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Oral infections

Professor Samar Burgan


PhD, MSc (University of London)
Oral medicine specialist
Primary herpes simplex
herpetic gingivostomatitis
 Herpes viruses are contagious
 It affects children under 3 yrs and young adults
 80% of herpes simplex infections are asymptomatic
 In immunocompromised patients, infections can cause life-
threatening complications
 Prodromal symptoms appear 1-2 days prior to oral lesions,
then vesicles appear and affects both free and attached gingiva
 A generalised marginal gingivitis may precede oral ulcers
 Primary infection in adolescents manifests as severe pharyngitis
 The lesions heal spontaneously within 2 weeks
 Once infected, the virus remains in the body for life
Aetiology

• Infection with HSV, usually type


I and less commonly type II
Generalised marginal gingivitis
Discrete ulcers
1ry herpes simplex
1ry herpes simplex
Coated tongue
Diagnosis

 Immunodot glycoprotein G-specific (IgG) HSV test

 It detects the presence or absence of past infection, and


whether past infection is due to HSV type 1, type 2 or both
Treatment

 Supporative
 Chlorhexidine MW and painkiller

 Systemic acyclovir only in


immunocompromised
 Avoid self-inoculation
Recurrent herpes simplex
herpes labialis or intraoral herpes
 After 1ry infection, HSV becomes latent in the nerve of face
 It may reactivates and recurrent blisters appear in the same
area
 Affects more the upper and lower lips
 The recurrent infection is often called herpes labialis
 Itching proceeds lesion, then blisters form within 24 hrs
which ruptures and form ulcers that crust over and heals
 Lesion disappears spontaneously in 1-2 weeks
 Infection may be severe if occurs in or near the eye, or in
immunocompromised patients
 Rarely, reinfection occurs inside mouth and affects hard
palate and gingiva, possibly accompanied by herpes
labialis
Aetiology

 Reactivation of the latent HSV that resides in the


sensory ganglion of the trigeminal nerve

 Precipitating factors include fever, stress, sunlight,


trauma, hormonal alterations and
immunosuppression
Blisters of herpes labialis
Infected herpes labialis
Crusted lesion
Infected lesion
Immunocompromised
Primary infection in adolescents
Intraoral herpes simplex stomatitis
Diagnosis

 By history and clinical examination


Treatment

 Sunscreen
 Ice pack for 90 minutes
 Acyclovir cream or zinc oxide cream
 Oral acyclovir if frequent or recurrent intraoral
together with topical corticosteroid
Herpetic whitlow
 It is a painful infection that affects more fingers or thumbs
 HSV-1 whitlow affects dental or medical workers exposed to
oral secretions
 It occurs in thumb sucking children due to autoinculation
 Adults may got it following contact with HSV-2 infected
genitals
 The skin of infected fingers become swollen and reddened
with fever and swollen lymph nodes
 Vesicles initially form individually then merge together
 The lesion usually heals in 2-3 weeks
Aetiology

 Caused by infection with HSV-1 or HSV-2


Herpetic whitlow
Diagnosis

 By history and clinical examination


Treatment

 Gloves should be worn routinely

Acyclovir cream
Chickenpox
varicella
 1ry infection that spreads by direct contact or by air
 Incubation period takes 1-3 weeks after exposure to develop
 Most common between the ages of 2-8 yrs
 It is contagious 1-5 days before skin rash appears and
continues until all blisters crust over forming scabs
 Presents in the mouth as oral ulcers mainly of the oropharynx
 Most common in winter and spring as an epidemic every 3 yrs
 Following 1ry infection the child becomes immune
Aetiology

 Caused by primary infection with VZV


Ulcers of the oropharynx
Vesicle
Skin blisters
Skin blisters
Scab formation
Diagnosis

 Clinical from skin rash

 By testing vesicle fluid or blood


Treatment

 MW

 Calamine lotion containing zinc


oxide for skin rash

 Painkillers or antihistamines
Oral acyclovir in adults
to be initiated early
Herpes zoster
shingles or zona
 Once chickenpox is resolved, VZV becomes latent in ganglia
 Reactivated virus travels down nerve axon causing a painful rash
 Affects more thoracic region
 Only 30% affects trigeminal nerve
 Most common branch to be involved is the ophthalmic
 The pain may be extreme in the affected dermatome
 Skin rash presented as a belt-like pattern that is limited to one
side of the body and does not cross the midline
 Oral lesions appear if maxillary or mandibular branches involved
 Patients older than 60 yrs are prone to postherpetic neuralgia
 There is a risk of developing cancer after herpes zoster infection
 It is extremely rare for patients to suffer more than 3 recurrences
Aetiology

 Reactivation of latent VZV


 Impaired immune system
Belt-like skin rash
Belt-like skin rash
Herpes zoster of opthalmic branch
Herpes zoster
Vesicular rash in herpes zoster
Herpes zoster of maxillary branch
Skin rash
Intraoral herpes zoster
Diagnosis

VZV-specific IgM
antibody during
infection
 Exclude malignancy and immune defect
Treatment

 Topical calamine lotion with zinc oxide for


itching
 Topical lidocaine or morphine for pain
 Oral acyclovir, valacyclovir, or famciclovir within 72 hrs
 Short-term course of oral corticosteroid for
neuralgia
 Live vaccine marketed as Zostavax
Herpes Zoster Oticus
Ramsay Hunt syndrome
 Involves the ear
 Shingles of the geniculate ganglion
 Since the vestibulocochlear nerve is in proximity to the
geniculate ganglion, it may also be affected
 Symptoms include acute facial nerve paralysis, earache, taste
loss, dry mouth and eyes, vesicular rash in the ear canal
 Patients may suffer from tinnitus, hearing loss, and vertigo
Aetiology

 Shingles of geniculate ganglion


 Vestibulocochlear nerve affected
Herpes zoster oticus
Herpes zoster oticus
Diagnosis

 Clinical findings
Treatment

 Complete recovery can be achieved in 75% of cases

ifprednisolone and
acyclovir started within 3
days
Hand, foot and mouth disease
 It is a childhood illness
 Affects children aged 10 years and under
 It is moderately contagious
 Spread through direct contact with mucus, saliva or faeces
 Occurs in small epidemics during summer and autumn
months
 Should not be confused with foot and mouth disease of
animals
 It manifests as painful vesicles on soles of feet and palms of
hand

 Affects the mouth as ulcers of


tongue or buccal mucosa !PT!
Aetiology

 Caused by Coxsackie virus A16


Vesicles on palm of hand
Vesicles on palm of hand
Vesicles on soles of feet
Oral ulcers
Diagnosis

 Clinical history and physical findings


Treatment

 Symptomatic
 Antipyretics
 Topical anaesthetics
(for painful ulcers!)
Herpangina
mouth blisters
 It is a painful mouth infection, most common in children
 Very contagious
 Can be asymptomatic
 Symptoms are usually high fever and sore throat
 Ulcers form in the back of mouth, particularly soft palate
 Lesions heal in 7-10 days
Aetiology

 Coxsackie A or B viruses, or echoviruses


Ulcers of soft palate
Diagnosis

 Clinical signs and symptoms


Treatment

 Supporative

 Hydration
 Antipyretics
 Topical anaesthetics
Focal epithelial hyperplasia
Heck’s disease
BY HPV 13 or possible HPV 32
speial for Czech!
 One of the most contagious oral papillary
lesions (also herpangina is very contagious)
 40% of children can be affected in isolated populations (??)
 Endemic among children, but lesions eventually disappear
 Sites more affected include labial, buccal, and lingual mucosa
 Lesions are papillary (??) but smooth-surfaced and flat-
topped
 DD from squamous papilloma, VV, and condyloma
 Lesions cluster and takes on a cobblestone or fissured
appearance
 No case has been reported to transform into carcinoma
 It may be an oral manifestation of AIDS
Aetiology

 HPV-13 and possibly HPV-32


Flat-topped papillary lesions
A cobblestone appearance
Diagnosis

 Excisional biopsy
Treatment

 Surgery or laser destruction for aesthetic reasons


 Topical 5% imiquimod cream (???)
Infectious mononucleosis
mono, kissing disease, glandular
 Very common illness
 Peak incidence is at the age 15-17yrs
 The designation mononucleosis refers to increase in
lymphocytes (viral infection!)
 Ab against EBV can be detected in most people by adulthood
 Anginose type (??) shows oral ulcers, spongy gums, and petechial
haemorrhages at the junction of hard and soft palate
 Cervical lymphadenopathy, oedema of face and eyelids, may be
present with fever, fatigue, and sore throat
 Tiredness may persist for months following acute illness
 Patients continue to have virus particles in saliva up to 18 m
 If symptoms persist more than 6 m, it is called chronic EBV
Aetiology

 It is caused by EBV
 Saliva is the primary method of transmitting mono
Oral ulcers
Petechial haemorrhages
Enlarged tonsils
Amoxicillin
non-allergic
rash
Amoxicillin rash
Diagnosis

 Spleenomegaly and adenopathy ????


 Prescence of 50% lymphocytes and 10% atypical lymphocytes

 A positive heterophile antibody (Paul-


Bunnel or monospot test) ???
 IgG (past infection) and IgM (current infection) Ab testing
 Elevated hepatic transaminase levels in up to 50% of patients
Treatment

 Self-limiting
 NSAIDs for fever
 Valacyclovir

 Streptococcus throat best Rx with


penicillin or erythromycin
 Avoid Amoxicillin (non-allergic rash)
 Avoid sport for 4 weeks
Necrotising ulcerative gingivitis
NUG, Vincent’s stomatitis
 A subclassification of necrotising periodontal disease
 Peak incidence is 20-25 yrs
 Presents as an acute infection of the gingiva
 If infection progressed deeper, it is subclassified as (NUP)
 NUP may presents as punched-out papillae, red marginal
gingiva, pseudomembranous formation, and halitosis
Aetiology

 Anaerobes (Prevotella intermedia, fusobacterium,


spirochetes)
 Poor oral hygiene, poor nutrition, smoking, stress, lifestyle
 May complicate periodontitis
 Drugs (immunosuppresants)
NUG
NUG
NUG
NUG
Diagnosis

• By smear and gram stain


• Response to treatment
Treatment

 Metronidazole or penicillin-V for 5 days


 Chlorhexidine MW, vitamin C, oral analgesics
 Removal of supragingival and subgingival deposits
 Gingivoplasty

 Correct nutritional deficiency , DM,


anaemia
Tuberculosis
Tubercle bacillus
 A chronic infectious granulomatous disease
 Affects any part of the body including the mouth
 Increase in TB may be due to HIV, poverty, resistant to
drugs
 Oral lesions are rare, may be 1ry or 2ry
 1ry- uncommon seen in younger patients and present as
single painless oral ulcer with lympadenopathy (like
SLE !!)
 2ry-common seen in middle aged and elderly with
pulmonary disease, and present as single painful ulcer of
dorsum tongue
 Clinically- cough, haemoptysis, fever, weight loss, malaise
Aetiology

 Mycobacterium tuberculosis (MTB)


Single painless ulcer
Lung TB
Single painful ulcer
Diagnosis

 Cultures of biopsy, and sputum smear, reveal acid fast bacilli


 Histopathologic examination of biopsy
 Chest x-ray
Treatment

Antibiotics for at least 6-9 months:


(isoniazid, rifampin,

ethambutol,
pyrazinamide)
Syphilis
It is a sexually transmitted infection of 3 distinct stages:
1ry phase- highly contagious; tongue is second to lip as site
for chancre which is painless (like SLE AND PRIMARY TB) ,
hard and punched out. Associated
cervical glands are hard and non-tender; lasts one week

2ry phase- highly contagious; develops 4-10 weeks after chancre


and may last up to 2 yrs. Mucous patches is seen on sides and tip of
Tongue that later coalesce to form snail track ulcers

3rd phase- less contagious than 2ry, but can be fatal. Presents as
gummas known as granulomas on hard palate or dorsum tongue. In
addition to a leukoplakia of dorsum tongue known as
syphilitic
glossitis which is premalignant
Aetiology

 Caused by Treponema palladium


 May transmit to faetus via placenta after 16 weeks of pregnancy
Lip chancre-1ry phase
Healing chancre
Healing chancre
Tongue chancre-1ry phase
Skin rash-2ry phase
Skin rash-2ry phase
Oral mucous patches-2ry phase
Snail track ulcers-2ry phase
Snail track ulcers-2ry phase
Gumma-3ry phase
Syphilitic glossitis
Syphilitic glossitis-3ry phase
Diagnosis

 Early cases: scrape the chancre and dark-field microscopy


 Advanced cases: blood sample for FTA-ABS (fluorescent
treponemal antibody absorption test) and TPPA
(treponema pallidum particle agglutination assay)
 If positive then refer to venereologist
Treatment

 Parenteral penicillin-G for


all stages
Actinomycosis
 A rare chronic bacterial infection
 Occurs in persons aged 30-60 yrs
 Affects face and neck, more mandible
 A favourable condition is required such as periodontal pockets,
fracture sites, and mainly post extraction
 Symptoms occur after trauma, oral surgery, dental abscess or
radiation therapy leading to weight loss, pain, and fever
 Once in tissue, it forms a painful abscess that breaks through
the skin surface to produce multiple draining sinuses
Aetiology

 Caused by anaerobic bacteria called Actinomyces israelii

 This organism found commonly in nose


and throat
Actinomycosis
Actinomycosis
A draining sinus
Diagnosis

• Smear and culture of tissue or fluid shows sulfur granules

•Positive Kveim test


confirms the diagnosis
????
Treatment

 Penicillin G (2-6w) followed by oral penicillin (6-12m)


 If allergic to penicillin then doxycycline
 Surgical drainage of abscesses or radical excision of sinus
tracts
Acute pseudomembraneous candidiasis
Moniliasis or thrush
 Tongue, palate, and buccal mucosa are most frequently affected
 Angular cheilitis is often found
 Soft, creamy white patches can be wiped off leaving erythema

 Distal spread may occur due to


underlying genetic defect,
endocrine deficiency, or
malignancy
Aetiology

 Candida albicans
 Precipitating factors-
(smokers, AB, steroids, immunosuppressive, CT(???),
irradiation, xerostomia, leukaemia, AIDS, malnutrition, DM,
neonates)
Thrush
Thrush
Angular cheilitis
Diagnosis

• By smear (gram or PAS stain) and culture swab


(Saboured’s medium)
Treatment

 Topical antifungal such as nystatin suspension or lozenges


 Systemic antifungal such as fluconazole for resistant cases
 Miconazole oral gel for angular cheilitis
Erythematous candidiasis
Two types:- acute and chronic

Acute erythematous candidiasis (acute atrophic candidiasis or


antibiotic sore mouth) is common in patients taking broad pectrum
AB. Manifested as erythema with atrophy of dorsal lingual papillae.
Red lesions are also seen on palate and BM. Excessive burning
sensation accompany the lesion

Chronic erythematous candidiasis (chronic atrophic candidiasis or


denture stomatitis) is seen in patients wearing ill fitting dentures for
prolonged duration, or through night. Erythema is limited to area
beneath upper denture. This lesion is not sore. Angular cheilitis or
stomatitis may be present
Aetiology

• Caused by Candida albicans


• PP- poor oral and denture hygiene, xerostomia, DM,

iron or
carbohydrate-rich diets,

vitamin B12 deficiency,


steroid, HIV infection, smokers
Chronic erythematous candidiasis
Chronic erythematous candidiasis
Chronic erythematous candidiasis
Angular cheilitis
Median rhomboid glossitis
Central papillary atrophy
A red depapillated rhomboidal area in the centre of
now believed to be
tongue dorsum,

associated with
erythematous candidiasis
Median rhomboid glossitis
Median rhomboid glossitis
Diagnosis

• By a smear (gram or PAS stain) and culture


swab (Saboured’s medium)
Treatment

 Topical antifungal therapy


 Miconazole oral gel for fitting surface and angular
cheilitis
 Soak dentures in 1% sodium hypochlorite, or if metallic
in 10% cetrimide
 Fluconazole for refractory cases
Acquired immunodeficiency syndrome
AIDS
 AIDS was recognised in 1981 in young men
 Today 75% of new infections are transmitted heterosexually
 Incubation period from 6m-2yrs up to 18yrs
 1/3 develop AIDS in 7yrs while 2/3 develop pre-AIDS symptoms
 HIV infected patients with no symptoms can transmit infection

 Pre-AIDS symptoms include chills, fevers, sweats, swollen


lymph nodes, weakness, weight loss

 Full blown AIDS is characterised by opportunistic infections


such as PCP, KS, Burkett-type lymphoma, unresolved candidal
infection, GIT infections, severe glomerulonephritis, renal
damage
 Oral symptoms are the first clinical
manifestations of HIV
 Commonest are florid candidiasis, KS, recurrent herpetic
infections, and to a lesser extent hairy leukoplakia (???),
NUG, SCC, and malignant melanomas
 All people infected with HIV eventually develop AIDS
 Some patients develop AIDS very slowly or never at all, and
called nonprogressors due to genetic factors
 Although treatments for AIDS and HIV can slow the course of
the disease but currently there is no known cure or vaccine
Aetiology

 A retrovirus known as HIV

direct contact of bodily


 Transmitted by

fluid containing HIV


Thrush
Kaposi’s sarcoma
Kaposi’s sarcoma
Kaposi’s sarcoma
Skin Kaposi’s sarcoma
Hairy leukoplakia
Hairy leukoplakia
Hairy leukoplakia
Gingivitis of AIDS
Diagnosis

 Smear and culture swab of candida


 Viral culture swab of dorsum tongue
 Tongue biopsy in hairy leukoplakia
 CBC, LFT, HBsAg, T4 and T4:T8 ratio, serology for Abs
(???????????????????????????????????????????????????)
 Barium swallow, bronchoscopy, and chest x-ray
Treatment

 HAART (highly active antiretroviral therapy)


reduces mortality and morbidity
 Treat opportunistic infections
 Prevention is the key

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