Fish & Invertebrate Gastroenterology

Question 1

Describe the gastrointestinal anatomy of teleost fish.

What species are agastric?

What species have a grinding organ?

What are pyloric ceca - what species are they present in?

How do pufferfish use their stomachs?

Answer 1

Gastrointestinal System

• Stomach size varies; some agastric (goldfish, koi, zebrafish), grinding organ (gizzard shad, sturgeon, mullet)
• Striated muscle (cardia) transitions to smooth (pyloric) and mucosa contains numerous mucus glands
• Pyloric ceca (diverticula off stomach) - present in salmonids, many other teleosts
  
  • Increase absorptive surface, not fermentative like in birds, mammals
• Variable intestinal length - fairly simple; colon minimal or not distinguishable; rectum present
  
  • Spiral-shaped in lungfish, sturgeon
• GI emptying times vary w/ both temp and volume
• Pufferfish can inflate w/ water or air - pump mouthfuls to stomach via modifications of pectoral girdle and head; skin distensible, ribs absent - in some spp. spines stand erect w/ inflation
• External intestinal and urogenital openings differ among spp. - most separate anus and repro opening/urogenital pore
  
  • Some fish have cloaca - lungfish, coelacanths
• Alimentary system
  
  • Cyprinids and many herbivores lack a stomach.
  • Intestinal length varies to reflect feeding habits.
  • Pyloric ceca in many spp – can range from few to hundreds.
  • Swim bladder – Derived from outpouching of esophageal wall.
    
    • Phsysostomous – Pneumatic duct communicates with esophagus.
    • Physoclistous – No pneumatic duct as adults, rely on vascular structures/gas gland to fill and empty the bladder.

Question 2

Describe the liver of teleost fish.

What side of the coelom is it typically on?

What species do not have a gallbladder?

How is the bile of carp different from other fish?

Answer 2

Liver and Gallbladder

• Liver fairly large (single or bilobed), typ. L side - orange to brown - if yellow/tan 🡪 fatty (r/o normal seasonal vs. abnormal high fat diet)
  
  • Separated from pericardial cavity by a septum
• Gallbladder - most spp. have (except burbot, others); b/w liver lobes in most, caudal coelom in rockfish
• Bile duct enters stomach or small intestine; most bile = bile salts and taurine conjugates of bile acids (except in carp - principal bile salt = alcohol sulfates)
• Hepatobiliary system
  
  • Liver – Usually lacks classic hexagonal pattern of lobule organization of mammals.
  • Most (except cod) have a gallbladder.
  • Proportions of glycogen and lipid may be species and diet dependent, caution in making diagnosis of hepatic lipidosis.

Question 3

Describe the differentials and management of fish with inappetence and weight loss.

What clinical signs might be seen (besides the anorexia)?

What are some potential cuases of a reduced feeding response?

What about a normal feeding response but the inability to prehend or ingest food?

What about weight loss despite normal intake of food?

How should these cases be worked up and managed?

Answer 3

INAPPETENCE, WEIGHT LOSS

Overview

• Inappetence and weight loss are common in fish
• Determine if problem is: lack of response to food vs. inability to prehend/ingest vs. normal appetite w/ weight loss
  
  • Acute vs. chronic; chronic usually carries guarded prognosis (unless obvious enviro cause)
• Can be difficult to determine when reduced appetite is concerning; species that normally feed frequently more likely to benefit from early nutritional support (know natural history!)

Signalment

• Any fish

Clinical Signs

• Lethargy, abnormalities around mouth, fecal output reduced, reduced BCS, reduced muscle mass and/or concave/pinched coelom, sunken eyes, poor muscle tone
• May see negative buoyancy in elasmobranchs d/t loss of lipid in liver (also longer resting periods, increased swimming effort, tail-down swimming)
• Small liver, empty GI tract, enlarged gallbladder (if present); lack of coelomic fat (bony fish)

Etiologies – Reduced Feeding Response

• Metabolic – nephrolithiasis
• Nutritional – many
• Infectious –
  
  • Viruses – esp. herpesvirus, rhabdoviruses, ranaviruses, megalocytiviruses, betanodaviruses, alphaviruses
  • Most bacteria
  • Fungi/Fungi-like – esp. atypical oomycetes, Exophilia, Fusarium, Paecilomyces spp., Microsporidia, Mesomycetozoea
  • Protozoa, metazoan, myxozoa, apicomplexans
• Inflammatory – any
• Idiopathic – egg-binding/retention
• Toxic – environmental, heavy metal, etc.
• Trauma
• Life support/environmental

Etiologies (Normal Feed Response, Inability to Prehend or Ingest Food)

• Neoplasia/hyperplasia – goiter, oral/pharyngeal
• Nutritional – many; myopathy (esp. seahorses, Syngnathidae)
• Infectious/inflammatory – esp. neurologic or musculoskeletal
• Trauma

Etiologies (Weight Loss in Spite of Normal Food Intake)

• Neoplasia – any; primary GI neoplasia in fish is rare
• Nutritional – many
• Infectious/inflammatory
  
  • Granulomatous disease – esp. Mycobacterium, Nocardia, Francisella, Streptococcus, Renibacterium, piscirickettsial-like spp.
  • Metazoa – esp. digenes, cestodes, nematodes
  • Myxozoa – esp. Ceratonova, Enteromyxum spp.
  • Apicomplexa – esp. Cryptosporidium, Eimeria

Diagnostic Approach

• Review history, check water quality
• Visually assess animal(s) – look for signs of displacement/inappropriate social groups, observe feeding
• Visually assess habitat – look for potential foreign bodies, species suitability
• Fecal sample exam – direct, float, diff-quick, Gram stain, acid-fast stain
• Necropsy
• Radiographs, culture(s), wet mounts, histology, other
• If cause still unknown -> handle live fish for diagnostics (recommend anesthesia)
  
  • Full clinical exam, body weight + measurements, consider ID to track changes if in group, skin/gill assessment, cloacal or rectal washes, radiographs, U/S, upper GI endoscopy, coelomic endoscopy or exploratory (examine/Bx liver, spleen, gonad, kidney), hematology/chemistry
    
    • Relatively common to see low glucose, protein, urea, PCV w/ hyponutrition and chronic disease
  • FW or SW dips to look for ectoparasites (diagnostic dips)
• Supportive care as indicated – may resolve signs even without known cause

Management Approach

• Treat any obvious primary cause
• Encourage free-feeding – food of excellent quality, appropriate, variable, and available; change delivery methods or locations; consider isolating fish if not additional stressor
• Supportive care
  
  • Fluid therapy for thin/inappetent SW fish (dehydrated) – PO most common, can do IV or ICe
  • Gavage (tube) feed – gradually increase volume to prevent potential refeeding syndrome (never reported in a fish)
  • Continue until able to meet caloric requirements via free-feeding
• Consider short courses of corticosteroids to reduce inflammatory response (Dex-SP 0.5-1 mg/kg IM)

Question 4

Describe the causes and management of coelomic distension in fish.

What clinical signs are typically present?

What are teh most common causes of distension in fish?

What fish are prone to polycystic kidneys?

What infectious diseases can lead to distension?

What reproductive conditions in elasmobranchs can produce coelomic distension?

How should these cases be diagnosed and managed?

Answer 4

COELOMIC DISTENSION

Overview

• Common; usually fluid or increased soft tissue
  
  • Most commonly – obesity, hepatomegaly, eggs, systemic infection
  • Occasionally due to gas – positive buoyancy
• Colloquially – dropsy, pinecone disease
• Usually individual, if multiple fish affected -> infectious higher concern

Signalment

• Any fish

Clinical Signs

• Coelomic distension may be only sign; may be generalized and symmetric (fat, effusion) or focal and asymmetric (neoplasia, renomegaly)
• Others – lethargy, reduced feeding, cloacal/anal protrusion or prolapse
• If skin erythema, hyperemia, or ulceration observed -> infectious/inflammatory higher on list (ulcer can form from pressure though)

Etiologies

• Most commonly – obesity, hepatomegaly, large ovaries, systemic infection/inflammation
• Developmental – goldfish, common carp, white sturgeon genetically predisposed to polycystic kidneys
• Metabolic – nephron/urolithiasis
• Nutritional – many, including micronutrient (Vit A, C, E) deficiency -> effusion, edema
• Infectious –
  
  • Most viruses and bacteria
  • Fungi/Fungi-like – esp. Exophilia, Microsporidia
  • Protozoa – esp. scuticociliates, Cryptobia, Hexamita/Spironucleus spp.
  • Metazoa – esp. cestodes, large nematodes, pentastomids, acanthocephalans
  • Myxozoa – esp. Ceratonova, Enteromyxum, Hoferellus, Tetracapsuloides spp.
  • Apicomplexa – esp. Eimeria spp.
• Inflammatory – vasculitis, DIC< hepatitis, steatitis, oophoritis, nephritis, enterocolitis, coelomitis (including vaccine-induced coelomitis)
• Idiopathic – multiple, including uterine mucometra and ovarian cysts in female rays
• Toxic – indomethacin, heavy metals
• Trauma
• Life support/environmental – high pH

Diagnostic Approach

• Review history, check water quality (esp. pH)
• Visually assess animal(s)
• Necropsy
• Culture(s), wet mounts, histology, other
• If cause still unknown -> handle live fish for diagnostics (recommend anesthesia – though can palpate or U/S some spp. w/out restraint)
  
  • Palpate coelom – assess for soft tissue vs. fluid vs. gas vs. foreign body
  • Examine cloaca/anus/urogenital openings for abnormalities; digital exam if big enough
  • Elasmobranchs – check abdominal pores and apply gentle pressure
    
    • In females w/ uterine effusion – can aspirate through red rubbed passed through cervix
  • U/S to differentiate between ST and fluid; can collect aspirates for cytology (direct, Diff-quick, gram, acid-fast staining)
  • Serosanguinous fluid often d/t contamination as true hemorrhagic effusion is uncommon in fish

Management Approach

• Treat any obvious primary cause
• Fluid and nutritional support; analgesia and anti-inflammatories
• Coeliocentesis may help reduce pressure effects, but does not help support respiration (unlike other vertebrates) – consider diuretics (use not commonly reported in fish)
• If mass/visceral pathology found:
  
  • Abnormal gonads – excised relatively easily in teleosts; more complicated in elasmobranchs
  • Hepatic masses – removal possible, but diffuse disease more common in fish
  • Renal, GI masses – difficult in fish

Question 5

Describe the dental disease of fish?

Dental overgrowth is common in what groups of fish?

What are the appreciable clinical signs?

What are the causes?

How should these cases be managed?

Answer 5

DENTAL DISEASE

Overview

• Dental overgrowth typically husbandry-related in fish evolved to feed or graze on hard items
• Other dental pathology – tooth loss, accretions on teeth, gingivitis
• Often present w/ reduced feeding, weight loss. Typically, individual fish problem

Signalment

• Dental overgrowth common in parrotfish, pufferfish, some rays (esp. eagle rays)
• Gingivitis common in some sharks (sand tigers)

Clinical Signs

• Overgrown teeth/beak/plates may be visible or mouth may not close normally
• Inappetence, reduced feeding, poor BCS, poor growth

Etiologies

• Most commonly – inappropriate diet
• Developmental
• Nutritional – soft diets, inappropriate composition of plaster of Paris used to make diet blocks
• Neoplasia, infectious/inflammatory, trauma

Diagnostic Approach

• Review history
• Visually assess animal(s)
• Handling of fish usually required for diagnosis and treatment (recommend anesthesia)
  
  • Check range of motion of jaws
  • Consider radiographs, CT of skull if indicated

Management Approach

• Trim overgrown dental plates – tissue is firm and high-speed dental burs or low-speed drills often needed
• Increase hard items in diet
  
  • If using plaster molds – use product w/ high setting strength (>6500 psi) to prevent concretions on pharyngeal teeth
  • Even with diet correction chronic management of dental plates often required

Question 6

Describe the causes and management of cloacal/anal prolapse in fish.

What species have true cloacas? What species have separate anal, urinary, and genital pores?

Are males or females more commonly affected?

What clinical signs are usually present?

What are some common causes of the prolapse?

How should these cases be diagnosed and managed?

Answer 6

CLOACAL/ANAL DISTENSION or PROLAPSE

Overview

• Elasmobranchs, lungfish, and coelacanths have true cloaca
• Most teleosts have separate anus, urinary and genital pores (urinary genital pores often very close)
• Often associated w/ coelomic distension, reproductive, and/or GI disease
• Often impossible to reduce prolapse or distension w/out fixing underlying problem

Signalment

• Any, but female may be more likely

Clinical Signs

• Lethargy, reduced feeding, abnormal swimming, hyperemia and skin ulcers, discharge from cloaca, anal or urogenital pores
• Mucosal changes may be seen – normal mucosa is pale, flat w/ no petechiae
• Prolapse tissue may be gonad, gonaduct, rectum, intestine (urinary bladder rare)

Etiologies

• Most commonly – large ovaries, oophoritis, cloacitis, enterocolitis, systemic inflammation
• Full list – anything causing coelomic distension (see above)
• Normal anatomy – may be mistaken for pathology – gonopodia, urogenital papillae

Diagnostic Approach

• Review history
• Visually assess animal(s)
• Necropsy, culture(s), wet mounts, histology
• If cause remains unknown -> handling of fish usually required (recommend anesthesia)
  
  • Palpate coelom and openings (as size allows)
  • Impression smears of distended tissue – direct, diff-quik, gram, acid-fast stains
  • U/S to look for effusion, evaluate coelomic organs
  • Plain and contrast radiographs +/- endoscopy

Management Approach

• Best managed by resolving underlying issue (e.g. ovariectomy, mass removal)
• Minor prolapses may self-resolve/not require treatment
• Manual replacement difficult and recurrence common in underlying problem not resolved, even with purse string sutures or -pexy surgeries
• Analgesia and anti-inflammatories
• Supportive care as indicated

Question 7

Describe the management of GI foreign bodies in fish.

What fish tend to be overrepresented?

How do these fish present?

What additional concerns may occur as a result?

Answer 7

• GI foreign bodies
  
  • Sometimes can be regurged or passed
  • Removal similar to other vertebrate classes
  • Signalment - larger mouthed fish, larger pufferfish tend to eat decor
  • Findings - inappetence, lethargy, regurg, oropharyngeal or ceolomic distention, abnormal fecal output, anemia d/t lead or zinc, neuro
  • Dx - imaging, endoscopy, measuring lead/zinc in blood
  • Husbandry - many gastric or esophageal ones can be regurgitated, if asymptomatic often appropriate to monitor
  • Medical tx
    
    • Retrieval via forceps, endoscopy, hand
    • Sx retrieval if in intestine
    • gastroprotectants/supportive care

Question 8

Describe iron overload in fish.

What environmental exposures appear to be correlated?

What lesions are found on necropsy?

Answer 8

Iron overload.

• FW and marine spp.
• Not understood.
• Fish exposed to high environmental iron, other exposure to heavy metal and PCB contaminated sites.
• Lesions – liver orange brown.
• Histo – visualization of stainable iron within hepatocytes.
• Potential indicator of contaminant exposure.

Question 9

How common is hepatic lipidosis in fish?

Answer 9

Hepatic lipid.

• Teleosts have a remarkable capacity for hepatocellular lipid storage without ill effects at levels that far exceed what would be considered life-threatening in other vertebrates.
• Often erroneous diagnosis of hepatic lipidosis.
  
  • Pathogenic condition associated with abnormalities of lipid metabolism and morbidity/mortality.
  • Lipid accumulation is essentially dietary in origin, reflects feeding practice in confinement systems.