A case series of post-infectious chikungunya myeloradiculoneuropathy.

Chikungunya fever is an arboviral illness caused by chikungunya virus (CHIKV) and transmitted by the bite of Aedes aegypti and Aedes albopictus. It is an RNA virus belonging to the genus Alphavirus and family Togaviridae. We present a case series of three patients with chikungunya illness developing para/post-infectious myeloradiculoneuropathy.These patients developed neurological symptoms in the form of bilateral lower limb weakness with sensory and bowel involvement after the recovery from the initial acute episode of chikungunya fever. Clinical examination findings suggested myeloradiculoneuropathy with normal Magnetic Resonance Imaging of the Spine, with the nerve conduction study showing sensorimotor axonal polyneuropathy. All the patients were treated with 1 g of methylprednisolone once a day for five days, and case 2 was given intravenous immunoglobulin also. In the follow-up, cases 1 and 2 showed complete recovery without recurrence, and case 3 did not show improvement at one month.

Case Report: A Case of Complicated Typhoid Fever with Rhabdomyolysis and Hemophagocytic Lymphohistiocytosis.

Typhoid fever can have diverse extra-intestinal complications including encephalitis, Guillain-Barré syndrome, endocarditis, myocarditis, osteomyelitis, renal abscess, and splenic abscesses. Secondary hemophagocytic lymphohistiocytosis with rhabdomyolysis is a rare complication of typhoid fever. Here, we present the case of an adolescent with typhoid fever complicated by rhabdomyolysis and hemophagocytic lymphohistiocytosis.

Occult paraquat poisoning causing pneumomediastinum and organizing pneumonia.

Pneumomediastinum is not an uncommon manifestation of lung toxicity in acute paraquat ingestion. The condition is almost invariably seen with other lung parenchymal abnormalities such as consolidations, ground-glass opacities and interlobular septal thickening. The diagnosis may be challenging in cases with no history of toxin exposure, presentation with a subacute illness and/or absence of typical local or systemic features of paraquat toxicity.

Cerebrospinal fluid adenosine deaminase for the diagnosis of tuberculous meningitis.

Background: A consensus on the diagnostic utility of cerebrospinal fluid adenosine deaminase (ADA) for tuberculous meningitis (TBM) is lacking. Methods: Patients aged ≥12 years admitted with CNS infections were enrolled prospectively. ADA was measured with spectrophotometry. Results: We enrolled 251 TBM and 131 other CNS infections. The optimal cutoff of ADA was calculated at 5.5 U/l against microbiological reference standard with area under curve 0.743, sensitivity 80.7%, specificity 60.3%, positive likelihood ratio 2.03 and negative likelihood ratio 3.12. The widely used cutoff value 10 U/l had specificity 82% and sensitivity 50%. The discriminating power was higher for TBM versus viral meningoencephalitis than bacterial or cryptococcal meningitis. Conclusion: Cerebrospinal fluid ADA has a low-to-modest diagnostic utility.

The diagnosis of tuberculosis (TB) of the brain is mainly made by testing cerebrospinal fluid, a clear liquid that flows in and around the brain and spinal cord. Adenosine deaminase (ADA) is a protein whose production and activity are increased in many diseases, such as TB. ADA testing in cerebrospinal fluid is widely used for the diagnosis of brain TB. However, the experts have split opinions regarding its confirmatory role. This study explores ADA measurement in cerebrospinal fluid for differentiating TB from other brain infections. The report says that this simple and inexpensive test can be helpful, but it cannot make or refute the diagnosis of brain TB and should only be considered along with other tests.

Severe copper sulphate poisoning: A case rescued with plasmapheresis.

Acute copper sulphate poisoning is associated with multi-organ failure and high mortality. Patients typically present with gastrointestinal symptoms, haemolysis, methaemoglobinaemia, acute liver injury, rhabdomyolysis and renal failure. Management is usually supportive, and the role of chelation therapy has not been established. Copper is not dialysable. Plasmapheresis has been shown to remove protein-bound copper, reducing plasma and intracellular concentrations. We present a case of severe copper sulphate poisoning, who did not improve with chelation therapy with D-penicillamine and supportive care, but with therapeutic plasma exchange (four cycles) showed rapid clinical recovery.