Fish Pathology: Diseases, Pathogenesis, and Treatment
1. Branchiomycosis and Saprolegniosis
Branchiomycosis
Cause
Branchiomycosis is a fungal disease of the gills, also known as “bad management disease.” It is caused primarily by Branchiomyces sanguinis and Branchiomyces demigrans.
Signs
The disease affects the gills. Fungal spores attach to the gills, germinate, and produce hyphae. These hyphae penetrate the gill epithelium or capillaries, reducing blood supply and causing tissue necrosis. Affected fish show respiratory distress, may gather near the water surface or inlet, and exhibit necrotic, pale, or mottled gill areas.
Diagnosis
Diagnosis is based on clinical signs, gross gill lesions, and microscopic examination of gill tissue showing fungal hyphae or spores. Histopathology can confirm fungal invasion and necrosis.
Saprolegniosis
Cause
Saprolegniosis is a fungal infection of fish skin, gills, and eggs caused by water molds of the class Oomycetes, order Saprolegniales. The fungi form branched, non-septate mycelium appearing as cotton-wool-like tufts.
Signs
The characteristic sign is a fluffy, cotton-like white to gray growth on the skin, fins, gills, or eggs. Hemorrhages, erosions, and ulcerations may occur. It is common following malnutrition, skin damage, external parasites, rough handling, overcrowding, or spawning stress. It may be secondary to fin rot, peduncle rot, MAS ulcers, or gill disease.
Diagnosis
Diagnosis is presumptive based on the cotton-like growth. Confirmatory diagnosis is achieved via microscopic examination of infected tissue or eggs showing branched, non-septate hyphae. Isolation on suitable fungal media may also be used.
2. Pathogenesis: Vibriosis vs. MAS
Vibriosis Pathogenesis
In Vibriosis, the pathogenicity of Vibrio anguillarum involves tissue invasion, particularly through skin injuries or the alimentary tract under stress. The organism can become septicemic, spreading to the blood, kidney, liver, and other organs. A major virulence mechanism is the ability to scavenge iron from host tissues via plasmid-mediated traits. The bacterium separates iron from transferrin or ferritin-binding proteins and damages tissues using haemolysins and proteases.
MAS (Aeromonas hydrophila) Pathogenesis
In Motile Aeromonas Septicemia (MAS), Aeromonas hydrophila multiplies in the intestine or at the site of invasion and spreads via the bloodstream. Pathogenicity is mainly attributed to toxigenic properties, including:
- Haemolysin
- Leucocidin
- Cytotoxin
- Dermonecrotic factor
- Protease
- Endotoxins
These toxins cause hemolysis, leukocyte damage, cytotoxicity, tissue necrosis, inflammation, and septicemia.
Key Differences
Vibriosis pathogenesis depends mainly on tissue invasion and iron-scavenging, whereas MAS is primarily toxin-mediated, causing systemic lesions and necrosis.
3. Stress and Stressors in Fish
Stress
Stress is the sum of all physiological responses by which a fish attempts to maintain or re-establish normal metabolism when faced with a physical or chemical force (a stressor).
Stressors
Stressors are factors that trigger exaggerated physiological responses.
Types of Stressors
- Physical: Temperature fluctuations, low dissolved oxygen, high ammonia, overcrowding, starvation, rough handling, and transportation.
- Chemical: Water pollution, toxic gases, pesticides, and industrial chemical wastes.
- Biological: Pathogens and domestic wastes.
Intensive culture methods increase exposure to environmental stressors. If fish cannot adapt, stress may be lethal; if less severe, it predisposes fish to disease.
4. Bacterial Environmental Gill Disease
Epizootiology and Pathogenicity
This disease is associated with poor environmental conditions and gill irritation. The primary cause is damage to gill membranes by water irritants, followed by invasion of opportunistic bacteria such as Flexibacteria, Pseudomonas, and Flavobacteria.
Unionized ammonia is a strong irritant to gill tissue. The disease has no specific temperature dependency. Transmission occurs through water or infected fish. Some bacteria produce extracellular hyperplasia-inducing factors; hyperplastic gill cells lack direct blood supply and become targets for bacterial invasion. Mortality may reach 20–30%.
Clinical Signs
- Fish remain near the water surface or inlet for air.
- Flaring of opercula.
- Increased respiratory rate.
- Excess mucus secretion (mucus strands may trail from gills).
- Swollen gills.
- Opercula may not close normally.
- Posterior part of the head may appear thickened.
- White to gray spots on the gills.
5. Columnaris Disease in Cultured Carp
Cause
Columnaris is a chronic to subacute bacterial disease caused by Flexibacter columnaris, also known as cotton-wool or saddleback disease.
Predisposing Factors
It occurs mainly in warm-water fish during summer. Overcrowding and poor environmental conditions favor the disease.
Clinical Signs
- Early thickening of mucus on the head, opercula, fins, and injured areas.
- Circular fluffy grayish-white growth on the skin.
- Small erythemic spots.
- Gill lesions: yellow-orange necrotic areas starting at the periphery and extending toward the base.
- Pale discoloration at the base of dorsal or pelvic fins.
- Lesions may enlarge to form a “saddleback” appearance.
- Skin, jaw, and mouth erosion exposing underlying muscle.
Diagnosis
Diagnosis is based on clinical signs, squash preparations from scrapings, and slide agglutination tests.
6. The Sandpaper Effect
The “sandpaper effect” is a characteristic sign of Ichthyophonus disease (Ichthyophonosis), a systemic granulomatous fungal disease caused by Ichthyophonus hoferi. In heavy infections, the skin becomes rough or granulomatous due to numerous infective units under the skin and muscles. Each unit forms a swollen necrotic lesion, which may rupture, leaving minute openings. It is often associated with scoliosis, lordosis, whirling, and internal gray-white granulomatous lesions in organs.
7. Streptococcal Septicaemia
This is a bacterial septicemic disease caused by Streptococcus species (Gram-positive, non-motile, facultative anaerobic cocci).
Causative Agents
S. agalactiae, S. dysagalactiae, S. equi, S. faecium, and S. pyogenes.
Clinical Signs
Erratic swimming, dark body coloration, unilateral or bilateral exophthalmia, corneal opacity, hemorrhages on the operculum and fin bases, and skin ulcers.
Diagnosis and Treatment
Diagnosis involves clinical signs, postmortem lesions (pale liver with focal necrosis, enlarged cherry-red spleen), and isolation of bacteria. Treatment may involve Erythromycin, while control focuses on reducing stress factors.
8. Vibriosis Treatment Calculation
Biomass Calculation
Total fish weight per pond: 520 kg. Total for 5 ponds: 2,600 kg.
Dosage Protocol (Sulfamerazine)
- Days 1–3: 264 mg/kg/day = 686.4 g/day. Total: 2.059 kg.
- Days 4–14: 154 mg/kg/day = 400.4 g/day. Total: 4.404 kg.
Total required: 6.463 kg of Sulfamerazine administered orally in medicated feed over 14 days.