The following case descriptions illustrate how complex respiratory disease can become in finishing facilities. Today it is extremely common to hear the report that Amy pigs are wrecking 5 to 7 weeks after they are placed in the finisher. This is due to multiple respiratory disease agents infecting a pig at the same time and resulting in a much worse disease than if pigs had been infected with just one organism or virus. This combination effect occurs with Mycoplasma hyopneumoniae and PRRS (porcine reproductive and respiratory syndrome) virus, porcine respiratory coronavirus (PRCV) and swine influenza virus, Streptococcus suis and PRRS virus, Pasteurella multocida and PRRS virus, and Haemophilus parasuis and PRRS virus-to name some of the combinations.

Case 1-6080 Head Off Site Nursery

Four buildings, each housing 1520 pigs, are operated on an all in/all out basis. Each building is filled with a single week's production from each of 3 sow farms, two of which were new 2000 sow units (18 months into production) and the third was a 1200 sow facility. The 3 sow farms supply 2 different, 6080 head, off site nurseries that developed the same clinical syndrome. An acute respiratory outbreak began in the nursery during August, 1995. By mid September, 40% of the nursery pigs had a very deep cough and 60% had thumping respiration. Mortality, cull pigs, and growth characteristics before and after the outbreak are listed in Table 1.

The 3 sow farms were vaccinated in September, 1994, for PRRS. In January, 1995, the sow herds were placed on a routine PRRS vaccination program. All sows now receive a full dose of RespPRRS 2 weeks prior to weaning. Replacement gilts are vaccinated at 9 weeks of age and again at 29 weeks of age before delivery to the farm. Parvo/Lepto/Erysipelas vaccination (a single product) is routinely used at weaning and the herds are vaccinated for PRV every 6 months. The two 2000-sow farms (A and C) were clinically normal during the nursery pig disease outbreak, while the 1200 sow unit (D) had an increase in the number of abortions and preg check negative sows during August and September, 1995. No unusual respiratory disease was observed in any of the farrowing units of the 3 farms during the nursery pig respiratory disease outbreak. Each sow herd and the off site nurseries were bled for the serologic tests described above. With 1 exception, at least 10 pigs (n=8-12) from each of 3 age groups of nursery pigs were bled at the 2 off site nurseries (BB and WP): 3-week-old pigs just moved to the nursery identified to sow farm origin, 7 and 9-week-old commingled (co) pigs. Lungs of poor-doing finishing pigs at a third site were sent for a complete diagnostic workup, which included histopathology, immunohistochemistry (IHC) for PRRS, swine influenza (SI) and porcine respiratory coronavirus (PRCV) when the appropriate histologic lesions were observed, bacterial culturing, and viral testing that included PRRS fluorescent antibody tissue section test (FATST), PRRS virus isolation (VI) in MARC-145 cells, SI capture enzyme-linked immunosorbent assay (ELISA), SI VI in primary swine kidney cell cultures and PRCV FATST.

Case 2-5000 Head Finishing Facility

The five 1000-head finishing buildings on the site are populated over a 2 week period of time from 1 of 2 off site nursery facilities that are supplied by 5 different sow farms. Ordinarily, 4000 pigs will be placed in the first week of delivery. The finishing buildings are curtain-sided, gutter flush units with solid concrete floors. The ceiling is open with ridge ventilation. Prior to an outbreak of acute respiratory disease, nursery death losses were consistently below 2% with an average daily gain of 0.9 lb and feed efficiency of 1.6. Cull rate on the finisher is usually below 5%, and the feeder pigs supplied to the farm will usually be 45 to 50 lb by 9 to 10 weeks of age. Each building is run on an all in/all out basis.

In September, 1995, the oldest group of finishing pigs developed acute respiratory disease characterized by a soft nonproductive cough 6 weeks after the floor was filled. Shortly after the coughing was observed, the pigs went off feed and began to scour. A poor response was obtained for aureomycin water medication and injection of individual pigs with procaine penicillin. Affected pigs did not die due to acute respiratory disease. Dead hogs usually had extensive gastric ulcers. Three acutely affected pigs were sacrificed for PRRS, SI, PRCV tests and salmonella culture. The same methods described for Case 1 were used for these samples. Death loss was between 4 to 5% and cull rate was 7-10%, which varied by building affected.

PRRS, PRCV and SI serology was performed on pigs at the 2 different off site nurseries that had provided feeder pigs for the finishing floors.. These nurseries, B and G, are supplied by the same sow farms. Ten pigs were bled in each nursery for the evaluation. Finishing pigs originating from the off site nurseries were also profiled at 16 weeks of age for the 3 viral pathogens to determine their prevalence on the farm.

For tabular reporting of results, nursery pig and finishing pig have been abbreviated as NP and FP.

Results of Laboratory Testing

PRRS serology is summarized below in a format similar to that described by Mike Snyder of the IDEXX Laboratories at the fall, 1995, swine diagnostics symposium held in Ames, Iowa. He presented a format for evaluation of antibody profiles based upon IDEXX's poultry ELISA interpretative software. For these case studies, that concept has been further refined as outlined in Table 2.

The adjustment made for titer groups as originally described by Snyder is due to correlation of clinical findings to PRRS ELISA in infected herds. Titer group 1 is observed in 3-week-old pigs from vaccinated or previously infected sows, and that level of antibody is typically found in a clinically normal nursery with endemic PRRS. Weaned pigs with titer group 2 results may very well have been infected in farrowing and are now a source of viral dissemination in the nursery facility. Nursery pigs older than 7 weeks with antibody levels in titer group 3 and 4 have been infected in farrowing or the nursery and are likely amplifiers of PRRS there and into the finishing facilities. RespPRRS-vaccinated sows with clinically normal reproductive parameters that have received 1 dose of the vaccine per farrowing cycle will usually have antibody levels between titer groups 1 and 2. Ideally, no more than 10% of the vaccinated breeding animals should have a titer group 0 response to past vaccination. Sows receiving 2 doses of vaccine per farrowing cycle will frequently be negative (up to 50% of the vaccinated sows). Those statements are based upon findings for previously infected herds with prior reproductive losses due to PRRS that no longer have clinical evidence of PRRS in the breeding herd, a "normal" herd. Finisher and breeding animals not vaccinated within the last 60 days that have antibody levels in titer groups 4 and 5, and possibly the upper end of group 3 have probably been recently infected. Animals with titer group 5 antibody levels may have been viremic at the time of blood collection.

Serologic Findings for Case 1:

Bacteriology, Virology, Histopathology:

49-day-old BB NP Lung: SI capture ELISA negative, VI negative (September 22) PRCV FATST negative, PRRS FATST negative, VI negative, IHC negative

Histopathology: moderate interstitial pneumonia suggestive of a viral etiology Bacteriology positive for Streptococcus suis 63-day-old BB FP Lung prominent peribronchiolar and perivascular (August 30) cuffing with attenuation and irregularity of the bronchiolar epithelium-bronchiolar damage suggestive of SI virus infection; SI IHC weak positive, PRCV IHC negative

2 Nasal swabs: SI capture ELISA positive, VI no test 17-wk-old BB FP

Lung Histopathology: moderate multifocal suppurative and histiocytic bronchointerstitial pneumonia characterized by moderate peribronchiolar and perivascular lymphocytic cuffing and nodule formation, moderate proliferation with less frequent and focal necrotizing bronchiolitis. Lesions are consistent with bronchopneumonia due to combined bacterial and mycoplasmal infection. The proliferative and focally necrotizing bronchiolitis is suggestive of resolving swine influenza virus infection.

PRCV, PRRS, SIV IHC negative Mycoplasma hyopneumoniae FATST-1of 2 lungs positive

Serologic Findings for Case 2:

Bacteriology, Virology:

17-week-old FP 3

Lungs: SI capture ELISA negative, 2 of 3 VI positive (September 26) PRCV FATST 3 of 3 positive PRRS FATST 1 of 3 positive Bacteriology positive only on 1 of 3 lungs that was SI and PRCV positive: 2+ Pasteurella multocida 1+ Streptococcus suis

NOTE: The PRRS FATST positive lung had a much more extensive PRCV infection, and the PRRS positive lung was negative for swine influenza.
*Titers expressed as geometric mean titer.
**Negative ^HNot Determined

The samples, herd histories and data are the result of a joint effort between or laboratory and Drs. Andy Holtcamp of Prestage Feeds, Randy Jones of Livestock Veterinary Service, C. L. Kanitz of the Purdue Animal Disease Diagnostic Laboratory (West Lafayette, IN) and Russell Bey of the Department of Veterinary Pathobiology of the University of Minnesota.

So What Do I Do?

There are obviously many negative interactions that can occur on a single farm, from the actual cases described. A producer's goal must be to minimize the impact of existing agents on his farm by managing his pigs to minimize the impact of any disease on them. One of the common ways used today for PRRS-infected farms is to vaccinate sows and/or pigs as prescribed by the herd veterinarian, or to use management to control the disease such as the McREBEL system of Dr. McCaw of the NCSU College of Veterinary Medicine.

It is obvious that swine influenza and PRCV are very common in North Carolina herds from the testing conducted at our laboratory. That means you must first determine if either or both are present, and then take the appropriate steps to minimize their impact on your pigs. Usually if either agent is present, many sows will be positive, and a blood sample from 20 randomly selected sows will confirm the infection(s).

PRCV can be a blessing and a curse. If a PRCV-positive sow herd is exposed to TGE by addition of infected gilts or boars, the disease will commonly be much milder and result in less baby pig deaths. However, when it is in a gilt developer, TGE can be masked by preexisting PRCV infection. That can mean shipping TGE with the next load of gilts. Finally, in the growing pig the ability of PRCV to cause pneumonia is highly variable, and can cause little or no disease to a very severe thumping cough. The more severe strains can make influenza infections much more severe than if the influenza occurred by itself.

What can you do about PRCV in the herd? There are no vaccines to use for this disease, meaning that you must resort to pig management to minimize its impact.

Swine influenza, on the other hand, can be managed by vaccination of either sows or growing pigs, but should be done under your veterinarian's guidance to maximize the benefit of vaccination for the least cost to your farm. It does not appear that the disease is decreasing at this time. Infected sow herds seem to maintain the infection on a 12 month basis, which is probably due to the high gilt replacement rates that are typical of today's swine production practices. The disease can be reduced in infected herds by gilt and boar immunization during their normal 45 to 60 day quarantine/isolation period after delivery to the farm when they are also vaccinated for PRRS when applicable.

Mycoplasma hyopneumoniae can also be a common disease agent in NC herds. When present, it is even more important to carefully control the impact of the viral diseases mentioned above. This agent is immunosuppressive, which means that any disease agent the pig is infected with following M. hyopneumoniae infection will commonly cause more severe disease.

The other swine bacterial disease agents described at the beginning of this article are commonly worse if a pig has an active PRRS infection. For that reason and the widespread occurrence of all these diseases in our industry, we must recognize the need for careful management of PRRS once it is introduced to our herds and most importantly, the need for very strict use of all in/all out pig flow management, limited cross-fostering and removal of backward pigs when indicated to reduce the disease load on the growing pigs. It is extremely important to consider needle management when treating or vaccinating pigs in a PRRS-infected herd. Using the same needle between litters or throughout a group of sows can spread an acute PRRS infection between piglets or breeding animals resulting in a catastrophic outbreak of disease in the herd.

References

Snyder ML. PRRS ELISA: A model for quantitative antibody determination. Proceedings, Diagnostic Serology and Viral Diagnostics Seminar, November 10-11, 1995, Ames, Iowa. Module I, Section D.

Lee BW, Bey RF, Baarsch MJ, Morrison RB, Freese, W. Determination of hemagglutination-inhibition titers to influenza A virus in porcine sera by use of an enzyme-linked immunosorbent assay. Am J Vet Res 54:1270-1276, 1993.

McCaw, M. PRRS Control: Whole Herd Management Concepts and Research Update, Proceedings of the North Carolina Healthy Hogs Seminar, 1995, p. 57-64.

Acknowledgments: Histopathology and immunohistochemistry were performed by the Iowa Veterinary Diagnostic Laboratory, Ames, Iowa.