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Viral exanthems

Keighley, Caitlin L.a,b; Saunderson, Rebecca B.a; Kok, Jena,c,d; Dwyer, Dominic E.a,c,d

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Current Opinion in Infectious Diseases: April 2015 - Volume 28 - Issue 2 - p 139-150
doi: 10.1097/QCO.0000000000000145
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Exanthems commonly accompany viral infections, but may also be caused by other infectious and noninfectious aetiologies. Although exposure to viruses may occur at mucosal surfaces or abraded skin sites, the presence of a rash in viral infections is generally not due to viral replication per se, but a hypersensitivity reaction to the virus. Viral exanthems may or may not be pruritic, and may be the first symptom or develop during the course of infection. In addition, they can occur during primary infection or following reactivation of a latent virus.

The spectrum of viral causes of exanthems and enanthems (in which mucous membranes are also involved) has increased with emergence of novel viruses and advances in laboratory diagnostic methods. Although some exanthems and enanthems may be nonspecific, others can be pathognomonic [1]. Pattern recognition and knowledge of epidemiology is pivotal in differentiating the likely pathogen and predicting the natural course and public health importance of cases (Fig. 1). In the absence of a specific pattern, arthropod exposure, travel and vaccination history may provide clues to the differential diagnoses. However, atypical patterns of exanthems can occur in immunocompromised patients or following vaccination. Herein, we describe common causes of viral exanthems and outline an approach to guide further investigation and management.

Flow chart of a practical clinical approach used to determine possible viral aetiologies of exanthems.
Box 1
Box 1:
no caption available


Syndromic rashes in viral infections can generally involve hands, feet and mouth; ‘gloves and socks’; and the face, limbs and buttocks with truncal sparing (Gianotti–Crosti syndrome).

Hand, foot and mouth disease

The enteroviruses have recently been reclassified (Table 1). Hand, foot and mouth disease (HFMD) is the commonest manifestation of human enterovirus infections (Table 2[2–14]), which are a major cause of rash and fever [1,15▪▪] (Fig. 2[16]).

Table 1
Table 1:
Recent reclassification of enterovirusesa
Table 2
Table 2:
Clinical features and diagnostic methods of endemic and vaccine-preventable viral infections
Table 2
Table 2:
(Continued) Clinical features and diagnostic methods of endemic and vaccine-preventable viral infections
(a) Following a mild prodrome, the clinical hallmark of HFMD is a deep-seated vesicular eruption affecting the palmar and plantar surfaces. There are vesicles with surrounding erythema, located on the fingers [16]. (n) The lesions on the palms and soles can be associated with an erosive stomatitis, fever and malaise. There is painful erosion on the lateral aspect of the tongue [16]. CMV, cytomegalovirus; EBV, Epstein–Barr virus; HHV, human herpesvirus; RSV, respiratory syncytial virus; VZV, varicella zoster virus.

Palmoplantar vesicular lesions and painful oral erosions (Fig. 2b) with the involvement of the buttocks/perineum may be seen. Less commonly, onychomadesis (painless spontaneous nail shedding) occurs after HFMD [17–19]. A more fulminant progression of HFMD associated with enterovirus-A71 has been recently described, resulting in the death of 170 children in an outbreak in Vietnam in 2011 [1,20,21].

Coxsackie virus-A6 is increasingly recognized to cause HFMD with atypical presentations in children [2–6,22–24]. In addition to hand, foot and buttock involvement, rash may be present periorally, truncally or with a predilection for areas of active atopic dermatitis, termed ‘eczema coxsackium’. Other reported morphologies include vesiculobullous eruption on the trunk, Gianotti–Crosti-like eruption, and petechial and purpuric eruptions [1,7▪▪,8,18–22,25–29]. Desquamation occurs in approximately 50% of cases, and rarely, a more severe form of infection occurs in the absence of rash [2–6,9,17,22–24].

In 2014, there has been a nationwide outbreak of enterovirus-D68 in the USA. Although respiratory illnesses are the predominant feature of enterovirus-D68 infections, rash may also be present [10,30].

Papular-purpuric ‘gloves and socks’ syndrome

Papular-purpuric ‘gloves and socks’ syndrome is most commonly associated with parvovirus B19 infection (Fig. 3). It is transmitted via respiratory droplets, blood products or in utero. The appearance of B19-specific immunoglobulin G coincides with onset of the rash, which is commonly pruritic [2,10]. Clinically, it can manifest as erythema infectiosum (Fig. 4), papular–purpuric ‘gloves and socks’ syndrome or purpuric exanthems. Unusual presentations include flagellate erythema [11,31]. Parvovirus is generally not infectious after the onset of the rash.

Papular–purpuric gloves and socks syndrome is seen in association with parvovirus B19 infection. Petechial purpura is seen on the palms in this patient, and such lesions are also seen on the soles of the feet [16].
(a) Erythema infectiosum, also known as fifth disease and ‘slapped cheek’ syndrome has a mild prodrome with low-grade temperature, myalgias and headache 7–10 days before the onset of the exanthem. This picture shows bilateral erythema of the cheeks, likened to ‘slapped cheeks’, with circumoral sparing [16]. (b) Following the development of the facial rash, there is progression over 1–4 days to the trunk/limbs where a lacy/reticulated pattern is seen, as seen on the inner thigh of this patient. The rash lasts 1–3 weeks and is exacerbated by heat and sunlight exposure [16].

Gianotti–Crosti syndrome

Gianotti–Crosti syndrome commonly occurs in children and resolves over 3–4 weeks [12–14,32,33]. It was initially described in children with hepatitis B infection, but has subsequently been associated with many other viral and bacterial infections [1–14,34▪▪,35▪▪].


Human herpesvirus (HHV) can cause a variety of viral exanthems, including vesicular, maculopapular, morbilliform, urticarial, scarlatiniform or purpuric rashes. Distinct patterns and persistent reactivation of latent herpesviruses [Epstein–Barr virus (EBV), cytomegalovirus and HHV-6] have also been observed following drug-induced hypersensitivity syndrome/Stevens–Johnson syndrome [1,15▪▪,36▪].

Herpes simplex virus

Herpes simplex virus (HSV)-1 and 2 typically produce vesicular lesions in the oral-labial or genital regions, although primary infection may cause a maculopapular rash. Vesicles may involve single or multiple anatomical sites following autoinoculation or in disseminated disease. Eczema herpeticum in patients with atopic dermatitis, herpes gladiatorum in athletes and erythema multiforme are also associated with HSV infection.

Varicella zoster virus

Primary and secondary varicella zoster virus (VZV) infection produces a classical and easily recognizable rash that is diffuse and dermatomal, respectively. However, herpes zoster may manifest as dermatomal pain or encephalitis in the absence of a rash (zoster sine herpete) [16,37▪▪], making the diagnosis more challenging. VZV is now vaccine preventable.

Cytomegalovirus and Epstein–Barr virus

Acute cytomegalovirus infection does not generally cause an exanthema, although it was the proposed cause in 4% of patients presenting with atypical exanthems as determined by serology and polymerase chain reaction; EBV was identified in another 8% [1,17–19,38]. Acute EBV infection may be associated with a maculopapular rash lasting up to a week that begins on the trunk and arms before spreading to the forearms and face [7▪▪]. It may be associated with an enanthem.

The use of penicillin and subsequent development of rash has been recently challenged in a prospective study of 184 patients with acute EBV infection [39,40]. Most of the 103 patients who received antibiotics were prescribed amoxicillin, and the presence of rash in those given penicillin derivatives was not significantly different from those that were not exposed.

Human herpesvirus-6 and human herpesvirus-7

Roseola infantum is a febrile illness predominantly caused by HHV-6 and occasionally HHV-7. It typically occurs in early childhood and presents with a febrile illness followed by rose-pink macules and papules on the neck, proximal extremities, trunk and occasionally on the face. An enanthem may be present. Using serology, HHV-6 was the most common cause in a prospective study of rash and febrile illness amongst patients less than 40 years of age presenting to clinics or hospitals [41].


Despite the availability of highly effective vaccines, reports of measles and rubella are increasing.


Measles incidence is rising, particularly in areas of low prevalence from imported cases where measles is endemic [42–44]. During 2011, more than 26 000 measles cases were reported in 36 European countries [45]. The USA has seen 20 outbreaks with 603 cases of measles in 2014 (until October 31) [46]. Following an influenza-like prodrome, Koplik spots usually precede a cephalocaudal morbilliform rash that appears 3–5 days after the onset of symptoms (Fig. 5).

(a) The prodrome of measles consists of fever, cough, rhinoconjunctivitis and a diffuse morbilliform rash that progresses cephalocaudally [16,34▪▪]. (b) Koplik spots, which are grey–white papules on the buccal mucosa, are highly predictive of confirmed measles [16,54].


There have been recent rubella outbreaks in Japan, China, India and Tunisia [12,47▪,48,49]. A 5-day prodrome of fever, headache and upper respiratory tract symptoms is associated with cephalocaudal progression of a maculopapular rash (Fig. 6). Infected individuals should be quarantined until 4 days after the rash subsides.

Rubella infection results in cephalocaudal progression of a nonspecific maculopapular rash. Petechial macules may be present on the soft palate (Forchheimer's spots) and tender lymphadenopathy, particularly in the head and neck region, may be present [16].


Although rash is uncommon in influenza, cutaneous manifestations have been reported with influenza A (H1N1)pdm09, A/H7N9 and influenza B [50–53]. A confluent maculopapular rash that spares the face and palmoplantar surfaces has been observed in influenza A (H1N1)pdm09 infection [51]. Influenza should remain in the differential diagnosis of children with fever and rash, particularly in the presence of respiratory symptoms during the influenza season.


With increased travel and population movements, imported viral infections with secondary local transmission are of great concern and outbreaks in susceptible populations may present containment issues.


Of the 754 recognized arboviruses, only Chikungunya, dengue, Japanese encephalitis and yellow fever viruses have evolved to primarily use humans as hosts. This implies that a large reservoir of other arboviruses in animals may affect humans. Table 3 details the clinical presentations, geographical distribution and diagnostic tests available.

Table 3
Table 3:
Arboviruses divided into clinical presentation/syndrome, geographic region, clinical features and current diagnostic test availability


Exanthems in alphavirus infections may appear anytime during the course of illness. Characteristic features include the cephalocaudal spread of rash in Barmah Forest virus (BFV) infection, and palmoplantar involvement in Ross River, Barmah Forest and Chikungunya virus.

Chikungunya virus

Chikungunya has spread to the Caribbean and Americas following large outbreaks in the Indian Ocean islands, Indian subcontinent and Europe [55–60]. The expansion of geographical areas of Chikungunya-competent vectors through climate change, and the spread of the virus into new vector species such as Aedes albopictus following importation from endemic areas have been responsible for the ongoing transmission of infection. Chikungunya virus rash is usually morbilliform, with or without acral and facial oedema, mucosal, genital and intertriginous ulceration. Vesiculobullous eruptions are more likely to occur in children.

Ross River and Barmah Forest virus

Ross River virus and BFV are endemic in Australia, with occasional outbreaks in the Pacific [11,61,62]. BFV is characterized by a rash in 90% of cases, whereas Ross River virus infection is more commonly associated with arthritis. However, around 40% of patients develop a rash [11,62,63▪,64–66]. The rash seen in BFV infection appears with the onset of illness and has cephalocaudal spread. It may be maculopapular, purpuric or vesicular [62–64].


The flaviviruses are structurally similar and serology may be cross-reactive (Table 3).

Dengue and Zika virus

Dengue virus transmission overlaps with that of Chikungunya virus and coinfection can occur. A faint morbilliform or scarlatiniform rash with islands of sparing occurs in 50% of individuals. Minor haemorrhagic lesions can occur. The rash rarely persists beyond 2 weeks [67]. Although secondary dengue carries a greater risk of dengue haemorrhagic fever, severe dengue also occurs with primary infections and some strains appear to diminish in severity with subsequent infection [68▪▪,69–71]. Zika virus is a flavivirus with an indistinguishable presentation from dengue infection. Outbreaks of Zika, dengue and Chikungunya have increased in frequency in recent years, particularly in the Pacific [60,72,73].

West Nile virus

Cutaneous manifestations in West Nile virus occur in 25% of patients and nonspecific erythematous macular or papular eruptions affecting the extremities predominate [74].

Murray Valley and Japanese encephalitis

Murray Valley encephalitis was first recognized in the Australian states of Victoria and South Australia in 1951. First isolated in Japan, Japanese encephalitis virus is now the leading cause of viral encephalitis worldwide. Most infections are subclinical or mild, with fever and an erythematous macular and/or papular rash that is more pronounced on the extremities [62,75].


The filoviruses responsible for viral haemorrhagic fevers include Ebola, Marburg and Lassa viruses. Ebola virus disease in West Africa has captured public attention with the largest recorded epidemic in 2014. Rash occurs in more than half of patients with Marburg virus infection after 4–5 days of symptom onset, but is uncommon in Ebola or Lassa virus infection. It develops over the upper limbs, face and trunk and resolves over days with desquamation and alopecia. It may be associated with enanthema involving the tonsils and palate with ‘tapioca granules’ on the soft palate with gingivitis, glossitis and fissuring [76–79].


In HIV infections, rash may be due to HIV per se, or from other infectious and noninfectious causes. HIV seroconversion illness may be associated with a generalized maculopapular rash, although this usually affects the palms and soles of the feet, with papules and nodules present on the trunk. Secondary syphilis should also be excluded. In HIV infection, HHV-8 can cause Kaposi's sarcoma, which may present as variegated macules, plaques or nodules. Multicentric Castleman's disease associated with HHV-8 infection can also result in a recurrent maculopapular rash of the limbs and trunk without mucosal involvement [69,80]. Other dermatoses in established HIV infection include papulo-pruritic eruptions, eosinophilic folliculitis, infective folliculitis, necrotizing vasculitis and drug reactions; skin biopsy is useful to differentiate these entities [81].


Hepatitis B and C are uncommon causes of viral exanthema. Manifestations are summarized in Table 4[35▪▪,82]. Treatment includes targeted antiviral therapy, and steroids and plasma exchange may have a role in the presence of serum sickness or vasculitis. Acute hepatitis E may also be associated with a rash [83].

Table 4
Table 4:
Skin manifestations of hepatitides

Bioterrorism agents

Smallpox was last reported in Somalia in 1977, but has gained notoriety as a potential agent of bioterrorism. It is highly contagious and carries a 30% mortality rate in unvaccinated populations. Smallpox causes a characteristic maculopapular rash that progresses to raised fluid-filled blisters, pustules and pocks. Scabs appear 10–14 days after onset of rash and fall off, leaving areas of hypopigmentation. Scarring may persist lifelong. Unlike pocks from VZV, pocks from smallpox usually occur in the limbs with palmoplantar involvement and are in the same stage of development.

New zoonotic viruses

A recent report describes Sosuga virus as the cause in a wildlife biologist who developed fever and a maculopapular exanthema after travel to South Sudan and Uganda [84▪]. This paramyxovirus is a rubella-like virus similar to others derived from fruit bats. Associated with an enanthem, the exanthema progressed to a petechial rash over sites of trauma or pressure. She recovered after 2 weeks.


Laboratory confirmation of viral exanthems is commonly made by virus-specific serology. The advantages of serology include its noninvasive nature and minimal sample degradation if transported and stored appropriately. Pathogen-specific immunoglobulin M is suggestive of an acute infection, but false-positive results can occur because of cross-reactivity with other viruses. Immunoglobulin G seroconversion (or a four-fold or greater rise in antibody titres between acute and convalescent sera) is regarded as definitive evidence of infection, but confirmation of infection may be delayed and a convalescent sera is not always collected. Measuring immunoglobulin G avidity to determine the maturity of the immunoglobulin G response may differentiate acute from previous infection. High immunoglobulin G avidity is indicative of previous infection, but low immunoglobulin G avidity is not necessarily suggestive of an acute infection as high avidity can take years to develop.

Where available, nucleic acid testing (NAT) on specimens including blood, fluid and tissues is generally the most sensitive and specific test, but specimen quality, storage and transport can affect the performance of NAT. Viraemia generally predates the onset of symptoms, but NAT of blood samples may be falsely negative if the period of viraemia is brief. In addition to qualitative assays, quantitative NAT, if available, can provide an assessment of disease progression and prognosis and guide treatment response. Antiviral resistance can also be detected using NAT. NAT is also useful for epidemiological purposes, which allows monitoring of phylogenetic secular trends and assay performance [34▪▪].

Immunofluorescence antigen detection is still used for the rapid diagnosis of HSV and VZV infections. Viral cultures are slow, time consuming, labour intensive and lack sensitivity, but remain the ‘gold-standard’ for diagnosis, which NAT assays are validated against.

Skin biopsies are not generally performed in viral exanthems as histological examination usually does not provide a definitive aetiological diagnosis. If the differential diagnosis includes a drug as the cause of the exanthem, then a skin biopsy should be performed as this may help elucidate the diagnosis. However, HHV infections have characteristic features including multinucleation, nuclei enlargement, nucleoli and intranuclear inclusions. Immunohistochemistry using specific monoclonal antibodies may also identify specific viruses [85▪▪,86▪▪].


The management of viral exanthems is largely supportive in the absence of specific antiviral therapy. Topical therapies such as steroid creams do not improve the natural history. Analgesia can be offered systemically, or via topical and viscous forms for painful enanthems and smaller areas of rash. Infection control measures remain an important strategy to limit further transmission of infection.


Viral exanthems are becoming more common with declining vaccination rates, increasing population and vector movements and emerging novel viruses. Vector control remains pivotal in preventing arboviral infections, and we eagerly await outcomes of Ebola, Chikungunya, dengue, HCV and enterovirus-A71 vaccination trials. New immunosuppressive treatments have led to higher rates of reactivation of latent viruses, and clinicians should be alert to atypical presentations of established viruses.


We have outlined pathognomonic features of endemic viruses causing exanthems and key epidemiological clues that are important where rash morphology is nonspecific. Diagnosis is generally secured via serology or NAT. Prevention and control measures are crucial in management.



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Conflicts of interest

There are no conflicts of interest.


Papers of particular interest, published within the annual period of review, have been highlighted as:

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1. Drago F, Paolino S, Rebora A, et al. The challenge of diagnosing atypical exanthems: a clinico-laboratory study. J Am Acad Dermatol 2012; 67:1282–1288.
2. Mage V, Lipsker D, Barbarot S, et al. Different patterns of skin manifestations associated with parvovirus B19 primary infection in adults. J Am Acad Dermatol 2014; 71:62–69.
3. Heegaard ED, Brown KE. Human parvovirus B19. Clin Microbiol Rev 2002; 15:485–505.
4. Katta R. Parvovirus B19: A review. Dermatol Clin 2002; 20:333–342.
5. Hashimoto H, Yuno T. Parvovirus B19-associated purpuric–petechial eruption. J Clin Virol 2011; 52:269–271.
6. Yermalovich MA, Hübschen JM, Semeiko GV, et al. Human parvovirus B19 surveillance in patients with rash and fever from Belarus. J Med Virol 2012; 84:973–978.
7▪▪. Di Lernia V, Mansouri Y. Epstein-Barr virus and skin manifestations in childhood. Int J Dermatol 2013; 52:1177–1184.

Thorough review of skin manifestations of EBV in childhood from a dermatological perspective.

8. World Health Organisation. Handbook Integrated Management of Childhood Illness. 2005. [Accessed 3 October 2014]
9. Tanaka-Taya K, Sashihara J, Kurahashi H, et al. Human herpesvirus 6 (HHV-6) is transmitted from parent to child in an integrated form and characterization of cases with chromosomally integrated HHV-6 DNA. J Med Virol 2004; 73:465–473.
10. Blauvelt A. Skin diseases associated with human herpesvirus 6, 7, and 8 infection. J Investig Dermatol Symp Proc 2001; 6:197–202.
11. Outhred AC, Kok J, Dwyer DE. Viral arthritides. Expert Rev Anti Infect Ther 2011; 9:545–554.
12. Messedi E, Fki-Berrajah L, Gargouri S, et al. Clinical epidemiological and molecular aspects of rubella outbreak with high number of neurological cases, Tunisia 2011–2012. J Clin Virol 2014; 61:248–254.
13. Harada T, Ohtaki E, Tobaru T, et al. Rubella-associated perimyocarditis: A case report. Angiology 2002; 53:727–732.
14. König AL, Schabel A, Sugg U, et al. Autoimmune hemolytic anemia caused by IgG lambda-monotypic cold agglutinins of anti-Pr specificity after rubella infection. Transfusion 2001; 41:488–492.
15▪▪. Zhu F, Xu W, Xia J, et al. Efficacy, safety, and immunogenicity of an enterovirus 71 vaccine in China. N Engl J Med 2014; 370:818–828.

Randomized double-blind placebo-controlled trial of enterovirus-71 vaccine in 10 007 infants and children demonstrating efficacy against enterovirus-71-associated disease.

16. Paller AS, Mancini A. Hurwitz Clinical Pediatric Dermatology. 4th ed.2011; Philadelphia: Saunders, Expert Consult.
17. Zhou H-T, Guo Y.-H, Tang P, et al. No exanthema is related with death and illness severity in acute enterovirus infection. Int J Infect Dis 2014; 28:123–125.
18. Feder HM Jr, Bennett N, Modlin JF. Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6. Lancet Infect Dis 2014; 14:83–86.
19. Mathes EF, Oza V, Frieden IJ, et al. Eczema coxsackium and unusual cutaneous findings in an enterovirus outbreak. Pediatrics 2013; 132:e149–e157.
20. Nguyen NTB, Pham HV, Hoang CQ, et al. Epidemiological and clinical characteristics of children who died from hand, foot and mouth disease in Vietnam, 2011. BMC Infect Dis 2014; 14:341.
21. Horsley E, Just E, Torres C, et al. Enterovirus 71 outbreak in Northern Sydney 2013: case series and initial response. J Paediatr Child Health 2014; 50:525–530.
22. Biao D, Ying Z, Huaping X, et al. Circulation of coxsackievirus A6 in hand-foot-mouth disease in Guangzhou, 2010–2012. Virol J 2014; 11:157.
23. Hongyan G, Chengjie M, Qiaozhi Y, et al. Hand, foot and mouth disease caused by coxsackievirus A6, Beijing, 2013. Pediatr Infect Dis J 2014; 33:1302–1303.
24. Puenpa J, Mauleekoonphairoj J, Linsuwanon P, et al. Prevalence and characterization of enterovirus infections among pediatric patients with hand foot mouth disease, herpangina and influenza like illness in Thailand, 2012. PLoS One 2014; 9:e98888.
25. Hubiche T, Schuffenecker I, Boralevi F, et al. Dermatological spectrum of hand, foot and mouth disease from classical to generalized exanthema. Pediatr Infect Dis J 2014; 33:e92–e98.
26. Puenpa J, Chieochansin T, Linsuwanon P, et al. Hand, foot, and mouth disease caused by coxsackievirus A6, Thailand, 2012. Emerg Infect Dis 2013; 19:641–643.
27. Montes M, Artieda J, Piñeiro LD, et al. Hand, foot, and mouth disease outbreak and coxsackievirus A6, northern Spain, 2011. Emerg Infect Dis 2013; 19:676–678.
28. Huang W-C, Huang L-M, Lu C-Y, et al. Atypical hand-foot-mouth disease in children: a hospital-based prospective cohort study. Virol J 2013; 10:209.
29. Lu Q-B, Zhang X-A, Wo Y, et al. Circulation of coxsackievirus A10 and A6 in hand-foot-mouth disease in China, 2009–2011. PLoS One 2012; 7:e52073.
30. Prevention ECFD, Team CEHCUEE. Continued seasonal circulation of enterovirus D68 in the Netherlands, 2011–2014. European Centre for Disease Prevention and Control (ECDC). 2014, 19.
31. Miguélez A, Dueñas J, Hervás D, et al. Flagellate erythema in parvovirus B19 infection. Int J Dermatol 2014; 53:3583–3585.
32. Iwasaki E, Takita M, Kishino R, et al. Adult Gianotti-Crosti syndrome caused by hepatitis B. Nihon Shokakibyo Gakkai Zasshi 2013; 110:1657–1662.
33. Stojkovic-Filipovic J, Skiljevic D, Brasanac D, Medenica L. Gianotti-Crosti syndrome associated with Ebstein-Barr virus and Parvovirus B-19 co-infection in a male adult: case report and review of the literature. G Ital Dermatol Venereol 2014;
34▪▪. Biesbroeck L, Sidbury R. Viral exanthems: an update. Dermatol Ther 2013; 26:433–438.

Review of viral exanthems from a dermatological perspective.

35▪▪. Kappus MR, Sterling RK. Extrahepatic manifestations of acute hepatitis B virus infection. Gastroenterol Hepatol 2013; 9:123–126.

Comprehensive review of extrahepatic manifestations of hepatitis B virus.

36▪. Ishida T, Kano Y, Mizukawa Y, Shiohara T. The dynamics of herpesvirus reactivations during and after severe drug eruptions: their relation to the clinical phenotype and therapeutic outcome. Allergy 2014; 69:798–805.

Retrospective analysis of 62 patients with herpesvirus reactivation differentiating pathogens associated with clinical drug eruptions.

37▪▪. Gershon AA, Gershon MD. Pathogenesis and current approaches to control of varicella-zoster virus infections. Clin Microbiol Rev 2013; 26:728–743.

Comprehensive review of VZV including clinical presentation, diagnosis, latency and reactivation, therapy and prevention.

38. Caseris M, Houhou N, Longuet P, et al. French 2010–2011 measles outbreak in adults: report from a Parisian teaching hospital. Clin Microbiol Infect 2014; 20:O242–O244.
39. Hocqueloux L, Guinard J, Buret J, et al. Do penicillins really increase the frequency of a rash when given during Epstein-Barr virus primary infection? Clin Infect Dis 2013; 57:1661–1662.
40. Chovel-Sella A, Ben Tov A, Lahav E, et al. Incidence of rash after amoxicillin treatment in children with infectious mononucleosis. Pediatrics 2013; 131:e1424–1427.
41. de Moraes JC, Toscano CM, de Barros ENC, et al. Etiologies of rash and fever illnesses in Campinas. Brazil J Iinfect Dis 2011; 204 (Suppl 2):S627–S636.
42. Tabak F, Murtezaoglu A, Tabak O, et al. Clinical features and etiology of adult patients with fever and rash. Ann Dermatol 2012; 24:420–425.
43. Sparrer KMJ, Krebs S, Jager G, et al. Complete genome sequence of a wild-type measles virus isolated during the spring 2013 epidemic in Germany. Genome Announcements 2014; 2:e00157–e214.
44. Weston KM, Dwyer DE, Ratnamohan M, et al. Nosocomial and community transmission of measles virus genotype D8 imported by a returning traveller from Nepal. Commun Dis Intell Q Rep 2006; 30:358–365.
45. Weekly Epidemiological Record [Internet]. 2011. [Accessed 8 November 2014]
46. CDC – Measles: cases and outbreaks [Internet]. 2014. [Accessed 3 October 2014].
47▪. Ujiie M, Nabae K, Shobayashi T. Rubella outbreak in Japan. Lancet 2014; 383:1460–1461.

Brief report of outbreak and measures implemented in Japan.

48. Singh MP, Kumar A, Gautam N, et al. Rubella outbreak in the union territory of Chandigarh North India. J Med Virol 2014; 87:344–349.
49. Xu H, Gao X, Bo F, et al. A rubella outbreak investigation and BRD-II strain rubella vaccine effectiveness study, Harbin city, Heilongjiang province, China, 2010–2011. Vaccine 2013; 32:85–89.
50. Koul PA, Khan UH, Shah TH, et al. Skin rash and subconjunctival haemorrhage in an adult with pandemic H1N1 influenza. Case Reports 2013; 1:bcr2013010216–6.
51. Rosenberg M, Tram C, Kuper A, Daneman N. Rash associated with pandemic (H1N1) influenza. CMAJ 2010; 182:E146.
52. Wiwanitkit S, Wiwanitkit V. Incidence of skin rash in the new H7N9 influenza. Indian J Dermatol 2014; 59:529.
53. Kaley J, Pellowski DM, Cheung WL, et al. The spectrum of histopathologic findings in cutaneous eruptions associated with influenza A (H1N1) infection. J Cutan Pathol 2013; 40:226–229.
54. Zenner D, Nacul L. Predictive power of Koplik's spots for the diagnosis of measles. J Infect Dev Ctries 2012; 6:271–275.
    55. Powers AM, Logue CH. Changing patterns of chikungunya virus: re-emergence of a zoonotic arbovirus. J Gen Virol 2007; 88 (Pt 9):2363–2377.
    56. Caglioti C, Lalle E, Castilletti C, et al. Chikungunya virus infection: an overview. New Microbiol 2013; 36:211–227.
    57. Mowatt L, Jackson ST. Chikungunya in the Caribbean: an epidemic in the making. Infect Dis Ther 2014; 3:63–68.
    58. Chusri S, Siripaitoon P, Silpapojakul K, et al. Kinetics of Chikungunya infections during an outbreak in southern Thailand, 2008–2009. Am J Trop Med Hyg 2014; 90:410–417.
    59. Robin S, Ramful D, Zettor J, et al. Severe bullous skin lesions associated with Chikungunya virus infection in small infants. Eur J Pediatr 2010; 169:67–72.
    60. Roth A, Mercier A, Lepers C, et al. Concurrent outbreaks of dengue, chikungunya and Zika virus infections - an unprecedented epidemic wave of mosquito-borne viruses in the Pacific 2012–2014. Euro Surveill 2014; 19:
    61. Smith DW, Speers DJ, Mackenzie JS. The viruses of Australia and the risk to tourists. Travel Med Infect Dis 2011; 9:113–125.
    62. Russell RC, Dwyer DE. Arboviruses associated with human disease in Australia. Microbes Infect 2000; 2:1693–1704.
    63▪. Hueston L, Toi CS, Jeoffreys N, et al. Diagnosis of Barmah forest virus infection by a nested real-time SYBR green RT-PCR assay. PLoS One 2013; 8:e65197.

    Analysis of the role of polymerase chain reaction assays for diagnosis of BFV infection.

    64. Dore A, Auld J. Barmah Forest viral exanthems. Aust J Dermatol 2004; 45:125–129.
    65. Lott JP, Liu K, Landry M-L, et al. Atypical hand-foot-and-mouth disease associated with coxsackievirus A6 infection. J Am Acad Dermatol 2013; 69:736–741.
    66. Centers for Disease Control. Notes from the field: severe hand, foot, and mouth disease associated with coxsackievirus A6 – Alabama, Connecticut, California, and Nevada, November 2011–February 2012. MMWR Morb Mortal Wkly Rep 2012; 61:213–214.
    67. Halsey ES, Williams M, Laguna-Torres VA, et al. Occurrence and correlates of symptom persistence following acute dengue fever in Peru. Am J Trop Med Hyg 2014; 90:449–456.
    68▪▪. Carod-Artal FJ, Wichmann O, Farrar J, Gascón J. Neurological complications of dengue virus infection. Lancet Neurol 2013; 12:906–919.

    Overview of dengue virus infection and thorough review of neurological complications including encephalitis, transverse myelitis, acute disseminated encephalomyelitis, Guillain–Barré syndrome, cerebravascular complications, muscle dysfunction and neuroophthalmic complications.

    69. Olkowski S, Forshey BM, Morrison AC, et al. Reduced risk of disease during postsecondary dengue virus infections. J Infect Dis 2013; 208:1026–1033.
    70. Guilarde AO, Turchi MD Jr, JBS, et al. Dengue and dengue hemorrhagic fever among adults: clinical outcomes related to viremia, serotypes, and antibody response. J Infect Dis 2008; 197:817–824.
    71. 2012; Simmons CP, Farrar JJ, van Vinh CN, et al. Dengue. N Engl J Med. 366:1423–1432.
    72. Grard G, Caron M, Mombo IM, et al. Zika virus in Gabon (central Africa) – 2007: A new threat from Aedes albopictus? PLoS Negl Trop Dis 2014; 8:e2681.
    73. Kutsuna S, Kato Y, Takasaki T, et al. Two cases of Zika fever imported from French Polynesia to Japan, December 2013 to January 2014 [corrected]. Euro Surveill 2014; 19:
    74. Rossi SL, Ross TM, Evans JD. West Nile virus. Clin Lab Med 2010; 30:47–65.
    75. Outhred AC, Kok J, Dwyer DE. Neuroviral Infections: General Principles and DNA Viruses. Singh SK, Ruzek D, editors. Boca Raton, FL: CRC Press; 2012.
    76. Kuhn JH. Filoviruses. A compendium of 40 years of epidemiological, clinical, and laboratory studies. Arch Virol Suppl 2008; 20:13–360.
    77. Bwaka MA, Bonnet MJ, Calain P, et al. Ebola hemorrhagic fever in Kikwit, Democratic Republic of the Congo: clinical observations in 103 patients. J Infect Dis 1999; 179 (s1):S1–S7.
    78. Lamunu M, Lutwama JJ, Kamugisha J, et al. Containing a haemorrhagic fever epidemic: the Ebola experience in Uganda (October 2000–January 2001). Int J Infect Dis 2004; 8:27–37.
    79. Team ROAWIS. Ebola haemorrhagic fever in Sudan, 1976. Bulletin of the World Health Organization. World Health Organiz 1978; 56:247.
    80. Wyplosz B, Carlotti A, Escaut L, et al. Initial human herpesvirus-8 rash and multicentric Castleman disease. Clin Infect Dis 2008; 47:684–688.
    81. Budavari JM, Grayson W. Papular follicular eruptions in human immunodeficiency virus-positive patients in South Africa. Int J Dermatol 2007; 46:706–710.
    82. Stone JH, Murali MR. Case records of the Massachusetts General Hospital. Case 10-2013. A 30-year-old man with fever, myalgias, arthritis, and rash. N Engl J Med 2013; 368:1239–1245.
    83. Al-Shukri I, Davidson E, Tan A, et al. Rash and arthralgia caused by hepatitis E. The Lancet 2013; 382:1856.
    84▪. Albariño CG, Foltzer M, Towner JS, et al. Novel paramyxovirus associated with severe acute febrile disease, South Sudan and Uganda, 2012. Emerg Infect Dis 2014; 20:211–216.

    Description of novel Sosuga virus presentation and identification.

    85▪▪. Molina-Ruiz AM, Santonja C, Rütten A, et al. Immunohistochemistry in the diagnosis of cutaneous viral infections-part I. Cutaneous viral infections by herpesviruses and papillomaviruses. Am J Dermatopathol 2015; 37:1–14.

    Overview of the use of immunohistochemistry in the diagnosis of herpesviruses and papillomaviruses.

    86▪▪. Molina-Ruiz AM, Santonja C, Rütten A, et al. Immunohistochemistry in the diagnosis of cutaneous viral infections-Part II: cutaneous viral infections by parvoviruses, poxviruses, paramyxoviridae, picornaviridae, retroviruses and filoviruses. Am J Dermatopathol 2015; 37:93–106.

    Overview of the use of immunohistochemistry in the diagnosis of parvoviruses, polyomaviruses, poxviruses, paramyxoviridae, picornaviridae, retroviruses and filoviruses.


    exanthem; Gianotti–Crosti syndrome; rash; viral infection; virus

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