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Two cases demonstrate failures to consider HSV-1 and VZV due to atypical anatomic locations and presentations. 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Atypical presentations further increase the risk of misdiagnosis or missed diagnosis.","Answer",{"name":65,"@type":60,"acceptedAnswer":66},"What do the two presented cases illustrate?",{"text":67,"@type":63},"They show HSV-1 and VZV lesions with atypical anatomic locations and presentations. In both cases, failure to consider the virus during laboratory test ordering led to missed or misdiagnosis.",{"name":69,"@type":60,"acceptedAnswer":70},"How does relying on typical epidemiology affect patient outcomes?",{"text":71,"@type":63},"Failure to order appropriate laboratory tests in atypical HSV or VZV presentations can impact a significant minority of cases. 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Buchan,1 Preeti Pancholi2  \nAUTHOR AFFILIATIONS See affiliation list on p. 7.  \nABSTRACT  \nBackground Herpes simplex virus (HSV) and varicella zoster virus (VZV) are common causes of clinically indistinguishable lesions. The epidemiology and clinical presentation, including anatomic site of lesion and patient age, differ between these viruses, which may influence physician ordering practices. Importantly, atypical presentation of either HSV or VZV can result in the potential for misdiagnosis or missed diagnosis.  \nCase Summary Two cases are presented illustrating atypical anatomic location and presentation of HSV-1 and VZV lesions that resulted in failure to consider the virus when placing orders for laboratory testing, leading to missed or misdiagnosis.  \nConclusion Atypical presentation of HSV or VZV resulting in failure to order the appropriate laboratory test impacts a significant minority of cases, which can lead to failure to prescribe appropriate therapy, extended symptoms, and additional interaction with the healthcare system.  \nKEYWORDS ulcerative lesion, varicella zoster virus, herpes simplex virus  \nH erpes simplex virus (HSV) and varicella zoster virus (VZV) are human pathogens  \nin the Alphaherpesvirinae subfamily (1, 2) . Primary infection with these doublestranded DNA viruses is often associated with the development of vesicular “herpetic”lesions, followed by lifelong latency characterized by periods of asymptomatic and symptomatic viral reactivation (1, 3) . All three viruses establish latency within sensory neurons; however, the clinical presentation and anatomic location of recurrent infection is influenced by both the cellular tropism of each virus and initial site of infection (1, 3) . Primary or recurrent lesions caused by HSV-1 and HSV-2 typically appear in localized clusters and are visually indistinguishable (4, 5) . Lesions caused by VZV appear similar to those caused by HSV though may be distinguished by their distribution across an entire dermatome, and the presence of multiple lesions at various stages of development (vesicular, ulcerative, crusted) (6) . Typical characteristics of HSV and VZV are presented in Table 1. Importantly, lesion appearance and presentation may be atypical. This is particularly evident in immunocompromised patients (7, 8) and individuals with darker pigmented skin (9), which may contribute to racial disparities in diagnosis of HSV and other infections in this population (10) . Further complicating clinical diagnosis is a shifting epidemiology. While historically associated with oral lesions (cold sores), HSV-1 is now a more common cause of primary genital infection than HSV-2 in some populations (11), and the impact of widespread varicella zoster vaccination has reduced the incidence of these infections in the pediatric population (12) .  \nEditor Nicholas M. Moore, Rush University Medical Center, Chicago, Illinois, USA  \nAddress correspondence to Blake W.  \nBuchan, [bbuchan@mcw.edu](bbuchan@mcw.edu), or Preeti Pancholi, [preeti.pancholi@osumc.edu](preeti.pancholi@osumc.edu).  \nBlake W. Buchan and Preeti Pancholi contributed equally to this article. B.W. B. was reponsible for drafting the manuscript and was designated first author. Both authors collected data, analyzed results, and reviewed and revised the manuscript text.  \nBW B and PP have received speaker's honoraria and  \nTABLE 1 Clinicopathologic features of herpes simplex and varicella zoster virusesa  \n\n| Characteristic | HSV-1 HSV-2 |  | VZV |\n| --- | --- | --- | --- |\n| Route of transmission\u003Cbr>Site of latency\u003Cbr>Seropositivity Primary infection\u003Cbr>Location of recurrent lesions (typical presentation)\u003Cbr>Lesion appearance (typical presentation)\u003Cbr>Systemic infections | Direct contact with virus in saliva, w","cbCaigJhoW3e6qcy","https://ap.wps.com/l/cbCaigJhoW3e6qcy","pdf",970842,"English","# Background\n# Case Summary\n# Conclusion\n# Clinical and Epidemiologic Factors\n## Typical vs Atypical Lesion Presentation\n## Shifting Epidemiology\n# Table 1: Clinicopathologic Features","[{\"question\":\"Why can HSV and VZV be confused during diagnosis?\",\"answer\":\"Their lesions may appear clinically indistinguishable, even though epidemiology and presentation differ by virus. Atypical presentations further increase the risk of misdiagnosis or missed diagnosis.\"},{\"question\":\"What do the two presented cases illustrate?\",\"answer\":\"They show HSV-1 and VZV lesions with atypical anatomic locations and presentations. In both cases, failure to consider the virus during laboratory test ordering led to missed or misdiagnosis.\"},{\"question\":\"How does relying on typical epidemiology affect patient outcomes?\",\"answer\":\"Failure to order appropriate laboratory tests in atypical HSV or VZV presentations can impact a significant minority of cases. This may result in delayed or inappropriate therapy, extended symptoms, and additional healthcare system interaction.\"}]","What you see is not always what you get - the influence of epidemiology on ordering practices for herpes simplex virus and varicella zoster virus | PDF",1790708590]