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This webpage will discuss several of the infectious diseases of the mouth, tongue, and parotid glands. These diseases include stomatitis due to the herpes simplex viruses and to Candida albicans and oral hairy leukoplakia, angular cheilitis, and parotitis.
This section of the handout will discuss several of the infectious diseases of the mouth, tongue, and parotid glands. These diseases include stomatitis due to the herpes simplex viruses and to Candida albicans and oral hairy leukoplakia, angular cheilitis, and parotitis.
Stomatitis is an inflammation of the mucosal surfaces in the mouth and on the tongue, and is most often caused by herpes simplex virus type 1 (HSV-1), HSV-2 and Candida albicans. If the inflammation includes the gingivae, it is called gingivostomatitis (common in HSV infections).
The most common cause of gingivostomatitis, or oral herpes, is HSV-1, and the most common cause of candidiasis is Candida albicans (oral candidiasis). HSV-2 can also cause oral herpes, but it is less common than HSV-1.
The incubation period of gingivostomatitis due to HSV-1 and HSV-2 is 1–2 days. The duration of illness is 2–3 weeks; during this time, the patient may experience fever, fatigue, muscle aches, and irritability. Pain, burning, tingling, or itching may occur at the site of infection before sores appear; clusters of blisters then erupt. The blisters break down rapidly, appearing as tiny, shallow, gray ulcers on a red base. The most intense pain caused by the sores occurs at the onset, causing eating and drinking to be difficult. Sores may occur on the lips, gingivae, front of the tongue, inside of the cheeks, the throat, and the roof of the mouth, and may also extend down the chin and neck. The gingivae may become red and mildly swollen and may bleed. Cervical lymph nodes often swell and become painful. Herpes may cause pharyngitis, with shallow ulcers and a grayish coating on the tonsils of persons usually in their teens and twenties.
Types of candidiasis
1. Acute pseudomembranous candidiasis, or thrush, is characterized by the presence of creamy-white plaques (pseudomembranes) that consist of superficial mucosal cells, neutrophils, and yeast cells. Plaques can be found on the tongue, soft palate, cheek, gingivae, and pharynx. Lesions often begin as tiny focal areas that enlarge to white plaques, or patches. Lesions are difficult to remove when scraped with a tongue blade, resulting in an inflamed base that is painful and may bleed. In neonates and infants, there is usually a white coating in the mouth and the infant may have difficulty feeding. Candidal infection in the diaper area may accompany acute pseudomembranous candidiasis. Candidiasis may spread to the esophagus in immunocompromised hosts.
2. Erythematous candidiasis consists of red lesions of varying sizes that can occur on any part of the oral mucosa. If present on the tongue, lesions can be painful, fiery red, and shiny, with evidence of depapillation. This disease can be acute or chronic.
3. Hyperplastic candidiasis, or candidal leukoplakia, is usually an individual lesion on the oral mucosa of the cheek near the commissure, at the angles of the mouth, or on the surface of the tongue. Lesions are chronic, discrete, raised, and may vary from a small, palpable, translucent, or whitish area to a large, dense, opaque plaque that is hard and rough to the touch. Homogeneous or speckled areas, which do not rub off, can be seen. Speckled red-white lesions have an increased chance of malignant transformation.
TMP-1. Predisposing Factors or Conditions for Candidiasis
Patients taking broad-spectrum antibiotics
Patients taking steroids (inhaled and systemic); children on inhaled steroids have increased incidence of oral candidiasis
Patients with polyendocrine disorders (e.g., diabetes mellitus)
Patients with xerostomia (dry mouth; Sjögren syndrome; after radiotherapy)
Patients with underlying immune dysfunction (e.g., HIV infection)
Smokers (30–70% are more likely to have Candida albicans in the oral mucosa)
Persons who wear dentures
Infants and neonates
Oral herpes results in painful sores on the lips, gingivae, tongue, roof of the mouth, and on the mucous membranes lining the cheeks. After infection, HSV-1 and HSV-2 have the ability to progress to the following stages.
1. During primary infection, the virus enters the skin or mucous membrane and reproduces in the mucosal cells. During this stage, oral sores and other symptoms such as fever may develop. The virus can cause asymptomatic infections, which occur twice as often as symptomatic disease.
2. The virus moves from the infected site to nerves in the region—the trigeminal root ganglion—and establishes itself latently in the host nerves. The virus reproduces and becomes inactive in the ganglion. HSV-1 and HSV-2 become latent in the ganglia of the host and remain in the host for a lifetime.
3. During times of emotional or physical stress, the virus can multiply in the ganglion, and viral particles can move to the skin and cause recurrence of the vesicular lesions on the skin around the mouth and nose. Recurrent lesions usually are seen in the skin around the nose and mouth, and rarely inside the mouth.
Acute pseudomembranous candidiasis results when there is a disturbance of the normal oral flora (e.g., antibiotic therapy, emotional or physical stress). C albicans will overgrow on the oral mucosa causing desquamation of epithelial cells and accumulation of bacteria, keratin, and necrotic tissue. This debris combines to form a pseudomembrane, which adheres closely to the mucosa.
Erythematous candidiasis can be an acute or a chronic condition. It is an inflammatory response to Candida overgrowth without the pseudomembrane or a candidal infection after the pseudomembrane sheds. It can occur following acute pseudomembranous candidiasis after the white plaques have shed, de novo in AIDS patients, in patients receiving prolonged topical steroids or broad-spectrum antibiotic therapy, or in persons who wear dentures.
Hyperplastic candidiasis is characterized by parakeratinization of areas in the mouth with marked hyperplasia and candidal hyphae invading the parakeratinized layer at right angles and superficial to the surface. Lesions may become malignant.
Diagnosis of herpes gingivostomatitis is usually based on clinical signs and symptoms; however, culture and serologic tests can be performed on the virus. Scraping the base of the ulcer usually results in a positive Tzanck test (presence of multinucleated giant cells).
Diagnosis of candidiasis is usually based on clinical signs and symptoms. Lesions can be swabbed and samples cultured on Sabouraud’s dextrose agar. The lesions can be scraped and stained with periodic acid–Schiff or Gomori methenamine silver stain to reveal the pseudohyphae of the yeast. Hyperplastic conditions should be biopsied for histology. Pseudomembranous lesions are removable; hyperplastic lesions are not.
Treatment and Prevention
Herpes gingivostomatitis is self-limiting and usually does not require treatment; however, if severe, penciclovir or valacyclovir can be given. Treatment is not curative, and the disease can recur. Treatment of candidiasis includes use of nystatin rinses, fluconazole, or itraconazole.
ORAL HAIRY LEUKOPLAKIA
Oral hairy leukoplakia is a disease of the lateral borders of the tongue. It is most commonly seen in immunocompromised patients (e.g., human immunodeficiency virus [HIV] infection), patients with malignant tumors, and in organ transplantation recipients.
Oral hairy leukoplakia is caused by a combination of at least two important factors: (1) The patient is severely immunocompromised. The most common cause of immunocompromise resulting in oral hairy leukoplakia is HIV infection. (2) and the patient has also been previously infected with the Epstein Barr virus (EBV).
Oral hairy leukoplakia is usually a nonpainful, white plaque that occurs along the lateral borders of the tongue. It is restricted to this region of the mouth and only rarely spreads to contiguous sites—the mouth floor, tonsillar pillars, ventral tongue, and pharynx.
Currently, there is very little information known about the pathogenesis of oral hairy leukoplakia, but what is known is that an individual with a history of infection with EBV becomes immunocompromised and the number of CD4+ T-lymphocytes decreases. During this time of immunosuppression, the patient who is latently infected with EBV cannot suppress EBV replication in the oral mucosa. EBV produces viral proteins important in viral replication and in tumor formation. These viral proteins contribute to the development of oral hairy leukoplakia and induction of many of the histologic features such as acanthosis (i.e., benign thickening of the mucosa) and hyperproliferation of the epithelial cells on the lateral surface of the tongue.
Diagnosis of oral hairy leukoplakia is based on clinical grounds. It is quite similar in appearance to pseudomembranous candidiasis (thrush). However, the white plaques associated with oral hairy leukoplakia cannot be removed like those of pseudomembranous candidiasis. The lesions of pseudomembranous candidiasis are usually more widespread in the mouth and are painful, whereas oral hairy leukoplakia is usually seen only on the lateral surface of the tongue and is painless. The white plague can be sampled using a sterile endocervical brush, and the sample stained using the Papanicolaou technique. Cells characteristic of oral hairy leukoplakia have Cowdry type A inclusions, a ground glass appearance, and nuclear beading.
Treatment and Prevention
Oral hairy leukoplakia is rarely treated unless the patient is infected with HIV. Patients infected with HIV are treated with highly active antiretroviral therapy (HAART), which helps resolve the plaque. When oral hairy leukoplakia is specifically treated, the following agents have been used: podophyllum resin and acyclovir in combination, or podophyllum resin, acyclovir, valacyclovir, famciclovir, ganciclovir, or foscarnet alone.
Angular cheilitis, also known as angular stomatitis or perlèche, is an inflammation of the angles of the mouth.
The most common cause of angular cheilitis is Candida albicans. If yellow crusting appears, Staphylococcus aureus is also likely to be involved.
The lesions of angular cheilitis affect the angles of the mouth; soreness, erythema, and fissuring are characteristic manifestations.
Angular cheilitis involves erythema and maceration of the skin adjacent to the angle of the mouth.
Diagnosis of angular cheilitis is usually determined based on signs and symptoms. The lesion can be swabbed and cultured to determine the organisms involved.
Treatment and Prevention
Treatment of angular cheilitis includes hydrocortisone 1% and clioquinol 3%. Prevention can include proper nutrition and referral to a dentist for proper fitting dentures.
The mumps virus and Staphylococcus aureus can cause inflammation in any of the salivary glands. However, because the parotid gland is affected most frequently, these two infections are called benign viral parotitis (mumps) and acute bacterial parotitis.
Benign viral parotitis (mumps)
Mumps is a common childhood inflammatory disease of the salivary glands with occasional serious complications. Although infection of the parotid glands is the most common manifestation, many other organs can be involved (e.g., epididymoorchitis, oophoritis, aseptic meningitis). The incidence of mumps has decreased dramatically since the introduction of the mumps vaccine.
Mumps is caused by an RNA virus in the paramyxovirus family, called the mumps virus.
Mumps is usually asymptomatic. If a clinically apparent case of mumps occurs, a prodrome of myalgia, anorexia, malaise, and a low-grade fever usually precedes the parotitis. The parotitis can include swollen and tender salivary glands, with the parotid gland most commonly affected. The patient may also complain of earaches, which last about 1 week and are usually bilateral. The orifices of the submandibular (Wharton duct) and parotid (Stensen duct) ducts become red and swollen with pinpoint petechial hemorrhages. Obstruction of these inflamed ducts by edema or cellular debris causes pain when chewing or drinking. The mumps virus can also infect and cause inflammation of the pancreas, thyroid, prostate, and lacrimal glands.
Other systems infected by the mumps virus include the central nervous system (CNS) and the male and female reproductive systems. Mumps virus infection of the CNS results in aseptic meningitis. Symptoms include fever, headache, nausea and vomiting, and lethargy, and usually subside within 3–10 days after onset. The virus can cause permanent damage to the vestibulocochlear nerve, which results in unilateral deafness in most cases. Mumps virus infection of the epididymis and the testis causes a bilateral inflammation of the testis called epididymoorchitis. Epididymoorchitis occurs abruptly and includes bilateral testicular swelling, tenderness, nausea, vomiting, elevated temperature, and chills. Sterility due to mumps orchitis is rare. The condition is usually seen in adolescent patients.
Mumps virus infection of the ovaries causes an inflammation of the one or both ovaries. Symptoms of oophoritis include abdominal tenderness and pain that can mimic appendicitis if the right ovary is involved. There is no evidence that the mumps virus causes impaired fertility in females. However, if the woman acquires the mumps virus during the first trimester, there is an increased chance of fetal death and abortion. If the mother acquires the mumps virus during the second or third trimester, there is little risk of congenital disease. Neonatal mumps infection is extremely rare.
The mumps virus usually enters the body through the upper respiratory tract and infects regional lymph nodes. A viremia occurs and disseminates the virus to the meninges, salivary glands, testes, pancreas, ovaries, kidneys (most patients have impaired renal function), thyroid, eyes, and mammary glands. The mumps virus has a tropism for glandular tissue and is neurotropic causing meningitis, encephalitis, myelitis, polyneuritis, polyradiculitis, and cranial neuritis.
The clinical signs and symptoms of mumps usually suffice for diagnosis of mumps parotitis. The parotid gland feels jelly-like; the overlying skin usually is not warm to the touch as occurs in bacterial parotitis. Orchitis, pancreatitis, and aseptic meningitis are often associated with high total white cell counts (above 20,000/mm3 with a high number of polymorphonuclear leukocytes). Rapid diagnosis can be made directly on pharyngeal cells or on urine sediment using an immunofluorescence assay for viral antigen.
Therapy and Prevention
Symptomatic treatment of mumps is recommended to alleviate distress associated with the patient’s symptoms. A live attenuated mumps vaccine is available for infants 12–15 months of age and is given in the MMR vaccine. A second dose of the MMR vaccine should be given to children at 4–6 years of age. The vaccine should NOT be given during pregnancy because the viruses in the MMR vaccine are live attenuated viruses that can cross the placenta, causing fetal damage.
Acute bacterial parotitis
Acute bacterial parotitis is an infection of the salivary glands. Previously, it was a frequent cause of mortality in terminally ill dehydrated patients and had a high mortality rate; however, with the advent of antibiotic and intravenous fluid therapy, the disease is now relatively uncommon.
The most common cause of acute bacterial parotitis is Staphylococcus aureus.
Patients with acute bacterial parotitis experience progressively painful swelling of the salivary glands. Chewing increases the pain. The swollen glands are tender to the touch, and the skin overlying the swollen glands is erythematous and warm. Massage of the affected glands results in purulent saliva.
If the flow of saliva is affected, bacteria can enter the ducts and ascend to the salivary gland, causing inflammation and pain.
Clinical presentation is helpful in determining the diagnosis of the patient with acute bacterial parotitis. In mumps, the glands are tender to the touch but the overlying skin is not erythematous, nor is it warm to the touch as it is in acute bacterial parotitis. Massaging the patient’s inflamed salivary glands expresses purulent saliva. The purulent saliva can be Gram stained and cultured to identify the causative agent.
Therapy and Prevention
Treatment of acute bacterial parotitis involves intravenous antibiotics (e.g., empiric therapy = vancomycin) and rehydration of the patient. The choice of antibiotics can be changed based on the results of culture and antibiotic sensitivity. If antibiotic treatment fails to resolve the infection, incision and drainage may be necessary. This infection can be prevented by ensuring proper hydration of chronically ill patients, elderly patients, and postoperative patients.
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