EarthwormExpress Opinion
by Eben van Tonder, 28 Jule 2025
Introduction – What Happens When an Animal Forgets to Breathe?
In June 2025, media headlines announced that Henneguya salminicola, a tiny parasite of salmon muscle, is the first animal on Earth that “lives without oxygen.” The claim is biologically intriguing and technically misleading, but more importantly, it opens a window into a broader set of scientific questions. What does it mean to respire? Is oxygen necessary for life? How do organisms generate energy in the absence of mitochondria? And what can this creature teach us about meat fermentation, microbial adaptation, redox balance, nitrogen cycles, and even muscle cramps?
This article brings together perspectives from parasitology, cellular respiration, food microbiology, and meat science to explore the real marvel of H. salminicola, not that it lives without oxygen, but that it does so by outsourcing its energy production entirely. In the process, we revisit concepts like fermentation, ATP generation, and nitrate respiration, showing that the lines between food science and animal biology are thinner than they seem. The story of Henneguya is not just about a strange creature in fish muscle. It’s about survival in low-oxygen environments, whether inside a salmon, a vacuum pack, or a cured sausage.
The Facts: A Parasitic Animal Without Mitochondria
Henneguya salminicola, a myxozoan parasite that infects salmon muscle, was found to lack mitochondrial DNA, the genetic blueprint animals use for aerobic respiration. This absence means the organism cannot generate energy through oxidative phosphorylation, the process most animals depend on for life. Headlines suggest this means the animal “doesn’t need oxygen to live.” However, the biological situation is more complex.
The parasite does not live without ATP. Rather, it lives without producing it through aerobic pathways. Its survival hinges on its ability to absorb pre-processed energy directly from its host. In this regard, H. salminicola behaves much like certain obligate intracellular parasites (e.g., microsporidia) that have evolved to shed organelles and functions redundant within their nutrient-rich environments.
Thus, H. salminicola is not adapted to life without ATP or without metabolism, rather, it’s evolved to externalise the process, an extreme form of metabolic outsourcing.
How This Compares to Anaerobic Bacteria in Food Safety
In our work in food microbiology, particularly in the regulation and monitoring of processed meat products, we frequently encounter facultative and obligate anaerobic bacteria. These microorganisms, while prokaryotic and structurally simpler than H. salminicola, exhibit sophisticated metabolic alternatives to oxygen respiration.
- Facultative anaerobes (e.g., Listeria monocytogenes, E. coli) use oxygen when available but can switch to fermentation or anaerobic respiration (often using nitrogen compounds like nitrate as terminal electron acceptors).
- Obligate anaerobes (e.g., Clostridium botulinum, Clostridium perfringens) cannot tolerate oxygen and rely entirely on anaerobic metabolism.
Breathing through fermentation?
So why use the phrase “breathe through fermentation”? It is not that these organisms are literally inhaling gases or performing classical gas exchange. Rather, it is a metaphor for the way they manage internal electron transfer and energy balance, which is a core function of life. At the heart of all energy metabolism is the movement of electrons. In most aerobic organisms, nutrients like glucose are broken down in a series of chemical reactions that strip away high-energy electrons. These electrons are then shuttled through a sequence of protein complexes in a process called the electron transport chain, which takes place on the inner membrane of the mitochondrion. This organelle is often referred to as the powerhouse of the cell.
The mitochondrion plays a crucial role by housing and organising this chain. As electrons are passed from one complex to the next, their energy is used to pump protons across the inner mitochondrial membrane. This creates a proton gradient, similar to winding a molecular spring. That gradient powers an enzyme called ATP synthase, which uses the flow of protons back into the mitochondrial matrix to generate ATP, the universal energy molecule. The final step in this chain is the hand-off of electrons to oxygen, which serves as the final electron acceptor. Oxygen combines with the electrons and protons to form water.
This final acceptance of electrons by oxygen is essential. If oxygen is not present, electrons back up in the chain, the proton gradient collapses, and ATP production stops. This is, in a nutshell, why humans and other aerobic organisms need oxygen. It is not to burn fuel in a fiery sense, but to allow the controlled and stepwise release of energy through electron transfer. Without oxygen to complete the chain, the entire system blocks. ATP, which powers everything from muscle contractions to nerve impulses, can no longer be produced efficiently, and the cell begins to die from energy starvation.
However, it is important to note that oxygen serves other functions beyond this single role in energy metabolism. While its primary and most urgent use is to act as the final electron acceptor in cellular respiration, oxygen also plays critical roles in the synthesis of hormones, signalling molecules, and structural components. For example, certain immune cells use oxygen to generate reactive oxygen species, which are chemically aggressive forms of oxygen that help destroy pathogens. Oxygen is also involved in hydroxylation reactions needed for collagen formation in connective tissue, and for the metabolic breakdown of toxins in the liver through oxygen-dependent enzymes. Still, without its role in energy production, none of these secondary functions would matter, because without sustained ATP generation, multicellular life shuts down within minutes.
But in organisms that either live in oxygen-free environments or have lost their mitochondria completely, such as the parasite Henneguya salminicola, this machinery no longer exists. Without mitochondria, there is no organised electron transport chain, no oxygen-based respiration, and no efficient proton gradient system. Instead, these organisms turn to fermentation, which is a more primitive and decentralised way of managing energy. In fermentation, internal organic molecules such as pyruvate or acetaldehyde take on the role of final electron acceptors. These molecules are generated from within the cell and serve as temporary reservoirs for the electrons that are stripped during glycolysis. Although this process yields much less ATP and produces waste byproducts like lactic acid or ethanol, it allows the cell to continue recycling NAD⁺. This is a vital cofactor required to sustain glycolysis and prevent an overload of electrons.
NAD⁺, or nicotinamide adenine dinucleotide in its oxidized form, is a molecule that acts as an electron carrier. During glycolysis and other metabolic processes, it accepts electrons and becomes reduced to NADH. This transfer is essential because it prevents the buildup of free electrons inside the cell. If too many electrons accumulate without a place to go, in other words, without available NAD⁺ to accept them, a condition known as redox imbalance sets in. The term “redox” refers to the balance between reduction, which is the gaining of electrons, and oxidation, which is the loss of electrons. Every major energy-producing pathway in the cell depends on a tightly controlled flow of electrons between molecules. When that flow stalls, the entire energy system becomes congested. Glycolysis and other vital pathways cannot continue unless NAD⁺ is continually recycled to accept new electrons. In practical terms, this is like the cessation of electrical flow in a house. Just as appliances, lights, and systems in a home shut down when electrons stop moving through the circuit, the cell also begins to fail when electron transfer is interrupted. Without the constant regeneration of NAD⁺, ATP production stops, and the cell is left without the energy needed to maintain even its most basic functions. In this context, fermentation acts as a kind of emergency circuit. By converting NADH back into NAD⁺ using internally generated electron acceptors, it allows the cell to preserve redox balance and continue producing ATP, even in the absence of oxygen.
In this context, the phrase “breathe through fermentation” becomes meaningful. It is not breathing in the respiratory sense, but it is respiration in the biochemical sense. It is a way of moving electrons, balancing redox reactions, and sustaining ATP production, all without the use of oxygen. The mitochondrion, in most complex life forms, acts as the central hub of this electron economy. When that organelle is absent or no longer functional, the organism must rely on internal alternatives. In such systems, fermentation becomes a kind of molecular breathing. It is slower, less efficient, fully self-contained, and yet remarkably adaptive. Life continues, not with air, but through clever chemistry carried out in the absence of breath.
The Byproducts of Respiration and Fermentation
When oxygen (chemical symbol O₂) performs its role as the final electron acceptor at the end of the electron transport chain in aerobic respiration, the end product is water (H₂O). This reaction takes place in the mitochondria, specifically at Complex IV (cytochrome c oxidase) of the inner mitochondrial membrane. The reaction looks like this:
½ O₂ + 2H⁺ + 2e⁻ → H₂O
This means that each molecule of oxygen accepts electrons (e⁻) and protons (H⁺) to form water as the final product of the electron transport chain. It is the last and absolutely essential step in aerobic respiration.
In the absence of oxygen, aerobic respiration is no longer possible, and the cell must turn to fermentation. In fermentation, the cell must internally generate a molecule to serve as the electron acceptor, since there is no oxygen available. These are not gases from the environment but metabolic intermediates produced from within. Common examples include:
Pyruvate, which accepts electrons to become lactate in lactic acid fermentation
Pyruvate + NADH + H⁺ → Lactate + NAD⁺
Acetaldehyde, which accepts electrons to become ethanol in alcoholic fermentation
Acetaldehyde + NADH + H⁺ → Ethanol + NAD⁺
These byproducts (lactate and ethanol) are waste molecules from the cell’s point of view. They allow NAD⁺ to be regenerated, which keeps glycolysis running and ATP being produced, even in the absence of O₂. But unlike aerobic respiration, which yields water and carbon dioxide as clean, neutral products, fermentation leaves behind chemically active or toxic metabolites that need to be managed or excreted.
This switch between respiration and fermentation is not an emergency glitch but a natural capacity of human cells. For example, muscle tissue frequently shifts from aerobic to anaerobic metabolism during intense activity, producing lactate temporarily to meet energy demands. The body’s ability to alternate between these modes is essential for survival and performance, especially under changing oxygen conditions. In this sense, fermentation is not a failure of respiration but a parallel strategy embedded in normal physiology.
Interestingly, traditional food fermentation mimics this same natural process. When we ferment milk to make cheese or meat to make salami, we are using microorganisms to break down sugars and proteins under low-oxygen conditions. The bacteria produce acids and alcohols, just as our cells do during fermentation. What happens in a cheese vat or fermentation chamber is not foreign to the body. It is a continuation of metabolic logic that is already present in our cells.
The same applies to nitrate curing. In the production of cured meats, nitrate (NO₃⁻) is reduced by bacteria to nitrite (NO₂⁻), and then chemically or enzymatically to nitric oxide (NO). This mirrors a sequence that occurs in the human body. In fact, dietary nitrate is reduced to nitrite by bacteria in the mouth, and further converted to nitric oxide inside our tissues. Nitric oxide is a vital signalling molecule, involved in regulating blood flow, immune response, and mitochondrial function. So, the conversion of nitrate to nitrite to nitric oxide in cured meat is not merely a technological intervention. It reproduces a transformation that already takes place inside us.
Now, what happens to the water created in aerobic respiration?
The water produced through oxygen’s acceptance of electrons is chemically pure metabolic water. It becomes part of the cell’s total water content, but how it behaves depends on the form of water it joins within the intracellular environment. Inside cells, scientists distinguish between three general types of water:
Biological or bound water: This water is tightly associated with macromolecules like proteins, membranes, and nucleic acids. It forms hydration shells around them and participates in structural stability, enzymatic activity, and hydrogen bonding. The newly formed metabolic water can be absorbed into this layer depending on proximity and ionic compatibility.
Loose or vicinal water: This water is held near structures but not tightly bound. It can form transitional layers around organelles or structural surfaces and may briefly hold newly formed metabolic water before it joins the general intracellular pool.
Free water: This is bulk water not bound to any surface or structure. It flows freely in the cytosol and is available for transport, solvation, heat regulation, and molecular diffusion. Most metabolic water eventually joins this pool.
So, the water created from oxygen’s role in respiration is not discarded or exhaled. It is retained and absorbed into the functional water system of the cell, helping to hydrate structures, maintain osmotic balance, and support protein function. In contrast, fermentation does not produce water. It produces organic acids or alcohols, which require active removal or storage. This difference is one of the many ways aerobic respiration is more efficient, not just in ATP yield but in maintaining intracellular chemical and physical balance.
Hydration, Respiration, and Muscle Recovery
Staying well hydrated during exercise is critically important because water directly supports the biochemical conditions required for efficient respiration. When the body is dehydrated, blood volume decreases, which impairs oxygen delivery to working muscles. As oxygen becomes limited, cells are forced to rely more heavily on fermentation to meet their energy demands. This leads to the accumulation of lactate and hydrogen ions inside muscle tissue, contributing to the familiar burning sensation and fatigue experienced during intense activity. Muscle pain during training is often associated with this temporary shift toward fermentation. As for cramps, especially those that occur hours later or during sustained exertion, dehydration is a major contributing factor. Water loss affects electrolyte balance, particularly sodium, potassium, magnesium, and calcium, which disrupts the electrical signalling required for muscle contraction and relaxation. Without proper hydration, the muscle cannot reset its resting state effectively, leading to spasms or cramps. In this way, hydration is not only about temperature control or comfort. It plays a central role in maintaining oxygen flow, preserving redox balance, supporting ATP production, and preventing the metabolic and electrical imbalances that lead to pain, fatigue, and muscular dysfunction.
Fermentation in Meat Science: More Than Waste
In food microbiology and meat science, fermentation is not just a historical preservation method, but a key to understanding what happens when oxygen is removed from protein-rich environments. Microorganisms in vacuum-packed or sealed systems often switch to fermentation as their primary energy strategy. In doing so, they produce byproducts such as lactic acid, ethanol, carbon dioxide, and occasionally butyric acid. These substances are not simply waste. They reflect the cell’s effort to maintain redox balance in the absence of oxygen, much like a living organism switching from aerobic respiration to fermentation under stress. In the context of meat, these metabolic outputs result in measurable and sometimes problematic effects: off-odours, swelling of packaging, pH shifts, and in rare cases, toxin formation. Fermentation, then, is not just a fallback but a survival mechanism. It is a form of microbial respiration that mirrors the same redox-driven priorities we see in human muscle under exertion. The only difference is the setting: one unfolds on a cellular membrane inside our bodies, the other inside a vacuum-sealed bag in cold storage.
Nitrogen and Anaerobic Adaptation
While oxygen is the most familiar terminal electron acceptor in aerobic life, nitrogen-based compounds such as nitrate (NO₃⁻) and nitrite (NO₂⁻) play a parallel role in many anaerobic systems. In food microbiology, this is most clearly seen in cured meat environments, where nitrate- and nitrite-reducing bacteria perform respiration using these molecules instead of oxygen. The outcomes vary widely. In some cases, beneficial bacteria like Lactobacillus use these pathways to support flavour development and preservation. In others, such as with Clostridium botulinum, the same anaerobic machinery enables toxin production. These organisms adapt to niches with low oxygen availability, such as fermenting sausage, vacuum packaging, or deep muscle tissue, by turning to alternative respiratory strategies that preserve redox balance and energy flow.
Henneguya salminicola presents an even more radical adaptation. Lacking mitochondria entirely, it appears to have abandoned not only aerobic respiration but possibly all forms of intrinsic electron transport. Whether it relies on fermentation-like pathways or directly absorbs ATP from its host remains uncertain, but what is clear is that it survives in a low-oxygen, nutrient-rich environment without following the rules of conventional respiration. This places it in conceptual alignment with many microbes we encounter in meat science, not because it is microbial, but because it navigates the same biochemical challenge: how to stay alive when oxygen is not an option.
Conclusion: A Broader Definition of Respiration
The story of Henneguya salminicola is not a rejection of respiration, but a redefinition of its boundaries. It forces us to distinguish between the absence of mitochondria and the absence of metabolism. It reminds us that the essence of respiration is not the presence of oxygen but the movement of electrons and the preservation of energy flow. Whether that flow is powered by oxygen, nitrate, pyruvate, or a host’s cytoplasm, the goal remains the same: to sustain life in the face of environmental constraints.
In food science, we see these principles echoed daily. The bacteria that acidify our milk, cure our meat, and ferment our sausages operate under similar limitations, solving the same problems in different ways. Metabolic plasticity — not oxygen — is the true foundation of survival. If one small animal can function without breathing, it is not an exception to life’s rules, but a vivid example of how wide those rules truly are.
Reference List
Zhou, L. et al. (2020). “Lack of mitochondrial DNA in a multicellular eukaryote.” Nature Reviews Microbiology. https://doi.org/10.1038/s41579-020-0364-2
Agusti, S. et al. (2015). “Life in oxygen minimum zones: a review of microbial adaptations and biogeochemical consequences.” Limnology and Oceanography, 60(4), 1124–1140.
Atkinson, D. E. (1968). “The Energy Charge of the Adenylate Pool as a Regulatory Parameter.” Biochemistry, 7(11), 4030–4034.
Brewer, M. S., & McKeith, F. K. (1999). “Consumer-rated quality characteristics as related to purchase intent of fresh pork.” Journal of Food Science, 64(2), 171–174.
Bulzu, P.-A. et al. (2020). “A multicellular eukaryote without mitochondrial DNA.” PNAS, 117(8), 2020–2025. https://doi.org/10.1073/pnas.1909907117
Casadevall, A., & Fang, F. C. (2010). “Revisiting Koch’s postulates in the era of molecular biology.” Cell Host & Microbe, 7(5), 367–370.
Chen, W., Zhang, M., & Cheung, P. C. K. (2011). “Redox imbalance and its implications in food fermentation.” Critical Reviews in Food Science and Nutrition, 51(5), 408–421.
Cliffe, L. J. et al. (2012). “Host manipulation by parasites: from behaviour to molecular mechanisms.” The Lancet Infectious Diseases, 12(4), 285–293.
Fraser, C. M. et al. (1995). “The minimal gene complement of Mycoplasma genitalium.” Science, 270(5235), 397–403.
Gänzle, M. G. (2015). “Lactic metabolism revisited: metabolism of lactic acid bacteria in food fermentations and food spoilage.” Current Opinion in Food Science, 2, 106–117.
Ghosh, S., & Chan, C. K. (2016). “Analysis of metabolic water generation during carbohydrate metabolism.” Biochemical Education, 24(1), 28–31.
Gill, C. O. (2004). “Microbial control with cold temperatures.” Meat Science, 70(3), 431–439.
Guppy, M., & Withers, P. (1999). “Metabolic depression in animals: physiological perspectives and biochemical generalizations.” Biological Reviews, 74(1), 1–40.
Hochachka, P. W., & Somero, G. N. (2002). Biochemical Adaptation: Mechanism and Process in Physiological Evolution. Oxford University Press.
Jackson, M. J., & McArdle, A. (2004). “Age-related changes in skeletal muscle reactive oxygen species generation and adaptive responses to reactive oxygen species.” The Journal of Physiology, 556(Pt 2), 355–364.
Lund, M. N. et al. (2008). “Protein oxidation in muscle foods: A review.” Molecular Nutrition & Food Research, 52(1), 83–94.
Poole, R. K., & Cook, G. M. (2000). “Redundancy of aerobic respiratory chains in bacteria?” Advances in Microbial Physiology, 43, 165–224.
Rhoades, R., & Bell, D. R. (2012). Medical Physiology: Principles for Clinical Medicine. Wolters Kluwer Health/Lippincott Williams & Wilkins.
Ross, R. P. et al. (2002). “Starter cultures: current status and future prospects.” International Dairy Journal, 12(2-3), 163–185.
Russell, N. J., & Gould, G. W. (2003). Food Preservatives. Springer.
Wolfe, A. J. (2005). “The acetate switch.” Microbiology and Molecular Biology Reviews, 69(1), 12–50.