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Background: Infections in the foot are more common with significant proportion of world’s population remaining bare foot, minor skin trauma is a frequent cause of local infection. The present study was conducted with an aim to study various foot infections and compare the findings in diabetic and non diabetic patients with reference to etiopathogenesis, clinical features, management, duration of hospital stay and outcome.Methods: The present study was conducted in Mamata General Hospital, Khammam, Telangana state from October 2016 to September 2018. A total of 50 cases were divided into 2 groups, Group A included 25 patients with diabetic foot infection and Group B included 25 patients with non diabetic foot infections.Results: In diabetics 6th decade and in non-diabetics 4th-6th decade was the most common age group presenting with foot infections. Cellulitis of the foot was the most common in both diabetics (40%) and non-diabetics (52%). Wagner’s grade 4 lesions were more common in diabetics (28%) than in non-diabetics (8%). The most common site of lesion in diabetics was dorsum (40%) and in non-diabetics was toes (40%). The incidence of neuropathy was significantly higher in diabetics (72%) than in non-diabetics (20%). Rate of amputation was high in diabetics (12%) compared to non-diabetics (8%). The average number days in a hospital stay in diabetics was 42.27 days and in non-diabetics it was 28.96 days.Conclusion: Diabetic patients have increased severity of infections, delayed healing process, need more active interventions. As compared to the non-diabetic patients, they do show high risk of amputations and prolonged hospital stay.

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Skin integrity is essential for protection from external stress and trauma. Defects in structural proteins such as keratins cause skin fragility, epitomized by epidermolysis bullosa (EB), a life-threatening disorder. Here we show that dominant mutations of KLHL24, encoding a cullin3eRbx1 ubiquitin ligase substrate receptor, cause EB. We have identified start-codon mutations in the KLHL24 gene in five patients with EB. These mutations lead to truncated KLHL24 protein lacking the initial 28 amino acids (KLHL24-DN28). KLHL24-DN28 is more stable than its wild-type counterpart owing to abolished autoubiquitination. We have further identified keratin 14 (KRT14) as a KLHL24 substrate and found that KLHL24-DN28 induces excessive ubiquitination and degradation of KRT14. Using a knock-in mouse model, we have confirmed that the Klhl24 mutations lead to stabilized Klhl24-DN28 and cause Krt14 degradation. Our findings identify a new disease-causing mechanism due to dysregulation of autoubiquitination and open new avenues for the treatment of related disorders.