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Viral Infections
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Differential diagnosis: This may include herpangina and varicella. In herpangina, another disease caused by a coxsackievirus, there is no viral exanthem, and oral lesions are primarily located in the posterior oropharynx. For varicella, the spread of the lesions is distinct from HMFD and is concentrated on the trunk and extremities with various stages of exanthem and vesicles that quickly crust over.
Enterovirus
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Herpangina is a febrile illness of infants and children associated with coxsackievirus A and other enteroviruses. It is characterized by sudden onset of fever with sore throat, headache, anorexia, neck pain, and vomiting, followed by oropharyngeal mucosal vesicular and ulcerative lesions, which usually heal without complications in about 7 days.
Section 5
Published in Padmanabhan Ramnarayan, MCQs in Paediatrics for the MRCPCH, Part 1, 2017
Herpangina is an infection of the fauces and pharynx, presenting with ulcération. Dermatitis herpetiformis is an immune-mediated skin condition, with no relation to herpes virus. It is treated with dapsone. Epidemic pleurodynia or Bornholm disease is an infection caused by coxsackie viruses, characterised by severe pleuritic pain in the chest.
An Atypical Case of Enterovirus Meningitis Presenting with Unilateral Optic Disc Swelling and Minimal Optical Symptoms
Published in Ocular Immunology and Inflammation, 2023
Efthymios Karmiris, Georgios Vasilakos, Konstantinos Tsiripidis, Evangelia Chalkiadaki
Enteroviruses constitute a genus of the picornavirus family which includes poliovirus, coxsackievirus and human enterovirus A, B, C and D.10 The non-polio human enteroviruses, which are transmitted via the fecal–oral route of infection, may completely shut down host translational machinery causing CNS dysfunction following infection, due to cytopathic effects.9 They can cause a broad spectrum of illnesses such as febrile disease, hand-foot-mouth, herpangina, aseptic meningitis, encephalitis, pancreatitis, chronic inflammatory myopathy, myocarditis and neonatal sepsis.9,10 Their clinical presentation may be varied, and symptoms such as fever, headache, neck stiffness, altered consciousness, seizures, and focal neurological findings often overlap various infectious agents.11 In uncomplicated viral meningitis, the clinical course is usually self-limited, with complete recovery in 7–10 days and no proven treatments.7 However enteroviruses have been linked to autoimmune-like diseases, including diabetes, chronic inflammatory myopathy and chronic myocarditis, perhaps in part due to the long-term presence of viral RNA potentially causing lasting neuropathology.10
Recent development of enterovirus A vaccine candidates for the prevention of hand, foot, and mouth disease
Published in Expert Review of Vaccines, 2018
Since 1998, outbreaks of enterovirus A infection have been reported and the most identified pathogens are EV-A71, CV-A16, CV-A6, and CV-A10 [4,5,12]. EV-A71 was first isolated from California, USA, in 1969 [13,14,19]. Several outbreaks of EV-A71-associated HFMD have been reported in Taiwan, Japan, Korea, Singapore, Vietnam, Thailand, Malaysia, India, China, Australia, France, Hungary, Spain, and the United Kingdom. CV-A16 was first isolated from South Africa in 1951 [13,19]. Although usually mild, CV-A16 infections can also lead to severe herpangina, major neurological complications, and fatal outcomes [20]. Several outbreaks of CV-A16-associated HFMD have also been reported in countries including Taiwan, Japan, Korea, Singapore, Vietnam, Thailand, Malaysia, India, China, Australia, and the United Kingdom [13,20]. The outbreaks of CV-A16 often co-circulate with EV-A71 [4,20,21].
Kingella kingae: from oropharyngeal carriage to paediatric osteoarticular infections
Published in Expert Review of Anti-infective Therapy, 2018
Raimonda Valaikaite, Nawal El Houmami, Vasiliki Spyropoulou, Gabriel Braendle, Dimitri Ceroni
The risk of young carriers to develop an OAI caused by K. kingae was calculated to be <1% per year [16], with no difference in the oropharyngeal bacterial load observed between healthy carriers and ill children [17]. Concomitant oropharyngeal viral infections caused by human rhinovirus, herpes virus simplex, or hand-foot-mouth disease/herpangina virus are commonly identified in children with K. kingae disease [18,19]. Damages to the mucosal layer caused by these viral agents are believed to trigger K. kingae invasive disease by facilitating the bacterial spread into the bloodstream and dissemination to distant sites [2]. Septic arthritis, osteomyelitis, and tenosynovitis represent the commonest manifestations of K. kingae disease [2]. While septic arthritis involving the knees and hips predominate, the bacterium presents also a peculiar affinity for uncommon anatomic sites such small joints and bones from the hand and wrist, foot and ankle, spine, or areas that are rich in growth plate cartilage such as epiphysis of long bones.