Diagnostic Approach to Fulminant Hepatitis in the Critical Care Unit
Cheston B. Cunha, Burke A. Cunha in 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.
Other viral infections
Hung N. Winn, Frank A. Chervenak, Roberto Romero in 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).
William Norman Pickles (1885–1969)
Neil Metcalfe in 100 Notable Names from General Practice, 2018
Pickles had an investigative nature and believed that general practitioners had unique opportunities to make valuable observations which other medical practitioners did not. It was James Mackenzie’s (1853–1925) book The Principles of Diagnosis and Treatment in Heart Affections (1918) which convinced Pickles that is was possible for a general practitioner to make important and original observations. In 1927, he attended a correspondence course in London, as he wanted to learn the latest methods of diagnosis and treatments from consultants. He would continue to take refresher courses to help keep his knowledge up to date. This proved useful in October 1928 when an epidemic of jaundice occurred in the Yorkshire Dales. Pickles kept records of all the 118 cases that he and Dunbar saw. By careful documentation and enquiry they were able to find 132 additional sufferers. In many cases, they were able to find the source of the infection and from this information Pickles accurately calculated the incubation period of the disease. Gertrude maintained and organised all of his charts and notes. His findings were published in the BMJ in 1930. Today the disease Pickles and Dunbar had been investigating is known as hepatitis A which is spread via the faecal–oral route. In 1933, Pickles documented an outbreak of epidemic myalgia, also known as Bornholm disease, in Wensleydale. The condition was practically unknown in the United Kingdom until his description of it. It is known today to be caused by Coxsackie B virus. Pickles also wrote important epidemiological descriptions of measles and farmer’s lung, the latter being a hypersensitivity pneumonitis caused by repeated inhaling of dust from mouldy hay.
A comparative analysis of immunogenicity and safety of an enterovirus 71 vaccine between children aged 3-5 years and infants aged 6-35 months
Published in Expert Review of Vaccines, 2018
Wei Gu, Gang Zeng, Yue-mei Hu, Yuan-Sheng Hu, Ying Zhang, Ya-ling Hu, Yang Wang, Jing-Xin Li, Feng-Cai Zhu
Hand, foot, and mouth disease (HFMD) is a highly contagious infectious disease in young children under 5 years of age, commonly caused by enterovirus 71 (EV71) and Coxsackie A virus 16 (CA16) [1,2]. Although most of the HFMD cases were mild or moderate, some severe HFMD cases can progress rapidly and lead to fatal cardiopulmonary and neurologic complications, especially the cases associated with EV71. In recent decades, EV71 infection has accounted for 70% severe HFMD cases and 90% fatal HFMD cases, becoming a serious public health threat and economic burden particularly in the Asian Pacific region [3,4]. In response to the large outbreak of HFMD in 2008 in China, HFMD has been designated as a category C notifiable infectious disease and is required to report in time [5,6]. From 2008 to 2012, 7200,092 probable HFMD cases, of which 267,942 (3.7%) were laboratory confirmed and 2457 (0.03%) were fatal, were reported in China and most were children under 5 years of age, with an average age of 27 months [7]. It is worth nothing that children aged 3–5 years accounted for approximately 30% of HFMD cases [8].
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].
Related Knowledge Centers
- Coxsackievirus
- Cytolysis
- Enterovirus
- Golgi Apparatus
- Picornavirus
- Poliovirus
- Echovirus
- Hand, Foot, & Mouth Disease
- Foot-and-Mouth Disease
- Asymptomatic