Oral Infections - Viral Infections PDF

Oral Infections Dr. Dilara Kazan Department of Oral&Maxillofacial Surgery Viral Infections • Primary Herpetic Gingivostomatitis • • It is caused by herpes simplex virus, type1 (HSV-1). The onset is abrupt. • Numerous oral vesicles and erosions,high fever and bilateral, cervical lymphadenopathy...

Oral Infections Dr. Dilara Kazan Department of Oral&Maxillofacial Surgery Viral Infections • Primary Herpetic Gingivostomatitis • • It is caused by herpes simplex virus, type1 (HSV-1). The onset is abrupt. • Numerous oral vesicles and erosions,high fever and bilateral, cervical lymphadenopathy are the main clinical features. • • Chills,nausea,anorexia,malaise,irritability,sore mouth, and headache are common. Oftenstartsaspharyngitisortonsillitis. • Resolves spontaneously in 10 to 15 days leaving partial immunity. • The pathogenesis of herpetic infections follows the course: • primary infection—latent phase—reactivation. • Primary herpetic gingivostomatitis is an acute infectious disease mainly affecting children (1–6 years), adolescents, and rarely adults. • Human herpes virus (HHV) family has eight members. • The cause is HSV-1 or, less often HSV-2, the latter being the most common cause of genital herpes. • Type 1 is transmitted through direct contact with saliva or other secretions, while type 2 is sexually transmitted. • Initial contact with HSV-1 may produce either acute primary disease (3–5%) or, most often, a subclinical asymptomatic infection. They both lead to partial immunity. Viral Infections • Primary Herpetic Gingivostomatitis • Clinical features • Characterized by systemic and local symptoms (high fever, 38–39°C, headache, malaise, loss of appetite, dysphoria, pain and a burning sensation in the mouth, and difficulty in swallowing), that precede the oral lesions by 1 to 2 days. • The oral mucosa is red and edematous, with numerous coalescing vesicles. • Within 24 hours, the vesicles rupture, leaving painful, small, round ulcers, covered by a yellowish-gray pseudomembrane and surrounded by an erythematous halo. • New vesicles continue to appear over 3 to 5 days. Lesions are painful and cause sialorrhea. The ulcers gradually heal in 10 to 14 days without scarring. • Bilateral painful, mandibular, and cervical lymphadenopathy is a typical clinical sign. Although localized involvement may be seen, oral lesions are usually widespread. • Both the movable and attached oral mucosa can be affected. Involvement of free and attached gingiva is a constant feature. • Limited involvement of the lips and perioral skin may be seen. • Lesions on the fingers, eyes, nose, ears, and the genitals may develop due to autoinoculation • Serious complications are rare, but include keratoconjunctivitis, pharyngitis, esophagitis, pneumonitis, meningitis, and encephalitis. • Diagnosis is made on clinical grounds and only rarely laboratory confirmation is required. Viral Infections • Primary Herpetic Gingivostomatitis • Differential Diagnosis • Herpetiform aphthous ulcers • Herpangina • Drug-induced stomatitis • Erythema multiforme • Stevens-Johnsonsyndrome • Hand-foot-and-mouthdisease • • Acutenecrotizingulcerativegingivitis Pathology is rarely necessary. • Treatment • Antiviral agents (acyclovir, famciclovir, valacyclovir) are the first-line therapy. • Treatment should be initiated during the first 3 to 4 days after the onset of symptoms. In children, oral suspension of acyclovir is administered. Concurrent administration of systemic corticosteroids, e.g., dexamethasone oral solution 2 mg/5 mL twice a day for 3 to 4 days, may offer rapid alleviation of symptoms. Dexamethasone should be avoided in children less than 5 years of age, as well as in immunosuppressed individuals. • Topical application of oral solutions with anti-inflammatory and anesthetic actions, contributes to pain relief Viral Infections • Secondary Herpetic Gingivostomatitis • Caused by reactivation of HSV-1. • It develops mainly on keratinized areas of the mouth (gingiva, hard palate, alveolar mucosa), as well as on the lips. • In transplant recipients and immunosuppressed patients, it may mimic primary herpetic gingivostomatitis. • Lesions self-heal in 4 to 6 days. • As antibodies against HSV-1 are present, symptoms are mild. • Predisposing factors include emotional or physical stress, febrile illness, cold, minor trauma of the oral mucosa, tooth extraction, or local anesthesia. • Clinical features • Clinically, localized, closely grouped vesicles develop. These later rupture, leaving superficial erosions that heal in about 1 week • However, in the immunosuppressed patients (leukemia, non-Hodgkin’s lymphoma, transplant recipients, active HIV infection) recurrent herpetic infection may persist for several weeks or months. • In such cases the erosions are of larger size with tendency to spread laterally and are surrounded by a whitish-yellow, raised halo • Most commonly affects adults • The diagnosis is based exclusively on the history and the clinical features. Viral Infections • Secondary Herpetic Gingivostomatitis • Differential diagnosis • Primary herpetic gingivostomatitis • Early herpes zoster • Aphthous ulcers • Hand-foot-and-mouthdisease • Streptococcal stomatitis • Primary and secondary syphilis (chancre, syphilitic plaques) • Traumatic erosions • Treatment is symptomatic. • Pospischill-Feyrter disease • Rare, severe form of gingivostomatitis herpetica. • Possible spread to pharynx and oesophagus, infestation of the fingertips. Viral Infections • Herpes Simplex Labiales-Herpes Labialis • The most common form of HSV-1 reactivation. • It is located on the vermilion border and the adjacent skin of the upper or lower lip. • It recurs frequently. • It involves the upper or the lower lip with equal frequency, and affects women more often than men in a ratio of approximately 2:1. • Clinical features • Clinically, herpes labialis is initially characterized by initial itching and burning, followed by edema and redness and the development of clusters of small vesicles located on the vermilion border and the adjacent perioral skin. The vesicles soon rupture, within 2 to 3 days, leaving small ulcers covered by crusts that heal spontaneously without scarring in 5 to 8 days. • In immunocompromised individuals, lesions can be more severe and extensive and may last for 1 to 3 months • Recurrences are a typical feature of herpes labialis and may be associated with fever, emotional or physical stress, menstruation, sun exposure, cold weather, or local trauma. The diagnosis is exclusively made on clinical grounds. • Differential diagnosis • Syphilitic chancre • Traumatic erosions • Impetigo • Treatment • Topical application of acyclovir or pencyclovir cream or ointment, during the early stages, may be helpful. Viral Infections • Oral Mucosal Herpes Viral Infections • Herpangina • It is caused by Coxsackie enteroviruses, group A, usually types 1 to 6, 8, 10, and 22. • The disease has a peak incidence during summer and autumn. • Typically, oral lesions are localized on the soft palate, uvula, and tonsils. • Diagnosis is based on the history and the clinical features. • More frequently, children and young adults are affected. • Clinical features • The disease has an acute onset, characterized by sudden fever, ranging from 38 to 40°C, headache, dysphagia, sore throat, nausea, and malaise. Within 24 to 48 hours, an acute inflammation of the posterior oral mucosa and oropharynx develops with concurrent appearance of numerous small vesicles, 2 to 5 mm in diameter. The vesicles become confluent and soon rupture, leaving painful shallow ulcers • The lesions characteristically involve the soft palate and uvula, tonsils, faucial pillars, posterior pharyngeal wall, and, rarely, the posterior tongue. The absence of lesions on the lips, gingiva, buccal mucosa, and the floor of the mouth is highly characteristic. The systemic symptoms resolve in 4 to 6 days while the oral ulceration heals in approximately 8 to 10 days. The diagnosis is based on the history and the clinical features. • Treatment • It is symptomatic. In most cases, the disease resolves spontaneously without complications. Viral Infections • Hand-Foot-and-Mouth Disease • It is caused by Coxsackie enteroviruses, mainlytype A16. less often, A5, A9, and A10. • The disease may occur in epidemics or isolated cases. • Clinical presentation and sites of involvement are typical. • It usually affects children and young adults. • Clinically, small vesicles appear on the oral mucosa, 5 to 30 in number, that soon rupture, leaving slightly painful, shal- low ulcers (2–6 mm in diameter), surrounded by a red halo • Any site on the oral mucosa may be involved, except the gingiva. • The skin lesions consist of small, turbid vesicles, 1 to 50 in number, surrounded by a narrow red halo and are localized on the lateral and dorsal aspects of the fin- gers, toes, palms, and soles • However, lesions may appear on the buttocks, knees, and extremities • The course is usually mild. Low-grade fever and general symptoms may be present. The disease lasts 5 to 8 days and resolves spontaneously without treatment. The diagnosis is based on clinical criteria. • Differential diagnosis • Herpangina • aphthous ulcers • Secondary herpetic stomatitis • Treatment is symptomatic. Viral Infections • Infectious Mononucleosis • • • • • EBV or HHV-4 is the cause Transmitted by saliva. Palatalpetechiae,uvularedema,oral lymphoid enlargement, and ulcerative gingivitis are the most common oral lesions. more common in children and young adults, aged 15 to 25 years. Intrafamilial spread of the virus is fre- quent In a healthy host, EBV remains latent in B cells, after the primary infection, for life. The incubation period is long, approximately 30 to 50 days, and the clinical presentation is variable. EBV appears to be implicated in the pathogenesis of Burkitt’s lymphoma, some other types of non-Hodgkin’s lymphoma, nasopharyngeal carcinoma, and lymphoepithelial carcinoma, as well as in other lymphohyperplastic disorders in transplant recipients and other immunosuppressed patients. It is also the causative agent of hairy leukoplakia. • Clinical features • Infectious mononucleosis is clinically characterized by low- grade fever, which persists for 1 to 2 weeks, söre throat, malaise, headache, generalized lymphadenopathy (mostly cervical and auricular), splenomegaly, and hepatomegaly. A maculopapular eruption, mostly located on the trunk, head and neck, and the extremities, may appear on day 4 to 6 and lasts for about 1 week • It is very characteristic that ampicillin causes exacerbation of the skin eruption in 80 to 100%. Oral manifestations are common and the most constant feature is palatal petechiae, solitary or grouped • The diagnosis is usually based on clinical grounds but should be confirmed by special laboratory tests. • Pathology • Identification of serum heterophile antibodies (monospot test) confirms the diagnosis. Increased titers of EBV DNA in serum are of diagnostic help. • Treatment • The disease is self-limited and the treatment is symptomatic. • • • • • • • Differential diagnosis Leukemia Secondary syphilis Streptococcal oropharyngitis Drug reaction HIVinfection Cytomegalovirus infection Viral Infections • Herpes Zoster • It is caused by the reactivation of herpes virus, type3 (VZV). • It usually affects sensory nerves, more often a single dermatome. • Involvement of the trigeminal nerve represents 20 to 30% of the cases. • Lesions characteristically exhibit a unilateral distribution. • It is most common among the elderly and the immuno-suppressed individuals. • Systemic antiviral drugs are the first line of treatment. • is an acute vesicular disease that is caused by the reactivation of latent VZV, also referred as herpes virus, type 3, in the partially immune host. • It mostly affects older individuals, over 50 years, and is very rare in infants and children. There is no gender predilection. An increased incidence of herpes zoster is observed in patients under long-term therapy with corticosteroids or other immunosuppressants, or during radiotherapy, as well as in patients with underlying malignancy, especially of the lymphoid tissue (Hodgkin’s disease, nonHodgkin’s lymphoma, leukemia). • The thoracic, cervical, trigeminal, and lumbosacral dermatomes are most frequently affected. Viral Infections • Herpes Zoster • Clinical features • Clinically, the first symptom of the disease is usually tenderness and pain in the involved dermatome. Constitutional symptoms such as fever, malaise, and headache may also oc- cur. After 2 to 4 days the eruptive phase follows, characterized by grouped maculopapules on an erythematous base, which rapidly form vesiclesand in 2 to 3 days evolve into pustules. Within 5 to 10 days the pustules crust and persist for 10 to 20 days. New lesions continue to appear for several days. The regional lymph nodes are usually tender and enlarged. • The unilateral distribution of the lesions is the most characteristic clinical feature of herpes zoster. Oral manifestations may occur when the second and third branches of the trigeminal nerve are involved. Frequently, intraoral involvement is associated with unilateral skin lesions on the face • Oral mucosal lesions are almost identical to the cutaneous lesions. • An itching sensation and pain, which may simulate pulpitis, precede the oral lesions. These begin as unilateral clusters of vesicles which in 2 to 3 days rupture, leaving ulcers surrounded by a broad erythematous zone • The ulcers heal without scarring in 2 to 3 weeks. • Postherpetic trigeminal neuralgia is the most common complication of oral herpes zoster. The diagnosis is based on clinical criteria. Viral Infections • Herpes Zoster • Differential diagnosis • Secondary herpetic stomatitis • Varicella • Erythema multiforme • Herpangina • Pathology Cytologic examination confirms virally modified epithelial cells with acantholysis and formation of multiple, free-floating Tzanck cells with nuclear margination of chromatin and multi- nucleation. The immunoglobulin G (IgG) antibody titer to VZV may risk between the acute and convalescent phases. • Treatment • Antiviral therapy is effective if started early, within 3 to 4 days from the onset of symptoms • Prednisolone (20–30 mg for 1 week, tapered for a further week) may alleviate acute symptoms and reduce the risk for postherpetic neuralgia. Analgesics, anticonvulsants, and sedatives are also administered to control the pain. Viral Infections • Papilloma Virus Infections (HPV) -Papilloma • A benign tumor of the surface epithelium. • In 50 to 60% of papillomas,humanpapillomavirus (HPV), types 6 and 11, are detected within the tumor. • It has a characteristic clinical presentation, comprising of multiple, small projections with a “cauliflower-like” appearance. • The final diagnosis is based on the histologic pattern. • Papilloma affects both sexes equally, most commonly be- tween the ages of 30 and 50 years. Clinically, it presents as an exophytic, well-circumscribed, pedunculated or sessile tumor. • The color varies between white, pale pink, or even normal mucosal, depending on the degree of keratinization. The size usually ranges between 3 and 6 mm and rarely grows above 1 cm. Papillomas are usually solitary, occurring more commonly on the tongue and the soft palate and less frequently in other sites. • Differential diagnosis • Verruca vulgaris Pathology • Condyloma accuminatum On histologic examination, the papilloma is characterized by • Verruciform xanthoma hyperplasia of the epithelial layers that give rise to • Verrucous carcinoma char- acteristic multiple, finger-like projections with a slender • Sialadenoma papilliferum fibrovascular core. Koilocyte-like cells can be observed in the prickle • Focal dermal hypoplasia syndrome cell layer and are indicative of viral infection. • Focal epithelial hyperplasia Treatment The treatment of choice is conservative surgical excision. Viral Infections • Papilloma Virus Infections (HPV) • -Focal Epithelial Hyperplasia(Morbus Heck) • The disease is caused by HPV types 13 and 32. • There is a predilection to American Indians,Eskimos, and South Africans. • It is sporadically observed in Europe. • Clinically, it is characterized by multiple, slightly elevated, small nodules that tend to disappear when the mucosa is stretched. • The final diagnosis is based on the histologic pattern. • The familial presentation and predilection to certain ages suggests that a genetic factor might be implicated. Additionally, cases have been reported in patients with AIDS. It is more commonly observed in children, but it can also appear in adults. • Presents as multiple, sessile, painless, and slightly elevated nodules of 1 to 10 mm in diameter and normal mucosa, pale pink, or white color • The surface is smooth or mildly granular. Characteristically, when the mucosa is stretched, the lesions tend to disappear. • The most commonly affected sites are the lower lip, tongue, and buccal mucosa, followed by the upper lip, gingiva, and palate. Rarely, conjunctival involvement may occur. • The diagnosis is based on the clinical features, but has to be confirmed by a biopsy and the histopathologic pattern. Viral Infections • Papilloma Virus Infections (HPV) -Focal Epithelial Hyperplasia(Morbus Heck) • Differential diagnosis • Condyloma accuminatum • Multiple verruca vulgaris • Multiple papillomas • Multiplefibromas • Focal dermal hypoplasia syndrome • Pathology • On histologic examination, the lesions show prominent acanthosis and elongated broad rete ridges. Koilocytes and sporadic mitoses may be observed particularly on the upper epithelial layers. HPV virus has been found with DNA in situ hybridization and PCR techniques. • Treatment • The lesions may spontaneously reverse after a few months and up to 2 years. For lesions that cause esthetic problem, conservative surgical excision or CO2 laser, or electrosurgery can be suggested. Recurrences after therapy rarely occur. Viral Infections • Papilloma Virus Infections (HPV) -Condyloma Acuminatum • Condyloma accuminatum is caused by HPV types 6 or 11 (HPV-6, HPV-11), which are considered to be low- risk types. • Condyloma accuminatum is most commonly observed on the genital mucosa and much less on the oral mucosa. • The final diagnosis is based on the histologic pattern. • Condyloma accuminatum is a common, sexually transmitted disease • Clinical features • Clinically, condyloma accuminatum appears as a sessile, painless, well-circumscribed exophytic tumor with a “cauliflower-like” surface and normal mucosal or pale pink color • The lesions are usually multiple, with size that ranges between 1 and 3 cm and have a tendency to coalesce and recur. Most commonly affected sites are the lips, buccal mucosa, tongue, lingual frenum, and soft palate. • Pathology • Histologically, condyloma accuminatum is characterized by parakeratosis, acanthosis, and elongation of the rete ridges. Koilocytes are frequently observed (small pyknotic nuclei sur- rounded by a clear cytoplasmic halo), indicating a microscopic feature of HPV infection. Verification of the virus infection can be proved by in situ hybridization and polymerase chain reaction (PCR) techniques. • Treatment • Conservative surgical excision or electrosurgery would be the preferred treatment for the oral lesions. Viral Infections • Papilloma Virus Infections (HPV) • -Verruca Vulgaris • Verruca vulgaris is associated with HPV, mainly types 1, 2, and 4. Lesions are very common on the skin, but are rarely observed in the mouth. • It is transmitted intraorally through self-inoculation from the existing lesions of the fingers. • The final diagnosis is based on the histologic pattern. • When it occurs intraorally, the sites most commonly affected are the lips, tongue, and gingiva. • Clinically, they present as small, painless, exophytic lesions with a “cauliflower-like” surface and white or pink-white color • They may be sessile or pedunculated, multiple or solitary. The clinical diagnosis has to be confirmed histopathologically. • Differential diagnosis • Condyloma accuminatum • Papilloma • Verruciform xanthoma • Verrucous carcinoma • Focal epithelial hyperplasia • Pathology • Histologically, the lesion is characterized by papillomatous projections of hyperplastic and hyperkeratotic squamous epithelium supported by a thin fibrous core. The rete ridges are elongated and tend to converge toward the center of the lesion (cupping effect). In the prominent granular cell layer, coarse, clumped keratohyalin granules are typically found, along with abundant koilocytes. • Treatment • Conservative surgical or electrosurgical excision of the oral lesions is the treatment of choice. Viral Infections • HIV/AIDS • Various oral lesions may occur at any stage of the infection; however, these lesions are indicative and not specific for HIV disease. • Alarming oral clinical manifestations suggestive of HIV infection are: oral hairy leukoplakia (OHL), necrotizing ulcerative gingivitis, necrotizing ulcerative periodontitis, and severe herpes zoster in young patients. • Some HIV-related infections may become apparent or worsen when the immune status improves during the cART therapy (combination antiretroviral therapy), such as herpes zoster, condyloma acuminatum—cytomegalovirus (CMV), Mycobacterium avium, a phenomenon termed 'immune reconstitution syndrome'.