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
always indicate presence of infectious virus. Although it
is considered that RNA will degrade in the absence of the
protective core protein, no information is available about
the time required for this in various types of samples.
Epidemiology
Groups A, B, and C RV infect pigs and humans
(Geyer et al. 1995; Kapikian, Hoshino, and Chanock
2001; Kim et al. 1999; Martella et al. 2001; Saif and Jiang
1990; Teodoroff et al. 2005; Winiarczyk et al. 2002; Yuan,
Stevenson, and Saif 2006). Both RV-A and nongroup
A have been detected in the same herd (Atii, Ojeh, and
Durojaiye 1990; Fitzgerald et al. 1988; Gatti et al. 1993).
group A
Group A RV is the main agent of viral diarrhea in
piglets, accounting for 53% of preweaning and 44% of
postweaning diarrhea in swine (Will et al. 1994). One
report attributes 89% of all RV diarrhea in commercial
pig operations to RV-A (Gouvea et al. 1991). Diarrheic
animals shed virus in high titer in feces (10 7 –10 8
infectious doses/g feces). In pigs, the infection is an
age- and husbandry-associated disease. Thus RV has
been associated with acute diarrhea in pigs weaned
at 2–8 wk of age and during different stages of the
suckling period, but not usually during the first 7–10
d of life (Bohl et al. 1978; Nagy et al. 1996; Wieler et al.
2001; Woode 1982). This difference has been attributed
to the level of passively transferred antibodies that
remains high during the first week of life, and to passive
antibodies in colostrum and milk maintained in the
gut. The occurrence of RV was significantly higher
in 22- to 28-d-old pigs than in younger pigs during
diarrhea outbreaks in 24 farms in Germany (Wieler
et al. 2001). Nagy and colleagues in Hungary (1996)
reported an 18.6% prevalence of RV-A in postweaning
pigs with diarrhea. In studies by Janke and colleagues
(1990), RV-A was detected in 76.4% of nursing pigs and
40.9% of weaned pigs during a diarrhea outbreak in
a conventional swine operation. Increased numbers
of outbreaks or outbreaks in pigs less than 1 wk old
can occur, if one or more risk factors such as the
introduction of a new RV strain, primiparous sows
with qualitatively and quantitatively poorer colostrum,
or poor farm management practices are present on
the farm. Farm expansion, early weaning, and all-in/
all-out production were associated with increased
numbers of outbreaks in Ontario between 1994 and
1998 (Dewey et al. 2003). A nonpreviously circulating
RV strain, primiparous sows, and high population
density were considered as the three major risk factors
that contributed to an outbreak of diarrhea by RV-A
affecting pigs from birth up to 28 d of age (53% of up
to 1-wk-old pigs, 60% of 8- to 21-d-old pigs, and 52% of
more than 21-d-old pigs) in Brazil (Barreiros et al. 2003).
group B and C rVs
The RV-B and RV-C have been identified in
humans and pigs. Geyer and colleagues (1996) reported
RV-B in 4.6% and RV-C in 10.8% by PAGE of samples
collected from 1- to 43-d-old pigs with diarrhea. In the
study by Janke and colleagues (1990), RV-B and RV-C
were detected in 7.4% and 7.5% of nursing pigs and in
18.2% and 22.7% of weaned pigs, respectively, by PAGE.
In the United States, RV-C was identified in fecal
samples collected from finishing pigs with diarrhea by
IEM, cell-culture IF, and RT-PCR (Kim et al. 1999).
Group C RV was the cause of enzootic neonatal
diarrhea in a swine herd in Quebec reported in 1990.
During the outbreaks of diarrhea, the morbidity rate was
100% and case fatality rates were 5 to 10% among 1- to
2-day-old piglets (Morin, Magar, and Robinson 1990).
Group RV-B and RV-C were reported as a cause of 12% of
120 outbreaks that occurred in Quebec during 1 yr in 2-d-
to 5-wk-old pigs (Magar, Robinson, and Morin 1991).
Most RV-B or RV-C in humans have been isolated
cases, but outbreaks have been reported worldwide
(Bridger, Pedley, and McCrae 1986; Castello et al. 2000;
Gabbay et al. 1999; Jiang et al. 1995; Maunula, Svensson,
and von Bonsdorff 1992; Penaranda et al. 1989; Rasool
et al. 1994; Tsunemitsu, Jiang, and Saif 1992). But the
finding of a low prevalence of antibody to RV-C in
humans (Nilsson, Sigstam, and Svensson 2000; Saif
and Jiang 1990; Tsunemitsu, Jiang, and Saif 1992) and
a higher prevalence in pigs (Bridger and Brown 1985;
Saif and Jiang 1990; Tsunemitsu, Jiang, and Saif 1992)
has led to the suggestion that RV-C could be a zoonotic
infection of humans (Will et al. 1994).