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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- crayfish plague
International Common Names
- English: crayfish aphanomyciasis; crayfish plague (fungus disease)
- French: la peste de l'écrevisse
Local Common Names
- Germany: Krebspest
- Sweden: Kräftpest
OverviewTop of page
Crayfish plague had a long history before the oomycete, Aphanomyces astaci, was finally established as the causative organism of the disease (Schikora, 1906; Schäperclaus, 1935; Nybelin, 1936; Rennerfelt, 1936). It was recognised as an infectious disease at the end of the 19th century. Early publications on the causative agent claimed that a bacterium, Bacillus pestis astaci, caused the disease (Hofer, 1898), but in 1903 Schikora identified a fungus, an Aphanomyces species, as the disease agent (Schikora, 1903). It was not until 1934 that A. astaci was finally determined to be the true infectious agent; the difficulty in isolating the fungus in pure culture was the reason for its prolonged obscurity. This problem is mainly due to the presence of bacteria and other fungi on the tissues used for cultivation. These contaminants can easily overgrow A. astaci, which itself is rather slow growing (Oidtmann et al., 1999b).
A. astaci is a member of a group of organisms commonly known as the water moulds. Although long regarded as fungi, this group, the Oomycetida, are now considered to be protists and are classified with diatoms and brown algae in a group called the Stramenopiles or Chromista. A. astaci belongs to the class Oomycetes and the order Saprolegniales, in which a number of aquatic animal pathogens can be found. It is a member of the family Leptolegniaceae.
A. astaci is the cause of crayfish plague in freshwater crayfish species susceptible to the disease, such as those of Europe and Australia. In contrast, in North American crayfish species, it acts as a benign parasite and these species can act as carriers of the pathogen (Unestam, 1969b; Unestam and Weiss, 1970; Unestam, 1972, 1975).
Crayfish plague is currently considered the most serious disease of freshwater crayfish.
A. astaci is thought to have been introduced into Europe in the middle of the 19th century (Cornalia, 1860; Alderman, 1996). Since then it has spread across large parts of Europe, leading to several outbreaks of crayfish plague in European crayfish populations, and is considered the most important reason for the decline of these species across Europe. The source of the original infections in the 19th century was never established; but the post-1960s spread is largely linked to the introduction and spread of North American crayfish introduced for purposes of crayfish farming.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Astacopsis fluviatilis||Experimental settings||Aquatic: Adult|
|Astacopsis gouldi||Experimental settings||Aquatic: Adult|
|Astacus astacus (European crayfish)||Domesticated host, Experimental settings, Wild host||Aquatic: Adult|Aquatic/Larval||Open water systems/Enhancements and culture-based fisheries (inc. ranching and stock enhacement)|Enclosed systems/Ponds|Enclosed systems/Raceways / running water ponds|
|Astacus leptodactylus (Danube crayfish)||Domesticated host, Experimental settings, Wild host||Aquatic: Adult|Aquatic/Larval||Open water systems/Enhancements and culture-based fisheries (inc. ranching and stock enhacement)|Enclosed systems/Ponds|Enclosed systems/Raceways / running water ponds|
|Austropotamobius pallipes (freshwater white-clawed crayfish)||Wild host||Aquatic: Adult|Aquatic/Larval|
|Austropotamobius torrentium||Wild host||Aquatic: Adult|Aquatic/Larval|
|Cambaroides japonicus||Experimental settings||Aquatic: Adult|
|Cherax destructor (yabby)||Experimental settings||Aquatic: Adult|
|Cherax papuanus||Experimental settings||Aquatic: Adult|
|Cherax quinquecarinatus||Experimental settings||Aquatic: Adult|
|Eriocheir sinensis (Chinese mitten crab)||Experimental settings||Aquatic: Adult|
|Euastacus clydensis||Experimental settings||Aquatic: Adult|
|Euastacus crassus||Experimental settings||Aquatic: Adult|
|Euastacus kershawi||Experimental settings||Aquatic: Adult|
|Faxonius limosus (Spiny-cheek crayfish)||Domesticated host, Subclinical, Wild host||Aquatic: Adult|Aquatic/Larval|
|Geocharax gracilis||Experimental settings||Aquatic: Adult|
|Pacifastacus leniusculus (American signal crayfish)||Domesticated host, Subclinical, Wild host||Aquatic: Adult|Aquatic/Larval|
|Procambarus clarkii (red swamp crayfish)||Domesticated host, Subclinical, Wild host||Aquatic: Adult|Aquatic/Larval|
Hosts/Species AffectedTop of page
To date, all species of freshwater crayfish have to be considered as susceptible to infection with A. astaci. The outcome of an infection varies depending on species. All stages of European crayfish species, including the Noble crayfish (Astacus astacus) of north-west Europe, the white clawed crayfish (Austropotamobius pallipes) of south-west and west Europe, the related Austropotamobius torrentium (mountain streams of south-west Europe) and the slender clawed or Turkish crayfish (Astacus leptodactylus) of eastern Europe and Asia Minor are highly susceptible (Unestam, 1969b; Unestam and Weiss, 1970; Unestam, 1975; Alderman et al., 1984; Rahe and Soylu, 1989; Alderman, 1996). Laboratory challenges have demonstrated that Australian species of crayfish are also highly susceptible (Unestam, 1975). North American crayfish such as the signal crayfish (Pacifastacus leniusculus), Louisiana swamp crayfish (Procambarus clarkii) and Orconectes spp. are infected by A. astaci, but under normal conditions the infection does not cause clinical disease or death. All North American crayfish species investigated to date have been shown to be susceptible to infection (Unestam, 1969b; Unestam and Weiss, 1970; Oidtmann et al., 2006) and it is therefore currently assumed that this is the case for any other North American species. The only other crustacean known to be susceptible to infection by A. astaci is the Chinese mitten crab (Eriocheir sinensis) but this was reported only under laboratory conditions (Benisch, 1940).
DistributionTop of page
The natural range of A. astaci is likely to be North America. It has been found in North American crayfish sampled in North America (Unestam and Weiss, 1970). Any occurrence of A. astaci outside of North America is currently considered as an exotic appearance of the pathogen.
The first evidence for the arrival of A. astaci in Europe is the first large crayfish mortalities, which were first observed in Italy in 1859 (Ninni, 1865; Seligo, 1895). These were followed by further reports of crayfish mortalities, where no other aquatic species were affected, in the Franco-German border region in the third quarter of the 19th century. From there a steady spread of infection occurred, principally in two directions: down the Danube into the Balkans and towards the Black Sea, and across the North German plain into Russia and from there south to the Black Sea and north-west to Finland and, in 1907, to Sweden. In the 1960s, the first outbreaks were reported in Spain and in the 1980s the disease spread further to the British Isles, Turkey, Greece and Norway (Alderman, 1996). The source of the original infections in the 19th century was never established. The spread of the disease post-1960s is largely linked to introductions of North American crayfish for crayfish farming (Alderman, 1996). Pacifastacus leniusculus, Faxonius limosus and Procambarus clarkii are now widely naturalised in many parts of Europe. Since North American crayfish serve as a reservoir of A. astaci, any areas where North American crayfish species are found have to be considered as areas where A. astaci is present (unless shown otherwise). Australia and New Zealand have not experienced any outbreaks of crayfish plague to date and are currently considered free of the disease (OIE, 2011b).
Some North American crayfish species, such as Procambarus clarkii, have been introduced for aquaculture purposes into many areas around the globe, like Central America, South America, Europe, Africa, China and other parts of east and south Asia. In most cases where P. clarkii has been introduced, it has escaped to the wild and established reproducing populations. It is not known whether all of these populations would still be carriers of A. astaci, but North American crayfish populations tested for carrier status in Europe have usually been found to be infected (Oidtmann et al., 2006; Kozubíková et al., 2009). The actual distribution of A. astaci is therefore likely to be far broader than the distribution table would suggest and is more likely to more or less coincide with the distribution of North American crayfish worldwide. If there are no susceptible species in the area to which the North American crayfish are introduced, there may be no impact of such introductions associated with A. astaci.
Details for introductions of North American crayfish species into new geographic areas can be obtained from Gherardi et al., 1999.
Distribution TableTop of page
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Lesotho||Absent, No presence record(s)||OIE (2009)|
|Sudan||Absent, No presence record(s)||OIE (2009)|
|Tunisia||Absent, No presence record(s)||OIE (2009)|
|Armenia||Absent, No presence record(s)||OIE (2009)|
|Azerbaijan||Absent, No presence record(s)||OIE (2009)|
|Bahrain||Absent, No presence record(s)||OIE (2009)|
|Bangladesh||Absent, No presence record(s)||OIE (2009)|
|China||Absent, No presence record(s)||OIE (2009)|
|Hong Kong||Absent, No presence record(s)||OIE (2009)|
|Indonesia||Absent, No presence record(s)||OIE (2009)|
|Iran||Absent, No presence record(s)||OIE (2009)|
|Israel||Absent, No presence record(s)||OIE (2009)|
|Japan||Absent, No presence record(s)||OIE (2009)|
|Kuwait||Absent, No presence record(s)||OIE (2009)|
|Malaysia||Absent, No presence record(s)||OIE (2009)|
|Turkey||Present||Introduced||Invasive||Rahe (1987); OIE (2009)|
|Austria||Present||Introduced||Invasive||Anon (1879); Pöckl and Pekny (2002)|
|Belarus||Absent, No presence record(s)||OIE (2009)|
|Belgium||Present||Introduced||CABI (Undated); Seligo (1895)||Original citation: ISSG (IUCN SSC Invasive Species Specialist Group) (2013)|
|Croatia||Absent, No presence record(s)||OIE (2009)|
|Cyprus||Absent, No presence record(s)||OIE (2009)|
|Czechia||Present||Introduced||Invasive||Kozubíková et al. (2006); OIE (2009)|
|Finland||Present||Introduced||Invasive||Westman and Savolainen (2001); OIE (2009)|
|France||Present||Introduced||Invasive||Raveret-Wattel (1885); Vivier (1951); CABI (Undated)|
|Germany||Present||Introduced||Invasive||Oidtmann et al. (1999); Tzukerzis (1964); OIE (2009)|
|Hungary||Absent, No presence record(s)||OIE (2009)|
|Iceland||Absent, No presence record(s)||OIE (2009)|
|Ireland||Present||Introduced||Invasive||Reynolds (1988); Matthews and Reynolds (1992); Demers and Reynolds (2002); OIE (2009)|
|Italy||Present||Introduced||Cammà et al. (2010); Cornalia (1860); OIE (2009)|
|Latvia||Present||Introduced||CABI (Undated); Tzukerzis (1964); OIE (2009)||Original citation: ISSG (IUCN SSC Invasive Species Specialist Group) (2013)|
|Lithuania||Present||Introduced||CABI (Undated); Mazylis and Grigelis (1979); OIE (2009)||Original citation: ISSG (IUCN SSC Invasive Species Specialist Group) (2013)|
|Netherlands||Absent, No presence record(s)||OIE (2009)|
|North Macedonia||Present||Introduced||CABI (Undated)||Original citation: ISSG (IUCN SSC Invasive Species Specialist Group) (2013)|
|Norway||Present||Introduced||Invasive||Hǻstein T. and Unestam (1971); Taugbøl et al. (1993); OIE (2009)|
|Poland||Present||Introduced||Seligo (1895); Własow et al. (2004)|
|Portugal||Present||Introduced||Bernardo and Ilheu (1997); OIE (2009)|
|Romania||Present||Introduced||Schrimpf et al. (2012)|
|Russia||Present||Introduced||CABI (Undated); Arnold (1900)||Original citation: ISSG (IUCN SSC Invasive Species Specialist Group) (2013)|
|Slovakia||Absent, No presence record(s)||OIE (2009)|
|Slovenia||Present||Introduced||Franke (1894); OIE (2009)|
|Spain||Present||Introduced||Invasive||Cuellar and Coll (1984); OIE (2009)|
|Sweden||Present||Introduced||Invasive||Alm (1929); Josefsson and Andersson (2001); Edsman (2004); OIE (2009)|
|Switzerland||Present||Introduced||CABI (Undated); Roch (1881); OIE (2009)||Original citation: ISSG (IUCN SSC Invasive Species Specialist Group) (2013)|
|Ukraine||Absent, No presence record(s)||OIE (2009)|
|United Kingdom||Present, Widespread||Introduced||Invasive||Alderman et al. (1984); OIE (2009)|
|Belize||Absent, No presence record(s)||OIE (2009)|
|Costa Rica||Absent, No presence record(s)||OIE (2009)|
|Cuba||Absent, No presence record(s)||OIE (2009)|
|El Salvador||Absent, No presence record(s)||OIE (2009)|
|Greenland||Absent, No presence record(s)||OIE (2009)|
|Guatemala||Absent, No presence record(s)||OIE (2009)|
|Martinique||Absent, No presence record(s)||OIE (2009)|
|Mexico||Absent, No presence record(s)||OIE (2009)|
|United States||Present||OIE (2011)|
|-Georgia||Absent, No presence record(s)||OIE (2009)|
|Australia||Absent, No presence record(s)||OIE (2009)|
|French Polynesia||Absent, No presence record(s)||OIE (2009)|
|New Caledonia||Absent, No presence record(s)||OIE (2009)|
|New Zealand||Absent, No presence record(s)||OIE (2009)|
|Argentina||Absent, No presence record(s)||OIE (2009)|
|Brazil||Absent, No presence record(s)||OIE (2009)|
|Chile||Absent, No presence record(s)||OIE (2009)|
|Colombia||Absent, No presence record(s)||OIE (2009)|
|French Guiana||Absent, No presence record(s)||OIE (2009)|
|Venezuela||Absent, No presence record(s)||OIE (2009)|
PathologyTop of page
Highly susceptible species
Depending on a range of factors, the foci of infection in crayfish may be seen by the naked eye or may not be discernable despite careful examination. Such foci can best be seen under a low power stereo microscope and are most commonly recognisable by localised whitening of the muscle beneath the cuticle (Oidtmann et al. 1996). In some cases a brown coloration of cuticle and muscle may occur, and in others, hyphae are visible in infected cuticle in the form of fine brown (melanised) tracks in the cuticle itself. Sites for particular examination include the intersternal soft ventral cuticle of the abdomen and tail, the cuticle of the perianal region, the cuticle between the carapace and abdomen, the joints of the pereiopods (walking legs), particularly the proximal joint, and finally the gills (Alderman and Polglase, 1986; Nyhlen and Unestam, 1980, Oidtmann et al. 1996).
North American crayfish species
Infected North American crayfish can sometimes show melanised spots in their soft cuticle, for example the soft abdominal cuticle. However, it must be stressed that these melanisations can be caused by mechanical injuries or infections with other water moulds and are very unspecific. Conversely, visible melanisation is not always associated with carrier status. Infected animals can appear completely devoid of visible melanisations.
Small pieces of soft cuticle excised from the soft abdominal cuticle and examined under a microscope may confirm the presence of aseptate fungus-like hyphae 7–9 μm wide (Oidtmann et al. 1996). In the case of North American crayfish, these are usually surrounded by melanin.
Unless the selection of tissue for fixation has been well chosen, A. astaci hyphae can be difficult to find in stained preparations. A histological staining technique, such as the Grocott silver stain counterstained with conventional haematoxylin and eosin, will make hyphae more visible in histological stains.
DiagnosisTop of page
Until recently, the diagnosis of crayfish plague from highly susceptible species strictly required the isolation and characterisation of the pathogen, A. astaci, using simple mycological media with antibiotics to control bacterial contamination. Isolation is only likely to be successful before or within 24 hours of the death of infected crayfish. However, there is no other disease or pollution effect that is known to cause such total mortality of crayfish while leaving all other animals in the same water unharmed. High mortalities in susceptible crayfish while all other invertebrates in the water course remain unharmed strongly suggest that the mortalities are due to a crayfish plague outbreak.
Clinical signs of crayfish plague include behavioural changes and a range of visible external lesions. The range of these lesions is so large that, except for the experienced eye, such clinical signs are of limited diagnostic value. Also, the lesions are not pathogen-specific and can be caused by mechanical lesions or invasion by other agents such as fungi or bacteria (Persson and Söderhäll, 1983).
The currently recommended method of diagnosis is single-round PCR assay, followed by sequencing (Oidtmann et al. 2006; OIE 2011a). This combination of methods provides a very quick and reliable result. Isolation of the pathogen using culture is time-consuming and can take several weeks. If it is successful, the identification of the isolate has to be further confirmed either by challenge of susceptible crayfish or by PCR and sequencing.
List of Symptoms/SignsTop of page
|Crustaceans / Cessation of feeding - Behaviour||Sign|
|Crustaceans / Changes in colour - Surface||Sign|
|Crustaceans / Changes in feeding behaviour - Behaviour||Sign|
|Crustaceans / Changes in swimming movement - Behaviour||Sign|
|Crustaceans / Failure to right / difficulty in righting - Behaviour||Sign|
|Crustaceans / General weakening - Behaviour||Sign|
|Crustaceans / Lethargy - Behaviour||Sign|
|Crustaceans / Mortalities - Miscellaneous||Sign|
|Crustaceans / Unusual activity during daytime - Behaviour||Sign|
Disease CourseTop of page
Highly susceptible species
Gross clinical signs are extremely variable and depend on challenge severity and water temperatures. The first sign of a crayfish plague mortality may be the presence of numbers of crayfish at large during daylight (crayfish are normally nocturnal), some of which may show evident loss of co-ordination in their movements, and easily fall over on their backs and remain unable to right themselves. Often, however, unless waters are carefully observed, the first sign that there is a problem will be the presence of large numbers of dead crayfish in a river or lake (Alderman et al., 1987).
In susceptible species, where sufficient numbers of crayfish are present to allow infection to spread rapidly, particularly at summer water temperatures, infection will spread quickly and stretches of over 50 km may lose all their crayfish in less than 21 days from the first observed mortality (D. Alderman, Centre for Environment, Fisheries, and Aquaculture Science, UK, personal communication, 2009). Crayfish plague has unparalleled severity of effect, since infected susceptible crayfish generally do not survive. Mortality or disappearance of other aquatic crustaceans as well as crayfish, even though fish survive, may indicate pollution rather than disease (e.g. insecticides such as cypermethrin have been associated with initial misdiagnoses).
North American crayfish species
Highly susceptible species
Infected crayfish of the highly susceptible species may leave their hides during daytime (which is not normally seen in crayfish), and have a reduced escape reflex and progressive paralysis. Dying crayfish are sometimes found lying on their backs. The animals are often no longer able to right themselves. Occasionally, the infected animals can be seen trying to scratch or pinch themselves.
North American crayfish species
Infected North American crayfish do not show any behavioural changes.
EpidemiologyTop of page
The life cycle of A. astaci is simple, with vegetative hyphae invading and ramifying through host tissues, eventually producing extramatrical sporangia that release amoeboid primary spores. These initially encyst, but then release a biflagellate zoospore (secondary zoospore), the infective stage. Biflagellate zoospores swim in the water column and, on encountering a susceptible host, attach, encyst and germinate to produce invasive vegetative hyphae. Free-swimming zoospores appear to be chemotactically attracted to crayfish cuticle (Cerenius and Söderhäll, 1984a) and often settle on the cuticle near a wound (Nyhlen and Unestam, 1980).
Release of the zoospores from the mycelium takes place when the mycelium grows out of the crayfish cuticle. This usually occurs when a susceptible crayfish is severely ill or dead, or, in the case of American species, during moulting or at death.
Zoospores are capable of repeated encystment and re-emergence, extending the period of their infective viability (Cerenius and Söderhäll, 1984b). Growth and sporulation capacity is strain- and temperature-dependent (Diéguez-Uribeondo et al., 1995).
It appears that A. astaci remains viable in the cuticle of North American crayfish for several months. In these species it infects the cuticle in a benign infection. Invading hyphae are surrounded by melanin, which is deposited as a result of the host’s immune system responding to the infection. The infection remains confined to the cuticle and does not – as in the highly susceptible species – break through the basal lamina and invade the body cavity and other host tissues.
Infection in highly susceptible species leads to the death of the host and subsequently, the generation of zoospores in order to find a new viable host.
A. astaci appears to be specifically adapted to grow in crayfish tissues. It has so far not been detected in any other host from the natural environment.
In the natural environment A. astaci does not survive well for long periods in the absence of a suitable host. Observations on the longevity of the various life stages have been presented (Unestam, 1969a; Svensson and Unestam, 1975). The authors observed that A. astaci cysts survive for 2 weeks in distilled water, and that zoospores remained motile for up to 3 days (Unestam, 1969a). As A. astaci can go through three cycles of zoospore emergence, the maximum life span outside of a host could be several weeks. Unestam found still-viable spores in a spore suspension kept at 2°C for 2 months (Unestam, 1966).
In principle, spread of crayfish plague can be through 3 pathways: 1) independent of crayfish host tissue (usually as zoospores or cysts), 2) infected cuticle/tissue of the highly susceptible crayfish species (e.g. any of the European species) and 3) spread with infected carrier (=North American) crayfish.
Spread independent of crayfish host tissue can be through contaminated water, and mechanical vectors or fomites that have been in contact with contaminated water. The likelihood of spread depends on several factors including the number of spores transmitted, the presence of susceptible crayfish at the site of release, the conditions the spores/cysts are exposed to during transfer etc. (Oidtmann et al., 2002; Oidtmann et al., 2005). The mechanical spread route is more relevant for relatively short durations of transfer due to the limited survival of the pathogen outside of a crayfish host. Examples of fomites that may be involved in mechanical transmission are: contaminated crayfish traps, angling equipment, and boots. It may also be possible that animals can carry the spores or cysts in their fur / feathers. Spread of A. astaci via water may occur for example during fish transport, or in ballast water of ships. Fish themselves may also serve as vectors in several ways: two independent studies have shown that A. astaci spores germinate on fish scales in vitro (Hall and Unestam, 1980; Ahne and Halder, 1988). However, it remains yet to be shown that transmission via fish skin occurs in vivo (Oidtmann et al., 2002). Mechanical spread would be most relevant from sites of current crayfish plague outbreaks during which a high number of spores and cysts would be present in the water.
Outbreaks of crayfish plague in the highly susceptible species are also a period during which spread via infected highly susceptible crayfish would be likely. Crayfish could be harvested without the person harvesting recognizing that there was an ongoing outbreak; the crayfish may also be emergency-harvested, or be preyed upon. In the course of the disease, susceptible crayfish become progressively paralysed and show abnormal behaviour such as daytime activity (normally crayfish are predominantly nocturnal). This makes them easy prey for an increased range of predators, which may eat the crayfish or abduct them to other locations. If eaten by fish, the pathogen may survive the gut passage and released with the fish faeces (Oidtmann et al., 2002).
American crayfish species carrying the pathogen as an unapparent infection can spread the disease into new areas by colonising new habitats. Commercial trade of live crayfish for human consumption, accidental co-transport during fish transport and crayfish used as bait for fishing may assist colonisation of new areas. Data from North American crayfish populations in Europe tested to date suggest that the majority of populations are carriers of the pathogen in their cuticle (Oidtmann et al., 2006; Kozubíková et al., 2009). Therefore every translocation of North American crayfish into previously A. astaci-free areas converts those areas into crayfish-plague-endangered areas; usually it is only a matter of time until susceptible crayfish in such areas develop the disease.
The risk of further spread of A. astaci varies depending on geographical region. A. astaci is already fairly widespread in many parts of continental Europe due to the spread of North American crayfish species, which may carry it as a subclinical infection. A broad range of potential pathways of spread exists in areas with North American crayfish presence in the wild. The range of transmission pathways is more limited in areas where North American crayfish do not occur in the wild. The extent of spread of North American crayfish species varies between European countries; accordingly the level of risk associated with the presence of carriers of the pathogen will vary.
Potential pathways of spread were summarized in a preliminary study. Sources of spread of carrier crayfish were identified for England and Wales, where they included fish farms, natural waters, crayfish farms, garden ponds, restaurants and aquaria. Modes of spread of A. astaci that were identified included live fish movements (anthropogenic), release of North American crayfish by the general public, crayfish migration, effluent water from rearing facilities, angling with crayfish bait, escapees, bulk water transfer, survey work, use of leisure equipment, angling equipment, birds, migratory fish and construction works (Oidtmann et al., 2005). Depending on customs in other countries these routes may vary.
Routes of introduction into new geographic areas will be most likely through the import of North American crayfish for food, the aquarium trade or for aquaculture purposes.
ImpactTop of page
The introduction of crayfish plague led to the disappearance of crayfish species native to Europe. Data on the economic impact of these historic introductions of crayfish plague are not available. However, across Europe, native crayfish have been widely used as food. Crayfish have historically provided food for the poor, since catching them was not regulated (in contrast to wild game). Crayfish have also been widely traded across Europe. Therefore, the livelihood of anyone involved in catching and trading of crayfish was affected.
Traditionally, five crayfish species have been considered indigenous to Europe:
- the Noble Crayfish Astacus astacus, centred in Germany and Poland.
- the narrow-clawed or Turkish Crayfish Astacus leptodactylus of south-eastern Europe.
- the Stone Crayfish Austropotamobius torrentium, which is found in the Alps and Balkans.
- the White-clawed Crayfish Austropotamobius pallipes (Lereboullet), which is found in Southern Europe and the British Isles.
- Astacus pachypus, which is restricted to the Black and Caspian Seas.
Of these, it is mainly Astacus astacus and Astacus leptodactylus that have been exploited for harvest. In medieval Europe crayfish caught in rivers were a highly esteemed food resource.
The impact of crayfish plague on harvest is probably best documented through its introduction into Turkey, where harvests declined from 8000 metric tonnes in 1984 to an average of less than 500 metric tonnes between 1990 and 1994 as a result of the disease (Ackefors, 1999).
Another area of economic impact to be considered is the costs of conservation of the native crayfish species that are affected by the spread of crayfish plague. Over the past 20 years, the costs of species conservation programs are likely to reach several million US$ for most economies in European countries. However, the costs of conservation attempts for native crayfish have never been collated to the knowledge of the author.
The consequence of an introduction of Aphanomyces astaci into the natural range of the highly susceptible European species is usually the disappearance of populations of these species in affected areas. In Europe, crayfish are considered a keystone species, due to the pivotal role they have in food webs and the ecology of the freshwater environment. If they are removed (for example as a result of a crayfish plague outbreak), the ecosystem is heavily affected. The proportions of most other species will be affected.
An example of the relevance of crayfish as a keystone species is Sweden. The water temperatures in many lakes in Sweden are too cold to support resident fish species. Native crayfish present in such lakes occupy this niche of ‘top predator’. When crayfish are removed as a result of crayfish plague, macrophytes and opportunistic invertebrates often expand, causing great fluctuations of species, imbalance and reduced biodiversity.
The impact of crayfish plague on a native crayfish species is fairly well documented in Sweden. It is estimated that out of 30,000 Astacus astacus populations present at the beginning of the 20th century, only 5% remained in the year 2000 (Edsman, 2000).
Austropotamobius pallipes is considered a flagship species of patrimonial value. Astacus astacus is highly valued – both from a recreational and economic point of view (Souty-Grosset, 2005).
The impact of the decline of the native crayfish as a result of spread of crayfish plague and spread of North American crayfish has been very well studied in Sweden, where crayfish fishery has a substantial social, cultural and economic value. Traditionally, crayfish parties take place in August of each year, which almost all Swedes participate in. The decline in the supplies of native Astacus astacus as the result of the introduction of crayfish plague in 1907 led to the introduction of North American crayfish to replace the Astacus astacus populations that had been lost to the disease. The crayfish parties still take place nowadays, but a large proportion of crayfish are now Pacifastacus leniusculus instead of Astacus astacus. In order to prevent the spread of crayfish plague to the remaining crayfish populations, a range of actions (including informing the public) have been taken (Edsman, 2000).
Disease TreatmentTop of page
No drug treatments are available.
Prevention and ControlTop of page
If crayfish plague is suspected or confirmed in European native crayfish populations, responsible authorities in some countries impose, to a greater or lesser extent, movement controls on the affected water body. In many European countries, the disease is often not diagnosed and also no action is taken to control the spread of the disease. Because crayfish plague is not a notifiable disease in the national legislation of most European countries, there is no direct obligation on the competent authorities to take measures to control the disease. Crayfish plague is currently (2009) a notifiable disease in Norway and Australia.
The only country that has informed the OIE that it has a national contingency plan for crayfish plague is Australia.
Currently, there is no evidence that vaccines offer long-term protection in crustaceans and even if this were not to be the case, vaccination of natural populations of crayfish is impossible.
Aphanomyces astaci may be transmitted via live North American crayfish traded for food. As a consequence, some countries have made efforts to control the import of live North American crayfish. To the knowledge of the author, the only European country that currently applies restrictions on the import of live North American crayfish is Sweden. The relevant legislation is based in the Species Protection Act connected to the environmental legislation and came into force in 2003. In short, all import, transportation, and storage of live freshwater crayfish from abroad was prohibited. These rules also apply to the aquarium trade (Edsman, 2004).
ReferencesTop of page
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Cammà C, Ferri N, Zezza D, Marcacci M, Paolini A, Ricchiuti L, Lelli R, 2010. Confirmation of crayfish plague in Italy: detection of Aphanomyces astaci in white clawed crayfish. Diseases of Aquatic Organisms, 89(3):265-268. http://www.int-res.com/articles/dao_oa/d089p265.pdf
Demers A, Reynolds JD, 2002. A survey of the white-clawed crayfish, Austropotamobius pallipes (Lereboullet), and of water quality in two catchments of eastern Ireland. Bulletin Francais de la Pêche et de la Pisciculture, 347:729-740. http://dx.doi.org/10.1051/kmae:2002062
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Kozubíková E, Petrusek A, Duri? Z, Kozák P, Geiger S, Hoffmann R, 2006. The crayfish plague in the Czech Republic - review of recent suspect cases and a pilot detection study. BFPP - Bulletin Francais de la Peche et de la Protection des Milieux Aquatiques:1313-1323
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Oidtmann B, Cerenius L, Schmid I, Hoffmann R, Söderhäll K, 1999. Crayfish plague epizootics in Germany - classification of two German isolates of the crayfish plague fungus Aphanomyces astaci by random amplification of polymorphic DNA. Diseases of Aquatic Organisms, 35(3):235-238
Oidtmann B, El-Matbouli M, Fischer H, Hoffmann RW, Klaerding K, Schmid I, Schmidt R, 1996. Light microscopy of Astacus astacus L. under normal and selected pathological conditions, with special emphasis to porcelain disease and crayfish plague. Freshwater crayfish [Freshwater crayfish XI : Proceedings of the International Association of Astacology eleventh symposium, Lakehead University, Thunder Bay, Ontario, Canada, 11-16 August 1996], 11:465-480
Oidtmann B, Thrush M, Rogers D, Peeler E, 2005. Pathways for transmission of crayfish plague, Aphanomyces astaci, in England and Wales. In: Meeting of the Society for Veterinary Epidemiology and Preventive Medicine, Nairn, UK, 30 March-1 April 2005. http://www.svepm.org.uk/posters/2005/Identification%20of%20pathways%20of%20transmission%20of%20crayfish%20plague%20in%20England%20and%20Wales.pdf
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OIE, 2011. Manual of Diagnostic Tests for Aquatic Animals 2011. Paris, France: OIE
Persson M, Söderhäll K, 1983. Pacifastacus leniusculus Dana and its resistance to the parasitic fungus Aphanomyces astaci Schikora. In: Freshwater Crayfish V, Papers from the Fifth International Symposium on Freshwater crayfish, Davis, California, USA, 1981 [ed. by Goldman, C. R.]. Westport, USA: The AVI Publishing Company, 292-298
Pöckl M, Pekny R, 2002. Interaction between native and alien species of crayfish in Austria. Bulletin Francais de la Pêche et de la Pisciculture, 367:763-776. http://dx.doi.org/10.1051/kmae:2002064
RENNERFELT E, 1936. Studies on the development and biology of the Crab fungus, Aphanomyces astaci Schikora. (Untersuchungen über die Entwicklung und Biologie des Krebspestpilzes Aphanomyces astaci, Schikora.) Medd. Undersokn. o. Forsoksanst. Sottvattensfisk, 10:21 pp
Schrimpf A, Pârvulescu L, Copilas-Ciocianu D, Petrusek A, Schulz R, 2012. Crayfish plague pathogen detected in the Danube Delta - a potential threat to freshwater biodiversity in southeastern Europe. Aquatic Invasions, 7(4):503-510. http://www.aquaticinvasions.net/2012/AI_2012_4_Schrimpf_etal.pdf
Unestam T, 1969. Resistance to the crayfish plague in some American, Japanese and European crayfishes. Report of the Institute of Freshwater Research, Drottningholm. Lund, Sweden: Carl Bloms Boktr, 202-206
Unestam T, 1975. Defence reactions in and susceptibility of Australian and New Guinean freshwater crayfish to European-crayfish-plague fungus. Australian Journal of Experimental Biology and Medical Science, 53:349-359
Unestam T, Weiss DW, 1970. The host-parasite relationship between freshwater crayfish and the crayfish disease fungus Aphanomyces astaci: responses to infection by a susceptible and a resistant species. Journal of General Microbiology, 60:77-90
Westman K, Savolainen R, 2001. Long term study of competition between two co-occurring crayfish species, the native Astacus astacus L. and the introduced Pacifastacus leniusculus Dana, in a Finnish lake. Bulletin Francais de la Pêche et de la Pisciculture, 361:613-627. http://dx.doi.org/10.1051/kmae:2001008
Arnold J, 1900. Short report on the spread of crayfish plague in Russia and on the present status of the crayfish fishery in the Volga area. (Kurzer Bericht über die Verbreitung der Krebspest in Russland und über den gegenwärtigen Zustand des Krebsfanges in dem Wolgagebiet.). Allgemeine Fischerei-Zeitung. 449.
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CABI, Undated a. CABI Compendium: Status as determined by CABI editor. Wallingford, UK: CABI
Cammà C, Ferri N, Zezza D, Marcacci M, Paolini A, Ricchiuti L, Lelli R, 2010. Confirmation of crayfish plague in Italy: detection of Aphanomyces astaci in white clawed crayfish. Diseases of Aquatic Organisms. 89 (3), 265-268. http://www.int-res.com/articles/dao_oa/d089p265.pdf DOI:10.3354/dao02207
Demers A, Reynolds JD, 2002. A survey of the white-clawed crayfish, Austropotamobius pallipes (Lereboullet), and of water quality in two catchments of eastern Ireland. In: Bulletin Francais de la Pêche et de la Pisciculture, 347 729-740. http://dx.doi.org/10.1051/kmae:2002062
Kozubíková E, Petrusek A, Duriš Z, Kozák P, Geiger S, Hoffmann R, 2006. The crayfish plague in the Czech Republic - review of recent suspect cases and a pilot detection study. BFPP - Bulletin Francais de la Peche et de la Protection des Milieux Aquatiques. 1313-1323.
Oidtmann B, Cerenius L, Schmid I, Hoffmann R, Söderhäll K, 1999. Crayfish plague epizootics in Germany - classification of two German isolates of the crayfish plague fungus Aphanomyces astaci by random amplification of polymorphic DNA. Diseases of Aquatic Organisms. 35 (3), 235-238. DOI:10.3354/dao035235
OIE, 2009. World Animal Health Information Database - Version: 1.4., Paris, France: World Organisation for Animal Health. https://www.oie.int/
Pöckl M, Pekny R, 2002. Interaction between native and alien species of crayfish in Austria. In: Bulletin Francais de la Pêche et de la Pisciculture, 367 763-776. http://dx.doi.org/10.1051/kmae:2002064 DOI:10.1051/kmae:2002064
Schrimpf A, Pârvulescu L, Copilaș-Ciocianu D, Petrusek A, Schulz R, 2012. Crayfish plague pathogen detected in the Danube Delta - a potential threat to freshwater biodiversity in southeastern Europe. Aquatic Invasions. 7 (4), 503-510. http://www.aquaticinvasions.net/2012/AI_2012_4_Schrimpf_etal.pdf DOI:10.3391/ai.2012.7.4.007
Westman K, Savolainen R, 2001. Long term study of competition between two co-occurring crayfish species, the native Astacus astacus L. and the introduced Pacifastacus leniusculus Dana, in a Finnish lake. In: Bulletin Francais de la Pêche et de la Pisciculture, 361 613-627. http://dx.doi.org/10.1051/kmae:2001008
OrganizationsTop of page
World: OIE (World Organisation for Animal Health), 12, rue de Prony, 75017 Paris, France, http://www.oie.int/
UK: CEFAS (Centre for Environment Fisheries and Aquaculture Science), Cefas Weymouth Laboratory, Barrack Road, Weymouth, Dorset DT4 8UB, Weymouth, UK, http://www.cefas.co.uk/
ContributorsTop of page
17/12/09 Original text by:
Birgit Oidtmann, Centre for Environment, Fisheries, and Aquaculture Science, Weymouth Laboratory, Barrack Road, Weymouth, Dorset, DT4 8UB, UK
Distribution MapsTop of page
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