SepticemicCutaneous Ulcerative Disease of Chelonians 

  Septicemiccutaneous ulcerative disease of chelonians was originally described by Kaplan in 1957 and is commonly referred to by its acronym SCUD.  The original causative agent was identified as the bacterium Escherichia freundii and the disease was referred to as Escherichiosis.  This organism has been renamed Citrobacterfreundii.

  This syndrome, which most often affects turtles in the families Trionychidae and Emydidae, is no longer attributed to a single bacterial species.  Today, SCUD is viewed more as a syndrome with many bacteria such as Citrobacterfreundii, Serratiaanolium, Beneckeachitonovora and other gram negative bacteria acting together with poor husbandry, poor water quality, abrasions and invertebrate predation to culminate in SCUD.  It has been hypothesized that the proteolytic and lipolytic actions of Serratia upon the plastron and carapace allowed the entry of Citrobacterfreundii, a gram negative rod normally found in soil, water and the intestinal tract of various animals, including chelonians and man.  New research has found infections devoid of Serratia and/or Citrobacter presenting with similar lesions and signs leading to the investigation of other contributing factors.

  The pathogenesis of SCUD involves a cutaneous insult either from an abrasion, enzyme degradation fromSerratia, invertebrate predation, shell rot from Benekeachitonovora or some other form of injury, allowing the entry of a gram negative bacteria, most commonly Citrobacterfreundii.  This infection develops into irregular, caseated, crateriform ulcers on the plastron, carapace and skin.  From this stage, the infection can become septicemic, causing multifocal hepatic and other visceral organ necrosis, hemolysis, limb paralysis, loss of digits or claws, cutaneousvasodilation and hemorrhage.  The animal presents with signs of lethargy, anorexia, reduced muscle tone, cutaneous ulcerations or death.  Erythrocytes may be vacuolated and contain numerous bacteria.

  The bacteria can be cultured on eosin-methylene blue agar from samples taken from cutaneous sores, blood, and visceral necrotic foci.  Spontaneous recovery has been reported but prognosis is poor if not treated.  Treatment entails debridement of ulcers and abscesses, use of antibiotics and shell support with fiberglass and resin if destruction is extensive.  Chloramphenicol has reportedly been effective at an initial dose of 8mg per 100g of body weight, IM or IP, followed by 4mg per 100g of body weight, IM or IP, twice a day for 7 days.  Gentamicin drops have also been applied topically along with Gentamicin IM, at 10mg/kg every 48 hours for 10 doses.  Shell lesions can take 1-2 years to heal.

 - By Frank Ridgley, Class of 2001

 - Edited by Kaori Sakamoto, DVM,

     ADDL Graduate Student