Last summer was exceedingly hot and dry in my home state of Oregon, with almost no snowpack in the mountains. By midsummer, many streams were just a series of stagnant pools. During the heat, when livestock crowded the streambanks for water, state and local officials issued stern warnings again and again.
Stay away. Be careful. Remove your animals. Don’t fish. Don’t drink the water! They were concerned about the sludge-colored blooms of algae in the stagnant water. And that’s definitely something we should talk about.
First, an eye-opener: Those toxic algae blooms are not algae. Those floating mats of sludge are actually huge colonies of bacteria. That’s right. You read it correctly. Bacteria. These bacteria are popularly called “blue-green algae,” which is confusing, but their proper name is cyanobacteria. The “cyan” term is derived from a Greek word meaning “dark blue.” (If you own an inkjet printer, you probably have come across a replacement cartridge bearing the word “cyan.” As far as I know, there is no other relationship between mat-forming bacteria and computer printers.)
So what are cyanobacteria?
Some background: The cyanobacteria comprise a huge array of species. Like all bacteria, they are single-cell organisms with cell walls and no nucleus. But unlike most bacteria, the cyanobacteria are capable of photosynthesis, which means they can manufacture their own carbohydrates by using solar energy. These bacteria contain pigments that convert atmospheric carbon dioxide into carbohydrates, just like the more complex green plants. Although some cyanobacteria species contain a version of green chlorophyll, their main light-capturing molecules are usually based on the pigment phycocyanin, which is blue.
In addition to photosynthesis, some cyanobacteria can fix atmospheric nitrogen. In the agricultural world, we are familiar with this nitrogen-fixing process because of the rhizobia bacteria that form nodules on legume roots. (Rhizobia are not cyanobacteria, but both groups have the same nitrogen-fixing metabolic machinery.) Nitrogen fixation – wow! Any bacteria that can capture both carbon and nitrogen from the atmosphere is certainly well-equipped to survive under harsh conditions.
And that is exactly what happens. The cyanobacteria are incredibly diverse, and they are found in nearly every environment on Earth. They are common in the open ocean, along shores, in rivers and streams, in wet areas on land, in soils, and on plants and animals. Some thrive in extreme conditions like hot springs and salt flats. One marine species may be the cause of much of the photosynthesis in the open ocean. Some cyanobacteria have formed symbiotic relationships with other species. Many lichens, for example, are actually interactive growths of cyanobacteria and fungi. Another example is a type of nitrogen-fixing cyanobacteria that lives on the aquatic fern azolla (sometimes called mosquito fern), which is routinely used as a biological nitrogen fertilizer in rice paddies.
Some cyanobacteria are nutritious and used as human food. The filamentous species spirulina is grown in ponds throughout the tropics, and its dried form is commonly sold in health food stores.
Where it can get ugly
But some cyanobacteria live on the dark side. These species produce toxins of various types, including some of the most lethal compounds known. This is where our cyanobacteria story meets the livestock world.
Cyanobacteria can produce a witch’s brew of horrors. Their toxins fall into four main categories:
- Cyclic peptides that damage the liver
- Polyketides that cause skin and respiratory inflammations
- Alkaloids that affect the liver, skin and nerves
- One unusual amino acid that damages the nerves and may be associated with certain human degenerative diseases
Sometimes these toxins are confined inside the bacterial cells, so that animals must consume the cells to be poisoned. Sometimes the toxins are released into the surrounding water, so that just being exposed to the water can result in toxic symptoms.
The cyclic peptides (microcystins and nodularins) are small molecules composed of amino acids linked in a ring, kind of like beads in a necklace. These compounds are extremely toxic. Not only do they cause irreversible liver damage, but they can accumulate up the food chain, so these toxins can poison people who eat fish and shellfish. Interestingly, the chemical structure of these toxins bears an uncanny resemblance to the cyclic peptide toxins of poisonous mushrooms like amanita.
The polyketide toxins (aplysiatoxins) are powerful irritants that cause severe contact dermatitis. Some polyketide toxins may be carcinogenic because they can promote tumor formation.
The alkaloid toxins are quite varied, and they can affect the liver, skin and nerves. One of these neural toxins is particularly lethal: anatoxin-a, which has also earned the nickname “Very Fast Death Factor.” Seriously. This toxin can kill in minutes. The reason lies in how nerves function. Typically, a neural impulse reaches the muscle in the form of acetylcholine, which is formed for a moment on the cell receptor. After the impulse is completed (causing the muscle to contract), the acetylcholine is split apart by the enzyme acetylcholinesterase. This returns the nerve receptor into a resting state until the next impulse. All of this, of course, occurs in milliseconds.
But anatoxin-a disrupts this sequence. Anatoxin-a outcompetes acetylcholine for the neural receptor and locks onto it, causing the circuit to complete. But then the acetylcholinesterase enzyme cannot break this molecule apart, so the toxin remains on the receptor and the nerve continues to fire. The resulting symptoms occur rapidly: muscle tremors, incoordination, convulsions, respiratory failure and death, sometimes within minutes. This toxin is quite similar to nerve gas, which works slightly differently but produces the same results. Nerve gas inhibits the acetylcholinesterase enzyme, so once the acetylcholine molecule is locked on the receptor, it cannot be removed. The physiological result is essentially the same as for anatoxin-a: a continuous firing of the nerve circuitry.
The unusual amino acid BMAA (short for beta-methylamino-L-alanine) is produced by a marine cyanobacteria and can accumulate in fish. It’s been found in some human foods like shark fin soup. BMAA is not involved in normal protein synthesis, but as a toxin it affects the nerves in various ways. One particularly disturbing characteristic of BMAA is that it may alter the three-dimensional structure of some neural proteins, causing protein tangles. There is some evidence that BMAA has been associated with human neural degenerative diseases like Lou Gehrig’s disease (ALS) and Parkinson’s disease.
A real-life look
These are all bad compounds, so what do we see in the field? The main thing is the “bloom” – a scum or foam mat that forms on the surface of still water. This mat is the result of the explosive growth of cyanobacteria due to favorable environmental conditions. These mats may be relatively thick, or they may look like a sheen of blue-green paint. They may not always be blue or green. The mats can contain more than one species of cyanobacteria, and they may or may not be toxic. It is not possible to identify a toxic bloom by just looking at it, so we should always assume the worst. (Although, ironically, a mat composed of true green algae is harmless.)
These mats may appear in a quiet eddy of a stream or river. Or on a lake, especially on the leeward side where the wind may have pushed them. (For completeness, I should mention the infamous “red tide” that occasionally appears in coastal waters. This is also a toxic bloom, usually red or brown, but it is not caused by bacteria. Red tide is caused by dinoflagellates, a type of plankton.)
What to do? Well, first, don’t drink the water. Or bathe or swim in it. This warning applies to livestock and people. Find alternative off-stream water sources for the livestock. One disturbing thing to note: City filtration systems don’t remove these toxins (an unpleasant thought). The good thing is that these blooms eventually go away.
But let me engage in some speculation. Most cyanobacteria toxins have not been well characterized. We don’t know exactly when or why the cyanobacteria decide to produce these compounds. We also don’t know much about toxin levels or dosages. Veterinarians and doctors are generally presented with patients showing the short-term effects, the obvious symptoms of acute toxicity. But what about long-term effects, especially for low dosages that may accumulate in body tissues? We know little or nothing about these. There are lots of possible scenarios: small mats or populations of cyanobacteria, low levels of toxins in water supplies, symbiotic cyanobacteria living on forages or animals or fish, no immediate toxicity symptoms. And then there is the unnerving potential connection of BMAA with some neural degenerative diseases in humans.
How does this affect our livestock? Well, we periodically find sick animals but can see no apparent cause. Or a dead animal in the field, maybe near a water source, again with no apparent cause. But there is always a cause. In warm weather, perhaps the potential of blue-green algae should come to mind.
The famous 1978 movie Jaws 2 had the tagline, “Just when you thought it was safe to go back in the water . . .” But I digress. That was just Hollywood.