Streptococcus equi subsp. equi

Characteristics of the symbiont/pathogen

The pathogen involved in this symbionic relationship Streptococcus equi. The bacterium S. equi subsp. equi infects Equus caballus, the horse, and causes a disease called Strangles.

S. equi is a gram positive bacterium. Irregularly shaped cocci are typical of the species. Its incubation period is 3-14 days. The bacterium, which is in Lancefield’s group C, also causes red blood cells to lyse [Sweeney et. al.]. The bacterium can be grown on blood agar at 37°C under aerobic conditions. The bacteria form β-haemolytic colonies, which appear mucousy with no pigment. They are catalase-negative and facultative anaerobes. In a study to determine species of an unknown bacterium, certain strains and other species of the Streptococcus genus were looked at. In this study, Fernandez et. al. looked at S. equi subsp. ruminatorum subsp. nov., but they also looked at general features of the S. equi species including other strains (subsp. equi and subsp. zooepidemicus). The scientists found several characteristics in the different species that distinguish them from each other, and they also found some characteristics unique to S. equi [1]. S. equi subsp. equi is thought to have evolved from S. equi subsp. zooepidemicus, which is usually harmless. Only S. equi subsp. equi actually causes Strangles, though [2].

S. equi produces a protein called SeM, which increases its virulence. The protein binds fibrinogen and immunoglobulin G in order to inhibit the deposition of C3b. This causes phagocytes to be destroyed. The protein contains a sub-typing region (the region in which alterations of amino acid codes are present), a fibrinogen binding region, and an IgG binding region [3].

The genome of S. equi contains 2253793 base pairs and contains circular DNA. The complete genome of the species has been discovered [2].

Characteristics of the host

The host of the bacterium Streptococcus equi subsp. equi is the horse, Equus caballus. The horse is an herbivore and its ancestors, the earliest of the Equidae family which horses are from, are known to have originated 45- 55 million years ago. About five million years ago, the modern equus species was born. Early horses ate leaves, but as the teeth evolved, they became grass eaters Horse. Ovis aries, the sheep, and Capra hircus, the goat, are two species which host other subspecies of the Streptococcus equi species [Fernandez].

The genome of the horse contains about 2,680,000,000 base pairs. It includes 64 chromosomes, including 31 pairs of autosomal chromosomes and the sex chromosomes. There is much known about the horse genome and it is completely mapped out [Chowdhary].

Host-Symbiont Interaction

The interaction is pathogenic. Streptococcus equi subsp. equi is a parasite to the horse as the bacterium survives and thrives while the horse suffers dramatically from its effects. The host acquires the disease called strangles form this bacterium. Strangles has many symptoms including a high fever, usually the first sign. The horse will develop nasal discharge. Lymph nodes can become very enlarged and abscesses will form in the submandibular and retropharyngeal lymph nodes. Lymph nodes will become swollen and painful after about one week of infection. These abscesses drain for several days or even weeks. The name "Strangles" actually came about because the enlarged lymph nodes of the horse obstruct the airway and cause suffocation in some cases. "Bastard strangles" occurs when the bacterium spreads to other organs of the thorax and abdomen.

Shedding of the bacteria begins one to two days after the horse has developed symptoms. The bacteria is shed through nasal discharge for two to three weeks in most cases. Transmission of the bacteria can be direct or indirect. It can be spread horse-to-horse or from contaminated objects. Contaminated barns, water troughs, clothes, tack or feed can spread the bacteria. Horses that seem healthy can actually incubate the disease and spread it, but only later develop symptoms themselves. Horses recovering from Strangles can still shed the bacteria for prolonged periods of time [Sweeney].

The relationship is facultative since Streptococcus equi subsp. equi is a pathogen, the horse does not benefit from the interaction at all. The bacteria can also sometimes survive without the horse under favorable conditions.There is little research performed on the ability of Streptococcus equi to survive outside the horse host. Weese et. al. found that very few bacteria survived even a few days on outdoor rubber, wood and metal surfaces. Another study showed that the organism can survive 63 days on wood at two degrees Celsius and 48 days on glass or wood at 20 degrees Celsius. It does not survive well with other bacteria from soil [Jorm].

Molecular Insights into the Symbiosis

Describe molecular/genetic studies on the symbiosis.

Ecological and Evolutionary Aspects

Streptococcus equi subsp. equi is derived from Streptococcus equi subsp. zooepidemicus. Several important genes involved with S. equi pathogenesis are also found in S. pyogenes, a bacteria affecting humans. Streptococcus equi subsp. equi or Se4047 contains an inversion from other Streptococcus species at about 14 kbp. This gene codes for capsule production, indicating why S. equi has high levels of hyaluronate capsule. S. equi has many pseudogenes, which are genes that are no longer expressed, which indicates that the bacterium has recent loss and gain of genes. Se4047 contains 58 partially deleted genes and 78 pseudogenes, much more than S. equi subsp. zooepidemicus. What is the evolutionary history of the interaction? Do particular environmental factors play a role in regulating the symbiosis?

Recent Discoveries

Describe two findings on the symbiosis published within the last two years.

References

[1] Fernandez, E., Blume, V., Garrido, P., Collins, M.D., Mateos, A., Dominquez, L., and Fernandez-Garayzabal, J.F. 2004 Streptococcus equi subsp. ruminatorum subsp. nov., isolated from mastitis in small ruminants. International Journal of Systematic and Evolutionary Microbioogy 54:2291-2296.

[2] Holden, M.T.G., Heather, Z., Paillot, R., Steward, K.F., Webb, K., Ainslie, F., Jourdan, T., Bason, N.C., Holroyd, N.E., Mungall, Kl, Quail, M.A., Sanders, M., Simmonds, M., Willey, D., Brooks, K., Aanensen, D.M., Spratt, B.G., Jolley, K.A., Maiden, M.C.J., Kehoe, M., Chanter, N., Bentley, S.D., Robinson, C., Maskell, D.J., Parkhill, J., and Waller, A.S. 2009. Genomic evidence for the evolution of Streptococcus equi: host restriction, increased virulence, and genetic exchange with human pathogens. PLoS Pathogens 5:1-14.

[3] Kelly, C., Bugg, M., Robinson, C., Mitchell, Z., Davis-Poynter, N., Newton, R., Jolley, K.A., Maiden, M.C.J., and Waller, A.S. 2006. Sequence variation of the SeM Gene of Streptococcus equi allows discrimination of the source of strangles outbreaks. Journal of Clinical Microbiology 44:480-486.

Sweeney, C.R., Timoney, J.F., Newton, J.R., Hines, M.T. 2005. Streptococcus equi infections in horses: Guidelines for treatment, control, and prevention of strangles. J Vet Intern Med 19:123-134.

[Sample reference] [[1] Seemanapalli SV, Xu Q, McShan K, Liang FT. 2010. Outer surface protein C is a dissemination-facilitating factor of Borrelia burgdorferi during mammalian infection. PLoS One 5:e15830.]

Edited by Brooke Reamer, students of Grace Lim-Fong