Another interesting post in prrscontrol.com. Check it here.
What WHO stands for? It is the World Health Organization.
Health? I encourage them to use the money and resources used in the study of some “probabilities” linked with meat consumption and cancer, in giving this food to the people who is dying because the y do not have meat to eat. They will save a lot of lives, instead of wasting their resources in dark communications with no clear purposes.
Organisation? They are really well organised. I would like to know the origin of the money supporting this study. Can someone tell where is the money coming from?
Concurrent infections with other pathogens, whether viruses and/or bacteria, are common in most PRRS virus infections in swine under field conditions.
Read more in http://www.prrscontrol.com/wps/portal/hipra/prrscontrol/news-on-prrs/news-detail/The+PRRS+role+on+concurrent+infections
Since the disease emerged on swine farms, the PRRS virus (PRRSV) has spread worldwide, gained genetic diversity and, in particular cases, increased its virulence. The basis for the virulence, however, remains unknown, despite being investigated with a variety of different approaches.
Porcine Reproductive and Respiratory Syndrome (PRRS) is characterized by reproductive and respiratory symptoms, a decrease in growth performance, and increased mortality in young pigs. The etiological agent, PRRSV belongs to the genus Artevirus within the family Arteriviridae, and its strains are divided into major genotypes. Type 1 viruses are related to the early European isolates (prototype Lelystad virus), whilst Type 2 genotype viruses are related to the North American strains (prototype VR-2332) isolated on swine farms.
It is now widely accepted that significant genetic variability can occur not only between but also within genotypes. This genetic variability of the PRRSV may correspond to the wide range of symptoms also observed on swine farms, extending from lack of clinical signs to fatal disease (highly virulent PRRSV). Multiple genomic regions may be responsible for the immunological behaviour and the virulence of the PRRSV. However, a link between specific molecular sequences and the degree of clinical severity among PRRS virus isolates on swine farms has not yet been identified. At the present time, molecular and antigenic characterization of isolates is used as an epidemiological tool rather than a virulence determinant or vaccine selection tool.
Although the most pathogenic outbreaks reported up to now have always been related to Type 2 isolates, highly virulent PRRSV strains of both genotypes have been isolated from severe clinical cases on swine farms all over the world. Some examples of virulent strains are described below:
Europe (Type 1; Subtype III): Karniychuk et al. (2010) investigated the pathogenesis and antigenic characteristics of type 1 Lena strain, which was isolated from a Belarusian farm with reproductive and respiratory clinical signs. The main conclusion of the study was that the Lena strain is a highly pathogenic PRRS virus strain belonging to subtype III (type 1).
North-America (Type 2): Numerous severe PRRS outbreaks have been reported from North-American farms, mainly in the U.S.A. In the last twenty years, three outbreaks have been particularly significant:
Isolates 142 (1996). Atypical PRRS clinical outbreaks known as swine abortion and mortality syndrome. It was mainly characterised by mid- or late-term abortions of 10-50% of the sows in a period of a few weeks. Sows and gilts had fever and were anorexic. Mortality was from 5% to 10% of the breeding herd. An increase in preweaning mortality and a decrease in nursery pig performance were also observed. The wild-type isolates involved were known as 142, because of their RFLP patterns.
Isolates 184 (2001 and 2006). RFLP 1-8-4 or Strain MN184. This caused high morbidity (50%) and mortality (20%) rates. ORF5 nucleotide sequence analysis and comparison with other type 2 PRRS virus strains demonstrated that MN184 were significantly different to previous strains. Three quite variable regions were identified, corresponding to nsp1β, nsp2 and ORF5. Nsp2 shared only 66-70% amino acid similarity to other North-American PRRS virus nsp2 proteins.
Asia (Type 2; Highly-pathogenic PRRS virus – HP-PRRSV): In June 2006, a very severe disease called porcine high fever syndrome emerged in Jiangxi province (People’s Republic of China) and rapidly spread throughout the country. By the end of that year, the disease had already been detected in 16 provinces affecting over 2 million pigs with about 400,000 fatal cases. Subsequent analysis demonstrated that the disease was caused by an atypical highly virulent strain of the PRRS virus. Since then, highly-pathogenic PRRS virus (HP-PRRSV) has been isolated around the East, South and North of Asia, including China, Vietnam, Bhutan, Cambodia, Indonesia, Laos, Malaysia, Myanmar, the Philippines, Russia, Singapore, etc. Nowadays, it has become endemic in some of these countries and continues to have a devastating economic impact in all of them.
According to ORF5 phylogenetic analysis, it seems that HP-PRRSV might have evolved from strains previously detected in China. Although the basis for HP-PRRSV virulence remains unknown, some authors have claimed that Nsp2, Nsp9 and/or Nsp10 may be involved in the fatal virulence of HP-PRRSV. Other studies have concluded that aberrant immune responses triggered by HP-PRRSV infection could be closely related to acute lung injury.
The risk of a new highly-pathogenic PRRS virus emerging and/or its worldwide spread is a real threat.
In my previous post I asked to do something about this matter. Well, I’m not sure if this is the answer, but better something than nothing. Even if it is a local initiative in Spain. At least, I’m confident in looking for a solution at European level. http://m.europapress.es/asturias/asturias-rural-00671/noticia-garcia-tejerina-anuncia-ayuda-directa-300-euros-vaca-ganaderos-rentabilidad-insuficiente-20150822122235.html
Check out this article explaining the current situation of milk prices throughout the world.
A global problem that should be solved soon or many producers everywhere are going to abandon their farms.
One hallmark of the PRRS virus in swine is its extremely high genetic diversity. This phenomenon has important implications for disease diagnosis and prevention and is one of the major causes of the partial or complete lack of protection against re-infections.
The PRRS virus is an RNA virus that belongs to the genus Arterivirus, the only genus in the family Arteriviridae, in the order Nidovirales. The PRRS virus contains a non-segmented, single-stranded, positive-sense RNA genome. The RNA genome is composed of ten open reading frames (ORFs).
Since the first outbreaks of PRRS in swine in America and Europe, two PRRS virus genotypes have been designated: European or Type 1 (prototype Lelystad virus) and North-American or Type 2 (prototype VR-2332). Interestingly, similarity between both prototype nucleotide sequences is as low as 55%. More importantly, intratype pairwise nucleotide sequence variation exceeds 20% (up to 30% in type 1 and around 21% in type 2).
A significant number of subtypes has been identified in both genotypes. Within type 1, there are at least 4 different subtypes; subtype I is predominant in Western Europe, whereas subtypes II-IV are isolated only in countries to the East of Poland. It seems that genetic variability within subtypes II-IV is higher than within subtype I (18.2% vs. 11.9% using ORF5, respectively). Regarding type 2, although subtypes have not been clearly defined, several lineages exist in two well-defined clades; seven lineages made up by North-American isolates and two lineages exclusively consisting of isolates from South-East Asia.
It has been described that the allocation of genetic diversity is not constant along the PRRS virus genome. Thus, it seems that diversity occurs more frequently in ORF1a, ORF3 and ORF4. However, it is important to note that phylogenetic analyses to determine subtypes and lineages have generally been based on ORF5, which represents a low percentage of the total viral genome. We cannot rule out that this classification may change in the future using the whole genome.
There are several causes that may explain why the PRRS virus in swine has such a highly genetic diversity:
Random mutations. As an RNA virus, the PRRS virus has an RNA polymerase that does not have the ability to correct the inherent common errors that occur during the transcription of RNA. Since these errors appear every 100-1,000 nucleotides, each new virus may be different to the previous one. The PRRS virus mutation rate is assumed to be the highest so far for a virus, being up to 40 times higher than the mutation rates of well-known viruses, such as the avian influenza virus or human immunodeficiency virus.
Recombination. Recombination among PRRS virus strains has frequently been demonstrated in both genotypes, indicating that this phenomenon is also very important in PRRS virus genetic diversity.
Immune selection. During infection, predominant variants would be those variants that possess changes in their genome which represent an advantage compared to the parental strain, such as the ability to escape from the immune response. Therefore, as PRRS virus variants are constantly created, producing new forms of antigens, host immune responses could cause selection pressure.
There are several consequences of such genetic diversity, all them implying a complication in diagnosis (false negatives in ELISA and PCR assays) and control (appearance of new highly pathogenic strains and immune escape mutants) of the PRRS disease in swine.
A PRRS control program cannot be conceived without implementing biosecurity measures. Whilst external biosecurity focuses on exclusion (not allowing it to enter) internal biosecurity focuses on containment (not allowing it to move).
The biggest problem today for the control of PRRS in pigs is that immunity induced against the strain circulating within the farm (called homologous immunity) will never confer 100% cross-protection against the arrival of a new strain (called heterologous strain). Understanding how good or bad the external biosecurity measures are is essential to be able to predict how high the risk of suffering the arrival of new strains is, but also very helpful in deciding the vaccine program strategy to be used.
The 3 main routes for new PRRS virus strains to break into farms are transport vehicles, live animals and airborne transmission. The risk of heterologous infections can be minimized by controlling these 3 main routes of transmission, but other routes of infection should also be taken into account such as semen, personnel, fomites and insects.
Once infection occurs, the virus will be shed from infected animals via blood, saliva, milk, colostrum, urine, faeces and semen. Moreover, some pigs have been reported to have been persistently infected for at least 200 days. Therefore, internal biosecurity refers to any type of measures implemented which manage to help to reduce the spread of the PRRS virus within the animals. These measures will be mainly related to management protocols and hygiene. The main factors to be considered when evaluating the internal biosecurity measures are the pig flow, personnel equipment, needles, fomites and insects. Obviously, personnel compliance is the key to successful implementation of such procedures for the control of PRRS in pigs.
Veterinarians can play an important role, not only as the team members who deliver science-based biosecurity to the farm, but also as teachers to educate personnel and auditors to ensure that compliance is maximized.