Normal flora of the mouth and upper respiratory tract

The oral cavity is sterile in utero and mucous membranes of the mouth and pharynx are often sterile at birth. During birth the neonate is exposed to all the complex microflora of the birth canal. But these organisms fail to colonize illustrating the highly selective environment of the mouth.

Within 4-12 hours after birth, streptococci become established as the most prominent members of the resident flora and remain so for life. Streptococci are numerically dominant, particularly S. salivarius, S. mitis, and S. oralis, which colonize the mucosal surfaces and dorsum of the tongue. Since the normal habitat of all these species is in humans, it seems most likely that the source of these will be an adult, most probably the mother or other primary carer. Earlier studies had indicated the mother to be the source of an infant's S. mutans, but a major advance was made when Caufield and his colleagues (1993) obtained genetic fingerprints of S. mutans isolated from mother-infant pairs.

S. mutans preferentially colonizes hard surfaces and hence, its appearance is delayed until the eruption of the first molar teeth. A majority of infants, therefore, acquire S. mutans during a 'window of infectivity' around the age of two. Early in life, aerobic and anaerobic staphylococci, gram-negative diplococci (neisseriae, Moraxella catarrhalis), diphtheroids, and occasional lactobacilli are added. When teeth begin to erupt, the anaerobic spirochetes, Prevotella, Fusobacterium species, Rothia and Capnocytophaga species, and some anaerobic vibrios and lacto­bacilli establish themselves. Yeasts (Candida species) occur in the mouth.

The flora of the nose consists of prominent coryne-bacteria, staphylococci (S. epidermidis, S. aureus), and streptococci.

In the pharynx and trachea, a similar flora estab­lishes itself, whereas few bacteria are found in nor­mal bronchi. Small bronchi and alveoli are normally sterile. The predominant organisms in the upper respi­ratory tract, particularly the pharynx, are non-hemolytic and alpha-hemolytic streptococci and neisseriae.

Grammar

Translate the sentences. Define the Objective-with-the-Infinitive constructions.

1. Earlier studies had indicated the mother to be the source of an infant's S. mutans. 2. We often find the pain in the temporo-mandibular joint to be of muscular origin. 3. The studies showed the drug to produce 20% stronger effect in the treatment of bleeding gums. 4. Damaging agents may act upon the organic structure of the enamel and cause it to disrupt. 5. The acid formed in the mouth corrodes the inorganic structure of enamel and dentin, causing cavities to form. 6. X-ray showed the tooth to be embedded in the soft tissues. 7. We have found this treatment procedure to give the most beneficial results in patients with various degrees of malocclusion.

Summary

Text I. Caries-producing microorganisms

Healthy tooth	Early decay	Advanced decay

Caries is a disintegration of the teeth beginning at surface and progressing inward. First the surface enamel, which is entirely noncellular, is demineralised. This has been attributed to the effect of acid products of bacterial fermentation.

Subsequent decomposition of the dentin and cement involves bacterial digestion of the protein matrix. An essential first step in caries production appears to be the formation of plaque on the hard, smooth enamel surface. The plaque consists mainly of gelati­nous deposits of high-molecular-weight glucans in which acid-producing bacteria adhere to the enamel. The carbohydrate polymers (glucans) are produced mainly by streptococci (Streptococcus mutans, peptostreptococci), perhaps in association with actinomycetes. There is a strong correlation be­tween the presence of S mutans and caries on specific enamel areas. The essential second step in caries pro­duction is the formation of large amounts of acid (pH < 5.0) from carbohydrates by streptococci and lactobacilli in the plaque. High concentrations of acid demineralize the adjoining enamel and initiate caries.

In experimental "germ-free" animals, cariogenic streptococci can induce the formation of plaque and caries. Adherence to smooth surfaces requires both the synthesis of water-insoluble glucan polymers by glucosyltransferases and the participation of binding sites on the surface of microbial cells. (Perhaps carbohy­drate polymers also aid the attachment of some strep­tococci to endocardial surfaces.)

Certain diphtheroids and streptococci can induce specific soft tissue damage and bone resorption typical of periodontal disease. Proteolytic organisms, including actinomycetes and bacilli, play a role in the microbial action on dentin that follows damage to the enamel. Periodontal pockets in the gingiva are particularly rich sources of organisms, including anaerobes. The development of caries also de­pends on genetic, hormonal, nutritional, and many other factors. Control of caries involves physical re­moval of plaque, limitation of sucrose intake, good nu­trition with adequate protein intake, and reduction of acid production in the mouth by limitation of available carbohydrates and frequent cleansing. The application of fluoride to teeth or its ingestion in water results in enhancement of acid resistance of the enamel.

Identification of the source of infection with the bacteria respon­sible for caries provides us with a potential way of developing a preventive strategy. It may not be feasible to achieve a lifetime free of S. mutans, but delaying the age at which a child becomes infected can reduce their subsequent caries risk.

Macrowiar P.A. The normal microbial flora. NEJM