Cleft Palate Microflora- Normal and Pathogenic



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Oral cavity is a house for more than 300 species of microorganisms which includes aerobic, non aerobic, spores, fungi etc. Though many microorganisms are commensal only few microorganism involve in pathogenic process due to predisposing or initiative factors like poor oral hygiene, medically compromised patients, dentate and non dentate mouth, dietary habit, clefts, etc,.

Cleft palate is one of the conditions in which commensal microorganisms can become pathogenic over time. There will be communication between nasal and oral microorganisms, which makes the habitat more suitable for few like Staphylococcus species. Even after the closure of due to exchange of microflora between oral and nasal cavity it can lead to wound dehiscence, which further leads to post operative complications.

Key words: cleft palate, oral microflora, wound dehiscence, staphylococcus, streptococcus, commensal, fistula


Clefts of the palate comprise a range of disorders affecting the oral cavity, the causes of which remain largely unknown1. Affected children have a range of functional problems which include feeding difficulties at birth due to problems with oral seal, swallowing and nasal regurgitation, hearing difficulties due to abnormality in the palatal musculature and speech difficulties due to nasal escape and articulation problems (Mossey and Little, 2009)2. Cleft may also predispose to alteration of normal flora at nose and oral cavity. Viridans streptococci were the first persistent colonizer of the human mouth and Streptococcus, Staphylococcus, and Neisseria spp were consistently found toward the end of the first year of life (Arief et al, 2005)3.


The world we live in contains unimaginable numbers of bacteria, representing the major diversity of life on our planet. The commensal bacteria are present on the epithelial surfaces of the skin and on the mucosal surfaces of the oral cavity, respiratory tract, esophagus, gastrointestinal tract and urogenital tract. An estimated 300 to 500 bacterial species (sp) coexist within the oral cavity, of which approximately 50% are currently uncultivable.4 In spite of this, only a relatively small number of bacteria cause infection in man (Henderson and Wilson, 1998)5.

Establishment of a normal flora occurs in a sequential manner: (1) the first exposure of the mucosal surfaces of a sterile neonate is to the maternal genital microflora during its passage through the birth canal, (2) a few hours later the organisms from the mother’s (or the nurse’s) mouth and possibly a few from the environment are established in the mouth, usually Streptococci spp, which bind to mucosal epithelium, (3) oral flora on the child’s first birthday usually consists of Streptococci, Staphylococci, Neisseriae and Lactobacilli, (4) the next evolutionary change in this community occurs during and after tooth eruption when two further niches are provided for bacterial colonization, (5) when all the teeth are lost as a result of senility, bacteria that colonize the mouth at this stage are very similar to those in a child before tooth eruption6,7,8.

The oral cavity, upper respiratory tract, and certain regions of the ears and eyes have an indigenous microflora. Because of the close anatomic relationship of these structures, the resident flora of these regions shares many common pathogens. Within a given microenvironment, however, certain microbes that constitute the normal flora are associated with distinct anatomic sites. Thus, the normal flora exists within complex ecosystems at different sites and interacts closely with different bacterial spp and with the host epithelial layers. This indigenous microflora is known to change over time and host age, congenital malformation, underlying disease and chemotherapeutic agents affect its composition4.

Microbial counts have been reported to vary from day to day9. A variety of conditions affect successful colonization of the mucosal surface in the oral cavity, including factors such as epithelial cell turnover, salivary flow, reduction in the oral pH environment following food intake and dentition. The predominant components of oral flora are Streptococcal spp, most commonly members of the Streptococcus group4,7,8. Increasing the amount of sugar intake would encourage growth of certain Streptococci that are able to tolerate a lower pH environment and also presence of teeth (Arief et al, 2005)3.

Organisms generally considered as commensals including palate are coagulase-negative staphylococci, nonhemolytic and viridans streptococci, Corynebacterium spp, Neisseria spp Candida spp and other cultivable and not-yet-cultivable spp of Streptococcus.10,11,12

Candida albicans (C. albicans) is the most prevalent yeast isolated from the human body as a commensal or as an opportunistic pathogen13. The presence of C.albicans in the oral cavity is not indicative of disease. In many individuals, C.albicans is a minor component of their oral flora, and they have no clinical symptoms. In healthy individuals, a large number of sites in the oral cavity can be colonized by C.albicans14.

A number of bacteria which populate the normal oral microflora are opportunistic pathogens capable of injuring or even killing the carrier, if conditions permit- organisms like Staphylococcus aureus (S.aureus), ?-hemolytic streptococci, Neisseria meningitides, Streptococcus pneumoniae,5 Klebsiella spp, Escherichia coli (E.coli) and Pseudomonas spp (Roscoe and Hoang, 2007)10. (Table 1)


Any wound is at some risk of becoming infected. One school of thought is that the density of microorganisms is the critical factor in determining whether a wound is likely to heal. However, a second school of thought argues that the presence of specific pathogens is of primary importance in delayed healing, while yet others have reported microorganisms to be of minimal importance in delayed healing15.

Wound contaminants are likely to originate from three main sources: (i) the environment; (ii) the surrounding skin; (iii) endogenous sources involving mucous membranes. The normal microfloras of the oral cavity are both diverse and abundant, and these supply the vast majority of microorganisms that colonize wounds15.

Bacterial infections after cleft palate surgery increase the risk of wound breakdown, palatal fistulas, poor speech, poor growth, poor aesthetic results and death. As the commensal oral bacteria in a normal young child change from birth as the child grows, factors that affect oral bacterial colonization include presence of antibodies that inhibit bacterial adherence, presence of teeth, formation of a biofilm, bacterial load in the saliva of attendants and frequency of exposure, prolonged hospital care and exposure to antibiotics (Chuo and Timmons 2005).3,16,17

The risk of infection is generally based on the susceptibility of a surgical wound to microbial contamination. Clean surgery carries 1 to 5% risk of postoperative wound infection and in dirty procedures that are significantly more susceptible to endogenous contamination, a 27% risk of infection has been estimated15.

Though, infection is not a very frequent complication following correction of the palate, when infection occurs, partial or complete dehiscence may be the consequence. All wound infections were diagnosed on the second to sixth postoperative day while most patients leave the hospital on the third postoperative day. However, the strong relationship with preoperative cultures and dehiscence indicates that pathogens causing infection do play a role. Moreover, patients with dehiscence showed pus and fever, both signs of an infectious complication18.

One might also argue that wound tension contributes to dehiscence and other causative factor. For example, too close to the incision edges may prevent the tissue from meeting and binding together properly. Sutures that are too tight can result in strangulation of the wound edges and poor blood supply to the wound, causing necrosis or sutures are removed too early.18

Wounds undergo a predictable alteration in microbial flora over time. Early on, the wound is colonized particularly by ?-hemolytic Streptococci and S.aureus, within the first 1 to 4 weeks, these are soon accompanied by that often infect wounds together in a synergistic fashion. After approximately 4 weeks, chronic wounds are more likely to become colonized by Pseudomonas spp Infections in older wounds are polymicrobial mixtures of aerobic pathogens usually associated with tissue necrosis, undermining and deep structure involvement (Gordon Dow, 2009).19

Invasive group A Streptococcal infections, once thought to be mainly a problem of the preantibiotic era, continue to be reported in many countries. In a multicenter general practice study in Denmark (1983 and 1984), group A ?-hemolytic streptococci detected in the throats of 10.9% of 99 asymptomatic children younger than 15 years old. Also the throat carrier rates of groups A, C and G ?-hemolytic streptococci decreased with increasing age of the individuals’ studied.16

The carrier ship of group A Streptococcus may predispose to infection and S.aureus ranks second among spp cultured from infected wounds18. Whilst the importance of Staphylococci as medical pathogens has been recognised for many years, it is now suggest that Staphylococci can be isolated frequently from the oral cavity of particular patients group such as children, elderly and in ill patients. Therefore, it is apparent that the oral cavity may present a hitherto poorly recognised reservoir of Staphylococci, some of which may, under appropriate conditions cause local or systemic infection.17

Nasal bacteria may be transmitted through an oronasal cleftfistula to the oral cavity, and it may be able to survive in the oral environment in children with cleft lip and palate (CLP) (Mims et al., 1993). S.aureus were identified in 53.1% of saliva samples and 40.6% of nasal samples. The oronasal fistula area was significantly higher in children who had S.aureus colonization in their oral cavity (Tuna et al, 2008).20

Recent data have shown that S.aureus is more frequently found in the oral flora of cleft patients than in normal children. Using saliva swabs, Arief et al. found that children with cleft palate showed more colonization by S.aureus compared to normal children of 3–39 months, which decreased significantly after operation.3

According to Aziz, Rhee, and Redai (2009), 5.5% of patients had nonlife-threatening complications (infection or wound dehiscence)21 and according to Hupkens and group (2007), they encountered 6.0% of wound dehiscence.18

The microbiological studies comparing flora between cleft and non-cleft sites in children with CLP by Brennan et al. (2001) determined that the oral bacteria colonize the cleft nasal floor in patients with unilateral oronasal fistulas. They reported that oral bacteria were not cultured in the nasal floor of the cleft in the majority of patients with oronasal fistula. The Investigators claimed that oral bacteria might occur only when the fistulae are sufficiently large to maintain a similar environment to the oral cavity.20

The study by Tuna et al. showed bacterial transmission was proven for large oronasal fistulas and a correlation was found with S.aureus counts in the children with CLP. It appears that as fistula size increases, significantly higher colony numbers of S.aureus were found in saliva samples. In addition, S.aureus tends to survive in the oral cavity as a result of transmission through the nasal passages as long as an unrepaired cleft exists.20

One study by Myburgh, and K.W. Butow (2009), swabs taken from their soft palates were made for days 0, 2, 4 and 6. The pathogenic organisms were: C.albicans, E.coli, Klebsiella pneumoniae, S. aureus, Pseudomonas aeruginosa and others.22 Another study from Finland showed that, Viridans Streptococci were the first persistent oral bacteria in babies (Kononen, 2000). Staphylococci were prevalent in more than 25% of children aged 0 to 6 months. The prevalence of Staphylococcus was lower in older children.16

Klebsiella spp are ubiquitous in nature and probably have two common habitats, one being the environment and the other being the mucosal surfaces of humans which they colonize. In humans, Klebsiella pneumoniae is present as a saprophyte in the nasopharynx and in the intestinal tract. Klebsiellae are opportunistic pathogens, can give rise to severe diseases such as septicemia, pneumonia, UTI, soft tissue infection and nosocomial outbreaks. The detection rate in the nasopharynx range from 1 to 6%, which differ considerably from study to study; Klebsiella spp are rarely found there and are regarded simply as transient members of the flora.23

According to the statistics of the Centers for Disease Control and Prevention, Klebsiella spp account for 8% of endemic hospital infections and 3% of epidemic outbreaks. The mortality due to Klebsiella spp bacteremia approaches 27–34% in adult patients. This data also showed a marked overall increase in the incidence of this infection during the study period and are in agreement with previous reports regarding the dynamics of gram-negative and Enterobacteriaceae bacteremias.24

During the 1980s and 1990s, the frequency of nosocomial Candidiasis has increased dramatically. Data from the USA National Nosocomial Infections Surveillance System shows that C.albicans was the most frequently isolated fungal pathogen (59.7%) in hospital environments. Transfer of Candida between individuals often occurs via the hands of health care workers, and nosocomial transmission can occur without Candidiasis outbreaks.14

Approximately 60% of the isolated recovered were gram-positive cocci (coagulase-negative Staphylococcus, ~31%), S.aureus (20%), and Enterococcus (9.5%). Over the past 5–10 years, most commonly isolated were gram-negative rods, such as E.coli, Klebsiella pneumonia, P.aeruginosa, and Enterobacter spp.23,25

It could be hypothesized that patient characteristics are primarily responsible for these differences. For example, genetic predilections, underlying diseases, social factors and economic factors and also differences in the virulence of individual microorganisms may be responsible for the manifestations of infection observed in cleft palate patients after surgery.26 (Table 2)


S.aureus and ?-hemolytic Streptococci are the commonest microflora which are responsible for wound dehiscence, it is always advised to do preoperative and postoperative culture. Though wound dehiscence is not always but frequent complication patient should be under proper care especially children. Alongside attention should be give to the other commensal microflora like Klebsiella, Candida, etc., which can become pathogenic over time in cleft patients.

Despite advances in preoperative care, the rate of surgical wound dehiscence has not decreased in recent years. Recognition of risk factors, prevention of wound infection and mechanical stress on the incision are important. Management of dehisced wounds may include immediate surgery. If surgery is not needed, management is essentially the same as that of any other wound through maintenance of a moist wound environment, reduction of bio burden and pain, and promotion of granulation tissue.

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