From: "Jernigan, Daniel B." To: dobos@math.utk.edu Cc: "Jernigan, Daniel B." Subject: Modeling of Infectious Diseases Date: Fri, 24 Feb 95 13:45:00 EST Message-Id: <2F4DABE2@SmtpOut.em.cdc.gov> Encoding: 20 TEXT X-Mailer: Microsoft Mail V3.0 Content-Length: 1051 Status: R Alek, I was forwarded your note regarding modeling of infectious diseases. There are a number of centers at CDC which currently use modeling to varying degrees. In our section, Respiratory Diseases Epidemiology Section of the National Center for Infectious Disease, our focus in the last year has been on drug-resistant Streptococcus pneumoniae. S. pneumoniae is responsible for most cases of bacterial pneumonia, meningitis, and otitis in the US and worldwide. In the last 10 years, resistance has rapidly emerged and has become a major public health problem. I am currently working with Bruce Levin and Rustom Antia to develop a model to describe the spread of pneumococcal resistance through a community and to determine the threshold of resistance at which antibiotic therapy should be altered. Let me know if there are specific questions that you have regarding antimicrobial-resistant Streptococcus pneumoniae if you are attempting to model bacterial community-acquired infections. Dan Jernigan, MD MPH CDC Atlanta, GA From brenda@jupiter.esd.ornl.gov Mon Mar 6 09:25:08 1995 Date: Mon, 6 Mar 1995 09:22:17 -0500 (EST) From: "Brenda L. Rashleigh" Subject: S. pneumoniae model (fwd) To: "Dr. Lou Gross" MIME-Version: 1.0 Content-Type: TEXT/PLAIN; charset=US-ASCII Content-Length: 1735 Dr. Gross: Attached is a reply from Dr. Jernigan at the CDC in response to my asking if their work was published. I called Eva Harris early this morning (at UT hospital) but apparently she will not be available until next Mon.--I will try again then. Brenda Rashleigh ---------- Forwarded message ---------- Date: Mon, 06 Mar 95 08:52:00 EST From: "Jernigan, Daniel B." To: brenda@jupiter.esd.ornl.gov Subject: S. pneumoniae model Unfortunately, the work is presently underway in collaboration with Bruce Levin and Rustom Antia at Emory University. There have not yet been any publications of it. Drs. Levin and Antia have a model for acute infection based mainly on work with E. coli. Their model takes in-host factors such as commensal populations etc and uses a modified Anderson-May model. They are working closely with the group at Oxford to develop a large model which would include in-host populations and populations of individual hosts in a community. This model will be interesting to see it's applicability to antimicrobial resistance. If you have a model that you need numbers, incidences etc to plug in I can provide some of those numbers for drug-resistant Streptococcus pneumoniae (DRSP). The topic you have chosen for your class is an important topic, that of antimicrobial resistance. It was in fact the topic of a meeting of mathematicians and epidemiologists 2 weeks ago following the Acad. Adv. Sci. meetings here in Atlanta. Let me know what the basic outline of your model is and I may be able to provide some numbers to support it. Antimicrobial resistance in the community is a tricky thing to define due to prevalence of antimicrobial use. Dan. ------------------------------------------------------------- Questions from Brenda to Dr. Jernigan These were my questions: 1. I have read that overuse/unnecessary use of antibiotics for colds and such has contributed to problems of resistance in bacterial diseases--how does this happen? Is it due to exchance of genetic material between viruses and bacteria? 2. I have read that antibiotic resistance decreases in a population when antibiotic use is decreased (i.e., penicillin in Hungary), although the link hasn't been firmly established. Is this simply due to the fact that fewer patients are developing resistance, or is there some sort of competitive interaction between bacterial strains? Response: Date: Mon, 06 Mar 95 11:11:00 EST From: "Jernigan, Daniel B." To: brenda@jupiter.esd.ornl.gov Subject: Re: S. pneumoniae model Inherent in most models is the assumption that there is a cost of resistance. This cost may be the carrying of a plasmid which infers resistance or chromosomal changes through acquisistion of transposons or free genetic elements in the environment. We usually assume that this cost exists and therefore, that resistance would decline given the removal of antimicrobials. Data to support this "cost" is not clear for S. pneumoniae. Drs. Levin and Antia have data to support the presence of a cost of resistance for E. coli. Their model allows one to vary the cost of resistance from 0 to 100% and explore the changes that occur in the outcome. In answer to your question re: antimicrobial use, most experts agree, although not so much from available data, that the major contributor to increased resistance is prophylactic antibiotic (Abx) use such as before surgery, and another contributor is empiric Abx use, such as giving ampicillin to a febrile child where the cause is not known, and won't be known because it is easier to treat than to find the cause. Abx-resistant TB is a different problem since the Abxs are only used to treat TB. There is no colonizing or commensal population of TB in people. Therefore, resistance develops in a host due to treatment, rather than development of resistance in commensal (non-pathogenic) bacteria which then serve as a reservoir of resistance genes for pathogenic bacteria. Specific questions regarding TB can be directed to Tom Kenyon or Patrick Zuber in the TB branch (404)639-8121. ------------------------------------------------------------------------------ REPLY FROM: Jernigan, Daniel B. Return-Path: Received: from msmail by SmtpIn.em.cdc.gov id <2F5AA176@SmtpIn.em.cdc.gov>;