Tonsillitis

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Tonsillitis is inflammation of the tonsils most commonly caused by a viral or bacterial infection. Symptoms of tonsillitis include sore throat and fever. While no treatment has been found to shorten the duration of viral tonsillitis, bacterial causes such as streptococcal pharyngitis are treatable with antibiotics. It usually takes one to three weeks to recover.

[edit]Symptoms
Common symptoms of tonsillitis include:[1][2][3][4]

red and/or swollen tonsils white or yellow patches on the tonsils tender, stiff, and/or swollen neck swollen lymph nodes sore throat cough headache sore eyes body aches earache fever chills nasal congestions ulceration

In cases of acute tonsillitis, the surface of the tonsil may be bright red and with visible white areas or streaks of pus.[5] Tonsilloliths occur in up to 10% of the population frequently due to episodes of tonsillitis.[6]

[edit]Causes
The most common causes of tonsillitis are adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus.[1][2][3][4] It can also be caused by Epstein-Barr virus, herpes simplex virus,cytomegalovirus, or HIV.[1][2][3][4] The second most common causes are bacterial. The most common bacterial cause is Group A hemolytic streptococcus (GABHS), which causes strep throat.[1][2][3][4] Less common bacterial causes include: Staphylococcus aureus ( including methicillin resistant Staphylococcus aureus or MRSA

),[7]Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, pertussis, Fusobacterium, diphtheria, syphilis, and gonorrhea.[1][2][3][4] A concomitant GABHS and influenza A virus pharyngotonsillitis can occur, as was evident by an increased in the ASO and anti-DNase B titers in a third of the patients who had both of these organisms isolated.[8] Anaerobic bacteria have been implicated in tonsillitis. These include pigmented Prevotella and Porphyromonas, Fusobacterium and Actinomyces spp. The possible role of anaerobes in the acute inflammatory process in the tonsils is supported by several clinical and scientific observations: anaerobes have been isolated from the cores of tonsils of children and adults with recurrent GABHSand non streptococcal tonsillitis, and peritonsillar and retropharyngeal abscesses in many cases without any aerobic bacteria, their recovery as pathogens in well-established anaerobic infectionsof the tonsils (Vincent's angina), the increased recovery rate of encapsulated pigmented Prevotella and Porphyromonas spp. in acutely inflamed tonsils, and the response to antibiotics in patients with non streptococcal tonsillitis.[9] Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils.[10][11] Within the tonsils, white blood cells of the immune system mount an attack that helps destroy the viruses or bacteria, and also causes inflammation and fever.[10][11] The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.[12] This is the area in the back of the throat that lies between the voice box and the tonsils. Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in this case called Vincent's angina or Plaut-Vincent angina.[13]

[edit]Laboratory

tests

The diagnosis of GABHS tonsillitis can be confirmed by culture. Samples are obtained by swabbing both tonsillar surfaces and the posterior pharyngeal wall are plated on sheep blood agar medium. The isolation rate can be increased by incubating the cultures under anaerobic conditions and using selective media. A single throat culture has a sensitivity of 90%-95% for the detection of GABHS. False-negative results are possible if the patient received antibiotics. The identification of GABHS requires 24 to 48 hours. The use of bacitracin disc provides presumptive identification. Attempts to identify beta hemolytic streptococci other than group A may be important in adults. Commercial kits containing group-specific antisera are available. Rapid methods for GABHS detection (1060 minutes), are available. Older antigen tests detect the surface Lancefield group A carbohydrate. Newer tests identify GABHS serotypes using nucleic acid (DNA) probes or polymerase chain reaction. Rapid detection kits have a sensitivity of 85 to 90. Bacterial culture should be performed in cases of a negative rapid streptococcal test.[14] True infection with GABHS, rather than colonization, is defined as the presence of >10 colonies of GABHS per blood agar plate. However, this method is difficult to implement because of the overlap between carriers and

infected patients. An increase in antistreptolysin O (ASO) streptococcal antibody titer 36 weeks following the acute infection can provide retrospective evidence of GABHS infection. [15] ASO titers are considered definitive proof of GABHS infection. When GAHBS is not isolated, the clinician should seek other potential pathogens. However, many of these organisms are part of the normal flora residing in the pharynx, making interpretation of the results difficult. A finding of a membrane in the throat should prompt a search for corynebacteria. Culture should be obtained from beneath the membrane, and use of a special moisture-reducing transport medium is necessary. The material may be inoculated on a Loeffler slant, tellurite plate, or blood agar plate. Identification by fluorescent antibody technique is also possible.Viral cultures are available, as well as rapid tests for some viruses (e.g., respiratory syncytial viruses). A heterophile slide test or other rapid test for infectious mononucleosis can provide a specific diagnosis.

[edit]Treatment
Treatments to reduce the discomfort from tonsillitis symptoms include:[1][2][3][4][12][16][17]

pain relief, anti-inflammatory, fever reducing medications (acetaminophen/paracetamol and/or ibuprofen) sore throat relief (warm salt water gargle, lozenges, and warm liquids)

If the tonsillitis is caused by group A streptococus, then antibiotics are useful with penicillin or amoxicillin being first line.[18] Cephalosporins and macrolides are considered good alternatives to penicillin in the acute setting.[19] A macrolide such as erythromycin is used for people allergic to penicillin. Individuals who fail penicillin therapy may respond to treatment effective against beta-lactamase producing bacteria[20] such as clindamycin or amoxicillin-clavulanate. Aerobic and anaerobic beta lactamase producing bacteria that reside in the tonsillar tissues can "shield" group A streptococcus from penicillins.[21] When tonsillitis is caused by a virus, the length of illness depends on which virus is involved. Usually, a complete recovery is made within one week; however, symptoms may last for up to two weeks. Chronic cases may be treated with tonsillectomy (surgical removal of tonsils) as a choice for treatment.[22]

[edit]Causes

of penicillin failure in the treatment of GABHS tonsillitis

Despite its excellence in vitro efficacy, the frequently reported inability of penicillin to eradicate GABHS from patients with acute and relapsing tonsillitis is a cause for concern. Over the past 50 years, the rate of penicillin failure has consistently increased from about 7% in 1950 to almost 40% in 2000.[23] There are several explanations for the failure of penicillin to eradicate GABHS tonsillitis (Table 1). One explanation is the poor penetration of penicillin into the tonsillar tissues as well as into the epithelial cells.[24] Other explanations relate to the bacterial interactions between GABHS and the other members of the pharyngo-tonsillar bacterial flora. It is hypothesized that the enzyme beta-lactamase which is secreted by beta-

lactamase-producing aerobic and anaerobic bacteria, that colonize the pharynx and tonsils, may shield GABHS from penicillins.[25] These organisms include S. aureus, Haemophillus influenzae, and Prevotella, Porphyromonas and Fusobacterium spp.,[26] A recent increase was noted in the recovery of MRSA which was isolated from 16% of tonsils, making it more difficult to eradicate this and other beta-lactamase producing organisms.[27] Another possibility is the coaggregation between Moraxella catarrhalis and GABHS, which can facilitate colonization by GABHS.[28] Normal bacterial flora can interfere with the growth of GABHS,[29][30] and the absence of such competitive bacteria makes it easier for GABHS to colonize and invade the pharyngo-tonsillar area.[31] GABHS can also be reacquired from a contact or an object (i.e., toothbrush or dental braces)[32] Table 1. Causes of Antibiotics Failure in Therapy of GABHS Tonsillitis

The presence of beta-lactamaseproducing organisms that protect GABHS from penicillins[33] Coaggregation between GABHS and M. catarrhalis[28] Absence of members of the oral bacterial flora capable of interfering with the growth of GABHS (through production of bacteriocins and/or competition on nutrients)[29][30]

Poor penetration of penicillin into the tonsillar cells and tonsillar surface fluid ( allowing intracellular survival of GABHS)[24]

Resistance (i.e., erythromycin) or tolerance (i.e., penicillin) to the antibiotic used Inappropriate dose, duration of therapy, or choice of antibiotic Poor compliance Reacquisition of GABHS from a contact or an object (i.e., toothbrush or dental braces)[34] Carrier state, not disease[35]

[edit]Implications

of microbial interactions on therapy

Penicillin is recommended by some guidelines as the antibiotic of choice,[36] although other antibiotics are more effective in the bacteriologic and clinical cure of acute and recurrent GABHS tonsillitis.[37][38][39][40][41] Lincomycin, clindamycin, and amoxicillin-clavulanate are more effective in relapsing GABHS tonsillitis.[37][42][43] Cephalosporins are superior to penicillins in both acute and relapsing GABHS tonsillitis.[44][45] In those who failed penicillin, the goal of therapy is to eradicate the beta-lactamase-producing bacteria that "shield" GABHS from penicillin, while preserving whatever "protective" interfering organisms (i.e., alpha hemolytic streptococci) that may colonize the tonsils. Cephalosporins have been successful in eradicating GABHS better,[46] and in some instances even faster[47] than penicillins. Their efficacy is explained by their activity against beat-lactamse producing aerobic bacteria, and sparing of interfering organisms.[48] Over 35 randomized studies had demonstrated cephalosporins of all generations to have a much higher success rate in eradicating GABHS than penicillin (a third of the failure rate of penicillin),[46] and 12 studies found equal or better success rate in 5 to 7 days of therapy as compared with 10 days of penicillin.[49][50]

[edit]Complications
Complications may rarely include dehydration and kidney failure due to difficulty swallowing, blocked airways due to inflammation, and pharyngitis due to the spread of infection.[1][2][3][4][12] An abscess may develop lateral to the tonsil during an infection, typically several days after the onset of tonsillitis. This is termed a peritonsillar abscess (or quinsy). Rarely, the infection may spread beyond the tonsil resulting in inflammation and infection of the internal jugular vein giving rise to a spreading septicaemia infection (Lemierre's syndrome). In chronic/recurrent cases (generally defined as seven episodes of tonsillitis in the preceding year, five episodes in each of the preceding two years or three episodes in each of the preceding three years),[51][52][53] or in acute cases where the palatine tonsils become so swollen that swallowing is impaired, a tonsillectomy can be performed to remove the tonsils. Patients whose tonsils have been removed are still protected from infection by the rest of their immune system. In very rare cases of strep throat, diseases like rheumatic fever[54] or glomerulonephritis[55] can occur. These complications are extremely rare in developed nations but remain a significant problem in poorer nations.[56][57] Tonsillitis associated with strep throat, if untreated, is hypothesized to lead to pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).[58]