Specific bacterial infections of the mouth are uncommon, with tonsillitis in children caused by Strep. pyogenes being the most common. Other bacterial causes of pharyngitis that are rarely diagnosed include C. diphtheriae and the fusospirochaetal complex associated with Vincent’s angina. Specific infections of the oral mucosa that are rare, and are usually manifestations of systemic infections, include diseases such as tuberculosis, syphilis, and gonorrhea. Sore throat is a common symptom of a number of specific infections and is accompanied by a variable degree of constitutional upset. Gonorrhea is a venereal infection with a worldwide distribution that has reached epidemic proportions in some countries. Although, at present, syphilis is not encountered frequently, it is an important disease with a variety of oral manifestations. Human-type and bovine-type tuberculosis are caused in man by Mycobacterium tuberculosis and Mycobacterium bovis, respectively. Other opportunist mycobacteria might also cause human infections. Leprosy is caused by an acid-alcohol-fast bacillus, Mycobacterium leprae, which in general prefers to grow near the cooler body surfaces of man. Tetanus is caused by a strictly anaerobic spore-bearing Gram-positive bacillus, Clostridium tetani.
Specific bacterial infections of the mouth are uncommon, with tonsillitis in children caused by Strep. pyogenes being the most common. Other bacterial causes of pharyngitis which are rarely diagnosed today include C. diphtheriae and the fuso–spirochaetal complex associated with Vincent’s angina. Specific infections of the oral mucosa which are rare, and are usually manifestations of systemic infections, include diseases such as tuberculosis, syphilis and gonorrhoea. Although many of these infections are uncommon in North America and Europe, the opposite is true in many other parts of the world.
Sore throat is a common symptom of a number of specific infections and is accompanied by a variable degree of constitutional upset. Although a specific diagnosis may be assisted by the clinical presentation, it is often necessary to perform laboratory tests. At least two-thirds of these infections are caused by viruses, the remaining one-third by bacteria, almost all due in the developed countries to Strep. pyogenes. It is noteworthy that Strep. pyogenes may cause rheumatic fever and carditis in susceptible individuals. Consequently, they may be at a higher risk of contracting infective endocarditis due to bacteraemias associated with surgical procedures such as tooth extractions. A summary of the clinical presentation, causative agents and microbial diagnosis of tonsillitis/pharyngitis is shown in Table 8.1.
|Causative agent||Clinical presentation||Sequelae and late complications if not treated||Laboratory diagnosis||Treatment|
|Steptococcus pyogenes(Lancefield Gp. A) Gram-positive cocci, 1 μm, in chains||Acutely inflamed tonsils with or without pus in crypts||Peritonsillar abscess, sinusitis, otitis media, scarlet fever, rheumatic fever and acute glomerulonephritis||Swab or saliva sample. Culture on blood agar, β-haemolytic colonies, Lancefield grouping and identification using API strep.||Penicillin, or erythromycin if hypersensitive|
|Corymebacterium diphtheriae Gram-positive rods 3 × 0.3 μm, ‘Chinese character’ arrangement with metachromatic granules||Inflamed fauces covered with grey-white serocellular membrane||Cranial and peripheral nerve palsies. Death due to (1) respiratory obstruction (mechanical blockage by membrane) (2) heart failure (cardiotoxin)||Swab of membrane and culture on blood tellurite and Loefflers medium. Identification by biochemical tests and toxin production (Elek plate)||Antitoxin, and tracheostomy if required. Penicillin or erythromycin|
|Fuso–spirochaetal complex, Treponema species and Fusobacterium nucleatum (see Chapter 5)||Necrotic ulcers on tonsils||Possibly chronic infection||Smear from ulcer stained by Gram’s method||Penicillin or metronidazole|
Gonorrhoea is a venereal infection with a worldwide distribution which has reached epidemic proportions in some countries. The causative agent Neisseria gonorrhoeae, a Gram-negative diplococcus, is transmitted by sexual activity, and lesions occur in the genitals, the anal canal, the oral cavity (particularly the pharynx), and combinations of these sites. The major risk factor for gonococcal pharyngitis is practice of orogenital sex. Gonococcal pharyngitis can be found in 10–20% of heterosexual women, 10–25% of homosexual men and 3–7% of heterosexual men who have urogenital gonorrhoea.
The disease is caused by the adherence of N. gonorrhoeae to either the genital or oral mucosa, and subsequent invasion into the deeper tissues between the surface epithelial cells. Spread may then occur by direct continuity, by lymphatics or haematogenously. Locally there is an intense inflammatory reaction with the production of pus which on microscopy reveals Gram-negative diplococci (0.6–1.0 μm), both extracellularly and within a proportion of polymorphonuclear leucocytes.
The oral mucosa is relatively resistant to infection by N. gonorrhoeae but gonorrhoeal stomatitis is diagnosed with increasing regularity in sexually active adults, especially homosexuals. The oral lesions of gonorrhoea are more commonly associated with primary infection of the mouth with N. gonorrhoeae than with spread of the pathogens to the mouth from a distant site.
The clinical presentation of primary oral gonorrhoea is varied, depending on the severity and distribution of the infection. The patient usually complains of a burning or itchy sensation or a dry hot feeling in the mouth, which in 24–48 hours changes to acute pain. The patient may also complain of a foul oral taste, the salivary flow may be increased or decreased, the breath may be foetid and the submandibular lymph nodes are usually enlarged and painful. The temperature may be raised if the infection is severe. Lesions have been reported on all parts of the oral mucosa and are usually described as consisting of a variable mixture of the following clinical signs: inflammation, oedema, vesiculation, ulceration, and pseudomembranes. These last are white, yellow or grey in colour, and easily removed by scraping which leaves a bleeding surface. In some patients a diffuse painful stomatitis occurs in which mucous membranes become fiery-red and oedematous. Speech, swallowing and simple mouth movements become extremely painful. The oral sites of primary infection which have been reported are the gingivae, the tongue, the buccal mucosa, the hard and soft palates and the oropharynx. N. gonorrhoeae have also been isolated from lesions of central papillary atrophy of the tongue. The tonsils and the oropharynx appear to be the commonest site of oral infection. However, as oral mucosa anterior to the pharynx is considered to be highly resistant to gonococcal infection, it is now thought that at least some of the previous reports of gonorrhoea in these locations are equivocal.
There is evidence that primary infection of the mouth can lead to disseminated lesions. Secondary gonorrhoeal infection of the parotid gland is rare but may occur in patients who have oral gonorrhoea or carry the organisms in their oropharynx. The significance of persistent oropharyngeal carriage of gonococci in asymptomatic individuals is not clear. Gonococcal arthritis of the temporomandibular joint is a not uncommon sequel if the primary infection is in the pharynx.
Gonorrhoeal infection of the urogenital tracts may result in haematogenous spread of gonococci to the skin and oral mucosa with resulting secondary infection. The oral manifestations of this type of infection can be split into two main groups, both of which appear to be rare: septic embolic phenomena and hypersensitivity reactions.
The recognition and diagnosis of oropharyngeal gonorrhoea is important for three main reasons: firstly, cases may act as a reservoir for the transmission of infection; secondly, they are a potential source of gonococcaemia giving rise to arthritis, meningitis and other septic embolic lesions in the body; and thirdly, they cause severe local tissue damage and discomfort.
The examination of Gram-stained films from oral lesions are of little direct diagnostic value due to the presence of oral commensal Neisseria species which cannot be differentiated from N. gonorrhoeae microscopically. The presence of numerous Gram-negative intracellular diplococci in a smear from a suspect lesion should be investigated further.
Swabs taken from the oral lesions should be placed in bacteriological transport medium and sent to the laboratory as quickly as possible. The requirement for culture is a semiselective medium, e.g. Thayer-Martin, containing antimicrobial agents, e.g. lincomycin, Colistin and nystatin, to inhibit the commensal flora. Incubation in 5–10% CO2 at 37 °C for 2 days results in colonies which can be identified using oxidase test, carbohydrate utilization (acid from glucose only) or fluorescent tests.
Standard treatment of 4.8 million units of procaine penicillin G, either by intramuscular injection alone or combined with 1.0 g probenecid orally, is effective for pharyngeal gonorrhoea. An alternative regimen is 0.5 g tetracycline orally four times a day for seven days. Amoxycillin or spectinomycin do not always eradicate pharyngeal infection.
Although syphilis is not encountered frequently today, it is an important disease with a variety of oral manifestations. At present in the West, it is most commonly seen among homosexuals. The causative organism Treponema pallidum is a motile spirochaete which can not be cultured in vitro. Spirochaetes have a helical structure which consists of a central protoplasmic cylinder bounded by a cytoplasmic membrane with an outer cell wall similar to that of Gram-negative bacteria. Beneath the outer membrane run axial filaments which can be regarded as internal flagella.
After the initial exposure to infection with Trep. pallidum, the spirochaetes pass through the mucous membrane or skin and are then carried in the blood throughout the body. After an incubation period of about three to four weeks there develops, at the site of entry, an ulcerated lesion called a primary chancre. The ulcer is round to oval with a regular bevelled margin and a base which is indurated, smooth and brownish red. The typical lesion is painless and oedema of the surrounding tissues is usually present. The regional lymph nodes become enlarged about two weeks after the appearance of the chancre and, on examination, are firm, painless and discrete with a rubbery consistency.
The normal site for the chancre is on the genitalia but extragenital primary lesions occur in some 10% of patients with syphilis. A chancre of the lip is the most common extragenital lesion and may present at the angles of the mouth. Other sites affected are the tongue and, to a lesser extent, the gingivae and tonsillar area (Table 8.2). Intraoral chancres are usually slightly painful due to secondary bacterial infection. The lesions are infectious and transmission may occur by kissing, unusual sexual practices and even by intermediate contact with cups, glasses and eating utensils. The chancre heals spontaneously about one to five weeks after appearing. The regional lymph nodes (submaxillary, submental and cervical) are enlarged. The differential diagnosis of primary syphilis includes ruptured vesicles of herpes simplex, traumatic ulcers and carcinoma.
|Primary||Chancre of lip, tongue gingiva||+ + +|
|Secondary||Mucous patches on tonsils, tongue, soft palate, cheek. ‘Snail track’ ulcers. Rubbery, enlarged cervical lymph nodes||+ +|
|Tertiary||‘Gumma’ of palate. Rarely osteomyelitis. Syphilitic leukoplakia leading to carcinoma||±|
|Congenital||Hutchinson’s incisors. ‘Mulberry’ molars. Facial deformities with open bite or dish face||–|