Background: Diagnosing the etiology of travel-associated febrile illness can be challenging due to the wide range of potential causes and the diverse geographic locations travelers may visit. Several factors contribute to this complexity including diverse pathogens, incubation period, multiple exposures, vector-borne diseases, immunization status, local outbreaks, and uncommon pathogens. The present study aimed to explore the characteristics and etiology of fever in returned travelers. Methods: A prospective observational study was carried out over one year which included patients presenting with fever, who had a recent travel history of not less than 1 week. Each patient was enquired regarding their basic demographics, comorbidities, etiology, symptoms on presentation, days of fever, and travel-related details. Patient-reported risk factors were noted. Results were statistically analyzed. Results: The study included 63 returned travelers who reported fever. The majority of the presentation was from the age group of 19–35 years, with the most common etiology being malaria (14.29%), followed by scrub typhus (9.52%) and typhoid (7.94%). While there were 6.34% cases of intercountry travel, 34.92% were cases of interstate travel and the rest were within the state. Average days of fever and symptom presentation widely varied with etiologies. Symptoms included rash, headache, hepatomegaly, anemia, chest abnormalities, leukocytosis, leucopenia, thrombocytopenia, hyperbilirubinemia, and transaminitis. Conclusion: It is important on the part of clinicians, especially, tropical medicine specialists to formulate pretravel consultation guidance and immunization strategies. Prompt evaluation and management of febrile illness among returned travelers is warranted.

Background: Apart from the traditional risk factors associated with stroke, several newer independent risk markers that are promising targets for modification, such as hyperhomocysteinemia, and elevated high-sensitive C-reactive protein (hs-CRP), may contribute significantly to the stroke risk. The role of elevated levels of inflammatory markers in predicting prognosis after a first ischemic stroke has been a gray area. The present study aimed to assess the clinical outcome of acute ischemic stroke patients in particular relation to hs-CRP and homocysteine (Hcy) levels within 48 hours of presentation. Methods: A prospective, observational study was carried out among admitted and diagnosed patients with acute ischemic stroke confirmed by CT/MRI scans where included patients were subjected to detailed history taking using pretested and predesigned pro forma along with thorough clinical examination using CT scan brain (non-contrast)/MRI brain. High-sensitive C-reactive protein and Hcy levels and other blood parameters were done within 48 hrs of hospital admission. Patients were scored based on the National Institute of Health Stroke Scale (NIHSS) at specified time points to assess the clinical outcome. Results were statistically analyzed. Results: Patients of cerebral infarction with elevated hs-CRP had a lower improvement score in contrast to those with non-elevated hs-CRP, who had a higher improvement. Also, patients with an elevated Hcy level had a lower mean improvement score at day 30 compared to those with normal Hcy levels. With the increasing size of the infarct, there was a lower improvement score. The higher the admission NIHSS score, the lower the improvement score in the study. High-sensitive C-reactive protein proved to be the strongest predictor for score improvement with other predictor variables like infarct size, NIHSS baseline score and Hcys also showing positive association. Conclusion: High-sensitive C-reactive protein alone comes out as the strongest predictor for the improvement in NIHSS score from the time of admission to a 30-day progress period with a prediction power of 98%.

Background: The mediastinum is known to be a space within the domain of the thorax housing the important organs, blood vessels, nerves, lymphatics along with the surrounding connective tissue, where the International Thymic Malignancy Interest Group (ITMIG) classification system based on cross sections derived by the CT into prevascular mediastinum, visceral mediastinum and paravertebral mediastinum. The diagnosis of mediastinal neoplasia and it is necessary treatment often becomes challenging owing to the complex anatomy. With the advancement in cross-sectional imaging using CT scan with or without contrasts, diffusion weighted and chemical shift MR imaging, FDG-PET scan, guided biopsies with microscopic examination aided by special stains, the diagnosis of such become unconstrained. Materials and methods: In our aim to focus on the clinico-pathology locus, diagnosis and treatment of mediastinal neoplasia, we perform a retrospective study in a tertiary care hospital spanning from January 2020 to December 2022, for a period of 3 years in the CTVS Department (IPGMER and SSKM) Hospital, with the number being 42 who had mediastinal masses and they were characterized using the age, gender, clinical stigmata, and were subjected to cross-sectional imaging of the thorax, guided biopsies, histopathological examination, targeted treatment using surgery or the standard therapeutic approach. Result: Statistical analysis was done using the software SPSS version 20/21, revealing 28 males and 14 females (M:F = 2:1) 28.57% patients for hydatid cyst, 26.19% patients of thymoma, 7% patients for thymic malignancy, 11.90% of patients for lymphoma, 14.28% for pleuropericardial cyst, 9.52% for dermoid, and 2.38% for teratomas. The follow-up period ranged from 1 to 5 years and the mean follow-up was 2.33 ± 1.28 (Mean ± SD). lesions were mostly found in the anterior compartment of the mediastinum (20%) with thymoma being the commonest followed by hydatid, pleuropericardial cysts, dermoid and the lymphoma. Conclusion: Since they are deemed to be slow growing and gradually would compress the great vessels, heart, spinal cord, vocal cords, stellate ganglion, brachial plexus, superior vena cava, or the diaphragm to explain the symptomology, we have generously discussed and documented the atypical lesions too which must be taken as the differential diagnosis namely atypical lesions namely retrosternal goiters invading the mediastinum, Langerhans cell histiocytosis, mesothelioma, squamous cell carcinoma, adenocarcinomatous lesion, pleomorphic sarcomas, melanomas, primary pleural liposarcoma, malignant epithelioid gastro intestinal stromal tumors, and even solitary fibrous tumors. To sum up, specific radiology with the needle diagnosis and targeted treatment would henceforth be a logical approach to aim a better patient care.

Antimicrobial resistance (AMR) poses a complex and interconnected global challenge affecting human health, animal health, and the environment. This comprehensive review explores the multifaceted dimensions of AMR and highlights the pivotal role of the One Health approach in addressing this pressing issue. The discussion emphasizes evidence-based strategies, integrated surveillance, and effective communication to inform decision-making and policy formulation. Furthermore, the economic implications of AMR and the need for a paradigm shift toward holistic One Health models are examined. The World Health Organization's (WHO) Global Action Plan and stakeholder engagement across various sectors are emphasized as critical components of AMR control. The review also delves into the importance of research and surveillance in understanding AMR drivers and developing alternatives to antibiotics. Promising approaches, such as microbiota modulation, gene editing, vaccines, antivirulence inhibitors, and bacteriophages, are explored as innovative means to combat AMR. Overall, this review underscores the urgency of a coordinated, multidisciplinary One Health approach in mitigating the global threat of AMR.

Poisoning by pesticides is the major public health problem in low-income and middle-income countries, and it is responsible for almost 20% of global suicides in the last decade. Paraquat (PQ) is a toxic bipyridyl compound commonly used in agriculture and it has potential ill-effects with high fatality if ingested even in very small amounts. The mode of poisoning is usually suicidal or accidental. Paraquat poisoning is still a nuisance faced in the rural and semiurban areas, attributable to wide availability and easy access to the poison as well lack of knowledge among the common people regarding its life-threatening effects. Paraquat is partially absorbed from the gastrointestinal tract and the toxic effects are mainly mediated by the production of reactive oxygen species (ROS) causing cell damage. It acts as a corrosive and erodes the gastrointestinal tract but majority of deaths occur due to acute lung injury (ALI). Renal failure and consequent multiorgan dysfunction are also common. The mainstay of management is supportive with paucity of human data on role of antioxidants and immunosuppressives. This review gives a comprehensive outlook on PQ poisoning, the probable mechanisms, available treatment options, and plausible recommendations while managing PQ toxicity.

Background: Vitamin B12 deficiency is widely known for its hematological and neurological manifestations. Neuropsychiatric manifestations of vitamin B12 deficiency include dementia, delirium, cerebellar ataxia, psychosis, neuropathy, and mood disorders. Dementia caused by vitamin B12 deficiency may not be accompanied by anemia and it may be the sole manifestation of cobalamin deficiency. Case description: A 70-year-old woman, premorbid normal, presented with rapidly progressive cognitive impairment over a period of 7 months in the form of short-term and episodic memory disturbances, decreased interaction, withdrawn behavior, apathy, wayfinding difficulties, and sleep disturbances. Neurologic examination revealed a mini-mental state examination (MMSE) score of 9/30. Tests for attention and sustained attention were impaired. Speech and language examination revealed reduced word output and impaired animal naming. Both immediate and recent memory was impaired. Lobar examination revealed frontal and temporal involvement. The patient's initial laboratory investigations indicated mildly decreased hemoglobin (10.2 gm/dL) and normal MCV - 98 fL. There were very low levels of vitamin B12 (116 pg/mL). Magnetic resonance imaging (MRI) of the brain showed age-related cortical atrophy. The patient was treated with parenteral methylcobalamin initially then switched to oral cobalamin. After a period of 3 months of treatment, MMSE was reassessed and was 16/30. She was fully oriented and had significant improvement in her memory and behavior. Conclusion: The role of vitamin B12 deficiency as one of the few treatable causes of dementia, however, is still controversial. The purpose of this case report is to show that if vitamin B12 deficiency remains undiagnosed, serious sequelae may occur. Assessment of B12 levels should be included as a standard evaluation in patients presenting with dementia. Therefore, prevention, early detection, and management of this reversible state are of profound importance.

Clinical features of cerebral venous sinus thrombosis commonly include headache, early and late seizures, and focal deficits. Cranial nerve (CN) involvement primarily includes the ocular motor nerves. Very few cases have been reported with isolated facial nerve involvement. Our case highlights a rare atypical clinical presentation of cerebral venous thrombosis (CVT). Facial nerve palsy in cerebral and cortical vein thrombosis is rare with an unclear pathophysiology and is rarely reported. We report a case of a 44-year-old male, a chronic alcoholic admitted with complaints of severe headache and raised intracranial pressure (ICP) features. He developed left-sided facial nerve palsy with impaired taste perception on the left side. Magnetic resonance imaging (MRI) of the brain and venography showed evidence of a late subacute stage of occlusion in the superior sagittal sinus, straight sinus, right transverse, and right internal jugular vein (IJV) with features of intracranial hypertension. Facial palsy in our patient is considered to be due to transient neuropraxia in the intracranial segment of the nerve. This case highlights facial palsy as a rare clinical presentation of cerebral venous thrombosis.

Introduction: Muscle-specific tyrosine kinase (MuSK) myasthenia gravis (MG) is a severe, subtype of MG with different pathogenesis, atypical clinical features, lack of symptom fluctuations, and acetylcholinesterase inhibitors failure making MuSK-MG diagnosis challenging. Such patients may suffer a worsening of symptoms upon exposure to a variety of medications such as fluoroquinolones. Fluoroquinolones of any generation may interfere with neuromuscular transmission and may lead to MG symptoms by simply unmasking a pre-existing mild case. This case report describes the development of myasthenic crisis and respiratory distress following the use of levofloxacin in a patient who was initially diagnosed as tuberculous meningitis with no previous diagnosis of MG. Case description: A 24-year-old woman presented with 1 month history of low-grade fever and headache without any raised intracranial pressure features or neck stiffness. All her routine laboratory investigations and brain imaging were normal. Cerebrospinal fluid analysis showed normal protein and sugar levels, zero cell count with mild cartridge-based nucleic acid amplification test (CB-NAAT) positivity for mycobacterium tuberculosis. She was started on routine anti-tubercular therapy (ATT) initially, later changed to modified ATT with levofloxacin, rifampicin, and ethambutol in view of deranged liver function tests. One month later, she returned with complaints of double vision, drooping of eyelids, unsteadiness while walking, dysphagia to solids and liquids, and shortness of breath. On examination, patient had bilateral ptosis and restricted extraocular movements in all directions. Curtain sign was present. Single breath count was eight. As the patient's clinical condition worsened despite adequate ATT regimen and in view of mild CB-NAAT positivity, evaluation for alternate diagnosis was considered. Ice pack test and neostigmine challenge test were done and both were positive. Repetitive nerve stimulation (RNS) showed more than 10% decremental response in facial and limb muscles. Acetylcholine receptor and MuSK antibody tests were sent. A working diagnosis of MG with myasthenic crisis was made and patient was started on intravenous immunoglobulin (IVIG) at a dose of 2 gm/kg for 5 days and oral pyridostigmine. Antibody testing came positive for anti-MuSK antibody. As the patient did not show any improvement to IVIG, she was given injection rituximab 1 gm and simultaneously started on mycophenolate mofetil. Even with rituximab, patient did not show adequate response, so she was taken up for plasma exchange with which her symptoms improved dramatically and was continued on mycophenolate mofetil. Conclusion: Muscle-specific tyrosine kinase-MG is a subtype of MG with atypical clinical presentations causing a delay in diagnosis. In such cases MuSK-Ab testing confirms the diagnosis. Fluoroquinolone exposure may result in potentially life-threatening myasthenia gravis in patients with underlying disease. Our case shows that levofloxacin can unmask MuSK-MG, which has not been much reported in the literature. Response to acetylcholinesterase inhibitors is often unsatisfactory from that expected in MG patients. Among all immunotherapies, plasma exchange can be considered as the cornerstone of treatment for MuSK-MG which was evident in our case where inadequate response was showed to IVIG and rituximab.

The relation between pulmonary embolism and hypercoagulable state has been a debate in medical literature. There have been articles describing role of hyperhomocysteinemia in vascular injuries leading to prothrombotic state. We herein present a case of unprovoked sub-massive pulmonary thromboembolism secondary to hyperhomocysteinemia due to hypovitaminosis B12. The patient was investigated thoroughly and was managed with proper anticoagulants.