The rod-shaped bacterium Pseudomonas syringae is a widespread and highly adaptable organism responsible for numerous diseases across a vast range of plant species. This pathogen is a significant concern in commercial agriculture and private horticulture due to the economic damage it causes to fruit trees, vegetables, and ornamental plants. Its ability to thrive in various environments and utilize multiple infection strategies makes it a persistent threat to plant health worldwide.
The Identity of the Bacterium
Pseudomonas syringae is classified as a Gram-negative bacterium, possessing a thin cell wall structure. This organism is ubiquitous in the environment, surviving in soil, water, and on plant surfaces without causing disease, a phase known as its epiphytic stage. From these environmental reservoirs, it is easily spread by wind-driven rain, insects, and contaminated pruning tools.
The bacterium can act as a biological ice nucleator. Specific strains produce an Ice Nucleation Active (INA) protein that migrates to the outer bacterial membrane. This protein acts as a scaffold, causing supercooled water to freeze at much warmer temperatures, often between -1.8°C and -3.8°C. This early freezing causes physical damage to the plant cells, leading to frost injury. The resulting cracks and wounds in the plant tissue provide entry points for the bacteria to transition to an invasive pathogenic state. This mechanism links cold weather events directly to disease outbreaks.
How P. syringae Causes Plant Disease
Once P. syringae gains entry into the plant’s internal tissues, it initiates a complex attack to overcome the host’s immune system. The bacterium employs a specialized molecular syringe called the Type III Secretion System (T3SS). This apparatus directly injects a repertoire of virulence proteins, known as effectors, into the host plant’s cells.
The primary function of these Type III effectors is to suppress the plant’s basal defense mechanisms. By interfering with the host’s signaling pathways, these effectors essentially disarm the plant. This allows the bacterium to multiply and spread unchecked within the tissue.
In addition to the T3SS effectors, many P. syringae strains produce potent chemicals called phytotoxins that directly damage the host cells. One prominent phytotoxin is coronatine, which structurally mimics the plant hormone jasmonic acid. This mimicry enables the toxin to disrupt the host’s hormonal defense signaling and forcibly reopen the stomata, which the plant typically closes to prevent bacterial entry. Another well-studied toxin is syringomycin, a substance that acts as a surfactant. Syringomycin disrupts the integrity of the plant cell membranes, leading to water-soaked lesions and necrosis.
Common Symptoms and Host Plants
The highly diverse nature of P. syringae, which includes over 50 distinct pathovars, results in a wide array of disease manifestations across its host range. The most common signs of infection fall into three categories: leaf spot, blight, and cankers.
Bacterial Leaf Spot
Bacterial leaf spot begins as small, water-soaked spots that eventually turn necrotic and brown. On plants like lilac, these spots often develop a noticeable yellow halo around the lesion. On maples, the infection can cause blackened veins and petioles.
Blight
Blight is characterized by the rapid death of flowers, buds, and young shoots. Flower blast, for instance, causes flower buds to turn brown or black, a symptom frequently seen on ornamental plants and fruit trees like cherry and apricot. Shoot-tip dieback is also a form of blight where black, dead tissue progresses down the twig from the tip.
Cankers
On woody plants, the infection often manifests as cankers, which are sunken, discolored, and necrotic areas on the bark or stems. These cankers are particularly damaging on stone fruit trees, such as peach, plum, and cherry. Cankers can girdle the stem and kill entire branches or the whole tree. The plant sometimes attempts to wall off the infection by exuding a gummy substance, a process known as gummosis.
Strategies for Managing P. syringae Infection
Management of P. syringae infections relies on integrating several preventive and mitigating practices, as the bacterium is widespread and opportunistic. Cultural controls are the first line of defense and involve minimizing conditions that favor bacterial entry and spread. This includes avoiding overhead irrigation, which can splash bacteria from the soil or infected leaves onto healthy plant parts.
Sanitation requires the prompt removal and destruction of infected plant material, such as cankered branches or blighted shoots. Pruning should only be conducted during dry weather, typically in the summer, to allow wounds to heal quickly. Tools must also be cleaned to prevent spreading the pathogen between plants.
For chemical management, copper-based bactericides, such as Bordeaux mixture or copper hydroxide, are the conventional treatment option. These products act as protectants, killing the bacteria on the plant’s surface during the epiphytic stage before they can enter the tissue. The timing of these applications is important, often requiring sprays in the autumn and spring to protect dormant buds and young growth.
However, copper spray efficacy can be inconsistent, and some strains have developed resistance. For a more sustainable approach, researchers are exploring biological controls, which involve using natural antagonists like bacteriophages. Bacteriophages are viruses that specifically target and kill bacteria, offering a promising alternative that is less harmful to the environment.