Lecture 1: Bacterial&fungal infection with damage of mucouse of oral cavity

student: Parisa Pour khosrow group 26, 4th years Dental faculty
Kiev 2011

Common Infections of the Oral Mucosa

Bacterial Infection 1) Streptococcal organisms 2) Syphilis 3) Gonorrhea

Streptococcal organisms:
Streptococcal organisms are by far the most commonly isolated microorganisms from the oral mucosa. Caries of the dentition is a streptococcal infection. Streptococcus viridans is the most prevalent organism. Streptococcal infections appear as very erythematous, inflamed and painful lesions of the oral mucosa.
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Streptococcus mutans
Streptococcus mutans is a facultatively aerobic, Gram-positive coccus-shaped bacterium commonly found in the human oral cavity and is a significant contributor to tooth decay.

Streptococcus vestibularis
Streptococcus vestibularis is a member of the salivarious group of viridans streptococci. Manyof the viridans streptococcal species are part of human normal microbial -ora. The commensal species aremost prevalent in the oral cavity. S. vestibularis has been accepted as an important nosocomial pathogen and an atypical cause of signifi cant septicemia in the presence of mucosal lesions, immune compromising states, malignancy, liver cirrhosis, renal failure or chronic diseases, such as diabetes mellitus. S. vestibularis has been reported to be associated with severe human infections, such as meningitis, endocarditis, bacteremia, and bone and joint infections.
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Syphilis

Primary syphilis of the oral mucosa appears as an erosive ulceration with erythema and raised margins which is non-tender and indurated. There is a non-tender, rubbery cervica lymphadenopathy. This characteristic lesion has been referred to as a chancre. In the oral cavity, the lips are the site of predilection with the commissures also exhibiting ulcerations, When appearing on the outer surfaces of the lips, ulcerations become crested in contrast to those found within the oral cavity which remain moist.
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PRIMARY SYPHILIS
The mouth, perhaps surprisingly, is rarely the site of primary syphilis, and because of its transient nature, the oral ulceration of primary syphilis often goes unnoticed by the patient or by any unsuspicious clinician. In addition, albeit rarely, the lesions of primary disease may be confused with other pre-existing mucocutaneous disease. A chancre develops within 1 to 3 weeks of acquisition. Primary syphilis is usually the consequence of orogenital or oroanal contact with an infectious lesion. Kissing may, very rarely, cause transmission; indeed, it has been suggested that intrafamilial oral acquisition of syphilis in a child may have occurred via this route, although more usually oral syphilis in a child is indicative of sexual abuse.Primary syphilis of the mouth manifests as a solitary ulcer usually of the lip or, more rarely, the tongue. The upper lip is more commonly affected than the lower in males, while the opposite occurs infemalesprobably reflecting the anatomy involved with fellatio and cunninlingus. The pharynx or tonsils may rarely be affected. The ulceration is usually deep, with a red, purple, or brown base and an irregular raised border. There is usually an accompanying Cervical lymphadenopathy. The ulceration of primary syphilis may be confused with other solitary ulcerative disorders, most notably traumatic ulceration, squamous cell carcinoma, and non-Hodgkin's lymphoma
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Treponemes
Treponemes are present in primary lesions and can be detected by dark field microscopy; however, this test is fraught with the risk of nosocomial transmission and is thus no longer considered suitable. In addition, there can be confusion between the spirochetes of T. pallidum with the normal commensals of the mouth. Histopathology is not always helpful, as there are no specific histopathological features, and the detection of T. pallidum with Warthin-Starry stain or silver nitrate stain may not be possible. Monoclonal anthodyl immunoperoxidase staining techniques can detect T. pallidum and is a relatively routine clinical investigation of biopsy material. However, molecular methods such as in situ and tissue PCR still remain nonroutine investigations for all types of syphilis. The tests used to detect IgM antibodies to T. pallidum may detect early infection.

MACULOPAPULAR LESIONS:

Macular syphilides: Macular lesions tend to arise on the hard palate and manifest as flat-to-slightly raised, firm, red lesions. Papular syphilides: These are rare. They manifest as red, raised, firm round nodules with a grey center that may ulcerate. The papules usually arise on the buccal mucosa or commissures.

Mucous patches: A variety of descriptions of mucous patches have been reported, but in general these manifest as oval-to-crescenteric erosions or shallow ulcers of about 1 cm diameter, covered by a grey mucoid exudate and with an erythematous border. The patches usually arise bilaterally on the mobile surfaces of the mouth, although the pharynx, gingivae, tonsils, and very rarely the hard palate can be affected. At the commissures, the mucous patches may appear as split papules, while on the distal and lateral aspects of the tongue, they tend to ulcerate or manifest as irregular fissures. The mucous patches may coalesce to give rise to, or arise de novo as, serpiginous lesions, sometimes termed snail track ulcers.
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Gonorrhea

This disease takes on varying appearances within the oral mucosa. It can resemble acute necrotizing gingivitis exhibiting a necrotic pseudomembrane covering ulcerations or a severe erythematous inflammatory response of the oropharyngeal mucosa. The lesions are painful and cause difficulty in swallowing. When appearing as ulcerations, it can easily be mistaken for streptococcal infections or multiple aphthous stomatitis.

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Oral gonorrhea (also termed pharyngeal gonorrhea) is defined as an STD infection of the pharynx with Gram-negative coccal shaped (round) bacteria named Neisseria gonorrhoeae. Infection is acquired from direct contact with white/yellowish pus-like fluid containing N. gonorrhoeae (also termed discharge or exudates) in one sex partner. This discharge is caused by N. gonorrhoeae. It mixes with a person's vaginal fluids, seminal fluids, or mucus membranes near the anus and rectum that come in contact with another person's oral mucus membranes. The bacterial infection then establishes itself in the pharynx and may be asymptomatic (cause no symptoms), but can cause symptoms of sore throat and discomfort when swallowing food. The affected throat resembles a strep throat with redness and occasionally may have some white spots or whitish/yellow discharge.
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Stomatitis
Oral inflammation and ulcers, known as stomatitis, may be mild and localized or severe and widespread. They are invariably painful. Stomatitis may involve swelling and redness of the oral mucosa or discrete, painful ulcers (single or multiple).

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Acute necrotizing ulcerative gingivitis causes severe inflammation and punched-out ulcers on the dental papillae and marginal gingivae. A severe variant called noma (gangrenous stomatitis) can cause full-thickness tissue destruction (sometimes involving the lips or cheek), typically in a debilitated patient. It begins as a gingival, buccal, or palatal (midline lethal granuloma) ulcer that becomes necrotic and spreads rapidly. Tissue sloughing may occur. Isolated oral gonorrhea very rarely causes burning ulcers and erythema of the gingiva and tongue, as well as the more common pharyngitis.
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RECURRENT APHTHOUS STOMATITIS

Recurrent aphthous stomatitis is a common condition in which round or ovoid painful ulcers recur on the oral mucosa. Etiology is unclear. Diagnosis is clinical. Treatment is symptomatic and usually includes topical corticosteroids. Recurrent aphthous stomatitis (RAS) affects 20 to 30% of adults and a greater percentage of children at some time in their life.
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Minor aphthae (Mikulicz's disease): account for 85% of cases. They occur on the floor of the mouth, lateral and ventral tongue, buccal mucosa, and pharynx; are < 8 mm (typically 2 to 3 mm); and heal in 10 days without scarring.

Major aphthae: (Sutton's disease, periadenitis mucosa necrotica recurrens) constitute 10% of cases. Appearing after puberty, the prodrome is more intense and the ulcers are deeper, larger (> 1 cm), and longer lasting (weeks to months) than minor aphthae. They appear in the lips, soft palate, and throat. Fever, dysphagia, malaise, and scarring may occur.

Herpetiform ulcers: (morphologically resembling but unrelated to herpesvirus) account for 5% of cases. They begin as multiple (up to 100) 1- to 3-mm crops of small, painful clusters of ulcers on an erythematous base. They coalesce to form larger ulcers that last 2 wk. They tend to occur in women and at a later age of onset than do other forms of RAS.

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Fungal Infections

ORAL CANDIDIASIS (MONILIASIS, THRUSH)

Candida albicans is the most frequent cause of fungal human disease in general and very much the most common cause of oral fungal involvement. The organism is a normal inhabitant of the oral cavity in 30 to 40% of the population. When the bacterial flora of the oral cavity is disturbed by antibiotic therapy, or in individuals who have diabetes mellitus, xerostomia (dry-mouth), weakened immunity (for example, AIDS), or severe debilitation, this otherwise harmless microorganism multiplies to cause overt lesions.
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The causes and the course the disease:

Oral Candidiasis takes the form of a superficial, curdy, gray to white membrane that can be readily scraped off to reveal an underlying erythematous inflammatory base. In the milder expressions, there is minimal ulceration of the mucosal surface and only a superficial subepithelial inflammatory infiltrate. More severe oral infections may produce mucosal ulceration and a correspondingly greater inflammatory reaction.In the debilitated, compromised host, the oral candidal infection may be spread into the esophagus by the introduction of a nasogastric tube. Even more threatening, in the vulnerable individual, is more widespread mucous-membrane infection with invasion of the fungi into the deeper tissues of the oral cavity, increasing the potential for bloodstream diffusion. Uncommonly, and in the vulnerable individual, oral candidiasis is followed by widespread mucous membrane infection that has greater potential for invasion and distribution.
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The clinical features:

The patient with candidiasis may complain of a burning sensation, tenderness, or sometimes pain around the affected mucosa. Spicy foods will cause occasional discomfort because of the increased sensitivity of the affected mucosa. These infections were more common in women and in patients over 40 years old. Fifty percent of the patients came to them with a chief complaint of oral burning. The patient may report having been on a prolonged course of broad spectrum antibiotics for a sore throat or other infection.
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Major types of oral candidiasis :

1)pseudomembranous; 2) hyperplastic; 3)erythematous (atrophic) 4) angular cheilitis.

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Pseudomembranous
Oral infection may show as fine whitish deposits on an ervthematous patch of mucosa or as more highly developed small, soft, white, slightly raised plaques that closely resemble to milk curds. The disease may range in severity from a single region to a diffuse whitish involvement of several or all the mucosal surfaces. The mucosa next to, or between, these whitish plaques appears red and moderately swollen. The plaques or pseudomembranes may be stripped off the mucosa, leaving a raw bleeding surface. When separate restricted sites are involved, the cheek mucosa and vestibule are the most frequent regions affectedfollowed by the dorsum of the tongue, palate, gum, floor of the mouth, and lips.
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Hyperplastic
hyperplastic is characterized by white plaques which cannot be removed by scraping. The most common location is the cheek mucosa. In patients infected with HIV, the hyperplastic candidiasis most often is found in the lip commissures.

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Erythematous
Erythematous is characterized by a red appearance. The color intensity may vary from fiery red to a hardly distinct pink spot. Common locations are the palate and dorsum of the tongue, as in the so-called multifocal candidiasis in patients who are not infected with HIV but who are heavy smokers. However, erythematous candidiasis may also appear as spotty areas of the cheek mucosa. This is a characteristic feature of the HIV infection, but is often overlooked.

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Angular cheilitis
Angular cheilitis is characterized by cracks radiating from the angles of the mouth, often associated with small white plaques. In the elderly, this is not an unusual lesion and may be because of anemia, loss of chewing vertical dimension, or vitamin deficiency. But it should be remembered that when it is noted in a young man, it could be the first sign of an HIV infection. Today it is recognized the most important etiologic cause is Candida albicans. However, Staphylococcus aureus may also be present in some patients.

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Treatment
The management of patients with oral candidiasis is two fold 1) to identify, correct, or eliminate predisposing or precipitating causes. 2) to provide antifungal therapy

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Drugs:
1) gentian violet 2) nvstatin 3) amphotericin B 4) miconazole 5) clotrimazole 6) ketoconazole

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REFERENCES

1. Lynch MA, et el. Burket's Oral Medicine: Diagnosis and Treatment. Philadelphia: J.B. Lippincott. 8 Ed., 1984. 2. Fiumera NJ, et al. Primary syphilis in the oral cavity. Brit J Vener Dis 1974; 50:463-464. 3. Meyer I, et al. The oral manifestations of acquired syphilis. J Oral Surg Oral Med Oral Pathol 1967; 23: 45-87. 4. Nahmias AJ, et al. Infection with herpes simplex viruses 1and 2. N Engl J Med 1973; 289:667-784. 5. Nally FF, et al. Herpes zoster of the oral and facial structures: Report of five cases and discussion. J Oral Surg 1971; 32(2):221-234. 6. Eisenber E. Intraoral isolated Herpes zoster. J Oral Surg 1978; 45(2):214219. 7. Lehner T. Oral thrush, or acute pseudomembranous candidiasis: A clinicopathologic study of forty four cases. J Oral Surg Oral Med Oral Pathol 1964; 18(1):27-37. 8. Klein RS, et al. Oral candidiasis in high risk patients as the initial manifestations of acquired immunodeficiency syndrome. N Eng J Med 1985; 311:354-358.
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