Typical presenting signs included a high fever Excessive salivation was commonly reported and the mucous membranes of the nares were inflamed with a nasal discharge which was initially mucus and later mucopurulent. A short explosive cough was also characteristic of the disease.
Morbidity in these herds was 7. Affected animals returned to normal fairly rapidly with evidence of the acute phase typically disappearing within one month. On post-mortem examination the most prominent and characteristic lesion was severe haemorrhagic tracheitis and bronchitis. While diarrhoea was not a clinical sign, severe enteritis of the small intestines and mucoid enteritis of the large intestines were reported.
The aetiology was believed to be viral and this report is now considered to be the first peer-reviewed description of infectious bovine rhinotracheitis IBR in cattle. The following year , a report was published [ 5 ] describing an emerging respiratory disease of feedlot and dairy cattle which it named infectious necrotic rhinotracheitis.
This was first observed in the autumn of in Colorado and consistent with the report from the previous year [ 4 ], was characterised by a high fever and acute inflammation affecting the upper respiratory tract down to and including the bronchi. Following its emergence in Colorado in , signs were observed in a number of feedlots between and with affected cattle to this point typically being mature animals. This changed in when the disease was recognised in calves as young as 3 weeks of age and also occurred in epizootic form in dairy herds.
Clinical signs were again similar to those described in the index case [ 4 ] with a sharp reduction in milk yield including cessation in some animals with recovery in 5—7 days and changes in the gastro-intestinal tract with mucosal ulceration in the abomasum, severe enteritis in the small intestine and mild inflammation in the large intestine.
Unlike the index case diarrhoea was reported as a presenting sign in some cases, with animals having fresh or digested blood in their dung which in some instances was linked to abomasal ulceration.
Based on the results of restriction endonuclease analysis, isolates of BoHV-1 can be subdivided into three subtypes. A second group of viruses, referred to as BoHV This grouping can be further subdivided into BoHV The potential for BoHV-1 infection to have a negative impact on fertility has been recognised for many years.
One of the earliest reports, published in described an experimental study to investigate the impact of the presence of BoHV-1 in semen used in artificial insemination AI , [ 9 ].
Initially, 4 heifers were inseminated with semen spiked with the U. Each heifer showed clinical signs of IPV, with 3 returning to oestrus 9—13 days later while the fourth conceived and ultimately produced a live calf at term. In a follow-up study 6 of 8 seronegative heifers inseminated in the same way had short oestrus cycles 11—15 days. Endometrial biopsies indicated the development of a chronic necrotising endometritis which was still evident 31—47 days after insemination. Histopathological changes were also observed in the vulva, vagina and oviducts of some animals at this stage and 5 of 8 animals examined had cystic corpora lutea.
A subsequent more detailed study, [ 11 ] investigated the effect of BoHV-1 on breeding by both AI and natural service. Seronegative heifers and cows were either inseminated with semen and an Australian strain of BoHV-1 or were mated naturally to bulls which had been inoculated preputially 2 days previously with the same virus. Following AI, when semen was deposited into the uterus, only 2 of 10 animals conceived to first service, with a further 2 animals conceiving to a second BoHVfree insemination.
In addition 4 of the 6 non-pregnant animals showed one or more shortened oestrus cycles. Overall there were 4. In contrast, breeding by natural service produced similar outcomes independent of infection status. All 10 animals bred by non-infected bulls were pregnant after 2 services whereas 9 of 10 bred by BoHVinfected bulls were in calf with respective services per conception of 1.
Irrespective of the means of service all animals receiving BoHVinfected semen developed lesions of IPV within 48 hours which regressed 9—11 days later, with the inoculated bulls developing IPB. In the artificially inseminated group, virus was recovered consistently from vaginal swabs from all animals with a mean duration of excretion of 8. Virus was intermittently recovered from some animals for as long as 40 days post insemination. Histopathological examination of the 6 non-pregnant animals in the AI group showed lesions of chronic endometritis ranging in nature from mild to severe.
The authors concluded that the route of infection is critical in determining whether endometritis and infertility occur. While the introduction of BoHV-1 by natural service does not appear to significantly affect fertility, the inoculation of BoHV-1 into the uterus can cause infertility due to endometritis and also increase the incidence of shortened oestrus cycles. The potential negative impact of the use of BoHVcontaminated semen was also highlighted by a field study which who reported that cows in 20 herds inseminated with contaminated semen had a non-return rate of In addition In the first of these [ 13 ], 12 seronegative heifers were inoculated by the intrauterine route one day after natural mating with a non-infected bull.
Animals were subject to post mortem examination 4—14 days later. The corpus luteum CL of 8 of the 12 virus-inoculated heifers, representing all 3 inocula, contained cysts. No gross or microscopic lesions were observed in the control heifers or those inoculated with the FI isolate.
In contrast, gross lesions of oedema, haemorrhage and necrosis were recorded in the uterine bodies or horns of the heifers that were inoculated with either of the other strains.
Microscopic lesions ranging from mild focal endometritis to severe diffuse necrotizing metritis were also observed in these groups. In addition to the luteal inflammation, 2 heifers had areas of necrosis in the contra-lateral ovary, with one having a severe, diffuse, necrotizing oophoritis. Based on these findings, the authors drew a number of conclusions.
Firstly, the absence of gross lesions in the cranial uterine horns, accompanied by minimal microscopic changes, were unlikely to interfere with blastocyst attachment in this area 3 weeks after conception and therefore the infertility associated with intra-uterine exposure is unlikely to be a direct consequence of the pathological effects of the virus on the uterine epithelium.
Secondly, BoHV-1 can produce inflammation and necrosis of the CL after intra-uterine exposure at oestrus. However, they concluded that the intra-luteal cysts are probably not a direct result of viral damage due to the lack of correlation between their presence and the detection of lesions or the isolation of virus which was not isolated from all corpora lutea in challenged cattle and their occurrence in some control animals also.
The difference in outcomes between BoHV-1 isolates is noteworthy. In a follow up study [ 14 ] the Colorado and Iowa isolates were used to infect seronegative heifers on the day after breeding by natural service.
For each virus isolate, 2 heifers were each inoculated by the intravenous i. Gross ovarian lesions were found in the ovaries of 4 heifers 3 i. Microscopic ovarian lesions were found in all 4 animals inoculated by the i.
No gross or microscopic lesions were detected in the ovaries of animals exposed by aerosol route and virus was not isolated from their ovarian tissue. The authors concluded that BoHV-1 readily gains access to ovarian tissue from the blood and that the immediate post-oestrus ovary is particularly susceptible to infection via this route.
They proposed that the absence of ovarian lesions following aerosol infection probably reflects the absence of a viraemia with the incidence of ovarian involvement related to the duration and height of post-infection viraemia. The Iowa and Colorado isolates were then used to conduct a further study [ 15 ] to investigate the effect of BoHVinduced oophoritis on ovarian function during an acute primary i.
Six heifers were inoculated by the i. Plasma progesterone was followed over subsequent cycles to monitor CL function and was found to be depressed in all heifers. The reduction in progesterone was more marked with the Iowa isolate. Two heifers had a normal next oestrus cycle whereas for 3, onset was delayed by a few days to a week and the one remaining heifer returned to normal cyclicity after 2 months. The authors concluded that while primary BoHV-1 infection at oestrus may cause severe oophoritis, the resulting functional impairment of the ovary is temporary.
None of the heifers became pregnant, although the authors were unable to state whether this reproductive failure was as a result of necrosis of the CL or lethal embryonic infection. Despite the i. No lesions were observed on the ovaries of any heifer and virus was only isolated from the ovarian tissue of one animal, suggesting that recurrent BoHV-1 infection does not directly interfere with ovulation or luteal function.
To compare the pathological changes induced in the ovaries by different modified live IBR vaccines administered during oestrus, 22 seronegative heifers were synchronised with 2 doses of prostaglandin and then administered double doses by the intravenous route of one of three modified live vaccines licenced in North America [ 16 ]. BoHV-1 was isolated from blood and nasal and vaginal secretions from each of the three vaccine groups.
The heifers were ovariectomized nine days after vaccination for histological investigation and virus isolation. In all three groups necrotic oophoritis with multifocal areas of ovarian tissue necrosis, haemorrhage and mononuclear lymphocytic infiltration was observed. While some differences were observed between vaccine strains these were not statistically significant.
It should be noted that studies e. Indeed the studies cited were typically conducted using early vaccines licenced for use outside Europe. The European Pharmacopoeia [ 18 ] that lays down the criteria for licensing of live IBR vaccines requires data from a minimum of 24 pregnant cows at various stages of gestation and administered ten times the vaccinal dose of virus to demonstrate the absence of either abortion or antibodies to BoHV-1 in pre-colostral sera.
A later study also investigated the impact of vaccine-induced changes on fertility [ 19 ], administering a modified live IBR vaccine i. Vaccine was given on the second of these treatment days at which time each animal in the trial was placed with a proven sire for 35 days and resulting conception rates were monitored.
The authors attribute the marked difference in conception rates to a profound negative influence of concurrently administered vaccine virus on fertility. All of the previous studies focused on infection with BoHV-1 at the time of oestrus. To evaluate the outcome of infection at different developmental stages of the bovine CL and conceptus, pairs of heifers were inoculated i.
In contrast to the severe oophoritis reported in earlier studies associated with infection at oestrus, heifers inoculated at 7 or 14 days post natural service had mild oophoritis with a few necrotic follicles in one or both ovaries. Those inoculated 21 or 28 days post breeding had no lesions in the corpus luteum but numerous necrotic follicles in their ovaries, with viral antigen observed in all lesions by immunohistochemistry.
The uterus of one heifer inoculated 7 days post-breeding contained a degenerating conceptus from which BoHV-1 was isolated. Heifers inoculated 14 days post-breeding were found not to be pregnant, but there was evidence that the post-breeding oestrus cycle had been longer than normal suggesting that conception followed by early embryonic death had occurred.
The uteri of heifers inoculated at 21 or 28 days post-breeding and the other heifer inoculated on day 7 contained normal-appearing concepti. Thus the results indicate that the pathogenic effect of BoHV-1 on the CL depends on the stage of development, with the severity of lesions decreasing as the interval from breeding to exposure increased. Shortly after ovulation, intense neo-vascularization develops in the follicular theca interna, and the authors speculate that infection occurring at oestrus can result in a large number of cells being simultaneously exposed to virus and leading to diffuse necrosis of the CL.
In contrast, infection when the CL is fully functional and less vascularized may result in a lower level of exposure and subsequent pathology. Having previously identified the diffuse necrosis of the CL and subsequent progesterone deficiency that accompanies infection at oestrus as one means by which BoHV-1 can prevent continued pregnancy, these authors considered cytocidal infection of the developing conceptus occurring when heifers are inoculated 7—14 days after breeding as a further mechanism by which infection may impact fertility.
In this case embryonic death is not the result of luteal damage but rather cytocidal infection of the trophoblast. In a subsequent study on the effect of BoHV-1 on fertility of heifers in the early embryonic period, the same researchers exposed 2 groups of recently served, seronegative heifers to BoHV-1 by the i.
Pregnancy occurred in all 5 control non-inoculated heifers, whereas only 1 of 8 inoculated heifers maintained pregnancy.
These results were attributed to early embryonic death rather than a failure to conceive with inter-oestrus periods typically normal or only slightly longer than would be expected in the absence of conception.
Virus was isolated from the adrenal glands of 7 out of 8 of the challenged heifers and from vaginal and nasal swabs of 5 and 3 of these heifers respectively. Virus was also isolated from the reproductive tissues of one ovary, infundibulum and uterine tube. Histological changes were observed only in the adrenal glands being characterised by a lymphohistiocytic infiltration accompanied less frequently by necrotic foci. In an earlier study, the same researchers had shown that isolate FI had reduced pathogenicity compared to Iowa and Colorado strains in terms of its ability to cause endometritis and oophoritis when challenge occurred at the time of oestrous [ 13 ].
To further characterise this isolate they conducted a study to test its effect on pregnancy and determine whether it was pathogenic for the developing corpus luteum in heifers [ 8 ]. Nine seronegative heifers were bred naturally and inoculated i.
Plasma progesterone was monitored to follow CL function with low values and failure to conceive being recorded for the 2 heifers inoculated at DPB 1. Luteal function was normal in heifers inoculated on DPB 7 and 14 with these 4 heifers producing healthy uninfected calves at term. The 3 heifers inoculated with FI at 6 months all produced a calf at term although one was delivered dead. No virus was isolated from this calf but it was cultured from the placenta.
The authors considered that BoHV-1 could be present in cotyledonary tissue without inducing lesions or infecting the foetus.
This was based on the observation that abortion is typically not seen in association with venereal disease which is typically attributed to BoHV Several epidemiological studies have investigated the impact of BoHV-1 on reproductive performance in dairy and beef herds. One of these [ 22 ] examined the impact of natural subclinical infections on fertility losses in a limited number of non-vaccinated dairy cows and heifers in Turkey.
The study comprised cows and 89 heifers cattle in different herds, all of which were inseminated by a single individual using semen from the same bull. The average days open for cows that were seropositive at the time of service Vaccinating latently infected animals may reduce the level of shedding from this group.
Marker vaccines are also available and recommended. These are based on glycoprotein E gE deleted mutants, with detectable antibodies present to the gE antigen in marker vaccinated individuals indicating wild-type viral infection. Kaashoek, M. Tvan A conventionally attenuated glycoprotein E-negative strain of bovine herpesvirus type 1 is an efficacious and safe vaccine. Vaccine , 12 5 ; Karstad, L. Lemaire, M. J Clin Microbiol, 38 11 ; 43 ref.
Mars, M. H et al Airborne transmission of bovine herpesvirus 1 infections in calves under field conditions. Veterinary Microbiology , 76 1 Veterinary Microbiology, 66 3 ; OIE, World Animal Health Information Database. Van, Oirschot, J. M Advances in the development and evaluation of bovine herpesvirus 1 vaccines.
Wyler, R. In: Wittmann G, ed. Herpesvirus Diseases of Cattle, Horse and Pigs. From WikiVet English. Bovine Herpesvirus 1. C Infectious bovine rhinotracheitis virus. Risk evaluation of cross-infection of cattle with ruminant alphaherpesviruses related to bovine herpesvirus type 1.
C Herpesviral abortion in domestic animals. M Bovine herpesviruses. Part I. Bovine herpesvirus 1. Veterinary Bulletin', J Clin Microbiol , Navigation menu Personal tools Create account Log in. Namespaces Page Discussion. Views Read View source View history.
Upload file Commons WhiteList. BRSV is a difficult virus to detect, although chances of isolation may improve when sampling animals in the incubation or acute phases of infection. Although virus isolation is difficult, PCR is a useful and rapid method commonly used to detect the antigen.
Other procedures that have proved useful in detection of BRSV antigen are fluorescent antibody and immunoperoxidase staining. Paired serum samples can be used to establish a diagnosis. However, the antibody titer of animals with well-developed clinical disease may be higher in the acute sample than in the sample taken 2—3 wk later, because the antibody response often develops rapidly, and clinical signs follow virus infection by up to 7—10 days.
Single serum samples with high antibody titers from a number of animals in a respiratory outbreak may help diagnosis if coupled with clinical signs. Calves that become infected with BRSV in the presence of passively derived antibody may not seroconvert.
Treatment focuses on antimicrobial therapy to control secondary bacterial pneumonia see Bacterial Pneumonia in Cattle Bacterial Pneumonia in Cattle Mannheimia haemolytica serotype 1 is the bacterium most frequently isolated from the lungs of cattle with BRD.
There is no specific treatment for the viral interstitial pneumonia. Supportive therapy and correction of dehydration may be necessary. Most animals will recover in several days without treatment. General control and prevention are discussed under Enzootic Pneumonia of Calves and Shipping Fever Pneumonia Enzootic Pneumonia of Calves and Shipping Fever Pneumonia Enzootic pneumonia and shipping fever pneumonia share many similarities in their respective etiologies and pathogeneses and in general measures for control and prevention.
Enzootic pneumonia Inactivated and modified-live vaccines are available and may serve to reduce losses associated with BRSV; however, there is a paucity of field trials to evaluate the efficacy of these vaccines.
Bovine herpesvirus 1 BHV-1 is associated with several diseases in cattle: infectious bovine rhinotracheitis IBR , infectious pustular vulvovaginitis IPV , balanoposthitis, conjunctivitis, abortion, encephalomyelitis, and mastitis. BHV-1 infections are widespread in the cattle population.
In feedlot cattle, the respiratory form is most common. The viral infection alone is not life-threatening but predisposes to secondary bacterial pneumonia, which may result in death.
In breeding cattle, abortion or genital infections are more common. Genital infections can occur in bulls infectious pustular balanoposthitis and cows IPV within 1—3 days of mating or close contact with an infected animal. Transmission can occur in the absence of visible lesions and through artificial insemination with semen from subclinically infected bulls.
Cattle with latent BHV-1 infections generally show no clinical signs when the virus is reactivated, but they serve as a source of infection for other susceptible animals. The incubation period for the respiratory and genital forms is 2—6 days. In the respiratory form, clinical signs range from mild to severe, depending on the presence of secondary bacterial pneumonia. Nasal lesions consist of numerous clusters of grayish necrotic foci on the mucous membrane of the septal mucosa, just visible inside the external nares.
They may later be accompanied by pseudodiphtheritic yellowish plaques. Conjunctivitis with corneal opacity may occur as the only manifestation of BHV-1 infection. In the absence of bacterial pneumonia, recovery generally occurs 4—5 days after the onset of signs. Abortions may occur concurrently with respiratory disease but may be seen up to days after infection. They can occur regardless of the severity of disease in the dam.
Abortions generally occur during the second half of pregnancy, but early embryonic death is possible. In genital infections, the first signs are frequent urination, elevation of the tailhead, and a mild vaginal discharge.
The vulva is swollen, and small papules, then erosions and ulcers, are present on the mucosal surface. If secondary bacterial infections do not occur, animals recover in 10—14 days.
With bacterial infection, there may be inflammation of the uterus and transient infertility, with purulent vaginal discharge for several weeks. In bulls, similar lesions occur on the penis and prepuce.
BHV-1 infection can be severe in young calves and cause a generalized disease. Pyrexia, ocular and nasal discharges, respiratory distress, diarrhea, incoordination, and eventually convulsions and death may occur in a short period after generalized viral infection. In uncomplicated IBR infections, most lesions are restricted to the upper respiratory tract and trachea. Petechial to ecchymotic hemorrhages may be found in the mucous membranes of the nasal cavity and the paranasal sinuses.
Focal areas of necrosis develop in the nose, pharynx, larynx, and trachea. The lesions may coalesce to form plaques. The sinuses are often filled with a serous or serofibrinous exudate. As the disease progresses, the pharynx becomes covered with a serofibrinous exudate, and blood-tinged fluid may be found in the trachea. The pharyngeal and pulmonary lymph nodes may be acutely swollen and hemorrhagic. The tracheitis may extend into the bronchi and bronchioles; when this occurs, epithelium is sloughed in the airways.
The viral lesions are often masked by secondary bacterial infections. In young animals with generalized BHV-1 infection, erosions and ulcers overlaid with debris may be found in the nose, esophagus, and forestomachs.
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