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BDS10033 Viral infections: non-HIV infections of the mouth Viral infections – non-HIV infections of the mouth Aim • The aim of this lecture is to review the common viral infections, other than HIV, that may give rise to oral manifestations Objectives: On completion of this lecture, the student sh...

BDS10033 Viral infections: non-HIV infections of the mouth Viral infections – non-HIV infections of the mouth Aim • The aim of this lecture is to review the common viral infections, other than HIV, that may give rise to oral manifestations Objectives: On completion of this lecture, the student should be able to: • Understand the risk factors, clinical presentation, diagnostic process and treatment of the herpetic group of viral infections • Understand the risk factors, clinical presentation, diagnostic process and treatment of the coxsackie group of viral infections • Be aware that other viral infections may rarely affect the mouth Viral infections of the oral mucosa I. II. III. IV. V. VI. Human Herpes virus family Coxsackie group Human papillomavirus Measles Mumps & Rubella HIV I. Human Herpes virus family There are 8 Human herpes family species Name of virus Abbreviation 1) Herpes simplex virus-1 HSV 1 2) Herpes simplex virus-2 HSV-2 Name of infection/disease 6) Human Herpes virus- 6 7) Human Herpes virus- 7 HHV-6 HHV-7 • 1ry herpetic gingivostomatitis. • Recurrent herpes labialis. • Recurrent intraoral herpes. Genital herpes • Chicken pox • Herpes Zoster (Shingles) Glandular fever-like illness (rare) • Infectious mononucleosis • Oral Hairy leukoplakia Roseola infantum Roseola infantum 8) Human Herpes virus- 8 HHV-8 • Kaposi sarcoma 3) Varicella Zoster virus VZV 4) Cytomegalo virus 5) Epstein bar virus CMV EBV HERPES SIMPLEX VIRUS HSV-1 HSV-2 A) Oral infection: 1) Primary herpetic givostomatitis. 2) Recurrent intraoral herpes. 3) Recurrent herpes labialis. A) Genital infection B) Dermatitis above the waist. C) Pharyngeal infection. D) Genital infection in 50% of cases. B) Dermatitis below waist C) Infection in new born From contact with vaginal lesion during normal labor. Dies on the 9th-12th day of life due to viremia 1) 1ry/Acute herpetic gingivostomatitis • Acute herpetic gingivostomatitis is the primary form of HSV-1. • 95-99 % are subclinical or are misdiagnosed as teething. • 1-5 % show clinical features of the disease. Fate: • Self limiting & resolves within 10-14 days. • Prolonged in immunosuppressed patients. Age: • Common in preschool children (2-3 years old) & teenagers. • Uncommon < 6 months of age because of maternal Ig G that can cross placental barrier. • Adults with immunodeficiency e.g. leukemia, HIV, immunosuppression & manifestations are more severe. Clinical features:1-Prodromal features (flu symptoms): • Fever, headache, malaise, submandibular & upper deep cervical lymphadenopathy & skin rash. • Occur before appearance of oral vesicles by 1-2 days. 2-Acute marginal gingivitis : • After 1-2 days gingiva is intensely inflamed & edematous. 3- Vesiculobullous lesion: • Once fever subsides, small multiple vesicles develop on both keratinized & non-keratinized mucosa (tongue, gingiva, all oral mucosa). • Vesicles rupture forming ulcers. 4- Oral ulceration : 1. Painful 2. Superficial 3. Small round regular & discrete then coalesce to form large irregular ulcers. 4. Surrounded by inflammatory halo 5. Covered by a greyish membrane. Gingiva: • Inflamed “boggy”, multiple vesicles rupture forming ulcers. • There is NO LOSS of interdental papillae. Tongue: • Inflamed, enlarged & scalloped. • Multiple vesicles on dorsal surface of tongue that rupture forming ulcers. • Ulcers coalesce resulting in large irregular ulcer. Circumoral : • Small multiple clusters of vesicles on the lip vermillion border & circumoral skin. • The vesicle when rupture they form an ulcer covered by crust of purulent exudates due to secondary infection. • In few cases lesions are ONLY on the lip & circumoral skin without intra-oral ulcers. Diagnosis: A) Case history 1. History of prodromal features. 2. History of contact with patient with 1ry or recurrent herpes. 3. Negative history of previous recurrent herpes. B) Clinical examination Gingivitis, Multiple small ulcers on mucosa, Lymphadenopathy. C) Special investigation (Rarely required). a) Viral swab - culture, EM, PCR b) Vesicular fluid - (historical) c) Viral antibody titers: appears by 7th day, reach max by 3rd week (4 folds rise during convalescence) Management of 1ry herpetic gingivostomatitis: 1) 1ry herpetic gingivostomatitis in childhood: It is self-limiting, so managed with supportive treatment only: 1. Bed rest & monitor temperature. 2. Fluid for dehydration. 3. Analgesic and antipyretic e.g. Paracetamol. 4. Paracetamol spray + benzydamine HCL m/w or lidocaine gel 1-2% 5. Antiseptic mouth rinse e.g. 0.2% chlorohexidine. 6. Antihistamines - sedation 2) 1ry herpetic gingivostomatitis in adults or immunodeficiency: 1. Bed rest, fluid for dehydration & monitor temperature. 2. Analgesic and antipyretic e.g. Paracetamol. 3. Acyclovir (Antiviral) < 12 years 100 mg 5 x daily for 5 days. > 12 years 200 mg 5 x daily for 5 days. • Immunodeficiency patients  400 mg 5 times/day till healing. • Avoid in first trimester (see therapeutics lectures) 2) Secondary HSV infection • After resolution of the primary lesion, HSV migrate through the trigeminal nerve to the trigeminal ganglion. • The virus remains latent in the ganglion until its reactivation by predisposing factors. “It is not a re-infection” • When reactivation is triggered, virus travels within sensory nerve to infect the oral-skin epithelium leading to: A. Recurrent intraoral herpes. B. Recurrent herpes labialis. • Transmission by salivary direct contact. • Occurs in young adults. • Both genders affected. • Incubation time: 7-14 days Recurrent herpes labialis • Recurrent herpes labialis is a secondary form of HSV-1 infection. Predisposing factors: 1. Exposure to sunlight. 2. Psychological stress. 3. Pregnancy/menstrual cycle 4. Trauma 5. Common cold or Fever 6. GIT disturbance 7. Immunosuppression. Fate: • The lesion is self limiting, heals without scar within 5-10 days. • Recurrent attacks once-twice/ month, once-twice/ year & decrease with age. Clinical features: 1) Prodrome: •Burning or itching sensation at site on which the vesicle will develop. •Followed by local erythema, edema & vesicle formation. 2) The vesicles are: 1.Small (1 mm) 2. In clusters 3. Surrounded by erythema 4. Tend to coalesce forming large lesions (1-2 cm) 5. On vermillion border of lips (mucocutaneous junction). 6. Vesicles rupture, ulcerate & covered by purulent crust due to 2ry bacterial infection. Diagnosis: 1. History 2. Clinical examination 3. Special investigation (VERY rare) identify HSV by culture, PCR or EM (serology is not helpful). Management: 1) Avoid exposure to sunlight if it is the predisposing factor. 2) Sun blocker or sun screen cream. 3) Acyclovir 5% ointment 5 times/day for 5 days 4) Penciclovir 1% cream every 2 hours • Started within 24 hours after the lesion’s onset, otherwise will be of no benefit. Recurrent intra-oral herpes • Recurrent intraoral herpes is a secondary form of HSV-1. Clinical features: • Multiple small vesicles in clusters. • On keratinized mucosa (Tongue, Palate, gingiva). • Rupture forming dozens of pin head-sized ulcers. • Coalesce to form large, irregular & extremely painful ulcers. Fate: • Lesion is self limiting & heal without scar within 7-14 days. Treatment: • 2% tetracycline mouth bath after meals & before bed time. Other disorders suggested to be associated with HSV-1: 1. Erythema multiforme minor 2. Bell’s palsy I. Human Herpes virus family There are 8 Human herpes family species Name of virus Abbreviation 1) Herpes simplex virus-1 HSV 1 2) Herpes simplex virus-2 HSV-2 Name of infection/disease 6) Human Herpes virus- 6 7) Human Herpes virus- 7 HHV-6 HHV-7 • 1ry herpetic gingivostomatitis. • Recurrent herpes labialis. • Recurrent intraoral herpes. Genital herpes • Chicken pox • Herpes Zoster (Shingles) Glandular fever-like illness (rare) • Infectious mononucleosis • Oral Hairy leukoplakia Roseola infantum Roseola infantum 8) Human Herpes virus- 8 HHV-8 • Kaposi sarcoma 3) Varicella Zoster virus VZV 4) Cytomegalo virus 5) Epstein bar virus CMV EBV VARICELLA ZOSTER VIRUS (VZV) • VZV causes two different diseases: 1. Chicken pox (primary infection). 2. Herpes Zoster (secondary infection/reactivation of virus). • Primary infection with VZV causes Chicken pox (a childhood illness). • The virus then migrates from the skin through the sensory nerves & remains latent within the ganglia of spinal cord & cranial nerves. • Predisposing factors trigger the latent virus “REACTIVATION” which spreads from the ganglion to infect specific dermatomes leading to Herpes Zoster. Chickenpox : Chicken pox (Varicella) is the primary infection of VZV. Epidemiology • It is a childhood diseases that occurs at earlier age of onset in temperate than tropical areas. • Risk of mortality & morbidity increases steeply with patient age. Clinical manifestation: • Pruritic vesicular rash. • Pustules and ulcers. • Fever and systemic illness. • Oral painless lesions at lips & palate. Treatment: • Prophylactic: Varivax vaccine. • Self limiting Analgesics & antipyretics Herpes Zoster (Shingles) Etiology: • Herpes Zoster (Shingles) is the secondary infection of VZV. • Occurs due to reactivation of latent VZV without an obvious cause. • Some predisposing factors : 1. Trauma/surgery of spinal cord. 2. Malignancy (lymphoma, leukemia) 3. Immunodeficiency: immunosuppressive drugs & AIDS. Epidemiology: • Both genders • No seasonal or climate variations. • Increased risk among elderly (>45 years old). • Racial variations. • Higher mortality rate than chickenpox. Clinical Features:1) Prodrome: Fever, malaise, headache & unilateral tenderness along the involved nerve. 2) Unilateral severe itching & neuralgic burning pain. 3) Skin vesicles appear after 2-5 days as unilateral dermatomal rash on skin & mm supplied by the affected nerve. • After 1 week vesicle rupture forming crust. • Mixed skin lesions such as papules, vesicles and pustules and crust. Orofacial involvement: • Trigeminal shingles: reflects reactivation of VZV within the trigeminal ganglion involving one or more branches of the trigeminal nerve: • Herpes zoster ophthalmicus (50%) • Mandibular and maxillary nerves (15%- 20%). • When maxillary & mandibular branches are involved, oral lesions are seen. Vesicles are:• Extremely painful (neuralgic pain) • Unilateral • Dermatomic distribution • Rupture to leave ulcers. • Ulcers are painful, unilateral, shallow, small, rounded with erythematous base •Healing may be associated by scarring. Ramsay Hunt Syndrome: • Reactivation of VZV affecting the facial nerve via infection of geniculate ganglion. • Prodrome: headache, malaise and fever, pain localized to ear or radiating to jaws or neck. • Herpetic Oticus : Small crops of vesicles on tragus of ear. • Lower motor neurone facial palsy (identical to Bell’s Palsy). • Oral manifestations: 1. Affect anterior two thirds of one side of the tongue & ipsilateral soft palate or fauces. 2. Unilateral localized pain followed by vesicles that soon rupture to ulcers. Post-herpetic neuralgia: • Most common complication of shingles. • Occurs to 30% of patients with shingles • Pain or dysesthesia persisting for 3 or more months after rash resolves. • Pain is due to inflammation and fibrosis of the affected nerve. • Localized, acute episodic and sharp pain. • Can be precipitated by light touch. • Skin can be erythematous. • Ophthalmic division is mot commonly affected in orofacial region Treatment 1. Gabapentin 2. Lidocaine patch 5% 3. Topical capsaicin cream 0.075% 4. Pregabalin 5. Amitriptyline 6. Opioid analgesics (oxycodone) Diagnosis: 1) Case history. 2) Clinical examination: unilateral, extremely painful vesicles & ulcers on skin & oral mucosa. 3) Special investigation: • FBC and/or HIV assessment (if relevant) • Rarely identify virus (e.g. PCR). Serology is generally unhelpful. Fate: • Healing within 3-4 weeks by scar formation (2ry infection is common). • These scars are diagnostic in case of post herpetic neuralgia. Management: • Potent analgesics. • 0.2% chlorhexidine mouthwash. • 5% Acyclovir ointment for skin and eye lesion. • Antiviral agents: Acyclovir 800 mg tablets 5 times per day for 7 - 10 days. or less commonly valaciclovir or famciclovir. I. Human Herpes virus family There are 8 Human herpes family species Name of virus Abbreviation 1) Herpes simplex virus-1 HSV 1 2) Herpes simplex virus-2 HSV-2 Name of infection/disease 6) Human Herpes virus- 6 7) Human Herpes virus- 7 HHV-6 HHV-7 • 1ry herpetic gingivostomatitis. • Recurrent herpes labialis. • Recurrent intraoral herpes. Genital herpes • Chicken pox • Herpes Zoster (Shingles) Glandular fever-like illness (rare) • Infectious mononucleosis • Oral Hairy leukoplakia Roseola infantum Roseola infantum 8) Human Herpes virus- 8 HHV-8 • Kaposi sarcoma 3) Varicella Zoster virus VZV 4) Cytomegalo virus 5) Epstein bar virus CMV EBV CYTOMEGALOVIRUS • 95% of adults have this virus – but it rarely causes disease unless the patient is immunocompromised. • Transmitted through biological fluids (saliva, blood, urine, semen, breast milk, vaginal secretions), transplant tissue and faeces. • Following primary infection, CMV can remain in latent state throughout the host’s life and very rarely becomes symptomatic. • Reactivation of the virus results in recurrent infection. • Most commonly involved structures include the lymphoid tissue, lungs, liver, gastrointestinal tract, retina, as well as salivary glands and central nervous system. • The majority of acute CMV infections are asymptomatic and only 5-10% may present a variety of signs and symptoms, similar to those of infectious mononucleosis. • Most common signs & symptoms are fever, sore throat, cough, pharyngitis, malaise, myalgia, joint pain, abdominal pain, diarrhoea, lymphadenopathy, hepatosplenomegaly, adenopathy & meningeal irritation. • Oral lesions (ulcers) are rare and occur mainly in severe immunosuppression. • Salivary gland swelling is rare, but possible. • The main relevance of CMV infection for the orofacial region is that it can give rise to a glandular feverlike illness – with notable cervical lymphadenopathy. • Diagnosis can often based upon raised levels of IgM class (in early infection) or IgG class antibodies; viral DNA detection may be possible • Management is directed towards treating the underlying causes plus appropriate anti-virals e.g. ganciclovir or valganciclovir (see therapeutics lectures). EPSTEIN-BARR VIRUS (EBV) • EBV gives rise to a spectrum of different disorders: 1. 2. 3. 4. 5. 6. Infectious mononucleosis (a type of glandular fever) Oral hairy leukoplakia Non-Hodgkin’s lymphoma Burkitt’s lymphoma Natural killer T cell lymphoma Nasopharyngeal carcinoma Non-Hodgkin’s lymphoma 1) Infectious mononucleosis (EBV related glandular fever) • Common • Both genders affected. • Teenagers/young adults • Long incubation time (35+ days) • Infection by salivary transmission. • Illness lasts 2-3 weeks – or more • Clinical features: • Fever, malaise, arthralgia & myalgia. • Profound lethargy. • Pharyngitis - white coating on tonsils • Oral petechiae & ulceration • Profound cervical lymphadenopathy • Hepatitis (right upper quadrant pain) • Splenomegaly (left upper quadrant pain) • Skin rashes (+ sometimes in response to ampicillin) Diagnosis: 1. Full blood count (FBC): • “atypical” lymphocytosis (EBV related) + neutrophilia. 2. Unstable liver function tests (hepatic biochemistry). 3. Heterophile antibodies: • Paul Bunnell & Monospot tests are positive. N.B. • Paul Bunnell test is negative with HIV, toxoplasmosis & CMV infection which have similar clinical picture of glandular fever. • Management 1. Bed rest & fluids 2. Analgesics/antipyretics 3. Acyclovir (?) Corticosteroids (?) Antibacterial (?) 2) Oral hairy leukoplakia: • • • • • Uncommon. Both genders. An epithelial proliferation related to EBV. Typically a feature of immunosuppression. Common with HIV disease, immunosuppression and less common in long term systemic or topical corticosteroids, diabetes mellitus. Clinical features: • Adherent white patches. • Bilateral, dorsum & lateral border of tongue, floor of mouth, very rarely in pharynx Diagnosis: • Usually based upon clinical features on a background of relevant medical history • Histopathology (demonstrates hyperkeratosis, acanthosis and koilocytic change) and immunohistochemistry to identify EBV. • Management: None – it is asymptomatic and not potentially malignant. • Suspect HIV infection in patients with oral hairy leukoplakia who are otherwise well. HUMAN HERPES VIRUS-8 • Transmitted sexually and non-sexually • Manifests as Kaposi’s sarcoma and Body cavity B cell lymphoma. • Usually gives rise to disease in immunocompromised patients. Kaposi’s sarcoma: • Classic (no oral disease) • Endemic • HIV • Immunosuppression. • Red, blue, purple. • Macule, papule, nodule, ulcer • Palate & gingivae most commonly affected sites. • Diagnosis with histopathology • Serology for HHV-8 not helpful • Managed by oncology teams. • HIV-related disease may regress with ART (see HIV lecture) • Iatrogenic disease may reduce with improved immune status. Viral infections of the oral mucosa I. II. III. IV. V. VI. Human Herpes virus family Coxsackie group Human papillomavirus Measles Mumps & Rubella HIV I. Human Herpes virus family There are 8 Human herpes family species Name of virus Abbreviation 1) Herpes simplex virus-1 HSV 1 2) Herpes simplex virus-2 HSV-2 Name of infection/disease 6) Human Herpes virus- 6 7) Human Herpes virus- 7 HHV-6 HHV-7 • 1ry herpetic gingivostomatitis. • Recurrent herpes labialis. • Recurrent intraoral herpes. Genital herpes • Chicken pox • Herpes Zoster (Shingles) Glandular fever-like illness (rare) • Infectious mononucleosis • Oral Hairy leukoplakia Roseola infantum Roseola infantum 8) Human Herpes virus- 8 HHV-8 • Kaposi sarcoma 3) Varicella Zoster virus VZV 4) Cytomegalo virus 5) Epstein bar virus CMV EBV II. COXSACKIE VIRUS INFECTIONS 1. Herpangina 2. Hand food and mouth disease 3. Acute Lymphonodular Pharyngitis 1) Herpangina • Caused by Coxsackie enteroviruses, group A, usually types 1-6, 8, 10 and 22. • Transmitted via droplet route • Disease has a peak incidence during summer and autumn. • Sudden fever, headache, dysphagia, sore throat, nausea, and malaise. • Within 24–48 hours, an acute inflammation of the posterior oral mucosa and oropharynx develops with concurrent appearance of numerous small vesicles, that become confluent, rupture and cause ulcers. • Lesions characteristically involve the soft palate and uvula, tonsils, faucial pillars, posterior pharyngeal wall, and, rarely, the posterior tongue. • Systemic symptoms resolve in 4-6 days while the oral ulceration heals in about 8-10 days. • Diagnosis is based on the history and the clinical features • Treatment is symptomatic reduction. 2) Hand Foot and Mouth disease • • • • • • • • • Caused by various types of Coxsackie virus, mainly A16 and, less often, A5, A9, A10. It usually affects children and young adults. Disease may occur in epidemics (e.g. within schools) or isolated cases. Small vesicles appear on the oral mucosa, 5-30 in number, that soon rupture, leaving slightly painful, shallow ulcers (2–6 mm in diameter), surrounded by a red halo. Any site on the oral mucosa may be involved, except the gingiva. Skin lesions consist of small, turbid vesicles, 1-50 in number, surrounded by a narrow red halo and are localized on the lateral and dorsal aspects of the fingers, toes, palms and soles – although lesions may appear on the buttocks, knees, and extremities . Low grade fever and general symptoms may be present. Disease lasts 5–8 days and resolves spontaneously without treatment. Diagnosis is based on clinical features Treatment is symptomatic reduction 3) Acute lymphonodular pharyngitis • • • • • • • • • An uncommon acute febrile disease Caused by Coxsackie virus, A10 Affects children and young adults. Presents with fever, ranging from 38°–41°C, mild headache, loss of appetite and sore throat, followed, after 2–3 days, by a characteristic non-vesicular eruption on the uvula, soft palate, anterior tonsillar pillars, and posterior pharynx. The lesions consist of multiple, raised, discrete papules, whitish to yellowish in colour surrounded by an erythematous halo. The size of the lesions varies from 3–6 mm in diameter. Clinical signs last 3-8 days (the papules represent hyperplastic lymphoid aggregates). Diagnosis is based on clinical features Treatment is symptomatic reduction III. HUMAN PAPILLOMAVIRUS (HPV) • • • • Double stranded DNA virus Over 200 genotypes, classified into dermatotropic and mucosotropic Only infect epithelial surfaces capable of proliferation. Transmitted via abrasions to the basal cells where viral proliferation occurs. Virus is released from the upper epithelial layers • Usually give rise to benign mucocutaneous disease, but some high risk genotypes are oncogenic • Transmitted by close contact • Clinical presentation varies with HPV genotype and geographic locale, sexual lifestyle, genetic predisposition and occupation of the host 1. Multifocal epithelial hyperplasia 2. Papillomas (see swellings lecture) 3. Oral squamous cell carcinoma (see cancer lectures) Multifocal epithelial hyperplasia Epidemiology • Few population based studies. • Rare worldwide. • Common only among Inuits, Indians and Eskimos resident in North Canada, North, Central, or South America, and South Africa. • More common in Females, Children and adolescence Lower socioeconomic groups, close living conditions. • Etiology: • HPV genotypes 13 and 32 are found in 75-100% of patients. • Also HPV genotypes 1, 6,11,16,18, and 55 have been detected • Genetic predisposition ? Clinical features: • Painless, sessile, flat-topped, smooth papules. • Typically multiple. • White, pink, or colour of normal oral mucosa. • 1-10 mm in diameter. • Most commonly affecting the lower labial mucosa and the buccal mucosa. • Two clinical forms: papulonodular and papillomatous. Diagnosis • • • • Social history (race, socio-economic, living conditions, and inter-familial infection). Clinical examination. Histopathological examination. Detection of HPV (In situ hybridization, Southern blot hybridization, PCR. Papulonodular Papillomatous Management: • Treatment is not always indicated. • Therapy indicated if lesions interfere with occlusion or for aesthetic consideration. • EXCISION: Scalpel excision Cryotherapy CO2 laser • MEDICAL THERAPY : Topical Systemic interferon ? intra-lesional intra-muscular Imiquimod ? Systemic retinoids ? Long term outcomes • Long term behaviour is unclear. • Spontaneous regression is possible. • Post-treatment recurrences can occur. • No difference in rate of recurrence between surgical and medical therapy. • No increased occurrence of oral epithelial dysplasia/OSCC. • May be more persistent or recurrent in immunocompromised patients. IV. MEASLES • Clinical features: • Transmission: droplet spread, highly infectious • Incubation period: 8-12 days • Prodromal signs: fever, cough, coryza (2-4 days) • Rash: maculopapular rash fade after 3-7 days • Oral manifestations: -Koplick’s spots -Candidosis suggested • Suggested links with : -Crohn’s disease -Hodgkin’s disease -Multiple sclerosis -RAS V. MUMPS • Clinical features : • • • • • Transmission: droplet spread, highly infectious (depends on close personal contact) Incubation period: 16-18 days Prodromal symptoms: fever, malaise, pain next to jaw angle Parotitis (after 1 day), (submand.=10%,sublingual= rare) Oral manifestations: Wharton’s and Stensen’s ducts redness and enlargement • Link with IBD, diabetes not proven • Also covered in salivary disease lectures. RUBELLA • Transmission: droplet spread • Incubation period: 14-21 days • Mild disease • Prodromal symptoms: fever, headache, sore throat (absent in children) • Cutaneous rash , lymphadenopathy • Oral manifestations: Forscheimer sign • Pregnancy: congenital rubella syndrome Summary of common viral infections of the mouth: • Most are related to Herpes simplex 1 and give rise to short-term oral ulceration and systemic symptoms. • Herpes labialis is the most common viral infection that will be present in patients attending for dental care. • Shingles of the orofacial region is uncommon but may reflect known or unknown immunosuppression. • Children and young adults may be liable to coxsackie infections – all of which are usually short-term. • The majority of common viral infections of the mouth do not require specific anti-viral therapy. Reading material Students are advised to review any relevant teaching provided in the earlier years. In addition they are advised to read relevant sections of the following texts: • Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 235-241 • Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp 28-32 • Scully C. Oral and Maxillofacial Medicine Churchill Livingstone 2008 pp 233-240 Viral infections – non-HIV infections of the mouth Aim • The aim of this lecture is to review the common viral infections, other than HIV, that may give rise to oral manifestations Objectives: On completion of this lecture, the student should be able to: • Understand the risk factors, clinical presentation, diagnostic process and treatment of the herpetic group of viral infections • Understand the risk factors, clinical presentation, diagnostic process and treatment of the coxsackie group of viral infections • Be aware that other viral infections may rarely affect the mouth