Background and Aims: There is an increasing recognition of reinfection in coronavirus disease 2019 (COVID-19). We studied the reinfection of COVID-19 disease among doctors at a tertiary care centre in Northern India. Methods: All COVID-19 patients readmitted for COVID-19 disease after any duration with at least a positive Real time- polymerase chain reaction (RT-PCR) for severe acute respiratory syndrome coronavirus 2 were included. Their clinical profile, vaccination status, outcome and Centre for disease control (CDC), Atlanta, USA reinfection criteria screening were recorded. Results: A total of 57 (0.53%) doctors were identified and 56 of them satisfied the CDC criteria. It included 13 (20.3%) females and 89.3% of cases were from clinical specialities; 98.2% of individuals had the first infection in 2020 and mean duration between 2 infections was 156.29 ± 76.02 (35–298) days. Duration between two episodes of the disease with more than 90 days apart was in 80.3% cases. One (1.8%) patient developed severe disease and two (3.6%) cases were of moderate severity. Symptoms were similar in both infections except significantly higher number of extra-respiratory complaints (2.2% vs. 9.1%). There were 37.5% cases who had received first dose of vaccination of any duration at the time of second infection. Nine (16.1%) and four (7.1%) patients with more than 4 weeks after the first and second dose of vaccination developed the second infection, respectively. Conclusion: Majority of reinfection were symptomatic and developed after 90 days and so majority followed CDC criteria. Breakthrough infections among vaccinated healthcare worker are real, and with sustained exposure to the virus, they should continue to use precaution including hand hygiene and mask in order to prevent reinfection.

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Background: In approximately 25% of peripheral neuropathy cases, diagnosis remains obscure. In India, leprosy continues to remain one of the most frequent causes of peripheral neuropathy. We, in this prospective evaluation, performed nerve biopsies in patients with peripheral neuropathy for early confirmation of the diagnosis. Materials and Methods: A total of 55 consecutive cases of peripheral neuropathy were included in this study. All patients were subjected to clinical and electrophysiological evaluation. Sural nerve biopsies were performed in all the patients. Result: After a nerve biopsy in 29 cases, we were able to identify the underlying cause of peripheral neuropathy. In 26 cases, the diagnosis remained obscure. The most frequent histopathological diagnosis was leprosy, which was seen in 20 cases. Other diagnoses were chronic demyelinating neuropathy (four cases), vasculitis (two cases), and amyloidosis in one case. In two biopsies, the findings were consistent with hereditary neuropathies. The demonstration of lepra bacilli was the most distinctive feature. In addition, foamy macrophages (100%) and granuloma (100%) formation, epineurial (83.3%) and endoneurial infiltration (69%) along with epineurial (87.5%) and perineurial thickening (77.3%) were also noted more frequently in leprosy-associated neuropathy. Conclusion: The nerve biopsies revealed that leprosy was the most common etiology in patients with peripheral neuropathy. In approximately 47% of the cases, even nerve biopsies failed to establish a confirmed diagnosis.

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Background: Guillain–Barré Syndrome (GBS) is an acute acquired autoimmune inflammatory disorder of peripheral nerves and roots. The pathogenesis is essentially an aberrant post-infectious immune response in a genetically susceptible host milieu. Single nucleotide polymorphisms (SNP) in genes encoding the inflammatory mediators like TNF-α, CD1A and CD1E can influence their expression and level and the susceptibility and clinical course of disease in GBS. Objective: We tried to study the susceptibility of single nucleotide polymorphisms of TNF-α and CD1 genes in Guillain–Barré Syndrome in Indian population and determine the association in terms of genotype, allele and haplotype distribution along with individual subtype, severity and clinical outcome. Methodology: In this case-control study, we investigated the single nucleotide polymorphism pattern in the promoter region of TNF-α (-308 G/A), TNF-α (-863C/A), CD1A and CD1E genes using real-time polymerase chain reaction in 75 GBS patients and analysed in comparison with 75 age and sex-matched healthy controls. Results: The findings revealed that the allelic distribution of TNF-α (-308 G/A) *A allele was associated with GBS ( P value 0.04, Odds Ratio 2.03, 95% Confidence Interval 1.01–4.07). There was no association found with genotype, haplotype combination and other allele distribution for GBS in the study. CD1A and CD1E SNPs did not reveal any susceptibility for GBS. The subtype analysis did not reveal any statistical significance, except for CD1A *G allele with AMAN subtype ( P value 0.026). The haplotypic combinations and mutant allele of TNF-α (-308 G/A), TNF-α (-863C/A), CD1A and CD1E were significantly associated with severe GBS in the study. However, there was no association of any SNP for mortality and survival of GBS in the study. Conclusion: TNF-α (-308 G/A)*A allele might confer genetic susceptibility for GBS in Indian population. CD1 genetic polymorphism could not be considered for susceptibility to GBS. TNF-α and CD1 genetic polymorphism did not affect mortality in GBS.