Abstract

The present report refers to a case that affected a population of five Port Jackson sharks, kept in Oceanário de Lisboa. The group consisted of four females, present in the aquarium since 1997 and a male, acquired July 2000. These sharks were maintained in a 21 m³ exhibit tank that has a mixed population of small elasmobranches and teleosts with a temperature range of 15-16°C. This tank has a sand filter, a protein skimmer with ozone injection, a biotower and no UV sterilization.

In July 1998, a Port Jackson female shark appeared with bilateral conjunctiva edema and hyperemia. A treatment with enrofloxacin (Baytril®) 15 mg/kg/every 2 days was administrated with no success. The animal died within two weeks.

At necropsy rupture of one eye with marked signs of bulbar conjunctiva inflammation was observed and a 2 cm diameter nodule was detected located in the dorsal midline between the spiracles. The subcutaneous tissue in the nodule was congested and edematous. The cerebrospinal fluid was hemorrhagic. Microscopic examination revealed that the nodule corresponded to granulomatous reaction within which thin and septated fungal hyphae were identified. The wall of the endolymphatic tubes showed inflammatory lesions with heavy cellular infiltration and fungal hyphae similar to the ones identified in the head nodule. In the brain non-purulent diffuse meningitis was observed. Fusarium sp. was isolated from the cerebrospinal fluid. In the past, Fusarium sp. skin infections had already been diagnosed in two hardnose houdsharks (Mustelus mosis) kept in the same tank.

In January 2000, a small supersaturation episode occurred. At that time, one of the Port Jackson sharks showed an agitated swimming pattern, with no other signs. Early in the beginning of the tank installation in 1997, a serious episode of supersaturation had also occurred, after which only teleosts showed signs of gas bubble disease.

In March 2000, another Port Jackson female shark showed a skin nodule in the dorsal midline between the spiracles, identical to the one described before, followed by unilateral eye lesions, such as corneal edema, iritis and median exophthalmia. She was transferred to an observation tank and after ceftazidime (Cefortan®) 30mg/kg/every 3 days and flunixin meglumine (Finadine®) 2mg/kg/IM/every 2-days/3 total, eye lesions regressed partially and the head nodule disappeared.

In January 2001, due to exhibit requirements, all animals but the three remaining Port Jackson sharks were taken from the tank and new teleosts were introduced. Two days after this event, the Port Jackson sharks appeared with mild to severe eye lesions consisting of corneal edema, iritis, hyphema or even corneal rupture. The swimming pattern was agitated and head nodules were observed in one female and in the male. Sharks with this nodule were transferred to the observation tank. The female with just corneal edema remained in the exhibit tank.

In April 2001, the female that was transferred in March 2000 was reintroduced in the exhibit tank. This female shark did not show any signs of disease until September 2001, when white skin patches appeared which did not regress after ceftazidime (Cefortan®) treatment. She was again transferred to the observation tank, where the unilateral eye lesions that were under control reappeared with severe exophthalmia, corneal edema and hyphema. A treatment with enrofloxacin (Baytril®) 15 mg/kg/every 2 days was administered but showed to be ineffective. Only after a prolonged treatment with ceftazidime (Cefortan®) the eye lesions regressed almost completely.

The female and male with the severe eye lesions and head nodules did not survive despite prolonged treatment with ceftazidime (Cefortan®). The male was also medicated with itraconazole (Sporanox®) PO, 20 mg/kg/every 48 hours, for 2 months.

Necropsy of the female showed a complete bilateral eye rupture with extended loss of tissue. The subcutaneous tissue in the nodule was congested and edematous. Endolymphatic tubes and membranous labyrinth tissues were also edematous and congested. Microscopic examination of the affected tissues revealed a set of lesions very similar to the case described above of the female that died in July 1998. Inflammation of the bulbar conjunctiva and retrobulbar tissue was marked by severe infiltration with eosinophilic granular cells. Soft tissues within and around the membranous labyrinth were equally infiltrated with inflammatory cells amongst which fungal hyphae could be identified. As in the previous case, the subcutaneous nodule corresponded to granulomatous inflammation, but with no evidence of fungal hyphae. Non-purulent meningitis was also diagnosed in the brain. Fusarium solani was isolated from the retrobulbar tissue and from the head nodule. The male shark was preserved intact for further anatomy studies.

All of the bacteria cultures both from needle aspirations of the head nodules and from material collected from necropsies were negative for pathogenic bacteria, including acid-fast bacteria. This may be due to the fact that these sharks were submitted to antibiotic therapy. The authors admit that, apart from the Fusarium, bacteria may also have been involved, because in the less severe cases the evolution of the disease was controlled with antibiotics. As theorized before by other authors, Fusarium fungal infections could be related to a compromised immunosystem. In one case described in the literature, raising water temperature was an efficient measure to solve this type of fungal infection in elasmobranches. In our tank raising temperature was not appropriated due to the characteristics of the co-habitant fishes. It's possible that the lack of UV disinfection system in the LSS and the supersaturation episodes previously referred could have contributed to the emergence and evolution of this process. It is important also to emphasize the non-existence of an efficient and practical drug for systemic fungal infections in fishes.

One hypothesis to explain the sequence of the lesions observed could be that the eye infection was the initial event, progressing to the brain, through the optic nerve, and to the otic capsule. In this last case, infection could have spread through the thin cartilaginous wall that separates the otic capsule from the eye. From this point infection may have evolved to the membranous labyrinth, endolymphatic tubes and subcutaneous tissues in the vicinity, creating the head nodules previously described. The initial infection may also have started simultaneously in the eye and the endolymphatic tubes openings, located in the dorsal midline between the spiracles, and may have spread from these points to the other organs affected.

References

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