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Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
Dengue hemorrhagic fever and dengue TSS are two deadly complications of dengue viral infection that occur during secondary infection. Dengue hemorrhagic fever is characterized by hemorrhage, thrombocytopenia, and plasma leakage. Dengue shock syndrome includes the additional complications of circulatory failure and hypotension [79,81,82].
The Pathogenesis and Pathology of the Hemorrhagic State in Viral and Rickettsial Infections
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
Dengue hemorrhagic fever (DHF) is but one of several clinical manifestations of dengue virus infection. DHF is usually transmitted by Aedes aegypti and is not transmitted by A. albopictus, a vector of mild endemic dengue.20 It occurs mainly in Asian children between the ages of 2 and 13 years, although children less than 1 year of age may also contract the disease. In the early stages, DHF resembles classic dengue fever with subsequent rapid deterioration. In some patients, dengue shock syndrome, which is defined by circulatory failure, may occur in the absence of hemorrhagic diathesis. DHF patients manifest a variety of clinical hemorrhagic findings including frequent cutaneous petechiae and ecchymoses, melena, and hematemesis, and (less often) epistaxis and bleeding in the gums, lungs, and urine.1,21-24 Evidence for increased vascular permeability include frequent pleural effusions.22 Pathologic hemorrhagic lesions are observed in skin, stomach, small intestine, heart, brain, liver, lungs, kidneys, skeletal muscle, and adrenal glands.21,23,25-27 Thrombi are noted in only a small proportion of necropsies (12 of 1 series of 100 necropsies with renal glomerular thrombi in only 5). Central or paracentral hepatocellular necrosis is commonly present, but may be due to ischemia or shock rather than viral hepatocellular injury.
Bites and stings
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Dengue hemorrhagic fever: This fatal hemorrhagic disease, primarily of children under 15 years of age, is characterized by sudden onset of fever, which usually lasts for 2–7 days. As the fever remits, characteristic manifestations of plasma leakage appear. Common hemorrhagic manifestations include skin hemorrhages such as petechiae, purpuric lesions, and ecchymoses (Figure 54.1). Epistaxis, bleeding gums, gastrointestinal (GI) hemorrhage, and hematuria occur less frequently.
Original antigen sin and COVID-19: implications for seasonal vaccination
Published in Expert Opinion on Biological Therapy, 2022
Original antigenic sin may reveal an asymmetric pattern of protective antibody cross-reactivity determined by exposure to previously existing strains of a given pathogen, and this phenomenon appears to occur more frequently in response to viruses [25–27]. Early work on immune imprinting focused primarily on the response to influenza [28–30]. This was due to the presumed influenza anamnesis of the human population born before 1956 – the year when A(H1NI) influenza viruses came out of circulation [31]. However, the phenomenon original antigenic sin has also been observed in response to dengue, a viral infection transmitted to humans through the bite of infected mosquitoes [32]. Symptoms typically occur 3 to 14 days after infection and may include fever, joint pains, rash, nausea, vomiting, and headache [33]. In some cases, the condition progresses to dengue hemorrhagic fever, which results in bleeding and severe hypotension that may be lethal [34–36].
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.
Repeated infections of dengue (serotype DENV-2) in lung cells of BALB/c mice lead to severe histopathological consequences
Published in Pathogens and Global Health, 2018
S. Sakinah, Sharmilah Kumari, Rusheni Munisvaradass, Pooi-Ling Mok, Hui-Yee Chee, Arivudainambi Seenichamy, Kiruthiga P.V, Akon Higuchi, Mariappan Rajan, K. Nataraja Seenivasan, Marlina, Palanisamy Arulselvan, Giovanni Benelli, S. Suresh Kumar
Dengue hemorrhagic fever (DHF) and DSS increase the rate of mortality, if compared to DF cases. Both of them are characterized by hemorrhages and shock syndrome [21]. DENV-2 infection raises the virus production within the body and affects most of the internal organs, as recently pointed out by researches conducted on liver tissues and blood cells from experimentally infected mice populations [9,10]. With its well know characteristics, DENV increases the permeability of endothelium bed of the vessel and leads to the fluid extravasations from the endothelium bed into the body cavity. This eventually reduces the blood pressure in the circulation, due to less circulating blood, resulting in low blood supply to all over the body, with highly detrimental consequences on vital organs. Moreover, the consumption of host mechanism by the DENV during its replication and host immunological storm results in organ malfunctioning. One of the organ malfunctions during DENV is bone marrow, results in low platelet production, increases the risk of bleeding and led to major complication to other vital organs [22].