Purulent Sinusitis can be caused when the ciliary clearancemechanism of the sinus is decreased, or by means of an obstructed ostium. As aresult, secretions are retained, sinus pressure is reduced to negative, alongwith a decrease in oxygen partial pressure as well. Sinus blockage and ciliarydysfunction are aggravated by allergic, non-allergic and/or viral attacks thatproduce an inflammatory response in the mucosa of the nasal- and sinuscavities, which produces an environment suitable for the growth of pathogens.Predisposing conditions such as cystic fibrosis, ciliarydyskinesia, allergic inflammation, immuno-compromisation and ostiomeatalobstruction (due to drug addiction and nasal polyps) should be seriouslyconsidered in those patients suffering from persistent or recurrent sinusitis.1 Acute viral rhinosinusitisThe majority of rhinosinusitis cases/episodes are caused byviral pathogens, the most common being Rhinovirus, along with Influenza andParainfluenza viruses, presenting in 3-15% of acute sinusitis cases. Otherviruses include Corona virus, Respiratory Syncytial virus, Adenovirus andenterovirus of which 0.5-2% can progress to acute bacterial sinusitis 2,3.
Of all other risk factors, Viral infections of the upperairway appear to be the most prevailing factor predisposing individuals to acutebacterial sinusitis. Of these patients, approximately 90% will present withsinus involvement, but a mere 5-10% of these individuals will have a bacterialsuperinfection. (4,5) Acute bacterial rhinosinusitisThere is a strong correlation between acute bacterialrhinosinusitis and upper respiratory tract infection.
The following factorscontribute to impaired mucocilliary clearance and bacterial infection: · Allergy · Trauma· Neoplasms· Granulomatous and inflammatory diseases· Midline destructive disease· Environmental factors· Dental infection· Anatomic variation S aureus, S Pneumoniaand H Influenza are the most common pathogenscontributing to sinusitis. After receiving the 7-valent pneumococcal vaccineintroduced in the year 2000, Paediatric cases infected with S Pneumonia in the United States, experienceda decline in recovery rate, but those infected with H Influenza experienced anincrease in recovery rate. 6,7 S pneumoniae penicillin-resistant strains’rate of recovery was different after vaccination.
P aeruginosa(amongst other gram-negative rods) have been observedin acute sinusitis of nosocomial origin. Patients with nasogastric- and/orcatheters in situ; immunocompromised persons; patients with HIV infection, andthose with cystic fibrosis were all frequent hosts of P aeruginosa. Sinus aspirates have produced proof that 66% of patientsdiagnosed with acute sinusitis are infected with at least one pathogenic bacterialspecies, while 26-30% show multiple predominant bacterial species. Normal floraare the bacteria most commonly involved in acute sinusitis and can become sinuspathogens when sneezing, coughing and/or direct invasion deposit thesepathogens into the sinuses, if conditions optimize their growth.
Streptococcuspneumoniae, Haemophilus influenzae and Moraxella catarrhalis are the predominate pathogens cultured from maxillarysinus aspirates. Streptococcus pyogenes,Staphylococcus aureus and anaerobes are found in less than 10% of patientswith acute bacterial sinusitis, despite the sufficient environment availablefor their growth. In Chronic Sinusitis, and sinusitis resulting from dental sources,anaerobic organisms were frequently isolated. S Pneumonia is a gram-positive, catalase-negative,facultative anaerobic cocci. Almost to 20- 43 % of acute bacterialrhinosinusitis episodes in adults result from this pathogen which is proving tobecome increasingly resistant to various antibiotics including penicillin. Intermediatepenicillin-resistance to Macrolides, Clindamycin, Trimethoprim-Sulfamethoxazoleand Doxycycline, than the complete penicillin resistant counter-part 8.
In the past, H Influenza type B(gram-negative facultativeanaerobic bacilli ) was one of the leading causes of meningitis, but this allchanged after the vaccine became extensively administered. Non-typeable strainsof H influenzae have found to be the cause of 22-35% of acute bacterialrhinosinusitis cases amongst adults. It develops antimicrobial resistance bymeans of Beta-lactamase production. Aspirates from the paranasal sinuses showedthat 32.7% of these patients, were infected with beta-lactamase–positive for Hinfluenza; other reports suggest a rate of 44%. M catarrhalis; a gram-negative, oxidase-positive, aerobicdiplococci; is responsible for 2-10% of acute bacterial rhinosinusitis cases inadults. It is yet another organism utilising Beta-lactamase production as themechanism of antimicrobial resistance.
Isolates from the paranasal sinusrevealed 98% to be beta-lactamase–positive for M catarrhalis. S aureus accounts for 10% of episodes of acute bacterialrhinosinusitis, and is now acknowledged to be an increasingly common pathogenin acute bacterial rhinosinusitis. 9 While methicillin-resistant S aureus(MRSA) still represents only a fraction of episodes of S aureus rhinosinusitis,increasing occurrences drug-resistant S aureus may alter future pharmacologicalrecommendations. 10 Gram-negative organisms are the leading cause in nosocomialsinusitis and include Pseudomonasaeruginosa (15.9%), Escherichia coli(7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species. They account for60% of cases.
Polymicrobial infection is observed in 25-100% of cultures. Otherpathogenic organisms found in nosocomial patients are gram-positive organisms(31%) and fungi (8.5%).10Acute invasive fungal rhinosinusitisOn the rare occasion, sinusitis is caused by fungalinfections. Fungal sinusitis (eg, allergic fungal sinusitis) may appear like alower airway disorder and allergic bronchopulmonary aspergillosis. Fungal agents associated with sinusitis include Aspergillus and Alternaria species. Bipolarisand Curvularia species are the mostcommon fungi seen in allergic fungal sinusitis, accounting respectively for 60%and 20% in most studies. CHRONICSINUSITIS(CRS)The etiological studies of sinusitis are gradually movingtowards focussing on ostiomeatal obstruction; allergies, polyps; occult- andsubtle immunodeficiency states; as well as dental diseases.
Microorganisms aremore often recognized as secondary invaders during Chronic RhinosinutitusBacterial involvementBacterial involvementThe bacteria involved in CRS are not the same as those involvedin acute rhinosinusitis. The following bacteria have been observed in samplesobtained via endoscopy and/or sinus puncture in those individuals with chronicsinusitis:• Staphylococcusaureus (both methicillin-susceptible S aureus MSSA and methicillin-resistantS aureus MRSA strains) 11• Coagulase-negativestaphylococci• Hinfluenzae• Mcatarrhalis• Spneumoniae• Streptococcusintermedius• Pseudomonasaeruginosa• Nocardiaspecies• Anaerobicbacteria ( Peptostreptococcus, Prevotella, Porphyromonas, Bacteroides,Fusobacterium species 12 ) The exact roles of these microbes in the aetiology ofchronic sinusitis is uncertain, as opposed to their well-defined role in AcuteRhinosinusitis. Various researchersdisagree on the microbial etiology of chronic sinusitis and much of the debatehas to do with varying research methodology. Studies that have used appropriatemethods for recovery of anaerobes have demonstrated their prominence in chronicsinusitis (50-70%), while many studies that utilised other techniques, failedto isolate them. 13 The variety growth of microbes in samples can also be attributedto patients’ previous exposure to various broad-spectrum antibiotics. During a study,Jyonouchi et al inoculated BacteriodesFragilis in rabbits by means of intra-sinus inoculation, therebysuccessfully inducing Chronic sinusitis.
Following the experiment, Immunoglobulin(IgG)was then identified againstB.Fragilis organism in the infected animals. 14 IgG antibodies to other anaerobicorganisms have been isolated in human cases of chronic sinusitis as well15, therebyreinforcing the suspected role of anaerobes in chronic sinusitis. In most cases, CRS patients present with 1-6 differentpathogens per specimen, thereby confirming the condition as a result of mostlypolymicrobial infection12. Antibiotic administration; past vaccinations; and normalflora suppressing the emergence of pathogenic species all influence themicrobial findings of chronic sinusitis. In some cases, acute exacerbation of chronic sinusitis isoften caused by polymicrobial infections, with the predominant pathogens beinganaerobic bacteria.
Aerobic bacteria usually associated with acute sinusitis(eg, S pneumoniae, H influenzae,M catarrhalis) may emerge at a later stage ofthe still emerge. 16Gram-negative facultative and aerobic bacteria, such as Paeruginosa, are mostly found in isolated post-endoscopic sinus surgery. 17Fungal involvementThe following fungal pathogens have been reported in samplesobtained by means of endoscopy or sinus puncture in patients with chronicsinusitis 18 :· Aspergillusspecies· Cryptococcusneoformans· Candidaspecies· Sporothrixschenckii· Alternariaspecies Risk factorsThe following conditions and risk factors are predisposingelements in the development of chronic sinusitis:· Anatomic abnormalities of the ostiomeatalcomplex (eg, septal deviation, concha bullosa, deviation of uncinate process,Haller cells)· Allergic rhinitis· Aspirin sensitivity· Asthma· Nasal polyps· Nonallergic rhinitis (eg, vasomotor rhinitis,rhinitis medicamentosa, cocaine abuse)· Defects in mucociliary clearance· Nasotracheal intubation· Nasogastric intubation· Hormonal (eg, puberty, pregnancy, oralcontraception)· Obstruction by tumor· Immunologic disorders (eg, common variableimmunodeficiency, immunoglobulin A IgA deficiency, IgG subclass deficiency,AIDS)· Cystic fibrosis· Primary ciliary dyskinesia, Kartagener syndrome· Wegener granulomatosis· Repeated viral upper respiratory tractinfections· Smoking· Environmental irritants and pollutants· Gastroesophageal reflux disease (GERD). Thereflux of gastric contents may play a contributing role in some cases of CRS;this relationship still needs to be better defined· Periodontitis/significant dental disease· Systemic diseases (ie, granulomatosis withpolyangiitis (Wegener granulomatosis), Churg-Strauss vasculitis, sarcoidosis)· Yellow nail syndrome