Acute hemorrhagic conjunctivitis due to enterovirus 70 in India.
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An outbreak of acute hemorrhagic conjunctivitis occurred in Delhi, India, during August and September 1996. The etiologic agent was confirmed as enterovirus type 70 by a modified centrifugation-enhanced culture method followed by immunofluorescence and neutralization tests. After nearly a decade, this virus is reemerging as a cause of acute hemorrhagic conjunctivitis in India. (+info)
Acute hemorrhagic conjunctivitis caused by coxsackievirus A24 variant, South Korea, 2002.
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In summer 2002, a nationwide outbreak of acute hemorrhagic conjunctivitis occurred in South Korea. The etiologic agent was confirmed as coxsackievirus A24 variant (CA24v) by virus isolation and sequencing of a part of the VP1 gene. Phylogentic analysis, based on the protease 3C sequences, showed that the Korean isolates were clustered into a lineage distinct from the CA24v isolates reported in previous outbreaks in Asia. (+info)
An outbreak of acute haemorrhagic conjunctivitis in Melaka, Malaysia.
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This paper reports a second outbreak of acute haemorrhagic conjunctivitis due to coxsackievirus A24 in peninsular Malaysia. Between June 2002 and early October 2003, 10,327 patients, comprising 3,261 children and 7,066 adults, were treated for acute conjunctivitis in 11 government health clinics in the Melaka Tengah district of the state of Melaka. The figure grossly underestimates the size of the outbreak; as no patients treated in private clinics in the same district were included. Institution and household surveillance showed that the commonest presenting clinical feature of the illness was eye-discharge (91.2%), followed by foreign body sensation (81.8%), pain (78.3%) and subconjunctival haemorrhage (74.4%). The mean duration of illness was 6.5 and five days for patients with and without subconjunctival haemorrhage respectively. (+info)
Acute hemorrhagic conjunctivitis (AHC) is an epidemic form of highly contagious conjunctivitis and is characterized by sudden onset of painful, swollen, red eyes, with conjunctival hemorrhaging and excessive tearing. Since 1981, when AHC was first detected in the Western Hemisphere, three major epidemics had occurred until 2003, all affecting the Caribbean. During August-October 2003, a fourth epidemic occurred in Puerto Rico (2000 population: 3.8 million). This report summarizes the outbreak investigation conducted by the Puerto Rico Department of Health (PRDOH), which documented an estimated 490,000 persons with illness, including >51,000 cases reported by physicians; demonstrated laboratory evidence of Coxsackievirus A24 (CA24); and determined that school-aged children (i.e., aged 5-18 years) and those living in crowded urban areas were at highest risk. To control outbreaks of AHC, prevention methods (e.g., frequent hand washing and avoidance of sharing towels and bedding) should be targeted to groups at highest risk, and information should be disseminated after the first report of AHC in the area. (+info)
Rapid identification of the coxsackievirus A24 variant by molecular serotyping in an outbreak of acute hemorrhagic conjunctivitis.
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We evaluated the clinical applicability of a molecular serotyping method for determination of the cause of epidemic acute hemorrhagic conjunctivitis. Seventy conjunctival swab specimens from individuals involved in a nationwide acute hemorrhagic conjunctivitis outbreak were tested. Viral culture and a molecular biology-based assay were compared by directly using clinical specimens. On the one hand, virus culture was done to isolate the enteroviruses, and serotyping was done by a coxsackievirus A24 variant-specific PCR. On the other hand, the original clinical specimens were directly screened for enterovirus by reverse transcription (RT)-PCR with panenterovirus-specific primers. Enterovirus screening-positive specimens were subjected to RT-PCR for detection of the VP1 region of enterovirus, and the amplicons were sequenced. Molecular serotyping was done by calculating the pairwise identity scores for the sequences with the maximum identities to the sequences of known prototype enteroviruses. Thirty-two specimens (45.7%) were culture positive, whereas 37 specimens (52.8%) were screening PCR positive (P < 0.001). The VP1 regions were amplified from 21 of the 37 specimens (56.8%), and the products amplified from 9 specimens were appropriately sequenced. These nine sequences were homologous with the sequence of the coxsackievirus A24 variant. Molecular serotyping by direct use of clinical specimens without cell culture could be applied for the rapid identification of the causative agent of epidemic acute hemorrhagic conjunctivitis. (+info)
Enterovirus 70 binds to different glycoconjugates containing alpha2,3-linked sialic acid on different cell lines.
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Enterovirus 70 (EV70), the causative agent of acute hemorrhagic conjunctivitis, exhibits a restricted tropism for conjunctival and corneal cells in vivo but infects a wide spectrum of mammalian cells in culture. Previously, we demonstrated that human CD55 is a receptor for EV70 on HeLa cells but that EV70 also binds to sialic acid-containing receptors on a variety of other human cell lines. Virus recognition of sialic acid attached to underlying glycans by a particular glycosidic linkage may contribute to host range, tissue tropism, and pathogenesis. Therefore, we tested the possibility that EV70 binds to alpha2,3-linked sialic acid, like other viruses associated with ocular infections. Through the use of linkage-specific sialidases, sialyltransferases, and lectins, we show that EV70 recognizes alpha2,3-linked sialic acid on human corneal epithelial cells and on U-937 cells. Virus attachment to both cell lines is CD55 independent and sensitive to benzyl N-acetyl-alpha-D-galactosaminide, an inhibitor of O-linked glycosylation. Virus binding to corneal cells, but not U-937 cells, is inhibited by proteinase K, but not by phosphatidylinositol-specific phospholipase C treatment. These results are consistent with the idea that a major EV70 receptor on corneal epithelial cells is an O-glycosylated, non-glycosyl phosphatidylinositol-anchored membrane glycoprotein containing alpha2,3-linked sialic acid, while sialylated receptors on U-937 cells are not proteinaceous. (+info)
Acute hemorrhagic conjunctivitis and coxsackievirus A24v, Rio de Janeiro, Brazil, 2004.
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An outbreak of acute hemorrhagic conjunctivitis (AHC) occurred in Rio de Janeiro in 2004. Coxsackievirus A24v (CA24v) was identified as the etiologic agent, and partial sequences from the VP1 gene show that the isolates are closely related to CA24v viruses that previously caused AHC epidemics in South Korea and French Guiana. (+info)
Acute haemorrhagic conjunctivitis outbreak in the city of Fortaleza, northeast Brazil.
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BACKGROUND/AIM: Between February and May 2003 an epidemic of acute haemorrhagic conjunctivitis affected more than 200 000 people in all five geographic regions of Brazil (north, south, midwestern, southeast, and northeast). The aim was to identify the aetiological agent and to describe clinical aspects of this outbreak in a group of patients treated at the ophthalmology department of the Hospital Walter Cantidio (OD-HWC) at the Universidade Federal do Ceara, in the city of Fortaleza, capital of the state of Ceara, northeastern Brazil. METHODS: Conjunctival swabs were collected from patients who spontaneously went to the laboratory of virology. Specimens were inoculated in HEp-2 and RD cell lines. The viral isolation was confirmed by performing reverse transcriptase polymerase chain reaction and indirect immunofluorescence assay. RESULTS: Viral conjunctivitis was diagnosed in 56 patients but only 24 of them allowed the collection of samples. Of 24 conjunctival swabs tested, 11 were positive for a variant of coxsackie virus A24 (CA24v) and one of the isolates reacted with anti-adenovirus monoclonal antibodies. CONCLUSION: CA24v was confirmed as the aetiological agent of this outbreak of acute haemorrhagic conjunctivitis in the city of Fortaleza. (+info)