Salmonid Rickettsial Septicemia

 
by  Chad Russell

    The purpose of this page is to provide some basic information about the fish disease Salmonid Rickettsial Septicemia and its causative agent Piscirickettsia salmonis. I have built this page as part of my class project in "Diseases of Fish", at Oregon State University. I have tried to include all of the relevant and interesting information regarding this topic, so I hope you find it interesting as well as informative. Welcome to the Salmonid Rickettsial Septicemia home page!

 

 
Introduction

    Rickettsial like infections have been reported since as early as 1939 in Egypt and later in British Columbia in 1970. However, because of the low mortality rate it was not considered very important (at least in an economical sense) and was never researched. This changed in the autumn of 1989 when, what was thought to be a new disease, broke out in Calbuco, southern Chile. An estimated 1.5 million market sized Coho salmon died from this unknown pathogen. Mortality rates ranged from 1 to 20% a month to 40% over a 10 week period. On certain farms mortality rates rose as high as 90%. In the following years, major losses were also attributed to the same organism among farmed Atlantic salmon. Because of the unusual nature of this disease, it was initially named U.A. (Unknown Agent), 'Coho salmon syndrome', or 'Huito disease'.
    The causative organism of the this Chilean outbreak has since been identified as Piscirickettsia salmonis, which is a rickettsial organism belonging to the order Rickettsiales. Today the most common names for this fish disease are known as Salmonid Rickettsial Septicemia (SRS), and Piscirickettsiosis. This disease is probably the most important disease affecting the Chilean salmon industry.
    Over the past few years, reports of ricketsial diseases infecting several different species of salmonids and non-salmonids in several different countries have surfaced.  This has increased concerns about the possible impact of this virulent organism in other fish cultures and wild fish stock.
 
 

Piscirickettsia salmonis

    P. salmonis is a Gram negative, acid fast, non-motile, non-capsulated, pleomorphic often spherical to coccoid organism ranging in size from 0.5 to 1.8 um in diameter. It is also an obligate intracellular organism and has been culture in 6 different cell lines. Typically, growth is determined by the appearance of cytopathic effect (CPE). Characteristic CPE include cell rounding and development of one or more large vacuoles within the cytoplasm of the host. Four of the six susceptible cell lines come from salmonid species. The other two lines come from warm water fish species. P. salmonis is very temperature sensitive, having a maximum range of 4 - 25 C and optimal growth at 15 - 18 C.  Click here to see picture
 

Pathology
    External signs of SRS include: lethargy, anorexia, darkening of the skin, surface swimming, and respiratory distress. External skin lesions are also common and include: hemorrhagic ulcers and white nodules measuring up to 1 cm in size. However, it has been reported that many heavily infected fish show no external lesions. Internal lesions are very characteristic of the disease. Commonly infected organs are liver, spleen, intestine, and hematopoietic tissue of the kidney. The most characteristic internal lesions are off-white to yellow nodules measuring up to 2 cm in diameter throughout the liver.  Click here to see picture
    P. salmonis a wide variety of cells including macrophages. Within the cell they replicate in membrane bound intracytoplasmic vacuoles of variable size. It has also been found extracellularly, apparently as a result of cell lysis. The mechanisms by which it infects and survives in the host cell is still not clear.
 
Transmission
    The mode of infection and transmission are still unclear. Experimentally, fish have been infected via the intraperitoneal, oral, and gill routes. Natural horizontal transmission seems to occur a few weeks after smolts are transferred to sea water. Infectivity of P. salmonis is greatly increased in sea water. It has been shown to survive up to 28 days in sea water at 5 C, while only surviving less than 30 min in fresh water at the same temperature. However, infections have occurred in fresh water tanks. Infected cells have been found in both the intestine and renal tubules, suggesting that the bacteria could be released into the water and survive to infect other fish.
    Intermediate vectors may also play a role in the natural transmission of the organism similar to terrestrial rickettsial diseases that are mainly transmitted by ticks to the host mammal. Preliminary studies show that invertebrates, non-salmonids, and salmonid parasites are able to carry the disease, and presumably act as vectors or reservoirs for the pathogen.
    Vertical transmission of P. salmonis has been considered unlikely. However, one study showed that 98.3% of fingerlings from positive brood stock were also positive. In contrast, only 26.7% of fingerlings from negative brood stock were positive. Due to the rick of vertical transmission, Chilean farmers have been screening brood stocks. Many different stains have been used to detect the organism in smears. Although this technique is not very specific, it is very fast and economical. Other more definitive techniques including cell line cultures, serotypes, PCR, and microwave radiation have been developed but are more costly.
 
Control
 
    P. salmonis has proven very sensitive to a large range of antibiotics used in vitro. However, results are far less encouraging in vivo. One possible explanation for this is that it is likely that the antibiotics can not reach the organism because of its intracellular nature. Another possibility is that the antibiotics are disabled by  the ionic nature of the sea water. However, some success has been made with antibiotics to control outbreaks of the disease. Among the antibiotics currently used, oxolinic acid and flumequine given orally are the most popular. Strategies to decrease transmission include injection of brood stock with antibiotics 30 to 60 days before spawning, and incorporation of antibiotics in the water while the eggs are hardening after fertilization.
    Other methods of control aside from antibiotics have proven quite successful as well. Decreases in unnecessary stress, quick elimination of dead or diseased fish, appropriate disposal of blood, and decreases in stocking densities have proven successful in limiting outbreaks.
 
Conclusion

    Piscirickettsia salmonis has continued to cause large losses in the Chilean salmon industry and reports continue to increase of rickettsial infections around the world. Due to the intracellular nature of the organism, the control of this disease has been difficult with antibiotics. Further research and information on the transmission, pathogenic mechanisms, and intracellular survival are needed to establish better preventative strategies.

 

  Bibliography

 MB 492 home page
 
If you have comments or suggestions, please email me at russelch@ucs.orst.edu
This page created with Netscape Navigator Gold