Postweaning multisystemic wasting syndrome produced in gnotobiotic pigs following exposure to various amounts of porcine circovirus type 2a or type 2b

In late 2005, a postweaning, high mortality syndrome spread rapidly through finishing barns in swine dense areas of the United States. Diagnostic investigations consistently detected porcine circovirus type 2 (PCV2) from diseased tissues. Subsequent genetic analysis revealed that the infectious agent was a PCV2 type termed "PCV2b". Prior to late 2004, only the PCV2a type, but not PCV2b, had been reported in North America. In this communication, we produce severe postweaning multisystemic wasting syndrome (PMWS) in gnotobiotic pigs using infectious PCV2a and PCV2b generated from DNA clones constructed from field isolates identified in the 2005 outbreak. Clinical signs exhibited by diseased pigs included anorexia, dyspnea and listlessness. Mortality was typically observed within 12h of onset of dyspnea. The most striking microscopic lesions in affected animals were severe hepatic necrosis and depletion of germinal centers in lymph nodes with associated abundant PCV2 viral antigen. Clinical signs and lesions observed in these studies were comparable to those reported in experiments with gnotobiotic pigs inoculated with a PCV2a isolate while concurrently receiving immune-stimulation or co-infection with porcine parvovirus or torque teno virus. The animals in these studies were confirmed to be free of detectable porcine parvovirus, porcine reproductive and respiratory syndrome virus, bovine viral diarrhea virus, swine hepatitis E virus, and aerobic and anaerobic bacteria. Seven out of 24 PCV2 inoculated pigs had a detectable congenital torque teno virus infection with no correlation to clinical disease. Thus, in these studies, both PCV2a and PCV2b isolates were singularly capable of inducing high mortality in the absence of any detectable infectious co-factor.     

Experimental reproduction of swine infertility and respiratory syndrome in pregnant sows.

The purpose of this study was to experimentally reproduce swine infertility and respiratory syndrome (SIRS). Six multiparous sows were intranasally inoculated at 93 days of gestation with lung homogenates from clinically affected pigs, and 3 additional sows were similarly inoculated with a virus isolated in cell culture from the lung homogenate (SIRS virus, isolate ATCC VR-2332). Inoculated sows developed transient anorexia, farrowed up to 7 days prematurely, and delivered a mean of 5.8 live pigs and 6.0 dead fetuses/litter. Clinical signs of disease were not observed in 3 sham-inoculated control sows that delivered a mean of 12.7 live pigs and 0.3 stillborn fetuses/litter. The SIRS virus was isolated from 50 of 76 live-born and stillborn fetuses from the 9 infected litters. Virus was not isolated from 26 autolyzed fetuses or 15 control pigs. Six of 9 inoculated sows developed neutralizing antibodies to SIRS virus. The reproductive effects found in these experiments were identical to those found in field cases. On the basis of our findings, virus isolate ATCC VR-2332 causes the reproductive failure associated with SIRS.     

Study of the potential involvement of pseudorabies virus in swine respiratory disease.

In order to investigate the potential involvement of pseudorabies virus (PRV) in swine respiratory disease, nine week old pigs were intranasally inoculated with the PRV strain 4892. Two doses of infection were used: 10(4.5) median tissue culture infectious doses (TCID50)/pig and 10(3.5) TCID50/pig, with ten pigs per group. In the group of pigs inoculated with 10(4.5) TCID50, seven out of ten pigs died within six days after inoculation. The mortality rate in the group of pigs inoculated with the lower dose was only two out of ten and, there were several pigs in this group that showed signs of respiratory distress besides some mild nervous signs. Pseudorabies virus was isolated from various tissues collected postmortem, including alveolar macrophages. Virus localization in tissues was also detected by in situ hybridization. The histopathological examination of the respiratory tract tissues revealed a pathological process that was progressing from mild pneumonia to severe suppurative bronchopneumonia. The isolation of virus from alveolar macrophages provides support to the hypothesis that replication of PRV during the course of infection produces an impairment of the defense mechanisms in the respiratory tract.     

Isolation of a cytopathic virus from weak pigs on farms with a history of swine infertility and respiratory syndrome.

Severe clinical signs of swine infertility and respiratory syndrome (SIRS) of unknown cause were observed in several Minnesota swine farms between November 1990 and March 1991. Forty-five lung samples of weak pigs were collected from 13 swine farms, and virus isolation was attempted using swine alveolar macrophage (SAM) cultures. A cytopathic virus was isolated from 19 lung samples collected from 6 different farms. Four pregnant sows were infected intranasally with a tissue suspension from which virus was isolated, and 4 6-week-old pigs and 2 contact pigs were infected intranasally with 1 of the isolates. The 4 sows farrowed 12 stillborn and 32 normal pigs. Virus was recovered from 10 of 19 pigs examined. Infected 6-week-old pigs were clinically normal except for slightly elevated rectal temperatures and mild respiratory signs. No or mild interstitial pneumonic lesions were observed in inoculated pigs, but the lesion was obvious in the 2 contact pigs. Seroconversion was observed in sows and pigs as measured by indirect fluorescent antibody (IFA). Serologic identification of the isolates was carried out by IFA using reference serum prepared from an experimentally infected sow. A cytoplasmic fluorescence was observed on the SAM monolayers infected with each of the 19 different isolates. Fluorescence was also observed when the monolayers were tested with SIRS virus ATCC VR-2332-infected sow sera. Replication of the isolates was not affected in the medium containing 5-iodo-2'-deoxyuridine but was inhibited by treatment with ether. The isolates were relatively stable at 56 C and did not agglutinate with various erythrocytes tested.(ABSTRACT TRUNCATED AT 250 WORDS)     

Experimental infection of European wild boars and domestic pigs with pseudorabies viruses with differing virulence

OBJECTIVE: To determine susceptibility of European wild boars (Sus scrofa) to infection with pseudorabies virus (PrV) and to characterize the virulence of a wildboar PrV isolate for wild and domestic pigs. ANIMALS: 18 wild boars and 16 domestic pigs. PROCEDURE: Three groups of 4 wild boars were inoculated with PrV Bartha, Kaplan, and a wild-boar isolate (BFW1) and housed with uninfected pigs. Two groups of domestic pigs (4 and 8 pigs/group, respectively) were inoculated with various doses of BFW1. Animals were observed daily for clinical signs, and samples were tested for PrV excretion and homologous antibodies. After reactivation of latent infection by induced immunosuppression, PrV was detected in tissues of necropsied animals, using cell culture and a polymerase chain reaction (PCR). RESULTS: Clinical signs depended on virulence of the PrV strain and dose of inoculum. Only infection with PrV Kaplan resulted in severe disease and death. Virus was isolated from nasal and genital swab specimens. Antibodies were first detected on day 7 after inoculation; a specific humoral immune response was delayed in BFW1-infected animals. Virus was isolated from various tissues of Kaplan-infected wild boars, whereas mainly viral DNA was detected in a few tissues of Bartha- and BFW1-infected animals, using PCR after immunosuppression. CONCLUSIONS AND CLINICAL RELEVANCE: European wild boars are susceptible to transmission of PrV infection from domestic pigs and vice-versa. The PrV isolate BFW1 is of low virulence and seems to be adapted to the wild boar population from which it was isolated.     

Pathogenesis of swine vesicular disease in pigs.

Pigs exposed to swine vesicular disease virus developed vesicular lesions by postinoculation day 2. Lesions first appeared on the coronary band and then on the dewclaw, tongue, snout, lips, and bulbs of the heels. The onset of viremia coincided with febrile response and the appearance of vesicles. Virus was isolated from the nasal discharge, esophageal-pharyngeal fluid, and feces as early as postinoculation day 1. Greater amounts of virus were isolated from samples collected during the first week of infection, and lesser amounts from samples collected during the second week. The appearance and the distribution of specific fluorescence in various tissues indicated that during the development of swine vesicular disease virus infection, the epithelial tissues were initially involved, followed by a generalized infection of lymph tissues, and subsequently, a primary viremia. Seroconversion was detectable as early as postinoculation day 4. A mild nonsuppurative meningoencephalomyelitis throughout the CNS was observed in both inoculated and contact-exposed pigs. The olfactory bulbs were most severely and were frequently affected, particularly in contact pigs. The most severe brain lesions were found in pigs 3 to 4 days after the onset of viremia; contact pigs showed more severe brain lesions than inoculated pigs. Microscopic changes were also found in the coronary band, snout, tongue, and heart.     

Evaluation of transmission of swine influenza type A subtype H1N2 virus in seropositive pigs

OBJECTIVE: To examine clinical signs, virus infection and shedding, and transmission of swine influenza virus (SIV) subtype H1N2 among seropositive pigs. ANIMALS: Eighteen 3-week-old pigs with maternal antibodies against SIV subtypes H1N1, H3N2, and H1N2. PROCEDURE: Ten pigs (principal) were inoculated intranasally with subtype H1N2 and 2 groups of contact pigs (n = 4) each were mixed with principal pigs on day 7 (group 1) or 28 (group 2). Two principal pigs each were necropsied on days 4, 14, 21, 28, and 42 days after inoculation. Four pigs in each contact group were necropsied 35 and 14 days after contact. Virus excretion was evaluated after inoculation or contact. Lung lesions and the presence of SIV in various tissues were examined. RESULTS: Mild coughing and increased rectal temperature were observed in principal pigs but not in contact pigs. Nasal virus shedding was detected in all principal pigs from day 2 for 3 to 5 days, in group 1 pigs from day 2 for 4 to 9 days after contact, and in group 2 pigs from day 4 for 2 to 6 days after contact. Trachea, lung, and lymph node specimens from infected pigs contained virus. Antibody titers against all 3 subtypes in all pigs gradually decreased. CONCLUSIONS AND CLINICAL RELEVANCE: Protection from viral infection and shedding was not observed in pigs with maternal antibodies, but clinical disease did not develop. Vaccination programs and good management practices should be considered for control of SIV subtype H1N2 infection on swine farms.     

Experimental infection of pigs with a thymidine kinase negative strain of pseudorabies virus

Sixteen 20 day old pigs, devoid of neutralizing antibody to pseudorabies virus (PRV), were divided into two groups of eight, and the animals of each group were housed in a separate unit. In each group 6 pigs were inoculated intranasally with the thymidine kinase (TK⁻) mutant (Group 1) or the field strain of PRV (Group 2), each pig receiving an inoculum of 4 ml. The remaining 2 pigs in each group served as uninoculated controls. The only clinical sign observed in the pigs of Group 1 was a transient febrile reaction, in the case of six pigs inoculated with the TK⁻ mutant of PRV, whereas no signs of disease were seen in the uninoculated controls. The virus was isolated from the 6 infected pigs of the group only on post infection day (PID) 2, whereas it was never isolated from the controls. By contrast, the pigs of Group 2, had a severe clinical response and one, among those that were inoculated with the field strain of the PRV, died on PID 9. Virus was consistently isolated from all pigs of Group 2, inoculated and control. On PID 30 all pigs, i.e. the 8 of Group 1 and 7 of the Group 2 which survived to the infection, were subjected to dexamethasone (DMS) treatment. After DMS treatment virus was never isolated from the nasal swabbings obtained from the pigs of Group 1, whereas it was consistently isolated from pigs of Group 2. After 30 d from the start of DMS treatment the pigs were killed and several tissues were collected from each pig for virus detection, by isolation in tissue culture and by PCR analysis. At necropsy no lesions were found in pigs of Group 1, whereas acute pneumonia and gliosis in the trigeminal ganglia were observed in pigs of Group 2. Virus was never isolated from any of the tissues taken from pigs of both, Group 1 and Group 2, nevertheless sequences of PRV were detected by PCR analysis in the trigeminal ganglia of the pigs of both Groups.     

Natural infections of pigs with bovine viral diarrhoea virus associated with signs resembling swine fever

Between 1976 and 1985 while using immunofluorescence in the laboratory diagnosis of swine fever (SF), 13 incidents of bovine viral diarrhoea virus (BVDV) infection were detected in the Netherlands. Ultimate differentiation between swine fever virus (SFV) and BVDV was based on herd evidence supported by comparative antibody studies on sera from pigs inoculated with the isolate and from contact pigs in the herd of origin, using reference strains of SFV and BVDV. Recently differentiation of SFV and BVDV has been facilitated by typing the isolates with monoclonal antibodies. Signs suspicious of SF were observed in pigs two to 16 weeks old and were always confined to animals of one litter. In most cases the affected litter died out gradually although once an animal recovered. Stillbirth and neonatal death as well as the late onset of disease and its limitation to a single litter in a herd suggested a congenital route of infection. Although transplacental infection of BVDV in pigs has been reported before, these cases are believed to be the first in which natural BVDV infections could be associated with clinical signs and pathological lesions indistinguishable from those observed in chronic SF.     

Experimental induction of bacterial gastritis and gastric ulcer disease in gnotobiotic swine inoculated with porcine Helicobacter-like species

OBJECTIVE: To determine whether 2 isolates of recently isolated swine-origin Helicobacter pylori-like bacteria are pathogenic in pigs and compare the signs of gastric disease induced by these isolates with those detected in H pylori- and Helicobacter heilmannii-infected pigs. ANIMALS: 36 neonatal gnotobiotic pigs. PROCEDURE: Groups of separately housed pigs were inoculated orally with swine-origin Helicobacter-like isolates 2662 or 1268, H pylori (human gastric pathogen), or a gastric homogenate from gnotobiotic swine containing H heilmannii. Noninoculated pigs were used as control animals. Clinical signs and development of homologous and heterologous antibodies against Helicobacter organisms were assessed. After euthanasia, gastric tissues were examined grossly and microscopically; Helicobacter organisms were detected by use of Warthin-Starry and immunohistochemical stains. RESULTS: Both porcine Helicobacter-like isolates colonized the stomachs of swine. Isolate 2662 was highly pathogenic; in 13 isolate 2662-inoculated pigs, gastroesophageal ulcerations developed in 9 and ulceration of the gastric glandular mucosa was detected in 5. Histologically, inflammatory gastritis consisting of multifocal to diffuse lymphocytic and plasmacytic cellular infiltrates and lymphoid follicle formation in the gastric lamina propria accompanied bacterial colonization of the gastric compartment. In contrast, H heilmannii was minimally pathogenic in that only modest inflammatory cell infiltrates were seen. Gastroesophageal or mucosal ulcers were not evident in pigs inoculated with H heilmannii. CONCLUSIONS AND CLINICAL RELEVANCE: These data indicate that swine-origin H pylori-like bacteria can be pathogenic in pigs and suggest that porcine gastric disease may be mediated, in part, by colonization of the stomach by swine-origin H pylori-like bacteria.     

某规模化猪场猪伪狂犬病的诊断

试验采用流行病学调查、临床观察和实验室检查对华北地区某疑似伪狂犬病发病猪场进行了诊断。猪场发病情况主要为母猪流产,新生仔猪死亡率较高,肥猪死亡率低。发病或死亡仔猪扁桃体充血出血、溃疡,肺脏出血、水肿,心肌色淡、心包积液,脑膜充血;表现为坏死性扁桃体炎、出血性淋巴结炎、出血性间质性肺炎、间质性心肌炎和非化脓性脑炎。发病猪扁桃体、肺脏、脑组织匀浆上清液接种家兔后出现奇痒等典型症状并很快死亡。发病猪脑组织可检出猪伪狂犬病毒gD基因特异性目的片段。猪场伪狂犬病野毒感染抗体阳性率为63%（63/100）。本试验结果表明,确诊该猪场发生了伪狂犬病。     

Transmissible Gastroenteritis in Feeder Swine: Clinical, Immunofluorescence and Histopathological Observations

Eight feeder swine (four to six months of age) were inoculated orally with 200,000 to 500,000 pig infectious doses (PID) of the Purdue strain of transmissible gastroenteritis (TGE) virus. Biopsies obtained from their small intestines were examined histopathologically and by fluorescent antibody tissue section technique at intervals that included 24, 48, 72 and 96 hours postexposure, and similar examinations were carried out at necropsy 168 hours postexposure. Evidence of virus infection was demonstrated in all segments of the small intestine except the upper duodenum and the viral antigen was found only in the cytoplasm of the absorptive cells covering the villi. Although six of the eight pigs failed to show clinical signs of TGE, typical microscopic lesions of villous atrophy with replacement of columnar absorptive cells by cuboidal cells were observed in seven pigs, and TGE virus antigen was demonstrated in the intestinal cells of four of eight pigs during the first week postexposure. The infection was usually mild to moderate and focal in the pigs without clinical signs of the disease and more severe and extensive in the pigs with clinical signs of the disease variable in severity. It was concluded that TGE virus probably replicated in all feeder swine exposed, and that the presence or absence of clinical signs of TGE in these pigs was related to the severity and extent of the villous atrophy and columnar cell replacement induced in their small intestines.     

Light and electron microscopic findings in the intestine of spontaneous and experimentally-produced African swine fever]

Light and electron microscopical studies were carried out after experimental induced and spontaneous infection with African swine fever virus. The experimental infection was performed in 18 pigs divided into two groups consisting of 9 animals. The pigs of group I were inoculated with virulent isolate E 70, those of group II with attenuated isolate E 75. Two infected pigs of group I and one control animal were killed on days 3, 5 or 7 p.i., two pigs of group II and one control animal were killed on days 9, 11 or 13 p.i. Additionally 19 spontaneous infected and seropositive animals and two seronegative pigs without clinical signs were examined. Infection with African swine fever virus resulted in slight morphological alterations of the intestine. The pathological findings showed a more intense involvement of the large intestine, especially the caecum and colon, than the small intestine, where the ileum was mostly affected. In all three groups edema and vacuolisation could be observed in endothelial cells. In spite of beginning degenerative signs, especially after spontaneous infection, the fenestrated structure of the endothelium was conserved in most of the cases. In animals infected with virulent isolate the vascular lumina contained aggregations of fibrin, which was severe pronounced in the pigs of the other groups. In the area of these alterations disturbance of permeability with extravasation could be found. In all groups single virions or virus aggregates could be identified in concave depressions of the erythrocyte membrane or free within the blood plasma, in some cases enveloped by a plasma-like material.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantitative aspects of the transmission of African swine fever

The contagiousness of pigs during different stages of infection with African swine fever virus was assessed by measuring the amount of virus excreted and the amounts of virus in the blood and other tissues, as well as determining the infectious dose of the virus by various routes. The virus was present in substantial amounts in secretions and excretions of acutely infected pigs for only 7 to 10 days after the onset of fever and was present in the greatest amount in the feces. Virus persisted in the blood of some recovered and clinically normal pigs for 8 weeks and in the lymphoid tissues for at least 12 weeks. The intranasal/oral ID50, and the IV/IM ID50 of a moderately virulent isolate of African swine fever virus were determined to be 18,500 and 0.13, 50% headsorbing units, respectively. A highly virulent isolate required approximately 10-fold more virus to cause infection by the intranasal/oral route.     

Classical swine fever: virulence and tissue distribution of a 1986 English isolate in pigs

Following the recurrence of classical swine fever in the United Kingdom in 1986, a virus isolated from a single outbreak was studied. A major factor in the spread of this disease is considered to be the presence of infectious virus in tissues taken from animals at certain stages of infection, although their condition may escape detection by routine inspection either before or after slaughter. Intranasal inoculation of the isolate into eight-week-old pigs reproduced the acute form of the disease. The pigs were killed or died between seven and 25 days after inoculation. The virus concentration was determined in a wide range of tissues taken at different stages of infection. Infectious virus was present at high concentrations in all the tissues taken and at all stages of infection. Any porcine tissue is therefore a potential source of infection even when it is taken either before the animal displays detectable signs of disease of after it develops serum neutralising antibodies.     

Synergism between porcine reproductive and respiratory syndrome virus (PRRSV) and Salmonella choleraesuis in swine

Porcine reproductive and respiratory syndrome virus (PRRSV) and Salmonella choleraesuis are two leading causes of economic loss in the swine industry. While respiratory disease is common in both S. choleraesuis and PRRSV infections, the factors that contribute to its development remain largely undefined. We investigated the interaction of PRRSV, S. choleraesuis, and stress in 5-week-old swine. All combinations of three factors (inoculation with S. choleraesuis on Day 0, PRRSV on Day 3, and treatment with dexamethasone on Days 3-7) were used to produce eight treatment groups in two independent trials. Fecal samples, tonsil and nasal swabs, serum samples and postmortem tissues were collected for bacteriologic and virologic examinations. No clinical signs were observed in pigs inoculated with only PRRSV or only S. choleraesuis. In contrast, pigs which were dually infected with S. choleraesuis and PRRSV exhibited unthriftiness, rough hair coats, dyspnea, and diarrhea. The pigs which received all three treatment factors were the most severely affected and 43% (three of seven) of the animals in this group died. Individuals in this group shed significantly higher quantities of S. choleraesuis in feces and had significantly higher serum PRRSV titers compared to other treatments (p < or = 0.05). In addition, S. choleraesuis and PRRSV were shed longer and by more pigs in this group than other groups and S. choleraesuis was recovered from more tissues in this group on Day 21 post inoculation. These results suggested that PRRSV, S. choleraesuis, and dexamethasone acted synergistically to produce a syndrome similar to that observed in the field.     

A sequential study of experimental infection of pigs with porcine circovirus and porcine parvovirus: immunostaining of cryostat sections and virus isolation

The sequential tissue distribution of virus was investigated using virus isolation and immunofluorescence tests in 1-day-old piglets inoculated with porcine circovirus 2 (PCV2) and/or porcine parvovirus (PPV). Enlarged mesenteric lymph nodes were seen in the pig inoculated with PCV2 alone and killed at 26 days post-inoculation (PI). One of the pigs inoculated with PCV2 and PPV and killed at 21 days PI had an enlarged liver. The pig killed at 26 days PI in this group had enlarged liver, kidneys and heart. Histopathological changes were seen in lymphoid tissues of the pigs inoculated with PCV2 alone and killed at 14 and 26 days PI. Similar, but more severe, lesions were observed in the pigs infected with PCV2 and PPV and killed from 10 days PI onwards. Histological lesions of nephritis, pneumonia and hepatitis were also apparent in these animals. Mild nephritis was also seen in the pigs infected with PPV alone and killed at 14 and 26 days PI. Moderate amounts of PPV antigen were detected in tissues from the pigs inoculated with PPV alone and killed at 14 days PI. Low levels of PCV antigen were detected, mainly in lymphoid tissues, in the pigs inoculated with PCV alone and killed at 14 days PI. Low to moderate amounts of PCV antigen were detected in a wider range of tissues in the pig in this group killed at 26 days PI. In the pigs inoculated with both viruses, PPV antigen was detected in tissues of pigs killed from 3 to 26 days PI with maximal amounts detected between 6 and 14 days PI. PCV2 antigen was detected in low to moderate amounts in the tissues of pigs killed at 14 days PI. Large amounts of PCV2 antigen were detected in most of the tissues from pigs in this group killed between 17 and 26 days PI. Virus isolation results for PCV2 generally correlated well with the results for immunofluorescent staining. PPV was isolated from almost all tissues from pigs inoculated with PCV2 and PPV, a much higher incidence of positive tissues than observed for immunofluorescent staining.     

Antiviral effectiveness of butylated hydroxytoluene against pseudorabies (Aujeszky's disease) virus in cell culture, mice, and swine

Butylated hydroxytoluene (BHT) was evaluated for antiviral effectiveness on pseudorabies virus (PRV) in cell culture, mice, and swine. When relatively small amounts of BHT were mixed with PRV and incubated at 37 C for 30 or 60 minutes before inoculation into cell cultures, the cell cultures did not become infected with virus. The PRV was not infectious when the virus was treated with BHT and then inoculated intraperitoneally into mice, but was infectious when BHT and PRV were inoculated simultaneously or when BHT was inoculated either 30 or 60 minutes before PRV. Swine fed BHT-medicated feed for 10 days before they were intranasally exposed with virulent PRV did not have overt signs of pseudorabies, had a lower concentration of PRV in nasal mucus than did control swine, and had acceptable blood enzyme and cholesterol concentrations during the experiment. The BHT was detected in tissues of 2 swine after they were fed BHT-medicated feed for 10 days, and higher concentrations of BHT were detected in tissues of 3 swine given BHT feed for 29 days.     

Evaluation of infectivity and transmission of different Asian foot-and-mouth disease viruses in swine

Most isolates of foot-and-mouth disease virus (FMDV) display a broad host range. Since the late 1990s, the genetic lineage of PanAsia topotype FMDV serotype O has caused epidemics in the Far East, Africa, the United Kingdom, France, the Netherlands, and numerous other countries throughout Europe and Asia. In contrast, there are several FMDV isolates that exhibit a more restricted host range. A Cathay topotype isolate of FMDV serotype O from the 1997 epizootic in Taiwan (O/TAW/97) demonstrated restricted host specificity, only infecting swine. Methods used to evaluate infectivity and pathogenicity of FMDV isolates in cattle are well-documented, but there has been less progress studying transmission and pathogenicity of FMDV isolates in pigs. In previous studies designed to examine pathogenicity, various chimeric viruses derived from O/TAW/97 were intradermally inoculated in the heel bulb of pigs. Subsequent quantitative scoring of disease and evaluation of virus released into nasal secretions and blood was assessed. Here we prove the usefulness of this method in direct and contact inoculated pigs to evaluate infectivity, pathogenicity and transmission of different Asian FMDV isolates. Virus strains within the Cathay topotype were highly virulent in swine producing a synchronous disease in inoculated animals and were efficiently spread to in-contact naive pigs, while virus strains from the PanAsia topotype displayed more heterogeneous properties.