RT-PCR is considered to be the standard gold diagnostic test for detecting COVID-19 causing SARS-CoV-2. Recent reports and recent pieces of evidence from scientific literature, however, tell a different story. There have been speculations of SARS-CoV-2 escaping the RT-PCR because of the series of mutations it has gone through. It is possible that host-dependent RNA editing and high person-to-person transmission have equipped the virus with mutations enabling it to spread faster and even evade the RT-PCR. Added to this is burnout among healthcare workers and technicians handling the RT-PCR machines and sampling. All of these factors may be working in unison to result in the deluge of false-negative cases India is facing during the second COVID-19 wave. The mutant strains are spreading to other parts, posing challenges to the whole world. These circumstances warrant supplementary diagnostic tests such as serological and radiological findings to deal with cases of high clinical suspicion. Even one misdiagnosed COVID-19 patient poses a risk to hundreds of others in the vicinity. Healthcare workers’ burnout also has to be dealt with. Erroneous staff should be re-trained.

Zika virus is an RNA virus belonging to the Flavivirus family that is chiefly transmitted by the female Aedes mosquito. The Zika virus first infected humans in Uganda and Tanzania in 1952. Since, it has spread to several parts of the world causing outbreaks of variable extent. In India, these outbreaks have been reported from Gujarat, Tamil Nadu, Madhya Pradesh, Rajasthan, Kerala, and Maharashtra. The most recent outbreak is from the most populous state of India, Uttar Pradesh, where the climate is conducive to the breeding and transmission of other arboviral infections such as Dengue, Chikungunya, and Malaria. These infections also happen to share similar incubation periods and overlapping clinical manifestations with Zika virus (ZIKV) infection, leading to misdiagnoses or delayed diagnosis. We aim to provide an account of the outbreak, its repercussions, errors made in attempting to contain the spread of the disease, and, measures to be taken in the future.

Antisynthetase syndrome is an autoimmune condition that manifests clinically through signs and symptoms, such as interstitial lung disease, myositis, Raynaud’s phenomenon, fever, hyperkeratotic fingertips (mechanic’s hands), and arthritis. It is associated with antibodies against aminoacyl tRNA synthetase enzyme, the most common autoantibody being the anti-Jo-1. An 18-year-old girl presented with weakness of both the upper and lower limb, swelling and generalized body pain, difficulty in swallowing. MRI of the thigh was highly suggestive of myositis with symmetrical bilateral involvement. Based on proximal muscle weakness, elevated creatine phosphokinase (CPK), and lactate dehydrogenase (LDH), strongly positive anti-nuclear antibodies human epithelial cell type-2 (ANA-HEp2), and a normal nerve conduction velocity test with precise MRI findings, a diagnosis of polymyositis was made. She was given bolus intravenous methylprednisolone for five days, followed by oral methylprednisolone with subcutaneous methotrexate weekly. She reported a 50% improvement in muscle weakness; however, partial bulbar weakness persisted at the time of discharge. On her next follow-up, her blood investigations for auto-antibodies were done. The autoantibodies anti-Jo-1 (3+), Ro-52 (2+), and Mi-2β (2+) were found to be positive. These investigations, coupled with the clinical features she was presenting, finally led us to conclude that it was a case of polymyositis complicated by the antisynthetase syndrome.

Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease that can affect almost every organ in the body. Its complications can often be fatal. The fatal complications include lupus cerebritis, lupus nephritis, and cardiac manifestations such as pericardial effusion. In this report, we discuss the case of a 23-year-old female who presented with complaints of high-grade fever, seizures, and altered mental state (AMS) and was found to have generalized lymphadenopathy (LAP). Various blood and urine analyses and radiological findings (chest X-ray, MRI of the head) were suggestive of lupus nephritis, lupus cerebritis, massive pericardial effusion, and thrombocytopenia. Her anti-double stranded DNA (anti-dsDNA) antibody was positive, and her pericardial fluid was positive for anti-nuclear antibodies (ANAs). She was administered IV glucocorticoids and phenytoin. She reported improvements in her symptoms gradually for a few days but eventually succumbed to the disease. Although generalized LAP is a rare initial presentation of SLE, it should be included in the differential diagnosis of the disease.