Vitreous cultures and antibiotic analysis in Puerto Rican endophthalmitis patients.
Objective: To analyze positive vitreous cultures and their
respective antibiotic sensitivities in patients with endophthalmitis in
Methods: We conducted a retrospective cohort study of vitreous cultures from all of the patients with a clinical diagnosis of endophthalmitis at the Puerto Rico Medical Service Administration Center in San Juan, Puerto Rico, from August 2009 to July 2010. Positive isolates were selected for analysis. A retrospective chart review was performed to establish the mechanism involved in the development of endophthalmitis.
Results: Forty-three patients underwent vitreous cultures for a diagnosis of endophthalmitis, of which 16 patients had positive cultures. Seventy-eight percent of the isolates were bacterial and 22% fungal. Staphylococcus genus was identified in 38% of patients. All of the Staphylococcus epidermidis and Streptococcus pneumonia isolates were resistant to oxacillin; 66% of the Staphylococcus aureus isolates were also resistant to oxacillin. All of the Gram-positive isolates in our study were sensitive to vancomycin. All of the gram-negative isolates were sensitive to ceftazidime. Twenty-nine percent of the post-traumatic endophthalmitis cases were fungal in origin.
Conclusion: The majority of endophthalmitis cases in our study were bacterial in origin, and the Staphylococcus genus was the most common type of organism identified. In our cohort, post-traumatic endophthalmitis was the most common mechanism leading to infection. Vancomycin in combination with ceftazidime appears to be adequate for the empiric treatment of all cases of bacterial endophthalmitis in our population. Anti-fungal agents should be considered as adjuvant empiric treatment in patients with post-traumatic endophthalmitis. [P R Health Sci J 2011;30:198-202]
Key words: Endophthalmitis, Ocular Trauma, Antibiotic resistance
Objetivo: Analizar los cultivos positivos de humor vitreo y sus respectivas resistencias a antibioticos en pacientes con endoftalmitis en Puerto Rico. Metodos: Hicimos un estudio de corte retrospectivo de los cultivos del humor vitreo de todos los pacientes con un diagnostico clinico de endoftalmitis en el Centro de Administracion de Servicios Medicos de Puerto Rico desde agosto del 2008 hasta julio del 2010. Los cultivos positivos fueron seleccionados para el analisis. Los expedientes medicos fueron revisados retrospectivamente para establecer el mecanismo que condujo a la endoftalmitis. Resultados: A cuarenta y tres pacientes se les hizo un cultivo del humor vitreo. Dieciseis de estos tuvieron resultados positivos en el cultivo. De los organismos aislados, 78% fueron de origen bacteriano y 22% de origen fungal. Staphylococcus fue el genero identificado en el 38% de los pacientes. Todos los Staphylococcus epidermidis y los Streptococcus pneumoniae fueron resistentes a oxacilina; 66% de los Staphylococcus aureus fueron resistentes a oxacilina. Todos los organismos Gram positivos aislados fueron sensitivos a vancomicina. Todos los organismos Gram negativos aislados fueron sensitivos a ceftazidima. Veintinueve por ciento de los casos de endoftalmitis post-traumatica eran de origen fungal. Conclusion: La mayoria de los casos de endoftalmitis en nuestro estudio eran de origen bacteriano, y estafilococo fue el genero mas comun de organismo identificado. En nuestro corte, el mecanismo mas comun que llevo a infeccion fue endoftalmitis post-traumatica. Vancomicina y ceftazidima aparenta ser una combinacion adecuada para el tratamiento de todos los casos de endoftalmitis bacteriana en nuestra poblacion. Agentes antifungales deberian ser considerados como tratamiento empirico adyuvante en pacientes con endoftalmitis post-traumatica.
|Article Type:||Perspectiva general de la enfermedad/trastorno|
Antibioticos (Uso terapeutico)
Antibioticos (Factores de riesgo)
Enfermedades de los ojos (Analisis de casos)
Enfermedades de los ojos (Investigacion cientifica)
Enfermedades de los ojos (Cuidado y tratamiento)
del Pilar Fernandez, Maria
Villegas, Victor M.
Oliver, Armando L.
|Publication:||Name: Puerto Rico Health Sciences Journal Publisher: Universidad de Puerto Rico, Recinto de Ciencias Medicas Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 Universidad de Puerto Rico, Recinto de Ciencias Medicas ISSN: 0738-0658|
|Issue:||Date: Dec, 2011 Source Volume: 30 Source Issue: 4|
|Geographic:||Geographic Scope: Puerto Rico|
Endophthalmitis refers to inflammation inside the eye. For over a
decade, the Endophthalmitis Vitrectomy Study (EVS) has served as the
main guideline for the treatment of post-operative endophthalmitis.
Since delaying the treatment of endophthalmitis can lead to long-term
visual impairment and even the loss of an eye, an initial, empirical
treatment with broad spectrum intraocular antibiotics is imperative to
assure the best possible prognosis for the patient being treated (1).
The emergence of new antibiotics with higher degrees of penetration to
the vitreous body, such as third-generation fluoroquinolones, has led
some physicians to add these agents as oral or intravenous adjuvants for
the treatment of endophthalmitis (2-4).
The main 3 mechanisms involved in the induction of endophthalmitis are post-surgical, post-traumatic, and endogenous infection. The most likely etiology of post-cataract surgery endophthalmitis is coagulase-negative staphylococci, which in some case series can represent up to 70% of the isolates (3-4). Chronic pseudophakic endophthalmitis is usually caused by Propionibacterium acnes (5). Streptococcus viridans and Streptococcus pneumonia are the most important pathogens in post-trabeculectomy-associated endophthalmitis (6-7). Posttraumatic endophthalmitis is mainly caused by Bacillus cereus and coagulase-negative staphylococci; however, Gram-negative infections and fungal infections can also be found in as many as 7% and 6% of patients, respectively (8-10). Thirty to fifty percent of endogenous endophthalmitis cases are caused by streptococci, while Staphylococcus aureus is responsible for 25% of cases and Gram-negative bacilli for 30% of cases (11-12).
It is common practice in our community to prescribe topical antibiotics to post-operative patients with the purpose of preventing endophthalmitis. The most commonly used agents are first- and third-generation quinolones as well as aminoglycosides, with the latter being used less commonly nowadays because of the availability of quinolones (which as a class have a higher rate of intraocular penetration and are less likely to provoke retinal toxicity) (13). In the last decade, the availability of third-generation quinolones, which are more effective against Gram-positive organisms, has led some surgeons to prefer these over the older quinolones such as ofloxacin (14). In addition, some surgeons in our community use subconjunctival injections of cefazolin or gentamicin at the end of surgery as endophthalmitis prophylaxis (15-17).
This study seeks to provide a better understanding of the organisms leading to endophthalmitis in Puerto Rico. We also recognize the fact that having an increased knowledge of the antibiotic sensitivity patterns of microorganisms in our community can lead to better institutional management protocols and antibiotic prophylaxis guidelines for ophthalmologists in our community.
We conducted a retrospective cohort study of vitreous cultures from all of the patients with a clinical diagnosis of endophthalmitis at the Puerto Rico Medical Service Administration Center (ASEM) in San Juan, Puerto Rico, from August 2009 to July 2010. To do so, we accessed the database at the microbiology laboratory at ASEM and requested the results of all of the patients who had microbiological cultures from which a diagnosis of endophthalmitis was made in the aforementioned time period. Patients with negative cultures were excluded from our analysis. The records of those patients with positive isolates were selected for careful retrospective chart review and in order to analyze the results from the antibiotic susceptibility tests. According to the institution's protocol, vitreous contents were cultured in blood agar, chocolate agar, Sabouraud's agar, and thioglycollate medium. Patients were stratified according to etiology, isolate, sex, and age at presentation. We also analyzed the results from the antibiotic susceptibility tests.
Forty-three patients underwent vitreous cultures for a diagnosis of endophthalmitis at the ASEM in the 1-year period of our study. Sixteen patients (37%) had positive cultures and were included in our analysis (Table 1). There were 12 men and 4 women. The mean age was 57 years, ranging from 6 to 101 years.
Fourteen patients (88%) had a single organism, and 2 patients had 2 organisms isolated. Of the organisms isolated, 78% were bacterial and 22% fungal. Staphylococcus genus was identified in 38% of patients and was the most common type of organism identified. We were able to retrospectively establish the mechanism leading to endophthalmitis in 94% of patients; among these patients, post-traumatic endophthalmitis was identified in 47% of cases and was the most common mechanism leading to infection.
Five isolates were related to endogenous sources. The etiologic microorganisms and their respective frequencies in this group were Staphylococcus aureus, 40%, Staphylococcus epidermidis, 40%, and Pseudomonas aeruginosa, 20%.
Three isolates were related to post-cataract extraction. The etiologic microorganisms were Streptococcus pneumoniae, Streptococcus mitis, and Aspergillus fumigates.
Eight isolates were related to eye trauma. The etiologic microorganisms for this group were Staphylococcus epidermidis, Streptococcus pyogenes, diphtheroids, Pseudomonas aeruginosa, Acremonium species, Scopulariopsis and Penicillium species, and an unidentified b-hemolytic non-group A, B, or D.
There were 2 isolates from a single patient in which the etiology for the endophthalmitis was not established; these were Staphylococcus aureus and Streptococcus agalactiae.
There were 13 isolates from which antibiotic sensitivity data were obtained; all of these were bacterial in origin: 11 (85%) were Gram-positive and 2 (15%) were Gram-negative. The antibiotic sensitivity data for these patients are shown in tables 2 and 3, respectively.
Of all of the gram-positive isolates in which sensitivity data were obtained, 100% were sensitive to vancomycin and 36% were resistant to clindamycin. Isolates from the Staphylococcus genus and Streptococcus pneumonia species were tested for oxacillin sensitivity; the overall resistance to this antibiotic in all these isolates combined was 86%. All of the Staphylococcus epidermidis and Streptococcus pneumonia isolates were resistant to oxacillin; 66% of Staphylococcus aureus isolates were also resistant to oxacillin. All of the staphylococci in our study were resistant to penicillin.
Staphylococci were also tested for fluoroquinolone (levofloxacin and gatifloxacin) antibiotic sensitivity. Overall, 33% of Staphylococcus aureus and 67% of Staphylococcus epidermidis were resistant to levofloxacin. Thirty-three percent of Staphylococcus aureus had intermediate resistance to levofloxacin. The resistance patterns to levofloxacin were identical to those of gatifloxacin across all the isolates that were tested for both of these antibiotics in our study.
All of the Gram-negative organisms in our study were sensitive to cefepime, amikacin, ceftazidime, ciprofloxacin, gentamicin, imipenem, levofloxacin, and tobramycin.
There were 4 fungal isolates in our study, representing 22% of the total isolates and being present in 19% of the endophthalmitis cases in our study. No sensitivities were established for these microorganisms.
This is the first study in the literature that describes the etiology and antibiotic resistance of endophthalmitis in Puerto Rico. In our study, the most common mechanism involved in the development of endophthalmitis was ocular trauma. Previous studies have suggested cataract surgery as the primary mechanism leading to endophthalmitis in developed countries (3, 18-20, 22). It is possible that our data are biased towards traumatic endophthalmitis. ASEM is the only level 1 trauma center in Puerto Rico, and, while some of the post-operative and endogenous endophthalmitis cases in our island are managed in other hospitals or by retinologists in private practice, most of the ophthalmology trauma cases in the island are sent exclusively to our center for management. Furthermore, trauma cases might have a larger inoculum, which facilitates having a positive culture (22).
Gram-positive organisms were the most common form of isolate in our study. This finding is consistent with other studies that suggest that the most likely organisms leading to overall endophthalmitis are gram-positive microorganisms (1, 20, 22). Gram-negative organisms were the least common isolates. In the EVS, Gram-negative isolates accounted for 5.9% of cases. (22) It appears that the patients with endophthalmitis who visit our institution have a low incidence of gram-negative infections, a rate that is similar to what has been found by other research studies in the United States (22, 27).
The initial empirical antibiotic treatment regimen for endophthalmitis in our institution consists of intravitreal vancomycin (1mg/0.1cc) and ceftazidime (2.5mg/0.1cc), which, according to our results, appears to be adequate to treat bacterial infections from all of the mentioned mechanisms identified. Our data also suggest that these 2 agents may also be effective for the empirical systemic treatment of patients in whom an endogenous source is suspected.
A significant percentage of the Gram-positive isolates in our study were fluoroquinolone (27%) resistant. Miller and colleagues suggested that fourth-generation fluoroquinolones have an efficacy of less than 80% in staphylococcal infections. (21-22) Concern exists about the emerging resistance of gram-positive isolates to third- and fourth-generation fluoroquinolones because of their common prophylactic use before and after intraocular surgery (23-26). For these reasons, we advise against the adjuvant use of topical, oral, or intravitreal fluoroquinolones in patients with established post-operative endophthalmitis who have received proper intraocular broadspectrum antibiotic coverage.
In our study 31% of the isolates were related to an endogenous source. In these patients, only infections by staphylococcal species and Pseudomonas species were isolated. Eighty percent of isolates were from the staphylococcal species. In the North American and European populations, streptococci account for 30-50% of endogenous endophthalmitis cases; Staphylococcus aureus causes 25% of cases and Gram-negative bacilli account for 30% of cases (11, 28). In Asia, Gram-negative bacilli, especially Klebsiella and Escherichia coli, cause the majority of cases of endogenous endophthalmitis (12, 29). Our study was too small to obtain a representative cohort of endogenous endophthalmitis cases in Puerto Rico.
Post-traumatic infection was the most common mechanism leading to endophthalmitis in our study. Results in our population are similar to the results of other studies done in the United States in which the organisms causing posttraumatic endophthalmitis include streptococci, Gramnegative bacilli such as Klebsiella and Pseudomona, molds, and coagulase-negative staphylococci (9-10). In our institution, because a significant proportion of cases with traumatic endophthalmitis appear to have fungal isolates, we recommend that patients in Puerto Rico with traumatic endophthalmitis be managed prophylactically with intravitreal and systemic antifungal therapy.
Fungal isolates in our study account for 17% of cases; of these, 66% were caused by post-traumatic endophthalmitis, and 33% were caused by post-cataract surgery endophthalmitis. In some countries with tropical climates such as ours, up to 50% of central corneal ulcers are caused by fungi (30-33). Exogenous fungal infections of the eye are of a particular concern mainly because of the increasing prevalence of contact-lens users (34). The tropical climate of our island also predisposes individuals to an increased annual incidence of fungal infection. Previous studies have revealed that when exogenous fungal endophthalmitis occurs, it is mostly caused by molds (mainly Fusarium and Aspergillus species) (34). Unsurprisingly then, in our study all of the fungal isolates were molds.
As in all retrospective studies, the data in this study must be interpreted with caution. A referral bias may exist because the cases forming the basis for our study came exclusively from the only trauma center in Puerto Rico. Infections caused by certain difficult-to-culture organisms (requiring methods, such as polymerase chain reaction, that were unavailable) may have gone unidentified, possibly leading to ascertainment bias. Other important limitations include the small sample size and the lack of historical population data. Further studies may allow us to obtain a broader picture of intraocular infections in Puerto Rico and help us detect changes in antibiotic resistance patterns over time.
(1.) Callegan MC, Gilmore MS, Gregory M, et al. Bacterial endophthalmitis: therapeutic challenges and host-pathogen interactions. Prog Retin Eye Res 2007;26:189-203.
(2.) Jensen MK, Fiscella RG, Moshirfar M, et al. Third- and fourth-generation fluoroquinolones: retrospective comparison of endophthalmitis after cataract surgery performed over 10 years. J Cataract Refract Surg 2008;34:1460-1467.
(3.) Speaker MG, Milch FA, Shah MK, et al. Role of external bacterial flora in the pathogenesis of acute postoperative endophthalmitis. Ophthalmology 1991;98:639-649.
(4.) Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol 1996;122:1-17.
(5.) Piest KL, Kincaid MC, Tetz MR, et al. Localized endophthalmitis: A newly described cause of the so-called toxic lens syndrome. J Cataract Refract Surg 1987;13:498-510.
(6.) Ciulla TA, Beck AD, Topping TM, Baker AS. Blebitis, early endophthalmitis, and late endophthalmitis after glaucoma-filtering surgery. Ophthalmology 1997;104:986-995.
(7.) Kangas TA, Greenfield DS, Flynn HW, et al. Delayed-onset endophthalmitis associated with conjunctival filtering blebs. Ophthalmology 1997;104:746-752.
(8.) Miller JJ, Scott IU, Flynn HW Jr, et al. Endophthalmitis caused by Bacillus species. Am J Ophthalmol 2008;145:883-888.
(9.) Abu el-Asrar AM, al-Amro SA, al-Mosallam AA, al-Obeidan S. Posttraumatic endophthalmitis: causative organisms and visual outcome. Eur J Ophthalmol 1999;9:21-31.
(10.) Benz MS, Scott IU, Flynn, HW JR, et al. Endophthalmitis isolates and antibiotic sensitivities: a 6-year review of culture-proven cases. Am J Ophthalmol 2004;137:38-42.
(11.) Okada AA, Johnson RP, Liles WC, et al. Endogenous bacterial endophthalmitis: Report of a ten-year retrospective study. Ophthalmology 1994;101:832-838.
(12.) Wong JS, Chan TK, Lee HM, et al. Endogenous bacterial endophthalmitis: An East Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology 2000;107:1483-1491.
(13.) Endophthalmitis Vitrectomy Study Group. Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial en dophthalmitis. Arch Ophthalmol 1995;113:1479-1496.
(14.) Jensen MK, Fiscella RG, Crandall AS, Moshirfar M, Mooney B, Wallin T, Olson RJ. A retrospective study of endophtalmitis [sic] rates comparing quinolone antibiotics. Am J Ophthalmol 2005;139:141-148.
(15.) Almeida DR, Miller D, Alfonso EC. Anterior chamber and vitreous concordance in endophthalmitis: implications for prophylaxis. Arch Ophthalmol 2010;128:1136-1139.
(16.) Fintelmann RE, Naseri A. Prophylaxis of postoperative endophthalmitis following cataract surgery: current status and future directions. Drugs 2010;70:1395-1409.
(17.) Soheilian M, Rafati N, Mohebbi MR, et al. Prophylaxis of acute posttraumatic bacterial endophthalmitis: a multicenter randomized clinical trial of intraocular antibiotic injection, report 2. Arch Ophthalmol 2007;125:460-465.
(18.) Baker AS, Durand M. The Endophthalmitis Vitrectomy Study. Arch Ophthalmol 1996;114:1025-1026.
(19.) Anand AR, Therese KL, Madhavan HN. Spectrum of etiological agents ofpostoperative endophthalmitis and antibiotic susceptibility of bacterial isolates. Indian J Ophthalmol 2000;48:123-128.
(20.) Bispo PJ, Melo GB, dAzevedo PA, Hofling-Lima AL, Yu MC, Pignatari AC. Culture proven bacterial endophthalmitis: a 6-year review. Arq Bras Oftalmol 2008;71:617-622.
(21.) Miller D, Flynn PM, Scott IU, Alfonso EC. In vitro fluoroquinolone resistance in staphylococcal endophthalmitis isolates. Arch Ophthalmol 2006;4:479-483.
(22.) Flynn HW Jr, Meredith TA. The Endophthalmitis Vitrectomy Study. Arch Ophthalmol 1996;114:1027-1028.
(23.) Kunimoto DY, Das T, Sharma S, et al. Microbiologic spectrum and susceptibility of isolates: Part I. Postoperative endophthalmitis. Endophthalmitis Research Group. Am J Ophthalmol 1999;128:240-242.
(24.) Deramo VA, Lai JC, Fastenberg DM, Udell IJ. Acute endophthalmitis in eyes treated prophylactically with gatifloxacin and moxifloxacin. Am J Ophthalmol 2006;142:721-725.
(25.) Goldstein MH, Kowalski RP, Gordon YJ. Emerging fluoroquinolone resistance in bacterial keratitis: A 5-year review. Ophthalmology 1999;106:1313-1318.
(26.) Kunimoto DY, Sharma S, Garg P, Rao GN. In vitro susceptibility of bacterial keratitis pathogens to ciprofloxacin. Emerging resistance. Ophthalmology 1999;106:80-85.
(27.) M Kernt, Kampik A. Endophthalmitis: Pathogenesis, clinical presentation, management, and perspectives. Clin Ophthalmol 2010;4:121-135.
(28.) Binder MI, Chua J, Kaiser PK, et al. Endogenous endophthalmitis: an 18-year review of culture-positive cases at a tertiary care center. Medicine (Baltimore) 2003;82:97-105.
(29.) Jackson TL, Eykyn SJ, Graham EM, Stanford MR. Endogenous bacterial endophthalmitis: a 17-year prospective series and review of 267 reported cases. Surv Ophthalmol 2003;48:403-423.
(30.) Dunlop AA, Wright ED, Howlader SA, et al. Suppurative corneal ulceration in Bangladesh. A study of 142 cases examining the microbiological diagnosis, clinical and epidemiological features of bacterial and fungal keratitis. Aust N Z J Ophthalmol 1994;22:105-110.
(31.) Polack FM, Kaufman HE, Newmark E. Keratomycosis. Medical and surgical treatment. Arch Ophthalmol 1971;85:410-416.
(32.) Srinivasan M, Gonzales CA, George C, et al. Epidemiology and aetiological diagnosis of corneal ulceration in Madurai, south India. Br J Ophthal mol 1997;81:965-971.
(33.) Thomas PA. Mycotic keratitis--an underestimated mycosis. J Med Vet Mycol 1994;32:235-256.
(34.) Wykoff CC, Flynn HW Jr, Miller D, Scott IU, Alfonso EC. Exogenous fungal endophthalmitis: Microbiology and clinical outcomes. Ophthalmology 2008;115:1501-1507.
Maria del Pilar Fernandez, BS *; Victor M. Villegas, MD ([dagger]); Armando L. Oliver MD ([dagger])
* Universidad Central de Caribe, Bayamon, Puerto Rico; ([dagger]) Department of Ophthalmology, University of Puerto Rico, San Juan, Puerto Rico
The authors have no conflict of interest to disclose.
Address correspondence to: Armando L. Oliver, MD, Department of Ophthalmology, University of Puerto Rico Medical Sciences Campus, PO BOX 365067, San Juan, PR 00966. Email: email@example.com
Table 1. Positive isolates by etiology, isolate, sex, and age Patient Etiology Isolate Sex Age 1 endogenous Staphylococcus aureus (BL+) M 36 2 endogenous Staphylococcus aureus (BL+) M 46 3 endogenous Staphylococcus epidermidis (BL+) M 42 4 endogenous Staphylococcus epidermidis (BL+) M 70 5 endogenous Pseudomona aeruginosa M 73 6 post-cataract Streptococcus pneumoniae M 75 7 post-cataract Streptococcus mitis M 72 8 post-cataract Aspergillus fumigatus F 82 9 post-traumatic Staphylococcus epidermidis (BL+) F 57 10 post-traumatic Streptococcus pyogenes (group A) F 101 11 post-traumatic Beta hemolytic non-group A/B/D M 62 12 post-traumatic Diphtheroids M 6 13 post-traumatic Pseudomona aeruginosa M 71 14 post-traumatic Acremonium species M 10 15 * post-traumatic Scopulariopsis Penicillium M 60 species 16 * undetermined Staphylococcus aureus (BL+) F 52 Streptococcus agalactiae * Patient had 2 isolated organisms Table 2. Gram-positive isolates and antibiotic sensitivity Organism Chloramphenicol Clindamycin Staphylococcus aureus (BL+) s Staphylococcus aureus (BL+) s Staphylococcus aureus (BL+) s Staphylococcus epidermidis (BL+) r Staphylococcus epidermidis (BL+) s Staphylococcus epidermidis (BL+) r Streptococcus pneumoniae s r Streptococcus pyogenes (group A) s s Streptococcus mitis s s Streptococcus agalactiae s Beta hemolytic non-group A/B/D s r Organism Cefotaxime Erythromycin Cefepime Staphylococcus aureus (BL+) r Staphylococcus aureus (BL+) s Staphylococcus aureus (BL+) s Staphylococcus epidermidis (BL+) r Staphylococcus epidermidis (BL+) s Staphylococcus epidermidis (BL+) r Streptococcus pneumoniae r Streptococcus pyogenes (group A) s Streptococcus mitis s s Streptococcus agalactiae s Beta hemolytic non-group A/B/D s s s Organism Linezolid Penicillin Staphylococcus aureus (BL+) s r Staphylococcus aureus (BL+) s r Staphylococcus aureus (BL+) s r Staphylococcus epidermidis (BL+) s r Staphylococcus epidermidis (BL+) r Staphylococcus epidermidis (BL+) r Streptococcus pneumoniae s Streptococcus pyogenes (group A) s Streptococcus mitis s Streptococcus agalactiae s Beta hemolytic non-group A/B/D s s Organism Tetracycline Vancomycin Staphylococcus aureus (BL+) s s Staphylococcus aureus (BL+) s s Staphylococcus aureus (BL+) s s Staphylococcus epidermidis (BL+) s s Staphylococcus epidermidis (BL+) r s Staphylococcus epidermidis (BL+) r s Streptococcus pneumoniae r s Streptococcus pyogenes (group A) s Streptococcus mitis i s Streptococcus agalactiae s Beta hemolytic non-group A/B/D r s Organism Gentamycin Levofloxacin Staphylococcus aureus (BL+) s i Staphylococcus aureus (BL+) s s Staphylococcus aureus (BL+) s s Staphylococcus epidermidis (BL+) r r Staphylococcus epidermidis (BL+) s s Staphylococcus epidermidis (BL+) r r Streptococcus pneumoniae Streptococcus pyogenes (group A) Streptococcus mitis Streptococcus agalactiae s Beta hemolytic non-group A/B/D Organism Gatifloxacin Oxacillin Staphylococcus aureus (BL+) i r Staphylococcus aureus (BL+) s s Staphylococcus aureus (BL+) s r Staphylococcus epidermidis (BL+) r r Staphylococcus epidermidis (BL+) s r Staphylococcus epidermidis (BL+) r r Streptococcus pneumoniae r Streptococcus pyogenes (group A) Streptococcus mitis Streptococcus agalactiae s Beta hemolytic non-group A/B/D Organism Quinupristin/ Trimethoprim/ dalfopristin Sulfamethoxazole Staphylococcus aureus (BL+) s s Staphylococcus aureus (BL+) s s Staphylococcus aureus (BL+) s s Staphylococcus epidermidis (BL+) s r Staphylococcus epidermidis (BL+) s Staphylococcus epidermidis (BL+) r Streptococcus pneumoniae r Streptococcus pyogenes (group A) Streptococcus mitis Streptococcus agalactiae s Beta hemolytic non-group A/B/D Organism Rifampin Staphylococcus aureus (BL+) Staphylococcus aureus (BL+) Staphylococcus aureus (BL+) s Staphylococcus epidermidis (BL+) Staphylococcus epidermidis (BL+) Staphylococcus epidermidis (BL+) Streptococcus pneumoniae Streptococcus pyogenes (group A) Streptococcus mitis Streptococcus agalactiae Beta hemolytic non-group A/B/D Table 3. Gram-negative isolates and antibiotic sensitivity Organism Cefepime Amikacin Ceftazidime Pseudomona aeruginosa s s s Pseudomona aeruginosa s s s Organism Ciprofloxacin Gentamycin Imipenem Pseudomona aeruginosa s s s Pseudomona aeruginosa s s s Organism Levofloxacin Tobramycin Piperacillin/ Tazobactam Pseudomona aeruginosa s s s Pseudomona aeruginosa s s s
|Gale Copyright:||Copyright 2011 Gale, Cengage Learning. All rights reserved.|