The aerobic and anaerobic oropharyngeal flora is the source of infections in and around the oropharynx.
The oropharyngeal flora as a source of infections
The aerobic and anaerobic organisms causing head and neck infections are listed in the table bellow:
Aerobes
|
Anaerobes
| |
Acute otitis media
|
S. pneumoniae, H. influenzae, M. catarrhalis
|
Rarely: Peptostreptococcus
|
Chronic otitis media &mastoiditis | S. aureus, E. coli, K. pneumoniae, P. aeruginosa | Peptostreptococcus spp, Prevotella spp, Porphyromonas spp, Fusobacterium spp, Bacteroides spp |
Acute rhinosinusitis | S. pneumoniae, H. influenzae,
M. catarrhalis
| Peptostreptococcus spp |
Chronic rhinosinusitis | a-hemolytic streptococci, S. aureus, Haemophilus spp | Peptostreptococcus spp, Prevotella spp, Porphyromonas spp, Fusobacterium spp, Bacteroides spp |
Acute Tonsillitis | Viruses, group A b-hemolytic streptococci (Streptococcus pyogenes) | rarely anaerobes |
Chronic tonsillitis Peritonsillar abscess | streptococci, staphylococci, M. catarrhalis, H. influenzae Group A b-hemolytic streptococci, Streptococcus milleri, Haemophilus influenzae, viridans streptococci | Bacteroides spp, Fusobacterium spp, Prevotella spp, Peptostreptococcus spp. Bacteroides spp, Fusobacterium spp, Prevotella spp, Peptostreptococcus spp. |
ACUTE AND CHRONIC OTITIS MEDIA AND CHOLESTEATOMA
The definitions and classification of otitis media are: 1Acute otitis media (AOM) is characterized by a rapid onset of signs and symptoms of middle ear inflammation. Earache, bulging of the tympanic membrane, and purulent exudate characterize the early phase of infection. Even though clinical signs and symptoms resolve rapidly, the effusion can persists. Otitis media with effusion (OME) refers to the presence of asymptomatic effusion. It may follow AOM or appear as silent or secretory otitis media. Chronic otitis media with effusion (COME) denotes a persistence of fluid for 3 months or longer. The fluid is more mucoid, so called glue ear. Chronic suppurative otitis media (CSOM) signifies chronic drainage through a perforation of the tympanic membrane.
Middle ear
Microbiology
Streptococcus pneumoniae and Haemophilus influenzae are the primary etiologic agents in AOM.2 These organisms are isolated from approximately 30% and 20% of patients respectively. Anaerobes have been isolated in 5-15% of patients with AOM2 and 42% of culture-positive aspirates of patients with serous OME.3 The predominant isolates in OME and OME were Peptostreptococcus spp. and Propionibacterium acnes. Gram-negative anaerobic bacilli were also found in OME. Persistent OME that fails to respond to antimicrobial therapy can lead to chronic infection that is associated with emergence of resistant anaerobes and aerobes. The transitional stages of persistent otitis from acute to chronic was demonstrated in a series children who had repeated aspirations of middle ear fluid over a period of 36-55 days.1
Anaerobes are present in about 50% of the patients with CSOM1,4 or cholesteatoma.5 The predominant anaerobes are Gram-negative bacilli and Peptostreptococci, and the aerobes were Pseudomonas aeruginosa and Staphylococcus aureus. Many of these organisms can produce beta-lactamase and might have contributed to the high failure rate of beta-lactam antibiotics in the therapy of this infection. Anaerobes are generally recovered, mixed with aerobic bacteria, and the number of isolates/specimen ranged between 2 and 6. Antimicrobial therapy directed at the eradication of anaerobic bacteria (clindamycin) was superior to therapies less effective against these organisms. 5 Anaerobes were isolated from 23 of 24 (96%) specimens of chronic mastoiditis,7 and from most patients with intracranial abscesses that complicate CSOM.
Tympanic membrane view of acute otitis media
Cholesteatoma
Management
AOM: Therapy includes analgesics, antipyretics, and local heat. Antimicrobials are administered to eradiate the pathogen(s), prevent recurrences and complications and to facilitate recovery. Although spontaneous resolution of AOME is common and may occur in about 2/3 of patients, it is impossible to predict which child will require antimicrobials to improve. 8
The duration of therapy is also controversial. Although most physician use 10 days of therapy, a shorter course of 5-7 days can be given to children older than 2 years, those who have no history of recurrences, or other serious medical problem clinical judgment and individualization of the length of therapy are imperative.9 The growing resistance to amoxcillin of H influenzae and M catarrhalis through the production of beta-lactamase, and S. pneumoniae through changes in the protein binding site increased the risk of antimicrobial failure. Increasing the dose of amoxicillin to 90mg/kg/d overcomes S. pneumoniae penicillin resistance. Effective agents against penicillin resistant aerobic and anaerobic bacteria is the combination of amoxicillin, plus clavulanic acid (a beta-lactamase inhibitor). The newer second-generation cephalosporins (cefuroxime, cefprozil, cefdinir and cefpedoxime) have also been effective in the treatment, mostly because of their effectiveness against Haemophilus and Moraxella and interemidately penicillin resistant S. pneumoniae. Azithromycin has improved activity against H influenzae. The anaerobes recovered in AOME are susceptible to penicillins and the other antibiotics commonly used to treat AOME. However, trimethoprim-sulfamethoxazole is effective against only 50% of anaerobic Gram-positive cocci isolates, the major anaerobe isolated in AOM.
CSOM: Treatment include clindamycin, cefoxitin, a combination of metronidazole plus either a macrolide, or amoxicillin, a penicillin (i.e. amoxicillin , ticarcillin ) plus a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam). In instances where P. aeruginosa is considered to be a true pathogen, parenteral therapy with aminoglycosides, cefepime or ceftazidime or a fluoroquinoline (only in postpubertal patients) should be added. Parenteral therapy with a carbapenem provides adequate coverage for all potential pathogens, anaerobes as well as aerobic bacteria.
Local instillation of appropriate antibiotic drops is sometimes effective. Cholesteatoma should be treated surgically when diagnosed.
Complications
Complications are uncommon and include: perforation of drum, resulting in CSOM, hearing loss, acquired cholesteatoma, mastoiditis, petrositis, meningitis, brain epidural and subdural abscesses, and chronic serous otitis (glue ear) are some of the complications of AOM. Fortunately, the intracranial suppurative complications are uncommon in recent years. These complications usually occur following CSOM or mastoiditis through direct extension or by vascular channels.
SINUSITIS
Sinusitis is defined as an inflammation of the mucous membrane lining the paranasal sinuses. Sinusitis can be classified chronologically into 5 categories: acute; recurrent acute; subacute; chronic; and acute exacerbation of chronic sinusitis. 10
Acute sinusitis is a new infection that may last up to 4 weeks and can be subdivided symptomatically into severe and non-severe. Recurrent acute sinusitis is diagnosed when four or more episodes of acute sinusitis, which all resolve completely, occur within 1 year. Subacute sinusitis is an infection that lasts between 4 to 12 weeks. Chronic sinusitis is diagnosed when signs and symptoms last for more than 12 weeks. Acute exacerbation of chronic sinusitis occurs when the signs and symptoms of chronic sinusitis exacerbate but return to baseline following treatment.
Plain x-ray showing opacification of right maxillary sinus
Micrbiology & Pathophysiology
Acute bacterial sinusitis has been shown to complicate 0.5%–5% of viral upper respiratory tract infections. It develops when there is an obstruction of the sinuses ostium, blocking aeration and drainage, due to allergy, viral infection, or anatomical malformations. S. pneumoniae, H. influenzae, and M. catarrhalis are the most commonly isolated pathogens (Table 1). Staphylococcus aureus predominates in sphenoid sinusitis.
Bacterial infection is likely to be secondary to a preceding viral infection viruses mentioned. The main viruses are : respiratory syncytial, rhino, parainfluenzae, ECHO , and Coxsackie.
Sinusitis occurs in a wide range of immunocompromised hosts, including neutropenic patients, diabetic patients, patients in critical care units, and patients with HIV infection. Neutropenia, is associated with infection due to Aspergillus spp., Mucor spp., Rhizopus spp., P. aeruginosa; Diabetes mellitus with the same organisms and also aureus, streptococci, P. mirabilis; Critical illness, especially in those who have Nasogastric or nasotracheal intubation with P. aeruginosa, S. aureus, anaerobes, and Candida albicans,12 and patients with HIV, with P. aeruginosa, S. aureus, Aspergillus species, cryptococci, microsporidia, cryptosporidia, Acanthamoeba species, atypical mycobacteria.102 Cystic fibrosis is associated with P. aeruginosa. 13
The infection is polymicrobial in about a third of cases of acute sinusitis. Although Anaerobes are isolated from 5-10% patients with acute sinusitis (mostly in infections originating from dental sources.
Anaerobes can be present in up to two-thirds of patients with chronic bacterial sinusitis. 14,15
The higher prevalence of anaerobes may be due to poor sinus drainage and increased intranasal pressure, resulting in reduced oxygen tension and increasing acidity, that support the growth of anaerobic organisms.
Anaerobes role in chronic sinusitis is supported by the detection of antibodies (IgG) to two anaerobic organisms commonly recovered from sinus aspirates (F. nucleatum and P. intermedia)16. Antibody levels to these organisms declined in the patients who responded to therapy and were cured, but did not decrease in those who failed therapy.
The transition in the flora and emergence of anaerobes was demonstrated in patients who failed antimicrobial therapy.
.
A growing number of aerobic and anaerobic organisms isolated from patients with acute and chronic bacterial sinusitis produce beta -lactamases. Beta-Lactamase activity was seen in 86% of sinus aspirates that contained beta -lactamase producing organisms. It has been suggested that the beta -lactamase present in sinus fluid may protect other non-beta-lactamase–producing organisms (BLPO).17 A greater role of methicillin resistant Staphylococcus aureus (MRSA) has been observed in both acute and chronic sinusitis. 17a
Studies of chronic sinusitis
The higher prevalence of anaerobes may be due to poor sinus drainage and increased intranasal pressure, resulting in reduced oxygen tension and increasing acidity, that support the growth of anaerobic organisms.
Oxygen concentration effects on the growth of anaerobes in sinusitis
Anaerobes role in chronic sinusitis is supported by the detection of antibodies (IgG) to two anaerobic organisms commonly recovered from sinus aspirates (F. nucleatum and P. intermedia)16. Antibody levels to these organisms declined in the patients who responded to therapy and were cured, but did not decrease in those who failed therapy.
Serum antibodies to Prevotella and Fusobacterium species in patients with chronic sinusitis before and after therapy
The transition in the flora and emergence of anaerobes was demonstrated in patients who failed antimicrobial therapy.
Dynamics of sinusitis with emergence of anaerobes over time
A growing number of aerobic and anaerobic organisms isolated from patients with acute and chronic bacterial sinusitis produce beta -lactamases. Beta-Lactamase activity was seen in 86% of sinus aspirates that contained beta -lactamase producing organisms. It has been suggested that the beta -lactamase present in sinus fluid may protect other non-beta-lactamase–producing organisms (BLPO).17 A greater role of methicillin resistant Staphylococcus aureus (MRSA) has been observed in both acute and chronic sinusitis. 17a
Microbiology of acute and chronic sinusitis (percent of patients)
Maxillary
|
Ethmoid
|
Frontal
|
Sphenoid
| |||||
Bacteria
|
Acute
N=NS*
|
Chronic
N=66
|
Acute
N=26
|
Chronic
N=17
|
Acute
N=15
|
Chronic
N=13
|
Acute
N=16
|
Chronic
N=7
|
Aerobes
S. aureus
S. pyogenes
S. pneumoniae
H. influenzae
M. catarrhalis
Enterobacteriaceaae
P. aeruginosa
Anaerobes
Peptostreptococcus
P. acnes
Fusobacterium
Prevotella & Porphyromonas
B. fragilis
|
4
2
31
21
8
7
2
2
-
2
2
-
|
14
8
6
5
6
6
3
56
29
17
47
6
|
15
8
35
27
8
-
-
15
12
4
8
-
|
24
6
6
6
-
47
6
59
18
47
82
-
|
-
3
33
40
20
-
-
3
3
3
3
-
|
15
-
-
15
-
8
8
38
8
31
62
15
|
56
6
6
12
-
-
6
19
12
6
6
-
|
14
-
-
14
-
28
14
57
29
54
86
-
|
Beta-Lactamase Detected in
| ||||||
Chronic Sinusitis Aspirates. 17
| ||||||
Patient No.
| ||||||
Organism
|
1
|
2
|
3
|
4
| ||
Staphylococcus aureus (BL +)
|
+
|
+
| ||||
Streptococcus pneumoniae
|
+
| |||||
Peptostreptococcus spp
|
+
|
+
| ||||
Propionibacterium acnes
|
+
| |||||
Fusobacterium spp (BL +)
|
+
|
+
| ||||
Fusobacterium spp (BL -)
|
+
|
+
| ||||
Prevotella spp (BL +)
|
+
| |||||
Prevotella spp (BL -)
|
+
|
+
|
+
| |||
Bacteroides fragilis group (BL +)
|
+
|
+
| ||||
Beta-lactamase activity in pus
|
+
|
+
|
+
|
+
| ||
BL + = Beta-lactamase-producing bacteria.
| ||||||
ACUTE SINUSITIS: Treatment goal is to establish good drainage by decongestants, nasal saline irrigation/spray, humidification and mucolytic agents. Systemic decongestants or antihistamines may be helpful, especially in allergic individuals. Anatomic deformities should be corrected.
Antimicrobials facilitate recovery and prevents septic complications. Patient who fails to show significant improvement within 48 hours or shows signs of deterioration, antral puncture surgical drainage may be needed, and sinus irrigation and culture of the aspirate is carried out.
The choice of therapy is similar to the one of AOM. The recommendations of the Sinus and Allergy Partnership guidelines for the optimal treatment of acute bacterial rhinosinusitis.18 are based on placing the patients into categories of expected clinical efficacy in adults and children with acute sinusitis. For adults, the most effective agents are bacterial efficacy rates are for gatifloxacin, levofloxacin, moxifloxacin, and amoxicillin/clavulanate (>90% efficacy) , for high-dose amoxicillin, cefpodoxime proxetil, cefuroxime axetil and trimethoprim-sulfamethoxazole (80% to 90%), for clindamycin, doxycycline, cefprozil, azithromycin, clarithromycin, and erythromycin (70% to 80%) , and for cefaclor and loracarbef (50% to 60%). Quinolones are not advocated in children. Azithromycin, clarithromycin, erythromycin, or trimethoprim-sulfamethoxazole are recommended in patients with hypersensitivity to beta‑lactams.
CHRONIC SINUSITIS: Repeated courses of decongestants and antibiotics may be required. Anti-inflammatory agents are used in allergic patients and include topical steroids
Antimicrobial agents used for chronic sinusitis therapy should be effective against aerobic and anaerobic BLPB; These include clindamycin, the combination of metronidazole and a penicillin or a macrolide, or the combination of penicillin (e.g. amoxicillin) and a beta-lactamase inhibitor (e.g. clavulanic acid), or the ‘newer’ quinolones with antianaerobic coverage (e.g. trovafloxacin, moxifloxacin). All of these agents (or similar ones) are available in oral and parenteral forms.
Other effective agents are available only in parenteral form (e.g. cefoxitin, carbapenems). If Gram-negative organisms, such as P. aeruginosa, may be involved, parenteral therapy with aminoglycosides, a fourth-generation cephalosporin (cefepime or ceftazidime) or oral or parenteral treatment with a fluoroquinolone (only in postpubertal patients) is added. Parenteral therapy with a carbapenem (e.g. imipenem) is more expensive, but provides coverage for most potential pathogens, both anaerobes and aerobes.
The length of therapy is at least 21 days, and may be extended up to 3 month. Fungal sinusitis can be treated with surgical debridement of the affected sinuses and antifungal therapy.
In contrast to acute sinusitis, which generally is treated vigorously with antibiotics, many physicians believe that surgical drainage and not antibiotics is the mainstay of therapy in chronic sinusitis.
Sinus infection when not treated promptly and properly may spread via anastomosing veins or by direct extension to nearby structures. Orbital complication include periorbital cellulitis, subperiosteal abscess, orbital cellulitis, and abscess. Sinusitis may extend also to the central nervous system, causing cavernous sinus thrombosis (CST), retrograde meningitis, and epidural, subdural, and brain abscesses.19 Orbital symptoms frequently precede intracranial extension of the disease.
Orbital complications of sinusitis
The most common pathogens in cellulites, CST, and abscesses are those seen in acute and chronic sinusitis, depending on the length and aetiology of the primary sinusitis. These include S. pneumoniae, H. influenzae, Staph. aureus, anaerobic bacteria (Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus spp.).19,20
The organisms recovered from brain abscesses as a complication of sinusitis are anaerobic, aerobic and microaerophilic streptococci. Anaerobes can be isolated in over two-thirds of the patients, and include pigmented Prevotella and Porphyromonas spp., Fusobacterium spp. and Peptostreptococcus spp.21
Although the need for judicious selection of antimicrobial agents is of utmost importance, it is essential to note that the treatment of the complications of sinusitis frequently requires surgical intervention.
MASTOIDITIS
Mastoiditis, a complication of otitis media and is defined as an inflammation of the mastoid antrum and air cells with bone necrosis. The acute form of the disease manifests itself with fever and tenderness around the mastoid cells, accompanied by pus. Chronic mastoiditis almost always associated with CSOM. It is insidious and generally not accompanied by acute findings.
Microbiology
ACUTE MASTOIDITIS S. pneumoniae, Streptococcus pyogenes, S. aureus, H. influenzae are the most common organisms recovered.22 Rare organisms and P. aeruginosa and other gram-negative aerobic bacilli, anaerobes and Mycobacterium tuberculosis.
CHRONIC MASTOIDITIS: P. aeruginosa Enterobacteriaceae, S. aureus and anaerobes are the predominante isolates. S. pneumoniae and H. influenzae are rarely recovered.7 Most infections are polymicrobial and the predominant anaerobic organisms are gram-negative bacilli (including pigmented Prevotella and Porphyromonas and B. fragilis group ), Gram-positive cocci (Peptostreptococcus spp., and microaerophilic streptococci), Actinomyces spp., F. nucleatum, P. acnes , and Clostridium spp. The main aerobes are S. aureus , P. aeruginosa), Escerichia coli , alpha-hemolytic streptococci , and K. pneumoniae . Many of the aerobic and anaerobic bacteria can produce beta-lactamase These included S. aureus, the B. fragilis group and the pigmented Prevotella and Porphyromonas.( Table 1)
Diagnosis
ACUTE MASTOIDITIS: Presents with pain, tenderness, edema, erythema of the postauricular area, and swelling or sagging of the posterosuperior canal wall. The pinna is displaced inferiorly and anteriorly. The eardrum usually shows changes of AOM and the child may be irritable and febrile. Radiographical studies including CT may be warranted.
CT showing mastoiditis
CHRONIC MASTOIDITIS: Symptoms include persistent painless, purulent, foul-smelling, scanty discharge. There is conductive hearing loss that is shown audiometrically.
Cultures and Gram and acid fast stains should be collected for aerobic and anaerobic bacteria, mycobacteria and fungi, and biopsy of suspicious tissue should be obtained. Radiographical studies including CT may be needed. An increase in thickness of the mastoid cells with a reduction in their size and sclerosis of the bone often occurs. Small abscess cavities may persist in the sclerotic bone.
Swelling and redness behind the ear lobe in mastoiditis
Management
ACUTE MASTOIDITIS: Treatment is guided by cultures and includes parenteral antimicrobials and myrinyotomy with tympanostomy tube. Cefuroxime, ceftriaxone, or the combination of a penicillin plus a beta-lactamase inhibitor (i.e. ticarcillin plus clavulumate) are appropriate.
With proper therapy improvement occurs within 48 hours. In this event, treatment should be continued for 7 to 10 days. However, if the toxicity increases, the disease progresses or does not improve within 48 hours, surgical intervention and drainage may be necessary.
CHRONIC MASTOIDITIS: Antimicrobial therapy should be directed at the eradication of both aerobic and anaerobic bacteria. Some of the anaerobes, such as B. fragilis, and many pigmented Prevotella and Porphyromonas and Fusobacterium spp. are resistant to beta-lactam antibiotics.
Clindamycin, metronidazole, cefoxitin, or the combination of a penicillin and a beta lactamase-inhibitor provide coverage for anaerobic bacteria. Therapy should also include antimicrobial agents effective against S. aureus ( oxacillin, vancomycin, or linezolide) and the Gram-negative aerobic bacilli including P. aeruginosa ( an aminoglycoside, ceftazidime, cefipime, or a fluroquinoline (i.e. ciprofloxacin, levofloxacin ) . The carbapenems (i.e. imipenem) provide therapy of all potential pathogens. Surgical drainage is indicated in many cases.
Complications
These include intracranial complications (meningitis, subdural empyema and brain abscess), subperiosteal abscess, bezold abscess, facial nerve paralysis, labyrinthitis, deafness, and osteomyelitis.
TONSILLITIS
Tonsillitis is a common disease of childhood. The diagnosis of tonsillitis generally requires the consideration of Group A beta-hemolytic streptococci (GABHS) infection. However, numerous other bacteria alone or in combinations (including S. aureus, and H. influenzae) viruses and other infections and non-infectious causes should be considered. Recognition of the cause and choice of appropriate therapy are important in assuring rapid recovery and preventing complications.
The role of anaerobes in this infection is hard to elucidate because anaerobes are normally prevalent on the surface of the tonsils and pharynx.
Microbiology
Anaerobic bacteria are abundant among the indigenous flora of the oropharynx and colonize the normal tonsills.23 Indirect evidence is supporting the involvement of anaerobes in acute and chronic tonsillitis. The evidence is derived from studies that show the major role of anaerobes in complications of tonsillitis. The organisms associated with the infection are Fusobacterium spp., gram-negative anaerobic bacilli, Peptostreptococcus spp. and Actinomyces spp.. Polymicrobial aerobic and anaerobic flora predominate in peritonsillar and retropharyngeal abscesses.24 These organisms can be isolated from 25% of suppurative cervical lymph nodes and are mostly associated with the presence of dental or tonsillar infections.25 Anaerobes have been associated with thrombophlebitis of the internal jugular veins, which often causes postanginal sepsis.26
The pathogenic role of anaerobes in the acute inflammatory process in the tonsils is also supported by several clinical observations: their recovery in tonsillar, peritonsillar or retropharyngeal abscesses in many cases without any aerobic bacteria,24 the isolation of anaerobes from tonsils in Vincent's angina,26 the recovery of encapsulated pigmented Prevotella and Porphyromonas spp. in acutely inflamed tonsils, the isolation of anaerobes from the core of recurrently inflamed non- GABHS tonsils,27 and the response to antimicrobials in patients with non-GABHS tonsillitis.28.29 Furthermore, immune response against P. intermedia can be detected in patients with non-GABHS tonsillitis;30 and an immune response can also be detected against P. intermedia and F. nucleatum in patients who recovered from peritonsillar cellulitis or abscesses31 and infectious mononucleosis.32
Therapy with metronidazole alleviated the symptoms of tonsillar hypertrophy and shortened the duration of fever in patients with infectious mononucleosis.28 Because metronidazole has no antiviral or aerobic antibacterial efficacy, suppression of the oral anaerobic flora may contribute to diminishing the inflammation induced by the Epstein-Barr virus. This explanation is supported by the increased recovery of P. intermedia and F. nucleatum during the acute phases of infectious mononucleosis.32 Clindamycin and metronidazole were more effective than penicillin in the therapy of patients with recurrent non-GABHS. 29
Anaerobes have been isolated from the cores of tonsils of children with recurrent GABHS 14,33,34 and non-GABHS tonsillitis. 27 Beta-lactamase-producing aerobic and anaerobic bacteria were recovered from 75% of tonsils of children with recurrent GABHS tonsillitis 13,40,41 and from 40% of those with non-GABHS tonsillitis.14,33 Similar organisms were recovered in the adenoides of patients with adenoiditis , adenoid hypertrophy, and recurrent otitis media.
Recurrent pharyngotonsillitis and penicillin failure to eradicate the GABHS can be a serious clinical problem. One explanation for penicillin failure is that repeated administrations result in selection of BLPB.14 The recovery of these bacteria in more than three quarters of the patients with recurrent GABHS tonsillitis,3,14 the ability to measure beta-lactamase activity in the core of these tonsils, and the response of patients to antimicrobials effective against BLPB (i.e., clindamycin or amoxicillin plus clavulanic acid )14,33-35support the role of these aerobic and anaerobic BLPB in the failure of penicillin to eradicate GABHS tonsillitis.
Recovery of beta-lactamse producing bacteria from tonsils
Diagnosis
Differentiation between viral and bacterial aerobic or anaerobic tonsillitis is difficult. The patients with anaerobic infection may manifest fever, malaise, and pain on swallowing. The tonsils are enlarged, and may be ulcerated. A foul-smelling discharge is frequently observed.
The classical findings of anaerobic tonsillitis are the presence of a thin white or gray film over the tonsils that can be detached to leave a superficial ulcer that bleeds. By the third or fourth day, the pseudomembrane is thick and caseous in appearance and contributes to a foul smell to the breath. With anaerobic tonsillitis enlarged submandibular lymph nodes, periadenitis, edema, and even trismus can be noted. The differential diagnosis includes GABHS infection, viral pharyngitis, diphtheria, and infectious mononucleosis.
Management
Penicillin is considered the antibiotics of choice for the therapy of GABHS tonsillitis. However, other antibiotics were found to be more effective in eradicating the infection in patients. These included lincomycin , Clindamycin , cephalosporins ( all generations) , macrolides , and amoxicillin-clavulanate .33 These agents were more effective than penicillin especially in treating patients who failed previous penicillin therapy. Treatment of tonsillitis in those who failed penicillin therapy, is aimed at the eradication of the BLPO that protect GABHS from penicillin.
The macrolides are also an alternative choice. However, their increased use has been associated with increased GABHS resistance. Clindamycin and amoxicillin-clavulante are effective against aerobic and anaerobic BLPB (except for M. cattarralis and H. influenzae by clindamycin ). They are also active against the anaerobic component of the oro-pharyngeal flora and should therefore be used in patients with recurrent or chronic tonsillitis, and those who had failed multiple therapies and are considers for elective tonsillectomy. Clindamycin has also been shown to be effective in the eradicating the GABHS carrier state. 36
Complications
These include peritonsillar abscess, bacteremia and sepsis. 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.
REFERENCES
1. Brook I, Frazier EH. Microbial dynamics of persistent purulent otitis media in children. J Pediatr. ;128:237-40. 1996.
2. Brook, I. Anthony, B.F.,Finegold, SM.: Aerobic and anaerobic bacteriology of acute otitis media in children. J. Pediatr. 92:13, 1978.
3. Brook, I. Yocum P, Shah K, Feldman B, Epstein S..: The aerobic and anaerobic bacteriological features of serous otitis media in children. Am. J. Otolaryng. 4:389, 1983.
4. Brook,
5. Brook,
6. Brook I. Management of chronic suppurative otitis media: superiority of therapy effective against anaerobic bacteria. Pediatr. Infect. Dis. J. 13:188-193, 1994.
7.Brook I, Aerobic and anaerobic bacteriology of chronic mastoiditis in children. Am J Dis Child. 135:478-9. 1981
8. R L. Wientzen, Jr, , C
9.
10. Clement, P.A.R., Bluestone, C.D., Gordts, F., et al.: Management of rhinosinusitis in children. Consensus Meeting,
11. Gwaltney, J.M., Jr., Scheld, W.M., Sande, M.A., Sydnor, A.: The microbial etiology and antimicrobial therapy of adults with acute community-acquired sinusitis: a fifteen-year experience at the
12. Brook,
13. Decker, C.F.: Sinusitis in the Immunocompromised Host Current Infectious Disease Reports, –32, 1999.
14. Nord, C.E.: The role of anaerobic bacteria in recurrent episodes of sinusitis and tonsilitis. Clin Infect Dis. 20:1512–24, 1995.
15. Brook,
16. Brook,
17. Brook,
17a. Brook I. et al. Increase in the frequency of recovery of MRSA in acute and chronic sinusitis.J Med Microbiology. 57:1015-17, 2008. 18. Sinus and Allergy Health Partnership.Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg. 2000 ;123:5-31
19. Brook,
20. Brook,
21. Brook,
22. .Niv, A., Nash, M., Peiser, J., Dagan, R., Einhorn, E., Leiberman, A., Fliss, D.M.: Outpatient management of acute mastoiditis with periosteitis in children. International Journal of Pediatric Otorhinolaryngology 46:9–13, 1998.
23. Socransky, S.S.,
24. Brook,
25. Brook,
26. Stammers, A.F.: Vincent's infection: observation and conclusions regarding the aetiology and treatment of 1017 civilian cases. Br. Dent. J. 76:147, 1944.
27. Brook,
28.
29. Brook,
31. Brook I, Foote PA, Slots J. Immune response to Fusobacterium nucleatum and Prevotella intermedia in patients with peritonsillar cellulitis and abscess. Clin infect Dis. 20:S220–S221, 1995.
33. Brook I, The role of beta-lactamase-producing bacteria in the persistence of streptococcal tonsillar infection.
Rev Infect Dis.;6:601-7. 1984.
34. Brook,
J Antimicrob Chemother.;24:227-33. 1989.
36. Tanz, R.R., et al.: Penicillin plus rifampin eradicate pharyngeal carrier of Group A streptococci. J. Pediatr. 106:876, 1985.
|