Bacteriology of chronic otitis media with effusion

1989 ◽  
Vol 103 (4) ◽  
pp. 369-371 ◽  
Author(s):  
C. Diamond ◽  
P. R. Sisson ◽  
A. M. Kearns ◽  
H. R. Ingham

AbstractSamples of middle ear effusions from 102 children with serous and mucoid otitis media were cultured for mycoplasmas and bacteria. No sample yielded mycoplasmas but bacteria were cultured from 48 (47 per cent). Organisms commonly regarded as pathogens were present in 25 samples (Haemophilus influenzae 17, Streptococcus pneumoniae four, other streptococci four). The only sample from which anaerobic bacteria were isolated was from a patient with cholesteatoma.

1994 ◽  
Vol 103 (5_suppl) ◽  
pp. 43-45 ◽  
Author(s):  
Steven K. Juhn ◽  
William J. Garvis ◽  
Chap T. Le ◽  
Chris J. Lees ◽  
C. S. Kim

Otitis media has a complex multifactorial pathogenesis, and the middle ear inflammatory response is typified by the accumulation of cellular and chemical mediators in middle ear effusion. However, specific biochemical and immunochemical factors that may be responsible for the severity or chronicity of otitis media have not been identified. Identification of factors involved in chronicity appears to be an essential step in the treatment and ultimate prevention of chronic otitis media. We analyzed 70 effusion samples from patients 1 to 10 years of age who had chronic otitis media with effusion for two cytokines (interleukrn-1β and tumor necrosis factor α) and total collagenase. The highest concentrations of all three inflammatory mediators were found in purulent otitis media, and concentrations were higher in younger than in older patients. Mediator concentrations were similar in samples obtained from patients having their first myringotomy for otitis media with effusion and in those who had had multiple previous myringotomies. The multiresponse star, which incorporates several biochemical parameters in one graphic illustration, may best characterize the complex nature of middle ear inflammation.


2003 ◽  
Vol 71 (6) ◽  
pp. 3454-3462 ◽  
Author(s):  
Kevin M. Mason ◽  
Robert S. Munson ◽  
Lauren O. Bakaletz

ABSTRACT The gram-negative bacterium nontypeable Haemophilus influenzae (NTHI) is the predominant pathogen in chronic otitis media with effusion and, with Streptococcus pneumoniae and Moraxella catarrhalis, is a causative agent of acute otitis media. To identify potential virulence determinants, bacterial gene expression was monitored by differential fluorescence induction during early disease progression in one specific anatomical niche of a chinchilla model of NTHI-induced otitis media. Genomic DNA fragments from NTHI strain 86-028NP were cloned upstream of the promoterless gfpmut3 gene. NTHI strain 86-028NP served as the host for the promoter trap library. Pools of 2,000 transformants were inoculated into the left and right middle ear cavities of chinchillas. Middle ear effusions were recovered by epitympanic tap at 24 and 48 h, and clones containing promoter elements that were induced in vivo and producing green fluorescent protein were isolated by two-color fluorescence-activated cell sorting. Insert DNA was sequenced and compared to the complete genome sequence of H. influenzae strain Rd. In a screen of 16,000 clones, we have isolated 44 clones that contain unique gene fragments encoding biosynthetic enzymes, metabolic and regulatory proteins, and hypothetical proteins of unknown function. An additional eight clones contain gene fragments unique to our NTHI isolate. Using quantitative reverse transcription-PCR, we have confirmed that 26 clones demonstrated increased gene expression in vivo relative to expression in vitro. These data provide insight into the response of NTHI bacteria as they sense and respond to the middle ear microenvironment during early events of otitis media.


1976 ◽  
Vol 85 (2_suppl) ◽  
pp. 145-151 ◽  
Author(s):  
Raymond W. Lang ◽  
David J. Lim ◽  
Yea S. Liu ◽  
Herbert G. Birck

Analyses of effusions and sera from patients with otitis media with effusion demonstrated local production in the middle ear of lysozyme, IgA and IgG. The effusion IgM was markedly elevated in some patients, also indicating local production. Complement C3 with rare exception was significantly lower in effusions than sera, suggesting utilization of complement in the middle ear, perhaps in conjunction with antibodies. The presence of high levels of lysozyme and immunoglobulins in effusions correlates with the low isolation rate of microorganisms in culture and may influence survival of organisms in the middle ear.


1994 ◽  
Vol 103 (5_suppl) ◽  
pp. 15-19 ◽  
Author(s):  
Joel M. Bernstein ◽  
William J. Doyle

A pathophysiologic model of otitis media with effusion secondary to IgE-mediated hypersensitivity is described. Specific mediators of inflammation are released by mucosal mast cells in the nasal mucosa following the interaction of antigen and specific IgE antibody. These mediators increase vascular permeability, mucosal blood flow, and, most important, mucus production. Furthermore, accessory cell types are recruited by colony-stimulating factors that in turn provide an autocrine-positive feedback for the influx of further inflammatory cells. The eustachian tube is then effectively obstructed by both intrinsic venous engorgement and extrinsic mucus plugs, isolating the middle ear space from the ambient environment The net result is the increased exchange of nitrogen into the middle ear mucosa from the middle ear cavity. This causes the development of a significant middle ear underpressure that disrupts tight junctions and allows for transudation of fluids into the middle ear space. The prolonged obstruction of the eustachian tube with mucus results in middle ear inflammation, mucosal metaplasia, and increased glandular activities, all of which are hallmarks of chronic otitis media with effusion.


1982 ◽  
Vol 90 (6) ◽  
pp. 837-843 ◽  
Author(s):  
Joel M. Bernstein ◽  
Diane Dryja ◽  
Erwin Neter

Twenty-eight middle ear effusions from 27 patients with chronic otitis media with effusion were studied for the presence of bacteria. The most common isolates were coagulase-negative staphylococci. However, biochemical and antibiotic sensitivity patterns demonstrated that these organisms represented a heterogenous group. At least three subtypes of coagulase-negative staphylococci were identified from the middle ear effusions, and in only one instance was the isolate from the ear canal identical with that of the middle ear effusion. The data presented suggest that coagulase-negative staphylococci from the middle ear effusions may not be contaminants; however, it cannot be determined from this study whether these organisms play a role as pathogens or as the result of indolent colonization.


2016 ◽  
Vol 273 (11) ◽  
pp. 3553-3560 ◽  
Author(s):  
Helen Van Hoecke ◽  
Ann-Sophie De Paepe ◽  
Edward Lambert ◽  
Jonas D Van Belleghem ◽  
Piet Cools ◽  
...  

1978 ◽  
Vol 87 (2) ◽  
pp. 197-201 ◽  
Author(s):  
Daniel M. Lewis ◽  
James L. Schram ◽  
Herbert G. Birck ◽  
David J. Lim ◽  
Gerald Gleich

To investigate the possible role of allergy in otitis media with effusion (OME), the immunoglobulin E (IgE) content of 138 middle ear effusions (MEE) and paired serum samples from patients with chronic otitis media with effusion was determined. The initial 62 paired specimens were assayed for IgE by the radioimmunosorbent test (RIST), while the later 76 paired specimens were assayed for IgE by the paper radioimmunosorbent test (PRIST). When the results obtained by these two techniques were compared, it was noted that the PRIST procedure gave significantly lower IgE values for effusions than the RIST method. When the effusion-to-serum ratios (E/S ratios) were computed from the PRIST data, the E/S ratio was less than one, while RIST data gave an E/S ratio greater than one. The results obtained with the PRIST procedure were confirmed by double antibody radioimmunoassay for IgE. Thus, the PRIST procedure appears to measure the IgE content of MEE more accurately, and the results obtained by this procedure fail to support the concept of allergy as a major causative factor in OME.


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