IndianJPaediatrDermatol1717-1118741_030627

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2016 Indian Journal of Paediatric Dermatology | Published by Wolters Kluwer - Medknow 7

cases occur during summer and early autumn.[1,2] Inmost instances, this is a mild self-limiting illness. Theskin lesions heal spontaneously without scarring. Theanalysis of the recent epidemics has shown a spectrum

INTRODUCTION

Hand, foot, and mouth disease (HFMD), a viralinfection which predominantly affects thechildren is characterized by a brief prodrome anderythematous papulovesicles mostly localized to palmsand soles with or without oral ulcerations. Involvementof buttocks, knees, elbows, and perioral skin is foundless commonly.[1,2]HFMD is usually been associated

with coxsackie A16, not uncommonly by coxsackie

A5, A10, and by human enterovirus 71.[3]The most

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DOI:

10.4103/2319-7250.173150

Hand, foot and mouth disease in children: A clinico

epidemiological study

K Bhumesh Kumar, A Geeta Kiran, B Udaya KumarDepartment of Dermatology, Venereology and Leprosy, Gandhi Medical College, Hyderabad, Telangana, India

ABSTRACT

Background:Epidemics of hand, foot, and mouth disease (HFMD) are increasing every year globally. The disease now

presents an increasing threat to public health worldwide. HFMD is a highly contagious viral infection characterized by a

typical maculopapular or vesicular eruptions on the hands and feet and in the oral cavity. It affects predominantly children

and/or immunocompromised adults and follows a benign self-limiting course. However, HFMD cases with severe or lethal

complications such as encephalitis, meningitis, pulmonary edema, and myocarditis have been reported mostly in children,

and also in immunocompromised adults. The common pathogens are coxsackievirus A16, enterovirus 71, and recently

coxsackieviruses A6 and A10 have been included. Differences in the course of HFMD have been observed depending on

the virus type, age, and immune status.

Aim:This study is to review the clinico epidemiological data for HFMD for early diagnosis and treatment, to prevent the

complications and to implement the precautionary measures during outbreaks.

Materials and Methods: A prospective observational study is conducted from August 2013 to January 2014. Consecutive

cases clinically diagnosed as HFMD, in the pediatric age group were taken up.

Results:We report the clinico epidemiological study of 50 cases of HFMD, their benign course and recovery among

immunocompetent children.

Conclusion: Early accurate diagnosis and treatment of HFMD along with monitoring is crucial to prevent severe

complications. Hence, a high index of suspicion is required to diagnose HFMD.

Key words: Coxsackievirus, hand, foot and mouth disease, immunocompetent children

ADDRESS FOR CORRESPONDENCEDr. K Bhumesh Kumar,

Department of Dermatology, Venereology and Leprosy, Gandhi MedicalCollege, Hyderabad - 500 003, Telangana, India.

E-mail: [email protected]

How to cite this article:Kumar K B, Kiran A G, Kumar B U. Hand, foot

and mouth disease in children: A clinico epidemiological study. Indian J

Paediatr Dermatol 2016;17:7-12.

This is an open access article distributed under the terms of the CreativeCommons Attribution-NonCommercial-ShareAlike 3.0 License, which allowsothers to remix, tweak, and build upon the work non-commercially, as long asthe author is credited and the new creations are licensed under the identicalterms.

For reprints contact: [email protected]

ORIGINAL ARTICLE

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Kumar, et al.: HFMD in children

Indian Journal of Paediatric Dermatology | Vol 17 | Issue 1 |Jan-Mar 20168

of central nervous system complications.[4]Mortalityis due to cardio-respiratory failure in severely affectedchildren.[5]

MATERIALS AND METHODS

A prospective observational study is conducted fromAugust 2013 to January 2014 in Hyderabad city.Consecutive cases clinically diagnosed as HFMD,in pediatric age group, attending DVL outpatientdepartment (OPD) were taken up.

Inclusion Criteria

All clinically diagnosed cases of HFMD children weretaken up for the study.

Exclusion Criteria

All above 18 years of age were excluded from thestudy.

Objectives

This study is to review the clinico epidemiologicaldata for HFMD for early diagnosis, to prevent thecomplications and to implement the precautionarymeasures during outbreaks.

RESULTS

A total of 50 cases were observed during an outbreakof HFMD. The youngest child among the casesstudied was 7-month-old and the oldest being

16 years [Chart 1]. The infection predominantlyaffected the children younger than 5 years (80%).Male to female ratio was 1:1. History of contact

with similar cases was found in 84% (42) ofcases [Chart 2]. All 50 cases presented with bothenanthemas and exanthemas either serially orsimultaneously, of which 44% (22) cases wereassociated with prodromal symptoms such as fever,irritability, etc. [Charts 3 and 4]. All the cases weremild in the form. There were no symptoms and signsof the primary immunodeficiency disorders such asrecurrent or atypical microbial infections, and they

were not on immunosuppressive medication.

Enathemas

Oral involvement [Figures 1 and 2] was found among48% (24) of 50 cases as a presenting complaint, of

which 70% (17) cases gave history of either droolingof saliva or refusal of feeds probably due to painfulerosions in infants. In seven cases (30%), painful oralerosions were seen on the soft palate, buccal mucosa,lateral side of the tongue, or on the dorsum of the

tongue in children [Chart 5]. Oral erosions were eithersingle or multiple in number.

Exanthemas

52% (26) cases presented with cutaneousmanifestations [Figures 3-5] as a presenting complaint

with itching and pain over the skin lesions in 6 and

2 cases, respectively. Remaining 70% (18) caseswere asymptomatic [Chart 6]. Exanthemas wereusually present in clusters of 310 maculopapules onerythematous skin involving the extremities either

80%(40)

20%(10)

0

10

20

30

40

Below 5 years Above 5 years

Chart 1:Predominantly affected age group is below 5 years (youngest age

was 7-month-old, and the oldest age was 16-year-old)

84%(42)

16%(8)0

10

20

30

40

50

History of contact No history of contact

Chart 2:History of contact with similar cases is seen in 42 (84%). No

history of contact in 8 (16%)

44%(22)

46%(28)

0

5

10

15

20

25

30

Prodromal symptoms No prodromal symptoms

Chart 3:22 cases (44%) were associated with prodromal symptoms like

fever and irritability. No prodromal symptoms in 28 (46%)



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Indian Journal of Paediatric Dermatology | Vol 17 | Issue 1 |Jan-Mar 2016 9

48%(24)

52%(26)

Enanthem as presenting

complaint

Exanthem as presenting

complaint

Chart 4:All 50 cases presented with both enathemas and exanthemas

of 23 days duration. Presenting complaint as enanthem is 48% and as

exanthema is 52%Figure 1:Erosion on soft palate

Figure 2:Erosion on tongue

Figure 3:Football shaped vesicle on erythmatous base on palm and sole

Figure 4:On buttocks

Figure 5:Extensive involvement on trunk

on the hand or palm then spreading to other partsof the body such as buttocks, legs, arms, and trunk.The dorsal aspect of the hands and sides of the fingers

were involved more often than the palmar aspect andfeet.

The diagnosis of HFMD was made based ondetailed clinical history and examination. Routineinvestigations of complete blood profile, erythrocytesedimentation rate, C-reactive protein, complete



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urine examination and chest X-ray were normal.Tzanck smears were negative ruling out other viral

infections such as herpes simplex virus, varicella, andmeasles.

All the children were treated with supportiveand symptomatic therapy such as cold sponging,antipyretics, plenty of oral fluids along withreassurance and counseling their parents. The lesionssubsided in 710 days without any significantcomplications such as dehydration, encephalitis,meningitis, myocarditis, and pulmonary edema. Allcases were treated on OPD basis, and none of thepatients required hospitalization.

DISCUSSION

HFMD is also known as vesicular stomatitis withexanthema caused by coxsackievirus which is highlycontagious.[6]During epidemics, the virus spread byhorizontal transmission with an incubation periodof 36 days. Initially, viral implantation occurs inthe buccal and ileal mucosa followed by spread tothe lymph nodes within 24 h. Oral lesions begin aserythematous macules that evolve into 23 mm

vesicles on an erythematous base. The vesicles mayinvolve the palate, buccal mucosa, gingival, lips andtongue. The vesicles are rarely observed because theyrapidly become eroded. They are painful with droolingof saliva and may interfere with the masticationand feeding as it observed in our study, especiallyin infants. In 44% of cases, tongue involvement isreported.[7] Viremia rapidly ensues, with spread tothe oral mucosa and skin. All lesions will be clearedover a period of 12 weeks because after 710 days,neutralizing antibody levels increase and the virus iseliminated.[8]

The same was noted in our study in the form of clinicalclearance of lesions in 1 to 2 weeks.

Normally there is no enteric virus flora in a humanbeing. In an individual, only one type of enterovirusmultiplies within the intestine at any given point oftime. Polio vaccination has been eliminated poliovirusesfrom the gut, thereby increasing the chances of otherenteroviruses like coxsackievirus and echo viralinfections. It is possible that the emergence of HFMDin India may be related to the mass polio vaccination.[9]The largest outbreak of HFMD occurred in an easternpart of India in 2007, where about 38 cases of HFMDin and around Kolkata was reported.[10]

Complications such as dehydration,meningoenchephalitis, myocarditis, pulmonary edemaand death occasionally occur in children with HFMD.[11]Complications mainly depend on the strain of theorganism, age and immune status of the child. Out ofall complications, dehydration was the most common.It may be due to hyperpyrexia and refusal of feedingdue to painful erosions, it may be easily prevented byplenty of oral fluids, cold sponging, and antipyretics.In our study of HFMD, we could not find any majorcomplications since this outbreak may be caused bycoxsackievirus A16. It is a benign and most commonstrain whereas enterovirus 71 is a rare strain commonlyassociated with severe complications. Hence, earlydiagnosis and treatment along with monitoring forsevere complication is mandatory because clinically wemay not know the strain of the virus.

Oral lesions of HFMD can be easily misdiagnosed asaphthous ulcers, varicella or herpangina. However,aphthous ulcers are multiple, more painful andrecurrent not associated with prodromal symptoms.

70%(17) 30%(7)

0 10 20 30

Symptoms

sign

Chart 5: Enanthemas: History of excessive crying, drooling of saliva

and refusal of feeds is seen in infants in 17 cases (70%) whereas painful

erosions on the soft palate, buccal mucosa, lateral, dorsal and ventral side

of the tongue is seen in children in 7 cases (30%)

30%(8)

70%(18)

0

5

10

15

20

Symptomatic Asymptomatic

Chart 6:Exanthemas: Asymptomatic in 18 (70%) cases and symptomatic

in 8 cases (30%)



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Indian Journal of Paediatric Dermatology | Vol 17 | Issue 1 |Jan-Mar 2016 11

Varicella rarely presents with oral lesions and theskin lesions are more concentrated on the trunk,rarely affecting the palms and soles. Herpangina isa viral infection of the children caused by a Type Acoxsackievirus which presents with similar types oforal ulcers extensively involving the tonsils, pharyngealmucosa, soft palate and the posterior part of buccal

mucosa.[12]Most of the parents come to us with thesuspicion of either measles or varicella infection.

Treatment

Medications are usually not needed as HFMD is a viraldisease that typically gets better on its own. Currently,there is no specific treatment for HFMD.[13] Diseasemanagement typically focuses on achieving symptomaticrelief. Pain from the sores may be eased with the useof analgesic medications like the topical application ofanesthetics and viscous lidocaine or dyphenhydramine.Infection in older children, adolescents, and adults is

typically mild and lasts approximately 1-week, but mayoccasionally run a longer course. Prodromal symptomslike fever can be treated with plenty of oral fluids, coldsponging, and antipyretics. A minority of individuals

with HFMD may require hospital admission due touncommon neurologic complications such as encephalitis,meningitis, or acute flaccid paralysis.[14]Nonneurologiccomplications such as myocarditis, pleural effusion, orbleeding into the lungs may also occur.[14]

Complications from the viral infections that causeHFMD are rare but require immediate medicaltreatment if present. HFMD infections caused byenterovirus 71 tend to be more severe and are more likelyto have neurologic or cardiac complications, includingdeath than infections caused by coxsackievirus

A16.[13] Viral or aseptic meningitis can occur withHFMD in rare cases and is characterized by fever,headache, stiff neck, or back pain.[13]The condition isusually mild and clears without treatment. However,hospitalization for a short time may be needed. Otherserious complications of HFMD include encephalitisor flaccid paralysis in rare circumstances.[13]

Fingernail and toenail loss have been reported in

children 48 weeks after having HFMD.[15] Therelationship between HFMD and the reported nailloss is unclear; however, it is temporary, and nailgrowth resumes without treatment.[15]

Prevention

Currently, there is no specific vaccine or antiviraltherapy against HFMD but such vaccines are beingdeveloped.[13] HFMD is highly contagious and istransmitted by nasopharyngeal secretions such as

saliva or nasal mucus, by direct contact, or by fecal-oraltransmission. Preventive measures include avoidingdirect contact with infected individuals, includingkeeping infected children home from school, propercleaning of shared utensils, disinfecting contaminatedsurfaces, and proper hand hygiene. These measureshave been shown to be effective in decreasing the

transmission of the viruses responsible for HFMD.[13]

CONCLUSION

Normally there is no enteric viral flora in human beings.Usually, only one type of enterovirus multiplies in anindividual at any given point of time. Polio vaccinationhas eliminated polio viruses from the gut therebyincreasing the chances of the coxsackievirus andenteroviral infections. It is possible that the emergenceof HFMD in India may be related to the mass polio

vaccination. Coxsackievirus A16 is more common and

has a benign course, whereas enerovirus 71 is rare andhas a lethal outcome. Early accurate diagnosis andtreatment of HFMD along with monitoring is crucialto prevent severe complications. Hence, a high indexof suspicion is required to diagnose HFMD.

Declaration of Patient Consent

The authors certify that they have obtained allappropriate patient consent forms. In the form thepatient(s) has/have given his/her/their consent for his/her/their images and other clinical information to bereported in the journal. The patients understand that

their names and initials will not be published anddue efforts will be made to conceal their identity, butanonymity cannot be guaranteed.

Financial Support and Sponsorship

Nil.

Conicts of Interest

There are no conflicts of interest.

REFERENCES

1. Miller GD, Tindall JP. Hand-foot-and-mouth disease. JAMA1968;203:827-30.

2. Ang LW, Koh BK, Chan KP, Chua LT, James L, Goh KT.Epidemiology and control of hand, foot and mouth diseasein Singapore, 2001-2007. Ann Acad Med Singapore2009;38:106-12.

3. Chen KT, Chang HL, Wang ST, Cheng YT, Yang JY.Epidemiologic features of hand-foot-mouth disease andherpangina caused by enterovirus 71 in Taiwan, 1998-2005.Pediatrics 2007;120:e244-52.

4. Ho M, Chen ER, Hsu KH, Twu SJ, Chen KT, Tsai SF, et al.An epidemic of enterovirus 71 infection in Taiwan. Taiwan



6/6



Enterovirus Epidemic Working Group. N Engl J Med1999;341:929-35.

5. Huang CC, Liu CC, Chang YC, Chen CY, Wang ST, Yeh TF.Neurologic complications in children with enterovirus 71infection. N Engl J Med 1999;341:936-42.

6. Buchner A, Mlinek A. Hand-foot-and-mouth disease inchildren in Israel. Harefuah 1973;84:321-2.

7. Thomas I, Janniger CK. Hand, foot, and mouth disease. Cutis

1993;52:265-6.8. Chang LY, King CC, Hsu KH, Ning HC, Tsao KC, Li CC, et al.

Risk factors of enterovirus 71 infection and associated hand,foot, and mouth disease/herpangina in children during anepidemic in Taiwan. Pediatrics 2002;109:e88.

9. Martin LA. Enteric viruses. In: Petersdorf RG, Adams RD,Braunwald E, Isselbacker KJ, Wilson JD, editors. HarrisonPrinciples of Internal Medicine. 10th ed. McGraw-HillInternational Book Company; 1983. p. 1125-32.

10. Sarma N, Sarkar A, Mukherjee A, Ghosh A, Dhar S, Malakar R.

Epidemic of hand, foot and mouth disease in West Bengal,India in August, 2007: A multicentric study. Indian J Dermatol2009;54:26-30.

11. Thomas J. Hand foot and mouth disease An overview. EJIndian Soc Teledermatol 2009;3:1-5.

12. Sterling JC. Viral infections. In: Burns T, Breathnach S, Cox N,Griffiths C, editors. Rooks Text Book of Dermatology. 7thed.,Vol. 25. Oxford: Blackwell Science; 2004. p. 1-83.

13. Sarma N. Hand, foot, and mouth disease: Current scenarioand Indian perspective. Indian J Dermatol Venereol Leprol2013;79:165-75.

14. Li Y, Zhu R, Qian Y, Deng J. The characteristics of bloodglucose and WBC counts in peripheral blood of cases of handfoot and mouth disease in China: A systematic review. PLoSOne 2012;7:e29003.

15. Hoy NY, Leung AK, Metelitsa AI, Adams S. New concepts inmedian nail dystrophy, onychomycosis, and hand, foot, and mouthdisease nail pathology. ISRN Dermatol 2012;2012:680163.


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