Investigating why oak trees are dying is helping scientists understand how infectious diseases work
This article by , Postdoctoral Research Officer, School of Natural Sciences is republished from under a Creative Commons license. Read the .
British oak trees are under threat from a disease known as . Mainly affecting mature trees, it can kill them within four to five years of symptoms appearing. However, while researchers like myself have been looking into , and trying to find a way to prevent it, our work has been hindered in part by the fact that we have to follow a set of scientific rules known as Koch鈥檚 postulates.
For more than 100 years, scientists have identified which single organism causes a disease according to these postulates. However, more recent research into both plant and animal illnesses has shown that these are too strict, and that we need to start considering in what is called a 鈥減athobiome鈥.
A pathobiome is essentially a community of interacting bacteria that together cause a disease in animals and plants. Acute Oak Decline, for example, arises from which together degrade the trees鈥 vascular tissues, preventing transport of water and nutrients to the branches and leaves. We two bacteria as causative agents of Acute Oak Decline 鈥 Brenneria goodwinii and Gibbsiella quercinecans 鈥 while others, including Lonsdalea britannica and Rahnella species, have been detected, although their role is currently unclear.
Alone, the bacteria are harmless, or are less severe. But when alongside other organisms the . This gives rise to 鈥渆mergent property鈥, meaning that the disease causing property is greater than the sum of the combined organisms.
The postulates problem
Prior to the pioneering work of 19th-century German biologist , the causes of disease were unknown. In 1890, building on the work of scientists and , Koch identified his as standardised guidelines . These are:
The parasite occurs in every case of the disease in question and under circumstances which can account for the pathological changes and clinical course of the disease.
The parasite occurs in no other disease as a fortuitous and non-pathogenic parasite.
After being fully isolated from the body and repeatedly grown in pure culture, the parasite can induce the disease anew.
The postulates were later adapted to incorporate viruses, and the occurrence of asymptomatic carriers 鈥 individuals who are infected but present no symptoms, such as .
In the 1980s, the postulates again, to acknowledge the discovery that a single gene can be responsible for disease. Pathologists have since exploited this discovery to find that removing a gene from a bacterial cell鈥檚 DNA causes it to lose its .
Bacterial communities
However, as mentioned above, bacterial diseases in both animals and plants are increasingly being recognised as being caused by a community of bacteria and not a single organism. In Bangladesh, investigated why some people fall dangerously ill with cholera (caused by the bacterium Vibrio cholerae) while others have much reduced symptoms. It was found that the bacterial species Ruminococcus obeum is highly abundant in those who have recovered from the disease 鈥 because it was able to outcompete V. cholerae using a communication system known as .
V. cholerae mass in the human gut by releasing small diffusible molecules, which 鈥渢alk鈥 to other bacteria and recruit them to the site in large concentrations. But R. obeum disrupts V. cholerae signalling by releasing its own signal, which prevents V. cholerae from reaching sufficient quantities to release toxins and cause disease. This means that the human gut鈥檚 bacterial community can dictate whether an individual falls victim to cholera or remains healthy.
Like humans, plants host multiple species of bacteria. They form intricate host-bacterial relationships which can be , or to plant health. Plants in favour of growth promoting species, by releasing hormones into the soil which encourage colonisation. But unhealthy plants are less able to do this 鈥 which leads to a changed community of resident microbes that can contribute to disease.
The opportunistic human and plant pathogen , for example, colonises and persists in host environments which would have previously been protected by the immune system or excluded from the environment by resident bacteria. This makes under the postulates as the passive bacterium can only cause disease in an already compromised host.
Taken together, it becomes clear why we need to start considering the . Each bacterium can cause different levels of disease according to whether other bacteria are present, and the level of disease . Perhaps scientists need a new set of postulates, ones which take into account the accumulated knowledge from the more than 100 years of scientific research since Koch鈥檚 original work.
Publication date: 14 January 2019