[USCC] Compost Digest, Vol 30, Issue 3 Adverse Health Effects (John Cline)

[Edo McGowan]

Re: Compost Digest, Vol 30, Issue 3
Adverse Health Effects from Land Application of Biosolids (John Cline) 


Some useful information for those discussing sludge now that we have an accepted authority speaking. The Jeff Soller paper (2006), --------see—

http://www.epa.gov/nheerl/articles/2006/waterborne_disease/microbial_risk_assessment.pdf

recently published within the Journal of Water and Health, whose editor is Charles P Gerba, notes the following, which is what some of us have been saying for years. The Soller paper is part of the basis for the EPA & CDC study of drinking water. In discussing health risk assessments based on dose response, he now also discusses the passage of antibiotic resistance from a few contaminants to vast numbers within the gut flora. I had previously commented on work by Soller in the area of risk assessment that it had neglected to consider the importance of transferred genetic information in dose response. I see that he has corrected that defect.

 “RELATIVE TO THE MICROORGANISMS THE FOLLOWING MAY BE IMPORTANT: THE VIRULENCE AND INFECTIVITY OF MICROORGANISMS CAN CHANGE DEPENDING ON THEIR INTERACTION WITH THE HOST AND ENVIRONMENT; GENETIC MATERIAL CAN BE TRANSFERRED BETWEEN MICROORGANISMS, LEADING TO THE TRANSFER OF CHARACTERISTICS SUCH AS ANTIBIOTIC RESISTANCE AND VIRULENCE FACTORS; AND/OR LOW DOSES OF SOME MICROORGANISMS CAN IN SOME CASES CAUSE SEVERE EFFECT.”  

>From my earlier work, we see much the same. These contaminant bacteria are thus able to colonize environmental niches, and animals, including humans, through ingestion. Once ingested, the plasmids may be transferred to normal flora, and subsequently to pathogenic bacteria found in humans or animals, making later treatment with particular antibiotics ineffective. Also one must consider transfer of genetic information from these organisms to more robust organisms as highlighted by Sjolund et al. (2005) [13] indicating that resistance in the normal flora, which may last up to four-years, might contribute to increased resistance in higher-grade pathogens through interspecies transfer. 

These authors go on to note that since populations of the normal biota are large, this affords the chance for multiple and different resistant variants to develop. This thus enhances the risk for spread to populations of pathogens. Furthermore, there is crossed resistance. For example, vancomycin resistance may be maintained by using macrolides [14]. 

This then brings into question the current paradigm on infection and its dose response to a certain load of a particular pathogen, i.e., ID and LD 50s. Lateral transfer of mobile genetic elements conferring resistance is not considered in this old paradigm. With the prodigious capacity for the gut bacteria to multiply, once the lateral transfer has taken place, very small original numbers---well below the old paradigms can be multiplied into impressive numbers. Since viruses and phages are also involved, their capacity to multiply, which dwarfs that of bacteria, must also be included. Thus there is a need for a new paradigm; unfortunately, the regulatory community seems not to recognize this. When one considers the multiplication within sewer plants and also within their byproducts, disbursement into the environment, the transfer to background organisms, hence to man and his animals, then the remultiplication within commensals, the emerging picture is worrisome.
[13]Emerging Infectious Diseases (Vol. 11, # 9, Sept 2005 @ p. 1389 et seq), 

[14]  Giacometti A, Cirioni O, Kamysz W, Silvestri C, Licci A, D'Amato G, Nadolski P, Riva A, Lukasiak J, Scalise G.  In vitro activity and killing effect of uperin 3.6 against gram- positive cocci isolated from immunocompromised patients. Antimicrob Agents Chemother. 2005 Sep;49(9):3933-6. Robertson GT, Zhao J, Desai BV, Coleman WH, Nicas TI, Gilmour R, Grinius L, Morrison DA, Winkler ME. Vancomycin tolerance induced by erythromycin but not by loss of vncRS, vex3, or pep27 function in Streptococcus pneumoniae. J Bacteriol. 2002 Dec;184(24):6987-7000. ].