|Created by the veterinary profession for you - find out more about WikiVet||NEW CONTENT!|
Caused By: Cryptobia branchialis — C. iubilans — C. salmositica — C. bullocki — C. borreli
- 1 Introduction
- 2 Distribution
- 3 Signalment
- 4 Clinical Signs and Pathology
- 5 Diagnosis
- 6 Treatment and Control
- 7 References
Cryptobia species are bi-flagellated protozoan that infect a range of vertebrate and invertebrate hosts. A few species are known for causing disease as both endoparasites and ectoparasites of fish. C. branchialis is the only ectoparasite of the five pathogenic species listed above. They may be found on the body surface or gills of host fish while endoparasitic species may reside within the intestine or the blood. A couple of blood parasites have ectoparasitic life stages on the external body surface.
The parasites are oval or ribbon-like in shape with both flagellae attached to their anterior end. One flagellum is recurrent and ends freely at the posterior end of the cell. They also have a very prominent kinetoplast. Replication is by binary fission.
Asia, North America and Eastern Europe and also in the Atlantic ocean in wild species.
C. bullocki is isolated in marine fish in the USA and Northern Gulf of Mexico.
C. iubilans is associated with the intestine and therefore transmitted faecally, while C. salmositica, C. bullocki and C. borreli are haematozoic species and therefore transmitted by bloodfeeding leeches. Some are also found in surface mucus. C. salmositica has been diagnosed where no leeches were found so transmission is poorly understood. It has been suggested that parasites enter the recipient fish via surface lesions or the gills. Transmission via the water in shared tanks is efficient and is only slightly reduced when infected and non-infected fish are separated by wire screens.
Many species of both marine and freshwater fish are infected. Although salmonids are often of prime concern, resident fish, such as flatfish in Chesapeake Bay are also affected. Interestingly, these native fish survive the disease if kept in water maintained at 10-13⁰C after infection but die if water is 5⁰ or below.
C. bullocki causes disease and mortality in marine fish. C. salmositica has also been found on fish in sea water. The remaining pathogenic species are parasitic to freshwater fish.
Leech numbers increase in November and so prevalence and severity of parasitaemia are higher in haematozoic infections during late Autumn and Winter in the northern hemisphere.
Clinical Signs and Pathology
C. branchialis – Respiratory Ectoparasite
Gills of fish infected with C. branchialis are abnormally red, their bodies are covered with copious mucus which often darkens shortly before death. Fish are anorexic and swim close to the water’s surface. The parasite attaches to the gill epithelium using its recurrent flagellum. Death eventually occurs due to thrombus formation.
C. iubilans – Gastrointestinal Endoparasite
C. iubilans causes lethargy, anorexia, stunted growth, emaciation and mortality, which can take variable amounts of time, as short as one week, but usually less than 3 months. Multifocal granulomas form in the liver, spleen, kidney, stomach and intestine.
C. salmositica – Haematozoic Endoparasite
Exophthalmia, splenomegaly, hepatomegaly, oedema, ascites, anaemia and marked emaciation are signs of infection with the blood-borne C. salmositica. Anaemia is usually microcytic and hypochromic, caused by haemolytic action of parasitic secretions (haemolysin, subsequently identified as a metalloprotease) and antigen release after immune destruction (immune complex driven). Obvious lesions are present in haematopoietic tissues of infected fish. Immunosuppression is also marked. Anorexia can be an important contributor to immunosuppression.
Infected fish are also more sensitive to environmental hypoxia due to the anaemia and occlusion of blood vessels by parasites and consequently impaired perfusion. This can be an important exacerbating factor of mortality when oxygen supply is already restricted due to overcrowding, slow flow or algal blooms.
Histopathological features include focal haemorrhages, vascular congestion and occlusion and oedematous changes in the renal glomeruli. Lesions can be present in the liver, gills and spleen also, and generalised inflammation progresses to mononuclear infiltration after 3 weeks. After this point, parasites are found extravascularly where they cause tissue necrosis.
C. borreli – Haematozoic Endoparasite
This parasite also causes anaemia. Diffuse degenerate changes are seen on pathological examination, with glomerulitis and tubulonephrosis and necrotic foci in the liver. Infection eventually destroys 40% of the renal tubules, causing renal and osmoregulatory failure. Mitochondrial deterioration is seen in late infection.
C. bullocki - Haematozoic Endoparasite
Anaemia, splenomegaly, lethargy and ascites in summer flounders is the typical presentation of C. bullocki infection. Mortality usually occurs within 11 weeks. Ascites and haemorrhaging in the ventral musculature often also occur around 5 weeks after infection. In acute infections, the parasite can be found extravascularly, often in adipose and haematopoietic tissues.
Necrotic foci form in the liver and diffuse splenic necrosis is also seen. Ulcers may be found in the abdomen and oedema and haemorrhage is common in the gastrointestinal tract. Focal lesions and congestion in the glomeruli may also feature.
Clinical signs and pathology as discussed individually above can be used for preliminary diagnosis.
Parasites are easily demonstrated in wet mounts from tissue samples during the acute phase of disease. Fresh samples from gills, mucus, viscera or blood/ascitic fluid depending on the species implicated, can be examined under cover slips using bright field or phase contrast microscopy for moving flagellates. Smears can also be fixed in ethanol and stained with Giemsa for confirmation under light microscopy.
Clotting techniques and haematocrit centrifuge techniques are useful for detecting low level parasitaemia of haematozoic species, e.g. in early or chronic disease stages.
Antibodies can be detected sensitively by either microscopic immunosubstrate enzyme technique (MIDET) or Immunofluorescent Antibody Testing (IFAT). ELISA is also available for C. borreli in carp and C. salmositica in salmonid fish.
Treatment and Control
Isometamidium chloride is effective against C. salmositica in Chinook salmon and can also be used prophylactically. It has also been used against other species.
A live vaccine is available which provides protection against C. salmositica for 2 years.
Selective breeding from resistant or asymptomatic breeds is also sensible.
|Cryptobiosis Learning Resources|
Test your knowledge using flashcard type questions
- Woo, P. T. K (1987) Cryptobia and cryptobiosis in fishes. Advances in Parasitology, 26:199-237
- Becker, C. D., Katz, M (1965) Distribution, ecology, and biology of the salmonid leech, Piscicola salmositica (Rhynchobdellae: Piscicolidae). J Fisheries Research Board of Canada, 22:1175-1195
- Bower, S. M., Margolis, L (1984) Detection of infection and susceptibility of different Pacific salmon stocks (Oncorhynchus spp.) to the haemoflagellate Cryptobia salmositica. J Parasitology, 70(2):273-278
- Kuperman, B. I., Matey, V. E., Barlow, S. B (2002) Flagellate Cryptobia branchialis (Bodonida: Kinetoplastida), ectoparasite of tilapia from the Salton Sea. Hydrobiologia, 473:93-102
- Woo, P. T. K., Wehnert, S. D (1986) Cryptobia salmositica: susceptibility of infected rainbow trout, Salmo gairdneri, to environmental hypoxia. Journal of Parasitology, 72(3):392-396
Woo, P. T. K (2001) Cryptobiosis and its control in North American fishes. International Journal for Parasitology, 31(5/6):566-574.
Woo, P.T.K. (2006) Diplomonadida (Phylum Parabasalia) and Kinetoplastea (Phylum Euglenozoa). In: Fish Diseases and Disorders Volume 1: Protozoan and Metazoan Infections (ed. P.T.K. Woo), CABI, Walingford, UK, pp. 46-115.
The datasheet was accessed on 15 July 2011.
This article has been expert reviewed by Prof Patrick Woo MSc PhD
Date reviewed: 24 August 2011
|WikiVet® Introduction - Help WikiVet - Report a Problem|