Respiratory disease

Sara Childs; Brent R. Whitaker

doi:10.22233/9781910443538.17

Respiratory disease

British Small Animal Veterinary Association , 135 (2001); https://doi.org/10.22233/9781910443538.17

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Respiratory disease

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Authors: Sara Childs and Brent R. Whitaker
From: BSAVA Manual of Ornamental Fish
Item: Chapter 17, pp 135 - 146
DOI: 10.22233/9781910443538.17
Copyright: © 2001 British Small Animal Veterinary Association
Publication Date: January 2001

Abstract

THIS MANUAL HAS BEEN REMOVED FROM SALE. IT REMAINS AVAILABLE TO THOSE WHO HAVE ALREADY PURCHASED ACCESS. INDIVIDUAL CHAPTERS MAY STILL BE PURCHASED

The anatomy and physiology of the respiratory system of fish differs markedly from those of mammals, birds or reptiles. Clinical signs of respiratory disease in fish species are often non-specific. Various features of the fish respiratory system predispose to disease. This chapter covers anatomy, physiology, clinical signs, investigations, systemic approach, normal gross appearance, colour change, visible ectoparasites and swellings.

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Figures

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Figure 17.1

Anatomy of the teleost gill. Water flows in through the mouth and over the primary and secondary lamellae. A vascular plexus providing a counter-current mechanism for gas exchange connects efferent and afferent blood vessels within the lamellae. Histologically, secondary lamellae are only a few cell layers thick, facilitating gaseous exchange and the elimination of metabolic wastes. (© Ken Probst, Johns Hopkins Art as Applied to Medicine.) © 2001 British Small Animal Veterinary Association

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Figure 17.1 Anatomy of the teleost gill. Water flows in through the mouth and over the primary and secondary lamellae. A vascular plexus providing a counter-current mechanism for gas exchange connects efferent and afferent blood vessels within the lamellae. Histologically, secondary lamellae are only a few cell layers thick, facilitating gaseous exchange and the elimination of metabolic wastes. (© Ken Probst, Johns Hopkins Art as Applied to Medicine.)

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Figure 17.2

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Figure 17.2 The normal gill of a koi. The tissue is bright red and the primary lamellae should be clearly visible on close inspection. (© W.H. Wildgoose.)

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Figure 17.3

Taking a gill biopsy. (A) The fish is held firmly and the operculum is lifted to expose the lamellae. (B) A small amount of lamellar tissue is cut, using scissors. (C) Artery forceps are used gently to crimp the cut tissue if haemorrhage occurs. (© Farheen Rahman, Johns Hopkins Art as Applied to Medicine.) © 2001 British Small Animal Veterinary Association

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Figure 17.3 Taking a gill biopsy. (A) The fish is held firmly and the operculum is lifted to expose the lamellae. (B) A small amount of lamellar tissue is cut, using scissors. (C) Artery forceps are used gently to crimp the cut tissue if haemorrhage occurs. (© Farheen Rahman, Johns Hopkins Art as Applied to Medicine.)

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Figure 17.4

The pale coloration of the gill in this koi is due to severe anaemia. The packed cell volume was 4%, whereas the normal value is about 30–35%. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.4 The pale coloration of the gill in this koi is due to severe anaemia. The packed cell volume was 4%, whereas the normal value is about 30–35%. (© W.H. Wildgoose.)

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Figure 17.5

Excess mucus in the gill is produced in response to many irritant agents. Unless severe, it is difficult to appreciate visually but produces a grey sheen on the filaments, as seen in the ventral part of this gill. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.5 Excess mucus in the gill is produced in response to many irritant agents. Unless severe, it is difficult to appreciate visually but produces a grey sheen on the filaments, as seen in the ventral part of this gill. (© W.H. Wildgoose.)

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Figure 17.7

Histological section illustrating damage caused by a severe infestation of white spot. There is extensive destruction of the gill, with loss of secondary lamellae. The parasites (arrowed) are packed between the remnants of the primary lamellae. (× 100 original magnification. H&E stain.) (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.7 Histological section illustrating damage caused by a severe infestation of white spot. There is extensive destruction of the gill, with loss of secondary lamellae. The parasites (arrowed) are packed between the remnants of the primary lamellae. (× 100 original magnification. H&E stain.) (© W.H. Wildgoose.)

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Figure 17.8

(a) Histological section of the gill showing normal primary and secondary lamellae. (b) Hypertrophy of the primary and secondary lamellae is seen in response to exposure to high levels of copper. (× 400 original magnification. H&E stain.) (© Brent Whitaker.) © 2001 British Small Animal Veterinary Association

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Figure 17.8 (a) Histological section of the gill showing normal primary and secondary lamellae. (b) Hypertrophy of the primary and secondary lamellae is seen in response to exposure to high levels of copper. (× 400 original magnification. H&E stain.) (© Brent Whitaker.)

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Figure 17.9

Extensive epithelial hyperplasia is visible as pale mottled areas in the dorsal part of the gill in this goldfish. Areas that are less severely affected are seen ventrally. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.9 Extensive epithelial hyperplasia is visible as pale mottled areas in the dorsal part of the gill in this goldfish. Areas that are less severely affected are seen ventrally. (© W.H. Wildgoose.)

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Figure 17.10

Severe necrosis due to bacterial gill disease in a koi. The characteristic blanched areas contained extremely high numbers of the filamentous bacteria, Flavobacterium. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.10 Severe necrosis due to bacterial gill disease in a koi. The characteristic blanched areas contained extremely high numbers of the filamentous bacteria, Flavobacterium. (© W.H. Wildgoose.)

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Figure 17.11

Saprolegnia infection in the gill. The collapsed fungal mass has a gelatinous appearance when the fish is out of water. Unicellular algae trapped among the hyphae give the lesion a green appearance. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.11 Saprolegnia infection in the gill. The collapsed fungal mass has a gelatinous appearance when the fish is out of water. Unicellular algae trapped among the hyphae give the lesion a green appearance. (© W.H. Wildgoose.)

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Figure 17.12

Polyopisthocotyle monogeneans (arrowed) use many suckers to attach to the gills. In large numbers these parasites can cover the lamellae, preventing normal gill function. (× 20 original magnification. Wet mount preparation.) (© National Aquarium in Baltimore.) © 2001 British Small Animal Veterinary Association

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Figure 17.12 Polyopisthocotyle monogeneans (arrowed) use many suckers to attach to the gills. In large numbers these parasites can cover the lamellae, preventing normal gill function. (× 20 original magnification. Wet mount preparation.) (© National Aquarium in Baltimore.)

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Figure 17.13

Epithelial cells of the gill are greatly enlarged (arrowed) due to infection by epitheliocystis in a flame angelfish. (× 20 original magnification. Wet mount preparation.) (© National Aquarium in Baltimore.) © 2001 British Small Animal Veterinary Association

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Figure 17.13 Epithelial cells of the gill are greatly enlarged (arrowed) due to infection by epitheliocystis in a flame angelfish. (× 20 original magnification. Wet mount preparation.) (© National Aquarium in Baltimore.)

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Figure 17.14

A severe hyperplastic response on the tips of primary lamellae produced a nodular appearance. This was thought to be due to nutritional deficiency since the young koi were reared on a homemade diet. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.14 A severe hyperplastic response on the tips of primary lamellae produced a nodular appearance. This was thought to be due to nutritional deficiency since the young koi were reared on a homemade diet. (© W.H. Wildgoose.)

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Figure 17.15

A histological section of the gill in Figure 17.14, revealing the extreme chronic hyperplastic change with consolidation and fusion of tips of adjacent primary lamellae. (× 40 original magnification. Bar = 500 μm. H&E.) (Courtesy of CEFAS, Weymouth.) © 2001 British Small Animal Veterinary Association

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Figure 17.15 A histological section of the gill in Figure 17.14, revealing the extreme chronic hyperplastic change with consolidation and fusion of tips of adjacent primary lamellae. (× 40 original magnification. Bar = 500 μm. H&E.) (Courtesy of CEFAS, Weymouth.)

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Figure 17.16

Squamous cell carcinoma. This koi was also affected with multiple papillomas on its head. The deeply invasive and proliferative tumour caused severe respiratory compromise. (Reprinted by permission of Veterinary Record.) © 2001 British Small Animal Veterinary Association

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Figure 17.16 Squamous cell carcinoma. This koi was also affected with multiple papillomas on its head. The deeply invasive and proliferative tumour caused severe respiratory compromise. (Reprinted by permission of Veterinary Record.)

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Figure 17.17

Multiple branchioblastomas in an adult koi. The tumours were found during a routine postmortem examination and caused no obvious clinical signs. (Reprinted by permission of Veterinary Record.) © 2001 British Small Animal Veterinary Association

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Figure 17.17 Multiple branchioblastomas in an adult koi. The tumours were found during a routine postmortem examination and caused no obvious clinical signs. (Reprinted by permission of Veterinary Record.)

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Figure 17.18

This opercular deformity was present in this goldfish when purchased 2 years earlier. The curled free edges of both operculae exposed the underlying gill tissue but caused no clinical problems. (© W.H. Wildgoose.) © 2001 British Small Animal Veterinary Association

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Figure 17.18 This opercular deformity was present in this goldfish when purchased 2 years earlier. The curled free edges of both operculae exposed the underlying gill tissue but caused no clinical problems. (© W.H. Wildgoose.)