17 research outputs found
Diagnosing acute infections of porcine reproductive and respiratory syndrome virus in swine
The goal of this paper is to illustrate which specimens and diagnostic methods have been the
most efficacious for the diagnosis of porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV)
infections by summarizing results from PRRS field investigations. In the fall of 1996 a number of swine
farms in the midwest USA experienced acute reproductive losses that were characterized by a high
incidence of sow mortality, abortions at all stages of gestation, stillborn and weak-born pigs, and
respiratory disease in young pigs. Except for the severity of the disease, the clinical signs
in these cases were compatible with PRRS although preliminary tests had not detected PRRSV. These cases
were initially referred to as Sow Abortion and Mortality Syndrome (SAMS) and diagnostic
investigations intensified. PRRSV was still the number one suspect etiology; however, serology was not
useful since most of these affected herds were seropositive for PRRSV due to previous
infections or vaccination. PRRSV was detected by immunohistochemistry in some of the affected pigs and
sows suggesting it had a role in SAMS. The syndrome became known as Atypical or Acute
PRRS and with the testing of adequate samples, PRRSV was isolated from these cases
indicating it played a
significant role in the reproductive failure. The best samples to demonstrate
reproductive failure (based on success of virus isolation) have been presuckle blood samples from
weak-born pigs followed by blood from stillborn pigs and fluids from aborted fetuses;
however, virus was isolated only rarely or almost never from fetuses aborted after or before 100 days of
gestation, respectively. The best sample to consistently demonstrate PRRSV infection in
a group of swine older than 3-5 days of age has been lung lavage fluid. During the course of this
investigation we visited 10 farms that had clinical signs compatible with Atypical PRRS.
PRRSV was isolated from each case using MARC-145 cells and all virus isolates had the same 1-4-2 RFLP
pattern; however, when sequenced there were genetic differences among the isolates
(nucleotide difference for OFR5 was 1-9%). An important factor in the success of isolating virus from
these cases was the collection of an adequate sample size since not all weak-born pigs
are infected with PRRSV in utero and PRRSV-induced abortions do occur without transplacental
infection of
fetuses (especially abortions earlier than 100 days of gestation). The severe disease
observed in the field has been reproduced in young pigs and pregnant gilts infected with Atypical PRRSV
isolates propagated in cell culture. This is in contrast to previous studies where swine
were not dramatically affected after experimental PRRSV infection. The application of diagnostic tests
for PRRS epizootiology is demonstrated with the following field study that started about August 1,
1998 when a veterinarian notified our laboratory that a number of swine farms in his practice experienced
epizootics of abortions and sick sows. We received or collected samples (sera from affected sows,
aborted fetuses, weak-born pigs, and affected neonatal pigs) from 7 of these affected farms and PRRSV was
isolated from at least one animal on each farm. All isolates from 6 of the 7 farms (Farms A,
B, C, D, E, and G) had a 1-4-1 RFLP pattern and the 7th farm (Farm F) had a 1-4-1 viral isolate in one
pig and a 1-7-1 viral isolate in a second pig. We were suspicious the epizootics on these
farms may have been related due to the fact that 6 of these farms were located relatively close to each
other (Farm D was located about 20 miles from this cluster of farms), the onset and
severity of reproductive failure was similar among farms, and the 1-4-1 RFLP pattern was found on each
farm. We continued the genetic analysis with nucleotide sequencing of ORF5 and comparison
of the amino acid sequence of each isolate on each farm. Farms A, D, E, and G had 100% homology and when
using the ORF5 sequence of these farms as a consensus sequence, farms B and C had 99.5%
homology. The 1-4-1 isolate and the 1-7-1 isolate from farm F had 97.25% and 96.75% homology with the
consensus sequence, respectively. Except for the fact that each farm had a group of
pregnant sows in the same stage of pregnancy, no common denominator or relationship was detected among
the farms that would account for the presence of a similar if not identical PRRSV isolate.
The findings from this cluster of PRRS epizootics suggests area spread of PRRSV without any direct
transmission by swine, humans, or fomites. We assume, as others have hypothesized, that
this area spread represents air borne transmission although the possibility of a biologic
or mechanical
vector (birds, insects) cannot be ruled out