic effects of sublethal cyanotoxin exposures are another important research area. There are indications that repeated exposures to low doses could lead to chronic liver damage and possibly carcinogenic effects.
These research approaches promise improved prevention, diagnosis, and treatment options for blue-green algae poisoning in the future, which is of great importance given the projected increase in cyanobacterial blooms due to climate change.
Frequently asked questions (FAQs)
1. How Do I Recognize if a Body of Water is Contaminated with Blue-Green Algae?
Blue-green algae blooms are often recognizable by a greenish-bluish discoloration of the water. The water appears cloudy, sometimes with foamy or slimy deposits on the surface. In cases of heavy infestation, carpet-like structures often form. A characteristic musty or foul odor can also indicate blue-green algae. When in doubt: It’s better to exercise caution and keep the animal away from the water.
2. Are Certain Dog Breeds more Susceptible to Blue-Green Algae Poisoning?
There is no specific breed predisposition for the toxicity itself; however, dogs with a high affinity for water, such as Labrador Retrievers, Golden Retrievers, or water dogs, are at a higher risk of exposure. Furthermore, animals with pre-existing liver or kidney diseases may react more sensitively to the toxins and show more severe courses.
3. How Quickly Do I Need to Act if My Pet Has Come into Contact with Blue-Green Algae?
Immediate action is crucial. The time until the first symptoms appear can range from 15 minutes to 24 hours, depending on the toxin type. Immediately rinse your pet thoroughly with clear water to remove adhering toxins, and seek veterinary help without delay, even if no symptoms are yet visible.
4. Can My Pet be Poisoned just by Swimming in a Contaminated Body of Water?
Yes, even if no water is ingested, poisoning can occur. Toxins can be absorbed through small skin lesions or by licking wet fur after bathing. Absorption is particularly possible in thin-skinned body areas such as the belly or paws.
5. Are Cats as much at Risk as Dogs?
Cats are generally less frequently affected than dogs due to their more selective drinking behavior and their lower tendency to bathe in natural waters. Physiologically, however, they react just as sensitively to the toxins and can develop severe poisoning symptoms upon exposure.
6. Can Blue-Green Algae Poisoning be Transmitted to Humans?
Direct transmission from animals to humans does not occur. However, you should thoroughly wash your hands after handling a potentially exposed animal, as toxin residues can remain in the fur. The main danger for humans lies in direct exposure to the contaminated water.
7. What Long-Term Consequences Can Surviving Blue-Green Algae Poisoning Have?
Animals that survive severe poisoning can suffer permanent liver damage, requiring lifelong medication and diet. Neurological residuals such as coordination disorders or a tendency to seizures are also possible. Regular veterinary check-ups are therefore important even after the acute phase.
8. Are there Seasons when the Risk is Particularly High?
The highest risk exists during the warm summer months from June to September, especially after prolonged heat periods without precipitation. However, in mild winters, blue-green algae blooms can also occur outside this main season. Climate change also leads to an extension of the risk season.
9. Are all Stagnant Waters Equally Dangerous?
No, the risk varies greatly. Particularly at risk are nutrient-rich, shallow waters with low mixing and direct sunlight. Small ponds and pools, but also calm bays of larger lakes, can be affected. Flowing waters with strong currents are generally less at risk.
10. How Can I Protect My Pet from Blue-Green Algae Poisoning?
During the summer months, avoid swimming and drinking from stagnant waters, especially if they appear cloudy or have an unpleasant odor. Carry enough drinking water for your pet on walks. Pay attention to warning signs near public waters and inform yourself about current blue-green algae contamination in the region before excursions.
Literature
- https://www.lubw.baden-wuerttemberg.de/wasser/blaualgen-cyanobakterien
https://www.schleswig-holstein.de/DE/Landesregierung/LASD/Aufgaben/Gesundheitsschutz/Download/data/Badegewaesser/VergiftungenDurchCyanobakterien.pdf?__blob=publicationFile&v=2 - Merel S, Walker D, Chicana R, Snyder S, Baurès E, Thomas O. State of knowledge and concerns on cyanobacterial blooms and cyanotoxins. Environment International. 2013;59:303-327.
- Puschner B, Humbert JF. Cyanobacterial (blue-green algae) toxins. In: Gupta RC, editor. Veterinary Toxicology: Basic and Clinical Principles. 3rd ed. Academic Press; 2018. p. 763-776.
- Fastner J, Beulker C, Geiser B, Hoffmann A, Kröger R, Teske K, et al. Fatal Neurotoxicosis in Dogs Associated with Tychoplanktic, Anatoxin-a Producing Tychonema sp. in Mesotrophic Lake Tegel, Berlin. Toxins. 2018;10(2):60.
- Rankin KA, Alroy KA, Kudela RM, Oates SC, Murray MJ, Miller MA. Treatment of Cyanobacterial (Microcystin) Toxicosis Using Oral Cholestyramine: Case Report of a Dog from Montana. Toxins. 2013;5(6):1051-1063.
- Löwe G, Löwe O. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd ed, Kreuztal: Kynos-Verlag. 2021; 208 pp.