Complications of tonsillitis include peritonsillar abscess, bacteremia and sepsis and Lemierre’s syndrome. Lemierre's syndrome or postanginal septicaemia (necrobacillosis) is caused by an acute oropharyngeal infection with secondary septic thrombophlebitis due to Fusobacterium necrophorum of the internal jugular vein and frequent metastatic infections. The most common sites of septic embolisms are the lungs and joints, and other locations can be affected. CT of the neck with contrast can detect internal jugular vein thrombosis. Treatment includes intravenous antibiotic therapy and drainage of septic foci. The role of anticoagulation is controversial. Ligation or excision of the internal jugular vein may be needed.
Peritonsillar abscess
CT of peritonsillar abscess
Peritonsillar, retropharyngeal and parapharyngeal abscesses are deep neck infections that are usually secondary to contiguous spread from local sites and can occur as a complication of tonsillitis. These abscesses share similar clinical features, and also present with distinctive manifestations and complications. When not recognized early, these abscesses are potentially life threatening.
A peritonsillar abscess ( PTA, or quinsy) afflicts more often children. It is a suppuration outside the tonsillar capsule and it is situated in the region of the upper pole of the tonsil and involves the soft palate. The infection generally starts in the intratonsillar fossa, which is situated between the upper pole and the body of the tonsil, and eventually extends around the tonsil. A quinsy usually is unilateral; but can occur rarely bilaterally.1
Peritonsillar abscess (Quinsy)
Tonsillar abscess is rare and implies an abscess within the tonsil following retention of pus within a follicle to produce pain and dysphagia. Retropharyngeal abscess occurs mostly in early childhood, and is caused by spread of an oral cavity suppuration to the retropharyngeal lymph glands.
This review describes the microbiology, diagnosis and management of peritonsillar, retropharyngeal and parapharyngeal abscesses in children.
Right peritonsillar abscess
Anatomy
Three major clinically important spaces exist between the deep cervical fascia. The parapharyngeal (or lateral pharyngeal, or pharyngomaxillary) space is situated in the upper neck, above the hyoid bone, between the pretracheal fascia of the visceral compartment medially and the superficial fascia, which invests the parotid gland, internal pterygoid muscle, and mandible laterally. This space is an inverted cone, with the skull at the jugular foramen forming the base, and the hyoid bone the apex.
The second space is located within the submental and submandibular triangles, and is situated between the mucosa of the floor of the mouth and the superficial layer of deep fascia of the regions.
Anatomy of peritonsillar abscess area
The retropharyngeal space is the third space. It extends longitudinally downward from the base of the skull to the posterior mediastinum; posterior border is the prevertebral fascia and anterior boundary is the posterior portion of the pretracheal fascia. It is connected to the parapharyngeal space, where its lateral border is the carotid sheaths.
Pathophysiology
The pathophysiology of this disease is unknown. The condition is usually the endpoint of a disease that starts with acute follicular tonsillitis, progresses to peritonsillitis, and ends with formation of an abscess.
An abscess can, however, develop without any preceding history of tonsillitis. The inflamed area prior to peritonsillar abscess is usually the supratonsillar space of the soft palate, above the superior pole of the tonsil and the surrounding muscles, especially the internal pterygoids. Pus collects between the fibrous capsule of the tonsil, generally at its upper pole, and the superior constrictor muscle of the pharynx.
Another explanation suggests involvement of the Weber glands. These are a group of salivary glands located above the tonsillar area in the soft palate that clear the tonsillar area of any trapped debris. Tissue necrosis and pus formation that result in an abscess which develops between the tonsillar capsule, lateral pharyngeal wall, and supratonsillar space. The resulting scarring and obstruction of the ducts that drain these glands may progress to abscess formation.
Microbiology
Most oro-pharyngeal abscesses are polymicrobial infections; the average number of isolates is 5 (range 1 to 10).1,2-8 Predominant anaerobic organisms isolated in peritonsillar,4-8 lateral pharyngeal,3,8 and retropharyngeal5,8 abscesses are Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus spp.; aerobic organisms are group A streptococcus ( GABHS ) , Staphylococcus aureus and Haemophilus influenzae. A recent increase was noticed in the isolation of methicillin resistant S. aureusmixed.8a Anaerobic bacteria can be isolated from most abscesses whenever appropriate techniques for their cultivation have been employed,2 while Streptococcus pyogenes is isolated in only about one-third of cases.4,6,6a More than two-thirds of deep neck abscesses contain beta-lactamase producing organisms.3,4 Retropharyngeal cellulitis and abscess in young children is more likely to have pathogenic aerobic isolates (groups A and B streptococcus, S. aureus), alone or mixed.9,10 Fusobacterium necrophorum is especially associated with deep neck infections that cause septic thrombophlebitis of great vessels and metastatic abscesses (Lemierre disease).11,12 Rarely, Mycobacterium tuberculosis13, atypical mycobacteria or Coccidioidis immitis14 is recovered.
Most oro-pharyngeal abscesses are polymicrobial infections; the average number of isolates is 5 (range 1 to 10).1,2-8 Predominant anaerobic organisms isolated in peritonsillar,4-8 lateral pharyngeal,3,8 and retropharyngeal5,8 abscesses are Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus spp.; aerobic organisms are group A streptococcus ( GABHS ) , Staphylococcus aureus and Haemophilus influenzae. A recent increase was noticed in the isolation of methicillin resistant S. aureusmixed.8a Anaerobic bacteria can be isolated from most abscesses whenever appropriate techniques for their cultivation have been employed,2 while Streptococcus pyogenes is isolated in only about one-third of cases.4,6,6a More than two-thirds of deep neck abscesses contain beta-lactamase producing organisms.3,4 Retropharyngeal cellulitis and abscess in young children is more likely to have pathogenic aerobic isolates (groups A and B streptococcus, S. aureus), alone or mixed.9,10 Fusobacterium necrophorum is especially associated with deep neck infections that cause septic thrombophlebitis of great vessels and metastatic abscesses (Lemierre disease).11,12 Rarely, Mycobacterium tuberculosis13, atypical mycobacteria or Coccidioidis immitis14 is recovered.
Finegold2 reviewed the literature up to 1977 summarizing many studies of the bacteriology of PTA. Hansen15 studied 153 aspirates from PTA and isolated 151 strains of anaerobic Gram-negative bacteria, including Gram-negative cocci, Bacteroides funduliformis, fusiform bacilli, and Bacteroides fragilis. Hallander, et al16 recovered anaerobes from 26 of 30 patients. The recovered Isolates included Bacteroides spp., Fusobacterium spp,, Peptostreptococcus spp., , microaerophilic cocci, veillonellae, and bifidobacteria. Sprinkle, et al17 isolated anaerobes from four of six patients with PTA. Anaerobes only were found in one instance, and the others yielded mixed aerobic and anaerobic flora. Lodenkämper and Stienen18 isolated Bacteroides spp. from six patients with retrotonsillar abscess, and Baba, et al19 recovered Peptostreptococcus spp from four patients. Ophir et al.20 isolated eight Bacteriodes spp. from 62 patients.
Several individual case reports described the isolation of anaerobic bacteria in PTA. Prévot21 isolated Ramibacterium pseudoramosum. Alston22 recovered Bacteroides necrophorus. Beerens and Tahon-Castel23 found B. funduliformis and Fusiformis fusiformis. Gruner recovered Actinomyces species,24 and Rubinstein, et al25 and Oleske, et al26 isolated Fusobacterium spp.
The microbiology of PTA in 16 children was reported by Brook.4 Anaerobes were recovered from all patients. There were 91 anaerobic and 32 aerobic isolates. The predominant isolates were pigmented Prevotella and Porphyromonas spp, anaerobic Gram-positive cocci, Fusobacterium spp., gamma-hemolytic streptococci, alpha-hemolytic streptococci, S. pyogenes, Haemophilus spp., clostridia, and S. aureus. Beta-lactamase production was detected in 13 isolates recovered from 11 patients (68%). These included all three isolates of S. aureus, eight (35%) of the 23 Prevotella melaninogenica, and two (40%) of the five Prevotella oralis.
Bacteria isolated in 16 children with peritonsillar abscesses. 4
Aerobic and facultative isolates
|
No. of isolates
|
Anaerobic isolates
|
No. of isolates
|
Gram-positive cocci (total)
|
27
|
Anaerobic cocci
|
22
|
Group A beta-hemolytic streptococci
|
4
|
Gram-positive bacilli (total)
|
12
|
Clostridium spp.
|
3
| ||
S. aureus
|
3
| ||
Gram-negative bacilli (total)
|
5
|
Gram-negative bacilli (total)
|
57
|
H. influenzae
|
4
|
Fusobacterium spp.
|
15
|
Bacteroides spp.
|
14
| ||
pigmented Prevotella and Porphyromonas spp.
|
23
| ||
Prevotella oralis
|
5
| ||
Total no. of aerobes
|
32
|
Total no. of anaerobes
|
91
|
Brook et al. evaluated 34 aspirates of pus obtained from adults and children with PTA.31 A total 107 isolates (58 anaerobic and 49 aerobic and facultative) were recovered, accounting for 3.1 isolates per specimen. Anaerobic bacteria only were detected in 6 (18%) patients, aerobic and facultatives in 2 (6%), and mixed aerobic and anaerobic flora in 26 (76%). Single bacterial isolates were recovered in 4 infections, 2 of which were GABHS and 2 were anaerobes. The predominant isolates were S. aureus (6 isolates), anaerobic gram negative bacilli (21 isolates, including 15 pigmented Prevotella and Porphyromonas spp.), and Peptostreptococcus spp. (16) and S. pyogenes (10). Beta-Lactamase-producing organisms were recovered from 13 (52%) of 25 specimens tested. This study highlights the polymicrobial nature and importance of anaerobic bacteria in PTA.
Aspirated pus samples from 124 patients with PTA were cultured quantitatively by Jousimies-Somer et al.28 Of the 550 isolates obtained (mean, 4.4 / patient), 143 were aerobes (representing 16 species or groups) and 407 were anaerobes (representing 40 species or groups). Aerobes were isolated from 86% of patients-alone in 20 cases and together with anaerobes in 87. The predominant aerobic isolates were GABHS (in 45% of patients), Streptococcus milleri group organisms (27%), H influenzae (11%), and viridans streptococci (11%). Anaerobes were isolated from 82% of the samples and as a sole finding from 15 abscesses. Fusobacterium necrophorum and Prevotella melaninogenica were both isolated from 38% of patients, Prevotella intermedia from 32%, Peptostreptococcus micros from 27%, F. nucleatum from 26%, and Actinomyces odontolyticus from 23%. The rate of previous tonsillar/peritonsillar infections was lowest (25%) among patients infected with S. pyogenes and highest (52%) among those infected with F. necrophorum (P < .01). Recurrences and/or related tonsillectomies were more common among patients infected with F. necrophorum than among those infected with S. pyogenes (57% vs. 19%; P < .0001) or with S. milleri group organisms (43% vs. 19%; P < .05). beta-Lactamase was produced by only 38% of the 73 isolates of Prevotella spp. tested; however, 56% of the 36 patients studied harbored one or more such strains.
Mitchelmore et al studied pus aspirated from 53 PTA.29 Cultures were positive in 45 (85%) instances: 7 yielded aerobic organisms, mainly GABHS (5/7), and 38 yielded anaerobes. Most anaerobes were recovered mixed with other aerobic and anaerobic organisms, and only in two cases F. necrophorum was isolated in pure culture. Peptostreptococcus micros and S. milleri were the predominant isolates in this study. Samples from ten patients (19%) grew beta-lactamase-producing isolates.
Kluget al.28a studied 36 PTA patients undergoing acute bilateral tonsillectomy and 80 electively tonsillectomised patients. F. necrophorum and GABHS were isolated significantly more frequently from the tonsillar cores of PTA patients, from both the abscessed and non-abscessed sides, than from the tonsillar cores of electively tonsillectomised patients. The authors concluded that F. necrophorum and GABHS are the prominent pathogens in PTA.
Several case reports describing the recovery of anaerobes in retropharyngeal abscess were summarized by Finegold.2 Myerson30 described a case of anaerobic retropharyngeal abscess that yielded an anaerobic Gram-positive bacillus and hemolytic streptococci. Recovered aerobes were Streptococcus viridans and Staphylococcus spp.. Prévot21 isolated Sphaerophorus gonidiaformans from a retropharyngeal abscess. Ernst31 isolated Bacteroides funduliformis among other organisms from a retropharyngeal abscess. Janecka and Rankow32 isolated Bacteroides spp. and anaerobic streptococci from a patient with a retropharyngeal abscess. Heinrich and Pulverer33 recovered P. melaninogenica from three patients with parapharyngeal abscess.
Aspiration of retropharyngeal abscesses was performed in 14 children5 and all yielded bacterial growth. Anaerobes were isolated in all patients; they were the only isolatee in two patients (14%) and were mixed with aerobes in 12 (86%). There were 78 anaerobic isolates (5.6 per specimen). The predominant anaerobes were Bacteroides spp., Peptostreptococcus spp., and Fusobacterium spp. There were 26 aerobic isolates (1.9 per specimen). The predominant aerobes were alpha- and gamma-hemolytic streptococci, S. aureus, Haemophilus spp., and GABHS. Beta-lactamase production was noted in 16 isolates recovered from ten patients (71%). These included all isolates of S. aureus, six of 18 pigmented Prevotella and Porphyromonas spp.(33%), and two of three P. oralis (67%).
Bacteria isolated in 14 children with retropharyngeal abscesses 5
Aerobic and facultative isolates
|
No. of isolates
|
Anaerobic isolates
|
No. of isolates
|
Gram-positive cocci (total)
|
22
|
Anaerobic cocci (total)
|
25
|
Group A beta-hemolytic streptococci
|
3
|
Peptostreptococcus spp.
|
18
|
Gram-positive bacilli (total)
|
7
| ||
S. aureus
|
5 (5)
|
Gram-negative bacilli
| |
Gram-negative bacilli (total)
|
4 (1)
|
Fusobacterium spp.
|
14
|
H. influenzae type B
|
3 (1)
|
Bacteroides spp.
|
11 (1)
|
pigmented Prevotella and Porphyromonas spp.
|
18 (6)
| ||
Prevotella oralis
|
3 (2)
| ||
Total no. of aerobes
|
26 (7)
|
Total no. of anaerobes
|
78 (9)
|
Coulthard and Isaacs studied 31 children with retropharyngeal abscess.34 The organisms isolated included pure growths of S. aureus (25%), Klebsiella spp. (13%), S. pyogenes (8%), and a mixture of Gram negative and anaerobic organisms (38%).
Because of a recent increase in retropharyngeal abscess cases due to community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA), a retrospective evaluation of the microbiology, clinical manifestations and treatment outcome of retropharyngeal abscess over the past 6-years (2004-2010) was performed at Children's Hospital of Michigan, Detroit, Michigan.28a The Findings were compared to those of a previous 11 year study (1993-2003) period.
One hundred eleven children with retropharyngeal abscess were treated representing a 2.8 fold increase in incidence (per 10,000 admissions) over the previous 11-year period. A total of 116 isolates (93 aerobes, 23 anaerobes) were isolated from 66 drained specimens (2/3 of the total). The study showed increased frequency of isolation of MRSA with an associated increase of S. aureus mainly CA-MRSA. S. aureus was recovered from 25 (38%) of 66 specimens compared to 2 (4.9%) of 41 in the previous 11 years; 16 (64%) of 25 were MRSA compared to none in the previous 11 years. Children whose abscess grew MRSA were younger (mean 11 months) than the others (mean 62 month) (p< 0.001). Five children had mediastinitis; all caused by MRSA. All MRSA isolates were susceptible to clindamycin.This is likely due to the overall increase in CA-MRSA infections in pediatric patients. Treatment with ceftriaxone and clindamycin in addition to surgical drainage was effective in most patients.
Obtaining appropriate specimens for cultures from pharyngeal abscesses is important, as a variety of organisms can be recovered. Specimens are best collected at the time of surgical drainage or through needle aspiration. Throat swab or swab obtained after drainage are inappropriate because they can be contaminated by oropharyngeal flora. Specimens should be transported promptly in media or transport systems that are supportive of growth of both aerobic and anaerobic bacteria; specimens should be inoculated and incubated into proper media to optimize recovery of these organisms.
Pathogenesis
The microbiology of deep neck abscesses are similar because the bacteria causing neck abscesses reflect the host's oropharyngeal (peritonsillar and pharyngeal lateral abscess) or nasopharyngeal (abscess retropharyngeal) flora. The microbiology of specific space infections generally is associated with the bacterial flora of the originating focus. The oropharyngeal flora is made of over 350 different species of aerobic and anaerobic bacteria; the number of anaerobic bacteria exceeds that of aerobic bacteria by a ratio of 10–100 to one.35 Most anaerobic bacteria recovered from clinical infections are found mixed with other organisms,36 and anaerobes generally express their virulence in chronic infections. Polymicrobial infections are known to be more pathogenic for experimental animals than are those involving single organisms.34 Elevated antibody levels to F. nucleatum and P. intermedia, known oral pathogens was recently found in children who had peritonsillar abscess or cellulitis, suggesting a pathogenic role for these organisms in peritonsillar infections.37
The microbiology of deep neck abscesses are similar because the bacteria causing neck abscesses reflect the host's oropharyngeal (peritonsillar and pharyngeal lateral abscess) or nasopharyngeal (abscess retropharyngeal) flora. The microbiology of specific space infections generally is associated with the bacterial flora of the originating focus. The oropharyngeal flora is made of over 350 different species of aerobic and anaerobic bacteria; the number of anaerobic bacteria exceeds that of aerobic bacteria by a ratio of 10–100 to one.35 Most anaerobic bacteria recovered from clinical infections are found mixed with other organisms,36 and anaerobes generally express their virulence in chronic infections. Polymicrobial infections are known to be more pathogenic for experimental animals than are those involving single organisms.34 Elevated antibody levels to F. nucleatum and P. intermedia, known oral pathogens was recently found in children who had peritonsillar abscess or cellulitis, suggesting a pathogenic role for these organisms in peritonsillar infections.37
Antibody titers to these organisms were measured by enzyme- linked immunosorbent assay in 19 patients with peritonsillar cellulitis and 19 with peritonsillar abscess patient, as well as in 32 controls. Serum levels in the patients were determined at day 1 and 42–56 days later. Significantly higher antibody levels to F. nucleutum and P. intermedia were evident in the second serum sample of patients with peritonsillar cellulitis or abscess, as compared to their first sample or the levels of antibodies in non-infected individuals.
Clinical Features of Peritonsillar, Retropharyngeal & Lateral Pharyngeal Abscesses
Usual Age |
Sites of Origin
| Location | Clinical Findings |
Complications/
Extension Site | Management | |
Peritonsillar Abscess
|
Adolescents, adults
|
Tonsillitis
|
Tonsillar capsule, & space below superior constrictor muscle
|
Swelling of one tonsil, uvullar displacement; trismus, muffled voice
|
Spontaneous rupture & aspiration; contiguous spread to pterygomaxillary space
|
Antibiotics, drainage
|
Retropharyngeal Abscess
|
<4 years
|
Pharyngitis, dental infection trauma
|
Between posterior pharynx & prevertebral fascia
|
Unilateral posterior pharyngeal bulging; neck, hyperextension drooling, respiratory distress
|
Spontaneous rupture & aspiration; contiguous spread to posterior mediastinum, parapharyngeal space
|
Antibiotics, drainage; artificial airway
|
Lateral Pharyngeal Abscess
|
>8 adolescents, adults
|
Tonsillitis ottitis media, mastoiditis, parotitis, dental manipulation
|
Anterior & posterior pharyngomaxillary space
|
Anterior compartment: swelling of the parotid area; trismus; tonsil prolapse/tonsillar fossa
Posterior compartment: septicemia; minimal pain or trismus
|
Carotid erosion; airway obstruction; intracranium, lung, contiguous spread to mediastinum; septicemia
|
Antibiotics, drainage, artificial airway
|
Diagnosis
Workup of the patient include Complete blood count (CBC) with differential, and culture and sensitivity via needle aspiration of purulent material. Most patients require no imaging studies. Intraoral ultrasound, may be used to exclude peritonsillar cellulitis and retropharyngeal abscess. This can confirm the presence of an abscess as well as its volume, location, and relationship to the carotid artery.
Workup of the patient include Complete blood count (CBC) with differential, and culture and sensitivity via needle aspiration of purulent material. Most patients require no imaging studies. Intraoral ultrasound, may be used to exclude peritonsillar cellulitis and retropharyngeal abscess. This can confirm the presence of an abscess as well as its volume, location, and relationship to the carotid artery.
CT of peritonsillar abscees ( early stages)
CT of peritonsillar abscess (late stage)
Bilateral peritonsillar abscesses (PTA)
A CT scan is used if the patient cannot open his/her mouth because of trismus. It is indicated especially when an abscess is suspected to extend into deep neck tissues. Regular x-rays are not as helpful as intraoral ultrasound or CT scanning.
CT of retropharyngeal abscess
CT of retropharyngeal abscess
Left parapahryngeal abscess
Management
Because of the similarity in their micrtobiology, the management of tonsillar, peritonsillar, and retropharyngeal abscesses is similar. Whenever these abscesses are diagnosed, systemic antimicrobial therapy should be administered in large doses. If treatment is started early, generally within the first 24 to 48 hours following the onset of pain when the infection is at the stage of cellulitis, the condition may resolve by fibrosis without abscess formation. Frank pus generally forms on about the fifth day. If the patient is not seen until pus has formed, or if the antibiotic therapy fails, the abscess must be drained. Because tonsillar and peritonsillar abscesses often tend to recur, tonsillectomy should be performed six to eight weeks following formation of the abscess. However, this approach is not always necessary in children25 as a recurrence rate of only 7% was observed in this age group, compared to 16% in adults. Ophir et al.20 demonstrated the ability to manage most patients with peritonsillar abscess on an outpatient basis, after needle aspiration of the abscess. However another study reported greater rate of recurrences in patients treated with needle aspiration.38
Tracheostomy
When present, airway obstruction may require immediate airway management. Therefore, equipment for intubation cricothyroidotomy or tracheotomy should be available. Supportive therapy to ensure adequate hydration and analgesia should be provided. Surgical drainage of an abscess is still the therapy of choice. However, administration of antimicrobial agents is also required. The isolation of aerobic and anaerobic beta-lactamase-producing bacteria from most abscesses mandates the use of antimicrobial agents effective against these organisms. Beta-lactamase-producing bacteria include Prevotella, Fusobacterium, Haemophilus and Staphylococcus spp. Efficacy antimicrobial agents include cefoxitin, a carbapenem (i.e., imipenem or meropenem), the combination of a penicillin (i.e., ticarcillin) and a beta-lactamase inhibitor (i.e., clavulanate), chloramphenicol, or clindamycin. Antimicrobial therapy can abort abscess formation if administered at an early stage of the infection. However, when pus is formed, antimicrobial therapy is effective only in conjunction with adequate surgical drainage.
Complications
Abscesses that are left untreated can rupture spontaneously into the pharynx leading to aspiration. Asphyxia resulting from direct pressure or from sudden rupture of the abscess and also from hemorrhage is the major complication of these infections. Other complications include extension of infection laterally to the side of the neck, or dissection into the posterior mediastinum through facial planes and the prevertebral space, cerebral abscess, meningitis, and sepsis. Death can occur from aspiration, airway obstruction, erosion into major blood vessels, or extension to the mediastinum.
Surgical drainage and antimicrobial therapy are essential for the prompt recovery and prevention of complications of these abscesses, such as bacteremia, aspiration pneumonia, and lung abscess after spontaneous rupture.
Conclusions
Peritonsillar, retropharyngeal and parapharyngeal abscesses are deep neck infections that share several clinical features, and also have distinctive manifestations and complications. They all are potentially life threatening if not recognized early. Large doses of systemic antimicrobial therapy should be given whenever the diagnosis is made. However, when pus is formed, antimicrobial therapy is effective only in conjunction with adequate surgical drainage.
Peritonsillar, retropharyngeal and parapharyngeal abscesses are deep neck infections that share several clinical features, and also have distinctive manifestations and complications. They all are potentially life threatening if not recognized early. Large doses of systemic antimicrobial therapy should be given whenever the diagnosis is made. However, when pus is formed, antimicrobial therapy is effective only in conjunction with adequate surgical drainage.
References
1. Brook, I. , Shah, K.: Bilateral peritonsillar abscess: an unusual presentation. South. Med. J. 74:514-5, 1981.
2. Finegold, S.M.: Anaerobic bacteria in human disease. New York
3. Brook, I. : Microbiology of abscesses of the head and neck in children. Ann. Otol. Rhinol. Laryngol. 96:429-33, 1987.
4. Brook, I. : Aerobic and anaerobic bacteriology of peritonsillar abscess in children. Acta Paediatr Scand 70:831–8, 1981.
5. Brook, I. : Microbiology of retropharyngeal abscesses in children. Am J Dis Child 141:202–4, 1987.
6. Jokipii, A.M.M, Jokipii L., Sipila P., Jokinen K.: Semiquantitative culture results and pathogenic significance of obligate anaerobes in peritonsillar abscesses. J Clin Microbiol 26:957–61, 1988.
6a. Risberg S, Engfeldt P, Hugosson S. Peritonsillar abscess and cellulitis and their relation to a positive antigen detection test for streptococcal infection. Scand J Infect Dis.;42:747-51, 2010.
6a. Risberg S, Engfeldt P, Hugosson S. Peritonsillar abscess and cellulitis and their relation to a positive antigen detection test for streptococcal infection. Scand J Infect Dis.;42:747-51, 2010.
7. Floodstrom, A., Hallander, H.O.: Microbiological aspects of peritonsillar abscesses. Scand J Infect Dis 8:157–60, 1976.
8. Dodds, B., Maniglia, A.J.: L Peritonsillar and neck abscesses in the pediatric age group. Laryngoscope 98:956–9, 98:1988.
8a. Abdel-Haq N, Quezada M, Asmar BI. Retropharyngeal abscess in children: The ising incidence of MRSA . Pediatr Infect Dis J. 2012 April. 2012 Apr 4
9. Asmar, B.I.: Bacteriology of retropharyngeal abscess in children. Pediatr Infect Dis J 9:595–6, 1990.
10. Asmar, B.I.: Neonatal retropharyngeal cellulitis due to group B streptococcus. Clin Pediatr 26:183–5, 1987.
11. Hughes, C.E., Spear, R.K., Shinabarger, C.E., Tuna I.C.: Septic pulmonary emboli complicating mastoiditis: Lemierre's syndrome. Clin Infect Dis 18:633–5, 1994.
12. Moreno
13. Neumann, J.L., Schlueter, D.P.: Retropharyngeal abscess as the presenting feature of tuberculosis of the cervical spine. Am Rev Resp Dis 110:508–11, 1974.
14. Barratt, G.E., Koopmann, C.F., Coulthard, S.W.: Retropharyngeal abscess. A ten year experience. Laryngoscopy 94:455–63, 1984.
15. Hansen, A.: Nogle undersøgelser over gram-negative aerobe ikke-spore-dannende bacterier isolerede fra peritonsillere abscesser hos mennesker. Copenhagen
16. Hallander, H.O., Floodstrom, A., Holmberg, K.: Influence of the collection and transport of specimens on the recovery of bacteria from peritonsillar abscesses. J. Clin. Microbiol. 2:504-9, 1975.
17. Sprinkel, P.M., Veltri, R.W., Kantor, L.M.: Abscesses of the head and neck. Laryngoscope 84:1143-8, 1974.
18. Lodenkämper, H., Stienen, G.: Importance and therapy of anaerobic infections. Antibiotic Medicine 1:653-9, 1955.
19. Baba, S., Mamiya, K., Suzuki, A.: Anaerobic bacteria isolated from otolaryngologic infections. Jpn. J. Clin. Pathol. 19 (suppl.):35-6, 1971.
20. Ophir, D., Bawnik J, Poria Y, Porat M, Marshak G.: Peritonsillar abscess. A prospective evaluation of outpatient management by needle aspiration. Arch. Otolaryngol. Head Neck Surg. 114:661-3, 1988.
21. Prévot, A.R.: Biologies des maladies dués aux anaerobies. Paris, Éditions Medicales Flamarion. 1955.
22. Alston, J.M.: Necrobacillosis in Great Britain
23. Beerens, H., Tahon-Castel, M.: Infections humaines à bactéries anaerobies nontoxigènes. Brussels
24. Gruner, O.P.N·: Actinomyces in tonsillar tissue: a histological study of tonsillectomy material. Acta Pathol. Microbiol. Scand. 76:239-44, 1969.
25. Rubenstein, E., Onderdonk, A.B., Rahal, J., Jr.: Peritonsillar infection and bacteremia caused by Fusobacterium gonidiaformans. J. Pediatr. 85:673-5, 1974.
26. Oleske, J.M., Starr, S.E., Nahmias, A.J.: Complications of peritonsillar abscess due to Fusobacterium necrophorum. Pediatrics 57:570-1, 1976.
27. Brook, I. , Frazier, E.H., Thompson, D.H.: Aerobic and anaerobic microbiology of peritonsillar abscess. Laryngoscope 101:289–92, 1991.
28. Jousimies-Somer, H., Savolainen, S., Makitie, A., Ylikoski, J.: Bacteriologic findings in peritonsillar abscesses in young adults. Clin Infect Dis Suppl 4:S292–8, 1993.
28a. Klug TE, Henriksen JJ, Fuursted K, Ovesen T. Significant pathogens in peritonsillar abscesses. Eur J Clin Microbiol Infect Dis. 30:619-27, 2011.
28a. Klug TE, Henriksen JJ, Fuursted K, Ovesen T. Significant pathogens in peritonsillar abscesses. Eur J Clin Microbiol Infect Dis. 30:619-27, 2011.
29. Mitchelmore, I.J., Prior, A.J., Montgomery , P.Q.
30. Myerson,M.C.:anaerobic retropharyngeal abscess. Ann.Otol.Rhinol.Laryngol.41:805-9,1932.
31. Ernst, O.: Zur bedetung des Bacteroides funduliformis als infektions-errerger. Z. Hyg. 132:352-7, 1961.
32. Janecka, I.P., Rankow, R.M.: Fatal mediastinitis following retropharyngeal abscess. Arch. Otolaryngol. Head Neck Surg. 93:630-3, 1971.
33. Heinrich, S., Pulverer, G.: Uber den Nachweis des Bacteroides melaninogenicus in Krankheitsprozessen bei Mensch und Tier. Z. Hyg. 146:331-8, 1960.
34. Coulthard, M., Isaacs, D.: Retropharyngeal abscess. Arch Dis Child 66:1227–30, 1991.
35. Socransky, S.S., Manganiello , S.D.
36. Brook, I. , Hunter, V., Walker , R.I.
37. Brook, I. , Foote, P.A .Jr., Slots, J.: Immune response to anaerobic bacteria in patients with peritonsillar cellulitis and abscess. Acta Otolaryngol 116:888–91, 1996.
38. Wolf, M., Even-Chen, I. , Kronenberg, J.: Peritonsillar abscess: repeated needle aspiration versus incision and drainage. Ann Otol Rhinol Laryngol 103:554–7, 1994.
