Explore chapters and articles related to this topic
Infectious Optic Neuropathies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Imran Rizvi, Ravindra Kumar Garg
Dengue virus is a flavivirus. Aedes mosquitos are responsible for its transmission in humans. The clinical spectrum of dengue fever ranges from mild self-limiting febrile disorder to severe life-threatening clinical syndromes, like dengue hemorrhagic fever and dengue shock syndrome. Ophthalmological complications, in dengue fever, occur in the form of subconjunctival hemorrhage, anterior uveitis, vitritis, retinal hemorrhages, retinochoroiditis, choroidal effusion, panophthalmitis and optic neuropathies.26 The reported incidence of optic neuropathy in dengue is up to 1.5%.27 Optic nerve involvement manifests with optic neuritis, optic disc swelling or neuroretinitis. Vision loss is often self-limiting.
Viral Pathogens: A General Account
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Vinod Joshi, Bennet Angel, Annette Angel, Neelam Yadav, Jagriti Narang
The virus belongs to the family Flaviviridae and is circulating worldwide in the form of four serologically different serotypes named DENV-1, DENV-2, DENV-3, and DENV-4. It is said that these serotypes have emerged from the sylvatic cycle circulating within the forests of South-East Asia (Wang et al., 2000). A fifth variant was discovered in 2013 and named DENV-5. It was identified in a 37-year-old farmerin Sarawak, Malaysia, in 2007 (Mustafa et al., 2015) (Fig. 3.8). Whole genome sequencing of the sample from the patient confirmed it tobe different from the existing ones but slightly similar to the DENV-2 strain (Normile, 2013). The virus is also known to have severe life-threatening effects in the form of dengue hemorrhagic fever and dengue shock syndrome. The virus is transmitted by Aedes mosquitoes. Different species of Aedes mosquitoes are responsible for its spread across countries, such as Aedes aegypti, Aedes albopictus, Aedes nivalis, Aedes polynesiensis, Aedes scutellaris, and Aedes africanus. Currently, there is no chemotherapy or licensed vaccine available against the dengue virus. Twenty-five candidates are under trials, but still a fully functional one is awaited (Back and Lundkvist, 2013).
Infections and Their Mimics in Returning Travelers in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Elise Kochoumian, Jonathon Moore, Bushra Mina, Kevin Cahill
Dengue shock syndrome can lead to alterations in glucose metabolism, electrolyte abnormalities, and acid-base disturbances, which must be monitored during treatment. Of note, patients with DSS may develop acute liver failure, with subsequent hepatic encephalopathy. Ammonia-clearing therapies are vital acutely, as well as correction of underlying electrolyte abnormalities.
The expression of circulating hsa-miR-126-3p in dengue-infected Thai pediatric patients
Published in Pathogens and Global Health, 2023
Methee Sriprapun, Jittraporn Rattanamahaphoom, Pimolpachr Sriburin, Supawat Chatchen, Kriengsak Limkittikul, Chukiat Sirivichayakul
Dengue virus (DENV) infection remains a major health problem in many parts of the world. Approximately 2.5–3 billion people live in its endemic areas and nearly 400 million suffer from infection [1,2]. It is a positive-sense single-stranded RNA virus in the family Flaviviridae (genus Flavivirus), which is composed of four distinct serotypes (DENV1-DENV4) and is transmitted via Aedes mosquitoes [2,3]. The genome consists of one open reading frame (ORF) with approximately 11 kb containing 3 structural (pre-membrane (prM), envelope (E) and capsid (C)) and 7 non-structural (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) genes [2]. Clinical symptoms are categorized as asymptomatic infection, undifferentiated fever (UF), dengue fever (DF) without hemorrhage, DF with unusual hemorrhage, dengue hemorrhagic fever (DHF), DHF with shock or dengue shock syndrome (DSS), and expanded dengue syndrome (EDS) or unusual manifestations with organ involvement [4]. Severe dengue infections commonly result from secondary infection with different serotypes from prior infection [5].
A hospital based cross-sectional study on platelet parameters in adult patients with dengue, its serological subgroups, and controls
Published in Platelets, 2022
Antony Gnana Shahila M, Prabhavati Jothilingam
Thrombocytopenia, a key feature of dengue, has been proposed to be due to antibody-mediated destruction, bone marrow suppression, toxic effect on megakaryocytes, functional defects of infected platelets and disseminated intravascular coagulation [10,11]. Kinetic description of platelet counts in uncomplicated dengue showed a mild-to-moderate decline from third to seventh days of fever with return to normal levels on the eighth to ninth days [10]. Antibodies produced in primary dengue infection are capable of neutralizing secondary infections caused by the same serotype. If the secondary infection is due to a different serotype, the antibody binds to the virus without neutralizing it, instead forming a complex which is recognized by the Fc receptors on cells allowing viral entry and replication. This enhances cytokine release and causes severe dengue with its syndromes of dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) [11–14].
Emerging Viral Infections Causing Anterior Uveitis
Published in Ocular Immunology and Inflammation, 2019
Moncef Khairallah, Padmamalini Mahendradas, Andre Curi, Sana Khochtali, Emmett T. Cunningham
The clinical presentation of dengue fever ranges from a fever to life-threatening dengue shock syndrome. Classically, the disease is characterized by symptoms that appear about 3–14 days after a bite from an infected Aedes group of mosquitoes. The main clinical features are an acute onset of high-grade fever lasting for about 2–7 days, accompanied by classical symptoms of headache, body ache, myalgia, arthralgia, and skin erythema. Nonspecific symptoms, such as anorexia, nausea, and vomiting are also commonly present. Hemorrhagic manifestations, such as petechiae and mucosal bleeding may also be observed.21 Reinfection is relatively common in endemic areas and increases the risk of dengue hemorrhagic fever. In dengue hemorrhagic fever, the virus causes increased vascular permeability that leads to a bleeding diathesis, and thrombocytopenia.22 In its most severe form, it may result in shock which can result in multiple organ failure of lungs, heart, kidneys, liver, and central nervous system.