Diagnosis can be made on the basis of clinical signs, serology, histopathology, and virus

isolation from sows and/or fetuses. Diagnosis on the basis of clinical signs is difficult to achieve
because of variable signs from pig to pig and from farm to farm. Secondary bacterial infections
can also complicate the diagnosis. However, PRRS should be suspected if during a 2-week
period there is an abnormal number of stillbirths (more than 20% of all farrowings), late-term
abortions and premature farrowings exceeding 8%, or an increase of ≥ 25% in mortality of pigs
in the first week of life.
A sequence of events that can be helpful in diagnosing this disease has been described. A few
gilts and/or sows become listless and anorectic and develop moderate respiratory illness and
fever (up to 107 F [41.6 C]). Other swine on the farm are then affected. The acute illness is
transient but appears to predispose animals to secondary infections. In pregnant swine, recovery
from acute illness is followed by serious reproductive complications, e.g., increases in stillbirths
and neonatal deaths followed by increased mortality in near-term fetuses and an increase in fetal
mummification.
No major gross lesions are seen on necropsy except for dilated heart and enlarged lymph nodes
(K. D. Rossow, unpublished). For histopathology, brain, heart, lung, spleen, lymph nodes, and
nasal turbinates are good samples. Interstitial pneumonia characterized by alveolar septa
thickened with macrophages is a cardinal lesion in this disease. Other viruses that can cause
interstitial pneumonia are swine influenza (H1N1 and H3N2 strains), atypical strain of influenza,
and porcine respiratory coronavirus. Other infections that can be confused with this syndrome
are PRV, EMCV, PPV, PCMV, Leptospira pomona, and L. bratislava. Direct fluorescent
antibody (DFA) test on frozen sections of lungs can also be used to make a diagnosis of PRRS.
However, fetal tissues do not yield satisfactory results on DFA (D. A. Benfield, personal
communication).
The detection of antibodies in fetal fluids or precolostral blood of stillborn and weak pigs and a
rise in antibody titers in sera taken 3 weeks apart are another indication of PRRS. Because the
prevalence of seropositive finishing pigs in infected herds is high, an infected herd can be
identified using a relatively small number of samples, especially after an acute outbreak. Thus, a
maximum of 12 paired serum samples from finishing pigs are used in the UK to make a
diagnosis.’ To achieve a 95% confidence level when the rate oinfection is 30% in a herd, a
minimum of 9 samples per barn should be tested from that herd. Howeverit may be appropriate
to sample a larger number of sows than young pigs because sows have a lower seroprevalence
than do the finishing pigs. A mini mum of 30 sows per barn has been recommended.
Seroconversion can be determined by using SN, IFA, IPMA, or ELISA tests. The IPMA titers
develop as early as 1-2 weeks postinfection and reach a peak of 1:40,000 at 5-6 weeks
postinfection. Antibodies persist for up to 1 year in sows, with some sows becoming
seronegative in 4-6 months. However, current serological tests for 1 particular strain of the virus
may not always be sensitive in the detection of other strains. Also, serology cannot always be
relied on for the dagnosis of viral infections and has often been abused. For example, all animals
do not seroconvert during anoutbreak. In 1 herd, 8% of the sows remained seronegative.
Similarly, the pigs can be viremic but seronegative at early stages of infection.
For virus isolation, numerous samples from pigs of various ages should be submitted. A weak
pig or an acutely infected pig with respiratory signs in the farrowing house is a good candidate
for virus isolation. Lungs, spleen, lymph nodes, and serum are appropriate samples for virus
isolation. Serum and plasma are better than buffy coat cells for virus isolation. The PRRSV has
been isolated. from sera of PRRSV-inoculated pigs for up to 41 dpi despite the presence of high
titers of antibody (IFA titers ≥ 1:1,280). Lung, spleen, heart blood, and thoracic fluids of stillborn
and aborted fetuses are also adequate for virus isolation. The virus can be isolated from lungs,
serum, plasma, and buffy coat cells for 6-8 weeks after infection and has been isolated from
tissues frozen for 2-4 years.30 Autolyzed and mummified fetuses are not suitable for virus
isolation.
The virus can be propagated in PAM or in CL2621 cells, but PAM appear to be the most suitable
for the isolation of many PRRSV isolates, especially from serum samples. The presence of
antibodies may enhance virus uptake by macrophages, because they possess Fc receptors. A
cloned line of MA-104 cells also supports the growth of PRRSV (H. S. Joo, personal
communication).

Penyebab penyakit reproduksi pada ternak babi disebabkan oleh beragam faktor termasuk aborsi
dan neonatus yang lemah, kelahiran mati (stillbirth), mumifikasi, kematian embrionik, dan
infertilitas. Pada umumnya, kasus mumifikasi terlihat lebih sering pada ternak babi, namun
disebabkan oleh beberapa sumber penyakit.
Peningkatan temperatur pada anus babi (> 32 °C) dapat dikaitkan dengan kadar progesteron yang
rendah khususnya pada musim panas, siklus estrus yang tidak teratur, peningkatan mortalitas
embrionik, penurunan laju penyebaran, dan keguguran kecil.
Mycotoxins zearalenone, estrogenik dan zearalenol dapat mengganggu konsepsi dan implantasi,
sehingga menyebabkan infertilitas, kematian embrionik, dan berkurangnya ukuran pada ternak
babi. Selain itu, antiparasit seperti kresol, dicumarol, dan nitrat bisa menyebabkan aborsi pada
ternak babi. Defisiensi vitamin A menyebabkan anomali kongenital dan kemungkinan aborsi,
sedangkan riboflavin menyebabkan kelahiran prematur dini (14 – 16 hari).

Deteksi Antibodi
Antibodi terhadap virus PRRS dideteksi menggunakan ELISA kit komersial Anigen PRRSV Ab
ELISA 2.0® (Anigen Animal Genetics Inc., Korea). Serum diencerkan 1:40 dengan larutan
pengencer yang telah tersedia. Serum yag telah diencerkan ditambahkan masing-masing ke
dalam sumuran mikroplate kode NHC dan PRRS yang sebelumnya telah dilapisi dengan antigen
rekombinan PRRS dan antigen NHC. Protokol yang sama dilakukan untuk kontrol positif dan
negatif. Mikroplate diinkubasikan pada suhu kamar selama 30 menit dan selanjutnya dicuci
sebanyak lima kali. Mikroplate ditambahkan anti-porcine-HRP dan diinkubasikan selama 30
menit. Mikroplate dicuci sebanyak lima kali. Substrat ditambahkan untuk setiap sumur dan
diinkubasikan selama 15 menit. Setelah itu stop solution ditambahkan 100 μL ke setiap sumur.
Nilai absorbansi dibaca dengan spektrometer pada panjang gelombang 450 nm dan panjang
gelombag referensi 620 nm. Validitas uji dinilai sesuai aturan pabrik. Cut-off criteria (S/P rasio)
dihitung sesuai dengan manual yag disediakan. Rasio S/P yang lebih besar atau sama dengan 0,4
dianggap positif, sedangkan rasio S/P yang kurang dari 0,4 diaggap negatif.
Deteksi Virus
Virus PRRS dideteksi dari sampel lapangan dengan menggunakan
reversetranscriptasepolymerase chain reaction (RT PCR). Primer yang digunakan adalah NSP2-
F5’-AAAGACCAGATGGAGGAGGA-3’, NSP2-R 5’-GAGCTGAGTATTTTGGGCGTG-3’,
ORF5-F 5’- ATGTTGGGGAAGTGCTTGACC-3’, dan ORF5 –R
5’CTAGAGACGACCCCATTGTTCCGC-3’(Feng et al., 2008). RNA genom diisolasi dari
serum atau jaringan menggunakan protokol ekstraksi Trizol (Invitrogen) setelah sampel jaringan
ditambahkan proteinase K dalam SDS 2%. RT-PCR untuk deteksi virus PRRS dilakukan dengan
menggunakan SuperScriptTMIII One-Step RT-PCR system dengan Platinum® Taq DNA
Polymerase (Invitrogen). Kondisi reaksi dilakukan dalam 0,2 mM dNTP, 1,6 mM MgSO4,
dengan konsentrasi masingmasing primer 600 μM. Setelah penambahan 1- 3 μL sampel RNA
dan enzim, tabung PCR dimasukkan ke dalam thermocycler (GenAmp PCR System 9700).
Siklus RT-PCR yang lengkap Suartha et al Jurnal Veteriner 26 adalah selama 60 menit pada
suhu 45OC, prapemanasan dan tahap aktivasi Tagpolimerase pada suhu 95OC selama tujuh
menit. Selanjut sebayak 40 siklus yang masing-masing 45 detik pada suhu 94OC, selama 45
detik pada suhu 50-55OC, dan pada suhu 72OC selama 60 detik. Tahap sintesis akhir pada suhu
72OC selama lima menit. Setelah RT-PCR, sebanyak 10-20% produk ditambahkan dengan 1-2
μL loading dye (Bromphenol-blue dan Cyline Cyanol), kemudian dimasukkan ke dalam sumur
cetakan gel agarose 1%, bersamaan dengan sampel, DNA ladder 100 bp (Ivitrogen) juga ikut
dielektroforesis. Gel agarose diwarnai dengan 25μg/ml ethidium bromida. Produk
divisualisasikan dalam kotak UV dan didokumentasikan menggunakan Photodoc-TIHood.

Prosedur Pemeriksaan Elisa Hog PRRS

1. Siapkan semua reagen, sampel dan catatan posisi sampel yang dalam plate.
2. Isikan 100 µl kontrol negatif pada lubang C1 dan D1, NHC pada lubang C2 dan D2.
3. Isikan 100 µl kontrol positif pada lubang A1 dan B1, NHC pada lubang A2 dan B2.
4. Tambahkan 100 µl sampel pada semua lubang mikroplate.
5. Tutup plate dengan penutup, inkubasi mikroplate pada temperatur kamar selama 30 menit.
6. Buang (kosongkan) semua larutan dalam mikroplate kemudian Cuci dengan larutan pencuci
(wash buffer) sebanyak 3 (tiga) kali dan kemudian setalah pencuacian terakhir pukulkan
mikroplate sampai terbuang sempurna.
7. Isikan 100 µl Konjugat (HPRO Anti E-2) pada semua lubang.
8. Tutup mikroplate dengan penutup dan inkubasi mikroplate pada temperature kamar selama 30
menit.
9. Ulangi langkah 6
10. Isikan 100 µ TMB Substrat pada semua lubang mikroplate.
11. Tutup plate dengan penutup, inkubasi mikroplate pada temperature kamar selama 15 menit.
12. Isikan 100 µl Stop Solutioan pada semua lubang mikroplate.
13. Baca OD semua lubang mikroplate dengan ELISA reader pada absorbance 450 nm.
Pembacaan Hasil Validasi
1. Hitung nilai S/P masing-masing sampel
2. Jika nilai S/P kecil dari 0.4 maka dikelompokkan sebagai negatif antibodi PRRS
3. Jika nilai S/P besar atau sama dengan dari 0.4 maka dikelompokkan sebagai positif antibodi
PRRS
Interpretasi
1. Hitung rata-rata kontrol negatif (NC : PRRS) 3. Hitung rasio S/P : ( sampel A : PRRSV ) –
( sampel A : NHC )
2. Hitung rata-rata control positif (PC : PRRS) ( PC : PRRSV ) - ( PC : NHC )

Aetiology and pathogenesis

Porcine Reproductive and Respiratory Syndrome (PRRS) is a highly contagious viral disease that
was first recognized almost simultaneously in Western Europe and North America in the late
1980s. It is caused by the Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), a
small single stranded, non segmented RNA virus. The virion is enveloped, spherical and ranges
in size from 45 to 80 nm in diameter. PRRSV is differentiated into two genetically distinct
genotypes: Type 1, or European genotype, with a predominant spread on the European continent
and Type 2, or North American genotype, that is mostly isolated on the American continent
(North and South), as well as in Asia. Even for RNA viruses, PRRSV shows a remarkable
genetic variability. Genetic differences between Type 1 and Type 2 of approximately 40% for
whole genome sequences are documented and the calculated rate of nucleotide substitution is the
highest reported so far for an RNA virus. These facts open up a wide field of research with
regard to virus phylogenesis, as well as to the immunology involved (Bahkan untuk virus RNA,
prrsv menunjukkan variabilitas genetik yang luar biasa. Perbedaan genetik antara tipe 1 dan tipe
2 sekitar 40% untuk seluruh urutan genom didokumentasikan dan laju substitusi nukleotida yang
dihitung adalah yang tertinggi yang dilaporkan sejauh ini untuk virus rna. Fakta-fakta ini
membuka bidang penelitian yang luas berkenaan dengan filogenesis virus, serta imunologi yang
terlibat.)
The PRRS virus compromises the cellular immune response and damages mucosal surfaces.
Primary virus replication takes place in local macrophages from where the virus rapidly spreads
to lymphoid organs and lungs. Other tissues may also be infected, but not as commonly (Jaringan
lain mungkin juga terinfeksi, tetapi tidak seperti biasanya.). Infection can occur via the
respiratory, oral and venereal routes, as well as intramuscular, intraperitoneal or intravenous
inoculation. Viraemia develops in pigs 12- 24 hours post infection, with the highest titres at 7-14
days. Most pigs are viraemic for no longer than 28 days. Congenitally and postnatally infected
piglets remain persistently infected, harbouring the virus in their tonsils and/or lymph nodes.
In the environment, PRRSV favours moist and cold conditions, at or below 20 0C, with a pH
range of 5.5-6.5. The virus is shed by infected pigs in all secretions, including faeces, saliva and
semen. Pork and pork products have been shown to be of negligible risk in the transmission of
PRRSV.
Virus Classification
Order : Nidovirales
Family : Arteriviridae
Genus : Arterivirus
Species : Porcine Reproductive and Respiratory Syndrome
Virus Genotypes Type 1: European genotype Divided into subtypes 1 (pan European), 2 and 3
(East European) Type 2: North American genotype
Treatment
There is no specific treatment for PRRS. Treatment can be symptomatic and aim to prevent
secondary bacterial infections.
Prevention: Strategies to prevent PRRSV introduction to production units have to build on two
main pillars. The most important, and not a disease specific prevention method, is the application
of basic biosecurity measures. Reducing the opportunities for virus introduction through animal
segregation, increased hygiene for visitors, application of animal quarantine for pigs entering a
herd and appropriate cleaning and disinfection at critical production stages will effectively
contribute to the prevention of disease introduction.
Additionally, both attenuated live and inactivated vaccines are commercially available, but it is
important to match the genotype of the vaccine with that circulating in the pig population. While
vaccination of pigs does not prevent PRRSV infection, it may reduce clinical disease and
transmission of the wild type virus. It is important to note that the modifi ed live vaccine virus
can persist in pigs and be disseminated through semen and oral fluids; it should therefore not be
used in naïve herds, pregnant sows or breeding gilts and boars.
Distinguishing infected from vaccinated animals is currently not possible. Furthermore, there is a
potential risk that vaccinal virus can revert to a more virulent form and cause disease.
The virus is shed in saliva (six weeks), urine (two weeks), semen (six weeks) and mammary
gland secretions. Transmission can be by inhalation, ingestion (including ingestion of infected
meat), coitus, transplacental, artificial insemination (also from vaccinated boars), pig bites and
needles and other inanimate objects (equipment, instruments, clothing) or substances (water,
food). Arthropod transmission has been suggested by some preliminary reports (Zimmerman et
al, 2006). PRRSV is highly infectious and easily transmitted through direct contact among pen
mates. Aerosol transmission is difficult, although it has been experimentally shown for distances
of up to 2.5 meters (Zimmerman et al. 2006).
PRRSV is unstable outside the pH 5.5-6.5 range. Low concentrations of detergents and solvents
such as chloroform and ether rapidly inactivate PRRSV. The virus survives in water for up to 11
days, but drying quickly inactivates it (Benfield et al, 1999a). As a result, the virus does not
survive in the environment or on fomites under dry conditions.
PRRSV can be isolated from muscle and lymphoid tissues up to 24 hours after slaughter (even
from muscle that had been frozen at 20°C for one month). Nevertheless, the virus titres decrease
with cooling, hardening and freezing, although PRRSV can survive several weeks at 4°C in bone
marrow (Bloemraad et al, 1994). Cooking, curing and rendering are sufficient to inactivate
PRRSV in meat, minimising the risk of spread in this way. The real threat occurs when
unprocessed infected meat is fed to susceptible pigs (swill feeding) (AHA, 2004).
The most likely path of entry into a farm or country is asymptomatically infected pigs, via semen
and swill feeding. If these are imported from countries where PRRS is known to be present,
appropriate procedures such as herd freedom certification, serological testing and quarantine
should be followed. It would be very difficult to contain the disease if the feral pig population
became affected (AHA, 2004).
5. PREVENTION AND CONTROL
The key elements of a PRRS control and eradication programme are early disease detection and
rapid laboratory confirmation; quick identification of the infected farms; and control of the
infection through different stamping out strategies. Control options will depend on pig density,
the degree of multisite structure of farms, the movement of pigs, and whether infected pig meat
is processed by cooking. Because PRRS is transmitted by direct contact, control measures are
advisable although not critical at slaughter plants, meat processing plants and sale yards (AHA,
2004).
2. GEOGRAPHICAL DISTRIBUTION
PRRS was first detected in North America in 1987 and in Europe in 1990 and has since then
been recorded in most major pig producing areas throughout the world (Table 1).
Table 1. Status of PRRS in affected countries (Source: OIE, WAHID)
Status
Infection present (with no clinical disease)
Infection present (with clinical disease)
Disease restricted to certain zone(s) / region(s) of the country
Countries reporting
Mexico, Slovakia Czech Republic, Lithuania,
Canada, Colombia, Costa Rica, France, Germany, Ireland, Japan, Republic of Korea,
Netherlands, Philippines, Portugal, Spain, United Kingdom, United States of America.
Bolivia, Chile, Dominican Republic, Romania
Viet Nam: Between March and August 2007, 44 outbreaks grouped into two main epidemics
were reported; the first in northern provinces between March and May, and the second in
southern provinces during June and July. About 44.000 pigs were affected, of which over 4.000
died (OIE, 2007a). At the end of August 2007, Viet Nam declared that the epidemic was under
control. However, during August and September 2007, nine new PRRS outbreaks were reported
in Khanh Hoa, Ca Mau and Lang Son provinces with mortalities of up to 24 percent (OIE,
2007b). Preliminary clinical experiments suggest that secondary or concomitant infections have
been the cause of high mortality and morbidity.
China: Two major (American-type) PRRS occurrences have been reported in China since the
mid 1990s. From June to September 2006, an atypical form of PRRS affected over two million
pigs, of which 400,000 died in 16 provinces according to the China Animal Disease Control
Center (CADC). Unlike other previous PRRS outbreaks in China and historical PRRS outbreaks
worldwide, this form of the PRRS virus was more virulent and many adult pigs and pregnant
sows died (Tian et al, 2007). Initially, a mixed infection of several agents (mainly PRRS,
classical swine fever and porcine circovirus) was suspected (OIE, 2006). At the beginning of
2007, the disease reemerged and since then, it is reported to have infected 310.000 pigs, of which
more than 81.000 have died in 26 provinces (ProMED, 2007b). Provinces along the Yangtze
River in the south of China have been the most affected (OIE, 2006). While the disease was
initially reported in both the commercial and backyard sectors, it now seems to be concentrated
in the latter, where control is a greater challenge, especially in remote areas. A compulsory
PRRS vaccination policy has been implemented in highrisk areas and in high value herds
(breeding pigs and large scale commercial farms), using a newly developed vaccine matching the
circulating strain. As of 22 August 2007, the authorities had administered 314 million doses of
vaccine to immunise more than 100 million pigs, one fifth of the nation’s total (Martin et al,
2007). The outbreak has caused considerable economic losses and a rise in pork prices in eastern
China (ProMED, 2007a). On 29 October 2007, the Ministry of Agriculture announced that PRRS
was under control (ProMED, 2007b)
South Africa: In Africa, the disease situation is unknown. The first official reports came from
South Africa in June 2004, when a total of 2.407 pigs from 32 infected farms (31 small farmers
and one commercial unit) were slaughtered in Western Cape Province (OIE, 2004). Two small
outbreaks were reported in the same area in October 2005 (OIE, 2005). In August 2007, the same
European strain was also reported in Western Cape, involving at least 21 farms and 8.000 pigs
(ProMED, 2007c). This outbreak was considered a resurgence of the 2004 outbreak (FAO field
officer).

PREVENTION AND CONTROL MEASURES FOR PRRS AND OTHER INFECTIOUS

DISEASES OF SWINE
5.1. Surveillance
The first step is to assess the extent of the infection. Veterinary officers or inspection teams
should perform clinical examination of pigs, take blood samples from a statistically significant
number of pigs, and examine production records for evidence of reproductive problems, such as
abortions and neonatal mortalities. Special attention should be paid to farms with a recent history
of pig purchases, sale of breeding or grower stock, and artificial insemination. Serosurveillance
is particularly valuable in asymptomatic herds and in those in contact with feral pigs, if such
populations become infected (AHA, 2004). Whenever an infected pig herd is found, its origin
should be traced back and contacts should be investigated. Passive surveillance and reporting
should be encouraged among pig owners through awareness campaigns. Because programmes of
investigation are often not implemented at local government and village levels, it is
recommended that epidemiological investigation should be carried out in villages by field
veterinary staff and extension personnel asking a single question: “Have you seen this disease
before?”.
5.2. Quarantine and movement controls Quarantine should be imposed on all farms with known
or suspected infection. In a free ranging or village situation, pigs should be enclosed. Movement
of pigs in and out of farms/villages should be prohibited, other than for those animals destined
for immediate slaughter. Movement controls should be applied to pigs and carcasses (for further
processing by cooking) inside and out of the infected zone. Vehicles used to transport infected
pigs should be decontaminated (see 5.6 Cleaning and disinfection).
5.3. Biosecurity Farmers should be encouraged to enhance their biosecurity levels: new animals
only from PRRS free herds, visitors kept to a minimum, perimeter fencing, removal of effluent,
pig loading facilities located at perimeter fences, and cleaning and disinfection of pig-carrying
trucks after unloading (AHA, 2004). Perimeter fencing will prevent the spread of disease from
domestic to feral pigs and vice versa. The access of wild pigs to domestic food scraps should be
prevented (AHA, 2004). Village settings, where pigs may roam freely, present additional
biosecurity challenges although the same biosecurity principles apply. Equipment and premises
should be periodically cleaned and disinfected. Pigs should be kept in fenced enclosures,
whenever possible. Sharing of equipment between farms/villages should be discouraged, unless
proper decontamination is performed. Pig owners/workers should avoid contacting other pig
populations and dedicated work clothing should be pro Focus on. Porcine reproductive and
respiratory syndrome 4 Issue No 2 2007 moted. Replacement breeding stock should come from
PRRS free and trusted sources. Casual visitors, particularly those who have contact with pigs,
should be discouraged. A sign at the farm/village entrance advising visitors not to come close to
pigs is also recommended. Entrails and other discarded parts of slaughtered pigs should be
disposed of in an appropriate manner such as composting, burying or burning. When the disease
is present in an area, decontamination instruments should be made available at village entry and
exit points (disinfectant, brush and a bucket of water or a foot bath).
5.4. Zoning If the disease is endemic in only part of a country it is possible to establish diseased
and disease free zones and enforce tight controls on the movement of pigs and products between
zones (AHA, 2004).
5.5. Stamping out Stamping out strategies can be considered depending on the epidemiological
situation. It should only be carried out in the first stage of the infection when the infected area is
limited and the number of pigs to kill is still low. Traditional stamping out has its limits in
developing countries because of the lack of funds for compensation. Without compensation,
stamping out is often rejected by pig owners, and this may contribute to more rapid
dissemination of the disease through illegal movement of sick animals. A flexible stamping out
approach is required. Modified stamping out consists of an initial quarantine followed by
slaughter of all marketable pigs at an abattoir. For the remaining pigs, several options are
available:
1) destroy unsaleable on-farm pigs and offer compensation
2) allow growing pigs to grow to market size, and/or
3) allow pregnant sows to wean their litters. Diseased pigs cannot be sent to abattoirs; they must
be destroyed or quarantined until the symptoms pass (AHA, 2004). The carcasses of destroyed
pigs must be disposed of in a safe manner after stamping out is completed. Reference should be
made to the FAO Manual on procedures for disease eradication by stamping out for more
information on on-site slaughter and disposal procedures.
5.6. Cleaning and disinfection For the decontamination of farms, vehicles and equipment, routine
cleaning and disinfection with almost any chemical is enough due to the low resistance of
PRRSV. Phenolic or organic acid disinfectants, chlorine, quaternary ammonium compounds and
lipid solvents (detergents) have all been reported to be highly effective in inactivating PRRSV
(AHA, 2004; Zimmerman et al, 2006). Either replace or put aside equipment which cannot be
easily disinfected.
5.7. Vaccination Vaccination is one of the most effective tools to control PRRS, although it does
not prevent PRRSV infection. Vaccines should contain the specific antigenic type to be effective.
Experience shows that vaccination with a homologous strain is more effective than vaccination
with a heterologous strain. In the United States there are approved modified live virus (MLV)
vaccines for the reproductive and respiratory forms of PRRS. MLV vaccines are used in piglets
from three weeks of age or sows and gilts 3-6 weeks prior to breeding. In Europe and United
States, an inactivated virus vaccine against the reproductive form of PRRS is also available on
the market (OIE, 2004). One recommended strategy is the vaccination of seronegative
replacement breeding stock 60–90 days before introduction (AHA, 2004). Animals vaccinated
with MLV vaccines shed the vaccine strain virus, which is then transmitted in the field,
complicating the problem of detecting infection with wild type virus, both through virology and
serology (Zimmerman et al, 2006).
5.8. Sentinel and restocking A minimum 14 day period after decontamination is required before
restocking to avoid reinfection. Serology on restocked animals should be carried out after two
months and again six weeks later (AHA, 2004). Given husbandry practices in many parts of the
world (Africa, Latin America and Asia), there is a potential danger that restocking aimed at
reestablishing former pig populations could contribute to creating the conditions for a new
outbreak..
5.9. Public awareness PRRS outbreaks should be well publicised, emphasising the dangers of
swill feeding, particularly to small pig holdings. Commercial farms should be encouraged to
enhance their biosecurity levels (AHA, 2004). In African, Eastern European and many Asian
countries, an early warning system encouraging early reporting, and consequently early reaction,
should be implemented in every state or region and at national level. Ensuring the cooperation of
pig owners can be facilitated through information/sensitisation events at village level meetings.
Civil administrative authorities should also be put on a state of alert with periodical
epidemiological information. The reluctance of villagers to implement control measures is
motivated by a number of different considerations, including the following:
1) Village pig populations play an important role in cleaning up human leftovers.
2) Pigs are a good source of income for families.
3) Villagers do not understand why, after having lost most of their pigs, they are asked to kill
those remaining.
4) Pigs have an important social function because they are slaughtered to meet family needs or
ritual/traditional ceremonies.
5) Villagers always harbour the hope that the disease will stop by itself and that some of their
pigs will escape death because they believe that there is no disease capable of killing all the pigs.

TINDAKAN PENCEGAHAN DAN PENGENDALIAN PRRS DAN PENYAKIT MENULAR

LAINNYA DARI Babi
5.1. Pengawasan
Langkah pertama adalah menilai luasnya infeksi. Petugas veteriner atau tim inspeksi harus
melakukan pemeriksaan klinis terhadap babi, mengambil sampel darah dari babi yang jumlahnya
signifikan secara statistik, dan memeriksa catatan produksi untuk mengetahui bukti masalah
reproduksi, seperti aborsi dan kematian neonatal. Perhatian khusus harus diberikan pada
peternakan dengan riwayat pembelian babi, penjualan pembibitan atau stok petani, dan
inseminasi buatan. Surveilans serosurvei sangat berguna pada kawanan tanpa gejala dan pada
mereka yang bersentuhan dengan babi liar, jika populasi tersebut terinfeksi (AHA, 2004).
Kapanpun kawanan babi yang terinfeksi ditemukan, asal-usulnya harus dilacak kembali dan
kontak harus diselidiki. Pengawasan dan pelaporan pasif harus didorong di antara pemilik babi
melalui kampanye kesadaran. Karena program investigasi sering tidak dilaksanakan di tingkat
pemerintah daerah dan desa, maka investigasi epidemiologi sebaiknya dilakukan di desa oleh
petugas veteriner lapangan dan petugas penyuluhan dengan mengajukan satu pertanyaan:
“Pernahkah Anda melihat penyakit ini sebelumnya?”.
5.2. Karantina dan kontrol pergerakan Karantina harus diterapkan di semua peternakan yang
diketahui atau dicurigai terinfeksi. Dalam lingkungan bebas atau situasi desa, babi harus
dikurung. Pergerakan babi keluar masuk peternakan / desa harus dilarang, selain dari hewan
yang akan segera disembelih. Kontrol gerakan harus diterapkan pada babi dan bangkai (untuk
diproses lebih lanjut dengan memasak) di dalam dan di luar zona yang terinfeksi. Kendaraan
yang digunakan untuk mengangkut babi yang terinfeksi harus didekontaminasi (lihat 5.6
Pembersihan dan desinfeksi).
5.3. Biosecurity Peternak harus didorong untuk meningkatkan tingkat biosekuriti mereka: hewan
baru hanya dari ternak bebas PRRS, pengunjung dijaga seminimal mungkin, pagar perimeter,
pembuangan limbah, fasilitas pemuatan babi yang terletak di pagar perimeter, serta pembersihan
dan desinfeksi truk pengangkut babi setelah bongkar muat (AHA, 2004). Pemagaran perimeter
akan mencegah penyebaran penyakit dari babi domestik ke babi liar dan sebaliknya. Akses babi
hutan ke sisa makanan domestik harus dicegah (AHA, 2004). Pengaturan desa, di mana babi
dapat berkeliaran dengan bebas, menghadirkan tantangan biosekuriti tambahan meskipun prinsip
biosekuriti yang sama berlaku. Peralatan dan tempat harus dibersihkan dan didesinfeksi secara
berkala. Babi harus disimpan dalam kandang berpagar, jika memungkinkan. Berbagi peralatan
antar pertanian / desa harus dicegah, kecuali dilakukan dekontaminasi yang tepat. Pemilik /
pekerja babi harus menghindari kontak dengan populasi babi lain dan pakaian kerja khusus harus
menjadi fokus profesional. Reproduksi babi dan sindrom pernapasan 4 Edisi No 2 2007 mot.
Bibit pengganti harus berasal dari sumber PRRS yang bebas dan tepercaya. Pengunjung biasa,
terutama mereka yang bersentuhan dengan babi, harus dicegah. Sebuah tanda di pintu masuk
peternakan / desa yang menasihati pengunjung untuk tidak mendekati babi juga
direkomendasikan. Isi perut dan bagian lain dari babi yang disembelih harus dibuang dengan
cara yang tepat seperti pengomposan, penguburan atau pembakaran. Jika penyakit ada di suatu
daerah, instrumen dekontaminasi harus tersedia di titik masuk dan keluar desa (disinfektan, sikat
dan seember air atau rendaman kaki).
5.4. Zonasi Jika penyakit endemik hanya di sebagian negara, maka dimungkinkan untuk
menetapkan zona bebas penyakit dan penyakit dan menegakkan kontrol ketat terhadap
pergerakan babi dan produk antar zona (AHA, 2004).
5.5. Strategi Stamping out dapat dipertimbangkan tergantung pada situasi epidemiologi.
Tindakan ini hanya boleh dilakukan pada tahap pertama infeksi ketika area yang terinfeksi
terbatas dan jumlah babi yang akan dibunuh masih rendah. Pemberantasan tradisional memiliki
batas di negara berkembang karena kurangnya dana untuk kompensasi. Tanpa kompensasi,
pemberantasan penyakit sering ditolak oleh pemilik babi, dan ini dapat berkontribusi pada
penyebaran penyakit yang lebih cepat melalui perpindahan hewan yang sakit secara ilegal.
Diperlukan pendekatan stamping out yang fleksibel. Pengepakan yang dimodifikasi terdiri dari
karantina awal yang diikuti dengan penyembelihan semua babi yang dapat dipasarkan di rumah
potong hewan. Untuk babi yang tersisa, tersedia beberapa pilihan:
1) memusnahkan babi on-farm yang tidak dapat dijual dan menawarkan kompensasi
2) membiarkan babi tumbuh tumbuh sesuai ukuran pasar, dan / atau
3) biarkan babi betina hamil menyapih anaknya. Babi yang sakit tidak dapat dikirim ke rumah
potong hewan; mereka harus dihancurkan atau dikarantina sampai gejalanya berlalu (AHA,
2004). Bangkai babi yang telah dimusnahkan harus dibuang dengan cara yang aman setelah
penginjilan selesai. Referensi harus dibuat untuk Manual FAO tentang prosedur pemberantasan
penyakit dengan stamping out untuk informasi lebih lanjut tentang prosedur pemotongan dan
pembuangan di tempat.
5.6. Pembersihan dan desinfeksi Untuk dekontami 5.6. Pembersihan dan desinfeksi Untuk
dekontami pertanian, kendaraan dan peralatan, pembersihan rutin dan disinfeksi dengan hampir
semua bahan kimia sudah cukup karena resistansi PRRSV yang rendah. Disinfektan asam
fenolik atau organik, klorin, senyawa amonium kuaterner dan pelarut lipid (deterjen) semuanya
telah dilaporkan sangat efektif dalam menonaktifkan PRRSV (AHA, 2004; Zimmerman et al,
2006). Ganti atau sisihkan peralatan yang tidak dapat didisinfeksi dengan mudah.
5.7. Vaksinasi Vaksinasi adalah salah satu alat yang paling efektif untuk mengendalikan PRRS,
meskipun tidak mencegah infeksi PRRSV. Vaksin harus mengandung jenis antigenik tertentu
agar efektif. Pengalaman menunjukkan bahwa vaksinasi dengan strain homolog lebih efektif
daripada vaksinasi dengan strain heterolog. Di Amerika Serikat, ada vaksin virus hidup yang
dimodifikasi (MLV) yang disetujui untuk bentuk reproduksi dan pernapasan PRRS. Vaksin
MLV digunakan pada anak babi dari umur tiga minggu atau induk babi 3-6 minggu sebelum
dikawinkan. Di Eropa dan Amerika Serikat, vaksin virus yang tidak aktif terhadap bentuk
reproduksi PRRS juga tersedia di pasaran (OIE, 2004). Salah satu strategi yang
direkomendasikan adalah vaksinasi bibit pengganti seronegatif 60–90 hari sebelum introduksi
(AHA, 2004). Hewan yang divaksinasi dengan vaksin MLV melepaskan vaksin strain virus,
yang kemudian ditularkan di lapangan, mempersulit masalah pendeteksian infeksi virus tipe liar,
baik melalui virologi maupun serologi (Zimmerman et al, 2006).
5.8. Sentinel dan penyetokan ulang Diperlukan waktu minimal 14 hari setelah dekontaminasi
sebelum penyetokan ulang untuk menghindari infeksi ulang. Serologi pada hewan yang distok
ulang harus dilakukan setelah dua bulan dan enam minggu kemudian (AHA, 2004). Mengingat
praktik peternakan di banyak bagian dunia (Afrika, Amerika Latin dan Asia), terdapat potensi
bahaya bahwa restocking yang bertujuan memulihkan populasi babi sebelumnya dapat
berkontribusi untuk menciptakan kondisi wabah baru.
5.9. Kesadaran publik bahwa wabah PRRS harus dipublikasikan dengan baik, dengan
menekankan bahaya pemberian pakan swill, terutama untuk kandang babi kecil. Peternakan
komersial harus didorong untuk meningkatkan tingkat biosekuriti mereka (AHA, 2004). Di
Afrika, Eropa Timur dan banyak negara Asia, sistem peringatan dini yang mendorong pelaporan
dini, dan akibatnya reaksi dini, harus diterapkan di setiap negara bagian atau wilayah dan di
tingkat nasional. Memastikan kerjasama pemilik babi dapat difasilitasi melalui acara
penyuluhan / penyuluhan di pertemuan tingkat desa. Otoritas administrasi sipil juga harus
disiagakan dengan informasi epidemiologi berkala. Keengganan warga desa untuk melakukan
tindakan pengendalian dilatarbelakangi oleh beberapa pertimbangan yang berbeda, antara lain
sebagai berikut:
1) Populasi babi desa berperan penting dalam membersihkan sisa-sisa manusia.
2) Babi adalah sumber pendapatan yang baik bagi keluarga.
3) Penduduk desa tidak mengerti mengapa, setelah kehilangan sebagian besar babi mereka,
mereka diminta untuk membunuh yang tersisa.
4) Babi memiliki fungsi sosial yang penting karena disembelih untuk memenuhi kebutuhan
keluarga atau ritual / upacara adat.
5) Penduduk desa selalu menaruh harapan bahwa penyakit akan berhenti dengan sendirinya dan
bahwa beberapa babi mereka akan lolos dari kematian karena mereka percaya bahwa tidak ada
penyakit yang mampu membunuh semua babi.

Clinical signs of PRRS vary with the strain of virus, the immune status of the herd and
management factors. The incubation period ranges from 3-37 days.
Dermatological signs: There may be a reddish to blue discolouration and blotching of the skin,
most often of the ears (which gives PRRS the name of ‘Blue ear disease’) and the vulva, and
may also include the trunk of the infected pigs. Subcutaneous oedema of the rear limbs and, in
neonates, of the eyelids and periorbital area, cranium, and snout, may also be present, especially
with the European genotype of PRRSV.
Reproductive failure in sows: The disease is first characterized by acute illness with lethargy and
reduced appetite and spreads quickly through a herd over 7–10 days. Clinical signs are infertility,
agalactia, lowered farrowing rates, a marked increase in late term abortions, and stillborn,
mummified or weak live born piglets. Respiratory disease may also be present. Sows can
transplacentally transmit PRRSV to their unborn piglets.
Respiratory disease in piglets and grower pigs: In piglets that survive the pregnancy and neonatal
phases, PRRS manifests as respiratory disease and is often complicated by secondary infections.
Concurrent infection with Pasteurella multocida, Porcine Circovirus Type 2 (PCV2),
Mycoplasma hyopneumonia, Streptococcus suis, Salmonella cholerasuis, Haemophilus parasuis
and swine infl uenza virus is common. High death rates can be observed, typically 30-50 percent
in young piglets and 4-20 percent in post-weaning pigs.
In post-weaning and grower pigs, clinical signs include dyspnoea, anorexia, lethargy, cutaneous
hyperaemia, rough hair coats, and decreased weight gain. Secondary infections are common.
Older pigs might show only minor respiratory signs.
Subclinical infection often occurs in finishing pigs, boars, gilts, and sows; in some herds,
infection is generally asymptomatic.
Post mortem lesions: Although PRRSV produces a multisystemic infection in pigs, gross lesions
are usually only observed in skin, respiratory and lymphoid tissues and vary depending on the
viral strain, the individual stress factors and the presence of secondary infections. Interstitial
pneumonia and enlarged lymph nodes can occur in all ages of swine. However, lesions are most
commonly observed in neonatal and young, weaned piglets. With severe disease, lungs are
mottled, tan and red, and fail to collapse; the cranioventral lobes tend to be most affected. Lymph
nodes are enlarged, sometimes haemorrhagic, and can range from solid to polycystic.
The body condition of foetuses from late-term abortions ranges from fresh to autolyzed;
umbilical haemorrhage has been reported to be a gross lesion of PRRSV infection.
Diagnosis and Treatment
Clinical diagnosis: Disease signs are similar to many other viral or bacterial swine diseases (see
list of differential diagnoses below) and the clinical picture can be blurred by co-infection with
other pathogens. Therefore, diagnosis of PRRS should be based on clinical signs and post-
mortem examination (noted above), in conjunction with laboratory tests. The disease should be
suspected with reproductive failure, high levels of neonatal mortality and respiratory problems in
pigs of any age.
Differential diagnoses for reproductive disease include classical swine fever (CSF), African
swine fever (ASF), leptospirosis, porcine parvovirus, porcine enterovirus, haemagglutinating
encephalomyelitis virus, Toxoplasma gondi, and Aujeszky’s disease.
For respiratory and postweaning disease, swine influenza, enzootic pneumonia, proliferative and
necrotizing pneumonia, Haemophilus parasuis infection, haemagglutinating encephalomyelitis
virus, porcine respiratory coronavirus, syncitial pneumonia and myocarditis, porcine circovirus-
associated disease, post-weaning multisystemic wasting syndrome and Nipah virus infection
should be considered.
Laboratory tests: A wide range of serological tests can be used for the detection of serum
antibodies, ideally performed during recent infections. However, these tests only indicate that a
pig has been exposed to the virus either naturally or through vaccination, but cannot tell if the pig
is still infected. The enzyme-linked immunosorbent assay (ELISA) has the advantage of being
able to test a large number of samples within a short period of time and has been developed to
distinguish between the American and European types. The European antigenic type can also be
detected with the immunoperoxidase monolayer assay (IPMA), using alveolar macrophages and
the American type with the indirect immunofluorescence assay (IFA), using MARC-145 cells.
To determine the actual presence of the virus, reverse-transcription polymerase chain reaction
(RT-PCR) is recommended. A multiplex PCR assay has been designed to differentiate between
North American and European PRRSV isolates. Confi rmation of PRRSV also includes
immunohistochemistry staining (IHC), fl uorescent antibody staining (FA) and in situ
hybridization of fi xed tissues.
Virus isolation (VI) is diffi cult, but can be attempted from serum, ascitic fl uid, and tissues
(lung, tonsils, lymph nodes and spleen). PRRSV is best cultured on porcine alveolar
macrophages and MARC-145 cells.

Tanda-tanda klinis PRRS bervariasi menurut jenis virus, status kekebalan kelompok dan faktor
manajemen. Masa inkubasinya berkisar antara 3-37 hari.
Tanda-tanda dermatologis: Mungkin ada perubahan warna kemerahan menjadi biru dan bercak
pada kulit, paling sering di telinga (yang memberi PRRS nama 'penyakit telinga biru') dan vulva,
dan mungkin juga termasuk batang babi yang terinfeksi. Edema subkutan pada tungkai belakang
dan, pada neonatus, pada kelopak mata dan area periorbital, kranium, dan moncong, juga dapat
muncul, terutama dengan genotipe PRRSV Eropa.
Kegagalan reproduksi pada induk babi: Penyakit ini pertama kali ditandai dengan penyakit akut
dengan kelesuan dan nafsu makan berkurang dan menyebar dengan cepat melalui kawanan
selama 7–10 hari. Tanda-tanda klinisnya adalah infertilitas, agalaktia, penurunan angka
kematian, peningkatan yang nyata pada aborsi jangka panjang, dan bayi lahir mati, mumi atau
bayi lahir lemah. Penyakit pernapasan juga mungkin ada. Induk dapat mentransmisikan PRRSV
secara transplasenta ke anak babi yang belum lahir.
Penyakit pernapasan pada anak babi dan babi dewasa: Pada anak babi yang selamat dari fase
kehamilan dan neonatal, PRRS bermanifestasi sebagai penyakit pernapasan dan seringkali
dipersulit oleh infeksi sekunder. Infeksi bersamaan dengan Pasteurella multocida, Porcine
Circovirus Tipe 2 (PCV2), Mycoplasma hyopneumonia, Streptococcus suis, Salmonella
cholerasuis, Haemophilus parasuis dan virus flu babi sering terjadi. Tingkat kematian yang tinggi
dapat diamati, biasanya 30-50 persen pada anak babi muda dan 4-20 persen pada babi pasca
penyapihan.
Pada babi pasca penyapihan dan pertumbuhan, tanda klinis termasuk dispnea, anoreksia, lesu,
hiperemia kulit, bulu kasar, dan penurunan berat badan. Infeksi sekunder sering terjadi. Babi
yang lebih tua mungkin hanya menunjukkan tanda-tanda pernapasan kecil.
Infeksi subklinis sering terjadi pada babi, babi hutan, gilt, dan babi betina; pada beberapa
kelompok, infeksi umumnya tidak bergejala.
Lesi post mortem: Meskipun PRRSV menyebabkan infeksi multisistemik pada babi, lesi berat
biasanya hanya terlihat pada kulit, jaringan pernapasan dan limfoid dan bervariasi tergantung
pada strain virus, faktor stres individu dan adanya infeksi sekunder. Pneumonia interstitial dan
pembesaran kelenjar getah bening dapat terjadi pada semua umur babi. Namun, lesi paling sering
ditemukan pada bayi baru lahir dan anak babi yang disapih. Pada penyakit parah, paru-paru
berbintik-bintik, cokelat dan merah, dan gagal untuk kolaps; lobus kranioventral cenderung
paling terpengaruh. Kelenjar getah bening membesar, terkadang berdarah, dan bisa berkisar dari
padat hingga polikistik.
Kondisi tubuh janin dari aborsi jangka panjang berkisar dari segar hingga autolisis; Perdarahan
pusar telah dilaporkan sebagai lesi parah dari infeksi PRRSV.

Diagnosis dan Perawatan

Diagnosis klinis: Tanda-tanda penyakit serupa dengan banyak penyakit babi akibat virus atau
bakteri (lihat daftar diagnosis banding di bawah) dan gambaran klinis dapat kabur karena
koinfeksi dengan patogen lain. Oleh karena itu, diagnosis PRRS harus didasarkan pada tanda-
tanda klinis dan pemeriksaan post-mortem (disebutkan di atas), dalam hubungannya dengan uji
laboratorium. Penyakit ini harus dicurigai dengan kegagalan reproduksi, tingkat kematian
neonatal yang tinggi dan masalah pernafasan pada babi dari segala usia.
Diagnosis banding untuk penyakit reproduksi termasuk demam babi klasik (LCS), demam babi
Afrika (ASF), leptospirosis, porcine parvovirus, porcine enterovirus, virus haemagglutinating
encephalomyelitis, Toxoplasma gondi, dan penyakit Aujeszky.
Untuk penyakit pernafasan dan pasca-penyapihan, flu babi, pneumonia enzootic, pneumonia
proliferatif dan nekrosis, infeksi Haemophilus parasuis, virus haemagglutinating
encephalomyelitis, virus corona pernafasan babi, pneumonia syncitial dan miokarditis, penyakit
terkait porcine circovirus, sindroma infeksi wasting multisistemik pasca-penyapihan Seharusnya
dipertimbangkan.
Tes laboratorium: Berbagai tes serologi dapat digunakan untuk mendeteksi antibodi serum,
idealnya dilakukan selama infeksi baru-baru ini. Namun, tes ini hanya menunjukkan bahwa babi
telah terpapar virus baik secara alami atau melalui vaksinasi, tetapi tidak dapat mengetahui
apakah babi tersebut masih terinfeksi. Enzim-linked immunosorbent assay (ELISA) memiliki
keuntungan karena dapat menguji sejumlah besar sampel dalam waktu singkat dan telah
dikembangkan untuk membedakan antara jenis Amerika dan Eropa. Jenis antigenik Eropa juga
dapat dideteksi dengan uji imunoperoksidase monolayer (IPMA), menggunakan makrofag
alveolar dan jenis Amerika dengan uji imunofluoresensi tidak langsung (IFA), menggunakan sel
MARC-145.
Untuk menentukan keberadaan virus yang sebenarnya, reaksi berantai polimerase transkripsi
balik (RT-PCR) direkomendasikan. Pengujian PCR multipleks telah dirancang untuk
membedakan antara isolat PRRSV Amerika Utara dan Eropa. Konfirmasi PRRSV juga
mencakup pewarnaan imunohistokimia (IHC), pewarnaan antibodi fluoresen (FA) dan hibridisasi
in situ jaringan tetap.
Isolasi virus (VI) sulit, tetapi dapat dilakukan dari serum, cairan asites, dan jaringan (paru-paru,
amandel, kelenjar getah bening, dan limpa). PRRSV paling baik dibiakkan pada makrofag
alveolar babi dan sel MARC-145.

Porcine reproductive and respiratory syndrome (PRRS) is an infectious viral disease of swine
that is easily transmitted through direct contact to susceptible pigs and vertically to foetuses.
PRRS is considered the most economically important viral disease of intensive swine farms in
Europe and North America. It is characterised by reproductive failure in sows and respiratory
distress in piglets and fattening pigs, which, combined with its potential for rapid spread, can
cause significant production and economic losses. PRRS, also known as Mystery Swine Disease,
Blue Ear Disease, Porcine Endemic Abortion and Respiratory Syndrome (PEARS) and Swine
Infertility Respiratory Syndrome (SIRS), is not known to be a zoonosis. The PRRS virus
(PRRSV) is an enveloped positive stranded RNA virus, classified in the order Nidovirales,
family Arteriviridae, and genus Arterivirus (Zimmerman et al. 2006). Two major serotypes of the
virus are currently described, the European and the American types. This classification is
significant in that vaccines made for one serotype will not completely protect against the other.
dan infeksi bakteri sekunder, seperti salmonella cholerasuis, haemophilus parasuis,
streptococcous suis, mycoplasma hyopneumonia dan virus flu babi (hill, 1996)
. Identifikasi dan karakterisasi virus dilakukan dengan immunostaining dengan antiserum
spesifik. Untuk konfirmasi laboratorium, imunohistokimia dan hibridisasi in situ pada jaringan
tetap dan transkripsi balik pcr (rt-pcr) digunakan (oie, 2004).