Bluetongue in ruminants; cause, symptom, prevention and control

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Bluetongue in ruminants; cause, symptom, prevention and control Bluetongue is caused by the pathogenic virus, Bluetongue virus (BTV),[3] of the genus Orbivirus, of Unlike other arboviruses, BTV lacks a lipid envelope.

Bluetongue is caused by the pathogenic virus, Bluetongue virus (BTV),[3] of the genus Orbivirus, of the Reoviridae family. Twenty-six serotypes are now recognised for this virus.[7]

The virus particle consists of ten strands of double-stranded RNA surrounded by two protein shells. The particle has a diameter of 86 nm.[8] The structure of the 70 nm core was determined in 1998 and was at the time t

he largest atomic structure to be solved.[9]

The two outer capsid proteins, VP2 and VP5, mediate attachment and pe*******on of BTV into the target cell. The virus makes initial contact with the cell with VP2, triggering receptor-mediated endocytosis of the virus. The low pH within the endosome then triggers BTV's membrane pe*******on protein VP5 to undergo a conformational change that disrupts the endosomal membrane.[8] Uncoating yields a transcriptionally active 470S core particle which is composed of two major proteins VP7 and VP3, and the three minor proteins VP1, VP4 and VP6 in addition to the dsRNA genome. There is no evidence that any trace of the outer capsid remains associated with these cores, as has been described for reovirus. The cores may be further uncoated to form 390S subcore particles that lack VP7, also in contrast to reovirus. Subviral particles are probably akin to cores derived in vitro from virions by physical or proteolytic treatments that remove the outer capsid and causes activation of the BTV transcriptase. In addition to the seven structural proteins, three non-structural (NS) proteins, NS1, NS2, NS3 (and a related NS3A) are synthesised in BTV-infected cells. Of these, NS3/NS3A is involved in the egress of the progeny virus. The two remaining non-structural proteins, NS1 and NS2, are produced at high levels in the cytoplasm and are believed to be involved in virus replication, assembly and morphogenesis.[3]

02/10/2022

Bluetongue (BT) is a haemorrhagic disease of wild and domestic ruminants with a huge economic worldwide impact on livestock. The disease is caused by BT-virus transmitted by Culicoides biting midges and disease control without vaccination is hardly possible. Vaccination is the most feasible and cost-effective way to minimize economic losses. Marketed BT vaccines are successfully used in different parts of the world. Inactivated BT vaccines are efficacious and safe but relatively expensive, whereas live-attenuated vaccines are efficacious and cheap but are unsafe because of under-attenuation, onward spread, reversion to virulence, and reassortment events. Both manufactured BT vaccines do not enable differentiating infected from vaccinated animals (DIVA) and protection is limited to the respective serotype. The ideal BT vaccine is a licensed, affordable, completely safe DIVA vaccine, that induces quick, lifelong, broad protection in all susceptible ruminant species. Promising vaccine candidates show improvement for one or more of these main vaccine standards. BTV protein vaccines and viral vector vaccines have DIVA potential depending on the selected BTV antigens, but are less effective and likely more costly per protected animal than current vaccines. Several vaccine platforms based on replicating BTV are applied for many serotypes by exchange of serotype dominant outer shell proteins. These platforms based on one BTV backbone result in attenuation or abortive virus replication and prevent disease by and spread of vaccine virus as well as reversion to virulence. These replicating BT vaccines induce humoral and T-cell mediated immune responses to all viral proteins except to one, which could enable DIVA tests. Most of these replicating vaccines can be produced similarly as currently marketed BT vaccines. All replicating vaccine platforms developed by reverse genetics are classified as genetic modified organisms. This implies extensive and expensive safety trails in target ruminant species, and acceptance by the community could be hindered. Nonetheless, several experimental BT vaccines show very promising improvements and could compete with marketed vaccines regarding their vaccine profile, but none of these next generation BT vaccines have been licensed yet.

Supportive care of blue toothPreventionThere is no specific treatment for animals with bluetongue apart from rest, provi...
02/10/2022

Supportive care of blue tooth
Prevention
There is no specific treatment for animals with bluetongue apart from rest, provision of soft food, and good husbandry. Complicating and secondary infections should be treated appropriately during the recovery period.
Prophylactic immunization of sheep remains the most effective and practical control measure against bluetongue in endemic regions. Attenuated and inactivated vaccines against BTV are commercially available in some countries. Three polyvalent vaccines, each comprising five BTV serotypes, are widely used in southern Africa and elsewhere. A monovalent (BTV type 10) modified live virus vaccine is available for use in sheep in the US. Use of vaccines with different serotypes does not provide consistent cross-protection. Live, attenuated virus vaccines should not be used during Culicoides vector seasons because these insects may transmit the vaccine viruses from vaccinated to nonvaccinated animals (eg, other ruminant species). The result may be reassortment of genetic material, giving rise to new viral strains. Passive immunity in lambs usually lasts 2–4 months.
Control of bluetongue is different in areas where the disease is not endemic. During an outbreak, when one or a limited number of serotypes may be involved, vaccination strategy depends on the serotypes causing infection. Use of vaccine strains other than those causing infection affords little or no protection and is not recommended. The potential risk from vaccine virus reassortment with wild-type viral strains, virus transmission by the vectors to other susceptible ruminants, and reversion to virulence of vaccine virus strains or even the production of new BTV strains of uncertain virulence should also be considered. The use of inactivated vaccines in BTV incursions into northern Europe has played a major part in controlling virus transmission in those regions where extensive vaccination rates (>80%) have been achieved.
Control of vectors by the use of insecticides or protection from vectors may lower the number of Culicoides bites and subsequently the risk of exposure to BTV infection. However, these measures alone are unlikely to effectively halt a bluetongue epidemic and should be regarded as mitigation measures to be used alongside a comprehensive and vigorous vaccination program.

Diagnosis of Bluetongue in RuminantsClinical evaluationPostmortem examinationVirus identificationSerologic testingThe ty...
02/10/2022

Diagnosis of Bluetongue in Ruminants
Clinical evaluation
Postmortem examination
Virus identification
Serologic testing
The typical clinical signs of bluetongue enable a presumptive diagnosis, especially in areas where the disease is endemic.
Suspicion is confirmed by the presence of petechiae, ecchymoses, or hemorrhages in the wall of the base of the pulmonary artery and focal necrosis of the papillary muscle of the left ventricle. These highly characteristic lesions are usually obvious in severe clinical infections; in mild or convalescent cases, however, they may be barely visible. These lesions are often described as pathognomonic for bluetongue, but they also occur occasionally in other ovine diseases, such as heartwater, pulpy kidney disease, and Rift Valley fever. Hemorrhages and necrosis are usually found where mechanical abrasion damages fragile capillaries, such as on the buccal surface of the cheek opposite the molar teeth and the mucosa of the esophageal groove and omasal folds. Other necropsy findings include subcutaneous and intermuscular edema and hemorrhages, skeletal myonecrosis, myocardial and intestinal hemorrhages, hydrothorax, hydropericardium, pericarditis, and pneumonia.
Laboratory confirmation of bluetongue is based on virus isolation in embryonated chicken eggs or mammalian and insect cell cultures, or on identification of viral RNA by PCR assay. The identity of isolates may be confirmed by group-specific antigen-capture ELISA, group-specific PCR assay, immunofluorescence, immunoperoxidase technique, serotype-specific virus neutralization tests, serotype-specific PCR assay, or hybridization with complementary gene sequences of group- or serotype-specific genes. For virus isolation, blood (10–20 mL) is collected as early as possible from febrile animals into an anticoagulant such as heparin, sodium citrate, or ethylenediaminetetraacetic acid (EDTA) and transported at 4°C (39.2°F) to the laboratory. For long-term storage when refrigeration is not possible, blood is collected in oxalate-phenol-glycerin (OPG). Blood to be frozen should be collected in buffered lactose peptone and stored at or below −70°C (−94°F). Blood collected later during the viremic period should not be frozen because lysing of the RBCs on thawing releases the cell-associated virus, which may then be neutralized by early humoral antibody. The virus does not remain stable very long at −20°C (−4°F). In fatal cases, specimens of spleen, lymph nodes, or red bone marrow are collected and transported to the laboratory at 4°C (39.2°F) as soon as possible after death.
A serologic response in ruminants can be detected 7–14 days after infection by BTV and is generally lifelong after a field infection. Current recommended serologic techniques for detection of BTV antibody include agar gel immunodiffusion (AGID) and competitive ELISA. The latter is the test of choice and does not detect cross-reacting antibody to other orbiviruses, especially anti-EHDV (epizootic hemorrhagic disease virus) antibody. Various forms of the serum neutralization test, including plaque reduction, plaque inhibition, and microtiter neutralization, can be used to detect type-specific antibody.

Clinical Findings of Bluetongue in RuminantsThe course of bluetongue in sheep can vary from peracute to chronic, with a ...
02/10/2022

Clinical Findings of Bluetongue in Ruminants
The course of bluetongue in sheep can vary from peracute to chronic, with a mortality rate of 2%–90%. Peracute cases die within 7–9 days of infection, mostly as a result of severe pulmonary edema leading to dyspnea, frothing from the nostrils, and death by asphyxiation. In chronic cases, sheep may die 3–5 weeks after infection, mainly because of bacterial complications (especially pasteurellosis) and exhaustion. Animals with mild cases usually recover rapidly and completely. The major production losses include deaths, unthriftiness during prolonged convalescence, wool breaks, and reproductive losses.
In sheep, BTV causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation, leading to edema, congestion, hemorrhage, inflammation, and necrosis. The clinical signs in sheep are typical. After an incubation period of 4–6 days, a fever of 40.5°–42°C (105°–107.5°F) develops. Affected animals are listless and reluctant to move. Clinical signs in young lambs are more apparent, and the mortality rate can be high (up to 30%). Approximately 2 days after onset of fever, additional clinical signs may be evident, such as edema of the lips, nose, face, submandibular area, eyelids, and sometimes ears; congestion of mouth, nose, nasal cavities, conjunctiva, and coronary bands; and lameness and depression. A serous nasal discharge is common, later becoming mucopurulent. The congestion of nose and nasal cavities produces a “sore muzzle” effect, the term used to describe the disease in sheep in the US.
Sheep eat less because of oral soreness and will hold food in their mouths to soften before chewing. They may champ to produce a frothy oral discharge at the corners of the lips. On close examination, small hemorrhages are visible on the mucous membranes of the nose and mouth. Ulceration develops where the teeth come in contact with lips and tongue, especially in the areas of most friction. Some affected sheep have severe swelling of the tongue, which may become cyanotic (hence the term "blue tongue”) and even protrude from the mouth. Animals walk with difficulty as a result of inflammation of the hoof coronets. A purple-red color is obvious as a band at the junction of the skin and the hoof. Later in the course of disease, lameness or torticollis develops due to skeletal muscle damage. In most affected animals, abnormal wool growth results from dermatitis.
Clinical signs of bluetongue in cattle are rare but may be similar to those that occur in sheep. They are usually limited to fever, increased respiratory rate, lacrimation, salivation, stiffness, oral vesicles and ulcers, hyperesthesia, and a vesicular and ulcerative dermatitis. Susceptible cattle and sheep infected during pregnancy may abort or deliver malformed calves or lambs. The malformations include hydranencephaly or porencephaly, which results in ataxia and blindness at birth. White-tailed deer and pronghorn antelope develop severe hemorrhagic disease leading to sudden death.
In many areas of the world, BTV infection in sheep, and especially in other ruminants, is subclinical. Although clinical signs in cattle are rare and limited, exposure to BTV can influence international trade and movement of serologically positive animals.

Epidemiology and Transmission of Bluetongue in RuminantsThere are at least 29 serotypes of BTV worldwide, although not a...
02/10/2022

Epidemiology and Transmission of Bluetongue in Ruminants
There are at least 29 serotypes of BTV worldwide, although not all serotypes exist in any one geographic area. Distribution of BTV throughout the world parallels the spatial and temporal distribution of vector species of Culicoides biting midges (the only important natural transmitters of the virus) as well as the temperatures at which BTV will replicate in and be transmitted by these vectors. Continued cycling of the virus among competent Culicoides vectors and susceptible ruminants is critical to viral ecology. In the US, the principal vectors are C sonorensis and C insignis, which limit the distribution of BTV to southern and western regions. In northern and eastern Australia, the principal vector is C brevitarsis, whereas in Africa, southern Europe, and the Middle East, it is C imicola. In northern Europe, the major vectors are species within the C obsoletus-dewulfi complex. In each geographic region, secondary vector species may attain local importance.
Vectors become infected with BTV by imbibing blood from infected vertebrates; transovarial transmission has not been reported. The high affinity of the virus to blood cells, especially the sequestering of viral particles in invaginations of RBC membranes, contributes to prolonged viremia in the presence of neutralizing antibody. The extended viremia in cattle (occasionally up to 11 weeks), as well as the host preference for cattle that some vector species of Culicoides display, provides a mechanism for year-round transmission in domestic ruminants in locations where the vector-free period (ie, winter) is relatively short. Mechanical transmission by other bloodsucking insects is of minor importance.
Vector-borne transmission through Culicoides spp is the primary way that BTV is transmitted. Virus concentrations in secretions and excretions are minimal, making direct, indirect, or aerosol transmission unlikely. However, in-contact transmission of BTV serotype 26 has been demonstrated in goats. The importance of this form of transmission in the ecology of this serotype is not known. Semen from viremic bulls can serve as a source of infection for cows through natural service or artificial insemination. Embryo transfer is regarded as safe, provided that donors are not viremic and an appropriate washing procedure for embryos is used. Transplacental transmission of field strains of BTV from dam to fetus, leading to the birth of viremic calves, is reported in cattle; however, the epidemiological importance of this mechanism is unclear. Bluetongue is listed by the World Organisation for Animal Health (OIE) as a notifiable disease. Bluetongue virus is not zoonotic.

Etiology and Pathogenesis of Bluetongue in RuminantsBluetongue virus is the type species of the genus Orbivirus in the f...
02/10/2022

Etiology and Pathogenesis of Bluetongue in Ruminants
Bluetongue virus is the type species of the genus Orbivirus in the family Reoviridae. The virion is a nonenveloped double-layered particle with an outer capsid that encloses a core containing a segmented double-stranded RNA genome.
Hosts typically become infected from the saliva of a biting midge. The virus spreads locally and replicates in regional lymph nodes, leading to viremia and systemic spread with virus replication in hematopoietic cells and endothelial cells, resulting in endothelial damage, hemorrhage, vascular occlusion, tissue edema, and epithelial sloughing due to loss of microvasculature.

Bluetongue is a viral disease of ruminants worldwide. Clinical signs in sheep result from vascular endothelial damage, i...
02/10/2022

Bluetongue is a viral disease of ruminants worldwide. Clinical signs in sheep result from vascular endothelial damage, including edema of the muzzle, tongue, and coronary bands. Diagnosis is made on clinical suspicion and viral identification. Control and prevention measures consist of vaccination, where available, and vector control.
Bluetongue is a noncontagious, infectious, arthropod-borne viral disease primarily of domestic and wild ruminants. Infection with bluetongue virus (BTV) is common in a broad band across the world, which until recently stretched from ~35°S to 40°–50°N. Since the 1990s, BTV has extended considerably north of the 40th and even the 50th parallel in some parts of the world (eg, Europe). The geographic restriction is in part related to the climatic and environmental conditions necessary to support the Culicoides vectors. Most infections with BTV in wild ruminants and cattle are subclinical. Bluetongue (the disease caused by BTV) is usually considered to be a disease of improved breeds of sheep, particularly the fine-wool and mutton breeds, although it has also been recorded in cattle and some wild ruminant species, including white-tailed deer (Odocoileus virginianus), pronghorn antelope (Antilocapra americana), and desert bighorn sheep (Ovis canadensis) in North America, and European bison (Bison bonasus) and captive yak (Bos grunniens grunniens) in Europe.

Bluetongue is a viral disease of ruminants worldwide. Clinical signs in sheep result from vascular endothelial damage, i...
02/10/2022

Bluetongue is a viral disease of ruminants worldwide. Clinical signs in sheep result from vascular endothelial damage, including edema of the muzzle, tongue, and coronary bands. Diagnosis is made on clinical suspicion and viral identification. Control and prevention measures consist of vaccination, where available, and vector control.

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