Beruflich Dokumente
Kultur Dokumente
J Antimicrob Chemother
doi:10.1093/jac/dkt128
Institute of Health and Society, Newcastle University, Newcastle upon Tyne NE1 7RU, UK; 2Department of Otolaryngology Head and
Neck Surgery, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK; 3Department of Medical Microbiology, Freeman Hospital,
Newcastle upon Tyne NE7 7DN, UK
Objectives: To perform a multifactorial exploration of the aetiology of peritonsillar abscess (PTA) in adults, in
order to develop greater clinical understanding of the condition and improve management.
Design: A literature review exploring key pathogens, predisposing host factors and current pathogenic hypotheses.
Methods: A PubMed search for articles published between January 1980 and January 2012 using the terms peritonsillar abscess AND microbiology, peritonsillar abscess AND pathophysiology and peritonsillar abscess AND
etiology.
Results: Major pathogens in PTA are opportunistic microflora. Group A streptococcal PTA infections present differently
from polymicrobial PTA. A number of host factors influence the conditions required for the pathogenesis of PTA.
Conclusions: PTA is clinically distinct from acute tonsillitis and occurs in people with a chronic underlying
susceptibility. Targeting host factors, including oral hygiene, antibiotic use and smoking, may prevent PTA. Reeducation of clinicians concerning the aetiology of PTA is necessary for appropriate disease management.
Keywords: quinsy, microbiology, aetiology
Introduction
Methods
Results
PTA microbiology
Microbiological overview
There is much inconsistency and controversy across the literature
in describing the microbiology of PTA. Table 1 displays the diverse
range of microbiological findings obtained from PTA pus samples
that were analysed in 15 papers.8,15 28 This is likely to reflect the
substantial diversity of natural flora within the oropharyngeal
spaces.29
# The Author 2013. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved.
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*Corresponding author. Department of OtolaryngologyHead and Neck Surgery, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK.
Tel: +44-(0)191-223-1086; Fax: +44-(0)191-223-1246; E-mail: janet.wilson@ncl.ac.uk
Review
29
Non-paediatric focus
Focus on PTA parameters
other than management
Focus on PTA parameters
other than disease
presentation
112
442
Peritonsillar abscess AND
etiology
Figure 1. Flow chart demonstrating the search method used to identify the relevant literature. The numbers in bold represent the number of papers
found and carried over for assessment.
The majority of PTAs, in most series, are polymicrobial infections containing common oropharyngeal microflora,5,15,16,22,30,31
with an average of three isolates per specimen.15,16,19 However,
Megalamani et al.32 describe all their identified aerobic infections
(65% of their isolated cultures) as being monomicrobial, and
72.3% of the patients studied by Snow et al.17 also had monomicrobial infections.
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Papers
read
Review
Study
15
Mixed aerobes
and anaerobes
(%)
Average
isolates/
specimen
Common aerobes
Common anaerobes
42
66.7
90.5
61.9
3.2
34
94.1
82.4
76.0
3.1
55
34.5
78.1
27.3
1.2
122
82.3
86.3
71.3
4.4
Mitchelmore et al.,
199519
Muir et al., 199520
Sakae et al., 200621
Zagolski and Gajda,
200728
Sunnergren et al.,
200822
45
84.4
62.2
46.7
3.2
GAS
39
26
12
48.0
73.1
50
29.0
96.2
50
69.2
50
2.9
1.5
GAS
GAS, other streptococcal sp.
streptococcal sp.
83
36.1
38.6
13.0
137
51.8
57.7
9.5
1.1
Repanos et al.,
200924
Rusan et al., 20098
Hidaka et al., 201125
119
23.5
43.7
26.9
streptococcal sp.
464
65
33.2
30.8
26.9
84.6
26.2
1.4
36
147
91.7
57
88.9
57.10
80.6
57.0
3.7
Weighted average
71
45
49
Jousimies-Somer
et al., 199318
GAS, non-haemolytic
streptococcal sp., S. aureus,
H. influenzae
GAS, SMG, H. influenza, viridans
streptococcal spp.
52.0
9.0
56.0
19.0
6.0
0.84
4.1
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JAC
b-Lactamaseproducing
cultures (%)
Review
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in 51% of samples. SMG most commonly coexists with anaerobes. Jousimies-Somer et al.18 observed that SMG was always
in mixed culture, although Hidaka et al.25 obtained aspirate cultures with pure SMG isolates. SMG thrives within polymicrobial
infections and is thought to promote virulence and accelerate inflammation.19,25,45 Given these findings, SMG is likely to have a
pathogenic role in the development of PTA.
We have clearly identified three key opportunistic bacteria
that are likely to be causative organisms in PTA: GAS, indigenous
Fusobacterium species and SMG. There seem to be predominantly two pathogenically different PTA subtypes. Type 1 contains a
pure culture of a single organism, most often GAS. Type 2 displays heavy polymicrobial growth, often containing a variety of
facultative and obligate anaerobes. Clinically, type 2 PTA often
appears to be more severe, probably due to synergistic microbial
interactions.15,49 The history of recurrent sore throat observed in
patients presenting with type 2 PTA is possibly representative of a
chronic underlying microfloral imbalance.18,23
PTA pathogenesis
Current hypotheses
Two hypotheses are currently described to explain the pathogenesis of PTA. The predominant theorydescribed in the majority
of medical textbooks and hence well known among cliniciansstates that PTA is a complication of AT.11 There seems,
however, to be no scientific literature that provides direct supporting evidence for this. The second is a hypothesis that has
been slowly gathering more recognition and supporting evidence
over the last 20 years and highlights the association between
damaged tissue and abscess development: the Weber gland
hypothesis.
A complication of AT
Recurrent episodes of ATand sore throat are commonly reported in
PTA.19,50 Marom et al.50 found that 79% of patients in their study
reported a sore throat preceding the development of PTA.
However, other studies have reported that up to 68% of patients
with PTA have no preceding history of tonsillitis or sore
throat.22,50,51 Some other recent observations question the true involvement of AT in the development of PTA.12 14 First, Passy12
observed in a study of 100 consecutive PTA patients that 96% of
patients had no exudate on the tonsils and very little tonsillar swelling. Furthermore, a study of resected tonsils by Chen et al.14
showed that the tonsils of patients with PTA were smooth and
healthy, while fibrosis was noted in the surrounding tissue.
Considering the bacteriology, isolates commonly found in PTA
are also found in the oropharynx of patients with AT and recurrent AT.52 54 As in PTA, there is great variation in the oropharyngeal bacteriology related to AT and recurrent AT.52,53,55 GAS are
found in statistically similar numbers,52 and anaerobic microflora
are becoming more recognized as potential causes of these diseases.53,54 However, other studies indicate significantly more
growth of S. aureus and H. influenza in the tonsils of patients
with AT than in those with PTA.52,55
A further area of discrepancy concerns the modal peak of incidence groups with the highest diagnoses of AT and PTA. The incidence of PTA is highest from the mid-teens to 40 years
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Review
Relation to pathogen
Host factor
Relation to PTA
incidence
Age:
highest PTA incidence
post-puberty
mid-teens to
40 years of age
Reference
(4, 8, 22, 23, 27, 41,
56 58, 62, 63)
Contributing effects
hormonal effect on local
immunity and/or microfloral
composition (8, 57)
GAS
lower incidences of GAS
infections in those over
40 years of age (8)
lifestyle
tonsillar crypt size (41)
Gender
Periodontal
disease
high incidence of
periodontal disease
coinciding with PTA
ear/nose/throat GAS
infections are more
common in males than
females (8)
Fusobacterium sp.
common organism
identified in
periodontal disease
and caries (69, 70,
76)
Smoking
in comparison with
population groups, a
high proportion of
PTA sufferers are
smokers
SMG
highest incidence of
fusobacterial PTA
infections is in
young adults (35)
high incidence of other
fusobacterial
infections in young
adults (8, 42, 44,
64)
fusobacterial infections high incidence of SMG
suggested to be
infections in males
more common in
(25, 47)
males (8, 64)
common organism
identified in
periodontal disease
and caries (69, 70,
76)
SMG takes advantage
of established
infectious damage
(47)
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Table 2. Host factors correlating with PTA incidence and, where possible, identified relationships to pathogens
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suggested that
antibiotic use
promotes
pathogenicity (49)
Antibiotic use
increased incidence of
PTA correlates with
increased prescribed
antibiotics for sore
throat
(19, 51)
inflammation as a result of
superficial infection can lead
to increased access of
pathogens (87)
Standardizing PTA pus sample analysis would provide more comparable, reliable microbiological data. The use of highly sensitive,
modern analytic tests such as PCR should identify the true PTA
microfloral composition more reliably.95 PCR of peritonsillar
swabs from healthy volunteers could provide comparative
control data to then determine the probable pathogenspossibly a more valid method than investigating the microflora of
tonsils excised from elective tonsillectomy patients, samples
that are unlikely to be representative of healthy individuals.
Immune assays of patients with PTA may allow for a more conclusive identification of pathogenic species.42 More data from a
wider cultural and populational spread would permit for a
more viable dataset and fairer analysis.
Investigating patients symptoms, sore throat experience and
history in relation to the microbiology of PTA could provide more
conclusive evidence in support of our proposal that there are
subtypes of PTA. Grouping patients into microbiologically similar
subtypes might allow for a more appropriate and more efficient
management.
Designing a tool that assesses throat health could be of use
both for disease prevention and for monitoring the efficacy of
PTA management. Our team have recently explored the use of
the Tonsillectomy Outcome Inventory 14 as such a tool, with positive outcomes for scoring throat-related quality of life.96
Conclusions
We have identified pathogens in PTA that are opportunistic species
native to the oropharynx. With the rapid evolution of generational
behaviour and lifestyle, it is likely that microfloral compositions are
continually changing. Therefore, it is probable that the organisms
considered to be major pathogens associated with PTA will fluctuate and change. For example, it has been suggested that the
increased prescription and dosage of b-lactamases is encouraging
pathogenic behaviour on the part of anaerobes.19 It is unclear
whether the rise in anaerobic infections seen in recent years
is linked to changes such as these or whether it is related to
more sensitive tests that actively search and identify species that
have been ever-present. Patients experience and history of
sore throat appear to differ according to whether their PTA is a
monomicrobial aerobic infection or a polymicrobial infection
containing anaerobes. This leads us to propose that there may
be pathogenically distinct PTA subtypes.
The establishment of PTA ultimately requires the disruption
of oropharyngeal commensal host homeostasis followed by
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Further research
Review
Viral tonsillitis
Smoking
Poor oral hygiene
Infectious
mononucleosis
Immunocompromised/deficient
Microfloral imbalance
Antibiotics
Gender*
Genetics
Age
Bacterial niche
Smoking
Suppurative infection
Genetics
Acute tonsillitis
Peritonsillar cellulitis
PTA
Figure 2. Summary of the effect of the interaction of host factors on the development of PTA. Solid outlined, non-shaded text indicates uncontrollable
factors. Dark grey outlined shading indicates factors that can be addressed and controlled. Light grey shading indicates factors that there may be
some control over. *Contradictory evidence.
localized tissue invasion. Certain host factors influence the development of PTA; some are controllable and therefore clinically targetable, whereas others are uncontrollable risk factors that may
be used by clinicians to indicate overall patient susceptibility
(Figure 2).
Current hypotheses concerning the pathogenesis of PTA are
likely to have some validity. Mild suppurative infection, such as
AT, could spread and result in tissue damage allowing localized
invasion by the already established pathogen. Blocked Weber
glands could lead to increased debris in the tonsillar crypts, subsequent poor oral hygiene and niches for suppuration. The
number of factors and variables affecting the development of
PTA, however, suggests that the combination of a variety of circumstances can trigger pathogenesis. It would seem that PTA
is, more often than not, a pathogenically separate entity from AT.
With the incidence of PTA rising worldwide and an increased
understanding of its aetiology, it is important to focus attention
on disease prevention in addition to appropriate management.
Re-education concerning the range of factors that promote
pathogenesis and invasion in PTA may facilitate disease
prevention.
Transparency declarations
None to declare.
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