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Other viral infections
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Less is known about neonatal infection with coxsackie A virus. There are case reports of in utero fetal death with disseminated coxsackie A virus. It is rare for coxsackie A virus to be passed to the fetus (42). There appears to be no association between echovirus or coxsackie B virus infection and an increased spontaneous abortion rate. Stillbirth in late pregnancy increases with both maternal echovirus and coxsackie B viral infection. The association between maternal coxsackie B virus infection and a slightly greater risk of fetal urogenital defects and congenital heart defects is tenuous (39,41). Coxsackie B virus, particularly serotypes B3 and B4, has been implicated in neonatal myocarditis (43).
Mouth, tongue, lips and ears
Published in Richard Ashton, Barbara Leppard, Differential Diagnosis in Dermatology, 2021
Richard Ashton, Barbara Leppard
This mild infection is due to Coxsackie A16 virus. Round erosions with a red margin are seen in the mouth. They look like small aphthous ulcers but are associated with small grey blisters with a red halo on the fingers and toes (seeFig. 13.03, p. 299). The condition gets better spontaneously in a few days.
Diagnostic Approach to Fulminant Hepatitis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Coxsackie B virus (COX B) belongs to a family of RNA viruses, Picornaviridae, that infects the heart, pleura, pancreas, and liver of early infancy, causing pleurodynia, myocarditis, pericarditis, and hepatitis. Coxsackie hepatitis is frequently associated with myocarditis [37]. The ALF develops as part of a disseminated viral infection, where fever, jaundice, and petechiae are the most consistent findings on admission. A biphasic fever pattern has also been reported. Jaundice and coagulopathy are poor prognostic indicators. Laboratory abnormalities include anemia, thrombocytopenia, prolongation of PT and activated thromboplastin time, marked transaminases elevation (AST > ALT), and elevated fibrin degradation product levels [38]. Diagnosis can be made by serological paired complement fixation antibody (IgG and IgM) titers for COX B, with at least a fourfold rise in titer between acute and convalescent phased [37]. The RT-PCR is diagnostic of infection, and cell cultures are useful when isolate serotyping is important. There is no specific therapy for COX B, and treatment includes fluids and supportive care.
Prediction, diagnosis, prevention and treatment: genetic-led care of patients with diabetes
Published in Expert Review of Precision Medicine and Drug Development, 2021
Watip Tangjittipokin, Nutsakol Borrisut, Patcharapong Rujirawan
Not all individuals with high-risk haplotypes develop T1DM. The majority of people with these haplotypes do not. The development of T1DM is likely partly influenced by environmental factors that play a role in triggering autoimmunity. A previous study reported that the development of autoantibodies against islet cells in high-risk individuals often occurs between 9 months to 2 years of age [18]. Viral infection is one of the most studied triggers of T1DM. Many viral infections are associated with T1DM development, including enteroviruses, such as Coxsackie B virus, cytomegalovirus, rubella virus, and rotavirus [19]. The mechanism by which enteroviruses induce autoimmunity remains unclear. However, it was proposed that the enteroviral P2-C protein sequence is similar to glutamic decarboxylase (GAD) in islet cells, and after infection, antibodies can cross-react with islet cells leading to islet cell destruction. Another study proposed that viral induction of T1DM might be due to molecular mimicry [20]. Other factors that continue to be explored are vitamin D deficiency, breastfeeding, milk formula, maternal age, preeclampsia, and childhood obesity.
Recent advances in the understanding of enterovirus A71 infection: a focus on neuropathogenesis
Published in Expert Review of Anti-infective Therapy, 2021
Han Kang Tee, Mohd Izwan Zainol, I-Ching Sam, Yoke Fun Chan
Unlike other receptors of EV-A71, HS has been previously reported to modulate neurotropism and neurovirulence in many viruses (Table 1). Overall, the mechanism of rapid virus clearance of HS-binding viruses leading to lower virus virulence has been supported by experiments in other viruses such as yellow fever virus, Japanese encephalitis virus, Murray valley encephalitis virus, West Nile virus, tick-borne encephalitis virus, Venezuelan equine encephalitis virus, coxsackie B3 virus, and dengue virus. In contrast, HS-binding viruses were associated with higher mortality in mice in Sindbis virus, Semliki Forest virus and eastern equine encephalitis virus (EEEV). Strong HS-binding EEEV antagonizes immune responses by inducing lower cytokines production, enabling higher virus replication leading to neurovirulence [131]. Interesti-ngly, EEEV with a strong HS-binding phenotype also showed higher neurovirulence in a mouse model when inoculated directly into the CNS but not by intraperitoneal injection suggesting an additional immune barrier exists during systemic infection. We have also provided a hypothesized model of EV-A71 heparin-dependent pathogenesis in humans whereby non-HS strains are associated with neurovirulence [66].
Immunosuppression in the Management of Presumed Non-infective Uveitis; Are We Sure What We are Treating? Notes on the Antimicrobial Properties of the Systemic Immunosuppressants
Published in Ocular Immunology and Inflammation, 2020
The first demonstrations of the antiviral activity of MPA took place in the 1960s, where initially it was found to have in vitro effect against Vaccinia virus, Measles virus, HSV and Newcastle disease virus.49 In vivo activity against these viruses in a mouse model was not shown, but activity against some oncogenic viruses was shown. Similarly in a chick embryo model, MPA was highly active against HSV and Vaccinia.50 Since these early demonstrations, a wider antiviral spectrum has been demonstrated: activity against a variety of orthopoxviruses including Camelpox virus, Cowpox virus, Monkeypox virus, and Vaccinia virus was shown in 2001 in a Vervet monkey renal model.51 Mycophenolate prevents Coxsackie-B3 virus-induced myocarditis in mice.52 It also inhibits the orthobunyaviruses which can cause human encephalitis.53 It is an inhibitor of HCV and is synergistic against it with both ciclosporin and interferon-α.54 It also may be synergistic with aciclovir in the prevention of herpetic keratitis recurrence following corneal graft.55