Vibrio coralliilyticus

by Megan Sawatzky and Emily Byrnes


Vibrio coralliilyticus is a gram-negative, rod shaped bacterium found globally in the marine environment. Gram-negative means the bacterium has an outer lipid membrane that can help it resist environmental and host defenses, thus making it more difficult to destroy. V. coralliilyticus is a temperature-dependent, opportunistic pathogen, predominantly to several genera of tropical corals. An opportunistic pathogen is one that, while non-harming in healthy organisms, may be threating to those weakened by other factors. For example, increasing sea temperatures decrease chlorophyll concentration in the coral’s algal symbionts, which subsequently decreases the coral’s food supply and induces stress. This cascade of events makes the coral more susceptible to infection (Figure 1). V. coralliilyticus directly benefits from the warmer temperatures as well, because of an upregulation in the pathogen’s motility, resistance, and virulence.

Figure 1. Factors contributing to increased host susceptibility to, and virulence of, V. coralliilyticus. Source: Megan Sawatzky, 2021.


V. coralliilyticus is associated with disease in a variety of marine organisms, including oyster and mussel larvae, rainbow trout, and most significantly, several genera of corals. The symptoms of disease vary depending on the species/organism that is infected. The disease progression in V. coralliilyticus infections has been principally studied in the coral, Pocillopora damicornis. In P. damicornis, V. coralliilyticus causes temperature-induced bleaching and tissue lysis. Bleaching is the disruption in the obligate symbiotic relationship between the coral and the dinoflagellates, i.e., algae, living in their tissues. This relationship can be damaged from environmental stress, or by a direct attack on the algae by V. coralliilyticus. The algae are the coral’s primary energy source, and when their relationship is damaged, it leaves the coral highly susceptible to other diseases.

When V. coralliilyticus enters the coral host, P. damicornis, it grows in the mucus and tissue. Next, bleaching occurs readily at temperatures between 25-29°C. Coral tissue lysis, promoted by extracellular bacterial proteases (enzymes that breakdown proteins), is apparent three to five days post infection and reaches completion after two weeks at temperatures above 27°C. Bleaching and tissue lysis are slowed at temperatures below 25°C, and virulence is significantly impaired at temperatures below 22°C.

In other coral species, V. coralliilyticus is the primary cause of White syndrome (WS). WS, or White Band Disease (WBD), is a term used to describe a class of coral tissue loss diseases characterized by acute and/or rapid tissue lysis leaving the coral as a bare skeleton. In non-coral hosts, V. coralliilyticus infections cause widespread mortalities. V. coralliilyticus is a highly infectious bacterial pathogen and can be transmitted through direct contact.


V. coralliilyticus is commonly located throughout the Indo-Pacific Ocean, as well as the Red and Mediterranean Seas (Figure 2). In the Red Sea, V. coralliilyticus was first shown to infect the coral, Pocillopora damicornis, in 2002. Since then, the bacterium has been the causative agent of numerous outbreaks of bleaching in the species. In the fall of 2006, there was an outbreak in the North-west Mediterranean Sea where V. coralliilyticus caused tissue loss in the coral, Paramuricea clavata. The minimum infectious dose, which is the minimum number of bacteria needed to cause fifty-percent of tissue lysis in infected corals, was 104 colony forming units (CFU)/mL. A CFU is defined as the number of bacteria that form in a given volume of culture.

In the Indo-Pacific Ocean, major outbreaks have been reported in Kāne’ohe Bay, Hawai’i, and the West Coast of the United States. In Kāne’ohe Bay, V. coralliilyticus was a prominent agent in an outbreak of Monitpora WS in the coral, Montipora capitata, from 2010 to 2011. The minimum infectious dose in this outbreak was between 107 and 108 CFU/mL, however this was exceeded in many of the infected coral. Outbreaks of V. coralliilyticus have also been observed in non-coral species, such as oysters, causing mass mortalities. In hatcheries in the West coast of the U.S, oyster larvae are frequently killed by this pathogen. Only hatcheries face this threat because V. coralliilyticus is only infectious to oyster larva in their stages before they stop being free-swimming, which is only the first 2 to 3 weeks. In the past couple years, two hatcheries on the West coast have lost over 80% of their larvae due to V. coralliilyticus.

Other outbreaks in the Indo-Pacific have been reported in Nelly Bay (Great Barrier Reef), Majuro Atoll (Republic of the Marshall Islands), and Nikko Bay (Republic of Palau). Since this bacterium is newly studied, outbreaks and diseases caused by V. coralliilyticus are still being discovered.

Figure 2: Outbreaks of V. coralliilyticus and their corresponding diseases. Source: Emily Byrnes, 2021.


The virulence of a pathogen refers to its ability to cause damage and/or disease in the host; virulence factors are structures, molecules, and/or cell systems that help it do so. The virulence of V. coralliilyticus is associated with chemotaxis/motility, i.e., movement directed by a chemical gradient, and host degradation. Very few virulence factors have been identified in V. coralliilyticus, and those that have demonstrate the temperature-dependent nature of the pathogen. A key temperature-dependent virulence factor of V. coralliilyticus is the flagellum (Figure 3). Flagella are “whip-like” surface structures used by motile bacteria to facilitate chemotaxis, adhesion, and invasion of host surfaces. V. coralliilyticus, and other Vibrio species, have a single flagellum at one end, known as a polar flagellum.

The first step in any bacterial infection is contact between the pathogen and the host. V. coralliilyticus uses its flagellum to follow a chemical gradient and facilitate contact with the coral host. Corals secrete copious amounts of mucus which covers their epidermis (outer “skin” layer) to help protect against surrounding pathogens. Ironically, the mucus of P. damicornis provides the chemical gradient that attracts V. coralliilyticus.

Figure 3. V. coralliilyticus flagellum as a key virulence factor. Source: Megan Sawatzky, 2021.

Mutants of V. coralliilyticus that are non-pathogenic have a single transposon insertion in the flhA gene. A transposon is a sequence of DNA that can “jump” to a different position in the genome. So, in the case of mutant V. coralliilyticus, a DNA sequence “jumped” into the sequence that codes for FlhA, thus rendering the gene inactive. FlhA is a membrane protein that is responsible for the export of flagellar proteins, so those that do not have the working gene do not have a flagellum.  With no flagellum the pathogen is unable to adhere to/invade the coral host and cause disease.


The main treatment plan currently being studied for organisms infected by V. coralliilyticus is bacteriophage, or phage, therapy. In bacteriophage therapy, specific viruses are used to kill a target bacterial pathogen. For V. coralliilyticus infected corals, bacteriophages stop tissue degradation and prevent the dissociation of the coral’s algal symbionts, thus preventing mortality. There are many bacteriophages that can infect V. coralliilyticus, and bacteriophages belonging to the Myoviridae family, including bacteriophage YC and vB_VcorM-GR28A, are the most effective.

Bacteriophage YC was discovered in Nelly Bay, Great Barrier Reef. It is an effective lytic phage in V. coralliilyticus, meaning it takes over the bacterium and destroys it. The other bacteriophage, vB_VcorM-GR28A, is a lytic phage which has been used for treatment in oyster larvae. Bacteriophage therapy is the main source of treatment against infections caused by V. coralliilyticus at this time.  


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