Microorganisms in Cheese: Fermentation and Safety

Cheese is one of the most microbiologically complex foods you can eat. A single wheel can harbor dozens of species of bacteria, molds, and yeasts, all interacting with each other and with the milk proteins and fats around them. Some of these organisms are deliberately introduced to drive fermentation and build flavor; others arrive uninvited and pose safety risks or cause spoilage. Understanding which microorganisms do what, and how cheesemakers manage them, turns cheese from a mysterious aged product into something that makes a lot of biological sense.

How Lactic Acid Bacteria Start the Process

The foundation of nearly every cheese is a group of organisms collectively called lactic acid bacteria, or LAB. These bacteria consume lactose, the natural sugar in milk, and produce lactic acid as a byproduct. That acid lowers the milk’s pH, which does two critical things: it causes milk proteins to clump together into curds, and it creates an environment hostile to many harmful bacteria. LAB function either as starter cultures added deliberately at the beginning, or as secondary microbiota that become important later during ripening.¹

The starter cultures used in commercial cheesemaking are carefully selected strains, often species like Lactococcus lactis or Streptococcus thermophilus. Their job is rapid acidification. They bring the pH down quickly enough that the window of vulnerability, when milk is warm and nutrient-rich but not yet acidic, stays as short as possible. An enzyme called rennet (traditionally from calf stomachs, though microbial and plant-based alternatives exist) works alongside this acidification to break down casein proteins and form the gel-like curd that becomes cheese.¹

Molds That Make Blue and Bloomy Rinds

If you have ever looked at a wedge of Roquefort or Gorgonzola and wondered whether it is safe to eat something so visibly moldy, the answer is that those blue-green veins are the intentional work of Penicillium roqueforti. This mold is introduced into the curd or injected into young wheels, and as it grows through the interior, it breaks down both proteins and fats. The fat breakdown, called lipolysis, releases free fatty acids that contribute sharp, pungent flavors. Penicillium roqueforti is more aggressive at this fat breakdown than its cousin Penicillium camemberti, which is the mold responsible for the white, bloomy rinds on Brie and Camembert.²

That difference in enzyme activity is part of why blue cheeses tend to have a much stronger taste than soft-ripened cheeses like Camembert. P. camemberti works mainly from the outside in, softening the paste beneath the rind through protein breakdown while producing fewer of those intense fatty-acid flavors. The result is a creamy, mild interior rather than the assertive punch of a good blue.

Surface Bacteria and the Orange Rind

Washed-rind cheeses like Munster, Époisses, Limburger, and Taleggio develop their distinctive orange or reddish surfaces thanks to bacteria that thrive in the salty, moist conditions on the cheese exterior. The most well-known of these is Brevibacterium linens, which cheesemakers often add to the milk or apply to the rind during aging.³ The color comes from carotenoid pigments the bacteria produce. On the French cheese Fourme de Montbrison, researchers identified eleven different carotenoids in the rind, most belonging to a family of aromatic carotenoids called isorenieratene derivatives.⁴

B. linens is also responsible for much of the pungent smell associated with washed-rind cheeses. It produces sulfur compounds as it metabolizes amino acids on the cheese surface. The same organism, incidentally, lives on human skin and contributes to foot odor, which is why people sometimes say these cheeses smell like feet. The comparison is not coincidental: it is literally the same bacterium doing the same chemistry in both places.

Ripening and the Slow Work of Nonstarter Bacteria

Once the starter cultures have done their initial acidification work, a second wave of bacteria begins to matter. These are called nonstarter lactic acid bacteria (NSLAB), and they were not added by the cheesemaker. They come from the raw milk, the equipment, or the aging environment. During months of ripening, NSLAB can reach very high populations, sometimes climbing to around a hundred million cells per gram of cheese within three to nine months.⁵

What these bacteria do depends entirely on which species and strains happen to dominate. Some contribute desirable flavors by breaking down proteins and fats into tasty smaller molecules. Others cause off-flavors, bitterness, or textural problems. A study on goat cheese found that two different NSLAB strains produced very different flavor profiles over a 60-day ripening period: one strain ramped up protein and fat breakdown, while the other drove a different fat-metabolism pathway, leading to distinct volatile compounds in the finished cheese.⁶ This is part of why two wheels of ostensibly the same cheese can taste noticeably different: the NSLAB populations were not identical.

Where the Holes Come From

Swiss-style cheeses like Emmental get their signature holes from a bacterium called Propionibacterium freudenreichii. After the initial lactic acid bacteria have done their work, P. freudenreichii takes over and ferments the lactic acid itself. The products of this secondary fermentation include propionic acid, which gives Swiss cheese its characteristic nutty, sweet flavor, and carbon dioxide. Because the bacterium prefers oxygen-free conditions, it grows inside the cheese wheel rather than on the surface, and the CO₂ it produces gets trapped, forming the bubbles that become eyes.⁷

When this process goes right, you get evenly distributed, round eyes. When it goes wrong, or when a different gas-producing organism is responsible, the results are less pleasant.

Late Blowing and Spoilage

One of the most costly defects in semi-hard cheeses like Gouda and Gruyère is called late blowing. Weeks or months into aging, the cheese suddenly develops cracks, irregular holes, and off-flavors from butyric acid, which smells rancid. The culprit is almost always Clostridium tyrobutyricum, a spore-forming bacterium whose heat-resistant spores survive pasteurization and then germinate later in the low-oxygen interior of the aging cheese.⁸ Researchers confirmed that C. tyrobutyricum was specifically responsible by testing 32 strains: 28 of them caused late blowing in experimental cheeses, while related Clostridium species did not.⁸ The defect leads to significant economic losses for the dairy industry, since an entire batch may need to be discarded.⁹

Listeria, E. coli, and the Pathogens That Worry Food Safety Experts

The organism that causes the most concern in cheese safety is Listeria monocytogenes. Unlike most foodborne pathogens, Listeria can grow at refrigerator temperatures, making aged cheese a plausible vehicle for infection. A risk assessment of soft raw-milk cheese estimated that while the probability of any given milk batch being contaminated was high (around two-thirds of batches), the percentage of finished cheeses carrying dangerous levels of the pathogen was low, about 1.4%.¹⁰ That sounds small, but Listeria infections can be severe or fatal in pregnant women, older adults, and people with weakened immune systems, so even a low percentage matters.

Raw-milk cheeses tend to carry higher Listeria concentrations than pasteurized-milk cheeses when contamination occurs. An Irish risk model found that contaminated raw-milk cheeses averaged far higher bacterial loads than their pasteurized counterparts, and that the critical factors driving risk were how long the cheese sat in storage, what temperature it was stored at, and how big a serving someone ate.¹¹ In other words, even with raw-milk cheese, proper cold-chain management dramatically changes the risk.

Escherichia coli O157:H7 is another pathogen of concern, and it is one reason many countries require raw-milk cheeses to be aged for at least 60 days before sale. The assumption behind that rule is that the combination of low pH, low moisture, and salt will kill off dangerous bacteria during aging. Research on this is mixed. One study found that E. coli O157:H7 populations in cheddar aged at refrigerator temperatures for 60 days dropped by less than one order of magnitude, and even at 120 days the drop was less than two orders, leading the researchers to conclude that the 60-day rule is inadequate for this pathogen.¹² However, a survey of 41 raw-milk cheeses that had been properly aged found no enteric pathogens in any sample, suggesting that the 60-day rule works adequately in practice when good manufacturing standards are followed.¹³ A larger Canadian study of 127 aged raw-milk cheddars similarly concluded that the cheeses did not pose a significant health risk, though fecal coliforms were detected in about 18% of samples at low levels.¹⁴

The honest read of the evidence is that the 60-day rule is imperfect. It works well enough most of the time, especially when paired with good hygiene and quality milk, but it should not be treated as a guarantee that all pathogens have been eliminated.

Biogenic Amines in Aged Cheese

Pathogens are not the only safety concern. As cheese ages and microorganisms break down proteins into amino acids, some bacteria convert those amino acids into compounds called biogenic amines. The two that show up most frequently at high concentrations in cheese are tyramine and histamine.¹⁵ In sensitive individuals, high intakes of histamine can trigger headaches, flushing, and digestive distress, while tyramine can cause dangerous spikes in blood pressure, especially for people taking a class of antidepressants called MAO inhibitors.

Total biogenic amine levels correlate with overall microbial counts in cheese, meaning that cheeses with higher bacterial populations tend to accumulate more of these compounds.¹⁶ Heavily aged and traditionally fermented cheeses generally contain the highest concentrations. This is why people on MAO-inhibitor medications are routinely warned to avoid aged cheeses. For most people, the amounts in a normal serving are not dangerous, but they can contribute to the headaches some people report after eating strong cheeses.

Mycotoxins in Blue Cheese

The Penicillium molds used in blue cheese are selected precisely because they are safe to eat, but they do produce small amounts of secondary metabolites classified as mycotoxins. The two main ones are roquefortine C and mycophenolic acid. A study testing 86 blue-veined cheeses from around the world found roquefortine C in nearly all of them (about 98%), while mycophenolic acid was detectable in roughly a third.¹⁷ Concentrations varied enormously from cheese to cheese. The good news is that no aflatoxin M1, a more dangerous mycotoxin associated with contaminated animal feed, was found in any sample.

Whether the roquefortine C and mycophenolic acid levels in blue cheese are high enough to harm people at normal consumption levels remains debated, but researchers are not waiting for the debate to settle. Using gene-editing tools, scientists have recently created strains of P. roqueforti that cannot produce either mycotoxin. Lab-scale cheeses made with these engineered strains had no detectable levels of the toxins while still developing normally.¹⁸ Whether consumers and regulators will accept gene-edited cheese molds is a separate question, but the technology is there.

Bacteriocins and Biopreservation

One of the more elegant safety strategies in cheesemaking is turning the microorganisms themselves into a defense system. Certain LAB strains produce antimicrobial peptides called bacteriocins, which kill or inhibit competing bacteria, including pathogens. The best-known bacteriocin is nisin, which has been used as a food preservative for decades.¹⁹

Rather than adding purified bacteriocins, some producers use bacteriocin-producing strains as their starter cultures, so the protective compounds are generated in place. In cottage cheese, for example, a nisin-producing strain of Lactococcus lactis successfully controlled Listeria monocytogenes growth when used as a starter.²⁰ This approach, sometimes called biopreservation, is appealing because it does not require synthetic additives and fits within the clean-label movement that many consumers prefer.

Bacteriophages and the Invisible Threat to Fermentation

The biggest day-to-day headache for cheese producers is not a pathogen but a virus. Bacteriophages, viruses that specifically infect bacteria, can attack and destroy starter cultures mid-fermentation. When phages wipe out a starter population, acidification stalls, the curd does not set properly, and the batch fails. This has been a problem in the dairy industry for as long as defined starter cultures have existed.

Dairy scientists manage phage risk partly through strain diversity. Research on complex starter cultures has shown large differences in phage resistance among strains, even among strains that are closely related genetically. That individual resistance to phage attack helps maintain diversity within the culture, since resistant strains survive and keep fermenting even when others are wiped out.²¹ Another approach is to develop phage-resistant mutants of important strains. Researchers isolated phage-resistant variants of Lactobacillus helveticus and tested them in hard cheese production. The resistant variants performed identically to the original strain in terms of cheese composition, microbial counts, and sensory quality, making them viable replacements in rotation programs designed to stay ahead of evolving phages.²²

Biofilms in Cheese Facilities

Listeria monocytogenes is not just a concern in the cheese itself but in the processing environment. The bacterium is notorious for forming biofilms, structured communities of cells encased in a self-produced protective matrix, on surfaces like stainless steel, plastic, and drains. Cells within biofilms are much harder to kill with standard cleaning and sanitizing than free-floating cells, which is why Listeria can persist in a facility for months or even years.²³

A study of L. monocytogenes strains from two Brazilian cheese plants found that every single isolate could form biofilms on polystyrene, and about a quarter also formed biofilms on stainless steel.²⁴ Interestingly, strong biofilm production did not always predict which strains persisted longest in the facility, suggesting that other survival strategies are also at play. Effective control requires not just routine sanitation but attention to hard-to-reach surfaces, aging equipment, and the design of drainage systems.

Wooden Boards and the Microbiology of Place

Many artisan cheeses are aged on wooden boards or shelves rather than stainless steel, and regulators have sometimes questioned whether this is hygienic. The science suggests the picture is more nuanced than either side of that debate assumes. Wooden boards develop their own resident microbial communities over time, dominated by salt-tolerant and cold-tolerant bacteria, including genera like Brevibacterium, Brachybacterium, and Staphylococcus.²⁵ An analysis of boards from cheese-processing facilities identified hundreds of distinct bacterial types, with a core group of seven that appeared on every board tested.²⁶

Far from being merely a sanitation risk, these board communities may actively help protect cheese. Researchers have identified seven bacterial species living on wooden boards that inhibit L. monocytogenes, belonging to genera including Bacillus, Staphylococcus, Serratia, and Lactococcus.²⁵ Similarly, studies of wooden shelves used for aging traditional Sicilian cheeses found LAB strains with strong activity against common dairy pathogens.²⁷ The wooden surface is not sterile, but it is colonized by organisms that may be doing useful defensive work, a kind of accidental biopreservation that traditional cheesemakers have relied on for centuries without knowing the mechanism.

The Rind as an Ecosystem

A large-scale sequencing project examined 137 cheese rind communities from ten countries and found 24 widely distributed genera of bacteria and fungi that dominated these communities.²⁸ What makes cheese rinds especially interesting to microbiologists is that they are complex, multi-species ecosystems that form reproducibly under known conditions. The same cheese style made in different parts of the world tends to recruit similar microbial communities, suggesting that the cheese recipe and aging environment exert strong selective pressure on which organisms thrive.

These rind communities are not just decoration. They contribute to flavor, texture, and moisture regulation of the cheese beneath them. They also act as a barrier. A healthy, established rind community can outcompete incoming contaminants simply by occupying the available surface space and nutrients. This is part of why traditional natural-rind cheeses, which develop their surface communities over months, sometimes resist contamination better than cheeses wrapped in plastic immediately after production. The microbes are doing defense duty whether anyone planned it that way or not.

Health-Promoting Compounds Formed During Fermentation

Beyond flavor and preservation, fermentation and aging generate a range of compounds with documented biological activity. As microorganisms break down milk proteins, they release bioactive peptides, short protein fragments that have been shown in laboratory studies to exhibit properties including antioxidant, blood-pressure-lowering, and antimicrobial effects.²⁹ The specific peptides produced depend on which organisms are present and how long the cheese ages, which is one reason the health profile of a fresh mozzarella differs from that of a two-year Parmigiano-Reggiano.

Research into these bioactives is still largely at the test-tube and animal-model stage, so it is premature to call any cheese a health food on this basis. But it does add another dimension to the microbiological story: the same organisms that create flavor and texture also generate molecules with genuine pharmacological interest. Whether those molecules survive digestion in meaningful amounts and reach human tissues at effective concentrations remains an active area of investigation.