Fate and Transport of Zoonotic Bacterial, Viral, and - The Pork Store ...

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Fate and Transport of Zoonotic Bacterial, Viral, and Parasitic Pathogens during Swine Manure Treatment, Storage, and Land Application
3 and genotype 4 strains of HEV, although not the sole
reservoir of all HEV.
Inactivation
Only limited information is available regarding
HEV resistance to inactivation by physical, chemical,
and environmental forces. Under laboratory conditions,
HEV is sensitive to CsCl gradient centrifugation and
low-temperature storage (Bradley et al. 1987; Purcell and
Emerson 2001). Iodinated disinfectants and autoclaving
normally will destroy the virus (Balayan 1997; Schlauder
and Dawson 2003). HEV virions are reportedly stable
when exposed to trifluorotrichloroethane (Ticehurst
1991). Like other nonenveloped small RNA viruses,
however, HEV can survive harsh environments. The
fecal–oral route of transmission indicates that HEV
is resistant to inactivation by acidic and mild alkaline
conditions in the intestinal tract. It recently has been
shown that HEV is more heat labile than the hepatitis A
virus (HAV), another enterically transmitted hepatitis
virus (Emerson, Arankalle, and Purcell 2005). When
fecal suspensions of wild-type HM175 strain of HAV
or Sar-55 strain of HEV were diluted in a phosphatebuffered
saline (PBS) buffer and compared in the
same test by heating for 1 hr at 45, 50, 56, 60, 66, or
70°C, HAV was inactivated only 50% at 60°C but
was almost totally inactivated at 66°C. In contrast,
HEV was approximately 50% inactivated at 56°C and
almost totally inactivated (96%) at 60°C. The in vitro
results were recently confirmed by an in vivo pig study
demonstrating that incubation of infectious HEV at
56°C for 1 hr did not abolish the infectivity of the virus
(Feagins et al. 2008).
Presence and Fate
As fecal–oral transmitted diseases, waterborne
epidemics are the characteristic of hepatitis E outbreaks
in humans (Purcell and Emerson 2001). Like human
HEV, swine HEV is thought to be transmitted via the
fecal–oral route under natural conditions. It has been
demonstrated that infected pigs shed large amounts
of viruses in feces (Halbur et al. 2001; Meng et al.
1998b; Williams et al. 2001), which likely is the main
source for virus spread within a herd. Fecal shedding
of HEV in pigs, ranging from 3 to 8 wk, lasts much
longer than viremia, and the infectious virus titer in
feces also is higher than that in blood (Halbur et al.
2001; Kasorndorkbua et al. 2002, 2004; Meng et al.
1998b). It generally is believed that pigs become infected
through ingestion of feces-contaminated water or feed
or through direct contact with infected pigs. Current
swine production procedures often flush water through
confinement housing either in open gutters or under
slatted floors, providing the opportunity for either
direct exposure of pigs to feces (open gutter system)
or indirect exposures via droplet aerosols (slatted
floor system) (Dickey, Brumm, and Shelton 1981). But
under experimental conditions, infection of pigs via
the oral route of inoculation with an infectious stock
of swine HEV proved to be more difficult than via the
intravenous route (Kasorndorkbua et al. 2004).
Because of the ubiquitous nature of swine HEV
in pigs and the large amount of viruses excreted in
feces, swine manure in swine production areas could
contaminate irrigation and drinking water in nearby
wells, rivers, ponds, or coastal water with concomitant
contamination of produce or shellfish (Smith et al.
2001). Consumption of contaminated shellfish has
been implicated in sporadic cases of acute hepatitis
E (Cacopardo et al. 1997; Koizumi et al. 2004). It
also has been shown that, in HEV endemic regions,
the use of river water for bathing, waste disposal,
and drinking purposes is a significant risk factor
(Sedyaningsih-Mamahit et al. 2002). In Southeast
Asia, a unique riverine ecology of HEV transmission
has been reported. Epidemic foci centered in riverine
environments (Corwin et al. 1999), the epidemic peaked
with heavy rains and flooding, and the attack rate was
significantly higher in villages supplied with river water
than in those relying on wells or ponds for water supply
(Bile et al. 1994). In these particular studies, the precise
origin of the HEV was undetermined.
Hepatitis E virus strains of both human and
swine origin have been detected in raw sewage water
(Clemente-Casares et al. 2003; Jothikumar et al. 1993;
Pina et al. 1998, 2000), and the recovered virus from
sewage water still is infectious in nonhuman primates.
Pina and colleagues (2000) found that the E11 strain of
HEV—likely of swine origin, recovered from sewage
water of pig slaughterhouses in Spain—has a close