As a young physician at Louisiana State University, Dr. Bonilla focused on the Clinical Management of HIV/AIDS and HCV, two neglected and stigmatized diseases for which effective therapies were in their infancy. While learning the clinical aspects of the two diseases, Dr. Bonilla saw a need to create and organize a support community to promote understanding and management of the conditions. Subsequently, he went to Summa Health System in Akron, Ohio, and he continued his work where he specialized in HIV/HCV as well as in Infectious Diseases Clinical Practice. In addition to teaching medical residents and students, Dr. Bonilla participated in numerous clinical trials and developed clinical research projects. Furthermore, he led the Infection Renal Transplant Program, HIV and HCV clinics, and he participated in several cooperative studies with Case Western Reserve University. Dr. Bonilla’s interest in academia led him to the University Of Pittsburgh Medical Center where he was an Assistant Professor, Clinician, and Medical Educator in the Department of Medicine in the Division of Infectious Diseases. Due to his interest in cytokines and immunological responses, Dr. Bonilla became a researcher at ImmunoScience Inc., a biotechnology company in California that works to develop a therapeutic HIV vaccine. Dr. Bonilla’s experience of treating HIV/HCV combined with his interest in inflammatory response is the driving force behind his desire to understand ME/CFS. Dr. Bonilla is a strong patient advocate, and he believes in integrated care—care in which physicians communicate and coordinate efforts to deliver the best medical outcome for patients. His ME/CFS patients are his inspiration, and he is committed to continuing research to seek answers to their health challenges.
- Infectious Disease
Clinical Associate Professor, Medicine - Infectious Diseases
Boards, Advisory Committees, Professional Organizations
Member, International Collaboration of Endocarditis (ICE) (2010 - Present)
Member, American Society of Microbiology (ASM) (1997 - Present)
Member, Infectious Diseases Society of America (IDSA) (1995 - Present)
Board Certification: Infectious Disease, American Board of Internal Medicine (1996)
Fellowship: University of Michigan Infectious Diseases Fellowship (1996) MI
Board Certification: Internal Medicine, American Board of Internal Medicine (1994)
Residency: Sinai Grace Hospital Internal Medicine Residency (1994) MI
Medical Education: Universidad Del Valle (1983) Colombia
MD, Universidad del Valle School of Medicine, Cali, Colombia, MD (1983)
Chief Medical Resident, Universidad del Valle, Internal Medicine (1988)
Visiting Physician, Henry Ford Hospital, Nephrology Department (1990)
Clinical Research, Sinai Hospital of Detroit, Clinical Research (1991)
Internship, Sinai Hospital of Detroit, Internal Medicine (1992)
Residency, Sinai Hospital of Detroit, Internal Medicine Residency (1994)
ID Fellow, University Of Michigan, Infectious Diseases (1996)
Beta-Glucanemia after Coronary Artery Bypass Graft Surgery: A Case Report.
Journal of fungi (Basel, Switzerland)
2018; 4 (4)
Blood salvage techniques are increasingly being used during surgical procedures to reduce the need for exogenous blood products. The blood recovered from the surgical field through aspiration or absorption by surgical sponges is reinfused into a patient. A 65-year old patient who underwent coronary artery bypass grafting using blood salvage techniques developed a fever on post-op day 3 and was noted to have an elevated beta-d-glucan level, a marker of systemic fungal infections. Ultimately, no fungal infection was identified, beta-d-glucan levels slowly decreased and the patient demonstrated clinical improvement. To determine whether blood salvage procedures led to his elevated beta-d-glucan levels, the surgical sponges were tested for elutable levels of beta-d-glucan. The beta-d-glucan content of the eluents was measured using the Fungitell IVD kit (Associates of Cape Cod, Inc.; East Falmouth, MA). The beta-d-glucan levels were found to be in concentrations 10,000-times greater than the limit of detection for human serum. While various studies have demonstrated both the immunomodulatory and pro-inflammatory effects of beta-d-glucan, the physiologic impact of such high levels of beta-d-glucan post-operatively remains unknown. Additionally, the persistence of detectable beta-d-glucan up to several weeks after surgical procedures presents a challenge for the diagnosis of invasive fungal infections. Further studies are needed to assess the beta-glucanemia-related safety of surgical materials and their potential biological effects.
View details for PubMedID 30279391
Defining the incidence and risk factors of colistin-induced acute kidney injury by KDIGO criteria
2017; 12 (3): e0173286
Acute kidney injury (AKI) remains a treatment-limiting toxicity of colistin. Recently developed clinical practice guidelines from the Kidney Disease: Improving Global Outcomes (KDIGO) group have harmonized definitions of AKI, but have not been widely applied to patients receiving colistin.We retrospectively defined AKI by KDIGO definitions among adult patients receiving intravenous colistin for ≥ 3 days. Risk factors for AKI within 48 hours and 7 days of initiating colistin were determined by multivariable logistic regression.Among 249 patients treated with colistin, rates of AKI were 12% and 29% at 48 hours and 7 days, respectively. At 48 hours, patients in the intensive care unit were at increased risk for AKI. Within 7 days, colistin daily doses >5mg/kg, chronic liver disease, and concomitant vancomycin were independent predictors. Seven percent of patients required renal replacement therapy at a median of 5 days (range: 3-7) following colistin initiation.Safe use of colistin is promoted by early detection of AKI with KDIGO criteria, avoiding nephrotoxins, and limiting duration of therapy.
View details for PubMedID 28267779
Atorvastatin and Fluvastatin Are Associated With Dose-Dependent Reductions in Cirrhosis and Hepatocellular Carcinoma, Among Patients With Hepatitis C Virus: Results From ERCHIVES
2016; 64 (1): 47–57
Statins are associated with delayed fibrosis progression and a reduced risk of hepatocellular carcinoma (HCC) in chronic hepatitis C virus (HCV). Limited data exist regarding the most effective type and dose of statin in this population. We sought to determine the impact of statin type and dose upon fibrosis progression and HCC in patients with HCV. Using the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES) database, we identified all subjects initiated on HCV antibody (anti-HCV) therapy from 2001 to 2014, and all incident cases of cirrhosis and HCC. Statin use was measured using cumulative defined daily dose (cDDD). Multivariable Cox's proportional hazard regression models were used to examine the relationship between statin use and development of cirrhosis and HCC. Among 9,135 eligible subjects, 1,649 developed cirrhosis and 239 developed incident HCC. Statin use was associated with a 44% reduction in development of cirrhosis (adjusted hazard ratio [HR]: 0.6; 95% confidence interval [CI]: 0.53, 0.68). The adjusted HRs (95% CI) of fibrosis progression with statin cDDD 28-89, 89-180, and >180 were 0.74 (0.59, 0.93), 0.71 (0.59, 0.88), and 0.6 (0.53, 0.68), respectively. Mean change in FIB-4 score with atorvastatin (n = 944) and fluvastatin (n = 34) was -0.17 and -0.13, respectively (P = 0.04), after adjustment for baseline FIB-4 score and established predictors of cirrhosis. Statin use was also associated with a 49% reduction in incident HCC (adjusted HR: 0.51; 95% CI: 0.36, 0.72). A similar dose-response relationship was observed.In patients with chronic HCV, statin use was associated with a dose-dependent reduction in incident cirrhosis and HCC. Atorvastatin and fluvastatin were associated with the most significant antifibrotic effects, compared with other statins. (Hepatology 2016;64:47-57).
View details for PubMedID 26891205
View details for PubMedCentralID PMC4917438
- Does Staphylococcus aureus Bacteriuria Predict Clinical Outcomes in Patients With Bacteremia? Analysis of 274 Patients With Staphylococcus aureus Blood Stream Infection INFECTIOUS DISEASES IN CLINICAL PRACTICE 2016; 24 (3): 151–54
Effect of addition of statins to antiviral therapy in hepatitis C virus-infected persons: Results from ERCHIVES
2015; 62 (2): 365–74
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been variably noted to affect hepatitis C virus (HCV) treatment response, fibrosis progression, and hepatocellular carcinoma (HCC) incidence, with some having a more potent effect than others. We sought to determine the impact of adding statins to antiviral therapy upon sustained virological response (SVR) rates, fibrosis progression, and HCC development among HCV-infected persons using the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), an established, longitudinal, national cohort of HCV-infected veterans. Within ERCHIVES, we identified those who received HCV treatment and a follow-up of >24 months after treatment completion. We excluded those with human immunodeficiency virus coinfection, hepatitis B surface antigen positivity, cirrhosis, and HCC at baseline. Our main outcomes were liver fibrosis progression measured by FIB-4 scores, SVR rates, and incident HCC (iHCC). Among 7,248 eligible subjects, 46% received statin therapy. Statin use was significantly associated with attaining SVR (39.2% vs. 33.3%; P < 0.01), decreased cirrhosis development (17.3% vs. 25.2%; P < 0.001), and decreased iHCC (1.2% vs. 2.6%; P < 0.01). Statins remained significantly associated with increased odds of SVR (odds ratio = 1.44; 95% confidence interval [CI] = 1.29, 1.61), but lower fibrosis progression rate, lower risk of progression to cirrhosis (hazard ratio [HR] = 0.56; 95% CI = -0.50, 0.63), and of incident HCC (HR = 0.51; 95% CI = 0.34, 0.76) after adjusting for other relevant clinical factors.Statin use was associated with improved virological response (VR) rates to antiviral therapy and decreased progression of liver fibrosis and incidence of HCC among a large cohort of HCV-positive Veterans. These data support the use of statins in patients with HCV.
View details for PubMedID 25847403
Patience Is a Virtue: An Argument for Delayed Surgical Intervention in Fulminant Clostridium difficile Colitis
2014; 80 (6): 614–19
Recently, the incidence and severity of Clostridium difficile infection (CDI) has increased. In cases of fulminant infection, surgery is a viable therapeutic option but associated with high mortality. We sought to examine factors associated with mortality in a large sample of patients with severe CDI that underwent surgery. A retrospective study was conducted in patients with severe CDI undergoing colectomy. Demographics, risk factors, comorbidities, clinical and laboratory data, and time between admission/diagnosis of CDI and colectomy were collected. Conventional markers of severity were evaluated as predictors of mortality. Sixty-four cases were included for analysis. The overall observed mortality rate was 45.3 per cent. Few conventional markers of severity were significantly associated with mortality. Risk factors that correlated with postsurgical mortality were vasopressor use (odds ratio, 3.08; 95% confidence interval, 1.00 to 9.92) and shorter time between diagnosis and surgery (median time, 2 vs 3 days, P = 0.009). This study suggests that a delay in surgery after diagnosis of severe CDI may improve overall outcomes. The finding regarding timing of surgery is contrary to traditional teaching and may be the result of improved medical treatment and stabilization before surgery. Consideration should be given to the importance of timing of colectomy in fulminant CDI, whereas prospective studies should be conducted to elucidate causal relationships.
View details for Web of Science ID 000337747600028
View details for PubMedID 24887802
Dissemination of a pSCFS3-Like cfr-Carrying Plasmid in Staphylococcus aureus and Staphylococcus epidermidis Clinical Isolates Recovered from Hospitals in Ohio
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
2013; 57 (7): 2923-2928
Nineteen linezolid-resistant Staphylococcus epidermidis and two Staphylococcus aureus isolates recovered from two medical institutions in northeast Ohio and an S. aureus cfr index strain previously collected in the same facilities during the 2007 SENTRY Antimicrobial Surveillance Program were investigated for the genetic basis of oxazolidinone resistance and the location of cfr. S. aureus isolates were typed by pulsed-field gel electrophoresis (PFGE), spa typing, and multilocus sequence typing (MLST). The location of cfr was determined by Southern blotting and hybridization. Plasmid sequencing was performed using the 454 Life Sciences (Roche) GS-FLX DNA platform. The two S. aureus isolates showed unique PFGE patterns but were multilocus sequence type 5 (ST5) and spa type t002, whereas the S. aureus index strain was ST239 and t037. Southern blot and hybridization experiments showed that cfr was plasmid located and that the S. epidermidis isolates, one of the S. aureus isolates, and the S. aureus index strain shared an identical cfr-carrying plasmid (39.3 kb). Sequencing results confirmed these findings. A 10-kb fragment containing cfr showed the highest identity (99.9%) to a 9.5-kb fragment of plasmid pSCFS3 from a bovine Staphylococcus lentus isolate from Germany. In addition, these 39.3-kb plasmids from human S. epidermidis and S. aureus exhibited BglII restriction profiles very similar to that observed for plasmid pSCFS3. The cfr-carrying plasmid detected in the remaining S. aureus isolate (7.9 kb) was distinct and showed the highest identity to the chromosomal cfr integrate found in the chromosomal DNA of a Proteus vulgaris isolate from a pig in China.
View details for DOI 10.1128/AAC.00071-13
View details for Web of Science ID 000320229600003
View details for PubMedID 23571552
View details for PubMedCentralID PMC3697371
- Can a vancomycin assay be utilised to predict plasma telavancin concentrations? INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS 2013; 41 (5): 495-497
Epidemiology and clinical outcomes of patients with Fusobacterium bacteraemia
EPIDEMIOLOGY AND INFECTION
2013; 141 (2): 325–29
This 10-year retrospective study assessed the epidemiology and outcomes of patients with Fusobacterium bacteraemia (FB) at a tertiary-care hospital in the USA - this is the second study focusing on FB in adults to be conducted in the USA in 30 years. Demographic, clinical, laboratory, treatment, and outcome data were collected and statistically analysed. Nineteen patients with FB were identified, representing 0·11% of bacteraemia cases. Mean age was 58·6 years with equal gender distribution. Common comorbidities included cardiovascular disease (CVD) and immunosuppression. Thirty-day mortality was 21·1%, and 68·4% of FB patients required intensive care unit (ICU) admission. Elevated creatinine levels and mental status changes were associated with higher mortality (P = 0·0181 and 0·0374, respectively). CVD, diabetes, and ICU admission were associated with increased length of hospital stay (P = 0·0017, 0·0010, and 0·0379, respectively). The prevalence of FB at our hospital was very low, with poor outcomes associated with increased creatinine level, mental status changes, CVD, diabetes and ICU admission.
View details for PubMedID 22717143
In Vitro Activities of LTX-109, a Synthetic Antimicrobial Peptide, against Methicillin-Resistant, Vancomycin-Intermediate, Vancomycin-Resistant, Daptomycin-Nonsusceptible, and Linezolid-Nonsusceptible Staphylococcus aureus
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
2012; 56 (8): 4478–82
LTX-109 and eight other antimicrobial agents were evaluated against 155 methicillin-resistant Staphylococcus aureus (MRSA) isolates, including strains resistant to vancomycin and strains with decreased susceptibility to daptomycin and linezolid, by microdilution tests to determine MICs. Time-kill assays were performed against representative MRSA, vancomycin-intermediate S. aureus (VISA), and vancomycin-resistant S. aureus (VRSA) isolates. LTX-109 demonstrated a MIC range of 2 to 4 μg/ml and dose-dependent rapid bactericidal activity against S. aureus. This activity was not influenced by resistance to other antistaphylococcal agents.
View details for DOI 10.1128/AAC.00194-12
View details for Web of Science ID 000306826300058
View details for PubMedID 22585222
View details for PubMedCentralID PMC3421571