Oral and Maxillofacial Viral Infections

Oral and Maxillofacial Viral Infections Stephen Porter, Jair C. Leão, and Luiz Alcino Gueiros Abstract Keywords A wide spectrum of viral infections can affect Viral diseases • Viral infections • the mouth and allied structures. In most Herpesviridae • Enterovirus • HIV • HPV instances, these give rise to short-term local illness (e.g., herpes simplex infections in Contents immunocompetent hosts); however, infections Introduction .......................................... 2 such as Human Immunodeficiency viruses Herpes Viruses ....................................... 2 (HIV), Epstein Barr virus (EBV), and the Herpes Simplex Virus (HSV-1 and HSV-2) . 2 oncogenic types of Human Papillomavirus Varicella Zoster Virus ................................. 6 (HPV) can cause significant orofacial disease Ramsay Hunt Syndrome .............................. 7 that will increase patient morbidity and possi- Epstein Barr Virus ..................................... 8 Cytomegalovirus ...................................... 10 bly lead to early death. The present chapter Human Herpes Virus 6 ................................ 10 details the viral infections that may commonly Human Herpes Virus 7 ................................ 10 affect the oral cavity and/or salivary glands in Human Herpes Virus 8 ................................ 10 patients worldwide. The epidemiology of viral Coxsackie Viruses .................................... 11 infections is ever changing; hence, health care Hand, Foot, and Mouth Disease ...................... 11 providers are encouraged to maintain knowl- Herpangina ............................................ 12 edge of virally driven infections that may Acute Lymphonodular Pharyngitis . 13 impact upon the health and clinical care of Rubella ................................................ 13 their relevant specialty. Human Immunodeficiency Viruses ................. 13 Human Papilloma Virus ............................. 16 Nononcogenic HPV Disease .......................... 16 Oncogenic HPV Disease .............................. 17 Viral Infections of the Salivary Glands ............ 19 Mumps ................................................ 19 S. Porter (*) Hepatitis C Virus ...................................... 20 UCL Eastman Dental Institute, University College HIV Salivary Gland Disease .......................... 21 London, London, UK e-mail: [email protected] Seasonal Viral Infections ............................ 21 J.C. Leão • L.A. Gueiros Emerging Viral Infections ........................... 22 Oral Medicine Unit, Departamento de Clínica e Odontologia Preventiva, Universidade Federal de Conclusions and Future Directions ................. 22 Pernambuco, Recife, PE, Brazil Cross-References ..................................... 23 e-mail: [email protected]; [email protected]; [email protected] References ............................................ 23 # Springer International Publishing AG 2017 1 C.S. Farah et al. (eds.), Contemporary Oral Medicine, https://doi.org/10.1007/978-3-319-28100-1_44-1 2 S. Porter et al. Introduction destruction and specific induction of a latent immune state. The β-herpervirinae viruses, on The oral mucosa is a common site for primary the other hand, have a long reproductive cycle viral infections particularly those of the human and may become latent in lymphoreticular cells. herpesvirus (HHV) and human papillomavirus CMV is the hallmark of this subfamily, being (HPV) families. More recently, HPV infections capable of inducing a plethora of clinical disor- have received particular attention as oncogenic ders, particularly in immunocompromised indi- types aetiologically linked to increasing numbers viduals. Finally, γ-herpesvirinae have an affinity of cases of oral squamous cell carcinoma. None- for T and B lymphocytes, become latent in lym- theless, many other viral infections may be found phoid tissues, and are closely associated with in the oral cavity of humans. This chapter dis- certain malignant diseases. EBV is the typical cusses viral conditions of the oral cavity, includ- member of this subfamily, being associated with ing HHV infection, HPV, coxsackievirus, mumps, acute infection (infectious mononucleosis) and measles, rubella, and those conditions/diseases being causative of malignant diseases that in- associated with HIV and HCV infection. Emerg- clude Burkitt’s lymphoma and nasopharyngeal ing viral diseases including Ebola and Zika virus carcinoma. are also briefly discussed. Herpes Simplex Virus (HSV-1 Herpes Viruses and HSV-2) The human herpesvirus (HHV) are a species- Clinical Features specific family of DNA virus that includes eight Herpes simplex virus 1 (HSV-1) is transmitted via types that can infect humans. The human herpes close contact with infected fluids (usually saliva) viruses are classified into three subfamilies (α, β, or lesions, and tends to give rise to disease of the and γ). The α-herpervirinae viruses are character- mouth and surrounding skin. In contrast, HSV-2 is ized by a relatively short reproductive cycle and usually transmitted by genital-to-genital contact irreversible destruction of infected cells and with infected fluids or lesions and predominantly include HSV1, HSV2, and VZV. β-Herpervirinae gives rise to genital disease. However, HSV-1 can viruses (CMV, HHV6, and HHV7) have a long cause genital disease and HSV-2 can give rise to reproductive cycle and a slow infection process. oral illness as a consequence of acquisition via Finally, γ-herpesvirinae (EBV and HHV8) repli- orogenital contact. Both HSV-1 and HSV-2 lead cate in lymphoblastoid cells and may establish to an initial primary infection with later episodes a latent or lytic infection in B or T lymphocytes. of less severe secondary infection in some, but not This classification is reflectedintheclinicalbehav- all, infected patients (Arduino and Porter 2008). ior of the associated diseases as discussed below. Primary HSV-1 infection typically affects the The human herpes viruses may promote a dis- mouth and arises within 1–2 weeks of acquisition ease state in three distinctive ways: (1) direct of the virus. The clinical features comprise initial destruction of cells and tissues, (2) induction of nonspecific features of malaise, pyrexia, and leth- immune responses, and (3) facilitation of neoplas- argy followed by the eruption of widespread tic transformation. The α-herpervirinae viruses ulceration of the oral mucosa and gingiva (Cun- typically present a short reproductive cycle with ningham et al. 2006). irreversible destruction of infected cells, follow- The ulcers are usually superficial, initially ing the ability to maintain latent infection in the small and spherical but may coalesce to give rise sensorial neural ganglion. Herpes simplex virus is to large sized, irregular outlined ulcers (Fig. 1). within this subfamily and causes rapid infection of The ulceration can arise on any oral mucosal epithelial cells with subsequent latency state and surface; indeed, typically all sites of the mouth recurrent flares, characterizing the direct cellular can be affected. The gingiva becomes swollen, Oral and Maxillofacial Viral Infections 3 Fig. 1 Initial aspect of intraoral herpes simplex infection, palatal ulcers observed 2–3 days following initial symp- with blister formation in the hard palate (a). Multiple toms of intraoral herpes simplex (b) Secondary HSV-1 infection of the mouth affects about 30% of patients with a history of probable primary infection. Many patients present with a likely secondary disease, however, cannot recall having the primary disease (Arduino and Porter 2008; Fatahzadeh and Schwartz 2007). Secondary HSV-1 infection of the mouth typically affects the vermillion of the lip termed herpes labialis (commonly known as “cold sores”) (Fig. 3) but can also arise on the perioral or peri- nasal skin. Sole involvement of the mouth (e.g., small numbers of superficial oral mucosal or gin- Fig. 2 Multiple ulcers due to herpes simplex infection gival ulcers) is a very rare manifestation of secondary HSV-1 infection (Figs. 4 and 5). Herpes erythematous, and ulcerated, with ulceration labialis is characterized by a clinical pattern of affecting the free and/or attached gingiva (Fig. 2) paraesthesia, followed by erythema, vesiculation, (and hence may mimic acute necrotizing ulcera- pustule formation, superficial ulceration, and tive gingivitis – ANUG). The ulceration causes eventual spontaneous healing. The complete clin- notable pain, dysphagia, dysarthria, and possibly ical disease lasts about 5–7 days (Arduino and drooling. There is usually bilateral cervical Porter 2008). lymphadenopathy and occasionally a generalized Herpes labialis may often, but not always, be macular cutaneous rash. The signs and symptoms precipitated by an identifiable precipitant that may usually spontaneously resolve within 7–10 days, include concomitant illness, (e.g., flu or other although the disease can be severe and prolonged infections) exposure to sunlight or UV light or in immunocompromised individuals (Elad et al. occasionally is associated with particular phases 2010). of the menstrual cycle or pregnancy. Immunosup- Primary HSV-2 infection of the mouth can give pression (e.g., iatrogenic, malignancy-associated rise to a similar clinical picture to that of HSV-1 or HIV-associated) can also lead to the onset of although it has been suggested that the illness may herpes labialis that may be severe and/or pro- be less severe and not as prolonged as that caused longed, but can also involve intra-oral sites

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