Venereal transmission of pseudorabies viruses indigenous to feral swine

Between 1995 and 1998, we designed a series of studies in which we attempted to determine the main routes of transmission involved in the natural infection of pseudorabies virus (PRV) indigenous to free-ranging feral swine (Sus scrofa). Naturally infected feral sows transmitted the infection to uninfected feral boars, with which they had been commingled for a 6-wk period. Pseudorabies virus was isolated from boar preputial swabs, but not from nasal swabs. Three of the same PRV-infected feral sows did not transmit the infection to domestic boars during a 16 wk commingling period, despite the fact that they became pregnant. Feral boars, naturally infected with PRV transmitted the virus to domestic gilts while penned together during 6 wk. Pseudorabies virus was isolated from vaginal swabs, but not from nasal swabs of gilts, after 2 and 3 wk of commingling. When the same infected boars were commingled with either feral or domestic boars for 13 wk, PRV transmission did not occur. None of the exposed boars developed neutralizing antibodies or yielded virus from their preputial or nasal swabs. Our results indicate that PRV indigenous to feral swine is preferentially transmitted to feral or domestic swine of the opposite sex by the venereal route. This mode of transmission differs from that seen in the natural transmission of PRV prevalent in domestic swine, where contaminated secretions, excretions and aerosols are responsible for the spread of the virus. Based on these results, we feel that as long as feral swine do not come into direct contact with domestic swine, PRV-infected feral swine probably pose only a limited risk to the success of the National Pseudorabies Eradication Program. The fact that PRV is usually transmitted from feral to domestic swine at the time of mating would indicate that the isolation of domestic herds by the use of a "double fence," should be adequate protection against reinfection with PRV.     

A serosurvey for Brucella suis, classical swine fever virus, porcine circovirus type 2, and pseudorabies virus in feral swine (Sus scrofa) of eastern North Carolina

As feral swine (Sus scrofa) populations expand their range and the opportunity for feral swine hunting increases, there is increased potential for disease transmission that may impact humans, domestic swine, and wildlife. From September 2007 to March 2010, in 13 North Carolina, USA, counties and at Howell Woods Environmental Learning Center, we conducted a serosurvey of feral swine for Brucella suis, pseudorabies virus (PRV), and classical swine fever virus (CSFV); the samples obtained at Howell Woods also were tested for porcine circovirus type 2 (PCV-2). Feral swine serum was collected from trapped and hunter-harvested swine. For the first time since 2004 when screening began, we detected B. suis antibodies in 9% (9/98) of feral swine at Howell Woods and <1% (1/415) in the North Carolina counties. Also, at Howell Woods, we detected PCV-2 antibodies in 59% (53/90) of feral swine. We did not detect antibodies to PRV (n=512) or CSFV (n=307) at Howell Woods or the 13 North Carolina counties, respectively. The detection of feral swine with antibodies to B. suis for the first time in North Carolina warrants increased surveillance of the feral swine population to evaluate speed of disease spread and to establish the potential risk to commercial swine and humans.     

Potential sites of virus latency associated with indigenous pseudorabies viruses in feral swine

Free-ranging feral swine (Sus scrofa) are known to be present in at least 32 states of the USA and are continuously expanding their range. Infection with pseudorabies virus (PRV) occurs in feral swine and the primary route of transmission in free-living conditions seems to be venereal. Between 1995 and 1999, naturally infected feral swine and experimentally infected hybrid progeny of feral and domestic swine, were kept in isolation and evaluated for occurrence of latent PRV indigenous to feral swine in sacral and trigeminal ganglia and tonsil. Sacral ganglia were shown, by polymerase chain reaction (PCR) amplification of the thymidine kinase (TK) gene of PRV, to be the most frequent sites of latency of PRV. Nine (56%) of 16 sacral ganglia, seven (44%) of 16 trigeminal ganglia, and five (39%) of 13 tonsils from naturally infected feral swine were positive for PCR amplification of TK sequences of PRV. These tissues were negative for PRV when viral isolation was attempted in Vero cells. DNA sequencing of cloned TK fragments from the sacral ganglia of two feral swine, showed only one nucleotide difference between the two fragments and extensive sequence homology to fragment sequences from various domestic swine PRV strains from China, Northern Ireland, and the USA. The hybrid feral domestic swine, experimentally inoculated with an indigenous feral swine PRV isolate by either the genital or respiratory route, acquired the infection but showed no clinical signs of pseudorabies. Virus inoculated into either the genital or respiratory tract could, at times, be isolated from both these sites. The most common latency sites were the sacral ganglia, regardless of the route and dose of infection in these experimentally infected hybrids. Nine of 10 sacral ganglia, six of 10 trigeminal ganglia, and three of 10 tonsils were positive for PCR amplification of TK sequences. No virus was isolated from these tissues in Vero cells. The demonstration of the sacral ganglia as the most common sites of latency of pseudorabies viruses indigenous to feral swine, supports the hypothesis that these viruses are primarily transmitted venereally, and not by the respiratory route as is common in domestic swine, in which the trigeminal ganglia are the predominant sites of virus latency.     

Increased prevalence of Brucella suis and pseudorabies virus antibodies in adults of an isolated feral swine population in coastal South Carolina

Two hundred twenty seven adult (> 8 mo) feral swine (Sus scrofa) trapped from April through July 1999 at three locations on a coastal South Carolina (USA) peninsula with restricted ingress and egress were tested for Brucella suis and pseudorabies virus (PRV) antibodies. Approximately 44% of the animals tested positive for B. suis antibodies and 61% tested positive for antibodies to PRV. Previous surveys (1976 and 1992) of feral swine at the same location with similar methods indicated lower seroprevalences (28% and 18% for B. suis and 0% and 19% for PRV). We also found 39% of feral swine seropositive (n = 179) for Trichinella spiralis and 49% seropositive (n = 181) for Toxoplasma gondii. Results of repeated sampling demonstrated that seroprevalence to pathogens can increase with time in an isolated, unhunted population of feral swine suggesting an increased risk to local domestic livestock and potentially to human health.     

Serologic evidence of Venezuelan equine encephalitis in some wild and domestic populations of southern Texas.

More than 2,500 sera from approximately 30 wild and domestic species in southern Texas were tested for neutralizing antibodies to Venezuelan equine encephalitis (VEE). Virus isolations were also attempted from blood and tissue samples of many of the wild specimens. VEE neutralizing substances were present in a variety of species collected prior to the 1971 epizootic, suggesting that VEE was present and perhaps enzootic in this area before the recent epizootic. Serologic results of this study suggest that deer (Odocoileus virginianus) and feral swine (Sus scrofa) may serve as good indicators or sentinels of VEE transmission. The reservoir of VEE was not established, but results of the study suggest that a number of species or a combination of animal host populations including deer, feral swine, and peccaries (Pecari angulatus) may be involved in the eizootiologyof VEE in southern Texas.     

A survey of wild swine in the United States for evidence of hog cholera

The results of surveillance for hog cholera (HC) in wild swine (Sus scrofa) collected from throughout the United States from 1979 to 1987 are presented. Sera collected from 1,218 wild swine and tissues from 637 were evaluated for HC antibodies and virus, respectively. Included within this surveillance were samples from Santa Cruz and Santa Rosa Islands, California, where HC virus had been deliberately introduced into wild swine during the 1950's in attempts to eradicate these animals. All evaluations were considered negative for HC. It appears that the HC virus does not maintain itself in dispersed swine populations and that wild swine have not remained a reservoir of HC since its eradication in domestic swine in the United States.     

Making Contact: Rooting Out the Potential for Exposure of Commercial Production Swine Facilities to Feral Swine in North Carolina

Despite North Carolina’s long history with feral swine, populations were low or absent in eastern counties until the 1990s. Feral swine populations have since grown in these counties which also contain a high density of commercial production swine (CPS) facilities. Sixteen of the highest swine producing U.S. counties also populated with feral swine are in North Carolina. Disconcertingly, since 2009, positive tests for exposure to swine brucellosis or pseudorabies virus have been found for feral swine. We surveyed 120 CSP facilities across four eastern counties to document the level and perception of feral swine activity around CSP facilities and to identify disease transmission potential to commercial stock. Nearly all facility operators (97%) recognized feral swine were in their counties. Far fewer said they had feral swine activity nearby (18%). Our inspections found higher presence than perceived with feral swine sign at 19% of facilities where operators said they had never observed feral swine or their sign. Nearly 90% expressed concern about feral to domestic disease transmission, yet only two facilities had grain bins or feeders fenced against wildlife access. Due to increasing feral swine populations, recent evidence of disease in feral populations, the importance of swine production to North Carolina’s economy and the national pork industry, and potential for feral-domestic contact, we believe feral swine pose an increasing disease transmission threat warranting a stringent look at biosecurity and feral swine management at North Carolina CPS facilities.     

Prevalence of antibody to Toxoplasma gondii and Trichinella spp. in feral pigs (Sus scrofa) of eastern North Carolina

Feral pigs (Sus scrofa) survive in many climates, reproduce year-round, and are dietary generalists. In the United States, the size and range of the feral pig population has expanded, resulting in greater interaction with humans and domestic swine and increased potential for disease transmission. We conducted a serosurvey in feral pigs from eastern North Carolina to determine exposure to the zoonotic parasites, Toxoplasma gondii and Trichinella spp. Between September 2007 and March 2009, blood serum was collected from 83 feral pigs harvested at Howell Woods Environmental Learning Center, Four Oaks, North Carolina, USA. We used a modified agglutination test to test for T. gondii antibodies and an enzyme-linked immunosorbent assay to test for Trichinella spp. antibodies. The prevalences of antibodies to T. gondii and Trichinella spp. were 27.7% and 13.3%, respectively and 4% (n=3) had antibodies to both agents. We detected an increased risk of T. gondii antibodies with age, whereas the risk of exposure to T. gondii across years and between sexes was similar. In eastern North Carolina, feral pigs have been exposed to T. gondii and Trichinella spp. and may pose a health risk to domestic swine and humans.     

Further Isolation of a Recombinant Virus (H1N2, Formerly Hsw1N2) from a Pig in Japan in 1980

In September 1980, an outbreak of febrile respiratory disease was observed in a herd of sows (1-2 years of age) in Ehime Prefecture, Japan. Most of the swine showed clinical signs of disease such as depression, anorexia, fever, nasal discharge, and cough. A hemagglutinating agent was isolated from a nasal swab from one of the diseased pigs. By cross-hemagglutination-inhibition and neuraminidase-inhibition tests with antisera to influenza viruses of swine origin, the isolate was identified as an influenza A virus of the H1N2 (former designation, Hsw1N2) subtype, and designated A/swine/Ehime/1/80 (H1N2). Significant antibody rises against the surface antigens of the isolate were found in convalescent swine sera. The distribution of antibody against H1N2 virus in swine sera in Ehime Prefecture was examined. Seven (8%) of 93 sera collected after the outbreak (in 1981) showed antibodies to only H1 and N2 antigens but none of the sera before the outbreak contained such antibodies, indicating that H1N2 virus had been restrictedly prevalent among swine but was not wide-spread until 1981.     

Hosts of Lutzomyia shannoni (Diptera: Psychodidae) in relation to vesicular stomatitis virus on Ossabaw Island, Georgia, U.S.A.

Abstract. Hosts of Lutzomyia shannoni Dyar, a suspected biological vector of the New Jersey serotype of vesicular stomatitis (VSNJ) virus, were determined using an indirect enzyme-linked immunosorbent assay (ELISA) of 333 blood-fed female sandflies collected from their diurnal resting shelters on Ossabaw Island, Georgia, U.S.A. Sandflies had fed primarily on white-tailed deer ( Odocoileus virginianus ) (81%) and to a lesser extent on feral swine ( Sus scrofa ) (16%), two species of host infected annually with VSNJ. Other hosts were raccoons ( Procyon lotor ) and horses ( Equus caballus ) or donkeys ( E. asinus ), with only two (<1%) mixed bloodmeals from deer/raccoon and deer/swine. A larger proportion of feedings on feral swine was detected in maritime live oak forests than in mixed hardwood forests. These findings are consistent with the hypothesis that L. shannoni is a primary vector of VSNJ virus on Ossabaw Island.     

Serologic survey for brucellosis in feral swine, wild ruminants, and black bear of California, 1977 to 1989.

A retrospective analysis of brucellosis serologic testing results in eight wildlife species in California from 1977 to 1989 was done. Samples were collected from 5,398 live-captured or hunter-killed animals and tested by combinations of up to six serologic tests for antibodies to Brucella spp. Twenty-three of 611 (3.8%) feral swine (Sus scrofa), one of 180 (0.6%) black bear (Ursus americanus), one of 355 (0.3%) California mule deer (Odocoileus hemionus californicus), and one of 1,613 (0.06%) blacktail deer (Odocoileus hemionus columbianus) samples were considered reactors. Suspect serologic reactions occurred in three of 619 (0.5%) desert bighorn sheep (Ovis canadensis nelsoni) and one of 355 (0.3%) California mule deer samples. Brucellosis is not considered an important wildlife health problem in California except in feral swine.     

Fascioloides magna (Bassi, 1875) in feral swine from southern Texas.

Between 1971 and 1975, Fascioloides magna was found in 46 of 67 (69%) feral swine (Sus scrofa) in southern Texas. Flukes were recovered from swine in areas where F. magna commonly has been recovered from white-tailed deer and cattle. One to 12 flukes were recovered from each infected animal. Their presence was indicated by black hematin pigment on the liver and various other internal organs. Eggs were not detected in the gallbladder or feces of infected animals although mature flukes and eggs were recovered in the livers suggesting that, like cattle, feral swine can be infected but are aberrant hosts for the parasite and do not disseminate eggs.     

Influenza exposure in United States feral swine populations

Swine play an important role in the disease ecology of influenza. Having cellular receptors in common with birds and humans, swine provide opportunities for mixed infections and potential for genetic reassortment between avian, human, and porcine influenza. Feral swine populations are rapidly expanding in both numbers and range and are increasingly coming into contact with waterfowl, humans, and agricultural operations. In this study, over 875 feral swine were sampled from six states across the United States for serologic evidence of exposure to influenza. In Oklahoma, Florida, and Missouri, USA, no seropositive feral swine were detected. Seropositive swine were detected in California, Mississippi, and Texas, USA. Antibody prevalences in these states were 1% in Mississippi, 5% in California, and 14.4% in Texas. All seropositive swine were exposed to H3N2 subtype, the predominant subtype currently circulating in domestic swine. The only exceptions were in San Saba County, Texas, where of the 15 seropositive samples, four were positive for H1N1 and seven for both H1N1 and H3N2. In Texas, there was large geographical and temporal variation in antibody prevalence and no obvious connection to domestic swine operations. No evidence of exposure to avian influenza in feral swine was uncovered. From these results it is apparent that influenza in feral swine poses a risk primarily to swine production operations. However, because feral swine share habitat with waterfowl, prey on and scavenge dead and dying birds, are highly mobile, and are increasingly coming into contact with humans, the potential for these animals to become infected with avian or human influenza in addition to swine influenza is a distinct possibility.     

Antibodies to vesicular stomatitis virus in populations of feral swine in the United States

From 1979 to 1985, 941 feral swine (Sus scrofa) from 53 locations in 15 states were serologically tested for antibodies to vesicular stomatitis virus (VSV). Antibodies to New Jersey serotype VSV were present in 75 swine from five locations in Arkansas, Florida, Georgia, and Louisiana. Within these populations, antibody prevalences ranged from 10 to 100%. No antibodies to Indiana serotype were detected.     

Isolation of feline parvovirus from peripheral blood mononuclear cells of cats in northern Vietnam.

Feline parvovirus (FPV) was isolated rather frequently from the peripheral blood mononuclear cells (PBMCs) of cats in northern Vietnam by coculturing with MYA-1 cells (an interleukin-2-dependent feline T lymphoblastoid cell line) or Crandell feline kidney (CRFK) cells (a feline renal cell line). Efficiency of virus isolation was higher in MYA-1 cells than in CRFK cells. Interestingly, among the 17 cats from which FPV was isolated, 9 cats were positive for virus neutralizing (VN) antibody against FPV, indicating that FPV infected PBMCs and was not eliminated from PBMCs even in the presence of VN antibodies in the cats.     

Comparison of enzyme-linked immunosorbent and virus neutralization assays for the serology of reovirus infections in laboratory animals

An enzyme-linked immunosorbent assay (ELISA) for the detection and quantification of reovirus-specific IgM and IgG serum antibodies in rodents, detecting reovirus group reactive antibodies, was compared with reovirus types 1, 2 or 3 specific virus neutralization (VN) assays. To this end, serum samples were collected from specific pathogen-free (SPF) BALB/c RIVM mice, after experimental infection with any of the three mammalian reovirus serotypes. The majority (seven out of twelve) of the reovirus type 1-infected and one third (two out of six) of the reovirus type 3-infected mice died within 15 days after infection, whereas all (six out of six) of the reovirus type 2-infected animals survived. Using reovirus type 2 antigen in the ELISA, reovirus-specific IgM antibodies could be demonstrated within 1 week after infection in all the mice infected with reovirus types 2 or 3 and in the majority of the mice infected with type 1. Similarly, reovirus-specific IgG could be detected within 3 weeks in all the surviving mice infected with reovirus types 2 or 3 and within 5 weeks in all surviving mice infected with reovirus type 1. These results coincided well with the data obtained in the VN assays, in which all the infected animals also could be detected within 1 week after infection. As expected, titers were detected most rapidly and to the highest levels in the homologous VN assays. Given the sensitivity and the specificity of the ELISA system demonstrated in this paper and its suitability for incorporation in automated systems, the ELISA system should be considered valuable for the routine serologic diagnosis of reovirus infections in rodents.     

Trichinella spiralis in an agricultural ecosystem. III. Epidemiological investigations of Trichinella spiralis in resident wild and feral animals

As part of a larger epidemiological study examining the transmission of Trichinella spiralis in an agricultural ecosystem, resident wild and feral animals were trapped to determine the extent of their involvement in the natural, on-farm cycling of the parasite among swine. During a 21-mo-study, seven of 15 skunks (Mephitis mephitis), one of three opossums (Didelphis virginiana), two of two feral domestic cats and a raccoon (Procyon lotor) were found to be infected, while five shrews (Blarina brevicauda) and 18 deer mice (Peromyscus spp.) were uninfected. Most of the former hosts probably became infected by scavenging dead infected swine or rats (Rattus norvegicus). However, infections obtained through predation of living rats, particularly with regard to the cats, cannot be excluded. Our observations do not suggest that there was transmission of T. spiralis from the wild animals to swine. Therefore, transmission of T. spiralis appeared to occur only from the farm's swine and rats to the associated wild and feral animals.     

Parasites of the feral sheep of Pitt Island,Chatham group

Abstract

Samples from the feral and domestic sheep on Pitt Island were examined for parasites. The feral sheep had never been treated against parasites, and most were due for extermination. The domestic sheep were examined by way of comparison. The sheep ked (Melophagus ovinus) and the chorioptic mange mite (Chorioptes bovis) were found on feral but not domestic sheep. The sheep body louse (Damalinia ovis) was found on domestic but not feral sheep. Lung nodules and liver lesions, presumed to be caused by parasites, were significantly more prevalent in domestic than in feral sheep. The prevalence of Cysticercus tenuicollis cysts and Sarcocystis spp. macrocysts was similar in feral and domestic sheep. The species of intestinal nematode and their relative abundance in feral sheep were similar to those in mainland sheep. Fewer feral sheep were found to have antibodies to Toxoplasma gondii when compared with other breeds; the proportion with antibodies to Sarcocystis ovicanis differed little from that in the mainland flocks, however. The data are compared with information from the Campbell Island feral sheep flock.     

Virus-neutralizing antibodies of immunoglobulin G (IgG) but not of IgM or IgA isotypes can cure influenza virus pneumonia in SCID mice.

The ability of monoclonal antibodies (MAbs) to passively cure an influenza virus pneumonia in the absence of endogenous T- and B-cell responses was investigated by treating C.B-17 mice, homozygous for the severe combined immunodeficiency (SCID) mutation, with individual monoclonal antiviral antibodies 1 day after pulmonary infection with influenza virus PR8 [A/PR/8/34 (H1N1)]. Less than 10% of untreated SCID mice survived the infection. By contrast, 100% of infected SCID mice that had been treated with a single intraperitoneal inoculation of at least 175 micrograms of a pool of virus-neutralizing (VN+) antihemagglutinin (anti-HA) MAbs survived, even if antibody treatment was delayed up to 7 days after infection. The use of individual MAbs showed that recovery could be achieved by VN+ anti-HA MAbs of the immunoglobulin G1 (IgG1), IgG2a, IgG2b, and IgG3 isotypes but not by VN+ anti-HA MAbs of the IgA and IgM isotypes, even if the latter were used in a chronic treatment protocol to compensate for their shorter half-lives in vivo. Both IgA and IgM, although ineffective therapeutically, protected against infection when given prophylactically, i.e., before exposure to virus. An Fc gamma-specific effector mechanism was not an absolute requirement for antibody-mediated recovery, as F(ab')2 preparations of IgGs could cure the disease, although with lesser efficacy, than intact IgG. An anti-M2 MAb of the IgG1 isotype, which was VN- but bound well to infected cells and inhibited virus growth in vitro, failed to cure. These observations are consistent with the idea that MAbs of the IgG isotype cure the disease by neutralizing all progeny virus until all productively infected host cells have died. VN+ MAbs of the IgA and IgM isotypes may be ineffective therapeutically because they do not have sufficient access to all tissue sites in which virus is produced during influenza virus pneumonia.