Abstract

A 3-4 year old wild female Hawaiian monk seal (Monachus schauinslandi) was brought into captivity due to poor body condition. She was moved to a captive display facility and housed in an enclosure with 2 other female seals; one monk and one harbor seal (Phoca vitulina). Overall her medical history was unremarkable. However, at 19 years of age she developed bilateral corneal opacities 2-3 mm in diameter with punctate ulcerations. Approximately 3 months later, small superficial erosions developed acutely on her ventrum, one on her thorax (1 cm) and the other on her abdomen (0.5 cm). Despite systemic and topical treatments, neither the eye nor skin lesions resolved.

Over the next 18 months both the eye and skin lesions progressed very slowly. The chronic keratitis progressed to involve most of the corneas (OD>OS). The skin lesions developed deeper ulcerations up to 1.5 x 2 x 2 cm on the thorax and 0.5 x 0.4 cm on the abdomen. Multiple rounds of topical and systemic antimicrobial therapies failed to significantly improve the lesions.

In February 2009, the abdominal lesion finally resolved. However, the thoracic lesion continued to expand in diameter and depth over the next 8 weeks and it was clear that the lesion had become much more aggressive. She was sedated with midazolam (0.15 mg/kg) and butorphanol (0.1 mg/kg) administered intramuscularly and multiple wedge and punch biopsies and cultures were obtained. Due to the possibility of a fungal etiology, a course of high dose fluconazole (4 mg/kg PO BID) was initiated. The treatment was tolerated very well and we saw minimal changes in her hepatic indices over the 2 weeks of treatment.

Histopathologic examination revealed invasive squamous cell carcinoma (SCC) in all of the samples submitted. Cultures revealed a variety of bacterial and a few fungal species, all of which appeared to be of environmental origin with highly sensitive susceptibility patterns. Viral PCR was negative for Hawaiian monk seal herpes, novel herpes, papilloma and parapox virus.

Thoracic radiographs were performed to evaluate for metastasis, but were inconclusive. A surgical resection of the lesion was performed under general anesthesia and a 26cm x 22cm x 6cm deep section was removed. The ventral margin of the lesion was excised, including multiple fascial layers, as well as thoracic muscle. The defect was closed by dissecting the blubber layer from underlying muscle and sliding it as an advancement flap utilizing 0-PDS to secure the blubber layer to the thoracic muscle. A second layer of 0-PDS attached the external skin, covering the blubber layer and securing it to the exposed muscle. The remaining 12 x 18 cm exposed muscle was left to heal by second intention. Piroxicam (0.2 mg/kg PO daily) was started the day after surgery and continued on a 5 days on and 2 days off dosing schedule. Due to the ulcerogenic potential of the piroxicam, misoprostol (2.8 mcg/kg PO TID) was given. She also received oral amoxicillin with clavulanic acid (22 mg/kg PO BID) and silver sulfadiazine cream was applied topically to the surgical site.

Over the next 3 months the surgical site healed slowly, but unremarkably. The seal was seen scratching at the surgical site as it healed and a small depression developed at the center of the wound. Two months after the surgery an area of swelling was observed along the caudal edge of the lesion. A superficial erosion developed, but began to heal after some suture was extracted. A second erosion developed along the lateral margin of the surgical field about 10 days later and again suture material was removed, however it did not follow the same pattern of healing.

Three months after the surgery a dark green focus developed in the center of the lesion. Within 5 days, the necrotic tissue eroded to reveal a deeper cavity. The lesion progressed rapidly and continued to undermine and subsequently erode the apparently healthy overlying epithelium. A second non-healing site also developed along the craniolateral margin which was more erosive in nature than the previous sites.

She was sedated again for a biopsy with the same protocol and intermittent retching was observed starting 5 minutes after the sedatives were administered, but subsided within 5 minutes. This had not been observed during the previous sedation and was thought to be a side effect of the butorphanol. Invasive SCC was again documented in all 5 punch biopsies. Within 8 weeks after the development of the green necrotic lesion, the 3 sites became confluent and an 8 x 5 x 2 cm deep cavity remained.

The treatment plan was changed to include carboplatin (300 mg/m², BSA=2.6 m²) administered IV as a bolus over 15 minutes. Prior to the treatment she was sedated with midazolam (0.15 mg/kg), butorphanol (0.06 mg/kg) and atropine (0.02 mg/kg) administered IM. Metoclopramide (0.3 mg/kg IM daily) was administered for 2 days. She showed no emesis during or after the procedure. This treatment appeared to arrest the growth of the tumor for several weeks.

A second surgical resection was discussed; however it was not pursued because the size, location and aggressive nature of the tumor made a positive long term outcome very unlikely. The piroxicam provided adequate pain relief when administered and tramadol (2 mg/kg PO BID) was added on the alternate days. The final outcome of the case is still pending.

Acknowledgements

The authors would like to acknowledge and thank the following: Jeff Pawloski, Celeste Cunningham and the Sea Life Park Hawaii Animal Care staff for their dedicated care and training with this animal, Dr. Ben Okimoto and the Honolulu Zoo for allowing us to use their surgical facilities and anesthesia equipment, Dr. Eric Jensen and the US Navy Marine Mammal Program for the use of their ventilator and Dr. Bob Braun and NMFS for consulting on this case.