Ever had a dodgy chicken sandwich that left your stomach in knots? Or heard of someone feeling numbness after a bout of food poisoning? It might have been down to a little mischief-maker called Campylobacter. In this post, we'll dive into what this bacterium is all about, why it loves to hide in chicken, and some of its peculiar habits like thriving in warm environments and being a bit shy around oxygen. Plus, we'll discuss a mysterious condition called Guillain-Barré Syndrome that might follow this food poisoning – a syndrome where your body's own defense system goes a bit rogue. And, of course, we'll give you some top tips to keep these unwanted dinner guests away from your plate. Ready to become a food safety expert? Let's dive in!

Understanding Campylobacter: A Domino Effect from its Habitat

 Before we dive into the details of Campylobacter, it might be helpful to first read our foundational article on Gram staining and microbial characteristics available on our blog. This background information will create a smooth flow for understanding Campylobacter, like a well-aligned row of dominos.

The Extraordinary Relationship between Gram Staining and Microbial Properties

Visual representation of Campylobacter jejuni habitat and characteristics in a domino effect format, illustrating its preference for the intestinal tracts of birds, microaerophilic nature, resistance to acids and antimicrobial agents, and susceptibility to dryness and high temperatures.
  1. Habitat of Campylobacter: This bacterium primarily inhabits the intestines of birds, which provide a moist environment.
  2. Type of Bacterium: Given its habitat, we understand that Campylobacter is a Gram-negative bacterium.
  3. Infection Nature: As a Gram-negative bacterium, Campylobacter is capable of causing infectious food poisoning.
  4. Unique Growth Temperature: What sets Campylobacter apart is its optimal growth temperature of 42°C, and its inability to grow below 30°C.
  5. Sensitivity to Conditions: Like other Gram-negative bacteria, Campylobacter is vulnerable to drying and high heat.
  6. Oxygen Requirements: Unlike many bacteria, Campylobacter doesn’t thrive in standard oxygen levels (20%) or complete oxygen absence. Instead, it grows best in environments with 3–15% oxygen, making it a “microaerophilic” bacterium. Unlike facultative anaerobes, which can switch metabolic processes depending on oxygen availability, Campylobacter requires moderate oxygen levels to sustain its energy production through the citric acid cycle.Campylobacter can be thought of as a bacterium that “needs sunlight but is easily sunburned.” It thrives with a specific oxygen range, but too much exposure is harmful.
Campylobacter growth types and oxygen requirements: Illustration showing aerobic, obligate anaerobic, facultative anaerobic, and microaerophilic bacteria types, with Campylobacter categorized as microaerophilic, requiring 5-15% oxygen.
Campylobacter’s oxygen metabolism: This image illustrates Campylobacter as microaerophilic, depending on the citric acid cycle for energy. While it requires oxygen, it’s sensitive to high levels, thriving best in low-oxygen environments, unlike fully aerobic or anaerobic bacteria.

For more on the difference between anaerobic and aerobic bacteria, see our article below:

Understanding Gram-Negative Bacteria: The Role of the OF Test

  1. Growth during Chicken Distribution: Because its minimum growth temperature is 30°C, Campylobacter does not multiply in standard storage temperatures used for chicken or chicken products.
  2. Laboratory Growth of Campylobacter: Being Gram-negative, Campylobacter can be selectively cultured using compounds that inhibit Gram-positive bacteria.

By understanding these points sequentially, as in a domino effect, we can better comprehend Campylobacter’s characteristics and its role in food safety.

The Spiral Shape of Campylobacter

Bacteria come in various shapes, but the two most common forms are spherical (coccus) and rod-shaped (bacillus). Campylobacter, however, stands out with its unique spiral or helical shape, unlike most bacteria.

This corkscrew-like form is rare among bacteria. Campylobacter shares this spiral shape with another well-known bacterium, Helicobacter pylori, which is associated with stomach ulcers.

Interestingly, there was a time when scientists believed that Helicobacter pylori was a type of Campylobacter. However, advances in molecular biology, particularly with the analysis of 16S ribosomal DNA, revealed that these two bacteria belong to different genera. It’s a fascinating twist in the story of microbiology!

Campylobacter and Helicobacter comparison: This image highlights the phylogenetic relationship between Campylobacter jejuni and Helicobacter pylori. While C. jejuni typically inhabits poultry intestines, H. pylori is known for causing stomach ulcers in humans. The image also shows the phylogenetic tree, emphasizing their close genetic relationship despite residing in different hosts.

The Natural Home for Campylobacter

It's widely believed that the primary natural hosts for Campylobacter are birds. Let’s explore why:

Widespread Presence in Birds

Campylobacter is commonly found in the gastrointestinal tracts of various bird species in the wild. Birds carry Campylobacter without showing any symptoms, while in pigs and cows, the bacteria might cause adverse effects, like miscarriages or dysentery.

Campylobacter habitat distribution and effects: This image illustrates the typical habitats of Campylobacter in birds and livestock, where it causes no symptoms, as well as in cattle and pigs, where it may lead to issues such as miscarriages and dysentery. The image also shows symptoms in humans, including diarrhoea, vomiting, and fever.

The Temperature Connection

Campylobacter thrives at a toasty 40-42°C, which aligns with the body temperature of birds. Birds need to maintain this higher body temperature—around 5°C above that of mammals—to stay active and counter rapid heat loss.

Optimum growth temperature for Campylobacter compared to bird body temperature: This image shows how the optimal growth temperature for Campylobacter (40–42°C) aligns with the body temperature of birds, which is approximately 5°C higher than that of mammals. The image also illustrates the high-energy demand associated with flight, contributing to the elevated body temperature in birds."

Given these reasons, it’s no surprise that the optimal temperature for Campylobacter matches the body temperature of birds. Looking at all the evidence, it's reasonable to say birds are the natural hosts for Campylobacter. Cool, right?

llustration showing birds as the likely natural hosts of Campylobacter, based on its optimal growth conditions and the unique relationship between Campylobacter and avian body temperatures.

The Culprit Behind Campylobacter Gastroenteritis: Chicken Meat

  When we talk about Campylobacter gastroenteritis, chicken is often the primary suspect. Most people don’t consume raw chicken, so cases of Campylobacter food poisoning typically result from undercooked dishes, like fried or grilled chicken. However, the risk doesn’t stop at cooking. Imagine this scenario: you chop raw chicken with a knife, and then use the same knife or cutting board on another dish without proper cleaning. This cross-contamination can easily lead to foodborne illness.

 In Japan, some people do enjoy eating raw chicken, which has led to Campylobacter being a primary cause of food poisoning there.

Illustration depicting different cultural practices linked to Campylobacter food poisoning: undercooked chicken in general contexts and raw chicken consumption in Japan. Just a single drop of chicken juice with around 500 Campylobacter cells can cause infection, highlighting the risk of cross-contamination.

Interestingly, once Campylobacter is transferred from a contaminated surface like a knife, it doesn’t multiply on other foods. This is because it requires a minimum temperature of 30°C to grow. However, Campylobacter, closely related to the stomach-acid-resistant Helicobacter pylori, can withstand stomach acid, making it particularly infectious. In fact, as few as 500 bacterial cells—equivalent to a drop of chicken juice—can cause illness.

Comparison of Campylobacter and Helicobacter pylori in terms of acid resistance. Helicobacter pylori thrives in the stomach, while Campylobacter also shows resistance to stomach acid, aiding its survival and infection potential.

 So, secondary contamination from tools and surfaces plays a significant role in Campylobacter gastroenteritis, even in cases where bacteria numbers are low. Globally, whether through raw or undercooked chicken or cross-contamination, Campylobacter on chicken remains a common culprit in foodborne illness.

American perspective on the Japanese practice of eating raw chicken, a potential source of Campylobacter infection.

Why It Takes So Long to Get Sick from Campylobacter

One tricky aspect of Campylobacter gastroenteritis is its delayed onset. Unlike infections caused by Salmonella or E. coli, which typically result in symptoms like bloody diarrhea within about 24 hours, Campylobacter can be sneaky. Symptoms may not appear until 2 to 7 days after consuming contaminated food.

Why the delay? Bacteria like Salmonella and E. coli multiply rapidly at body temperature, doubling every 20 to 30 minutes. But Campylobacter is slower—it takes a full hour to divide at 37°C. Below 30°C, it can’t divide at all.

Due to this slower growth rate and higher temperature requirement, it can take longer for Campylobacter to reach levels that trigger illness. This lag time means Campylobacter gastroenteritis symptoms might not appear until well after the initial exposure. It’s a long wait that nobody wants, but it’s a characteristic that makes Campylobacter distinct from other foodborne pathogens.

Comparison of growth rates and onset times of Campylobacter, E. coli, and Salmonella at 37°C, highlighting Campylobacter's slower growth rate and delayed onset of infection symptoms (2-7 days). Minimum growth temperature for Campylobacter is shown as 31°C.

Why Campylobacter Might Be Sneakier Than You Think

   When Campylobacter infects the cells lining our intestines, it disrupts normal absorption and secretion processes, leading to an increased release of fluids and, ultimately, diarrhea.

Illustration of Campylobacter infection in intestinal epithelial cells, showing how the bacterium disrupts water absorption, leading to diarrhoea.

 

nitially, symptoms from Campylobacter poisoning might not seem severe, and most people recover within 2 to 5 days.

Illustration showing typical recovery time for Campylobacter food poisoning, which is 2–5 days, with a humorous character asking, 'Oi, fancy some raw bird?'

But here’s the twist: about 10 days after recovery, approximately 1 in 1,000 people may develop Guillain-Barré Syndrome (GBS), a condition where nerves in the arms and legs become paralyzed, potentially affecting movement, walking, and even breathing in severe cases.

Illustration depicting the mechanism of Guillain-Barré Syndrome, showing immune cells attacking the nerves after a Campylobacter infection, leading to neuron damage and potential paralysis.

 Why does this happen after a Campylobacter infection? Scientists believe that GBS is triggered when our immune system mistakenly targets our own nerve cells. This misidentification occurs because certain sugars (polysaccharides) on our nerve cells resemble those found on the outer layer of Campylobacter. When we’re infected, our immune system goes into action to fight Campylobacter by targeting these sugars. Although the immune cells successfully fend off the bacteria, they sometimes remain activated and misidentify our own cells as foreign, leading to GBS.

It’s fascinating—and a bit alarming—how such a small bacterium can have such significant effects on our bodies, highlighting the complex interplay between pathogens and our immune system.

Diagram showing the similar antigenic structures between the cell surface layers of Campylobacter and human nerve cells, illustrating how immune system misidentification can lead to Guillain-Barré Syndrome.

Guillain-Barré Syndrome: Not Just After Food Poisoning, But COVID-19 Too?

  Remember Guillain-Barré Syndrome (GBS), the condition that can cause paralysis in the arms and legs after a Campylobacter infection? It turns out that food poisoning isn’t the only potential trigger for GBS. Other infections, such as the flu, have also been linked to this syndrome, with Campylobacter being the most commonly reported precursor.

Diagram illustrating the potential triggers for Guillain-Barré Syndrome, including infection with Campylobacter and influenza viruses, as well as vaccination, with symptoms developing within 3 to 6 weeks post-exposure.

  Recently, there have been reports suggesting that COVID-19 might also be linked to GBS in some cases. Ongoing studies continue to investigate this possible connection, as researchers examine the wider effects of viral infections on our immune system and their potential to trigger conditions like GBS.

 Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases

IThis surprising link between foodborne and respiratory infections like COVID-19 reminds us of the complex and interconnected relationship between our immune responses and various pathogens.

Illustration of a person experiencing fatigue and headache with the text 'Long COVID?' highlighting symptoms associated with long-term effects of COVID-19."

Food Distribution & Campylobacter

When it comes to foodborne bacteria, Campylobacter stands out for several reasons. First, it thrives in warmer environments—about 42°C, which is higher than the optimal growth temperature of most foodborne pathogens. However, Campylobacter won’t grow at temperatures below 30°C, meaning it doesn’t proliferate even if chicken is left out at room temperature. This sets it apart from bacteria like Salmonella and E. coli, which can grow at temperatures as low as 10°C.

Illustration of a chicken packaging with the message 'Is this poster correct?' followed by a caution text 'Caution: Campylobacter Risk! Refrigerate poultry.' Emphasizes food safety and the risk of Campylobacter contamination in raw chicken if not properly refrigerated.

Even if there’s a lapse in temperature control during chicken distribution, Campylobacter won’t multiply. Moreover, as a "microaerophilic" bacterium, it doesn't grow well on most foods, including chicken. So, keeping chicken refrigerated or controlling its temperature won’t directly affect Campylobacter levels. Instead, the focus needs to be on managing the initial contamination levels at chicken farms and processing facilities.

Diagram showing Campylobacter levels during poultry processing and distribution. An image of a poultry slaughterhouse is on the left, followed by a distribution truck, with a graph indicating expected vs. actual Campylobacter levels, suggesting control measures should prevent bacterial increase during transportation.

In the U.S., poultry processing plants often use sodium hypochlorite to reduce Campylobacter contamination. Newer methods combine peracetic acid with organic acids for potentially more effective results. The EU, however, bans the use of such chemical treatments in poultry processing. They argue that strong disinfectants may mask hygiene issues in the earlier stages of the supply chain.

This insight into Campylobacter highlights the unique challenges in controlling its spread and the importance of comprehensive hygiene management across the entire food processing system.