We investigated mass mortalities of koi, Cyprinus carpio Linnaeus, 1758, experienced in South Indian fish farms by virus isolation, electron microscopy, PCR detection, sequencing of capsid protein gene and transmission studies. Samples of moribund koi brought to the laboratory suffered continuous mortality exhibiting swimming abnormalities, intermittent surfacing and skin darkening. Irido-like virus was isolated from the infected fish in the indigenous snakehead kidney cell line (SNKD2a). Icosahedral virus particles of 100 to 120 nm were observed in the infected cell cultures, budding from the cell membrane. Virus transmission and pathogenicity studies revealed that horizontal transmission occurred associated with mortality. PCR analysis of infected fish and cell cultures confirmed the presence of Ranavirus capsid protein sequences. Sequence analysis of the major capsid protein gene showed an identity of 99.9% to that of largemouth bass virus isolated from North America. Detection and successful isolation of this viral agent becomes the first record of isolation of a virus resembling Santee-Cooper Ranavirus from a koi and from India. We propose the name koi ranavirus to this agent.

Increase of MDA and IMA levels with decreased antioxidant status indicate the presence of OS in hypothyroid patients, which was more pronounced in OHT patients. Elevated levels of IMA can be a clinically useful marker of protein oxidative damage and OS in hypothyroidism.

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Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but lethal manifestation of hypersensitivity reaction precipitated by certain drugs and viral infections. Among the drugs, it is more common with antibiotics, antiepileptics and nonsteroidal anti-inflammatory drugs. We report the case of a 14-year-old male who presented to the medicine out-patient department with a history of fever since the previous day. Four days before this, he had developed an episode of generalised tonic–clonic seizures and was initiated on oral phenytoin since then. Following admission to the medical intensive care unit, fever persisted on the 2nd day as well. The patient developed a maculopapular rash over face and trunk, ulceration over lips and skin peeling involving >10% <30% body surface area suggestive of SJS/TEN overlap syndrome. Oral phenytoin was stopped, and he was started on oral levetiracetam. He was treated with intravenous corticosteroids, topical antibiotics and symptomatic management. The patient recovered, skin lesions subsided and he discharged in a stable condition after 2 weeks of in-hospital stay. The present case documents the rare occurrence of SJS/TEN overlap syndrome as an adverse drug reaction caused by phenytoin. Early identification and stopping of offending drug will aid in better management of the patient.