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18 Fate and Transport of Zoonotic Bacterial, Viral, and Parasitic Pathogens during Swine Manure Treatment, Storage, and Land Application Table 2.2 examples of the effects of biological and physical variables on bacterial pathogens in wastes Physical Biological Chemical Variable Significant Conditions Effect on Pathogens References Temperature 1–9°C vs. 40–60°C Increased survival of Salmonella and E. coli O157:H7 at lower temperatures 8°C vs. 20°C vs. 37°C Increasing survival of Salmonella as temperatures were lowered Moisture 2% DM vs. 7% DM Increased survival of E. coli O157 and Salmonella at higher moisture content. No effect on Listeria and Campylobacter survival Aeration Conditions not specified Decreased survival of Salmonella and E. coli O157:H7 in solid manures when manures were aerated Turning solid manure heap Removal of solids from liquid fraction Time interval not provided Removal of 98% of total suspended solids from swine wastewater Turning swine manure heap increased survival of E. coli O157 and Salmonella, but had no effect on Listeria and Campylobacter survival Rogers and Haines 2005 Guan and Holley 2003 Nicholson, Groves, and Chambers 2005 Rogers and Haines 2005 Nicholson, Groves, and Chambers, 2005 Reduced Salmonella 0.5 to 1 log10 Vanotti et al. 2005a Sunlight Ultraviolet-B λ=285-315 Inactivates E. coli (indicator bacteria, pathogenic E. coli not measured) Anaerobic mesophilic lagoon treatment Actinomyces bacteria Removal of biological nitrogen Not applicable Reduces Salmonella 0.8-1.8 log10 and enterococci 1.8 log10 Hill 2003 Hill and Sobsey 2003; Vanotti et al. 2005a, c Antibiotic production Antagonistic to Salmonella spp. Hill 2003 Denitrification resulting in removal of 95% of TKN Reduction of Salmonella by 2.4 log10 and enterocci by 4.1 log10 High pH Average pH value over 10 Reduction of Salmonella and enterococci by over 1.5 log10 Vanotti et al. 2005a, c Vanotti et al. 2005a, c
3. Common Viruses of Swine inf l u e n z a Influenza viruses are enveloped, segmented, single-stranded (ss), negative-sense ribonucleic acid (RNA) viruses belonging to the family Orthomyxoviridae (Lamb and Krug 2001). The Orthomyxoviridae family consists of four genera: influenza A virus, influenza B virus, influenza C virus, and thogotovirus (Lamb and Krug 2001). Swine influenza virus belongs to the influenza A virus genus. Type A influenza viruses cause disease in lower mammals, birds, and humans (Wright and Webster 2001). Although type B influenza viruses primarily have been associated with disease in humans, there is evidence for rare type B influenza infections outside humans reported in the United Kingdom (U.K.) and China in pigs that were shown to possess antibodies against influenza B virus (Brown, Harris, and Alexander 1995; Mu et al. 1988), and a single report of an infection in a marine mammal (Wright and Webster 2001). Type C influenza viruses are isolated only occasionally, and although they can infect humans, dogs, and swine, there is little evidence that they circulate widely in swine (Brown, Harris, and Alexander 1995; CDC 2005; Matsuzaki et al. 2002; Youzbashi et al. 1996). Because swine influenza is caused primarily by influenza A viruses, this genus will be discussed in detail in this chapter. The influenza A virus genome consists of eight RNA genes (Lamb and Krug 2001) that encode for 11 different viral proteins (Chen et al. 2001; Gibbs et al. 2003). Two of the genes—hemagglutinin (HA) and neuraminidase (NA)—encode for surface glycoproteins that project from the viral envelope, and because they possess distinct antigenic properties, they are used to subtype influenza viruses into 16 HA types (1–16) (Fouchier et al. 2005) and 9 NA types (1–9) (Lamb and Krug 2001). Two internal genes—nucleoprotein and matrix—are conserved highly within the three types (A, B, and C) of influenza viruses and often are targeted in detection assays. 3. COMMON VIruSeS OF SwINe Influenza A viruses are named by their HA and NA type, (e.g., H1N1), and often are given “strain” names that include their genus or type, host species if other than human, location of isolation, arbitrary laboratory number, and year of isolation (e.g., A/Swine/ Iowa/15/1930). Epidemiology Swine influenza virus (SIV) has evolved from a seasonal disease caused by a stable genotype to a yearround endemic respiratory disease caused by multiple genotypes undergoing continual change (Erickson and Gramer 2003). These changes are caused by two mechanisms: antigenic shift (or reassortment) and antigenic drift (Lamb and Krug 2001). Antigenic shift is a dramatic change that occurs when virus gene segments are exchanged between two viruses infecting the same host cell (Hilleman 2002). Antigenic drift is a more subtle change that occurs through accumulations of point mutations made during replication of the virus genome (Schweiger, Zadow, and Heckler 2002). For 80 yr, pigs in North America had only one endemic strain of SIV, classical H1N1, until 1998 when a human reassortant H3N2 SIV was detected in U.S. swine (Brown 2000). In 1998, reassortant H3N2 SIVs emerged in the swine population that either were double reassortant with human and avian strains of influenza (A/Sw/NC/98) or triple reassortment with human, avian, and swine influenza strains (A/Sw/TX/98). In early 1999, the HA of the preexisting classical H1N1 SIV reassorted with H3N2 SIV virus to create a second reassortant virus, H1N2 (Karasin, Olsen, and Anderson 2000). Control then was complicated further as evidenced by multiple outbreaks of swine influenza resulting from H1N2 infection despite possible preexisting vaccinal immunity against classical H1N1 SIV (Erickson and Gramer 2003; Karasin, Olsen, and Anderson 2000). Further reassortment occurred in late 2002 when both the HA and NA of H3N2 SIV were replaced by the classical H1 and N1 genes, thereby creating a reassortant novel H1N1 SIV with avian internal (PA and PB2) genes (Webby et al. 2004). 19
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