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Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Infectious or postinfectious SSPE.Arbovirus encephalitis.Herpes simplex encephalitis.Human T-lymphotropic virus 1.Whipple's disease.West Nile virus encephalitis.Postinfectious encephalopathy.Progressive multifocal leukoencephalopathy.
Contaminated blood
Published in Mélinée Kazarian, Criminalising Medical Malpractice, 2020
From March 1983, scientists worldwide were aware that there was a risk of HIV infection through sexual contact.73 The first reports of AIDS cases in PWH were found in the Annals of Internal Medicine in March 1983.74 At that time, 10 cases of AIDS had already been reported in France, and 6 cases had been reported in the UK.75 Very soon after, in April 1983, the risk of contamination in FCs was being discussed in the scientific world.76 By the end of July 1983, 14 cases of AIDS were reported to the Communicable Disease Surveillance Centre in England, of which one case was a PWH who had received FVIII imported from the US.77 In August 1983, a British Medical Journal article was reporting that ‘the risk from blood products, imported into Britain seems at present very small’.78 In England and Wales, in the summer of 1983, the transmission of AIDS through blood was reported in medical and scientific journals.79Human T-lymphotropic virus III (HTLV-III) was officially recognised as the virus causing AIDS in 1984.80Lymphadenopathy associated virus (LAV)/HTLV-III was later renamed HIV.
Prostaglandins and Semen
Published in Murray D. Mitchell, Eicosanoids in Reproduction, 2020
Further work from this group has demonstrated that an in vitro culture of a T-cell line (MT-4) infected with type III human T-lymphotropic virus produced 2.5 times more virus than control groups when 5 μm (1.7 μg/ml) PGE2 was added.85 Such a concentration is well below the concentration found in normal human semen.
Escherichia coli: a rare cause of meningitis in immuno-competent adult
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Maryam Zafar, Abubakar Tauseef, Muhammad Sohaib Asghar, Narmin Khan, Nabeeha Farooqui, Mustafa Dawood, Tanvir Alam, Durre Naman
The incidence of idiopathic community-acquired Escherichia Coli (E-Coli) meningitis in immune-competent adults is rare across the globe and a total of forty-five cases have been reported so far since 1945, making an average of less than one case per year [1]. The risk factors identified to develop E-Coli meningitis include diabetes mellitus, alcoholism, cirrhosis, HIV infection, Chronic Obstructive Pulmonary Disease (COPD), chronic organ dysfunction in decreasing order of their associations [2,4]. Rarely, it is associated with human T-lymphotropic virus 1(HTLV-1), Marfan Syndrome, Hemochromatosis, myelodysplasia, and B-cell lymphoma. Previously, reports have shown that the source of its spread is from blood, urine, joint aspirate and ascitic fluid [2,4]. Retropharyngeal abscess [3,4] and neurosurgical intervention were also found to be the route of the entrance of E-Coli in few cases [4,5]. In 40% of the cases, the cause or source of its spread remained unknown as was shown in our patient [2]. E-Coli meningitis was found to be a disease in immunocompromised patients and the elderly age group [3]. E-coli being the most common pathogen in causing meningitis among the neonatal age group [6], It is one of the rare causes of meningitis in immune-competent adults as was seen in our patient.
Exploring the interplay between autoimmunity and cancer to find the target therapeutic hotspots
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Neeraj Kumar, Heerak Chugh, Ravi Tomar, Vartika Tomar, Vimal Kishor Singh, Ramesh Chandra
Certain lymphomas transformations are reported to have a consistent pattern of significant positive association with viral infections due to human herpes virus 8, human T-lymphotropic virus type I. Conditions can get more severe due to infection with Plasmodium falciparum, Campylobacter jejuni, and with certain hepatitis virus like HBV, HCV. These infections can further cause autoimmune disorders which cause chronic immune stimulation that can lead to defective apoptotic mechanisms towards B-cells and hence cause lymphoma [31]. Viruses that can cause lymphocyte infection are evidently associated with lymphoproliferative disorders and hence cause severe consequences like lymphomagenesis [32]. Hence, it can be concluded that chronic infections, chronic inflammations and lymphomas are some severe consequences of autoimmune diseases [33,34].
Two cases of annular erythema without bullous lesions by autoimmune blistering diseases
Published in Modern Rheumatology, 2018
Miho Kabuto, Noriki Fujimoto, Toshihiro Tanaka
An 80-year-old Japanese male visited our hospital in 2014. He had noticed multiple annular erythemas on his trunk and upper arms one month before, which repeatedly improved and relapsed spontaneously. Physical findings demonstrated multiple annular indurated erythemas with slight pruritus on his trunk and extremities (Figure 1d). No bullous or mucosal lesion was observed. Histopathological findings of a cutaneous biopsy specimen from the annular erythema on the abdomen revealed only perivascular lymphocytic infiltration (Figure 1e). Laboratory examinations showed that the number of eosinophils increased (6.8 × 104 μl−1). Anti-human T-lymphotropic Virus-1 antibody and ANA were not detected. Autoantibodies against BP180-NC16A were detected with high titer (356 U/ml), and no other autoantibodies against SS-A/Ro and SS-B/La were detected using ELISA. Direct IF examination demonstrated linear deposition of IgG (Figure 1f) and C3 on the BMZ. Indirect IF using 1 M NaCl-split skin examination showed a deposition on the epidermal side of BMZ. Based on these findings, we diagnosed the patient with bullous pemphigoid. Since clinically no bullae were found, we initiated treatment with topical corticosteroids. Multiple annular erythemas gradually disappeared, and autoantibodies against BP180-NC16A decreased to 152 U/ml six months later. Although the eruptions are not completely improved, no bullae have been observed for nine months.