http://archotol.ama-assn.org/cgi/content/full/133/2/110

Biofilm Surface Area in the Pediatric Nasopharynx
Chronic Rhinosinusitis vs Obstructive Sleep Apnea

James Coticchia, MD; Giancarlo Zuliani, MD; Crystal Coleman, BS;
Michael Carron, MD; Jose Gurrola II, BS; Michael Haupert, DO; Richard
Berk, PhD

Arch Otolaryngol Head Neck Surg. 2007;133:110-114.

INTRODUCTION

Chronic rhinosinusitis (CRS) in the pediatric population is a complex
disease with a considerable effect on the US economy. The health care
expenditure in the United States in 1996 for rhinosinusitis in the
pediatric population was estimated to be $1.8 billion.1 Most
otolaryngologists agree that the cornerstone of treating CRS is a
prolonged course of a broad-spectrum -lactamase stable oral antibiotic
in an attempt to cover the varied pathogens that may be present in the
sinuses. These are not the same well-defined set of organisms that may
exist in acute sinusitis. Anaerobes are cultured from the paranasal
sinuses of children diagnosed as having CRS at rates ranging from 2%
to 100%.2

Alternatives to the standard course of oral antibiotic therapy include
adenoidectomy, functional endoscopic sinus surgery, and long-term
intravenous antibiotic therapy. Adappa and Coticchia3 achieved a 91%
long-term success rate in treating 22 patients with CRS during a mean
of 5 weeks of intravenous antibiotic therapy with concurrent
adenoidectomy. Recent findings suggest that adenoidectomy by itself
may provide benefits for patients with CRS. In a study by Vandenberg
and Heatley,4 58% of children demonstrated near or complete symptom
resolution of CRS after adenoidectomy. These authors suggest that
adenoidectomy improves sinonasal symptoms by eliminating airway
obstruction and secretion stasis, as well as by removing a nidus for
chronic bacterial infection.

Biofilms are increasingly associated with chronic infectious
processes. Using a simple light microscope, Antonie van Leeuwenhoek
(1632-1723) was the first to describe the concept of microorganisms
bound to a surface in the form of dental plaque.5 In the 1970s, there
was a reemergence of the notion of the bacterial biofilm when
Characklis6 studied microbial slime in industrial water systems and
noted its resistance to disinfectants. A transition in thinking has
begun in that bacteria are no longer thought to exist singularly as
mere planktonic organisms but rather as well-organized ecosystems even
within a human host. These complex ecosystems are well suited for
conditions of environmental stress such as crowding and altered oxygen
tension. It is believed that, at any given time, 99% of bacteria exist
in the form of a hydrated matrix of polysaccharides and protein slime
known as a biofilm.7 According to a recent public announcement from
the National Institutes of Health, more than 60% of human bacterial
infections involve biofilms.8 Different nosocomial infections related
to the use of urinary catheters, orthopedic devices, prosthetic heart
valves, and central venous catheters are associated with the adherence
of biofilms to a surface.9 Infectious processes attributed to
bacterial biofilms are increasingly difficult to treat secondary to
resistance to antimicrobial therapy, and in the case of artificial
heart valves and indwelling catheters, removal is the only means of
eradication.

Biofilms are difficult to eradicate, and their formation on adenoid
surfaces provides a mechanism for persistent infection seen in CRS.10
Biofilms form when individual planktonic bacteria coalesce and adhere
to various surfaces via glycoconjugate moieties.11 The life cycle of
biofilms can be divided into 3 parts, namely, attachment, growth, and
detachment.12 During the attachment phase, the substrate must be
adequate to be adsorbed for the bacteria to irreversibly attach to the
surface. As the cells divide, an exopolysaccharide matrix is formed.
The biofilm then begins to form towers and water channels through the
matrix. These channels aid in the elimination of waste and contribute
to a pH gradient within the matrix. Finally, the individual bacteria
begin to shed from the biofilm to colonize another surface. The oxygen
tension gradient present in the biofilm allows for increased metabolic
activity in superficial layers of the matrix while the underlying
layers persist in a quiescent phase. Chemical signaling, known as
quorum sensing, allows for cell-cell communication within the biofilm.
Antibiotics may temporarily reverse symptoms caused by shedding of
planktonic bacteria; however, unless the colonized surface is also
removed, the infection will recur.13

To demonstrate a new paradigm in the pathogenesis of CRS, our
laboratory set out to quantitatively describe the anatomical
microstructure of adenoids removed from children with CRS vs children
with obstructive sleep apnea (OSA). Because microscopy is the only
technique whereby bacterial biofilms can be studied at the single-cell
level, scanning electron microscopy (SEM) was used to detect and help
quantify biofilm architecture.14 Despite the use of standard measures
in attempting to eradicate CRS from our pediatric population, we
encounter many treatment failures. Therefore, we contend that biofilm
formation might play an important role in the pathogenesis of this
disease.

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Results  Adenoids removed from patients with CRS had dense mature
biofilms covering the mucosal surface; they had a mean of 94.9% of
their mucosal surface covered with mature biofilms, compared with a
mean of 1.9% coverage on the adenoids removed from patients with OSA.
This difference was statistically significant at P<.001.

Conclusions  Adenoids removed from patients with CRS had almost their
entire mucosal surface covered with biofilms vs scant coverage for
patients with OSA. Biofilms in the nasopharynx of children with CRS
may act as a chronic reservoir for bacterial pathogens resistant to
standard antibiotics. The mechanical debridement of the nasopharyngeal
biofilms may explain the observed clinical benefit associated with
adenoidectomy in this subset of pediatric patients.

The whole artical is a good read.

http://archotol.ama-assn.org/cgi/content/full/133/2/110