Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6

2014 ◽  
Vol 14 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Henry M Feder ◽  
Nicholas Bennett ◽  
John F Modlin
Keyword(s):  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Foot And Mouth

scholarly journals A Clustering Outbreak of Hand, Foot, and Mouth Disease Caused by Coxsackie Virus A10

1983 ◽  
Vol 27 (11) ◽  
pp. 929-935 ◽  
Author(s):  
Asao Itagaki ◽  
Junko Ishihara ◽  
Kyo Mochida ◽  
Yoshihiro Ito ◽  
Koichi Saito ◽  
...  
Keyword(s):  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Foot And Mouth

scholarly journals Epidemiological Study of Hand, Foot and Mouth Disease in Al-Kindy Teaching Hospital/ Baghdad

2019 ◽  
Vol 14 (2) ◽  
pp. 84-88
Author(s):  
Suha N. Al-Wakeel ◽  
Khansa A. Al Rubiae ◽  
Suha N. Al-Wakeel ◽  
Basil M. Hanoudi
Keyword(s):  
Clinical Features ◽  
Teaching Hospital ◽  
Specific Treatment ◽  
Foot And Mouth Disease ◽  
Viral Disease ◽  
Skin Lesions ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Cross Sectional ◽  
Foot And Mouth

Background: Hand, foot, and mouth disease is viral disease caused commonly by coxsackie virus A16 virus. It is a mild disease and children usually recover with no specific treatment within 7 to 10 days. Rarely, this illness may be associated with aseptic meningitis were patient may need hospitalization. Objective: To determine significance of clinical features of hand, foot and mouth disease. Methods: A cross sectional study of cases with clinical features of hand, foot and mouth disease visiting the dermatological consultation unit of Al Kindy teaching hospital. Sampling was for Zyona and Edressi Quarter patients over the period of 1st December 2017 to 30th of November 2017. Aim: To determine significance of clinical features of hand, foot and mouth disease Results: The mean age of patients (100 patients) was 29.99 months. Males were 65 (65%) and females were 35 (35%), (P 0.23). Tenderness of skin lesions, Malaise and decreased Appetite were the most frequent symptoms. Winter months illness was common .Cases were diagnosed two days before seeking medical help, while home contact of patients was most common place for infection transmission .Involvement of palms and soles was universal and indifferent (100%). Groin was more commonly affected (67%), (P 0.015). Fever was present in 81%.

scholarly journals Hand, Foot and Mouth Disease (HFMD): An Update

2017 ◽  
Vol 40 (2) ◽  
pp. 115-119 ◽  
Author(s):  
Probir Kumar Sarkar ◽  
Nital Kumar Sarker ◽  
Md Abu Tayab
Keyword(s):  
Enterovirus 71 ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Asia Pacific ◽  
Human Enterovirus ◽  
Small Scale ◽  
Human Enterovirus 71 ◽  
Mild Disease ◽  
Foot And Mouth

Hand, foot, and mouth disease (HFMD) also known as vesicular stomatitis with exanthema, first reported in New Zealand in 1957 is caused by Coxsackie virus A16 (CVA16), human enterovirus 71 (HEV71) and occasionally by other HEV-A serotypes, such as Coxsackie virus A6 and Coxsackie virus A10, are also associated with HFMD and herpangina. While all these viruses can cause mild disease in children, EV71 has been associated with neurological disease and mortality in large outbreaks in the Asia Pacific region over the last decade. It is highly contagious and is spread through direct contact with the mucus, saliva, or feces of an infected person. This is characterized by erythrematous papulo vesicular eruptions over hand, feet, perioral area, knee, buttocks and also intra-orally mostly in children, typically occurs in small epidemics usually during the summer and autumn months. HFMD symptoms are usually mild and resolve on their own in 7 to 10 days. Treatment is symptomatic but good hygiene during and after infection is very important in preventing the spread of the disease. Though only small scale outbreaks have been reported from United States, Europe, Australia Japan and Brazil for the first few decade, since 1997 the disease has conspicuously changed its behavior as noted in different Southeast Asian countries. There was sharp rise in incidence, severity, complications and even fatal outcomes that were almost unseen before that period. There are reports of disease activity in different corners of India since 2004, and the largest outbreak of HFMD occurred in eastern part of India in and around Kolkata in 2007and Bhubaneswar, Odisha in 2009. In recent years there are cases of HFMD have been seen in Bangladesh also. Although of milder degree, continuous progress to affect larger parts of the neighboring may indicate vulnerability of Bangladesh from possible future outbreaks.Bangladesh J Child Health 2016; VOL 40 (2) :115-119

Outbreak of hand, foot and mouth disease with onychomadesis caused by Coxsackie virus A16 in Granada

2015 ◽  
Vol 82 (4) ◽  
pp. 235-241
Author(s):  
E. Navarro Moreno ◽  
D. Almagro López ◽  
R. Jaldo Jiménez ◽  
M.C. del Moral Campaña ◽  
G. Árbol Fernández ◽  
...  
Keyword(s):  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Foot And Mouth

scholarly journals Coxsackie Virus Induced Graves’ Disease in an Immunocompetent Patient

2021 ◽  
Vol 6 (10) ◽  
pp. 731-734
Author(s):  
Wesley Tang, DO, MPH ◽  
Sulagna Das, MD ◽  
Zoltán Krudy, MD
Keyword(s):  
Foot And Mouth Disease ◽  
Immunocompetent Patient ◽  
Thyroid Stimulating Hormone ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Graves Disease ◽  
Autoimmune Thyroid Diseases ◽  
Recent Infection ◽  
Autoimmune Thyroid ◽  
Foot And Mouth

Enteroviruses, such as Coxsackie virus, have been implicated in the past as a pathogen associated with subacute thyroiditis, also known as de Quervain’s thyroiditis. Less commonly are viruses associated with autoimmune thyroid diseases such as Hashimoto’s thyroiditis and Graves’ disease. We present a case of a healthy 43 year old female who presented to the emergency department complaining of several months of weakness, nausea, loose bowel movements, anxiousness, and shortness of breath. Physical exam revealed tachycardia, tremors, and a non-tender thyroid gland to palpation. Skin exam showed a rash on the palms of her hands and soles of her feet bilaterally with dark papules, suggestive of Hand, foot, and mouth disease. Laboratory workup would reveal an undetectable thyroid stimulating hormone (TSH), and levels of T3 & T4 too high to quantify. Thyroid receptor antibodies would return as positive, diagnostic of Graves’ disease. Coxsackie virus (the causative agent of Hand, foot, and mouth disease) IgM titers also returned positive suggesting recent infection. Although the etiology of Graves’ disease is still not clear, this case report provides evidence that environmental triggers such as Coxsackie viral infection may be involved in its pathogenesis.

Case of hand, foot and mouth disease by Coxsackie virus A6 infection mimicking disseminated herpes zoster

2014 ◽  
Vol 41 (3) ◽  
pp. 273-274 ◽  
Author(s):  
Hisashi Nomura ◽  
Shohei Egami ◽  
Hiroko Kasai ◽  
Tomoaki Yokoyama ◽  
Atsushi Fujimoto ◽  
...  
Keyword(s):  
Herpes Zoster ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Foot And Mouth

scholarly journals Hand-foot-and-mouth disease virus receptor KREMEN1 binds the canyon of Coxsackie Virus A10

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuguang Zhao ◽  
Daming Zhou ◽  
Tao Ni ◽  
Dimple Karia ◽  
Abhay Kotecha ◽  
...  
Keyword(s):  
Conformational Changes ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Coxsackie Virus ◽  
Virus Surface ◽  
Virus Particles ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Severe Infections ◽  
Entry Receptor

AbstractCoxsackievirus A10 (CV-A10) is responsible for an escalating number of severe infections in children, but no prophylactics or therapeutics are currently available. KREMEN1 (KRM1) is the entry receptor for the largest receptor-group of hand-foot-and-mouth disease causing viruses, which includes CV-A10. We report here structures of CV-A10 mature virus alone and in complex with KRM1 as well as of the CV-A10 A-particle. The receptor spans the viral canyon with a large footprint on the virus surface. The footprint has some overlap with that seen for the neonatal Fc receptor complexed with enterovirus E6 but is larger and distinct from that of another enterovirus receptor SCARB2. Reduced occupancy of a particle-stabilising pocket factor in the complexed virus and the presence of both unbound and expanded virus particles suggests receptor binding initiates a cascade of conformational changes that produces expanded particles primed for viral uncoating.

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