Pathogens and acute respiratory distress syndrome
Dear editor: Acute respiratory distress syndrome (ARDS), represented mainly by the common cold, pharyngitis, nasopharyngitis, pharyngotonsillitis, laringitis, otitis media, sinusitis, bronchitis, bronchopneumonia, and pneumonia,1 is the most common reason for seeking medical attention and the fourth cause of mortality in Mexico.2 The principal agents associated with this syndrome are viral;3 however, bacterial agents are associated with increased mortality, and the most common microorganisms are Streptococcus pneumoniae, Haemophillus influenzae, Moraxella catarrhalis and Streptococcus pyogenes.4 In our community there is an increase in failures of common treatments, presumably provoked by an increase in resistant microorganisms or by the presence of uncommon ones.
In order to determine the pathogens most frequently associated with ARDS, their prevalence, and resistance patterns to common antimicrobials, we conducted a clinical survey of 194 students with acute respiratory infection who had not previously received treatment. The students were selected from five high schools belonging to the Universidad Autónoma del Estado de México (UAEM). A clinical diagnosis and appropriate bacteriological culture from the affected sites was conducted for each case.
The clinical distribution of ARDS was: pharyngitis (60.8%), pharyngotonsillitis (34.5%), nasopharyngitis (4.1%) and rynitis (0.5%). The agents associated with these were; S. pyogenes (23%), M. catarrhalis (55.1%) and S. aureus (49.4%). In addition, no bacterial pathogen could be isolated in 27 of the cultures. A high bacterial resistance to common antimicrobials was found: S. pyogenes showed a resistance pattern to pefloxacine (86.7%) and trimethoprim-sulfamethoxazole (51.1%), whereas the resistance of M. catarrhalis to ampicilin, trimethoprim-sulfamethoxazole, and carbenicillin was higher than 60% and lower than 21% to gentamicyn, metilmicin, and nitrofurantoin. The microbial resistance of S. aureus to cefotaxime, ampicillin, penicillin, dicloxacin, and cefatazidime was higher than 80% and lower than 21% for trimethoprim-sulfamethoxazole, gentamicyn, cefalotine, and erytromicin. Strains S. pyogenes producing b-lactamase were not found.
ARDS is well recognized as a serious public health problem among specific age groups.4, 5 Free access to antibiotics and self-medication in most cases, regardless of etiology,6 have favored an increase in the rate of bacterial resistance in the three most common pathogens: S. pneumoniae, H. influenzae and M. catarrhalis.7 It has been suggested that the use of microbiologic tests, such as cultures of the affected sites, can improve diagnostic and therapeutic accuracy and avoid the emergence of resistant strains.8
S. pyogenes was the most common pathogen isolated in a single form; however, the indentification of M. catarrhalis in all clinical diagnoses, with the exception of nasopharyngitis, was not expected in this population. Currently, it is accepted that M. catarrhalis is the third most common pathogen agent in children9 and in adults with immunologic compromise9 or chronic obstructive pulmonary disease.10 Its role as an etiology agent in healthy adolescents, however, has not been reported.11 Only a low prevalence rate in carriers of M. catarrhalis has been reported in this age group.11-13
]]> This finding merits some consideration. First, the current rate in carriers of M. catarrhalis must be established in this age group, and specifically, in those who present with ARDS, in order to discard its pathogenic role. Second, even though the rates of colonization were naturally elevated and not associated with disease, M. catharralis is associated with a high betalactamase production index. This can favor the persistence of strains sensitive to betalactamic antibiotics through a synergetic effect with non-producing strains (as is the case for S. pyogenes), 14 prolong the clinical course of the disease, and force a change in the selection of the antibiotic in order to avoid the appearance of resistant strains.The study had some limitations. We were not able to dismiss an etiologic role of M. catarrhalis because all subjects were symptomatic. Although we were not able to test the production of the BRO15 b-lactamase enzyme by M. catarrhalis, it was the second pathogen most commonly isolated. We also cannot dismiss the role of those pathogens previously described as commensals in the etiology of ARDS. This needs further investigation. Recently, S. aureus has been recognized as an invasive pathogen of the upper tract respiratory16 and also has been documented in the familiar transmission of disase17 and as a responible of recurrent disease for drug resistant.18
The most important fact in this study was the high resistance of S. pyogenes to trimethroprim-sulfamethoxazole, which explains the high degree of failure of antibiotic treatment in our community. Cultures and office visits, despite the costs, should be considered as a strategy before the use of antibiotics.
María del Socorro Camarillo-Romero.
Laboratorio de Análisis Bioquímico Clínicos.
Centro de Investigación en Ciencias Médicas.
Universidad Autónoma del Estado de México.
Jesús Carranza 200, Colonia Universidad.
CP 50130, Toluca, Estado de México, México. ]]>
Teléfono y Fax: 01-722-219-4122.
Email: sococamarillo@yahoo.es
Aurora Maravilla.II
Eneida Camarillo Romero.I
Juan O. Talavera.I,III
Gerardo Huitrón-Bravo.I
ILaboratorio de Análisis Bioquímico Clínicos. Centro
de Investigación en Ciencias Médicas. Universidad
Autónoma del Estado de México.
IICoordinación de Investigación y Estudios ]]>
de Postgrado Facultad de Medicina. Universidad
Autónoma del Estado de México.
IIIUnidad de Investigación Médica en Epidemiología
Clínica, Hospital de Especialidades
Centro Médico Nacional Siglo XXI, IMSS.
References
1. Solórzano-Santos F, Miranda Novales G. Resistencia de las bacterias respiratorias y entéricas a antibióticos. Salud Publica Mex 1998;6:510-516.
2. Sistema Nacional de Evaluación - Tercera vigilancia de los progresos en la aplicación de estrategias de salud para todos en el año 2000, SPT/2000- México, DF: INEGI/DGEIE, 1994.
3. Avila MM, Carballal G, Rovaletti H, Ebekian B, Cusminsky MM, Weissenbacher M. Viral etiology in acute lower respiratory infections in children from a closed community. Am Rev Resp Dis 1989;140:634-637.
]]> 4. Fenddrick AM, Saint S, Brook I, Jacobs MR, Pelton S, Sethi S. Diagnosis and treatment of upper respiratory tract infections in the primary care setting. Clin Ther 2001;10:1683-1706.5. Lavoie F, Blais L, Castilloux AM, Saclera A, LeLorier J. Effectiveness and cost-effectiveness of antibiotic treatments for community acquired pneumonia (CAP) and acute exacerbations of chronic bronchitis (AECB). Can J Clin Pharmacol 2005;2:e212-e217.
6. Stratchounski LS, Andreeva IV, Ratchina SA, Galkin DV, Petrotchenkova Na, Demin AA, et al. The inventory of antibiotics in Russian home medicine cabinets. HYPERLINK "javascript:AL_get(this, 'jour', 'Clin Infect Dis.');" Clin Infect Dis 2003;37(4):498-505.
7. Doern GV, Jones RN, Pfaller MA, Kugler K. and The sentry Participants Group. Haemophilus influenzae and Moraxella catarrhalis from patients with community-acquired respiratory tract infections: antimicrobial susceptibility patterns from the SENTRY antimicrobial surveillance program (United States and Canada, 1997) Antimicrob. Agents Chemother 1999;2:385-389.
8. Gunnarsson RK, Holm SE, Söderström M. The prevalence of potentially pathogenic bacteria in nasopharyngeal samples from individuals with a long standing cough-clinical value of nasopharyngeal sample. Family Practice 2000;2:150-155.
9. Murphy TF. Branhamella catarrhalis: epidemiology, surface antigenic structure, and inmune response. Microbiol Rev 1996;2:267-279.
10. Carr B, Walsh JB, Coakley D, Mulvihill E, Keane C. Prospective hospital study of community acquired lower respiratory tract infection in the elderly. Respiratory Medicine 1991;85:185-187.
11. García Rodríguez JA, Fresnadillo Martinez MJ. Dynamics of nasopharyngeal colonization by potencial respiratory pathogens. J Antimicrob Chemother 2002;(Suppl 2):S59-S73.
12. Chi DH, Hendley JO, French P, Arango P, Hayden FG, Winther B. Nasopharingeal reservoir of Bacterial Otitis media and sinusitis pathogens in adults during wellness and viral respiratory illness. Am J Rhinol 2003;4:209-214.
13. Leaños-Miranda B, Miranda-Novales MG, Solórzano-Santos F, Ortiz-Ocampo L, Guiscafré-Gallardo H. Prevalencia de colonización por Moraxella catarrhalis en portadores asintomáticos menores de seis años. Salud Publica Mex 2002;43:27-31.
]]> 14. Hol C, Van Dijke EE, Verduin CM, Verhoef J, Van Dijk H. Experimental evidence for Moraxella –induced penicillin neutralization in pneumococcal pneumonia. J Infect Dis 1994;170:1613-1616.15. Schmitz FJ, Beeck A, Perdikouli M, Boos M, Mayer S, Scheuring S, et al. Production of BRO lactamases and resistance to complement in European Moraxella catarrhalis isolates J Clin Microbiol 2002;4:1546-1548.
16. Andrade MA, Hoberman A, Glustein J, Paradise JL, Wakd ER. Acute otitis media in children with bronchitis. Pediatrics 1998;101 (4 Pt 1):617-619.
17. Gross-Schulman S, Dassey D, Mascola l, Anaya C. Community-acquired methicilinn-resistant Staphylococcus aureus. JAMA 1998;280:421-422.
18. Nyquist AC, Gonzales R, Steiner JF, Sande MA. Antibiotic prescribing for children with colds, upper respiratory tract infections and bronchitis. JAMA 1998;279:875-877.
]]>