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Investigating why oak trees are dying is helping scientists understand how infectious diseases work



British oak trees are threatened by an illness known as acute decay of oaks. Mainly influencing mature trees, it can kill them within four to five years from the onset of symptoms. However, while researchers like me have examined how they are causing it and trying to find a way to prevent it, our work has been hampered in part by the fact that we have to follow a set of scientific rules known as Koch's postulates.

For more than 100 years, scientists have identified which single organism causes an illness according to these postulates. However, more recent research on both plant and animal diseases has shown that these are too harsh and we need to start considering how more bacteria interact to cause a disease in what is called a "patobioma".

A pathobiome is essentially a community of interacting bacteria that together cause disease in animals and plants. The acute decline of the oak, for example, comes from several bacteria that together degrade the vascular tissues of the trees, preventing the transport of water and nutrients to the branches and leaves. We have recently identified two bacteria as agents responsible for the decline of the acute oak ̵

1; Brenneria goodwinii and Gibbsiella quercinecans – while others, including Lonsdalea Britannica and Rahnella were detected, although their role is not clear at the moment.

Alone, the bacteria that form the pathobiome are harmless, or are less severe. But when next to other organisms it increases the likelihood, the incidence and the severity of the disease. This gives rise to "emergent properties", which means that the disease that causes properties is greater than the sum of the combined organisms.

The Postulate Problem

Prior to the pioneering work of 19th century German biologist Robert Koch, the causes of the disease were unknown. In 1890, based on the work of scientists Louis Pasteur and John Snow, Koch identified his postulates as standard guidelines to demonstrate the cause of the disease. These are:

  1. The parasite occurs in each case of the disease in question and in circumstances that may explain the pathological changes and the clinical course of the disease.

  2. The parasite does not manifest itself in any other disease as a fortuitous case and not a pathogenic parasite.

  3. After being completely isolated from the body and repeatedly
    grown in pure culture, the parasite can induce the disease again.

Robert Koch works in his laboratory in Kimberley, South Africa.
Wellcome Collection, CC BY

The postulates were subsequently adapted to incorporate viruses, and the presence of asymptomatic carriers – infected individuals but no symptoms such as Typhoid Mary.

In the 1980s, the postulates were again extended, to recognize the discovery that a single gene can be responsible for the disease. Since then, pathologists have exploited this discovery to discover that the removal of a gene from the DNA of a bacterial cell causes the loss of its disease-causing abilities.

Bacterial communities

However, as mentioned earlier, bacterial diseases in animals and plants are increasingly recognized as being caused by a community of bacteria and not by a single organism. In Bangladesh, a study in 2014 examined why some people fall ill with cholera (caused by the bacterium Vibrio cholerae ) while others have very reduced symptoms. It has been discovered that the bacterial species Ruminococcus obeum is very abundant in those who recovered from the disease – because it was able to overcome V. cholerae using a communication system known as quorum sensing.

V. cholerae mass in the human gut by releasing small diffusible molecules, which "speak" to other bacteria and recruit them into the site in large concentrations. But R. obeum upsets V. cholerae signaling by releasing its own signal, which prevents V. cholerae from reaching sufficient quantities to release toxins and cause disease. This means that the bacterial community of the human gut can determine if an individual falls victim to cholera or remains healthy.

Like humans, plants host more species of bacteria. They form complicated host-bacterial relationships that can be beneficial, passive or harmful to plant health. Plants can directly model their resident bacteria in favor of species that promote growth by releasing hormones into the soil that encourage colonization. But unhealthy plants are less able to do so – which leads to a mutated community of resident microbes that can contribute to the disease.

The opportunistic human and plant pathogen Pseudomonas aeruginosa PA14, for example, colonizes and persists in host environments that previously would have been protected by the immune system or excluded from the environment by bacteria residents. This makes it difficult to prove the cause of the disease under the postulates as the passive bacterium can only cause the disease in an already compromised host.

Taken together, it becomes clear why we need to start considering pathobiome as a central factor in disease. Each bacterium can cause different levels of disease depending on whether other bacteria are present and the level of disease can be measured on a scale. Perhaps scientists need a new set of postulates, which take into account the knowledge accumulated by over 100 years of scientific research from Koch's original work.


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