Herp Gastroenterology Flashcards

1
Q

Describe the liver anatomy of reptiles.

How many lobes do they have?

What are teh liver ligaments in chelonians?

What is the blood supply to the liver?

What are the five cell types that make up the reptilian hepatic sinusoid?

A
  1. Liver Anatomy
    1. Bilobed in most reptiles (except snakes)
    2. Chelonian liver ligaments: gastrohepatic (right lobe to stomach), hepatoduodenal (left lob to duodenum), coronary (liver to transverse septum)
    3. Blood Supply = hepatic v. + portal v. (anastomosis of anterior abdominal, gastric, leingastric, intestinal v.)
      1. +/- dorsal gastroesophageal, parietohepatic v.
  2. Cells in the reptilian hepatic sinusoid
    1. Hepatocyte: simlar to mammalian counterpart
    2. Endothelial: Line the sinusoids
    3. Kupffer: intraluminal macrophage attached to the endothelium
    4. Melanomacrophage: perisinusoidal location for removal of free radicals
    5. Stellate/Ito/Lipocyte: Between endothelium and hepatocyte to store vitamin A
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2
Q

Describe the physiology of the reptile liver.

What type of bile acids do reptiles have?

What is unique about indigo snake bilirubin?

What important proteins are synthetsized in the liver?

What are the end products of protein metabolism in the reptilian liver?

A
  1. Physiology
    1. Hepatic function declines linearly with core body temperature
    2. Supplies glucose via glycogenolysis (aerobic) or gluconeogenesis
    3. Extensive anaerobic metabolism produces lactic acid, which decreases heart rate and blood pH
    4. Fat is stored in discrete intracoelomic fat bodies
    5. Liver stores fat and exports phospholipids and cholesterol
    6. All reptiles have 3-alpha-hydroxyl bile acids
    7. Indigo snakes have very high amounts of unconjugated bilirubin
    8. Protein synthesis occurs in the endoplasmic reticulum of the hepatocytes
      1. Albumin
      2. Fibrinogen, prothrombin, factors V, VII, VIII, IX, XI
      3. Transferrin, ferritin, hormone-transporting proteins
    9. Liver urea production is low
    10. Nucleic acids of purine origin are degraded to uric acid by the liver and secreted in the proximal renal tubules
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3
Q

How are liver diseases in reptiles diagnosed and treated?

What are the typical clinical signs?

What are some potential exposures that could result in hepatic disease?

What might you find on physical examination or clinical pathology?

What imaging modalities are useful for liver pathology?

What medications are commonly used with liver disease in reptiles?

A
  1. Clinical Investigation
    1. History and Physical Examination
      1. Ingestion of aflatoxins or pyrrolizidine alkaloids
      2. NSAIDs or glucocorticoid administration
      3. Clinical signs: anorexia, lethargy, vomiting, coelomic distension
      4. Chronic hepatic disease may lead to GI ulceration (hematemesis, coelomic pain, melena)
      5. Obesity followed by anorexia → hepatic lipidosis
    2. Physical Examination
      1. Icterus may be present
    3. Clinical Pathology
      1. AST, ALT, LDH, and SDH are consistent with the initial phase of acute liver injury
      2. Chronic liver disease → hypoalbuminemia
      3. Hepatitis → hypergammaglobulinemia, decreased alpha and beta globulins
      4. Hepatic failure/shunting → hyperammonemia
      5. Hyperbilirubinemia can occur in snakes with ability to reduce biliverdin to bilirubin
      6. Need to fast reptiles, then a pre-prandial and post-prandial sample
      7. Hypercholesterolemia may occur with cholestasis, and hepatic lipidosis
    4. Imaging
      1. Radiology is not sensitive for hepatic abnormalities in reptiles
      2. Ultrasound is the most helpful for diagnosing hepatic abnormality
      3. Endoscopy provides direct visualization and ability to biopsy
  2. Treatment
    1. Anorectic animal with mild to moderate hepatic lipidosis can often be treated with oral fluids
    2. Severe hepatic disease may require parenteral fluids
    3. Other treatments should be based on medical diagnosis
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4
Q

What are some of the most common heptic diseases of reptiles?

What are some of the more common causes of infectious hepatitis in reptiles?

Hepatic neoplasia is common in which group of reptiles?

How do reptiles present with hepatic lipidosis? How is it diagnosed?

How is hepatic lipidosis treated?

A
  1. Hepatic Diseases
    1. Hepatic Lipidosis
      1. Potentially caused by high fat diet, obesity, decreased exercise
      2. Presents with chronic anorexia
      3. Diagnose with elevated triglycerides, cholesterol, and lipoproteins +/- increased BA or hypoalbuminemia and hyperechoic liver
      4. Treat with nonlactated, nonglucose fluids and nutritional suppoer +/- vitamin K +/- L-carnitine
    2. Hepatitis
      1. Caused by:
        1. Viruses: herpesvirus, orthoreovirus, hepatitis B, WNV, adenovirus
        2. Bacteria: Chlamydia in crocodiles; Microscopiridia in bearded dragons
    3. Present with acute lethargy, depression, weakness
    4. Diagnosis with increased AST, ALT, LDH, SDH, +/- leukocytosis → biopsy is best
    5. Treat the underlying cause based on culture and MIC, plus supportive care
  2. Toxic Hepatopathy
    1. Caused by heavy metals, pesticides
    2. Present with lethargy, hyporexia, and weight loss
      1. Chelonians with ivermectin toxicity had neurologic signs
    3. Diagnosis with hepatocellular enzymes, bile acids, biopsy, toxicology sampling
    4. Treat with supportive care
  3. Cholangitis, Cholecystitis, Cholecystolithiasis
    1. Caused by metazoan and protozoan parasite migration from GI tract
    2. Present with icterus when obstructed
    3. Ultrasound is most helpful
    4. Treat with supportive care, cholecystectomy and/or parasitic treatment
  4. Hepatic Neoplasia
    1. Most common in snakes
    2. +/- liver enzyme and BA elevations
    3. Biopsy required for diagnosis

MARMS – 151. Hepatic Lipidosis

  1. Hepatic lipidosis = Metabolic derangement of the liver causing accumulation of intrahepatic fat
    1. Some fat may be normal in reptile liver (before hibernation or folliculogenesis)
    2. Can be associated with many disease and syndromes
  2. Clinical Presentation and Diagnosis
    1. Chronic, gradual reduction in appetite, fecundity, and fertility
    2. Elevated triglycerides, cholesterol, lipoproteins, bile acids
    3. +/- Decreased albumin?
    4. Ultrasound shows a hyperechoic liver
    5. CT shows hypoattenuation
    6. Biopsy required for confirmation
  3. Preferred Treatments
    1. Correct dehydration
    2. Nutritional support
    3. +/- Vitamin K, if coagulopathy
    4. +/- L-carnitine to improve hepatic metabolism of fat
    5. SAMe (antioxidant)
  4. Prognosis and Prevention
    1. Good prognosis if diagnosed early
    2. Guarded prognosis if clinical signs and severe disease
    3. Prevent with a large enclosure, no excessive feeting, allow hibernation/reproduction
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5
Q

Describe the upper GI anatomy of reptiles.

Oral Cavity

  • What taxa have lips?
  • How many dental arcades do various taxa have?
  • What are the three tooth types in reptiles? Give taxonomic examples of each.
  • What are the four fang types in snakes? Give taxonomic examples of each.
  • What taxa have telescoping tongues?
  • What are glands are present in the oral cavity? Give taxonomic samples of each.
  • What is crocodilian dentition like?

Esophagus

  • What is an additional funciton of the snake esophagus?
  • What is the antomy of the sea turtle esophagus like?
  • What lymph anatomy is present in the esophagus? How is this used clincially?

Stomach

  • What are the three regions of the reptile stomach?
  • What are the two regions of the crocodilian stomach?
  • What is the typical pH of the reptilian stomach?
  • Describe the gastric hypertrophy of snakes.
A

Anatomy & Physiology

  • Ectothermic, use approx 10% of energy that mammals/birds do
  • Oral Cavity
    • Squamates- lips
    • Dental arcade
      • Lizards- 2 mandibular and 2 maxillary dental arcades
      • Snakes-2 additional palatal arcades (6 total arcades)
    • Dentition
      • Lizards- either acrodont (fused to ridges) or pleurodont (seated in grooves)
        • Acrodont- Agamid (bearded dragons & chameleons)
        • Pleurodont- Iguanid
      • Snakes- Modified pleurodont dentition (teeth shed and replaced throughout life)
        • Aglyphous- no specialized fangs
        • Solenoglyphous- viperids- hollow fangs, folded
        • Proteroglyphous- elapids- fangs are fixed, erect
        • Opisthoglyphous- rear-fanged, erect, found caudal to eye
    • Vomeronasal organ- rostral maxilla
    • Choana- tubular larynx sits when mouth is closed
    • Tongue- Varanid lizards & snakes- specialized telescoping, forked (helps with prey trails) tongues with keratinized epithelium
    • Mucous glands
      • Lizards- lots and lots of salivary glands
        • Labial venom glands of helodermatid and varanids
      • Snakes similar, but dental salivary glands are absent (still have all the others)
        • Venom glands (assoc with maxillae)
    • Crocs- teeth exposed when mouth closed, tongue fills entire intermandibular spaced and is immobile and fixed ventrally.
      • Palatal fold comes from base of tongue to seal pharynx for opening of mouth in water
        • Thecodont dentition - seated in sockets, replaced throughout life
  • Esophagus
    • Can be a storage organ in snake (small stomach)
    • Sea turts- Papillae, conical and keratinized, caudally directed
    • Submucosal lymphoid aggregates throughout esophagus in reptiles
      • Some species these orgainze into esophageal tonsils
        • Boid snakes- great placed to biopsy and look for arenavirus
  • Stomach
    • Cardiac, fundic, and pyloric regions
    • Crocs- fudic (muscular with keratinized mucosa similar to aian ventriculus); gastroliths are common
    • Mucosal glands- HCl and pepsinogen
      • pH during digestion (2-2.5)
    • Range in gastric anatomy and function
      • Sit & wait burmese pythons- stomach is atrophied, no acid, and quiescent state
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6
Q

Describe the infectious diseases of the upper GI tract of reptiles.

Viral Diseases

  • What are the lesions associated with herpesvirus? What taxa are affected?
  • What species get oral lesions from adenovirus?
  • How does West Nile present in the oral cavity of alligators?
  • How does nidovirus affected the upper GI of ball pythons? What are the other lesions?
  • How does ranavirus present in the upper GI of chelonians?

Bacterial Diseases

  • What bacteria commonly affect the GI tract?
  • What bacteria is a commensal of the bearded dragon oral cavity that is lethal to chuckwallas?
  • Regurgitation in emerald tree boas is commonly due to what bacterial infection?

Mycotic Diseases

  • What fungal diseases can affect the upper GI of reptiles?

Parasitic Diseases

  • What is the most significant protozoal disease of the reptile GI tract? What are the signs? How is it diagnosed and treated?
A

Clinical Diseases

  • Stomatitis, esophagitis, and gastritis
  • Viral diseases
    • Herpesvirus
      • Chelonians- well described, predelection for muco-epithelial cells and assoc with stomatits/glossitis
      • Lizards- predispose them to oral squamous cell carcinoma (some species)
    • Adenovirus
      • Sulawesi tortoises- mucosal ulcerations/erosions
    • Flaviviurs (West Nile Virus)
      • American alligators- necrotizing stomatitis and glossitis
    • Nidovirus
      • Ball pythons- esophagitis, tracheitis, and pneumonia
    • Atadeoviral
      • Colubrids- gastritis and path to other organs
    • Ranavirus
      • Chelonians- necrotizing stomatitis and esophagitis
  • Bacterial diseases
    • Gram-negatives: Pseudomonas spp., Aeromonas spp., Alcaligenes spp, Acinetobacter spp, Stenotrophomonas spp., and Salmonella spp.
    • Gram-positives: Staphylococcus spp. and Clostridium spp.
    • Devriesea agamarum is considered a facultative pathogenic bacterium and is found in the oral cavity of some healthy bearded dragons
    • Mycobacteria
    • Chlamydophila- assoc dz- emerald tree boas with “regurg syndrome”- common
  • Mycotic diseases
    • Metarhizium viride and Metarhizium granulomatis are reported to cause disseminated mycosis in chameleons and bearded dragons, including granulomatous glossitis and stomatitis
    • Candida
    • Purpureocillium lilacinum- saprophyte
  • Parasitic diseases
    • Helminthiasis- digenetic trematodes, ascarids and strongyles
    • Cryptosporidiosis- can be devastating; GI signs- chronic wasting syndrome
      • Seem species specific
      • Snakes- anorexic with palpable firm stomach (can have mass effect)
        • Hypertrophic gastritis to fibrosis and maldigestion
        • Progressive and death; carriers exist
        • DX: Direct smear, float, acid-fast staining, gastric lavage (2-3 days post feed); beware of hitchhikers from diet
          • PCR is sensitive and specific
        • Tx: Can try Paromomycin (likely recur after done)
          • One report of total clearance from beardie
          • Dissinfectoin: 3% hydrogen prerox or ammoniom hydrox for 20-30 mins
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7
Q

Describe the noninfectious diseases of the reptile upper GI tract.

A

Noninfectious Disease

  • Malnutrition
    • Hypovitaminosis A
    • Nutritional Secondary Hyperparathyroidism
  • Maldigestion secondary to environmental and dietary issues
    • Too large or when animal is cold and/or dehydrated
    • Putrefaction of food items
    • Potential endotoxemia or septicemia; gas- producing bacteria
      • Bloating
  • Handling/stress
  • Foregn Bodies
  • Neoplasia
    • Gastric neuroendocrine sarcomas (beardies); mets to liver
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8
Q

What reptile tooth type is predisposed to periodontal disease.

What are some risk factors for periodontal disease.

How do the bacterial populations differ between acute and chronic periodontal disease?

What diagnostics should be performed in these cases?

How are these cases treated?

What is the general prognosis?

A

MARMS – 159. Periodontal Disease

  • Bacterial or fungal invasion
  • Acrodont dentition, specifically agamids

Clinical Significance & Known Etiological Causes

  • Thin layer of gingival tissue, fragile
  • Potentially diet related
  • Early plaques- gram +, aerobic, cocci population
    • Advanced- comes anaerobic orgs, including gram- neg & spirochetes

Clinical Presentation and Diagnostic Confirmation

  • Present anorexic, soft tissue swellings, irregular labial closure
  • OR..no clinical signs
  • Biopsy of bone and or assoc. soft tissue is most definitive method for identifying pathogens
  • Imaging, RADS/CT

Treatment(s)

  • Clean and debride
  • Culture and biopsy, histopathology
  • Broad spectrum ATBs 4-6 wks

Prognosis

  • Fair to poor
  • Lifetime dental prophylaxis
  • Feeding hard-bodied insects and more fibrous veggies help strengthen and keep gingiva healthy and clean.
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9
Q

Describe reptile stomatitis.

Are there any predisposing factors to developing stomatitis?

What are some common sequalae to these infections?

What parasitic adn viral pathogens are associated with stomatitis?

How do these animals typically present?

How are they managed?

A

MARMS – 167. Stomatitis

  • Inflammation and infection in oral cavity
  • May extend and become cellulitis, sinusitis/rhinitis, osteomyelitis and then down to pneumonia

Clinical significance and known etiological causes

  • Often systemic
  • Usually secondary to something else
    • Immunosuppression, poor husbandry, malnutrition, or trauma
    • Vit A deficiency and squamous metaplasia
    • Nutritional secondary hyperparathyroidism
    • 2ndary infection with normal microbes of mouth
  • Parasitic disease
    • Nematodes
      • Spirorchid nematodes lay eggs and can embolize small vessels
    • Flukes (monogenic and digenic trematodes) specialize in oral cavity and exacerbate existing stomatitis
  • Viral Pathogens with tropism for oral mucosa
    • Herpesvirus
    • Ranavirus
    • Nidovirus (ball pythons)

Clinical Presentation & Diagnostic Confirmation

  • Define pathology in oral cavity
  • Perioral or intra oral swelling, ptyalism, disruption of lip margins, inability to close mouth, mucosal hyperemia, petehication, ulceration, mucosal plaques….ect….
  • Examine tongue in snakes, varanid lizards, and chameleons- glossal abnorms

Preferred treatments

  • Husbandry corrections
  • Gavage feedings or esophagostomy
  • Debridement, marsupialization of deep tracts
  • Systemic therapy antimicrobial and antiinflammatories

Prevention- Husbandry, diet, biosecurity; application of beeswax, p jelly, silver sulfadiazine cream, dilute chlorhex, tri-edta soln…

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10
Q

Describe the oral surgery of reptiles?

What species are prone to glossal prolapse? What are some causes of it? How is this managed surgically?

Stomatitis in chameleons may progress to what oral issue? How is it managed?

How are facial masses and osteomyelitis addressed?

A

MARMS – 94. Oral Cavity Sx

Glossitis and Glossal Prolapse

  • Chameleons can prolapse and swallow their tongue. Emergency.
    • Related to nutritional deficiencies
    • Spay hook can replace, but if any necrosis…amputate
  • Partial and complete glossectomy
    • No tension on glossal epithelium
    • With long narrow tongue- tranfix circumferential ligature
    • Chelonians/lizards- large fleshy tongues
      • Multiple mattress sutures may be needed

Oral Masses & Stomatitis

  • Temporal glands located at commisures of mouth in some old-world chameleons- may present asymmetrical. (common in Jackon’s chameleons), green exudate often Pseudomonas.
    • Explore, marsupialize, check for bony involvement

Facial Masses & Osteomyelitis

  • Rarely resolve with lance & flush
  • Total surgical removal is likely required; less skin to close on facial structures
  • Bilat mandibular swellings- nutritional secondary hyperparathyroidism
  • Osteomyelitis (acrodont teeth)- agamids with unilateral swelling, discoloration
    • Usually needs aggressive surg debridement/marsup//medical combo
  • Overgrown Beak (Rhamphotheca- rhinotheca (maxillary) & gnathotheca (mandible))
    • Multifactorial (husbandry, nutrition, trauma, infection, or congenital)
    • Outer nares can become occluded
  • Fractures (Beak, maxilla, and mandible)
    • Ventral temporomandibular joint in chelonians (do not mistake for fracture)
    • Freshen wound edges if >12 hours old
    • Place esophagostomy tube
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11
Q

Discuss regurgitaiton and vomiting in reptile species.

What taxa rarely vomit or regurgitate?

What are some differentials for vomiting? List four infectious and five noninfectious causes.

What are some differentials for regurgitation?

How should these cases be worked up?

A

MARMS – 173. Regurgitation and Vomiting

  • Turtles and tortoises rarely vomit or regurgitate – very concerning if present
  • Nervous snakes may vomit/regurg due to stress
  • Reptiles usually vomit rather than regurgitate
  • Differentials for vomiting:
    • Consumption of too large a meal
    • Maintenance of the reptile at temperatures not conducive to proper digestion
    • Ingestion of partially autolyzed prey items
    • Medication administration
      • Apomorphine, levamisole, xylazine, miticides, and organophosphates
    • Toxins
      • Bufo toxicity
      • Organophosphates
    • GI foreign body
    • Obstructive neoplasm or granuloma, stricture, intussusception
    • Congenital defects/atresia
    • Infectious
      • Bacterial
        • Ex - chlamydia
      • Fungal
      • Parasitic
        • Cryptosporidiosis
          • Common cause of vomiting and midbody (gastric) swelling in snakes  poor prognosis, no tx
        • Ascariasis
        • Cestodiasis
        • Amebiasis
      • Viral
        • Adenoviruses
        • Inclusion body disease (reptarenavirus) of boid snakes
  • Differentials for regurgitation:
    • Similar to vomiting
    • Esophageal, pharyngeal, or oral lesions
      • Stomatitis
      • Esophagitis
      • Neoplasia
      • Esophageal laceration or perforation, strictures, granulomas, and foreign bodies
  • Diagnostics
    • Survey and contrast rads
    • Advanced imaging – CT, MRI
    • Endoscopy
    • Infectious disease testing
      • Gastric crypto – acid fast stain, gastric biopsy and histopath
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12
Q

Describe the intestinal anatomy of reptile species.

How does it differ by diet (carnivore v herbivore)?

How do insectivorous reptiles digest chitin?

How does pancreatic anatomy differ across taxa?

A

MARMS – 74. Gastroenterology 2 (SI/LI)

Anatomy and Physiology:

Carnivorous

  • Shorter GI tract

Insectivore

  • Pancreatic chitinase made by pancreas

Herbivores

  • Longest GI tract
  • Higher optimal body temperature range to promote microbial fermentation
  • Sacculated colon
    • Iguanas – saccules more defined in adults
      • Protozoa Nyctotherus sp – commensal in iguana colon for complex car digestion

Small intestine

  • Longitudinal muscular folds
  • Primary site for absorption
  • No clear divide between the duodenum, jejunum, and ileum
  • SI tract shorter than in mammals

Species differences:

  • Chelonians
    • SI located in caudal coelomic cavity
    • Cecum not well developed, usually found in right caudal coelomic cavity
    • Pancreatic and bile ducts enter the pylorus instead of the duodenum
    • Pancreatic alpha and beta cells equally present
  • Snakes
    • SI empties directly into colon
      • Exception  boid snakes - small cecum located at proximal colon
    • Pancreas - located caudal to stomach in area of gallbladder and spleen
      • Pyramidal in shape and more consolidated
      • Alpha and beta cells equally present
      • Splenopancreas in some snake species
  • Lizards
    • Cecum usually found in right caudal coelomic cavity
    • Trilobed pancreas – lobe extending to gallbladder, duodenum, and spleen
    • Pancreatic alpha cells more abundant
  • Crocodilians
    • Pancreatic alpha and beta cells equally present
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13
Q

What are some of the most common nematodes affecting the repitle intestinal tract?

What are typical clinical signs of nematodiasis?

How are they diagnosed?

How are they treated?

A
  • Nematodiasis
    • May be asymptomatic
    • Signs - anorexia, emaciation, diarrhea, regurgitation, vomiting, coelomic discomfort, colonic prolapses through the cloaca, stunted growth, and death
    • Heavy burdens of ascarids or strongylids can cause intussusception, ulceration, avascular necrosis and fatal intestinal impactions
    • Visceral migration can damage other tissues
    • Often no treatment recommended unless high burden or clinical signs
    • Ascarids
      • Undergo extensive tissue migration - significant pathology
      • Ophidiascaris and Polydelphis present in snakes feeding on amphibians and rodents (intermediate hosts)
      • Common finding in crocodilians
    • Rhabditid nematodes
      • Inhabit areas outside the intestinal tract
      • Stronglyoides can be found in small intestine of snakes
      • Signs – diarrhea, weight loss
      • Hemorrhagic ulceration, malabsorption, diarrhea, and obstruction can be seen with heavy burdens
    • Diagnosis
      • Fecal
        • Collection – voided, during soak, cloacocolonic flush
    • Treatment:
      • Routine prophylactic treatment for enteric parasites not advised
      • Benzimidazoles – commonly used
        • Fenbendazole
          • Metabolized by liver to more active – oxfendazole
          • Lower doses over few days better than single higher dose
          • Toxicity reported - radiomimetic signs
      • Levamisole – narrower margin of safety, toxicity causes neuro signs
      • Ivermectin – not recommended, toxic to chelonians
      • Clean environment and prevent access to feces to control parasites with direct life cycle
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14
Q

Describe trematodiasis and cestodiasis of reptiles.

What is the general lifestyle of trematodes? What intermediate host is needed? How are these controlled?

What are the common tapeworms found in snakes and lizards? What species are they found in?

A
  • Trematodiasis (flukes)
    • Aspidogastreas – chelonians
    • Require an intermediate host in their life cycle - aquatic snails
      • Only a concern in wild caught animals
    • No clinical signs
    • Diagnosis - adult fluke in the feces, cloaca, or mouth; fecal exam
    • Tx – praziquantel
    • Amphibians fed to pt should be frozen _>_3 days before feeding to prevent transmission
  • Cestodiasis (tapeworms)
    • Require intermediate host
    • Ophiotaenia
      • Proteocephald tapeworm
      • Most common tapeworm found in wild-caught North American snakes
      • Intermediate host - frogs
      • Dx – fecal exam to see eggs or adult tapeworms
    • Diphyllobothrid tapeworms (Bothridium sp.)
      • Found as adults in pythons
      • Other species use reptiles as intermediate hosts
    • Mesocestoidid tapeworms
      • Found as adults in GI tract of snakes and lizards
        • Most tapeworms of this family use them as intermediate hosts
    • Signs - often symptomatic but can cause enteritis, malnutrition, and intestinal obstructions
    • Diagnosis – fecal exam
    • Tx – praziquantel
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15
Q

Discuss cryptosporidiosis in reptile species.

What are the two organisms that affect repiles? What is their tissue tropism?

How is this disease transmitted?

How is it diagnosed adn treated?

What disinfectants are needed to reduce infection of other animals?

A
  • Cryptosporidiosis
    • Coccidian parasites
    • Pathogenicity due to reduced immunocompetence of host or presence of concurrent disease
    • Species:
      • Cryptosporidium serpentis - gastric disease in snakes
      • C. varanii and C. saurophilum - enteric disease in lizards
        • Signs - anorexia, diarrhea, weight loss, passing undigested food and regurgitation, death
    • Direct life cycle
      • Also able to replicate within the host
    • Transmission – fecal-oral, autotransmission
    • Shed intermittently
      • Cysts shed in feces are immediately infective and are extremely resistant in env
    • Diagnosis – fecal exam, stain kit, PCR, histo
      • Immunofluorescent antibody testing
    • Organisms reside in brush border of epithelial cells, marked infiltrative enteritis
    • No treatment
      • Paromomycin – prevented shedding in bearded dragons
      • Bovine hyperimmune colostrum – reduce shedding and histopathological resolution of disease after a course of treatment in monitors
        • Less efficacious in geckos
      • Euthanasia may be recommended
      • Environmental control important
    • Very resistant in environment
      • Ammonia (5%) and formalin (10%) appear effective with a contact time of 18 hours at 4°C
      • Moist heat (45°–60°C for 5–9 minutes), freezing, or desiccation most effective ways to clear environment
    • Poor prognosis if clinical signs
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16
Q

Describe ameobiasis in reptile species.

What is the offending pathogen? What clinical signs does it cause?

How is it diagnosed?

What are the histologic lesions?

How is it treated? How do the two forms of the pathogen require different treatment?

What is the general prognosis?

A
  • Amoebiasis
    • Entamoeba invadens
    • Causes mucoid dysentery
      • Also see anorexia, wasting, dehydration, and eventual death
      • Can invade tissue – GI ulcers, liver abscesses
    • Direct life cycle
    • Transmission – fecal oral
      • Can have asymptomatic carriers who shed intermittently
    • Diagnosis:
      • Fecal exam
        • fresh fecal wet prep stained with Lugol’s iodine - detection of cysts or trophozoites
      • PCR
    • Lesions
      • Thickening and edema of the intestine wall, erosions, ulcers, and infection
      • Possible liver abscesses
      • Histo – marked enteritis +/- hepatitis
    • Treatment
      • Metronidazole – treats trophozoites but not cysts
      • Paromomycin, diloxanide furoate, or iodoquinol - treats cysts
    • Prognosis
      • Morbidity and mortality can be high in lizards and snakes
      • Chelonians often reservoir hosts, asymptomatic
    • Trophozoites and cysts resistant, can survive in environment for >14 days
17
Q

Describe coccidiosis in reptile species.

What is the coccidia of bearded dragons? How does it affect them?

What is the typical lifecycle of coccidian parasites?

How is it treated?

A
  • Coccidiosis
    • Eimeria oocysts - four sporocysts
    • Isospora and Sarcocystis oocysts – two sporocysts
      • Isospora amphiboluri
        • Common in young bearded dragons
        • Enteritis with heavy burden
        • Heavy burden can be associated with concurrent adenovirus infection
        • Signs - anorexia, lethargy, weight loss, diarrhea, tenesmus, prolapses, and death may occur
        • Stunting of juveniles with heavy burden
    • Caryospora oocyst – one sporocysts
    • Oocyst ingested  releases sporozoites that invade cells  mature into schizonts  cell ruptures and releases merozoites  merozoites invade more cells  merozoites also undergo sexual reproduction, form zygotes  zygotes release oocysts
    • Asymptomatic unless high number with immune compromise
    • Diagnosis – fecal exam
    • Treatment – toltrazuril, TMS, clazuril
    • Oocysts can be inactivated by freezing or exposure to high temperatures
18
Q

Describe the following infectious causes of enteritis in reptiles.

What are some of the typical nonpathogenic protozoa found in the reptile GI tract? When should they be treated?

What bacteria may cause bacterial enteritis?

What fungi may cause enteritis?

What viruses have been implicated in enteritis?

A
  • Nonpathogenic Protozoa (Amoeba, Flagellates, and Ciliates)
    • Various amoebae, flagellates (typically Trichomonas, Hexamita, or Giardia), and ciliates (such as Balantidium and Nyctotherus)
    • Treat only if signs of enteritis
  • Bacterial enteritis
    • Rare
    • Salmonella can be isolated from reptile feces, considered normal flora
      • Can be pathogenic in some cases (Nile crocodile outbreak, red tail boas)
    • Reported bacterial enteritis organisms
      • Clostridium perfringens
      • Mycobacterium
      • Chlamydia
    • Infections caused by gram-negative aerobes are generally considered more common
    • serology, cytology, or histopathology (ideally) required to confirm pathogenicity of an organism identified in GI tract
  • Fungal enteritis
    • Typically opportunistic
    • Yeasts considered part of normal flora, particularly in herbivorous species
      • Overgrowths often associated with prolonged antibiotic therapy
      • Isolates identified include: Aspergillus, Fusarium, Mucor, Candida, Penicillium, Basidiobolus, and Paecilomyces/Purpureocillium
    • Diagnosis – fecal culture, fecal cytology
    • Treatment
      • Nystatin - locally acting antifungal agent
      • Itraconazole or voriconazole – systemic for advanced or disseminated infection
  • Viral enteritis
19
Q

Discuss the noninfectious causes of intestinal disease in reptiles.

What are the gastrointestinal effects of nutritional secondary hyperparathyroidism?

How does environment affec the GIT?

What foregin bodies are common in reptiles? How do those animals present?

What are some of the neoplasms that have been reported in the reptile intestinal tract and pancreas?

A
  • Nutritional disorders
    • Nutritional secondary hyperparathyroidism
      • GI transit and motility dependent on calcium
      • Reduced ionized calcium levels can lead to reduced GI motility and ileus
        • Can lead to increased fermentation of digesta with gas production
        • Can lead to dehydration of bowel contents, obstipation, fecoliths
    • Low environmental temperatures
      • Reduction in appetite and fecal output
      • Reduced metabolic rate and GI motility
    • Sudden dietary change
      • Can cause diarrhea - due to increased water or simple carb content of food
      • Dysbiosis in herbivores
      • Greater levels of dietary fiber increase GI transit time
  • Foreign bodies
    • Risk factors
      • Sand substrate
      • Chelonians prone to ingesting rocks and wood materials, bright colored objects
      • Reproductively active females - ingestion of stones
      • Feeding snakes on substrates
      • Dermatophagy
    • Signs - anorexia, weight loss, and lethargy, can be for weeks to months
      • Vomiting with SI FB
      • Constipation, reduced/absent feces, bloating, cloacal prolapse, diarrhea possible
  • Neoplasia
20
Q

Discuss the pancreatic diseases of reptiles.

What protozoal diseases have been documented to affect the pancreas?

What viral diseases have been documents to affect the pancreas?

Pancreatic islet cell tumors have been documented in what lizard species?

A
  • Pancreatitis
    • Uncommon in reptiles but reported
    • Intranuclear coccidiosis
      • Chelonian species
      • Clinical signs - anorexia, lethargy, wasting, oculonasal discharges

Multiple organs including liver, kidneys, and pancreas

  • Diagnosis - histopath
  • Treatment - standard anticoccidials ineffective for non-intestinal coccidiosis
  • Cryptosporidium reported in pancreas of corn snakes
  • Pancreatitis associated with nematode infection in red-eared slider turtles
  • Migratory nematodes and trematodes found in pancreatic tissue
    • Typically walled off and phagocytized
    • Cause minimal damage to pancreas but can result in secondary infection
    • Diagnosis - often incidental at postmortem examination
  • Inclusion body disease (IBD, arenavirus)
    • Common condition in boas and pythons
      • Some colubrids and vipers
    • Signs - neurological disease, regurgitation, weight loss
    • Eosinophillic intracytoplasmic inclusion bodies
    • Diagnosis – histopath  inclusion bodies in pancreas, kidneys, liver, CNS
  • Herpes viral inclusion bodies in pancreas found in boa constrictors
  • Subacute/chronic pancreatitis associated with orthoreovirus in rough green snakes
  • Pancreatic neoplasia
    • Rare
    • Multihormonal pancreatic islet cell carcinomas found in one female and two male captive geriatric Komodo dragons
21
Q

Discuss gastrointestinal surgery in reptile species.

When is it indicated?

What are some general principles of GI surgery in reptiles?

What is closure like of the GI tract?

What suture is recommended? What type of needle should be used?

What is the prognosis if a resection & anastomosis is needed?

When shoudl animals be fed again following GI surgery?

A

MARMS – 103. GIT Sx

  • Indications: gastrointestinal foreign bodies, intraluminal impactions, neoplasia, abscesses or granulomas, and intussusceptions, volvulus, or stricture, diagnostic biopsy

Principles of Gastrointestinal Surgery in Reptiles

  • Magnification beneficial
  • Wound healing takes longer
  • Standard practice to provide intraoperative (IV or IO) antimicrobials prior to entering the nonsterile gastrointestinal tract
    • More effective at reducing postsurgical complications and reducing antibiotic resistance then post-op therapy
    • Ex - cefazolin
  • Stomach incisions should be closed in two layers:
    • Initial, full-thickness closure - simple continuous or simple interrupted pattern
    • Inverting pattern (Cushing or Connell pattern) overtop
  • Antemesenteric, longitudinal intestinal incisions closed end to end result in a larger diameter and reduced constriction
  • Colotomy incisions - close in two layers
    • First layer - appositional or inverting
    • Second layer – inverting
  • Closing intestinal incisions challenging - thin wall and small luminal diameter
    • Single layer of accurately placed simple interrupted sutures usually sufficient
  • Recommended suture material - monofilament absorbable suture material
    • Polydoxanone or poliglecaprone 25
    • Antimicrobial impregnated ideal for intestinal closure, reduces risk of infection
    • Tapered, swaged needle recommended
      • Cutting needles create too much trauma
  • RNA
    • Simple interrupted, appositional pattern is preferred
    • Place initial sutures at mesenteric and antimesenteric aspects of wall
    • Prognosis usually guarded after RNA
      • Type of lesion that necessitate this and amount of intestine removed
    • Enterostomy can be performed in lower GI if RNA not possible, guarded px
  • Post op care
    • No feeding for minimum of 3-7 days, several weeks in snakes
      • Refeed gradually, start with small highly digestible meals
22
Q

Discuss diarrhea in reptiles.

What are some common causes of acute diarrhea? What are the sequalae of chronic diarrhea?

What are some of teh differentials?

How are these cases managed?

A

MARMS – 145. Diarrhea

  • Reptiles – longer GI transit time so most normal feces well formed, even desiccated
  • Diarrhea
    • Acute - sudden onset, self-limiting, short duration
      • Ddx - dietary indiscretion, sudden diet changes, inadequate temperatures
    • Chronic - longer duration, recurrent
      • More concerning – dehydration, electrolyte imbalances
    • Steatorrhea and melena - often indicate small-bowel problem
    • Fresh blood and mucus - more likely large-bowel problem
    • DDX
      • Infectious enterocolitis (parasitic, bacterial, viral, mycotic)
      • Inflammatory
      • Infiltrative diseases of the bowel (neoplasia)
      • Intestinal malfunction (partial obstruction)
    • Diagnostics – full workup recommended
      • Fecal exam – both direct and floatation
      • CBC/chem
      • Imaging - radiography, ultrasonography, CT, MRI
      • Endoscopy
      • Biopsy
    • Treatment
      • Treat underlying disease
      • Fluid therapy
      • Assess and correct husbandry concerns
23
Q

Discuss salmonellosis in reptiles.

How is it diagnosed? Is testing recommended in a healthy reptile?

What are some of the more common serovars implicated in reptile illness?

What is a common finding in snakes with salmonellosis?

A

MARMS – 166. Salmonellosis

  1. Salmonella is commonly found in reptile gastrointestinal tracts
    1. Zoonotic risk
  2. Human salmonellosis → Gi signs
  3. Diagnosis by PCR has a higher sensitivity and specificity than culture or ELISA
  4. Not recommended to test a clinically healthy reptile because intermittent shedding causes false negatives
  5. Elimination of Salmonella from reptiles has been unsuccessful
  6. Osteomyelitis can be treated with surgical debridement, but advanced spinal cases have a poor prognosis
24
Q

Discuss the anatomy of the reptile cloaca.

What are the three compartments? What structures are present in each?

How does this vary by taxa?

A

MARMS – 75. Gastroenterology 3 (Cloaca)

  • Anatomy:
    • 3 compartments, between caudal colon and vent.
      • Coprodeum (cranial)
        • Receives outflow of LI.
        • Chelonians – ventral surface coprodeum and urodeum also location of male copulatory organ or female clitoral organ.
      • Urodeum (midsection).
        • Openings to ureters (urinary pores). Bladder if present.
        • Genital openings of oviduct/vas deferens (genital pores).
          • Genital ducts arise from mesonephric Wolffian duct, paramesonephric Mullerian ducts.
            • Males, WD develops but remnants of MD may remain.
        • May be separated by an incomplete partition where the ureters end.
      • Proctodeum (caudal).
        • Opens outside at vent.
        • Outflow of bladder, urodeum, coprodeum, genital organs, ureters.
        • Reservoir for fecal/urinary waste before excretion.
        • Opening of musk glands.
    • Snakes.
      • Divisions less defined than other reptiles.
      • No urinary bladder.
        • Ureters empty into urodeum via urinary pores.
        • Paired hemipenes – invaginations inside the mucocutaneous junction medial to the lateral edges of the vent.
          • Functional surface is the lumen of the invagination.
          • Evert through the vent when erect.
          • Scent glands, anal sacs empty into the caudal proctodeum.
          • Specialized exocrine glands elaborate behaviorally active chemicals.
    • Lizards.
      • If bladder is present, empties via short urethra into ventral urodeum.
      • Hemipenes evert similar to snakes.
      • Some males retain remnants of Mullerian duct.
      • Some geckos have cloacal bones.
    • Chelonians.
      • Cloacal divisions well defined.
      • Bladder empties via urethra into ventral urodeum.
        • Accessory bladders or bursae empty into lateral wall of urodeum.
      • Copulatory organ originates from ventral urodeum.
        • Protrudes through vent when engorged.
      • Extensive physiological interactions with bladder and LI for fluid recycling, esp in uricotelic and hibernating spp.
25
Q

Discuss the physiology of the reptile cloaca.

How well do reptile kidneys concentrate urine? How do reptiles concentrate their urine?

What species have a bladder?

A
  • Physiology:
    • Kidneys cannot form urine hyperosmotic to plasma.
      • Greater renal water loss with excretion of solutes in solution.
      • Losses balanced by fluid resorption in lower urinary tract.
    • Uricotelic reptiles – excrete uric acid and urates.
      • Typically arid environments, hibernate.
      • Uric acid barely soluble and can be excreted with minimal water.
      • Mainly excrete urea.
    • Ureo-uricotelic reptiles – uric acid and urea.
    • Amino-ureotelic – excrete ammonia and urea.
      • Aquatic or FW spp.
    • Excess Na and K may precipitate in cloaca as urate salts.
      • Urine may be directed either to urodeum or proctodeum after exiting the ureters.
        • Depends on spp, hydration status.
        • Water resorption in colon or proctodeum.
        • Urine may direct into bladder for electrolyte and fluid exchange.
          • In spp without bladder, urine mixes with fecal material and is voided simultaneously.
    • Chelonians – bladder connects with cloaca.
      • May hold large volumes.
      • Postrenal modification of urine occurs as fluid is resorbed across bladder wall, ions i.e. K excreted opposite.
        • Dehydration can be addressed with soaking.
      • Some semiaquatic spp absorb O2 through cloacal bursae for underwater hibernation.
    • Crocodilians and snakes – no bladder.
      • Postrenal modification of urine in urodeum or proctodeum.
        • Accessory bladders may play role in water and electrolyte regulation, respiration, absorption of solutes.
26
Q

How is cloacal prolapse (any type) managed in reptiles?

What are some of the causes of cloacal prolapse?

A
  • Cloacal Organ Prolapse:
    • Untreated prolapses involving colon, bladder, and oviduct likely fatal.
      • Ischemic tissue necrosis, compromised body system functions.
      • Addressing underlying cause also important.
    • Chelonians commonly have normal engorged clitoris or phallus protrude during handling, bathing, urination, chemical restraint.
      • Usually return to cloaca quickly without assistance prior to presentation, whereas pathologic prolapse does not.
    • Clinical Presentation:
      • Structures that may prolapse – cloaca, colon, bladder, oviduct, intestine, rectum, copulatory organs.
      • Goal of intervention is threefold:
        • Provide analgesia, emergency stabilization.
        • ID, clean, protect anatomic structure, replace or remove.
        • ID, plan, tx underlying cause.
    • Triage:
      • Following emergency stabilization:
        • Temporary prolapse protection, reduction, prolapsed retention, removal of a prolapsed organ, pexy of reduced structure, euthanasia may occur.
    • Prolapse Protection:
      • Clean with saline or warm water.
      • Wrap caudal body and prolapse in cling film, moist toweling, or dampened swabs.
        • Can tape in place or retain with veterinary dressings.
        • Osmotic reduction solution, lubrication, local anesthetic agents.
    • Dx – full workup should include hx, PE, CBC/chem, fecal, rads, US +/- cytology, histo, CT scan, MRI, endoscopy.
      • Rads recommended in all cases of cloacal organ prolapse.
      • Obtain history about husbandry and nutrition.
      • Immediate management of core temp, pain, hydration status, sepsis or toxemia, electrolyte derangements equally important as protecting and dealing with the prolapse.
        • Fecal/urine output may be impaired resulting in severe metabolic derangements.
          • Hypocalcemia assoc with nutritional or renal secondary hyperparathyroidism may have predisposed the patient to the presentation.
          • Parasitic, protozoan, or bacterial infection may contribute as underlying cause.
            • Direct microscopy, cytology, examination of cloacal washes may be helpful.
      • Imaging.
        • Assessment for cystic calculi, eggs, or space-occupying masses present.
        • If free fluid in coelom, FNA and cytology may be beneficial.
    • Prognosis:
      • Depends on underlying cause, patient condition, prolapse viability and duration.
    • Treatment:
      • Analgesia.
      • Protection of prolapse - lavage, lubricant, osmotic gels, protective wraps.
      • If in distress, sedation or GA.
      • Cystic calculi – celiotomy indicated.
      • Prolapse of LI and oviduct invariably surgical.
      • Prolapse reduction.
        • Clean with sterile fluid or warm water.
        • Osmotic reduction, lubricant, physical manipulation.
        • May add local anesthetic agents to gel.
        • Osmotics – sugar, honey, dextrose solution.
        • Male reproductive organs can also be removed if needed.
        • All tubular intussuscepted prolapses require coeliotomy to correct and retain via sutures.
27
Q

Describe the management of phallic and hemipenal prolapses in reptiles.

What are some of the common causes of these prolapses?

What differentials need to be considered?

How can these cases be managed?

A
  • Phallus, chelonian.
    • Causes – courtship trauma, balanoposthitis, dystocia, chronic sexual activity, constipation, paraphimosis, neuro dysfunction, substrate contamination, hypothermia, hypocalcemia, dehydration, cloacoliths, neoplasia.
    • Not life-threatening.
    • Single large, engorged nontubular structure protruding through the vent.
      • No lumen.
      • Rads recommended.
      • Px good depending on etiology.
      • Lubricate, reduce.
      • Temporary retaining sutures can be applied across vent.
      • Surgical removal preferred for avascular traumatized, necrotic, or infected prolapses where reduction is not feasible or if relapsing.
  • Hemipenises, squamate.
    • Causes – same as above.
    • Single or paired small, nontubular structure protruding through the vent at lateral edges.
    • No lumen.
    • Rads recommended.
    • Do not confuse with cloacitis, cloacal trauma, hemipenile plugs, or scent gland secretion.
    • Px is good depending on etiology.
    • Plugs or contaminating material should be gently removed.
    • Lubricate, reduce, temp sutures may be helpful.
    • Can remove if indicated.
  • Phallus (chelonian), Hemipenis (squamate) prolapse:
    • Most common prolapse type of reptiles.
    • Phallus does not contain a lumen and is relatively small, originates within caudolateral vent in squamates and may be bilateral in squamates.
      • Ddx in squamates – hemipenile plugs and infections.
    • Chelonians – single large structure centrally from the cranial cloaca.
    • Usually can defecate and urinate around prolapse.
      • Male copulatory organ contains no urethra.
    • Tx – reduction or amputation. Rehydration, warmth, analgesia.
      • Does not affect output of the urinary system.
      • Squamates can still reproduce with 1 hemipenis.
      • Good prognosis.
      • Application of topical local anesthetics mixed with lube may reduce straining and aid reduction.
        • Can also do an intrathecal block.
      • If unable to reduce manually, vent may be surgically enlarged with lateral releasing incisions and surgical closure after reduction.
        • Cloacal suture or staples prevent further prolapse and allow normal urination and defecation.
      • If traumatized, severely swollen, or necrotic, amputation is favorable.
        • Can be done with sedation, GA, local block.
28
Q

Describe the management of oviductal prolapse in reptiles.

What are some of the common causes?

How can you determine that the prolapsed structure is the oviduct?

How are these treated?

What is the general prognosis?

A
  • Oviduct (oviparous spp).
    • Causes – hypocalcemia, dehydration, dystocia, infection, uroliths, neoplasia.
    • Most will have follicular stasis, urinary calculi, or dystocia.
    • Life-threatening.
    • Modest flaccid, intussuscepted structure.
    • Usually solid and linea with a lumen.
    • Large in size vs size of animal.
    • Rads recommended.
    • Px is poor.
      • Few will return to normal quality of life.
      • If recent it may be reduced and removed via celiotomy.
    • Tx – celiotomy and entire ovariosalingectomy advised.
      • Alternatively, prolapse can be amputated and residual tissue addressed via coeliotomy.
      • Endangered spp, minimum of unilateral salpingectomy advised and must include ipsilateral ovariectomy.
  • Oviduct prolapse:
    • Reported in lizards and chelonians.
    • Tubular prolapsed structure.
      • Smooth surface with occasional longitudinal striations.
      • Lumen is present.
      • May pass fecal and urinary excretion products around the prolapse.
      • Bilateral prolapses not reported.
      • Chronic prolapses become traumatized, strangulated, necrotic.
        • Ddx – Colon prolapse.
        • Examination of cloaca with otoscope or endoscope may help ID source of tissue.
      • Tx – protection of organ, analgesia, rehydration, warmth. Local blocks.
        • Coeliotomy (open reduction) with multimodal analgesia advised.
          • Radiographic evidence of dystocia or urinary calculi can also be addressed.
        • Amputation usually necessary before coeliotomy.
          • Prevents drawing necrotic, infected tissues back into the vent and cloaca.
        • Euthanasia may also be considered.
        • Closed reduction of oviduct and temporary retention is possible but usually will recur.
      • Females all have a bicornuate repro system and two ovaries.
        • Recommended to remove the portion of affected repro tract and accompanying ovary.
        • If future reproduction is not a concern, bilateral ovariohysterectomy is preferred to unilateral.
        • Squamates – right ovary is close to vena cava.
        • Post-op complications – infection, hemorrhage, thromboembolism, paresis, ovarian remnant.
        • Culture swab from coelom should be taken prior to lavage and closure.
29
Q

Discuss the management of colonic prolapse in reptiles.

What are some of the common causes?

How can you determine the prolapsed structure is the colon?

How are these cases managed?

What is the prognosis?

A
  • Colon (all spp).
    • Causes – hypocalcemia, dehydration, constipation, infection, neoplasia.
    • Bladder stones, fecoliths, or uroliths within urodeum or dystocia may contribute.
    • Emaciated animals are overrepresented.
    • Large, rigid, engorged and intussuscepted structure.
      • Usually solid and linear, has a lumen, may have become traumatized and necrotic.
      • Rads recommended.
        • Px generally grave.
        • If fresh may be able to reduce via coelomic celiotomy approach.
      • Once reduced, colopexy.
  • Large Intestine (Rectal/Colonic) Prolapse:
    • Ddx in female is oviductal prolapse.
    • Smooth linear structure with a lumen, feces or gas may be present.
      • May be rigid and inflexible.
      • Tx – coeliotomy with multimodal analgesia is advised.
        • Euthanasia may be considered.
        • Milking the intussusceptum slowly out of the intussuscipiens is important.
          • Risk of iatrogenic perforation.
          • Colopexy following correct reduction.
            • Partial thickness sutures.
            • Colon can also be incorporated into the body wall closure.
            • RNA can be performed.
            • Culture swab prior to lavage and closure.
      • A fresh nontraumatized prolapse can be hydrostatically reduced with warm water local irrigation after osmotic reduction.
      • Contrast rads, US, and endoscopy may be needed to confirm placement.
      • It is unusual to reduce a colon prolapse without persistence of inversion or recurrence.
      • Anastomosis can be performed without coeliotomy after insertion of a smooth, tubular object into the lumen.
        • Monitor for ability to urinate and defecate and for recurrence or breakdown.
30
Q

Discuss the management of bladder prolapse in reptiles.

What are some of teh common causes?

How do you dtermine the prolapsed structure is the bladder?

How are these managed?

What is the prognosis?

A
  • Bladder (all chelonians, some lizards).
    • Causes – Hypothermia, hypocalcemia, dehydration, uroliths, ectopic eggs, bladder and cloacal infections, neoplasia.
      • Emaciated animals overrepresented.
    • Life-threatening.
    • Large, engorged, fluid-filled structure.
    • May be thin-walled.
      • No lumen, not tubular.
      • Urate deposits may pe apparent with cystic structures across mucosa.
      • If ruptured may present as long, stringy, nonspecific, nontubular structure.
      • Rads recommended.
      • Px is grave.
    • Recent, viable prolapses can be reduced and replaced.
    • Fluid can be infused into cloaca to reverse organ involution.
    • Scope can be used.
    • Temporary retaining sutures.
    • Surgical replacement preferred for avascular traumatized, necrotic, infected prolapses, and where reduction is not feasible.
      • Part of bladder wall can be resected if needed.
      • Braided suture material should be avoided in uricotelic spp.
  • Bladder Prolapse:
    • Amorphous translucent structure from cloaca, may contain fluid, no lumen.
    • Because ureters empty into urodeum without direct connection to the UB, usually not damaged during prolapse.
      • But outflow may be obstructed.
      • Attempt to salvage as much viable tissue as possible.
    • Bladder is easily traumatized.
    • Can try closed reduction with hydrostatic pressure of warm water enema.
    • Exposed necrotic tissue must be surgically resected.
      • Double-layer inverting suture line proximal to a clamp to seal the UB.
      • Endoscopy can confirm bladder placement following hydrostatic reduction.
      • If substantial portion of the bladder is damaged, open reduction via coeliotomy is advised.
      • Culture swab prior to lavage and closure.