Saprolegnia Infection in Fish – Gross Pathology and Histopathology

Saprolegnia sp. is classified within Oomycetes, a group of pathogens similar to fungi but which are more closely related to golden-brown algae and are part of the Chromista or chromoalveolates and therefore are not “true fungi”.

Saprolegnia can infect amphibia, molluscs, crustacea, fish and their eggs causing the disease known as Saprolegniasis. The most frequently affected fish are salmonids, which are especially vulnerable to Saprolegnia. Several species of Saprolegnia can be involved as fish pathogens, including Saprolegnia australis, S. parasitica, S. delica, S. diclina, and S. ferax. S. parasitica is considered the most virulent causative agent, leading to devastating infections in freshwater. S. diclina has been considered as the main threat for fish eggs.

Infections with a particularly pathogenic strain may cause huge losses of both fish and eggs. Therefore, specific identification of Saprolegnia strains involved in outbreaks is important in order to decide whether the infection is caused by a pathogenic or saprophytic strain.

Stress factors such as poor water quality, temperature variations, malnutrition, physical injury, reduction in oxygen levels and high density of fish, are well-known risk factors for Saprolegnia infection.

Saprolegnia often presents as a secondary infection that is diagnosed by the appearance of white or grey cotton-like tufts that, when out of water, have a somewhat mucoid appearance. Typical disease signs are visible circular or crescent-shaped, cotton-wool like, white or grey patches of filamentous mycelia on the fish skin. The lesions appear mainly around the head and the caudal, adipose and anal fins. Lesions may spread across the body until adjacent lesions coalesce.

The most virulent strains can penetrate organs causing damage to the underlying muscles and respiratory difficulties may also present when infection is associated with the gills.

In eggs, mould is detected by the thick layer of mycelium that spreads from dead eggs to healthy eggs, which leads to death by suffocation.

Histologically, the oomycete pathogen usually establishes itself focally, invading the stratum spongiosum of the dermis and then extending over the epidermis, eroding it as it spreads. Superficial invasion of the dermis rapidly leads to osmotic imbalance and peripheral circulatory failure (shock). Also, beneath this superficial mat of mycelium are areas of degenerate tissue ranging from superficial dermal necrosis and oedema to deep myofibrillar necrosis and extensive haemorrhage.

Normally, little inflammation is present, but a more marked response may appear when concomitant bacterial infection occurs. Intestinal infection and peritoneal saprolegniasis are common and non-septate hyphae can be found invading different internal organs such as stomach and kidney. In those cases where invasion is via the gastric lumen with primary mucosal necrosis, likely associations, particularly in larval fish, would be dietary alterations and/or heavy environmental contamination, often due to poor cleaning practices of tanks and feeding equipment.

The oomycete hyphae are PAS-positive and are also easily demonstrated by silver impregnation methods, such as Grocott’s technique.

Diagram 1. Life cycle of Saprolegnia parasitica.


Figure 1. Smolt. S. salar. Evident white “cotton-like” patches attached to fish skin.
Figure 2. Egg. S. salar. Filamentous mycelia covering egg surface.
Figure 3. Rainbow trout fry showing abdominal distension due to fungal invasion of the gastro-intestinal tract. In these cases, the source of the infection can often be contaminated feed or feeders, or excess debris in the tanks.
Figura 4. Speckled trout showing severe mycotic dermatitis. Note the sharp demarcation between infected and normal skin.
Figure 5. S. salar. Evident “cotton-like” tufts covering pectoral fin base.
Figure 6. S. salar. Evident “cotton-like” tufts surrounding the operculum.
Figure 7. S. salar. Saprolegnia infection secondary to mechanic damage in skin.
Figure 8. Trout fry showing severe focally extensive mycotic dermatitis on the head. Note that the skin has ulcerated, and the fungi have penetrated down throughout the sub-cutis into the cartilage
Figure 9. Mycotic dermatitis in trout showing early invasion of epidermis prior to ulceration. Note the severe hydropic and ballooning degeneration of the epidermis leading to almost total loss of integrity. Early inflammation can be seen just above the basement membrane.
Figure 10. H&E. S. salar. Skin. Abundant hyphae invading epidermis, dermis and muscle.
Figure 11. Pocket of fungal hyphae sitting within necrotic skeletal muscle.
Figure 12. H&E. S. salar. Muscle. Muscle degeneration due to the action of toxins.
Figure 13. Inflammatory response to fungal hyphae can often involve giant cells. In Saprolegnia infections, which are very frequently dermal, inflammatory responses are dominated and over-whelmed by necrosis, loss of integrity of the osmotic defences and subsequent water-logging, no doubt diluting inflammation-inducing factors. Giant cell responses are therefore uncommon, but can sometimes be seen, notably in systemic invasions.
Figure 14. Histopathology of fry from figure above showing presence of brown-stained fungal hyphae within the lumen, throughout the gastro-intestinal tract and within the peritoneal cavity. Oedema and haemorrhage accompany the infection.
Figure 15. Histopathology of fry with mycotic peritonitis showing the brown-stained hyphae penetrating into and through all visceral organs.
Figure 16. Grocott. S. salar. Muscle. Hyphae invading muscular tissue.
Figure 17. Grocott. S. salar. Stomach. Abundant hyphae invading stomach and abdominal cavity.
Figure 18. H&E. S. salar. Gills. Adundant hyphae invading gills.
Figure 19. H&E. Acipenser transmontanus. Skin. Abundant hyphae invading skin and muscle.
Figure 20. Grocott. S. salar. Liver. Hyphae invading liver parenchyma.
Figure 21. PAS. S. salar. Skin. Abundant hyphae invading epidermis and dermis.


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By: Hugh Ferguson

Dr Ferguson earned his veterinary degree from the Royal (Dick) School of Veterinary Studies, Edinburgh, Scotland and held a Wellcome Research Fellowship at the Institute of Aquaculture, Stirling University where he obtained his PhD. He then worked for 4 years as a diagnostic pathologist at the Veterinary Research Laboratories, Belfast, Northern Ireland, prior to moving to Canada. He left Ontario Veterinary College after 19 years as a full professor of veterinary pathology, to return to Scotland to become head of diagnostic pathology in Stirling. During all this time he became board-certified in the American college of veterinary pathology (ACVP), and a Fellow of the Royal College of Pathologists (FRCPath, London). After Scotland he moved to become chair of veterinary pathology, and Senior Research Fellow in Windward Islands Research and Education Foundation (WINDREF), St George’s University (SGU), Grenada, West Indies. He has published more than 230 papers in refereed journals.