Masters class

MASTERS IN INFECTIOUS DISEASES 2011

STUDY GUIDE

Epidemiology 1
Inglis TJ. Principia aetiologica: taking causality
beyond Koch’s postulates. J Med Microbiol. 2007; 56:1419-22.

There is no single accepted method to establish a causal relationship between an infective agent and its corresponding infectious disease. Different biomedical disciplines use a patchwork of distinct but overlapping approaches. To a greater or lesser extent these are based on criteria known as the Koch-Henle postulates, or ‘Koch’s postulates’ for short. Deficiencies in Koch’s postulates were recognized by their principal author shortly after their formulation. Now, over a century later, a more rigorous method to test causality has still to be finalized. One contender is a method that uses molecular methods to establish a causal relationship (‘molecular Koch’s postulates’). Recognizing the wider range of contemporary approaches used to build an argument for a causal relationship, the use of a more inclusive approach to establish proof of causality is proposed. This method uses an argument built from a series of assertions:

1:  congruence or reproducible correlation of a taxonomically defined life form
with the clinico-pathological and epidemiological features of infection.

2:  consistency of the demonstrable biological response in the subject to an
encounter with the prospective infective agent.

3:  progressive or cumulative dissonance as an explanation for pathophysiological
processes at every known level of biological organization in the subject.

4:  curtailment of that pathophysiological process on the deliberate introduction
of a specified biomedical intervention.

Evidence to implicate the candidate biological entity as an initiator of
or primer for cumulative dissonance places it in a subcategory of
micro-organisms to be known as ‘priobes’. A priobe is the sufficient and
necessary antecedent cause of a pathophysiological process evident as an
infectious disease.

Epidemiology 2
Key examples of how it plays out:

  • Acinetobacter in intensive care

Snelling AM, Gerner-Smidt P, Hawkey PM, Heritage J, Parnell P, Porter C, Bodenham AR, Inglis T. Validation of use of whole-cell repetitive extragenic palindromic sequence-based PCR (REP-PCR) for typing strains belonging to the Acinetobacter calcoaceticus-Acinetobacter baumannii complex and application of the method to the investigation of a hospital outbreak. J Clin Microbiol. 1996; 34: 1193-202.

  • Melioidosis

Inglis TJ, Garrow SC, Henderson M, Clair A, Sampson J, O’Reilly L, Cameron B.
Burkholderia pseudomallei traced to water treatment plant in Australia.
Emerg Infect Dis. 2000; 6: 56-9.

Inglis TJ, O’Reilly L, Merritt AJ, Levy A, Heath C. The aftermath of the Western
Australian melioidosis outbreak.
Am J Trop Med Hyg. 2011; 84: 851-7.

  • Listeriosis

Inglis TJ, Clair A, Sampson J, O’Reilly L, Vandenberg S, Leighton K, Watson A. Real-time application of automated ribotyping and DNA macrorestriction analysis in the setting of a listeriosis outbreak. Epidemiol Infect. 2003; 131: 637-45.

  • Pseudomonas hospital infections

Inglis TJ, Benson KA, O’Reilly L, Bradbury R, Hodge M, Speers D, Heath CH. Emergence of multi-resistant Pseudomonas aeruginosa in a Western Australian hospital. J Hosp Infect. 2010; 76: 60-5.

  • German STEC

http://micrognome.priobe.net/2011/06/new-stec-in-europe/

  • H1N1/09 influenza

Iwasaki Y, Abe T, Wada K, Itoh M, Ikemura T. Prediction of directional changes of influenza A virus genome sequences with emphasis on pandemic H1N1/09 as a model case. DNA Res. 2011; 18: 125-36.

Ingram PR, Inglis T, Moxon D, Speers D. Procalcitonin and C-reactive protein in severe 2009 H1N1 influenza infection. Intensive Care Med. 2010; 36: 528-32.

3 Diagnostics

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