Jose Montoya

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Source: SanfordHealthCare

Jose Montoya is an Infectious disease doctor and Professor of Medicine (Infectious Diseases and Geographic Medicine) at Stanford University Medical Center. His special areas of clinical focus include: Chronic Fatigue Syndrome, Infectious Disease, Toxoplasmosis, Infection in the setting of solid organ transplantation, and Infection as a trigger of chronic diseases.[1]

Dr. Montoya heads the Stanford ME/CFS Initiative.

Education[edit]

  • 1994, Fellowship:Stanford University School of Medicine,California, USA[1]
  • 1990, Residency:Tulane University School of Medicine, Louisiana, USA[1]
  • 1988, Internship:Tulane University School of Medicine[1]
  • 1985, Medical Education:Universidad Del Valle, Colombia[1]

Clinical practice[edit]

Dr. Montoya and his team at the Stanford ME/CFS Initiative have short term goals of Patient Care, Research and Discovery, and Education. They, also, have a long term goal of establishing an inpatient center, apart from a hospital where patients with chronic conditions could receive long-term treatment.

At present there is a waiting list to see Dr. Montoya. If you would like to be placed on the waiting list, please contact the New Patient Coordinator at (650) 736-5200.

Clinic address[edit]

2nd Floor of Hoover Pavilion, 211 Quarry Road, Palo Alto, CA 94304. Phone: (650) 736-5200.

Awards[edit]

  • 2016, Infectious Disease Specialist Jose G. Montoya, MD, to be Recognized as a 2016 Top Doctor in Stanford, California
  • 2013, Selected as one of the 100 Colombians who have exceled abroad, 2013 Edition., 100 Colombianos en el exterior[1]
  • 2011, Fellow of the American College of Physicians (FACP), American College of Physicians[1]
  • 2011, Fellow of the Infectious Diseases Society of America (FIDSA), Infectious Diseases Society of America[1]
  • 2011, The Arthur L. Bloomfield Award for Excellence in the Teaching of Clinical Medicine, Stanford University School of Medicine[1]
  • 2003, Chief Residents Teaching Award for exemplary teaching at Stanford Resident's report, Department of Medicine, Stanford University School of Medicine[1]
  • 2002, The Kenneth Vosti Teaching Award for Excellence in Teaching, Division of Infectious Diseases, Department of Medicine, Stanford University School of Medicine[1]
  • 2001, The David A. Rytand Teaching Award for Excellence in Clinical Teaching., Department of Medicine, Stanford University School of Medicine[1]
  • 2000, The Kenneth Vosti Teaching Award for Excellence in Teaching, Division of Infectious Diseases and Geographic Medicine, Stanford University School of Medicine[1]
  • 1998, The David A. Rytand Teaching Award for Excellence in Clinical Teaching, Department of Medicine, Stanford University School of Medicine[1]
  • 1997, The Arthur L. Bloomfield Award for Excellence in the Teaching of Clinical Medicine, Stanford University School of Medicine[1]
  • 1995, The Henry J. Kaiser Award for Excellence in Clinical Teaching, Stanford University School of Medicine[1]
  • 1995, The Franklin G. Ebaugh, Jr. Award for Advising Medical Students, Stanford University School of Medicine [1]
  • 1990, Outstanding Senior Resident Awar, Department of Medicine, Tulane University School of Medicine[1]
  • 1990, The Department of Medicine Outstanding Teaching Award, Tulane University School of Medicine[1]
  • 1990, The Owl Club Award for Outstanding Clinical Teaching, Tulane University School of Medicine[1]
  • 1988, Outstanding Intern Award, Department of Medicine, Tulane University School of Medicine[1]

Notable Studies[edit]

  • 2017, Patients diagnosed with Myalgic encephalomyelitis/chronic fatigue syndrome also fit systemic exertion intolerance disease criteria
    Abstract - Background: Myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) remains undiagnosed in up to 91% of patients. Recently, the United States-based Institute of Medicine (IOM) developed new diagnostic criteria, naming it systemic exertion intolerance disease (SEID). Purpose: We examined how subjects fit SEID criteria and existing ME/CFS case definitions early in their illness. Methods: A total of 131 subjects fitting 1994 Fukuda CFS criteria at the time of study recruitment completed a survey of symptoms they experienced during their first 6 months of illness. Symptoms were drawn from SEID and existing criteria (1994 Fukuda, 2003 Canadian Consensus Criteria (CCC), and 2011 Myalgic Encephalomyelitis-International Consensus Criteria (ME-ICC)). We calculated and compared the number/percentage of subjects fitting single or combinations of case definitions and the number/percentage of subjects with SEID experiencing orthostatic intolerance (OI) and/or cognitive impairment. Results: At 6 months of illness, SEID criteria identified 72% of all subjects, similar to when Fukuda criteria (79%) or the CCC (71%) were used, whereas the ME-ICC selected for a significantly lower percentage (61%, p < .001). When severity/frequency thresholds were added to the Fukuda criteria, CCC and ME-ICC, the percentage of these subjects also fitting SEID criteria increased to 93%, 97%, and 95%. Eighty-seven percent of SEID subjects endorsed cognitive impairment and 92%, OI; 79% experienced both symptoms. Conclusions: SEID criteria categorize a similar percentage of subjects as Fukuda criteria early in the course of ME/CFS and contain the majority of subjects identified using other criteria while requiring fewer symptoms. The advantage of SEID may be in its ease of use.[2]
  • 2017, Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome (FULL TEXT)
    Abstract - Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained persistent fatigue, commonly accompanied by cognitive dysfunction, sleeping disturbances, orthostatic intolerance, fever, lymphadenopathy, and irritable bowel syndrome (IBS). The extent to which the gastrointestinal microbiome and peripheral inflammation are associated with ME/CFS remains unclear. We pursued rigorous clinical characterization, fecal bacterial metagenomics, and plasma immune molecule analyses in 50 ME/CFS patients and 50 healthy controls frequency-matched for age, sex, race/ethnicity, geographic site, and season of sampling. Results: Topological analysis revealed associations between IBS co-morbidity, body mass index, fecal bacterial composition, and bacterial metabolic pathways but not plasma immune molecules. IBS co-morbidity was the strongest driving factor in the separation of topological networks based on bacterial profiles and metabolic pathways. Predictive selection models based on bacterial profiles supported findings from topological analyses indicating that ME/CFS subgroups, defined by IBS status, could be distinguished from control subjects with high predictive accuracy. Bacterial taxa predictive of ME/CFS patients with IBS were distinct from taxa associated with ME/CFS patients without IBS. Increased abundance of unclassified Alistipes and decreased Faecalibacterium emerged as the top biomarkers of ME/CFS with IBS; while increased unclassified Bacteroides abundance and decreased Bacteroides vulgatus were the top biomarkers of ME/CFS without IBS. Despite findings of differences in bacterial taxa and metabolic pathways defining ME/CFS subgroups, decreased metabolic pathways associated with unsaturated fatty acid biosynthesis and increased atrazine degradation pathways were independent of IBS co-morbidity. Increased vitamin B6 biosynthesis/salvage and pyrimidine ribonucleoside degradation were the top metabolic pathways in ME/CFS without IBS as well as in the total ME/CFS cohort. In ME/CFS subgroups, symptom severity measures including pain, fatigue, and reduced motivation were correlated with the abundance of distinct bacterial taxa and metabolic pathways. Conclusions: Independent of IBS, ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity. However, our findings indicate that dysbiotic features that are uniquely ME/CFS-associated may be masked by disturbances arising from the high prevalence of IBS co-morbidity in ME/CFS. These insights may enable more accurate diagnosis and lead to insights that inform the development of specific therapeutic strategies in ME/CFS subgroups.[3]
  • 2015, Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome
    Abstract - Methods: Fifteen patients with CFS were identified by means of retrospective review with an institutional review board–approved waiver of consent and waiver of authorization. Fourteen age- and sex-matched control subjects provided informed consent in accordance with the institutional review board and HIPAA...Results: In the CFS population, FA was increased in the right arcuate fasciculus (P = .0015), and in right-handers, FA was also increased in the right inferior longitudinal fasciculus (ILF) (P = .0008). In patients with CFS, right anterior arcuate FA increased with disease severity (r = 0.649, P = .026). Bilateral white matter volumes were reduced in CFS (mean ± standard deviation, 467 581 mm3 ± 47 610 for patients vs 504 864 mm3 ± 68 126 for control subjects, P = .0026), and cortical thickness increased in both right arcuate end points, the middle temporal (T = 4.25) and precentral (T = 6.47) gyri, and one right ILF end point, the occipital lobe (T = 5.36). ASL showed no significant differences...Conclusions: Bilateral white matter atrophy is present in CFS. No differences in perfusion were noted. Right hemispheric increased FA may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS.[4]
  • 2015, Distinct plasma immune signatures in ME/CFS are present early in the course of illness FULL TEXT
    Abstract: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an unexplained incapacitating illness that may affect up to 4 million people in the United States alone. There are no validated laboratory tests for diagnosis or management despite global efforts to find biomarkers of disease. We considered the possibility that inability to identify such biomarkers reflected variations in diagnostic criteria and laboratory methods as well as the timing of sample collection during the course of the illness. Accordingly, we leveraged two large, multicenter cohort studies of ME/CFS to assess the relationship of immune signatures with diagnosis, illness duration, and other clinical variables. Controls were frequency-matched on key variables known to affect immune status, including season of sampling and geographic site, in addition to age and sex. We report here distinct alterations in plasma immune signatures early in the course of ME/CFS (n = 52) relative to healthy controls (n = 348) that are not present in subjects with longer duration of illness (n = 246). Analyses based on disease duration revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines as well as dissociation of intercytokine regulatory networks. We found a stronger correlation of cytokine alterations with illness duration than with measures of illness severity, suggesting that the immunopathology of ME/CFS is not static. These findings have critical implications for discovery of interventional strategies and early diagnosis of ME/CFS.[5]
  • 2014, Conference paper, EEG peak alpha frequency is associated with chronic fatigue syndrome: A case-control observational study (FULL TEXT)
    Abstract - The purpose of this study was to look at the electrophysiology of the brain in patients with chronic fatigue syndrome (CFS) and compare their electrophysiology to that of healthy controls. Using EEG peak alpha frequency (PAF) in a resting-state eyes-closed condition, EEG was recorded from 19 scalp locations using linked-ear reference from 50 patients and 50 matched controls age 28 to 74 years. The Multidimensional Fatigue Inventory (MFI-20) and the Fatigue Severity Scale (FSS) were used to evaluate fatigue. PAF was computed within the 8-12 Hz frequency band based on each participant’s EEG. Differences between patients diagnosed with the Fukuda criteria and healthy controls were evaluated using a mixed effects analysis of variance and regression analyses to evaluate the relationship between PAF and fatigue within each fatigue measure. A small but significant difference was observed with control PAF being higher than participants’ PAF. Bonferroni-corrected follow-up tests indicated significant differences in PAF at multiple (11) electrode sites (p<.05) in frontal, left temporal, central and parietal regions of interest (ROIs), consistently exhibiting a direct relationship between qEEG and fatigue. Linear regression model fits using PAF to predict each fatigue scale and each subscale of the MFI-20 were statistically significant (p=.000). These novel neuropsychological relationships attest to the use of qEEG as a novel and objective measure of fatigue and neurocognitive impairment (NCI) in CFS. Moreover, resting-state PAFs may indicate its potential for use in diagnosis and to evaluate treatment progress in the clinic.[6]
  • 2013, Daily cytokine fluctuations, driven by leptin, are associated with fatigue severity in chronic fatigue syndrome: evidence of inflammatory pathology
    Abstract - Methods: Ten women meeting the Fukuda diagnostic criteria for CFS and ten healthy age- and body mass index (BMI)-matched women underwent 25 consecutive days of blood draws and self-reporting of symptom severity. A 51-plex cytokine panel via Luminex was performed for each of the 500 serum samples collected. Our primary hypothesis was that daily fatigue severity would be significantly correlated with the inflammatory adipokine leptin, in the women with CFS and not in the healthy control women. As a post-hoc analysis, a machine learning algorithm using all 51 cytokines was implemented to determine whether immune factors could distinguish high from low fatigue days. Results: Self-reported fatigue severity was significantly correlated with leptin levels in six of the participants with CFS and one healthy control, supporting our primary hypothesis. The machine learning algorithm distinguished high from low fatigue days in the CFS group with 78.3% accuracy. Conclusions: Our results support the role of cytokines in the pathophysiology of CFS.[7]
  • 2013, Randomized Clinical Trial to Evaluate the Efficacy and Safety of Valganciclovir in a Subset of Patients With Chronic Fatigue Syndrome
    Abstract: There is no known treatment for chronic fatigue syndrome (CFS). Little is known about its pathogenesis. Human herpesvirus 6 (HHV-6) and Epstein-Barr virus (EBV) have been proposed as infectious triggers. Thirty CFS patients with elevated IgG antibody titers against HHV-6 and EBV were randomized 2:1 to receive valganciclovir (VGCV) or placebo for 6 months in a double-blind, placebo-controlled trial. Clinical endpoints aimed at measuring physical and mental fatigue included the Multidimensional Fatigue Inventory (MFI-20) and Fatigue Severity Scale (FSS) scores, self-reported cognitive function, and physician-determined responder status. Biological endpoints included monocyte and neutrophil counts and cytokine levels. VGCV patients experienced a greater improvement by MFI-20 at 9 months from baseline compared to placebo patients but this difference was not statistically significant. However, statistically significant differences in trajectories between groups were observed in MFI-20 mental fatigue subscore (P = 0.039), FSS score (P = 0.006), and cognitive function (P = 0.025). VGCV patients experienced these improvements within the first 3 months and maintained that benefit over the remaining 9 months. Patients in the VGCV arm were 7.4 times more likely to be classified as responders (P = 0.029). In the VGCV arm, monocyte counts decreased (P < 0.001), neutrophil counts increased (P = 0.037) and cytokines were more likely to evolve towards a Th1-profile (P < 0.001). Viral IgG antibody titers did not differ between arms. VGCV may have clinical benefit in a subset of CFS patients independent of placebo effect, possibly mediated by immunomodulation and/or antiviral effect. Further investigation with longer treatment duration and a larger sample size is warranted."[8]
  • 2012, Response to valganciclovir in chronic fatigue syndrome patients with human herpesvirus 6 and Epstein-Barr virus IgG antibody titers.
    Abstract: Valganciclovir has been reported to improve physical and cognitive symptoms in patients with chronic fatigue syndrome (CFS) with elevated human herpesvirus 6 (HHV-6) and Epstein-Barr virus (EBV) IgG antibody titers. This study investigated whether antibody titers against HHV-6 and EBV were associated with clinical response to valganciclovir in a subset of CFS patients. An uncontrolled, unblinded retrospective chart review was performed on 61 CFS patients treated with 900 mg valganciclovir daily (55 of whom took an induction dose of 1,800 mg daily for the first 3 weeks). Antibody titers were considered high if HHV-6 IgG ? 1:320, EBV viral capsid antigen (VCA) IgG ? 1:640, and EBV early antigen (EA) IgG ? 1:160. Patients self-rated physical and cognitive functioning as a percentage of their functioning prior to illness. Patients were categorized as responders if they experienced at least 30% improvement in physical and/or cognitive functioning. Thirty-two patients (52%) were categorized as responders. Among these, 19 patients (59%) responded physically and 26 patients (81%) responded cognitively. Baseline antibody titers showed no significant association with response. After treatment, the average change in physical and cognitive functioning levels for all patients was +19% and +23%, respectively (P < 0.0001). Longer treatment was associated with improved response (P = 0.0002). No significant difference was found between responders and non-responders among other variables analyzed. Valganciclovir treatment, independent of the baseline antibody titers, was associated with self-rated improvement in physical and cognitive functioning for CFS patients who had positive HHV-6 and/or EBV serologies. Longer valganciclovir treatment correlated with an improved response."[9]
  • 2012, A Multicenter Blinded Analysis Indicates No Association between Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and either Xenotropic Murine Leukemia Virus-Related Virus or Polytropic Murine Leukemia Virus (FULL TEXT)[10]

Talks & Interviews[edit]

Notable quotes[edit]

Back in 2005, while attending a conference on toxoplasmosis in Paris, Montoya told his mentor that he wanted to research ME/CFS. His mentor scoffed at the idea, pointing to a homeless person lying in a Parisian gutter. 'That’s going to be you if you go into chronic fatigue research,' the mentor told him.[11]

Online presence[edit]

Learn more[edit]

See also[edit]

References[edit]

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 Montoya, Jose G., Stanford Medicine Bio 
  2. Chu, Lily; Norris, Jane; Valencia, Ian J.; Montoya, Jose G. (2017), "Patients diagnosed with Myalgic encephalomyelitis/chronic fatigue syndrome also fit systemic exertion intolerance disease criteria", Fatigue: Biomedicine, Health & Behavior, 5, doi:10.1080/21641846.2017.1299079 
  3. Nagy-Szakal, Dorottya; Williams, Brent L.; Mishra, Nischay; Che, Xiaoyu; Lee, Bohyun; Bateman, Lucinda; Klimas, Nancy G.; Komaroff, Anthony L.; Levine, Susan; Montoya, Jose G.; Peterson, Daniel L.; Ramanan, Devi; Jain, Komal; Eddy, Meredith L.; Hornig, Mady; Lipkin, W. Ian (2017), "Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome", Microbiome, 5 (44), doi:10.1186/s40168-017-0261-y 
  4. Zeineh, Michael M.; Kang, James; Atlas, Scott W.; Raman, Mira M.; Reiss, Allan L.; Norris, Jane L.; Valencia, Ian; Montoya, Jose G. (Feb 2015), "Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome" (PDF), Radiology, 274 (2): 517-526, doi:10.1148/radiol.14141079 
  5. Hornig, M; Montoya, JG; Klimas, NG; Levine, SM; Felsenstein, D; Bateman, L; Peterson, DL; Gottschalk, CG; Schultz, AF; Che, X; Eddy, ML; Komaroff, AL; Lipkin, WI (2015), "Distinct plasma immune signatures in ME/CFS are present early in the course of illness", Science Advances, 1 (1), doi:10.1126/sciadv.1400121 
  6. Zinn, Marcie L; Zinn, Mark A; Norris, Jane; Valencia, Ian; Montoya, Jose G; Maldonad, Jose R (2014), "EEG peak alpha frequency is associated with chronic fatigue syndrome: A case-control observational study", Conference: 2014 Stanford Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome Symposium 
  7. Stringer, Elizabeth Ann; Baker, Katharine Susanne; Carroll, Ian R; Montoya, Jose G; Chu, Lily; Maecker, Holden T; Younger, Jarred W (9 April 2013), "Daily cytokine fluctuations, driven by leptin, are associated with fatigue severity in chronic fatigue syndrome: evidence of inflammatory pathology", Journal of Translational Medicine, 2013 (11): 93, doi:10.1186/1479-5876-11-93 
  8. Montoya, JG; Kogelnik, AM; Bhangoo, M; Lunn, MR; Flamand, L; Merrihew, LE; Watt, T; Kubo, JT; Paik, J; Desai, M (2013), "Randomized clinical trial to evaluate the efficacy and safety of valganciclovir in a subset of patients with chronic fatigue syndrome.", Journal of Medical Virology, 85 (12): 2101-9, PMID 23959519, doi:10.1002/jmv.23713 
  9. Watt, T; Oberfoell, S; Balise, R; Lunn, MR; Kar, AK; Merrihew, LE; Bhangoo, MS; Montoya, JG (2012), "Response to valganciclovir in chronic fatigue syndrome patients with human herpesvirus 6 and Epstein-Barr virus IgG antibody titers", Journal of Medical Virology, 84 (12): 1967-1974, PMID 23080504, doi:10.1002/jmv.23411 
  10. Alter, Harvey J.; Mikovits, Judy A.; Switzer, William M.; Ruscetti, Francis W.; Lo, Shyh-Ching; Klimas, Nancy; Komaroff, Anthony L.; Montoya, Jose G.; Bateman, Lucinda; Levine, Susan; Peterson, Daniel; Levin, Bruce; Hanson, Maureen R.; Genfi, Afia; Bhat, Meera; Zheng, HaoQiang; Wang, Richard; Li, Bingjie; Hung, Guo-Chiuan; Lee, Li Ling; Sameroff, Stephen; Heneine, Walid; Coffin, John; Hornig, Mady; Lipkin, W. Ian (2012), "A Multicenter Blinded Analysis Indicates No Association between Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and either Xenotropic Murine Leukemia Virus-Related Virus or Polytropic Murine Leukemia Virus", mBio, 3 (5): e00266–12, doi:10.1128/mBio.00266-12 
  11. Immune System Disruption - Stanford Med


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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history