Chapter 21 Viruses of relevance to dentistry
Human papillomavirus (HPV) mainly causes skin warts (verrucae); it is also associated with a number of lesions including oral papillomas, oral verrucous carcinomas and focal epithelial hyperplasia. There are more than 70 serological types of HPV, some of which are more closely associated with lesions (both benign and cancerous) than others.
Acute respiratory disease is the most common adenovirus infection. It is an influenza-like illness seen commonly in military training camps. Clinically, the main symptoms are pharyngitis and conjunctivitis. Although self-limiting, acute respiratory disease may be complicated by pneumonia in some cases. Other infections caused by these viruses include pharyngoconjunctival fever (a disease of infants and children), epidemic keratoconjunctivitis, pneumonia and gastroenteritis.
There are a range of different human herpesviruses, currently numbered 1–8 (see Table 4.3). All of them are structurally similar (enveloped, icosahedral with double-stranded DNA) and infect both humans and animals. They are the most common causes of human viral infections. All have the important property of remaining latent, with the ability to reinfect the host a variable period after the primary infection. Important human pathogens include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV) and Epstein–Barr virus (EBV) (see Chapter 4). Students of dentistry should be thoroughly conversant with the herpes group of viruses as the majority of them either cause oral infection or are intimately associated with orofacial tissues and saliva.
Recurrence or reactivation of HSV entails activation of the non-infectious form of the latent virus residing in the neurons of either the trigeminal ganglion (Fig. 21.3) or the sacral ganglia. Reactivation is provoked by menstruation, stress, sunlight (possibly ultraviolet rays), local trauma, etc.; the lesions tend to recur at the site of the primary lesion. HSV has been implicated in Bell’s palsy.
Humans are the only known reservoir for HSV-1 and HSV-2; experimental infection can be induced in animals and cell cultures. As the virus is highly labile, most primary infections are acquired through direct contact with a lesion or contaminated secretions. In general, HSV-1 causes orofacial lesions or lesions ‘above the belt’, while HSV-2 causes lesions ‘below the belt’, i.e. genital herpes (Fig. 21.4). However, because of sexual promiscuity or for other reasons, this may not be always true. HSV-1 is acquired early in life, while HSV-2 appears after the onset of sexual activity.
As recurrent infection is common in the presence of high antibody titres, circulating antibodies appear to be unhelpful in controlling HSV infection. One reason for this may be the contiguous cell-to-cell spread of the virus, which cannot be prevented by antibody. Reactivation is not accompanied by a rise in herpes antibody titre.
Fig. 21.5 Positive immunofluorescence of a smear taken from the lip lesion shown in Figure 21.3B (stained with anti-herpes antibody tagged to a fluorescing chemical), indicating that the patient has herpes labialis.
Control is difficult because of the high frequency of asymptomatic infection. It is important to avoid contact with acute herpetic lesions and contaminated body fluid (e.g. saliva) by routine wearing of gloves. No vaccine is available.
This organism causes both varicella (chickenpox) and herpes zoster (shingles) – two different diseases due to an identical organism. Chickenpox is the primary infection, and herpes zoster is the reactivation of illness.
A common childhood fever, varicella is mild and self-limiting. The disease is more severe if contracted in adulthood. After a 2-week incubation period, fever develops, followed by a papular rash of the skin and mucous membranes, including the oral mucosa. The papules rapidly become vesicular and itchy but painless (in contrast to the rash in zoster).
Occurs primarily as a reactivation of the virus in dorsal root or cranial nerve (usually trigeminal) ganglia (Fig. 21.6). The disease usually affects adults, and the virus is reactivated despite circulating antibodies. Zoster is triggered by trauma, drugs, neoplastic disease or immunosuppression.
The virus remains latent in ganglionic nerve cells and, after activation, travels back along the nerve fibre to the skin. Thoracic nerves supplying the chest wall are most often affected, and the lesion presents as a unilateral, painful vesicular rash, which extends in a horizontal strip from the middle of the back around the side of the chest wall (‘belt of roses from hell’). Fever and malaise accompany the lesion. The rash may last for 2–4 weeks, with pain (post-herpetic neuralgia) persisting for weeks or months.
The trigeminal nerve is affected in about 15% of cases, with involvement of the ophthalmic, maxillary and mandibular divisions (in that order of precedence). Severe localized oral pain precedes the rash and may be easily confused with toothache (see Chapter 35). Involvement of the ophthalmic nerve may lead to eye lesions and sometimes blindness.
Shingles is primarily a disease of older adults and immunocompromised persons; it is rare in children. The incidence increases with advancing age and with decreasing degree of immunocompetence. It is a highly contagious infection in a host not previously exposed to the virus. Transmission occurs by direct contact with skin lesions or droplet infection from infectious saliva.
The clinical picture is pathognomonic, as the lesion distribution overlaps and accurately maps the distribution of the sensory nerve (Fig. 21.7). Serology, if needed, entails detecting a fourfold rise in antibody titre in paired sera (compare herpes simplex reactivation, where antibody rise is not significant).
Chickenpox is self-limiting and requires symptomatic treatment, if any. Disseminated zoster in immunocompromised patients requires antiviral drugs (e.g. aciclovir, vidarabine), which interfere with herpesvirus DNA replication. Varicella-zoster virus is less sensitive to aciclovir than is HSV, and hence, a higher dosage is required; therapy should start within 72 h of onset. Systemic aciclovir may reduce the duration of the early infective phase and the associated pain. In addition, it may reduce the prevalence of post-herpetic neuralgia.
EBV is widespread in humans, and most adults have antibody to the virus. The virus persists in latent form within lymphocytes after primary infection (lymphotrophic, unlike HSV and varicella-zoster virus, which are neurotrophic). The genome resides in a latent form in B cells; latent EBV infection is common in the population. It is the aetiological agent of a number of diseases:
An acute infection affecting lymphoid tissue throughout the body, infectious mononucleosis is commonly seen in teenagers, with a peak incidence at 15–20 years of age. The organism is present in saliva and is postulated to be transmitted during kissing – hence, it is called the ‘kissing disease’.
Low-grade fever with generalized lymphadenopathy and abnormal lymphocytes in the blood (note that a similar illness, glandular fever-like syndrome, develops during the first fortnight after infection with human immunodeficiency virus (HIV)). Fever, tonsillitis and fatigue are common, and many patients have splenomegaly. Lymphocytosis is a characteristic feature, hence the term ‘mononucleosis’; some 10% of the lymphocytes are atypical, with enlarged misshapen nuclei and increased cytoplasm (Fig. 21.8).
The virus is ubiquitous, and humans are its only known host. Spread of EBV is via respiratory secretions, primarily through oral contact. Those from lower socioeconomic classes are exposed to EBV at an early age and typically develop asy/>