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Case Report
Lecturer, Department of Pedodontics,Himachal Pradesh Government Dental College, Shimla, Himachal Pradesh.
Senior Lecturer, Department of Conservative Dentistry & Endodontics,Himachal College of Dental Sciences, Himachal Pradesh.
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Professor & H.O.D, Himachal Pradesh Government Dental College, Shimla, Himachal Pradesh.
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Lecturer, Department of Pedodontics,Himachal Pradesh Government Dental College, Shimla, Himachal Pradesh.
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Abstract
Primary Herpetic Gingivostomatitis(PHG) is a common infection of oral mucosa in children due to viral origin. PHG is accompanied with several
prodromal symptoms like fever, anorexia, irritability, malaise and headache. Intraorally there is severe stomatitis (inflammation of oral mucosa),
presence of several pin point vesicles that rupture to give raise to ulcers.Several oral conditions occur commonly that resemble PHG leading to
wrong diagnosis of the condition. Improper diagnosis can lead to improper treatment planning in children.The authors propose a treatment
algorithm for management of PHG.
Key Words
Primary Herpetic Gingivostomatitis, HSV 1, teething, acyclovir.
Introduction
Primary Herpetic Gingivostomatitis (PHG) is a common
infection of oral mucosa in children due to viral origin. It is
referred to as primary because the oral manifestation of disease
commonly occursduring the 1stepisode of Herpes simplex
virus (Herpes hominis virus, type I and II, with type I more
common). Other terms used to describe this condition is canker
sores.[1] About 1% of primary care consultations are for cold
sores. In US, 57.7% of population is infected with HSV-1.[2]
Worldwide, the rate of infection is over 85% after levels of
passively acquired maternal antibodies have diminished;
infants and young children are at increased risk for acquiring
infections.
After an incubation period of 3-7 days, the symptoms of the
disease start to appear. Virus enters epithelial lining of oral
mucosa and starts to replicate. Further these epithelial cells full
of virions breakdown pouring out their contents. Now newly
formed virions are free to invade neighbouring cells or
transmit to new sites or infect other people.[3] PHG is
accompanied with several prodromal symptoms like fever,
anorexia, irritability, malaise and headache. Intraorally there is
severe stomatitis (inflammation of oral mucosa), presence of
several pin point vesicles that rupture to give raise to ulcers.
These ulcers are usually covered by a yellow-grey membrane,
several in number, pinpoint in size. There is presence of linear
gingival erythema of gums, coated tongue, presence of plaque
due to ensuing improper oral hygiene and halitosis. Other
findings include halitosis, drooling saliva and refusal to drink
are usual concomitant findings.[4]
Case Report
A 2 year old child was accompanied by parents to the clinic.
The accompanying mother complained of inability/refusal of
the child to consume food from past 3 days. On general
examination, the child appeared to be malnourished. Weight
and height of the child did not coincide with Indian Standard
height-weight charts. The child was lethargic, irritated and not
oriented (must have occurred due absence of food intake from
past 3 days), severe halitosis (must have occurred due to lack of
oral hygiene), and pyrexia. Intraoral examination revealed
severe gingivitis (marginal, papillary and attached gingiva)
with linear marginal erythema characteristic of the disease
(Figure 1). Other regions of the mouth especially the upper
and lower lip was also erythematous with multiple ulcers
(Figure 2). The tongue showed peculiar strawberry
appearance (may be due to malnutrition and ensuing vitamin
deficiency) with several coalesced areas of depapillation and
ulcers (Figure 3). There was presence of pinpoint multiple
ulcerations in the gingiva and buccal mucosa also (Figure 4).
The ulcer was covered with grey-yellow membrane and
surrounded by a small area of inflammation. Palpation of the
small ulcers and surrounding region was painful.
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Diagnosis
Based on history, symptoms, and signs - a diagnosis of Primary
herpetic gingivostomatitis was ascertained.
Treatment
The patient was hospitalised immediately to treat for severe
dehydration immediately. Prescription of acyclovir to treat
infection, paracetamol to treat pyrexia was done. Topical
application of glycerine to oral mucosa was advised to
alleviate painful ulcers. Mother was instructed regarding care
of patient and hygiene practices to decrease the chances of
spread of infection to mother as well. Instructions regarding
Journal of Dental Herald (January 2015 Issue:1, Vol.:2).
Discussion
Herpetic gingivostomatitis is a highly contagious disease of
children. The general course is 10-14 days, although it is a selflimiting disease; it can cause several complications in children
and especially individuals with weak immunity. Viral
shedding can occur up to 60 hours after the onset of
symptoms.[5] Exchange of oral secretions can lead to
transmission of organisms from a child to other children.
Sharing of cups, baby bottles, nipples, spoons, plates, teething
toys or even mouth touching or kissing can easily lead to
spread of infection. All this accounts to higher infectious rate
of HSV among children. Reactivation of the dormant virus can
occur, often precipitated by factors such as sun exposure,
s t r e s s , i l l n e s s , m e n s e s , f e v e r, o r i m m u n e
suppression.Especially it is common to see sudden epidemics
in schools or day care centres. There are several complications
of untreated herpes virus-, viz Simplex keratitis- Constant touching of lesions and eye
can relocate organisms from oral cavity to eyes. It is
characterised by conjunctivitis, uveitis, (red eyes, watering
eyes), callousness to light and in severe cases can lead to
blindness. [6]
Genital lesions- Characterised by presence of painful
ulcers on genitals. HSV-1 can also be transferred to the
genitals through oral sex when mouth sores are present,
causing genital sores.
Herpes Zoster-Virus involving trigeminal neuralgia can
lead to neuralgias.
Bell's palsy- Bell's palsy is paralysis of facial muscles
affecting facial nerve.
Recurrent infections can lead to herpes labialis.[7]
Recurrent lesions at same site may sometimes alsoleads to
atrophy and scarring.
Secondary bacterial infection like impetigo may also
occur.
Several oral conditions occur commonly that resemble PHG
leading to wrong diagnosis of the condition. Improper
diagnosis can lead to improper treatment planning. The
conditions that mimic PHG are1. Teething- Teething is a common condition that occurs
during childhood. Symptoms of teething are similar to
PHG such as inability to eat, fever, irritation, lethargy.
Also, a milder form of PHG occurs when there is presence
of residual maternal antibodies leading to wrong diagnosis;
hence dismissed as teething problem because of absence of
classical signs of PHG in such cases.[8]
2. Aphthous stomatitis- Can be differentiated by presence of
lesions only in non-keratinizsed mucosa. There is no
history of vesicles and no prodromal symptoms.[9]
3. Herpangina- caused by Coxsackie A virus. This condition
is differentiated by presence of ulcers in soft palate and
anterior pillar of the mouth.[10]
4. Chickenpox- Caused by Varicella zoster. Presence of
vesicular rash mainly on head and body.
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2.
Treatment of infection.
3.
4.
5.
6.
7.
8.
4.
5. Chronic elemental mercury poisoning- Characterised by
severe inflammation of gums and oral mucosa. It is
differentiated by presence of additional neurological
problems like tremors, paraesthesia and psychiatric
problems like forgetfulness & mood disturbances.
6. Hand, foot, and mouth disease- Caused by Coxsackie viral
disease. This is differentiated by presence intra-oral and
extra-oral vesicles over other parts of body.
7. Stevens-Johnson Syndrome/ Erythema multiformeDifferentiated by presence of bothintra & oral lesions.
8. Impetigo.
Laboratory Investigations
Commonly used investigations are full blood count, culture
testsand serological tests.
1. In addition to the clinical picture associated with PHGS, a
complete blood count may reveal leucocytosis or
neutropenia associated with viral infections.
2. Culture of herpes simplex virus Isolation of the HSV-1
virus can be done using cell culture techniques.
Commercial kits are available. Careful swabbing of lesions
can be done with careful effort not to invoke trauma on
painful lesions.
3. Serology assaysAn indirect immunofluorescence
antibody test can be performed. newer fluorescent staining
or monoclonal antibodies can be performed.
4. Immunoassay techniques such as enzyme immunoassay
(EIA) or (ELISA) can identify viral DNA.
5. Rapid detection based on polymerase chain reaction (PCR)
is available when required (e.g., immunocompromised
patients, severe infection).[5]
6. Nucleic acid probes.
5.
6.
7.
8.
Treatment
The authors propose a treatment algorithm for management of
PHG (Table 1).
Nonpharmacologic comfort measures may include ageappropriate distraction techniques, cutaneous stimulation, and
the presence of significant caregivers to hold or rock children.
References
1. Kolokotronis A, Doumas S. Herpes simplex virus
infection, with particular reference to the progression and
complications of primaryherpetic gingivostomatitis. Clin
Microbiol Infect. 2006 Mar;12(3):202-11.
2. Xu F, Sternberg MR, Kottiri BJ, et al. Trends in herpes
simplex virus type 1 and type 2 seroprevalence in the
United States. JAMA. 2006 Aug 23;296(8):964-73.
3. Arduino PG, Porter SR. Herpes Simplex Virus Type 1
infection: overview on relevant clinico-pathological
features.J Oral Pathol Med. 2008 Feb;37(2):107-21.
4. Chandrasekar PH. Identification and treatment of herpes
lesions. Adv Wound Care. 1999 Jun;12(5):254-62.
5. Vogel JL, Kristie TM; The dynamics of HCF-1 modulation
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