Pediatric Annals

Special Issue Article 

Exanthematous Eruptions in Children

Trevor K. Young, BS; Vikash S. Oza, MD

Abstract

Childhood exanthems are commonly encountered by pediatricians in the hospital and the office. In the last several decades, we have seen a shift in the epidemiology of many of these diseases. After being deemed eliminated at the turn of 21st century, measles has experienced a resurgence secondary to falling vaccination rates, raising public health concerns. A new variant of hand, foot, and mouth disease caused by coxsackievirus A6 has been associated with more widespread and atypical disease, which can present diagnostic challenges to clinicians. Parvovirus B19, which is traditionally associated with fifth disease, is also the leading cause of papular purpuric gloves and socks syndrome, a rare condition with which providers may be unfamiliar. Since the introduction of routine vaccination, there has been a shift in the epidemiology and clinical presentation of primary varicella and herpes zoster. Finally, the recently described phenomenon of Mycoplasma pneumoniae-induced rash and mucositis will be discussed. [Pediatr Ann. 2020;49(3):e116–e123.]

Abstract

Childhood exanthems are commonly encountered by pediatricians in the hospital and the office. In the last several decades, we have seen a shift in the epidemiology of many of these diseases. After being deemed eliminated at the turn of 21st century, measles has experienced a resurgence secondary to falling vaccination rates, raising public health concerns. A new variant of hand, foot, and mouth disease caused by coxsackievirus A6 has been associated with more widespread and atypical disease, which can present diagnostic challenges to clinicians. Parvovirus B19, which is traditionally associated with fifth disease, is also the leading cause of papular purpuric gloves and socks syndrome, a rare condition with which providers may be unfamiliar. Since the introduction of routine vaccination, there has been a shift in the epidemiology and clinical presentation of primary varicella and herpes zoster. Finally, the recently described phenomenon of Mycoplasma pneumoniae-induced rash and mucositis will be discussed. [Pediatr Ann. 2020;49(3):e116–e123.]

The exanthem is often the medical trainee's first introduction to the field of dermatology. In its simplest form, an exanthem is a cutaneous eruption driven by an underlying disease state. Most childhood exanthems reflect underlying viremia in which the virus seeds the skin and a cutaneous inflammatory response ensues, resulting in a characteristic dermatologic pattern (Table 1).

Common Childhood Exanthems

Table 1.

Common Childhood Exanthems

Our understanding of childhood exanthems dates to the earliest recordings in medicine and is continually evolving. In the year 910 AD, Rhazes was first credited with pairing exanthems with specific infections: measles and smallpox. In modern medical literature, classic childhood exanthems were named in order of their discovery (ie, rubella or “third disease” was the third exanthem to be described). Today, the landscape of childhood exanthems is continually shifting, driven by vaccinations, immigration and travel, and the continual evolution of viral genomes. For the clinician, the importance of timely and accurate identification cannot be overstated. Many of the infections serve as public health threats, have serious systemic symptoms, and have important implications for close contacts. The goal of this article is to present an up-to-date review of select infectious exanthems of childhood with an emphasis on newly described manifestations that can aid in diagnosis.

Measles

A landmark achievement of 20th century medicine was the development of vaccines against common and potentially deadly infections. The measles vaccine was introduced in 1963, and the second dose was routinely recommended in 1990 after an outbreak among vaccinated children. Prior to routine vaccination, 3 to 4 million people were infected in the United States annually, resulting in 300 to 400 deaths per year.1 Due to widespread vaccination efforts, measles was deemed eliminated in 2000.2 However, in large part due to the falling rates of vaccination, particularly in certain enclaves, we have seen a resurgence of measles both within the US and throughout the world over the past several years.3 The largest number of measles cases since it was “eliminated” occurred between 2018 and 2019. The outbreak began after an unvaccinated child returned from Israel to a largely unvaccinated Orthodox Jewish community in Brooklyn, leading to 702 cases in New York City.4 There were a total of 1,487 cases in the US between September 30, 2018 and October 1, 2019.4

In temperate climates, measles is a seasonal disease with the highest rates in late winter and early spring. Theories for why this seasonality exists include environmental factors favoring virus transmission as well as social patterns that promote transmission, such as close contact of susceptible children in schools.5 Risk factors for measles include children younger than age 1 year who have not yet received their first vaccine; unvaccinated older children or adults; people with immunocompromised status; and unvaccinated travelers from areas where there are active outbreaks.

Clinically, measles presents with a prodrome of fever up to 104°F along with cough, coryza, and/or conjunctivitis, often lasting 2 to 4 days. During the prodrome, Koplik spots—small white papules with a surrounding erythematous ring on the buccal mucosa—may be present (Figure 1). Koplik spots typically present 48 hours prior to the onset of the exanthem and only last 12 to 72 hours. Therefore, they may be resolved by the time a patient with measles exanthem is evaluated. The hallmark feature of measles is a cranial to caudal spreading exanthem, starting on the face and spreading to the trunk and extremities (Figure 2). Many routine childhood exanthems do not start on the face. As the rash evolves, it coalesces on the trunk and often adopts a brownish color in patients with lighter skin complexion. The rash fades in 6 to 7 days. Patients are contagious from approximately 5 days before appearance of the rash until 4 days after rash onset. Patients should be isolated during this time to prevent transmission. The incubation period for measles is believed to be between 6 and 21 days. Clinicians should question the diagnosis of measles if the eruption spares the face, occurs in the absence of fever, or occurs in a fully vaccinated person, although cases of an attenuated form of measles termed “modified measles” have been described.6

Koplik spots: numerous white macules on the upper buccal mucosa near the second molar representing “grains of sand.”

Figure 1.

Koplik spots: numerous white macules on the upper buccal mucosa near the second molar representing “grains of sand.”

Morbiliform eruption of measles: 3- month-old infant with extensive morbilliform eruption throughout the trunk during the New York City measles outbreak of 2019.

Figure 2.

Morbiliform eruption of measles: 3- month-old infant with extensive morbilliform eruption throughout the trunk during the New York City measles outbreak of 2019.

Complications attributed to measles include pneumonia, acute otitis media, encephalitis, laryngitis, and severe vomiting and diarrhea causing dehydration. Serious complications are more common in children younger than age 5 years and patients who are malnourished. Encephalitis, which occurs during the acute infection, is seen in about 1 in 1,000 cases. This contrasts with subacute sclerosing panencephalitis, which occurs an average of 7 years after the acute infection and is almost always fatal. Measles has also been implicated in causing prolonged immunosuppression for years,7 and can result in an increase in all-cause childhood mortality for communities affected by measles outbreaks.8,9

In general, measles should be diagnosed clinically with prompt isolation and treatment while awaiting diagnostic confirmation. The current recommendation from the Centers for Disease Control and Prevention ( www.cdc.gov) is to obtain a throat swab specimen and a blood specimen for immunoglobulin (IgM) and reverse transcription polymerase chain reaction (PCR) testing. Providers should reach out to their local health department to determine where the samples should be sent.10 Treatment is usually supportive, although ribavirin is sometimes used in severe cases. Children should be carefully monitored for dehydration and signs of secondary bacterial infection. Immediate vitamin A supplementation is recommended for all patients regardless of nutritional status or country of origin, as it has been shown to decrease mortality.11 In otherwise healthy children, oral vitamin A should be given in 2 doses (one immediately upon diagnosis and a second dose 1 day later). Recommended doses are 50,000 IU for infants younger than age 6 months, 100,000 IU for infants age 6 to 11 months, and 200,000 IU to children older than age 12 months.12

Hand, Foot, and Mouth Disease

Hand, foot, and mouth disease (HFMD) was first termed “Toronto disease” in 1957 after a Toronto-based pediatrician described a reproducible eruption defined by oral aphthae and vesicles on the palms and soles. In the US, it has historically been caused by the picornaviruses coxsackievirus 16 (CVA16) and enterovirus 71 (EV71). It classically presents as prodromal fever and malaise followed by the development of oral aphthae as well as oval-shaped erythematous macules and vesicles limited to the palms, soles, and buttocks. Transmission usually occurs via ingestion of the virus with the highest transmission occurring in the summer and fall. Although CVA16 typically only causes HFMD, epidemics of EV71 with severe neurological and pulmonary complications have been reported in the Asia-Pacific region.13 For unclear reasons, these complications are not frequently seen in the US.

In 2008, coxsackie virus A6 (CVA6) was first described to cause an outbreak of HFMD in Finland followed by outbreaks in the US in 2011.14 Since that time CVA6 has become an increasingly common cause of the eruption, which can occur at any point of the year. CVA6 HFMD is characterized by palmoplantar involvement in addition to a more widespread eruption involving the upper and lower extremities as well as the perioral region. Large bullae on acral surfaces are seen in children younger than age 1 year, and purpuric macules may be seen in older patients. The eruption typically lasts for approximately 5 to 10 days. Despite the marked cutaneous findings, children with CVA6 infection generally do not have severe systemic symptoms. Families should be counseled about the potential for acral desquamation 1 to 2 weeks after resolution and onychomadesis (shedding of the nail plate from its proximal end) several months later. CVA6 has a predilection for areas of underlying atopic dermatitis, and patients with atopic dermatitis can present with “eczema coxsackium”—extensive erosions mimicking eczema herpeticum (Figure 3). However, in contrast to eczema herpeticum, eczema coxsackium should be a bilateral, symmetric eruption with palmoplantar involvement.

Eczema coxsackium: widespread erosions symmetrically involving the extremities in an infant with atopic dermatitis.

Figure 3.

Eczema coxsackium: widespread erosions symmetrically involving the extremities in an infant with atopic dermatitis.

Due to the varied morphology of CVA6 infection, the eruption can be confused for several diseases including bullous impetigo, autoimmune blistering diseases, and leukocytoclastic vasculitis. Clinicians should question the diagnosis of CVA6-induced HFMD if the exanthem does not involve the palms and soles. It should also be noted that the absence of oral aphthae cannot exclude HFMD, as oral lesions are only seen in 50% of cases caused by CVA6 compared to nearly all cases of classic HFMD.15

Diagnosis of classic HFMD is usually clinical. For more widespread cutaneous disease caused by CVA6, clinical diagnosis may be difficult, and PCR is the recommended method for diagnostic confirmation. Respiratory viral panels that report enterovirus can also be used. Treatment is generally supportive with wound care for skin lesions. In patients with eczema coxsackium, topical corticosteroids should be used to control the atopic dermatitis.

Parvovirus B19

Parvovirus B19 is a small DNA virus inadvertently discovered in 1974 when the hepatitis B antigen was being studied. Most people are exposed as children, and transmission occurs most commonly in the spring with associated school outbreaks. It is transmitted via respiratory droplets and blood exposure.

Erythema infectiosum, or fifth disease, is the most common manifestation of parvovirus B19 infection. The disease presents with nonspecific symptoms including fever, headache, and coryza. This is followed by the appearance of erythematous, edematous, confluent malar plaques, commonly referred to as “slapped cheeks,” and a lacy erythematous rash on the trunk and extremities that can be quite pruritic. Of note, the rash of fifth disease, which is believed to arise from immune complex deposition within blood vessels, is usually an indicator that the patient is appropriately clearing the infection and is no longer contagious.16 The rash resolves within about 1 week but can recur weeks to months later with certain triggers such as sunlight, warm temperature, and exercise. Approximately 10% of children who are affected develop arthralgias. Although the proximal interphalangeal and metacarpophalangeal joints are most commonly affected in adults, children most commonly present with involvement of large joints, particularly the knees.17 This is thought to be immune-related; parents can be reassured that children with arthralgias are not actively contagious and that symptoms typically resolve within 3 weeks.

Papular purpuric gloves and socks syndrome (PPGSS) was first described in 1990 as a dermatosis of unknown origin and was later found to be associated with parvovirus B19.18 Although usually seen with parvovirus B19, rare cases associated with other viruses have been observed.19 It is more commonly seen in adults and adolescents but has been described in younger children as well.20 It presents as a prodrome of mild fever, arthralgia, and myalgia followed by rapid development of symmetric edema and erythema of the hands and feet in a “gloves and socks” distribution. Purpuric papules and/or petechiae are also seen (Figure 4), and the affected areas are often very painful and pruritic. There is often a sharp demarcation at the wrists and ankles. Scattered erythematous papules on the trunk and extremities, palatal petechiae, oral erosions, and hyperemia of the lips and pharynx may also be seen. In younger children, the hands may be more involved than the feet and the petechial component may be less prominent. Fever and oral erosions may also be less common in younger children.20 The disease resolves within several weeks and there are no long-term complications. Duration of illness may be longer in younger children. In contrast to erythema infectiosum, in which patients are not infectious during the exanthem, patients with PPGSS are still thought to be contagious during the eruption.21

Parvovirus infection resulting in petechial eruption involving bilateral lower legs in a sock-like distribution.

Figure 4.

Parvovirus infection resulting in petechial eruption involving bilateral lower legs in a sock-like distribution.

Diagnosis of parvovirus B19 infection is usually clinical, as fifth disease is the most common clinical presentation and is self-limiting. In patients with aplastic crisis of unknown origin or PPGSS, IgM titers can be checked for diagnostic confirmation. PCR for viral DNA can also be done and is very sensitive. PCR should be used in an immunocompromised patient in whom there is concern for parvovirus B19 infection, as IgM titers may be unrevealing due to the underlying immunodeficiency.

Varicella

Varicella, or chickenpox, is caused by the varicella zoster virus. It is transmitted via respiratory droplets and close contact with vesicular fluid from active lesions. Like most respiratory viruses, transmission is most common in the winter and spring. Primary varicella is quite contagious, with >90% of susceptible household contacts acquiring the disease from a person who is infected. An attenuated vaccine was introduced in the US in 1995, and the second dose was added in 2006. Prior to the vaccine, 4 million children were diagnosed annually with over 10,000 hospitalizations and more than 100 deaths per year. Since introduction of the vaccine, there have been significant drops in total disease, hospitalization, and mortality, even among those who cannot receive the vaccine.22

Today, groups at risk include those who are unvaccinated or immunosuppressed, and immigrants from countries that do not routinely vaccinate for varicella. Severe varicella has been reported in patients on high-dose corticosteroids, particularly among patients who receive steroids during the incubation period,23 and in oncology patients. Patients with malignancy (particularly hematologic) who become infected are more likely to develop severe symptoms (including increased mortality), remain contagious for longer, and can become infected even if they have a history of vaccination or prior infection. This has led to outbreaks on pediatric oncology wards.24

Clinically, varicella has an incubation period of 1 to 2 weeks followed by a nonspecific prodrome of fever, malaise, and decreased appetite. This is followed by development of pruritic macules that quickly evolve into vesicles and crust over. Lesions can be found throughout the body but are typically most concentrated on the face and trunk. It is classic to see crops of vesicles and/or pustules in various stages of healing. New lesions should stop forming after about 4 days, and the crusts should fall off within 1 to 2 weeks. The most common complications in children are cutaneous bacterial superinfection and dehydration.

“Breakthrough varicella” is a much milder form of the disease that occurs when a previously immunized person is exposed to the virus. It presents with fewer lesions that are predominantly papular rather than vesicular, and it is seen more commonly in people who received one dose of the vaccine rather than two. Patients with breakthrough varicella can still transmit the virus, but much less so than with primary infection. Because of its varied and atypical presentation, it can be difficult to diagnose.

Diagnosis of varicella is usually clinical. When diagnostic confirmation is sought in the case of atypical or severe presentations, PCR of a sample of vesicular fluid is the preferred method. This can also be used to determine if an infection is from a wild-type or vaccine strain.

In general, children who are immunocompetent with classic symptoms can be treated with supportive therapy. There should be emphasis on decreasing scratching with oral antihistamines and topical preparations, as scratching is a significant risk factor for bacterial superinfection. People at higher risk for complications such as patients who are immunosuppressed and adolescents who are unvaccinated should be considered for oral antiviral therapy. If in the hospital, patients with varicella should be isolated with airborne precautions until all lesions have crusted over. Some evidence has suggested that patients who are immunocompromised may remain contagious even after lesions have crusted.24

Since the introduction of the varicella vaccine and coinciding decrease in childhood varicella infection, there has been a decrease in the incidence of herpes zoster in children.25 Approximately one-half of cases in children who are vaccinated are from wild-type strain and the other one-half are from the Oka vaccine strain. Vaccine-strain zoster is typically seen at an earlier age and may have a predilection for occurring on the same limb to which the vaccine was administered (Figure 5). In general, zoster should be a self-limiting disease, and recurring bouts of zoster should raise concern for an underlying immunodeficiency. Disseminated zoster is generally only seen in people who are immunocompromised and is defined as involving three or more dermatomes. Unlike in adults, children do not typically develop postherpetic neuralgia, so management decisions are often not made on preventing this complication. Children who are immunocompetent with zoster can be given antiviral therapy within 72 hours of disease onset to reduce symptom duration. All patients who are immunocompromised should receive antiviral therapy regardless of time since symptom onset.

Herpes zoster: grouped vesicles on an erythematous base in a dermatomal distribution.

Figure 5.

Herpes zoster: grouped vesicles on an erythematous base in a dermatomal distribution.

Mycoplasma Pneumoniae-Induced Rash and Mucositis

Mycoplasma pneumoniae is a common cause of atypical pneumonia and has been considered an infectious cause of Stevens-Johnson syndrome (SJS) in children since the 1960s.26 Most commonly drug-induced, SJS is characterized by a prodrome of fever and malaise followed by the development of epidermal necrosis and detachment, which manifests as confluent vesiculobullous lesions and sloughing of the skin. Drug-induced SJS can have internal organ involvement, lead to long-term morbidity, and has an estimated mortality rate of 16% if it progresses to toxic epidermal necrolysis (bullae involving greater than 30% of the body surface area).27 In contrast to drug-induced SJS, mycoplasma-induced mucocutaneous disease typically affects children (median age of 12 years), has prominent mucositis with limited cutaneous involvement, and has an excellent prognosis. This led to the proposal of a distinct entity, M. pneumoniae-induced rash and mucositis (MIRM), in 2015 to better characterize the mucocutaneous eruption seen in some people with mycoplasma pneumonia.28

MIRM begins with a prodrome of atypical pneumonia (fever, malaise, cough). This can be similar to the prodrome seen in drug-induced SJS, and providers should carefully investigate new medication exposures during this period. Approximately 1 week later, mucocutaneous lesions appear. Oral erosions and/or ulcerations are seen in almost all cases and may be quite severe, leading to confluent sloughing of the lips (Figure 6). Ocular involvement, characterized by purulent conjunctivitis with possible eyelid edema, and urogenital involvement are also commonly seen. Urogenital involvement can be characterized by vesiculobullous lesions and/or erosions.28 The nares and gastrointestinal tract can also be affected.29 Cutaneous involvement is seen in only about half of cases. When present, it is sparse and characterized by vesiculobullous and/or targetoid lesions with predilection for the extremities (Figure 7).28

Mycoplasma pneumoniae-induced rash and mucositis: mucosal erosions coalescing on the lower lip.

Figure 6.

Mycoplasma pneumoniae-induced rash and mucositis: mucosal erosions coalescing on the lower lip.

Mycoplasma pneumoniae-induced rash and mucositis: Erythematous targetoid papules on the dosral hand with central vesiculation.

Figure 7.

Mycoplasma pneumoniae-induced rash and mucositis: Erythematous targetoid papules on the dosral hand with central vesiculation.

Because of the variable presentations of MIRM, Canavan et al.28 proposed a set of diagnostic criteria. A patient should have clinical and laboratory evidence of atypical pneumonia, as evidenced by mycoplasma IgM, culture from oropharyngeal or cutaneous lesion, PCR, or serial cold agglutinins. There should be involvement of at least two mucosal sites and few vesiculobullous lesions with or without targetoid lesions. Skin detachment should not exceed 10% of body surface area. MIRM sine rash is used to describe MIRM without cutaneous involvement, and extensive widespread blisters or flat atypical target lesions are referred to as severe MIRM.28

There is no specific treatment for MIRM. The atypical pneumonia should be treated with a macrolide antibiotic, but it is not known if this intervention leads to improvement of MIRM. Similarly, although immunosuppressants such as corticosteroids and intravenous immunoglobulin are sometimes given, it is unclear if this is beneficial.28 Supportive care should be given with an emphasis on nutritional support, adequate wound care, and pain control such as medicated mouthwash for mucosal lesions. Ophthalmology consultation is essential as up to 10% of patients may have mucosal complications including conjunctival shrinkage, ocular synechiae, and blindness. Oral and urogenital synechiae have also been described and should be monitored. Transfer to a burn unit may be indicated if there is extensive involvement, although this would be unusual and should prompt thorough investigation for an alternate cause such as drug-induced SJS. Mucosal complications can be severe and necessitate prolonged hospital stays.30 However, most patients experience a full recovery. More recently, the diagnosis of reactive infectious mucocutaneous or mucosal-predominant eruption has been suggested to encompass similar mucositis-predominant eruptions caused by other respiratory pathogens, with Chlamydia pneumonia and influenza B being the most reported.31,32

References

  1. Centers for Disease Control and Prevention. Measles history. https://www.cdc.gov/measles/about/history.html. Accessed February 20, 2020.
  2. Wharton ME. Measles elimination in the United States. J Infect Dis. 2004;189(suppl):S1–S3. doi:10.1086/377693 [CrossRef]
  3. Feemster K, Szipszky C. Resurgence of measles in the United States: how did we get here?Curr Opin Pediatr. 2020;32(1):139–144. doi:10.1097/MOP.0000000000000845 [CrossRef]
  4. Patel M, Lee AD, Clemmons NS, et al. National update on measles cases and outbreaks United States, January 1-October 1, 2019. MMWR Morb Mortal Wkly Rep. 2019;68(40):893–896. doi:10.15585/mmwr.mm6840e2 [CrossRef] PMID:31600181
  5. Fine PE, Clarkson JA. Measles in England and Wales—I: an analysis of factors underlying seasonal patterns. Int J Epidemiol. 1982;11(1):5–14. doi:10.1093/ije/11.1.5 [CrossRef] PMID:7085179
  6. Komabayashi K, Seto J, Tanaka S, et al. The largest measles outbreak, including 38 modified measles and 22 typical measles cases in its elimination era in Yamagata, Japan, 2017. Jpn J Infect Dis. 2018;71(6):413–418. doi:10.7883/yoken.JJID.2018.083 [CrossRef] PMID:29962488
  7. Mina MJ, Metcalf CJE, de Swart RL, Osterhaus AD, Grenfell BT. Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality. Science.2015;348(6235):694–699. doi:10.1126/science.aaa3662 [CrossRef]
  8. Aaby P, Samb B, Simondon F, Seck AM, Knudsen K, Whittle H. Non-specific beneficial effect of measles immunisation: analysis of mortality studies from developing countries. BMJ.1995;311(7003):481–485. doi:10.1136/bmj.311.7003.481 [CrossRef]
  9. Welaga P, Hodgson A, Debpuur C, Aaby P, Binka F, Azonga D, Oduro A. Measles vaccination supports millennium development goal 4: increasing coverage and increasing child survival in Northern Ghana. Front Public Health. 1996–2012. 2018;6(28). doi:10.3389/fpubh.2018.00028 [CrossRef]
  10. Centers for Disease Control and Prevention. Collecting and shipping specimens for suspected measles cases. https://www.cdc.gov/measles/lab-tools/rt-pcr.html. Accessed February 20, 2020.
  11. Hussey GD, Klein M. A randomized, controlled trial of vitamin A in children with severe measles. N Engl J Med.1990;323(3):160–164. doi:10.1056/NEJM199007193230304 [CrossRef] PMID:2194128
  12. [No authors listed]. Measles vaccines: WHO position paper - April 2017. Wkly Epidemiol Rec. 2017;92(17):205–227. PMID: 28459148
  13. McMinn PC. An overview of the evolution of enterovirus 71 and its clinical and public health significance. FEMS Microbiol Rev. 2002;26(1):91–107. doi:10.1111/j.1574-6976.2002.tb00601.x [CrossRef] PMID:12007645
  14. Kimmis BD, Downing C, Tyring S. Hand-foot-and-mouth disease caused by coxsackievirus A6 on the rise. Cutis. 2018;102(5):353–356. PMID:30566537
  15. Mathes EF, Oza V, Frieden IJ, et al. “Eczema coxsackium” and unusual cutaneous findings in an enterovirus outbreak. Pediatrics. 2013;132(1):e149–e157. doi:10.1542/peds.2012-3175 [CrossRef] PMID:23776120
  16. Anderson MJ, Higgins PG, Davis LR, et al. Experimental parvoviral infection in humans. J Infect Dis. 1985;152(2):257–265. doi:10.1093/infdis/152.2.257 [CrossRef] PMID:2993431
  17. Nocton JJ, Miller LC, Tucker LB, Schaller JG. Human parvovirus B19-associated arthritis in children. J Pediatr. 1993;122(2):186–190. doi:10.1016/S0022-3476(06)80111-3 [CrossRef] PMID:8429430
  18. Harms M, Feldmann R, Saurat JH. Papular-purpuric “gloves and socks” syndrome. J Am Acad Dermatol. 1990;23(5 Pt 1):850–854. doi:10.1016/0190-9622(90)70302-X [CrossRef] PMID:2147699
  19. Gutermuth J, Nadas K, Zirbs M, et al. Papular-purpuric gloves and socks syndrome. Lancet. 2011;378(9786):198. doi:10.1016/S0140-6736(11)60554-0 [CrossRef] PMID:21742170
  20. Hsieh MY, Huang PH. The juvenile variant of papular-purpuric gloves and socks syndrome and its association with viral infections. Br J Dermatol. 2004;151(1):201–206. doi:10.1111/j.1365-2133.2004.05946.x [CrossRef] PMID:15270892
  21. Fölster-Holst R, Kreth HW. Viral exanthems in childhood – infectious (direct) exanthems. Part 2: other viral exanthems. J Dtsch Dermatol Ges. 2009;7(5):414–419. doi:10.1111/j.1610-0387.2008.06869.x [CrossRef]
  22. Bialek SR, Perella D, Zhang J, et al. Impact of a routine two-dose varicella vaccination program on varicella epidemiology. Pediatrics. 2013;132(5):e1134–e1140. doi:10.1542/peds.2013-0863 [CrossRef] PMID:24101763
  23. Reiches NA, Jones JF. Steroids and varicella. Pediatrics. 1993;92(2):288–289. PMID:8337033
  24. Manistarski M, Levin D, Dvir R, et al. Lessons from an outbreak of varicella infection in pediatric hemato-oncology patients. Pediatr Infect Dis J. 2018;37(7):649–653. doi:10.1097/INF.0000000000001920 [CrossRef] PMID:29373475
  25. Harpaz R, Leung JW. The epidemiology of herpes zoster in the United States during the era of varicella and herpes zoster vaccines: changing patterns among children. Clin Infect Dis. 2019;69(2):345–347. doi:10.1093/cid/ciy954 [CrossRef] PMID:30496366
  26. Katz HI, Wooten JW, Davis RG, Griffin JP. Stevens-Johnson syndrome. Report of a case associated with culturally proven Mycoplasma pneumoniae infection. JAMA. 1967;199(7):504–506. doi:10.1001/jama.1967.03120070116027 [CrossRef] PMID:6071288
  27. Hsu DY, Brieva J, Silverberg NB, Paller AS, Silverberg JI. Pediatric Stevens-Johnson syndrome and toxic epidermal necrolysis in the United States. J Am Acad Dermatol. 2017;76(5):811–817. doi:10.1016/j.jaad.2016.12.024 [CrossRef] PMID:28285784
  28. Canavan TN, Mathes EF, Frieden I, Shinkai K. Mycoplasma pneumoniae-induced rash and mucositis as a syndrome distinct from Stevens-Johnson syndrome and erythema multiforme: a systematic review. J Am Acad Dermatol. 2015;72(2):239–245. doi:10.1016/j.jaad.2014.06.026 [CrossRef] PMID:25592340
  29. Norton SA. Diagnosing Mycoplasma pneumoniae-induced rash and mucositis (MIRM) in the emergency room. J Am Acad Dermatol. 2015;73(2):e67. doi:10.1016/j.jaad.2015.03.060 [CrossRef] PMID:26184002
  30. Olson D, Watkins LK, Demirjian A, et al. Outbreak of Mycoplasma pneumoniae-associated Stevens-Johnson syndrome. Pediatrics. 2015;136(2):e386–e394. doi:10.1542/peds.2015-0278 [CrossRef] PMID:26216320
  31. Mayor-Ibarguren A, Feito-Rodriguez M, González-Ramos J, et al. Mucositis secondary to chlamydia pneumoniae Infection: expanding the Mycoplasma pneumoniae-induced rash and mucositis concept. Pediatr Dermatol. 2017;34(4):465–472. doi:10.1111/pde.13140 [CrossRef] PMID:28568680
  32. Goyal A, Hook K. Two pediatric cases of influenza B-induced rash and mucositis: Stevens-Johnson syndrome or expansion of the Mycoplasma pneumoniae-induced rash with mucositis (MIRM) spectrum?Pediatr Dermatol. 2019;36(6):929–931. doi:10.1111/pde.13921 [CrossRef] PMID:31576583

Common Childhood Exanthems

Peak Transmission Period Pathogen and Disease Key Clinical Features Period of Contagiousness
Winter and spring Varicella zoster virus (chickenpox) Prodrome: fever, malaise, and decreased appetite Exanthem: crops of vesicles and/or pustules concentrated on the face and trunk. Will classically see crops of lesions in various stages of healing Breakthrough varicella: seen in children who were previously immunized. Milder, predominantly papular, presentation Several days before rash onset until all lesions have crusted over
Late winter/early spring Rubeola virus (measles) Prodrome: fever, cough, coryza, conjunctivitis, and Koplik spots (small white papules resembling “grains of sand” on the buccal mucosa adjacent to the 1st and 2nd upper molars) Exanthem: starts on the face and spreads downward Approximately 5 days before appearance of the rash until 4 days after rash onset
Spring and winter (although can occur year-round) Mycoplasma pneumonia (M. pneumoniae-induced rash and mucositis) Prodrome: atypical pneumonia Mucositis, which may be severe, of at least 2 mucosal sites Limited cutaneous involvement characterized by targetoid and vesiculobullous lesions Approximately 10 days during the pneumonia
Spring Parvovirus B19 Fifth disease   Prodrome: fever, headache, and coryza   Exanthem: “slapped cheeks” rash and lacy truncal rash May have arthralgias (especially of the knees in young children) PPGSS   Symmetric erythema and edema of the hands and feet with sharp demarcation at the wrists and ankles   Purpuric papules and/or petechiae of the hands and feet Resolves within several weeks Fifth disease   Approximately 1 week prior to rash onset. Usually no longer contagious after the rash appears PPGSS   Thought to be contagious through- out the duration of the eruption
Summer and fall Year-round CVA16 and enterovirus 71 Classic HFMD   Prodrome: fever and malaise   Exanthem: Oral aphthae and vesicles limited to the palms, soles, and buttocks CVA6 HFMD   Palmoplantar vesicles   More widespread eruption involving the arms, legs, and perioral region   Oral aphthae may not be seen   Predilection for underlying atopic dermatitis (“eczema coxsackium”) Both classic and atypical HFMD are most contagious for the first week of illness, but may remain contagious for several weeks via shedding in the stool
Authors

Trevor K. Young, BS, is a Medical Student, New York University School of Medicine. Vikash S. Oza, MD, is an Assistant Professor of Dermatology and Pediatrics, The Ronald O. Perelman Department of Dermatology, New York University School of Medicine.

Address correspondence to Vikash S. Oza, MD, The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, 240 38th Street, 11th Floor, New York, NY 10016; email: Vikash.Oza@nyulangone.org.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/19382359-20200220-01

Sign up to receive

Journal E-contents