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Liver disease



  • Cause: infectious agents, inflammation/immune-mediated, nutritional/metabolic disorders, biliary obstruction, toxins, neoplasia, trauma, idiopathic, iatrogenic.
  • Signs: can be mild and non-specific (lethargy, dysrexia/anorexia, weight loss/poor body condition), emesis, altered mentation, jaundice/icterus, coelomic enlargement.
  • Diagnosis: clinical examination, CBC/biochemistry, urinalysis, coelomic fluid analysis, imaging, celioscopy, hepatic biopsy.
  • Treatment: parenteral fluid therapy, analgesia (if indicated), treatment of underlying cause, manage secondary effects (gastrointestinal ulceration and emesis, hepatic encephalopathy, coelomic effusion, coagulopathy, protein-calorie malnutrition), hepatic support using antioxidants.
  • Prognosis: dependent on etiology, can range from fair to poor.



Bacterial infection

  • Can be associated with ascending spread from the gastrointestinal tract through the bile duct or from hematogenous spread.
  • Mycobacteriosis: occasionally reported in various reptile species.
  • Salmonellosis (Salmonella spp): reported in tortoises (Testudo spp).
  • Specific bacterial hepatitis reported in various reptiles but in many cases, liver involvement is thought to secondary and reflect systemic infection and generalized sepsis. Primary acute hepatitis reported: Chlamydia presumed to be C. psittaci isolated from the livers of farmed hatchling Nile crocodiles (Crocodylus niloticus).

Viral infection

  • Various reports of viral hepatitis described in reptiles:
    • Herpesvirus Herpes virus infection in monitor lizards (Varanus spp).
    • Atadenovirus Atadenovirus infection in a boa constrictor (Boa constrictor).
    • Hepatitis B virus in turtle (Mauremys spp).
    • West Nile Virus in an alligator.

Fungal infection

  • Cryptococcosis: occasional reports noted in reptiles.​​
  • Occasional cases of mycotic hepatitis (Coccidioides, Penicillium) reported in reptiles.

Parasitic infection

  • Toxoplasma gondii Toxoplasmosis: clinical disease rare; clinical signs reflect organ involvement.
  • Microsporidiosis in Bearded dragons.
  • Entamoeba Amebiasis in snakes and tortoises.
  • Hepatozoon meronts resulting in granulomatous hepatic lesions in water snakes.

Nutritional and metabolic disorders

  • Hepatic lipidosis Hepatic lipidosis:
    • Overwhelming fatty acid accumulation within hepatocytes.
    • Can be associated with obesity but also in catabolic states where there is alteration in the insulin-glucagon ratio and subsequent mobilization of fatty acids and glycerol from body fat stores for energy production.
    • Anorexic Anorexia and obese Obesity animals most at risk.
    • Physiologic increase in intrahepatic fat levels in reptiles can occur prior to hibernation and in preparation to vitellogenesis:
      • Lack of natural fasting periods, eg during hibernation in captivity together with annual cycles of increased fat deposition may increase likelihood of obesity.
      • Female reptiles that do not have the opportunity to reproduce and thus lose this fat store through egg production are thought to be more predisposed to obesity and thus hepatic lipidosis in captivity.

​​Biliary obstruction


  • Aflatoxins.
  • Drugs, eg itraconazole Itraconazole, azathioprine, diclofenac, amoxicillin-clavulanate, ivermectin Ivermectin in tortoises. 



  • Liver lobe torsion.


  • Vacuolar hepatitis.

Predisposing factors



  • Contact with infected conspecifics or exposure to a contaminated environment with pathogen(s) implicated in hepatopathy.
  • Exposure to hepatotoxins.
  • Obese animals in late gestation.
  • Neoplasia more common in aged animals.


Primary hepatic insult

  • Pathophysiology will vary depending on etiology.
  • Direct hepatocellular damage:
    • Certain hepatotoxins can have a direct effect on hepatocytes or through enzyme-toxin binding.
    • Results in cellular and/or membrane dysfunction, and cytotoxic T-cell response.
  • Cholestasis: injury to canalicular membrane and transporters.
  • Immune-mediated:
    • Immunoglobulin E response induced by enzyme-toxin or enzyme-pathogen binding on hepatocytes.
    • Auto-immune cytotoxic lymphocyte response directed at hepatocyte membrane components.
  • Granulomatous: infiltration of hepatic lobules by macrophages and lymphocytes.
  • Steatosis/lipidosis:
    • Increased uptake and/or reduced hepatic clearance of fatty acids.
    • Acquired or congenital alteration in mitochondrial metabolism and subsequent β-oxidation of fatty acids.
    • Hepatocyte macrovesicular vs. microvesicular lipid accumulation and subsequent degeneration. Varies depending on etiology.
    • Acute liver failure can occur from overwhelming hepatocyte degeneration.
    • Prolonged hepatic lipid accumulation may progress to chronic liver failure through hepatic metabolic dysfunction and oxidative stress, inflammation, and fibrosis.
  • Fibrosis:
    • Activation of hepatic stellate cells into proliferative fibrogenic myofibroblasts and subsequent deposition of extracellular matrix.
    • Stimulated by production of pro-inflammatory mediators during hepatocyte damage and disruption of the extracellular matrix.
    • Release of chemokines and other leukocyte chemoattractants by activated hepatic stellate cells also upregulates expression of inflammatory receptors and mediators.
    • Perpetuation of inflammation and activation of hepatic stellate cells.
  • Vascular collapse: ischemic or hypoxic injury.
  • Oncogenesis.
  • Mixed pathogenesis is typical for most acute liver injuries.

Secondary to multi-organ failure (MOF)

  • Initiation of innate immune response caused by sepsis.
  • Production of reactive oxygen species (a subset of free radicals) and pro-inflammatory mediators.
  • Stimulation of a systemic inflammatory response syndrome and subsequent MOF.
  • Direct hepatocyte damage.
  • Dysregulation of systemic vascular tone leading to low systemic vascular resistance and reduced hepatic perfusion.

Chronic liver failure

  • Continuous and progressive hepatic fibrosis, liver tissue architectural distortion, and regeneration nodule formation.
  • Hepatic cirrhosis represents end-point of chronic liver failure.

Portal hypertension

  • Most commonly occurs secondary to hepatic fibrosis and cirrhosis:
    • May also be prehepatic (portal vein thrombosis), or post hepatic (infrequently reported in veterinary medicine) in origin.
    • Results in congestion of splanchnic vessels with pooling of blood in the splanchnic circulation.
    • Resultant drop in circulating blood volume and systemic arterial blood pressure causes a reduction in glomerular filtration rate and therefore stimulation of the renin-angiotensin-aldosterone system:
      • Leads to further fluid retention precipitating formation of ascites.
      • Reduced venous return due to increased pressure of the caudal vena cava.
    • Creates a vicious cycle of renal sodium retention and ascites.

Clinical manifestations of hepatopathy

  • Gastrointestinal (GI) disorders:
    • Emesis, diarrhea Diarrhea and anorexia Anorexia.
    • Thought to be associated with local inflammation, portal hypertension, hepatic encephalopathy (HE).
    • Hematemesis and melena may be seen with upper GI ulceration caused by portal hypertension:
      • Vascular congestion and fragility.
      • Poor GI mucosal perfusion and reduced epithelial cell turnover resulting in GI ulceration Gastric ulceration.
  • Protein-calorie malnutrition:
    • Result of reduced food intake caused by anorexia, vomiting and diarrhea.
    • Increased loss/wastage of calories caused by hypermetabolism and liver dysfunction.
    • Malnutrition may also predispose to GI ulceration and HE due to muscle catabolism (body protein).
  • Polyuria and polydipsia:
    • Underlying mechanisms poorly understood. Possible causes may include:
      • Altered sense of thirst due to HE.
      • Changes in the function of portal vein osmoreceptors demonstrated in humans and rodents.
      • Loss of the renal medullary-concentrating gradient for urea due to decreased hepatic production.
  • Coelomic effusion:
    • Associated with increased venous hydrostatic pressure caused by portal hypertension with or without decreased intravascular oncotic pressure from reduced serum albumin concentration due to reduced functional hepatic mass.
    • Effusion is typically a transudate or a modified transudate.
    • Altered vascular permeability in SIRS can also contribute to ascites.
  • Hepatic encephalopathy:
    • Neurologic dysfunction.
    • Caused by derangement to neurotransmitter systems from defective hepatic metabolic processes.
    • Ammonia is most important toxin implicated.
  • Jaundice/icterus:
    • Yellow-staining of tissues or serum caused by hyperbilirubinemia.
    • Associated with impaired excretion of bilirubin and other constituents of bile by diffuse hepatocellular or biliary disease (cholestasis).
    • Only some reptiles (some snakes) can convert biliverdin into bilirubin. Hyperbilirubinemia not a frequent feature of reptilian hepatopathy.
  • Coagulopathy:
    • Reduced synthesis of clotting factors.
    • Acquired vitamin K deficiency due to biliary obstruction and resultant reduced or absent bile acid-dependent fat absorption.
    • Hemorrhage and loss of clotting factors through hematemesis and melena (see above).
    • Disseminated intravascular coagulopathy (DIC) as a consequence to SIRS.


  • Varies with etiology.
  • Can range from days (eg most bacterial hepatitis, some viral etiologies, pregnancy toxemia, hepatoxic drugs) to months or years (inflammatory conditions, systemic amyloidosis, neoplasia).


  • Manifestations of infectious hepatopathies in many exotic animals can be a sequela of inappropriate husbandry and sanitation measures resulting in stress and immunocompromise.
  • Hepatic lipidosis in reptiles can be a consequence of captivity:
    • Lack of natural fasting periods, eg during hibernation together with natural annual cycles of increased fat deposition may increase likelihood of obesity.
    • Female reptiles that do not have the opportunity to reproduce are thought to be more predisposed to obesity and thus hepatic lipidosis in captivity.
The reader is encouraged to become familiarized with normal reptilian hepatogastrointestinal anatomy and physiology Chelonia anatomy and physiology Lizard anatomy and physiology Snake anatomy and physiology, which can confer particular considerations when diagnosing and managing reptilian patient with liver disease


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Dong V, Nanchal R & Karvellas C J (2020) Pathophysiology of acute liver failure. Nutr Clin Pract 35 (1), 24-29 PubMed.
  • Giuseppe M D, Oliveri M, Morici M et al (2017) Hepatic encephalopathy in a Red-Tailed Boa (Boa constrictor imperator). J Exotic Pet Med 26 (2), 96-100 SciDirect.
  • Lopez Panqueva R D P (2016) Useful algorithms for histopathological diagnosis of liver disease based on patterns of liver damage. Revista Colombiana de Gastroenterología 31 (4), 436-449 SciELO (pdf download).
  • Bexfield N & Watson P (2009) Treatment of canine liver disease 1. Diagnosis and dietary management. In Pract 31 (3), 130-135 WileyOnline.
  • Bexfield N & Watson P (2009) Treatment of canine liver disease 2. Managing clinical signs and specific liver diseases. In Pract, 31 (4), 172-180 WileyOnline.
  • Simpson M (2006) Hepatic lipidosis in a Black-Headed Python (Aspidites melanocephalus). Vet Clin North Am Exotic Anim Pract (3), 589-598 PubMed.
  • Rutgerus C (1996) Liver disease in dogs. In Pract 18 (9), 433-444 WileyOnline.

Other sources of information

  • Sharma A & Nagalli S (2021) Chronic Liver Disease. StatPearls Publishing, USA. Website:
  • Stephen J D (2019) Hepatology. In: Mader's Reptile and Amphibian Medicine and Surgery E-Book. 3rd edn. Eds: Stephen J D & Scott J S. Saunders, USA.
  • Watson P J (2019) Clinical Manifestations of Hepatobiliary and Exocrine Pancreatic Disorders. In: Small Animal Internal Medicine - E-Book. 6th edn. Eds: Nelson R W & Couto C G. Elsevier, USA.
  • Watson P J (2019) Diagnostic Tests for the Hepatobiliary and Pancreatic System. In: Small Animal Internal Medicine - E-Book. 6th edn. Eds: Nelson R W & Couto C G. Elsevier, USA.

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