Over a period of 6 months, dozens of moon jelly (Aurelia aurita) medusae from a single-species exhibit at the California Science Center (CSC) developed exumbrellar ulcers. Ulcers were progressive, causing umbrellar creases that expanded radially to the bell rim and occasional adoral erosions that extended into gastrovascular cavities. Husbandry interventions, including addition of ultraviolet light sterilizers, repopulation with fresh cultures, and enclosure disinfection, did not arrest the recurrence of lesions. Biopsies or whole specimens representing 17 medusae (15 affected and 2 grossly unaffected) from CSC and 2 control medusae from Aquarium of the Pacific were submitted to a private diagnostic laboratory and processed for light and electron microscopy. Microscopic lesions were present in all CSC medusae and were not observed or negligible in control medusae. Lesions included ulceration, necrosis, and hyperplasia in all umbrellar layers, with most severe lesions in the exumbrella and amoebocyte infiltration in the underlying mesoglea. Special stains, electron microscopy, and fungal culture did not associate microorganisms with the lesions. Bacterial cultures from the CSC population consistently grew Shewanella and Vibrio spp, both of which were considered commensal. Trauma and environmental stress are proposed as possible causes for the ulcers.

Histopathology of 61 captive American horseshoe crabs (HSCs; Limulus polyphemus) is reviewed. HSC organs evaluated histologically included body wall (chitin, epidermis, dermis, and skeletal muscle), hepatopancreas, gut, gonads, book gills, eyes, heart, brain, and coxal gland. In descending order, lesions were most frequently identified in compound eye, body wall, book gills, hepatopancreas, chitinous gut, nonchitinous gut, heart, and brain; lesions were not observed in coxal gland or gonads. Hemocytes (also called amoebocytes) surrounded infectious agents and occluded ulcers. Large hemocyte aggregates had a central eosinophilic coagulum (ie, hemocyte coagulum). Cutaneous ulceration (34/60 cases), branchitis (29/48 cases), and ophthalmitis (17/20 cases) were common lesions and consistently associated with fungi, which were invasive into subjacent tissues, and/or bacteria, which were usually superficial. Fungal culture was performed in 3 cases and isolated Fusarium spp., although fungal morphology varied and multiple fungal species may have been present. Presumptive green algae were associated with ulceration in 1 case with minimal to no inflammation. Presumptive cyanobacteria were identified within a biofilm overlying the gills in 4 of 48 cases and were not invasive. Multifocal, random hepatopancreatitis was identified in 16 of 57 cases, 10 of which were associated with bacteria. Metacercarial cysts were identified in 25 of 61 cases and associated with minimal to no inflammation. Depleted eosinophilic globules in hepatopancreatic interstitial cells were interpreted as decreased nutritional status in 12 of 57 cases.

Odontogenic lesions are well described in domestic cats, but published literature describing these lesions in nondomestic felids is limited. This study reports oral lesions in 109 captive, non-domestic felids. Ten cases of odontogenic lesions were diagnosed, including 9 with fibromatous epulis of periodontal ligament origin (FEPLO) and one odontogenic cyst in a cougar. FEPLO was common in lions. FEPLO did not recur after surgical removal in any of the 3 cases for which follow-up information was available. Increased occurrences of oral papillomas in snow leopards and eosinophilic granulomas in tigers were identified, which is consistent with the reported literature. With the exception of oral papillomas in snow leopards and FEPLO in lions, the spectrum of oral lesions in nondomestic felids was similar to what is reported in domestic cats, with squamous cell carcinoma being the most common oral malignancy, and stomatitis/gingivitis/glossitis accounting for approximately one third of all cases. Rare diagnoses with one case each included hemangioma, fibrosarcoma, melanoma, cleft palate, and glossal amyloidosis.

A retrospective study was performed by reviewing all Heloderma spp. submissions to Northwest ZooPath from 1996 to 2019. Necropsy and biopsy specimens from 106 captive Gila monsters (Heloderma suspectum) and 49 captive beaded lizards (Heloderma horridum) were reviewed. Inflammatory diseases were the most frequently diagnosed condition in Heloderma spp., and were diagnosed in 72% of all animals examined, including 76% of Gila monsters and 63% of beaded lizards. The most common cause of inflammation was bacterial infection, which was present in 52% of all Heloderma spp. with inflammation. Enterocolitis was common in Gila monsters (20%) and beaded lizards (14%), but the underlying causes were different for each species. Cryptosporidium spp. was the most common cause of enterocolitis in Gila monsters (36%) but was not identified in beaded lizards. Amoebiasis was a common cause of enterocolitis in Gila monsters (27%) and was the most common cause of enterocolitis in beaded lizards (57%). Deposition diseases were diagnosed in 34% of all Heloderma spp. The most frequently diagnosed deposition disease in beaded lizards was urolithiasis-nephrolithiasis (12%). This disease was not diagnosed in Gila monsters. Deposition diseases that were common in Gila monsters and beaded lizards included hepatic lipidosis and renal gout. Neoplasia was diagnosed in 17% of all Heloderma spp., including 17% of Gila monsters and 18% of beaded lizards. The most common neoplasm of Heloderma spp. was renal adenocarcinoma, which was equally common in Gila monsters and beaded lizards. Less common diagnoses included degenerative diseases, trauma, nutritional disease, nonneoplastic proliferative disease, nondegenerative cardiovascular disease, and congenital malformation.

Invertebrates, including arachnids, are a common taxon in zoological collections. Invertebrate medicine and pathology are emerging subspecialties, but there is limited reference material or published resources describing histologic lesions in arachnids. Histopathology of 26 captive arachnids (20 spiders and 6 scorpions) from institutional collections was reviewed. Most animals were found dead with limited clinical signs. Tissues evaluated included body wall (cuticle and epidermis), skeletal muscle, book lungs, digestive tract (pharynx, esophagus, sucking stomach, midgut tube, midgut diverticula, and stercoral pocket), central and peripheral nervous system, heart, hemolymph vessels and sinuses, Malpighian tubules, coxal glands, and gonads. Inflammation was frequent (24/26, 92%), and seen in multiple organs (18/24, 75%) with the midgut diverticulum most commonly affected (14/24, 58%) followed by the book lungs (13/24 arachnids, 54%), and body wall (8/24 arachnids, 33%). Inflammation comprised hemocyte accumulation, hemocytic coagula, melanization, and nodulation. Infectious agents, including bacteria (11/26, 42%), fungi (10/26, 38%), and parasites (2/26, 8%), were seen within inflammatory aggregates. Coinfection with multiple infectious agents was common (6/24, 25%). No etiologic agent was identified in 7/24 (29%) cases with inflammatory lesions. Lesions suggestive of decreased nutritional status or increased metabolic rate included midgut diverticula atrophy in 11/26 (42%) animals and skeletal muscle atrophy in 6/26 (23%) animals. Atrophic lesions were seen in combination with infection (8/11, 73%), pregnancy (2/11, 18%), male sex (2/11, 18%), or without other lesions (1/11, 9%). Other suspected contributors to death included dysecdysis-associated trauma (2/26, 8%) and uterine intussusception (1/26, 4%). No animals had neoplasia.