5.4 Bacterial infections

Some pathogens can cause a local infection (e.g. Mycobacterium tuberculosis can rarely initiate the development of primary tuberculosis – TBC of the oral cavity), others just participate in local diseases of the oral mucosa during systemic diseases. Of the systemic infections, we can find oral manifestations in bacillar (typhus, diphteria, whooping cough) and coccal infections (scarlet fever).

5.4.1 Necrotizing diseases of the periodontium

Ulcerative gingivitis and ulcerative stomatitis fall according to the classification of the American Dental Association (both 1999 and 2018 issues) into the category of the „necrotizing periodontal diseases“.

Acute necrotizing ulcerative gingivitis


Anaerobic microflora of the subgingival plaque is generally considered to be the provoking cause of the disease. In particular, the oral spirochete of the Treponema, Borrelia (Vincenti) genuses and other periodontal bacteria (rod-shaped gram-negative bacteria of the Tanarella, Prevotella, Porphyromonas, Fusobacterium, Aggregatibacter, Parvimonas genuses). Proliferation of these bacteria most likely occurs in predisposed individuals when several local (insufficient oral hygiene, tartar, poorly made fillings, semi-retained teeth, smoking) and systemic factors (physical and psychological stress, tiredness, physical exertion, insufficient nutrition, hormonal changes, immune dysbalance, acute respiratory infection) combine.

The primary form occurs suddenly in generally healthy young individuals (17-25 years). The disease is acute and extremely painful, always preceded by the plaque-induced gingivitis. When proper treatment is administered and the patient cooperates, the healing is without complications.

The secondary form assumes immunodeficiency in the organism caused by a systemic disease (HIV, haemoblastosis). The course of the disease in such cases is protracted, atypical, the destruction of the periodontium is quick and the disease responds only slowly to therapy, often recurring.

Clinical picture of the primary form: The disease is not associated with any systemic symptoms. From full health, a sudden onset of catarrhal gingivitis occurs without any prodromal symptoms (which is important for differentiation from herpetic gingivostomatitis!). The catarrhal gingivitis is localized in a certain region of the dentition only, typically in the frontal section of the dentition around incisors and canines, or in the region of lower third molars. Sites with local irritation of gingiva are usually the most affected. Initially, the gingiva is erythematous, very painful (spontaneously as well as to touch) and bleeds slightly. Later, the picture changes, showing greyish necrotic areas on the tips of interdental papillae that may progress circumdentally into the whole marginal gingiva. After separation of the necrotic tissue, ulcerated margins with typical “bevelled” interdental papillae can be found. The process is usually limited to the gingiva but it can also spread to the alveolar mucosa, buccal, lingual and palatine mucosa – ulcerative gingivostomatitis. If proper therapy is not initiated, the disease can recede spontaneously (albeit with a risk of recurrence) or become chronic – either as a painless ulcerative gingivostomatitis or as a very painful ulcerative gingivoperiodontitis associated with rapid destruction of the alveolar bone. Swelling of submandibular nodes, hypersalivation and bad breath are typical concomitant symptoms. Major subjective difficulties occur while eating or when performing oral hygiene (that becomes very difficult or even impossible, thus potentially further deteriorating the condition).

Dg.: The diagnosis can be established on the basis of the clinical findings (changes on the papillae occur as soon as the 2nd or 3rd day).

Dif. dg.: For differential diagnosis, it is necessary to check the blood count (leukaemia, agranulocytosis, etc.) and anti-HIV antibodies (secondary form)!

Th.: Depending on the intensity, extent and duration of the disease, local or systemic therapy may be needed. Local therapy is based on the effect of aerial oxygen on anaerobic bacteria. At the clinic, the necrotic tissue is carefully removed using cotton swabs soaked with 30 % hydrogen peroxide and the patches bearing signs of early development of the disease are washed by the same solution using a syringe with a blunt cannula. Such treatment shall be repeated every day for 2-5 days. In the acute phase of the disease, any surgical procedures (including tartar removal) are contraindicated. At home, a gentle but proper oral hygiene (a single tufted brush) is recommended, along with application of 6 % H2O2 on the patches. Treatment can also include antiseptic washes (hexetidine, chlorhexidine) and the application of a local anaesthetic spray before a meal. A pulpy and non-irritating diet is recommended. When subjective difficulties disappear, local irritating factors such as dental crowns and overhanging fillings are removed, aiming at reducing the subgingival plaque.

In the chronic form of the disease, it is beneficial to complement the local therapy with systemic administration of ATBs (metronidazole, tetracycline) in the usual dosage and symptomatic therapy (painkillers).

Necrotizing ulcerative periodontitis


This rapidly progressing disease leads to premature loss of teeth within a very short period (approx. 6 months from diagnosis). Only some (groups of) teeth can be affected but affliction of the entire dentition is not uncommon.

Clinical picture: The periodontium is not affected evenly; a purulent exudation from the periodontal pockets is common. Soft alveoli-covering tissues are prone to the necrosis as well. Severe gingivitis with necrotic disintegration of the papillae is always present. The disease is very painful. X ray examination will prove an uneven loss of bone, sometimes even osteonecrosis with a formation of sequesters.

Th.: Initially, analgesia is necessary (approximately for 2 weeks). Systemic antimicrobial therapy needs to be administered (nitroimidazol, TTC – be careful about the possibility of development of secondary oral candidasis due to dysmicrobia in the GIT). Surgical treatment is not indicated.

5.4.2 Contagious impetigo (impetigo contagiosa)


Contagious impetigo counts among pyodermas, often affecting the perioral region and vermilion zone. Impetigo contagiosa streptogenes is a highly contagious disease caused by beta haemolytic streptococci and affects predominantly children in groups. It occurs seasonally with a maximum in the summer and autumn months. Primarily, tiny blisters erupt, the roof of which soon breaks and erosions appear, covered by honey yellow crusts. Regional lymphatic nodes are usually swollen. Impetigo can spread continuously further to the facial skin. In adolescence, both conscious and unconscious mechanical trauma to the corners of the mouth often occurs, resulting in the development of angular cheilitis. Atopic eczema represents a significant predisposition for contagious staphylococcal impetigo (impetigo contagiosa staphylogenes) as Staphyloccocus aureus is present on the skin in approximately 90% of patients with atopic eczema (compared to 10% in healthy population), which can facilitate the invasion. The primary manifestation of this disease is a small blister that soon becomes purulent and once the roof is torn down, dirty greenish crusts are formed. After healing, pigmentation may persist on the affected area for some time.

Th.: The local therapy is managed by a dermatologist; the prevention of underlying factors is however of utmost importance.

5.4.3 Syphilis


The causative agent of this disease is a spirochaete bacterium Treponema pallidum. The clinical picture of syphilis in the oral cavity is varied and can resemble many afflictions of various etiologies. The oral mucosa can be affected in all stages of acquired syphilis and many of such manifestations can be highly contagious! In the congenital forms of syphilis, intraoral manifestations can be also present but do not affect the oral mucosa – rather, teeth and bones of the jaws can be affected (keratitis, labyrinthitis and Hutchinson’s teeth constitute a typical Hutchinsonʼs triad).

The disease is transmitted almost exclusively through a direct contact with an infected person. The most common route is sexual intercourse (oral cavity can be affected after oral sex). When the infection manifests in the oral cavity, other forms of the contact such as kissing can lead to the transmission, indirect transmission is uncommon but possible. The oral cavity is the most common site of the extragenital localization of the primary infection (10 % of cases!) – if the primary route of entry of the infection into the body is in the oral cavity (including lips), the primary manifestation (chancre) occurs there. It appears approximately three weeks after an oral sex as a shallow ulcer with rolled margin. Initially, it is a flat, erythematous papule approx. 1 cm in diameter, gradually turning into a pink, lard-like, glossy ulcer with rolled borders or an erosion with a mushy surface that can be coated with a tissue detritus and precipitated blood proteins. On the vermilion, it can manifest as a crust. A noticeable oedema surrounds the ulcer – so-called initial sclerosis. A complete painlessness of the defect and the hardness of the floor of the erosion when examined by palpation (in gloves!) are typical. The discrepancy between the clinical finding and appearance of the lesion and the subjective problems reported by the patient is striking. The chancre heals spontaneously in 6-8 weeks after the infection. While the chancre persists, lymphangitis and regional lymphadenitis develop. The lymph nodes are mobile, elastic, painless and together with the chancre, they form so-called primary complex.

The disease enters the early latency period, after which the secondary stage follows. At this stage, the disease is already generalized and manifests after 8-10 weeks from the infection by mild non-specific prodromes resembling a viral infection, followed by general lymphadenopathy associated with spleen enlargement, specific laryngitis and tonsillitis. The non-specific prodromes may include fatigue, elevated temperature, headache, loss of appetite and weight loss, polyarthralgia and polymyalgia. Macular exanthema (roseola syphylitica) develops. Other skin symptoms may be varied, it is however unusual for more than one type of lesions to be present on the skin or mucosa at the same time (monomorphic exanthema). In the oral cavity, enanthema (red spots) can be found, other types of lesions include smooth patches in the physiological coating of the tongue (plaques lisses), yellow-white, slightly elevated patches with an opalescent surface on the dark red base (plaques opalines) that later transform into erosive plaques (plaques muqueuses).

In the mouth corners, macerated mucosa can be found, similar to that of the primary stage (i.e., painless bilateral angular cheilitis with crevices) or warts resembling condylomas on the outer genital or in the perianal region can appear in the oral region, which are highly infectious. About of strikingly painless tonsillitis can appear (syphilitic tonsillitis) Tonsils are red, oedematous, coated or not, sometimes accompanied by hoarseness (syphilitic laryngitis). Systemic symptoms are usually missing in this stage! It is necessary to emphasize again that all the above-described syphilitic lesions are painless and can vary in appearance. The manifestations of the second stage syphilis in the oral cavity are frequent and very contagious! After the second stage, the duration of which can vary (2-5 years), the disease enters so-called late latency period that may take many years (at least 3 years). After that, the third stage (non-infectious) with localized organ impairment follows. In the early third stage, the dermal manifestation of the facial skin can propagate into the oral cavity in syphilis tubero-serpiginosa or ulcero-serpigninosa, forming infiltrations of various extents that tend to necrosis and scarring. Both circumscribed (gummas) and non-circumscribed infiltrations of soft tissues can develop, as can also non-circumscribed infiltrations of soft tissues or even jaw bones with decays resembling benign tumours.

Syphilitic gummas of the tongue result in its enlargement. The enlargement is usually irregular and lobed (lingua lobata) with hyperplastic growths of cauliflower-like character. The mucosa of the dorsum of the tongue is smooth, without papillae (clinical picture resembles atrophic glossitis).

The colliquation and decomposition of the infiltrates leads to a development of fistulas and scars. Oronasal communication can form when the hard palate is affected. Syphilitic glossitis represents another manifestation of the tertiary syphilis in the oral cavity. Its symptoms include leukoplakic changes in the atrophic epithelium of the tongue dorsum that can succumb to malignant transformation. Two types of syphilitic interstitial glossitis (glossitis interstitialis luetica) can be distinguished – superficial (with protruding infiltrations, mucosal hyperkeratosis/leukoplakia and occurrence of atrophic patches) and deep (glossitis interstitialis luetica profunda). The latter affects the entire tongue, which grows stiff and limits its mobility. Atrophy of lingual muscles or even scarring can occur, which can eventually lead to development of squamous cell carcinoma. In the past, the terminal stage of the disease was associated with cardiovascular and nervous systems (tabes dorsalis, progressive paralysis).

Examination: To be able to confirm the primary infection in the oral cavity, dark field microscopy of the native material must be performed (the mucosal lesion must be free of antiseptic/antimicrobial agents for at least two days prior to the sample collection; repeated examinations are necessary). At this stage, the serological examination would still return negative results. A suspicion on the secondary stage of syphilis can be verified (or disproved) by serological tests for the presence of specific antibodies. Serological and histopathological tests can be used to confirm the third stage of syphilis.

Th.: The treatment is managed by department of dermatology/venereology; various schemes and algorithms with precisely defined criteria for successful treatment can be used. Reporting patients with this disease to the regional health administration is mandatory!

Dif. dg.: All three stages of syphilis may pose difficulties in establishing the correct diagnosis as there are multiple diseases that can be misdiagnosed for syphilis. In the first stage, a traumatic ulcer of the oral mucosa can be mistaken for syphilis. It can be differentiated from the primary stage of syphilis on the basis of being painful and short-term, of patient-provided information about a trauma and missing (or only mild) induration of the floor of the ulcer. So-called neurodystrophic ulcer is caused by damage to the oral mucosa insensitive due to the application of a local anaesthetic (and occurs mostly in children where acquired syphilis is not a typical diagnosis). Recurrent aphthae major are usually associated with multiple lesions, very painful and (as the name suggest) recur. Similarly, labial herpes (herpes labialis, usually associated with prodromes) or skin pyoderma (boils on the cutaneous side of the lips) are very painful, show tendency to colliquation, are reflected in the regional lymph nodes and often come with fever.

The differential diagnosis of the secondary stage does not need to be difficult if the physician considers it a possibility. A proper case history taking and detailed examination of the oral mucosa with subsequent serological verification are usually sufficient for diagnosis. The lesions can resemble many congenital mucosal disorders such as geographic tongue (lingua geographica; usually known from the patient history), recurrent aphthae, herpetic stomatitis, EEM or autoaggressive diseases.

Manifestations of the third stage of syphilis in the oral cavity must be in particular distinguished from the tubercular symptoms (at this stage, the diagnosis is usually already established), lingual tumours and cysts, leukoplakia and carcinoma.

5.4.4 Tuberculosis


Tuberculosis is caused by Mycobacterium tuberculosis or, rarely, M. bovis. The prevalence of this systemic disease has grown again over the last years. Malnutrition, immunosuppression and cachexia of various origins (HIV, drug addiction) constitute predisposing factors. The oral cavity is only rarely affected but there are three scenarios of possible occurrence: if the primary route of entry of mycobacteria into the organism was through a damaged oral mucosa, secondarily as a result of autoinoculation during active TBC (usually pulmonary) or during spreading of cutaneous TBC into the oral mucosa.

Clinical picture: In case of a primary infection, a painless ulcer develops anywhere on the oral mucosa in two weeks. Regional lymph nodes are affected (enlarged and painless, may be subject to colliquation) and a so-called primary complex (of the ulcer and a regional node) is formed. Subsequently, the primary complex either heals with only negligible systemic manifestations, or a generalized miliary TBC develops. If secondary inoculation of mycobacteria into mucosal defects occurs during active pulmonary tuberculosis (the dorsum of the tongue, buccal mucosa, or gingiva are most commonly affected), a single, deep and painful ulcer with rolled margins (tuberculoma) develops. The standard therapy with neutral substances has no effect and the ulcer can spread slowly into the surroundings (acting like a carcinoma – it cannot be distinguished clinically). If such an ulcer develops deep in the muscles, a fistula may form. If the gingiva is affected, bleeding granulations and growths can be present. Diagnosis of active TBC is usually known – patients are cachectic, weak and have distinct general symptoms. There is a risk of occupational TBC infection in health professionals! The cutaneous form of TBC (tuberculosis cutis luposa, lupus vulgaris) is very rare nowadays. It presents in the oral cavity as erythematous patches, sometimes with greyish nodes that tend to break down and bleed. Lupus vulgaris is generally considered a precancerous lesion.

Th.: Therapy is managed by specialized clinics of pulmonary medicine.

So-called atypical mycobacteria (M. avium, M. kansasii, M. scrophulaceum, M. ulcerans) can also cause mucosal defects with the appearance of ulcers in the oral cavity; this type of lesions is usually only found in HIV-positive patients.