A canine parainfluenza viral vaccine: immunogenicity and safety.

A canine parainfluenza viral vaccine was developed and shown to be safe by absence of clinical disease in vaccinated dogs and by inability to isolate vaccine virus from blood or nasopharyngeal swabs. Backpassage in susceptible dogs, using blood of vaccinated dogs, could not be demonstrated. The vaccine produced neutralizing antibody when administered either intramuscularly or subcutaneously; however, a significantly higher immune response was obtained by intramuscular inoculation. Differences in the antibody response were not produced by tenfold dilutions of vaccine virus ranging from 10(2.9) to 10(5.9) median tissue culture infective doses. The presence of neutralizing antibody was associated significantly with decreased respiratory shedding period of challenge virus by vaccinated dogs compared to seronegative control dogs. Six days after aerosol exposure to virulent challenge virus, 100% of the controls (n = 5) but only 15% of the vaccinated dogs (n = 3) shed virus. Seven days after challenge exposure, virus could not be recovered from the vaccinated dogs, but 80% of the control dogs shed virus. An anamnestic response occurred in vaccinated dogs but not in the seronegative control dogs following challenge exposure. A mild clinical disease was produced in 3 of the 5 seronegative control dogs but not in the 20 vaccinated dogs.     

Equine rhinopneumonitis virus infection in New Zealand

Abstract

Extract

Sir,—Japanese workers (Matumoto el al., 1965 Matumoto, M., Ishizaki, R. and Shimuzu, T. 1965. Serologic survey of equine rhinopneumonitis virus infection among horses in various countries. Arch, f. Viruslorsch., 15: 609–624.  [Google Scholar]) have examined 388 horse sera from 17 countries including New Zealand and have found evidence of a high incidence of infection with equine rhinopneumonitis virus. The New Zealand material was supplied between 1957 and 1960, by Dr J. D. Manning, then of the National Health Institute, Wellington.     

Equine rhinopneumonitis virus (herpesvirus type 1): attenuation in stable monkey cell line.

An isolate of virulent equine herpesvirus (EHV) type 1 was adapted to Vero stable cell line by 13 serial passages at 37 C and 50 serial passages at 26 C. Characteristics of the attenuated EHV-1 were found to be avirulent, but immunogenic in horses if injected intramuscularly. The attenuated virus was regularly isolated from peripheral leukocytes in inoculated horses, but was not recovered from nasal turbinate tissues. A mild leukopenia was noticed. The attenuated virus produced characteristic large syncytia on primary isolation in rabbit kidney (RK13) or Vero cells at 37 C in contrast to cell rounding observed with virulent EHV-1. The syncytial marker was stable through 20 serial passages in Vero cells at 37 C. New application of double immunodiffusion test for distinguishing between EHV-1 and EHV-2 also is described.     

Safety and immunogenicity of a delta inulin-adjuvanted inactivated Japanese encephalitis virus vaccine in pregnant mares and foals

In 2011, following severe flooding in Eastern Australia, an unprecedented epidemic of equine encephalitis occurred in South-Eastern Australia, caused by Murray Valley encephalitis virus (MVEV) and a new variant strain of Kunjin virus, a subtype of West Nile virus (WNV_KUN). This prompted us to assess whether a delta inulin-adjuvanted, inactivated cell culture-derived Japanese encephalitis virus (JEV) vaccine (JE-ADVAX™) could be used in horses, including pregnant mares and foals, to not only induce immunity to JEV, but also elicit cross-protective antibodies against MVEV and WNV_KUN. Foals, 74–152 days old, received two injections of JE-ADVAX™. The vaccine was safe and well-tolerated and induced a strong JEV-neutralizing antibody response in all foals. MVEV and WNV_KUN antibody cross-reactivity was seen in 33% and 42% of the immunized foals, respectively. JE-ADVAX™ was also safe and well-tolerated in pregnant mares and induced high JEV-neutralizing titers. The neutralizing activity was passively transferred to their foals via colostrum. Foals that acquired passive immunity to JEV via maternal antibodies then were immunized with JE-ADVAX™ at 36–83 days of age, showed evidence of maternal antibody interference with low peak antibody titers post-immunization when compared to immunized foals of JEV-naïve dams. Nevertheless, when given a single JE-ADVAX™ booster immunization as yearlings, these animals developed a rapid and robust JEV-neutralizing antibody response, indicating that they were successfully primed to JEV when immunized as foals, despite the presence of maternal antibodies. Overall, JE-ADVAX™ appears safe and well-tolerated in pregnant mares and young foals and induces protective levels of JEV neutralizing antibodies with partial cross-neutralization of MVEV and WNV_KUN.     

Equine respiratory viruses in foals in New Zealand

AIMS: To identify the respiratory viruses that are present among foals in New Zealand and to establish the age at which foals first become infected with these viruses. METHODS: Foals were recruited to the study in October/ November 1995 at the age of 1 month (Group A) or in March/ April 1996 at the age of 4-6 months (Groups B and C). Nasal swabs and blood samples were collected at monthly intervals. Nasal swabs and peripheral blood leucocytes (PBL) harvested from heparinised blood samples were used for virus isolation; serum harvested from whole-blood samples was used for serological testing for the presence of antibodies against equine herpesvirus (EHV)-1 or -4, equine rhinitis-A virus (ERAV), equine rhinitis-B virus (ERBV), equine adenovirus 1 (EAdV-1), equine arteritis virus (EAV), reovirus 3 and parainfluenza virus type 3 (PIV3). Twelve foals were sampled until December 1996; the remaining 19 foals were lost from the study at various times prior to this date. RESULTS: The only viruses isolated were EHV-2 and EHV-5. EHV-2 was isolated from 155/157 PBL samples collected during the period of study and from 40/172 nasal swabs collected from 18 foals. All isolations from nasal swabs, except one, were made over a period of 2-4 months from January to April (Group A), March to April (Group B) or May to July (Group C). EHV-5 was isolated from either PBL, nasal swabs, or both, from 15 foals on 32 occasions. All foals were positive for antibodies to EHV-1 or EHV-4, as tested by serum neutralisation (SN), on at least one sampling occasion and all but one were positive for EHV-1 antibodies measured by enzyme-linked immunosorbent assay (ELISA) on at least one sampling occasion. Recent EHV-1 infection was evident at least once during the period of study in 18/23 (78%) foals for which at least two samples were collected. SN antibodies to ERBV were evident in 19/23 (83%) foals on at least one sampling occasion and 15/23 foals showed evidence of seroconversion to ERBV. Antibodies to ERAV were only detected in serum samples collected from foals in Group A and probably represented maternally-derived antibodies. Haemagglutination inhibition (HI) antibody titres 1:10 to EAdV-1were evident in 21/23 (91%) foals on at least one sampling occasion and 16/23 foals showed serological evidence of recent EAdV-1 infection. None of the 67 serum samples tested were positive for antibodies to EAV, reovirus 3 or PIV3. There was no clear association between infection with any of the viruses isolated or tested for and the presence of overt clinical signs of respiratory disease. CONCLUSIONS: There was serological and/or virological evidence that EHV-1, EHV-2, EHV-5, EAdV-1 and ERBV infections were present among foals in New Zealand. EHV-2 infection was first detected in foals as young as 3 months of age. The isolation of EHV-2 from nasal swabs preceded serological evidence of infection with other respiratory viruses, suggesting that EHV-2 may predispose foals to other viral infections.     

Studies on the immunogenicity of Streptococcus equi vaccines in foals.

The ability of either formalin-treated or heat-inactivated whole Streptococcus equi cell vaccines or partially purified M-protein of S. equi to give rise to protective antibody levels was studied in Standardbred foals by serological means. Two commercial preparations, i.e. a beta-propiolactone killed whole S. equi cell bacterin and a cell-free extract of S. equi cells were included in the study. The mean passive hemagglutination antibody titers (10 X log2) in sera of foals given either four doses of formalin-treated whole cell vaccine or an initial dose of formalin-treated followed by three doses of heat-inactivated vaccine with or without levamisole were significantly higher two weeks after the final dose. These passive hemagglutination antibody titers were higher in foals given formalin-treated whole cell vaccine (6.7 +/- 1.5) than given commercial bacterin (4.5 +/- 2.1). The passive hemagglutination antibody titers in all the groups decreased at 12 to 16 weeks after fourth dose of the vaccine. Foals given a commercial cell-free extract did not show a significant increase in passive hemagglutination antibody titers even up to four weeks after third dose. A group of six pony foals immunized with partially-purified M protein showed mean passive hemagglutination antibody titers lower than those observed in foals given whole cell vaccines. In a challenge experiment with S. equi, two of six foals vaccinated with partially-purified M-protein and all three controls developed clinical disease. The passive hemagglutination antibody of vaccinated foals increased after challenge, while at 28 days postchallenge the passive hemagglutination antibody titers of vaccinates and recovered controls were similar.     

Clinical, haematological and biochemical findings in foals with neonatal Equine herpesvirus-1 infection compared with septic and premature foals.

A retrospective multicentre study comparing historical, clinical, haematological, acid-base and biochemical findings of foals with Equine herpesvirus-1 (EHV-1) infection, septicaemia or prematurity was performed to determine if early diagnosis of EHV-1 foals was possible. Fifty-three foals were studied and were assigned to one of 2 groups: herpes positive (n = 14) or herpes negative (n = 39). The latter group included 20 septic, 11 premature, and 8 premature and septic foals. The presence of herpes antigen was confirmed by immunoperoxidase histochemical staining of tissues from necropsied foals. A nonparametric statistical analysis followed by a backwards elimination logistic regression was performed to establish a model at a P value of <0.05. All herpes positive foals died, while 47% (9/19) of the septic foals survived. Based upon our analysis, herpes positive foals were more likely to have total white blood cell counts less than 3 x 10(9)/l and to be icteric as compared to the septic and premature foals. Despite profound hepatic necrosis in the herpes positive foals, liver enzymes were not elevated and were not significantly different from the controls.     

Equine epitheliogenesis imperfecta in two american saddlebred foals is a lamina lucida defect

Necropsy of two American Saddlebred fillies diagnosed with epitheliogenesis imperfecta (EI) revealed missing patches of epithelium of the skin and oral mucosa as well as dental abnormalities. Examination of the digestive tract did not reveal signs of pyloric atresia in either foal. Histopathologic examination revealed separation of the epidermis from the dermis. In both foals a division within the lamina lucida of the basal lamina was observed by transmission electron microscopy. In comparison with an age-specific control, the ultrastructure of intact skin from the EI-affected foals showed abnormal hemidesmosomes, which lacked a subbasal plate. The morphological and ultrastructural defects observed in the EI-affected American Saddlebred foals were similar to those observed in Herlitz junctional epidermolysis bullosa-affected human newborns, which is caused by a defect in one of the subunits of laminin-5. The close similarity of lesions of the human and equine diseases suggests that EI may be caused by a laminin-5 defect.