Viral Bovine Disease Of Rinderpest Biology Essay

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The causative agent of rinderpest is a single-stranded RNA virus belonging to the order Mononegavirales and family Paramyxoviridae of the genus Morbillivirus (Iowa State University 2008). The Office international des epizooties or OIE (2009) explained there are three lineages of rinderpest virus (RPV) affecting Asia and Africa. The virus can tolerate temperatures of 56°C and 60°C for a period of 60 and 30 minutes, respectively. Moreover, RPV remains stable in both acidic and alkaline conditions (pH of 4-10). However, RPV exhibits susceptibility to disinfectants such as sodium hydroxide, β-propiolactone, cresol, and phenol as well as lipid solvents. The virus could be rapidly inactivated when exposed to ultraviolet radiation, dry temperatures, and intense light.

Species affected

Degree of susceptibility to RPV varies from species to species. Yaks (Bos grunniens), water buffalo (Bubalus bubalis), and domestic cattle (Bos domesticus) exhibit higher susceptibility. Bos primigenius taurus commonly known as the European cattle shows more susceptibility than Bos primigenius indicus or zebu. Other wild animals were also shown to be susceptible like Syncerus caffer (African buffalo), Giraffa cameloparadalis (giraffe), Taurotragus oryx (eland), Tragelaphus strepsiceros (kudu), Connochaetes sp. (wildebeest) and various antelope species. Other domesticated animals such as pigs, goats, and sheep may also be affected but are unimportant epidemiologically (OIE 2009).

Geographic distribution

Recorded cases of RPV Lineage 3 infection were in Yemen, Sri Lanka, Turkey, Saudi Arabia, Russia, Pakistan, Oman, Kuwait, Iraq, Iran, India, and Afghanistan. While evaluations are yet to be fully accomplished, eradication of the virus has been successful and the last country declared rinderpest-free was Pakistan in 2003 (OIE 2009).

Surveillance method used

For rinderpest surveillance, five points are addressed following the provisions stipulated in Chapter 2.1.15 of the Terrestrial Manual and Appendix 3.8.2 of the Terrestrial Code. First is clinical suspicion where a summary table on the number of suspected cases, samples tested for RPV, species affected, sample type, testing procedure and results of differential diagnosis. Serological surveillance is second. Detailed information on serological surveys performed should be furnished. The third is on demographics and economics of livestock where tables highlight the frequency of herds, flocks, and the like of each susceptible species for every country as well as its distribution. Fourth focuses on wildlife demographics and current measures in place to prevent physical contact between domesticated and wild species. Fifth provides information on markets and slaughterhouses looking into principal collection or marketing centres for livestock, patterns on the transport and movement of livestock in the country, and the mode of transporting and handling livestock in these transactions (OIE, 2008).

Transmission

Transmission could either be direct or close indirect contact with the infected animals. It is though faeces, eye and nasal secretions that the virus could be spread. Highly contagious exposure occurs one to two days prior to presentation of clinical signs to eight to nine days after manifestation of the clinical signs (Iowa State University 2008).

Incubation

Period of incubation of the rinderpest virus is from three to fifteen days but typically range from four to five days (Iowa State University 2008).

Clinical Signs

Basing on strain virulence and immune resistance of the animal infected, infections could be classified into three: peracute, acute, or subacute. In its peracute form, which is observed in young and highly susceptible animals, clinical signs presented may include reddened eyes and gums, high fever, and death in two to three days. In the classic or acute form, signs begin with fever, appetite loss, depression, and elevated heart and respiration rates, then progressing to oral sores coupled with salivation, clear to cloudy nasal and eye discharges, and reddened eyes and gums. Two to three days after, gastrointestinal signs begin to appear at the same time fever subsides. Infected species may either experience profuse bloody or watery diarrhoea which contain dead tissue and mucus, inability to rise, pain in the abdominal region, dehydration, and straining during defecation. Within a period of eight to twelve days, death could occur. In some instances for the acute type, there is regression of clinical symptoms in the tenth day and recovery within another ten to fifteen days. For the subacute form, low death rate has been recorded and very few of the classic symptoms are manifested. Among non-bovine species like pigs, goats, and sheep, the signs include anorexia, fever, and in some cases, diarrhoea. Oral sores and reddened eyes characterize the subacute form among pigs (Iowa State University 2008).

Morbidity

Illness rate of rinderpest is high (Iowa State University 2008).

Mortality

High death rates were registered for rinderpest; however it could vary from strain to strain (Iowa State University 2008).

Diagnosis

For rinderpest, consideration should be accorded to cattle showing acute fever which causes a highly communicable disease with gastrointestinal signs and/or oral erosions. Differentials diagnosis include arsening poisoning, paratuberculosis, necrobacillosis, salmonellosis, vesicular stomatitis, foot-and-mouth disease, malignant catarrhal fever, bovine herpes virus-1, and bovine viral diarrhea- mucosal disease. Bovine viral diarrhea-mucosal disease may less likely be observed occasionally since it principally affects species age four months to two years old; rinderpest affect cattle regardless of age (Iowa State University 2006).

Isolation of RPV is using marmoset lymphoblastoid cell line. Confirmation may be done by demonstrating RNA or viral antigens in the clinical samples. Detection of rinderpest antigens can be achieved through immunocapture enzyme linked immunosorbent assay (ELISA).

The immunocapture ELISA is a definitive diagnosis that differentiates rinderpest from peste des petits ruminants; on the other hand, AGID though useful in the field could not distinguish these mentioned diseases from each other. Immunofluorescence or immunoperoxidase staining can identify antigens in the tissue samples. Reverse transcription polymerase chain reaction (RT-PCR) assays can identify RPV, differentiates the three lineages, or discriminate RPV from peste des petits ruminants virus. Serology is also being utilized such as virus neutralization or competitive ELISA. Though employ for surveillance purposes, it possesses no capability of distinguishing the infected from the vaccinated animals (Iowa State University 2008).

Treatment

No treatment for this disease.

Recommendations

To quickly respond to a rinderpest outbreak, a veterinarian should be consulted. Quarantine should be in place in the affected area. Slaughter of infected livestock or wildlife is likewise recommended. Common disinfectants such as sodium hydroxide, cresol, and phenol should be prepared in order to kill rinderpest virus; however, virus can survive in frozen or chilled tissues. Vaccination should be directed by the local veterinary authorities should it be desired.

Bovine Ephemeral Fever

Aetiology

First recorded cases of bovine ephemeral fever were in South Africa during the middle of the nineteenth century then spread worldwide to Japan, Australia, most African nations and the Middle East (Abu-Elzein, Al-Afaleq, Housawi and Al-Bashier 2006, 1147). Bovine ephemeral fever is caused by a single-stranded RNA virus of the genus Ephemerovirus belonging to the family Rhabdoviridae. It is sensitive to the action of ether and contains five structural proteins and exhibits antigenic relationship to at least three of these non-pathologic viruses in cattle: Adelaide River, Berrimah virus, Kimberley virus and two viruses producing ephemeral-fever like signs, the Puchong and Kotonkan viruses in Malaysia and Africa, respectively. The virus is pH-liable and changes in the pH levels recorded in the muscles after death and atmospheric temperature inactivates the virus; thus survivability of virus outside the host is lessened. Virus can be best isolated in defibrinated blood-inoculated mosquito cultures then transferred to cell cultures such as Vero cells and BHK21 15 days after. Chuang, Ji, Chen, Lin, Hsieh and Liu (2007, 84) have successfully suppressed BEFV using RNA interference.

Species affected

Only the water buffalo (Bubalus bubalis) and cattle (Bos sp.) show the clinical signs of bovine ephemeral fever. All ages for cattle show susceptibility but more commonly it affects those between six to 24 months old. However, there are reported antibodies in domesticated goats and deer as well as giraffes, antelopes, kudu, wildebeest, waterbuck, hartebeest, and Cape buffalo. Majority of these seropositive ruminants are endemic to Africa. In sheep, experimental infections were established; however the infections outside the laboratory have not been documented (Iowa State University 2008).

Geographic distribution

Countries lying on both sides of the equator are most affected by bovine ephemeral fever and this include all the nations in the African continent and most Asian countries particularly in the Middle East (Iran, Iraq, Syria, Israel), South Asia (Bangladesh, India, Pakistan), central and southern China, southern Japan to Southeast Asian countries and Australia. There were no reports of BEF virus infections in Papua New Guinea, New Zealand, Pacific Islands, North and South America, and Europe. (Iowa State University 2008)

Surveillance method used

Serosurveillance method is used.

Transmission

Transmission of bovine ephemeral fever is established to be arthropod-mediated. However these arthropods still remain unknown; however, isolates of BEFV were found in mosquitoes of the genera Culex and Anopheles, A. bancroftii,in Australia and Culicoides in both Australia and Africa. Therefore, suspected as most important vectors are mosquitoes. Bovine ephemeral fever may also be transmitted through intravenous inoculation of blood in small amounts. No reports suggest that BEF could be transmitted via aerosol droplets, body secretions or close contact. Semen does not serve as vehicle for BEF transmission and virus can be inactivated in the meat. No known carriers were also established (Iowa State University 2008).

Incubation

In the laboratory, incubation of bovine ephemeral fever ranges from one to ten days, with majority of the cases developing three to five days following exposure. The natural incubation period can only be inferred but may also be similar (Iowa State University 2008).

Clinical Signs

Clinical signs observed in affected species may either be mild or severe; the most severe of cases occurs in high-producing cows and bulls. There are also subclinical infections noted. There appears to be variation in individual animal's presentation of symptoms but it usually starts with a biphasic, triphasic or polyphasic fever. Spikes in temperature occur 12 to 18 hours apart. At the first temperature surge, there is a dramatic drop in milk production; however the other clinical symptoms remain mild. Some of the animals may show reluctance to move, stiff or depressed. During the second day, which probably coincide with the second upsurge in temperature, the severity of symptoms become more progressive. Animals typically become depressed and inappetent and depressed, with mucoid or serous discharges in the nose, tachypnea, and elevated heart rate. Watery discharges in the eyes, shivering, muscle twitching, and profuse salivation could also be observed. Some affected animals may develop periorbital or submandibular edema or cephalic patchy edema. Commonly observed signs include joint pain, stiffness, and shiftness lameness; swollen joints may also be seen. Severity of the lameness can mimic a dislocation or a fracture. In severe cases, rales and pulmonary emphysema can be found. Healthy bulls and cows may develop recumbency between eight hours to days. Majority of animals are in a state of sternal recumbency, but in extreme cases, lateral recumbency may develop. There is a temporary loss of reflex and inability to rise in some of the animals. Animals in recumbency may exhibit bloatedness, ruminal stasis, or loss of swallowing reflex. These signs may be exacerbated by forced exercise or severe environmental stress. Improvement on the animals' health occurs after one to two days following the appearance of the first symptoms and full recovery within another one to two days. For severely affected lactating cows and other healthy animals, recovery may be achieved in one week. During the course of the illness, the animals generally lose their weight but slowly regain lost weight slowly. Complications are rare but may include subcutaneous accumulation of air on the back, mastitis, emphysema, aspiration pneumonia, and gait impairment. Many of the complications mentioned above may be due to recumbency or trauma. Infertility and abortion can occur in bulls and cows respectively. The infertility however is temporary for six months at the most. Rare cases of permanent infertility were reported. When the animals recover, milk production decreases by 10-15% during the remainder of the lactation period, but may be stable or normalize in the succeeding pregnancies. For cows that succumbed to the fever in lactation, production may not return. Though death is not common, occurrence may be either on the febrile or convalescent phase. The usual causes of deaths are either trauma or pneumonia. Water buffalo may share similar symptoms, but milder. Experimental infection of sheep showed no symptoms (Iowa State University 2008).

Morbidity

Frequency of susceptible cattle in a herd and intensity of epidemic partly influence morbidity. The disease may affect the herd for a period of three to six weeks. Very often, the occurrence of a major wave of clinical cases is in a week or more after one case or small assemblage of cases. Morbidity can range from 1% to 80% (Iowa State University 2008).

Mortality

In numerous outbreaks, mortality rate is between 1-2%. However, it could rise to 30% in very fat cattle (Iowa State University 2008).

Diagnosis

Most of the BEF cases are confirmed using serological surveys. To indicate a positive case, a rising titer with either enzyme-linked immune-sorbent assay (ELISA) or virus neutralization should be demonstrated; both a blocking ELISA and neutralization assay can discriminate BEFV from other viral species of the genus Ephemerovirus. Also, complement fixation can be utilized; however, this test only identifies antibodies specific only to Ephemerovirus. At the first exposure, anamnestic responses to BEFV could be observed if the animal had a previous exposure to another viral species of the genus Ephemerovirus. Polymerase chain reaction (PCR) assays are regularly utilized in a number of countries like Australia. From the blood samples, virus isolation was attempted but often resulted in failure. The most suitable cells in the initial isolation are the cell lines in Aedes albopictus. The Vero cells and BHK-21 are used in the propagation of the virus isolated. Confirmation on the virus identity is through blocking ELISA, virus neutralization, or immunofluorescence; on the other hand, immunofluorescence may only identify the virus as Ephemerovirus. BEF is also confirmed through intracerebral inoculation of unweaned mice (Iowa State University 2008).

Treatment

The Bangladesh Livestock Research Institute (2006) mentioned the absence of a specific treatment since it is caused by a virus. However, treatment should be administered symptomatically and check for secondary infections. Phenyl butazone could be used in treating inflammation and calcium borogluconate for signs of hypocalcaemia. For secondary infections, antibiotic treatment should be in place.

Recommendations

If bovine ephemeral fever is reported, animal health authorities should be notified. Should an outbreak occur in imported animals, they should be placed in an area that is insect-proof and spraying area with insecticides.

Bovine Viral Diarrhoea-Mucosal Disease Complex (BVD-MD)

Aetiology

The cause of bovine diarrhoea is the BVD virus belonging to the family Flaviviridae under the genus Pestivirus. Diameter of pestiviruses range from 40-60 nm and therefore are numbered among the smaller virus groups. The capsid is icosahedral composed of a single capsid protein and enclosed by three virus coded membrane proteins in the envelope. Common disinfectants inactivate the virus. The virus loses it infectivity at 37°C after four days while at 56°C, infectivity is lost after 45 minutes (Stahl 2006, 11). The virus has two distinct genotypes (types 1 and 2) based on their antigenic properties, and the viral isolates in these groups show significant variability biologically and antigenically (OIE 2008).

Species affected

Aside from cattle, other artiodactyls such as pigs, wild ruminants, goats, and sheep can also be infected. All ages showed susceptibility (Institute of Veterinary Virology 2006).

Geographic distribution

Virus is spread worldwide.

Surveillance method used

Serosurveillance is performed.

Transmission

Cattle that are persistently infected shed copious amounts of BVDV in their excretions and secretions and therefore easily transmit the virus to other susceptible members of the herd. BVDV can also be spread via wild ruminants, biologic products, semen, fomites, and insect bites (Kahn, 2008).

Incubation

Incubation is between two to fourteen days.

Clinical Signs

The course of BVDV infection in cattle could be asymptomatic, classic or acute, peracute, and pneunoenteritis complex. In the asymptomatic infections, signs are mild or benign that the livestock owner does not usually notice them. BVD in its classic or acute form results in the following symptoms: diarrhoea containing mucus or blood, anorexia, fever, eye and nasal discharges, and erosions in the mouth, muzzle, vaginal mucosa and interdigital cleft. This occurs four to eight days after infection. The immunosuppressive action of BVDV results in secondary infections. Bulls that are acutely infected suffer from a transient decrease in the quality of the sperm. In the peracute form, leukopenia and thrombocytopaenia were observed. Most of the cases are associated with the genotype II BVDV. Among fattening calves, BVDV significantly contributes to pneumoenteritis-complex which is a multiple infection of bacteria, mycoplasmas, and viruses. Only cattle that are persistently infected develop mucosal disease. During foetal development, infection was transplacental with the ncp BVD virus. Because immune system is not fully mature at that stage, the animals have not developed the antibodies against BVDV. Rather, the animals developed immunotolerance against the virus for the rest of their lives (Institute of Veterinary Virology 2006).

Morbidity

Stevens (2009) found that cattle not exposed to persistently infected individuals displayed a 19% morbidity which was significantly lower than those observed in pens exposed to PI-BVDV calves during feeding.

Mortality

Mortality in cattle is significant according to JaeKu, BangHun, SangHo, Kyoungki, SeongHee, HyeRyoung, ChoiKyu, and YiSeok (2009, 356).

Diagnosis

Numerous methods of diagnosing BVDV are available. Isolation of the virus remains to be the gold standard. Many clinical species may be submitted. Frequently, the specimen submitted is either a serum or tissue. The specimen that can be extensively studied is white blood cell fraction from a whole sample of blood. Serum use can produce variable outcomes because of neutralizing antibodies which may be potentially present. After processing is the transfer of the aliquot from the specimen to a cell culture system. Most common cell lines in BVDV virus isolation are the bovine testicle (Btest) cells, bovine turbinate (BT) cells, and Mandin Darby Bovine Kidney (MDBK) cells. After incubation which typically range from three to five days, cells can be visualised to determine whether there is BVDV infection. The cytopathic strains can be easily identified because they destroy the monolayer of cells. In contrast, the non-cytopathic strain exhibits a normal monolayer. Thus, using a monoclonal body is necessary for identifying and confirming BVDV. When tissues are to be utilized for viral isolation, lymphoid organs which include the thymus, mesenteric lymph nodes, Peyer's patch, and spleen are ideal for this method. A faster and economical method involves detection of BVDV antigen. One concern in this method is the lack of reliability and sensitivity in comparison to virus isolation. Thus, in screening animals, antigen detection techniques are most likely used. Currently, antigen detection can be done in any of these three: PCR, immunologic staining of tissue either fresh or fixed in formaldehyde, and antigen capture enzyme linked immunosorbent assay (ACE). Because these methods are used in screening, they are likewise used in identifying persistently infected animals. One drawback is the tests' inability to differentiate an acute or persistently infected animal. Immunologic staining of ear notch biopsies could also be performed. With the introduction of polymerase chain reactions (PCR), numerous valid PCR tests have been employed by various test centres. Since BVDV is an RNA virus, the PCR technique that is most applicable is reverse transcriptase PCR (RT-PCR). Most of the samples can be subjected to RNA isolation; however, for tissues fixed in formaldehyde it is a different story. One study found that ten-day formalin fixation of BVDV-infected tissues resulted in detectability loss. In the said study, 10% formalin was used; however in 5 % formalin, shelf-life of tissue was extended to three months. The high cost of the PCR seemed to be a barrier. In order for PCR costs to be reduced, samples are usually pooled. Pooling often occurs when serum samples are to be analysed and in bulk tank testing in identifying a PI animal. Another advantage of the PCR is its development of the real time PCR (rtPCR). In real time PCR, the critical reagent is the Taq polymerase. Aside from using two standard primers 5' and 3', another primer which is fluorochrome-labelled is needed. This supplementary primer is complementary to the area occupied between the 5' and 3' primers. The presence of the target in the sample results in the binding of all primers to the DNA. As nucleotides are added by the Taq polymerase in creating the complementary DNA, the fluorochrome in the additional primer is cleaved then released in the rtPCR solution. The fluorochome released will then be measured using a spectrophotometer then graphically analysed. This method does not only identify but also quantify the number of viral transcripts. Another technique used is serology which aims to measure antibody response in the animals naturally exposed to infection and post-vaccination. Commonly employed serological techniques are serum neutralization and ELISA. Of the two, less preference is given to ELISA because of the considerable diversity of viruses. In contrast, serum neutralization assay has pitfalls of its own. Variability of the results in a serum neutralization assay could be due to the BVDV strain used and test cells employed. Lastly, since there is no standardisation in diagnostic centres, not all laboratories employ similar BVDV and cells. Thus, discrepancies between diagnostic laboratories are very likely. As for its strengths, serum neutralization assay when appropriately applied is able to evaluate efficacy of the vaccine, compliance to vaccination protocol, status of herd in terms of BVDV exposure, and relate BVDV with observed clinical signs (Stevens 2009).

Treatment

At present, there is no cure for bovine viral diarrhoea-mucosal disease. For secondary infections like pneumonia, antibiotics should be given. When the animal develops the mucosal disease, IV fluids can be administered to prevent diarrhoea and dehydration. Euthanasia of persistently infected cattle should be done to prevent more infection and contamination to other herd mates. The best treatment available is the screening of the animals.

Recommendations

Animals displaying the clinical signs of BVDV-MD should be isolated and prevented direct contact with the rest of the herd. In treating, the infected cattle should be handled last. It is still recommended to take care of the pregnant cows before the infected animals. Pens of cattle should constantly meet sanitary standards since BVDV can be killed by normal disinfectants.

Foot-and-Mouth Disease

Aetiology

The virus causing foot-and-mouth disease belong to the family Picornaviridae and genus Aphthovirus. Seven serotypes of the FMDV exhibiting immunologic variations exist and these are Asia 1, SAT3, SAT 2, SAT 1, C, A, and O. Within each of these serotypes are at least 60 strains. Occasionally, there are new strains that spontaneously develop. The serotypes and strains of FMDV differ from one geographic region to another though the most common serotype on a global scale is Serotype O. This serotype was the cause for the pan-Asian epidemic that struck in 1990. Some serotypes likewise caused serious outbreaks. An animal might be immune to a certain serotype; however it could not provide cross-protection to the other serotypes. Against the other strains, there is variability in cross-protection due to antigenic similarity (Iowa State University 2007).

Species affected

Affected species are all artiodactlys and some species from other orders. There is a species variability in susceptibility towards FMDV infection and clinical disease and the ability of transmitting the virus to other individuals in the population. Susceptible livestock include reindeer, water buffalo, goats, sheep, pigs, and cattle. Experimental infection was noted in camels, alpacas, and llamas; however are insusceptible. More than 70 wild animal species can be infected by FMDV including gazelles, antelopes, impala, kudu, warthogs, blackbuck, wildebeest, giraffes, chamois, moose, elk, bison (Bison spp.) and African buffalo (Syncerus caffer).Other non-Artiodactyla manifest FMDV susceptibility such as mice, rats, guinea pigs, capybaras, nutrias, kangaroos, armadillos, and hedgehogs. There were also infections documented in Asian and African elephants in zoos; however, the latter cannot be considered susceptible in their natural habitat (Iowa State University 2007).

Geographic distribution

The OIE Report in 2009 indicated that FMD is endemic in Middle East countries. Clinical infections were noted in Yemen, Turkey, Sudan, Saudi Arabia, Oman, Lebanon, Kuwait, Jordan, Israel, Iran, Egypt, Bahrain, and Afghanistan.

Surveillance method used

Sero-surveillance are under way. The objectives of sero-surveillance programmes vary from country to country; Iran, assessment on the prevalence level of FMD where two provinces were analysed using the framework of a project of EUFMD; Egypt, evaluation on the immune status and post vaccination responses; and in Cyprus, detection of virus introduction. In terms of frequency, some countries conduct the surveillance regularly while others occasionally in the case of Jordan, Lebanon, Bahrain, and Syria (Primot 2009).

Transmission

According to Gloster, Jones, Redington, Burgin, Sorensen, Turner, Dillon, Hullinger, Simpson, Astrup, Garner, Stewart, D'Amours, Sellers, and Paton (2008), FMD is transmitted through direct contact with infected animals, animal products (semen, meat, milk), mechanical transfer on fomites or people or airborne route.

Incubation

Incubation of the virus varies according to species. In cattle, it ranges from two days to two weeks, depending on the infection route and virus load; pigs, at least two days or could be between 18 to 24 hours; sheep, typically three to eight days (Iowa State University 2007).

Clinical Signs

Manifestation of clinical signs of affected species depends on the serotype and species. The disease may be asymptomatic in some species. Typical the signs include high fever then vesicles develop in the tongue or gums, teats, interdigital space, coronary area, and rostrum. Then the vesicles that develop rupture and secondary infections may be noted in underlying tissue. The lesions cause lameness and salivation. It is common for infected animals to lose their hooves. In the early phase of the infection, there is discontinuity in the junction between the skin and hoof resulting in the abnormal wearing of the horn and development of a double-hoof structure. Impalas are the species exhibiting this abnormal structure and takes between five to six months before abnormality is not present due to normal wear and growth. Myocard necrosis (tiger heart) which results in acute death is reported among the young non-domestic and domestic artiodactylids, elephants, and camels. In the elephants, foot sole loss is partial as reported. Only the ruminants serve as the carriers after the infection (Schaftenaar 2009).

Morbidity

Morbidity is almost 100% among susceptible livestock (Iowa State University 2007).

Mortality

Usually a mortality of less than 1% is recorded (Iowa State University 2007).

Diagnosis

As mentioned earlier, FMD symptoms differ from one species to another but the presence of erosions and vesicles in the oral cavity, teats, feet, and other regions are suggestive. Cattle farmers should be suspicious when cattle are lame and at the same time salivating, specifically when there is a suspected vesicular lesion. In sheep or pigs, it is not common to observe profuse salivation; however, lameness is a more typical sign. Febrile or suspect animals need to be closely examined for the presence of lesions. When sudden death is noted among the young artiodactylid livestock, the mature animals should undergo examination; young

individuals dying of heart disease may be devoid of vesicular lesions. It is also a necessary measure to tranquilise the animal so that the examination is more thorough since vesicles are painful and imperceptible. Confirmation in the laboratory should also be in place since all vesicular diseases almost have the same clinical signs. FMD cannot be clinically distinguished from vesicular exanthema, swine vesicular disease, vesicular stomatitis and other vesicular diseases. Among domesticated animals, symptoms may be similar to thermal or chemical burns, traumatic stomatitis, and foot rot. For cattle, the oral lesions may be considered a symptom of epizootic hemorrhagic disease, malignant catarrhal fever, bovine viral diarrhoea, infectious bovine rhinotracheitis, and rinderpest. In sheep, the lesions may be misdiagnosed to be caused by leg and lip ulceration, contagious ecthyma, and bluetongue. Laboratory analysis to confirm infection with FMDV is through virus isolation, viral antigen or nucleic acid detection, and serology. Isolation of FMDV can be done in primary porcine or bovine thyroid cells or primary porcine, lamb, or calf kidney cells. Also used are IB-RS-2 or BHK-21 cells but the cell lines exhibit lower sensitivity than the primary cells. When necessary, virus may be inoculated to unweaned mice. When cell cultures are employed, identification of FMDV is achieved through reverse transcription polymerase chain reaction, complete fixation, or enzyme-linked immunosorbent assay (ELISA). While complement fixation is less sensitive and specific, the possibility of direct identification of viral antigens in tissues is high in ELISA. There are also RT-PCR techniques available for FMDV. Serotype of the virus can be resolved using RT-PCR or ELISA. There are instances that electron microscopy is utilized in distinguishing FMDV from the other viruses in the lesions. Serological tests can also be used in the diagnosis and certification of animals for exportation. The antibodies to the structural proteins of FMDV are employed in determining previous or current infections among the unvaccinated animals using serotype-specific virus neutralization tests and ELISAs. Serological tests detecting antibodies to non-structural proteins (NSP) can aid in the diagnosis of previously or currently vaccinated animals. These tests for anti-NSP include ELISAs and are not specific to any serotype. Some animals that have undergone vaccination then become infected persistently may be negatively detected by anti-NSP tests. Identification of the carrier animals can be done through virus isolation from fluids taken from the esophageal-pharyngeal region; however the virus may be occurring in small numbers and intermittently shed. Therefore it is necessary to repeatedly obtain samples. RT-PCR is likewise able to identify can also be used to identify these animals (Iowa State University 2007).

Treatment

No cure is known in the treatment of FMD. Animals that have recovered uncommonly return to pre-infection performance and production levels. At least half of infected animals are chronic carriers of the virus which complicate surveillance measures. In order that the discomfort of the animal is relieved, palliative care should be implemented; however it does not help in preventing the spread of the causative agent.

Recommendations

The following are recommended: 1. Prevent movement of the animals or products in affected area(s); 2. Surveillance should be strictly imposed in order to discriminate the carrier individuals; 3. Known contact and infected animals should both be slaughtered and their carcasses properly disposed; 4. Disinfect people or vehicles leaving the infected area(s); 5. Conduct communication and education strategies in the community; and 6. Financially indemnify the losses to the producer.

Bluetongue

Aetiology

The pathogen causing bluetongue is of the genus Orbvirus, family Reoviridae. Bluetongue viruses (BTV) show close relatedness to the epizootic haemorrhagic disease (EHD) serogroup. Viral genome contains ten double stranded (ds) RNA, localised in a core consisting of major (VP3, VP7) and minor (VP1, VP4, VP6) proteins. The core in a mature particle is enclosed by two capsid proteins (VP2, VP5). VP2 which is the protein most exposed in the mature virion confers host-specific immunity, haemagglutinating property, and causes binding to the receptor.VP5 penetrates the cell in the initial phases of the infection (Bhattacharya, Noad and Roy 2007). This icosahedral virus has 24 different serotypes (Zhen, Changyuan, Lulu, Dong-E, Guoming, Ming and Jun 2010). Replication of BTV occurs in the endothelial cells of the small blood vessels and capillaries. The hyperplastic, necrotic, and degenerative changes elicited by the virus are responsible for exudation, stasis, and vascular occlusion.

Species affected

Wild and domesticated ruminants are infected by BTV- antelope, deer, buffalo, cattle, goats, and sheep (Iowa State University 2006).

Geographic distribution

Aside from the Middle East, BTV has been an economically important concern in some countries in Asia, South Pacific, North America, South America, Australia, and Europe (Iowa State University 2006).

Surveillance method used

Vector surveillance and sero-surveillance for BT are employed.

Transmission

BTV transmission is vector-mediated. Principal vectors are biting midges of the genus Culicoides; in the US, it is C. varipennis var sonorensis; Australia, C. brevitarsis; Middle East and Africa, C. imicola. Though, non-communicable, it can be spread mechanically on needles and surgical instruments (Iowa State University 2006). Mayo, Crossley, Hietala, Gardner, Breitmeyer, and MacLachlan (2010) confirmed that BTV and viral nucleic acids are disseminated to newborn cattle via colostrums ingestion.

Incubation

In cattle, viraemia develops four days after infection but symptoms uncommonly present itself (Iowa State University 2006).

Clinical Signs

Many affected animals specifically cattle appear to be subclinically infected. Occurence of clinical disease, symptoms resemble other contagious diseases which include decreased milk production, inappetence, malaise, and pyrexia in the lactating cows. These signs may all or almost be present in cattle: lacrimation, conjunctivitis, nasal discharge, salivation, haemorrhages and hyperaemia on the ocular mucosal, nasal, and oral surfaces, ulcerations and erosions in the mucosal and oral surfaces, shedding and crusting of muzzle mucosa, appearance of petechia in teats and udder, ulceration and reddening of teats, coronitis, tenderness and warmness of feet, lameness, and reddening of skin and serous crusting above and along coronary band, respectively. Chronic infections result in secondary infections, aspiration pneumonia, pressure points, economic loss brought about by high wool break, severe weight loss, and depressed milk production, and reproductive problems such as reduced rate of conception and azoospermia (Williamson, Woodger and Darpel 2008, 243).

Morbidity

Only 5% of cattle may be ill (Iowa State University 2006).

Mortality

Rare deaths occur (Iowa State University 2006).

Diagnosis

Cattle owners should suspect infection with BTV when common clinical symptoms are presented during times when the insect vectors are active. Another supportive data in the diagnosis is the current history of herd foot rot and wasting. Differential diagnosis include Oestrus ovi infection, foot rot, sheep pox, contagious ecthyma, parainfluenza-3 infection, infectious bovine diarrhoea, malignant catarrhal fever, plant photosensitisation, peste des petits ruminants, vesicular stomatitis, and FMD. In deer and cattle, EHD also would have similar signs and symptoms. Virus isolation can be employed using cell cultures or embryonated chicken eggs. The drawback of using cell cultures is that it is less sensitive compared to the latter. In the laboratory, cell cultures used are Aedis albopictus (AA) cells, Vero, BHK21, and mouse L cells. Inoculation into sucking hamsters or mice and sheep can also isolate BTV. Identification of BTV serotype is possible by applying Immunospot test, ELISA, antigen capture, and immunofluorescence,. PCR has also seen wide usage in analysing clinical samples. Sometimes, serological methods are used which include virus neutralization, competitive ELISA, and agar gel immunodiffusion (AGID) (Iowa State University 2006).

Treatment

No treatment is available for bluetongue.

Recommendations

Preventing virus from being spread between the animals cannot be curbed; however, when disinfection is necessitated, NaOCl and 3% NaOH have been proven to be effective. Because it is a vector-borne disease, Culicoides containment is best achieved by spraying with organophosphates or synthetic pyrethroids.

Akabane Disease

Aetiology

This disease is caused by the virus of the genus Orthobunyavirus and the Simba sero-group under the family Bunyaviridae. Some viruses are closely related and considered isolates or strains of the Akabane virus as follows: Yaba-7 virus, Sabo virus, and Tinaroo virus (Iowa State University 2009). Genomic characteristics of negative sense RNA in Orthobunyavirus is composed of three segments- large (L), medium (M), and small (S). Encoded by the L-segment is the polymerase protein; M, the glycoproteins, Gc and Gn, and non-structural protein (NSm); and the S, NSs proteins and nucleocapsid (N) in overlapping reading frames (Mohamed 2007, 2). Kono, Hirata, Kaji, Goto, Ikeda, Yanase, Kato, Tanaka, Tsutsui, Imada and Yamakawa (2008) mentioned its teratogenicity since it causes congenital abnormalities with arthrogryposis-hydranencephaly syndrome, premature births, still births, and abortions in cattle. Through postnatal infection, induction of encephalomyelitis by the pathogen is rare.

Species affected

Only goats, sheep, and cattle manifest symptomatic infections. While Akabane virus can infect wild ruminants, no cases have been reported in literature. Antibodies to this virus have been noted in camels, deer, buffalo, donkeys, and horses. In Taiwan, an isolate (NT-14) was reported to be widely distributed among swine in Taiwan. Experimental infections can be demonstrated in hamsters and mice (Iowa State University 2009).

Geographic distribution

In calves, Akabane virus is the primary cause of hydrancephaly and congenital arthrogryposis in Australia, Middle East, Africa, and Asia (Smith and Sherman 2009, 112).

Surveillance method used

Monitoring of the disease through sentinel surveillance systems have been successful since the 1970s in Saudi Arabia and Oman (Racloz, Griot and Stark 2006).

Transmission

Transmission of Akabane virus is through biting midges (Culicoides spp.). It can also be transmitted to the foetus through the placenta and primarily the effect is suffered by the offspring of the infected cow. Casual contact is not apparent; horizontal transmission is via insect vectors. Ruminants, however do not carry the virus in the long-term (Iowa State University 2009).

Incubation

In the adults, infection is asymptomatic, but viremia occurs between one to six days following infection and there is evidence of a placental transmission of the virus (Iowa State University 2009).

Clinical Signs

Depending on the species and infection time, clinical signs vary. In a cattle herd with a year-round or extended calving period, abnormalities can be seen in full range. After infection of susceptible cows between 80 to 150 days in gestation, the most severe defects are presented. However the calves may be infected most of the time after the first two months of gestation. While calves are infected in late pregnancy may be born, but movements are not coordinated and in necropsy, manifest disseminated encephalomyelitis. Those which are earlier infected between four to six months of gestation typically exhibit arthrogryposis and at in some instances, scoliosis, kyphosis, and torticollis coupled with neurogenic muscle atrophy due to spinal motor neuron loss. These defects cause dystocia and severe obstetric complications which occasionally result in infertility and death among the cows. Those first calves afflicted with arthrogryposis have less severe defects compared to the later-borns after four to six weeks. Only one to two joints are fixed initially in one limb, but later cases involve multiple joints in several limbs or all the limbs. Inability to stand, uncoordinated gait, depression and blindness are observed in calves infected between 80 to 120 days of gestation. Among these calves, extent of cavitation of the cerebral hemispheres may vary from porencephaly to the severe case, hydranencephaly. Occurrence of the latter is widespread especially those infected early in the pregnancy. Some of the calves may have both arthrogryposis and hydranencephaly (Khan 2008).

Morbidity

In cattle, morbidity varies from 5% to 50%. Highest rates are noted at the onset of the susceptible period (Iowa State University 2009).

Mortality

High mortality rate is noted among the newborns (Iowa State University 2009).

Diagnosis

Outbreaks of aborted, stillborn, premature, or mummified foetuses with arthrogryposis and hydranencephaly should be suggested of the Akabane disease. Among the postnatal animals, encephalomyelitis may be reported; however outbreaks of this disease can occur in farms having no proof of congenital disease caused by the Akabane virus. Differential diagnosis include an array of toxic, genetic, or nutritional diseases, Wesselsbron disease, Border disease, bovine viral diarrhoea, Cache Valley virus infections, and Aino virus. Laboratory tests may include serology in the presuckle neonate or the foetus. Frequently used are ELISA and virus neutralization. Other serological methods may be employed like haemolysis inhibition, haemagglutination inhibition, and agar gel immunodiffusion assays. Other diagnostic tests include nucleic acid and antigen detection and virus isolation. In detecting nucleic acids, RT-PCR is used whereas for antigens, immunohistochemical or immunofluorescent staining may be done. In the isolation of the Akabane virus, cell lines including BHK-21 and hamster lung (HmLu-1) are appropriate (Iowa State University 2009).

Treatment

No treatment exists for Akabane disease.

Recommendations

Vector control is accomplished by disrupting breeding sites, applying pesticides, and protecting the host population from feeding by vectors. Furthermore, breeding animals should have been vaccinated.

Rift valley fever

Aetiology

The virus causing this condition in cattle is Phlobevirus of the family Bunyaviridae. Phleboviruses are spherical and icosahedral with a diameter between 80 and 120 nm (Freiberg, Sherman, Morais, Holbrook and Watowich 2008, 10341; Overby, Pettersson, Grunewald and Huiskonen 2008, 2375). As previously described, it possesses a tripartite genome system- the L, M, and S segments. Gerard and Nichol (2007, 124) revealed that the M segment codes for the glycoprotein precursor cleaved by host proteases in the GN and GC domains. Coded by the S fragment are non structural protein NSs and nucleoprotein NP protein. The nucleoprotein is composed of 245 amino acids that bind to replicative intermediates and genomic RNA forming circular ribonucleoproteic complexes (RNP). Under high humidity and moderate temperature, the virus is fairly stable; however virus is susceptible to highly acidic pH. Disinfection using 4% citric acid solution has proven very useful but a reduced efficacy is noted when organic matter is present. Low concentrations of formaldehyde inactive the virus (Oberem 2008).  

Species affected

Aside from cattle.gray squirrels, other rodents, monkeys, camels, buffalo, goats, and sheep are affected. Cattle and sheep appear to be the primary amplifying hosts. Viraemia can be observed in some monkeys, horses, dogs, and adult cats in mild cases; however, severe disease can be seen in newborn kittens and puppies. No viraemia is noted in hedgehogs, chickens, guinea pigs, pigs, and rabbits (Iowa State University 2006).

Geographic distribution

Though most widely distributed in Africa; however outbreaks of rift valley fever in both livestock and humans have recently occurred in Saudi Arabia and Yemen.

Surveillance method used

Vector surveillance aside from evaluation of climatic indicators especially rainfall are done.

Transmission

An animal-to-animal transmission forms the primary mode of spreading the virus through Monsosmia, Erepmapodites, Anopheles, Culex, and Aedes. In maintaining the disease in endemic areas, both vertical and trans-ovarial transmission in mosquitoes play a significant role. Trans-ovarial transmission appears to be important in causing the epidemics. Mechanically, Stomoxys, Tabanus and midges transmit the causative agent (Musser, Burnham and Coetzer 2006).

Incubation

The length of incubation is three days in cattle, dogs, goats, and sheep (Iowa State University 2006).

Clinical Signs

In the calves, depression, anorexia and fever are the signs while in the adults, decreased milk production, abortion, fetid diarrhoea, profuse salivation, weakness, anorexia and fever (National Agricultural Biosafety Center 2011).

Morbidity

RVF epidemics tend to follow a regular pattern, usually during heavy rains which cause hatching of infected mosquito eggs. Infections may be asymptomatic in indigenous species of cattle while in exotic species, the more severe form of the disease may be observed (Iowa State University 2006).

Mortality

In water buffalo, abortion rate is 50%. In cattle calves, mortality approaches 10-70% while less than 10% in adult (Musser, Burnham and Coetzer 2006; Iowa State University 2006).

Diagnosis

Virus isolation is one diagnostic method in Rift Valley fever using the blood of the febrile animals. Recovery of the virus can be done from tissues of dead and aborted animals; brain, spleen and liver are analysed. Cell lines appropriate in growing the virus include primary cultures of cattle, chicken embryo reticulum, Vero, and BHK-21. Viral titres in the tissues are typically high, thus diagnosis may proceed rapidly applying either agar gel diffusion or complement fixation on the tissue suspensions. Detection of antigens in the virus can be done via immunofluorescent staining of impression smears from the brain, spleen and liver. Blood samples may be analysed using immunodiffusion and immunoassay. RT-PCR detect the presence of viral RNA. Serology tests most widely used are haemogglutination inhibition, ELISA and virus neutralization (Iowa State University 2006).

Treatment

There is no specific treatment for Rift Valley Fever except for supportive therapy.

Recommendations

On the ground, vector control could either utilize ground or aerial ultra low volume insecticide application. Mists or thermal fogs that are generated on the ground may also be considered. If the area is wide, systematic or topical insecticide may assist in the reduction of potential vector populations.

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