ABSTRACT
Neurocysticercosis (NCC), one of the most important neuroparasitic diseases in humans, is caused by Cysticercus cellulosae, the metacestode stage of digenetic zoonotic cestode Taenia solium. The present study aims at the detection of anti-cysticercus antibodies in the sera of epileptic patients (n=26) visiting a tertiary care hospital in Nagpur, Maharashtra state, India, by an in-house developed indirect IgG-ELISA and enzyme-linked immunoelectro transfer blot (EITB) assay using different antigens (namely, Whole Cyst Antigen (WCA), Cystic Fluid Antigen (CFA), Scolex Antigen (SA), Excretory-Secretory Antigen (ESA) and Membrane-Body Antigen (MBA)) prepared from T. solium metacestodes to find out the status of NCC. An attempt has also been made for molecular detection of NCC from blood samples of those patients by Polymerase Chain Reaction (PCR) assay targeted at large subunit rRNA gene of T. solium. The IgG ELISA level of anti-cysticercus antibodies against WCA, CFA, SA, ESA and MBA antigens were as follows: 19.23 %, 23.07 %, 38.46 %, 30.76 % and 15.38 %. The seroreactivity to CFA, SA and ESA was found in equal proportions in patients with ring-enhancing lesions. In the EITB assay, the lower and medium molecular weight protein bands of SA and ESA were immunodominant compared to the higher WCA and CFA peptides. PCR positivity could be observed in 34.6 % (9/26) of the patients under study. It is the first report of detecting NCC among epileptic patients of the Nagpur region of Maharashtra state in India using serological and molecular tools.
ABSTRACT
The sodium channels SNS/PN3 and NaN/SNS2 are regulated by the neurotrophic factors-nerve growth factor (NGF) and glial-derived neurotrophic factor (GDNF), and may play an important role in the development of pain after nerve injury or inflammation. These key molecules have been studied in an amputated causalgic finger and control tissues by immunohistochemistry. There was a marked increase in the number and intensity of SNS/PN3-immunoreactive nerve terminals in the affected finger, while GDNF-immunoreactivity was not observed, in contrast to controls. No differences were observed for NGF, trk A, NT-3 or NaN/SNS2-immunoreactivity. While further studies are required, these findings suggest that accumulation of SNS/PN3 and/or loss of GDNF may contribute to pain in causalgia, and that selective blockers of SNS/PN3 and/or rhGDNF may provide effective novel treatments.
Subject(s)
Causalgia/metabolism , Fingers/physiopathology , Nerve Growth Factors , Nerve Tissue Proteins/deficiency , Neurons, Afferent/metabolism , Neuropeptides/metabolism , Nociceptors/metabolism , Radial Nerve/metabolism , Sodium Channels/metabolism , Aged , Amputation Stumps/pathology , Amputation Stumps/physiopathology , Causalgia/physiopathology , Female , Fingers/innervation , Fingers/surgery , Glial Cell Line-Derived Neurotrophic Factor , Humans , Immunohistochemistry , Mechanoreceptors/metabolism , Mechanoreceptors/pathology , NAV1.8 Voltage-Gated Sodium Channel , Nerve Fibers/metabolism , Nerve Fibers/pathology , Nociceptors/physiopathology , Postoperative Complications/metabolism , Postoperative Complications/physiopathology , Radial Nerve/physiopathologyABSTRACT
BACKGROUND: As human immunodeficiency virus (HIV) infection primarily impairs cellular immunity, the immune responses of HIV-infected individuals to tuberculous bacilli may be inadequate. The features of pulmonary and abdominal tuberculosis evident in HIV-positive (HIV-P) patients with severe immunosuppression are markedly different from those seen in HIV-negative (HIV-N) patients. However, such differences have not been reported in tuberculous meningitis (TBM). Here, we therefore compared the clinical, radiological and pathological features of TBM in patients with and without HIV infection. METHODS AND RESULTS: Twenty-two HIV-P patients with TBM, seen over 5 years, were studied and compared with 31 HIV-N patients with TBM. Although clinical features were similar, cognitive dysfunction was more common amongst the HIV-P group. Pathological features were markedly different in the HIV-P group reflecting severely reduced and atypical inflammatory response, and extensive vasculopathy. This manifested as absence or minimal meningeal enhancement and absence of communicating hydrocephalus on CT scan in HIV-P patients. Mortality was higher within the HIV-P group and depressed levels of consciousness and hemiplegia were associated with poor prognosis. CONCLUSION: The clinical, radiological and pathological features of TBM in HIV-P patients are distinctly different from those without HIV infection; a finding previously unreported.
