Clinton, NC •
October 29, 2004
DISEASES OF THE RESPIRATORY SYSTEM
Dr. R.B. Baker
College of Veterinary Medicine
Carolina State University
modern swine systems respiratory disease has evolved to more of a Porcine
Respiratory Disease Complex (PRDC). This
term is frequently used in lay and scientific text today. This complex of disease expression has likely
developed because of industry management strategies that have focused on
economies of scale and values created by food chain integration.
these strategies have eliminated many problems associated with continuous flow
systems and associated diseases it has produced very large populations of mixed
immune status pigs often on the same site.
This has favored new syndromes by changing the ecology and evolution of
a new set of economically important agents.
This is a dynamic situation that is both complex and evolving.
· Although each of the
various specific disease agents will be discussed many will be found together
or in rapid succession in modern pig rearing facilities. Some of these agents when alone cause little
disease or productivity impact but if present with PRRS virus serious
consequences often occur. This is a
challenge to the modern swine veterinarian who is limited by a decreasing number
of antimicrobials and often ineffectual vaccines.
· Clinical signs of swine
respiratory disease are little different from respiratory disease in other
species. There can be a wide range of
symptoms even in the same barn or production system. Multi-site production has led to a more age
dependent onset of many agents and associated signs.
· Porcine respiratory
disease is best compared to human respiratory outbreaks. Population size and contact rates affect both
species. For example, whooping cough in
daycare centers or seasonal influenza outbreaks spreading globally best mimic
the respiratory issues faced in modern pig production.
· Coughing is common in
pigs of all ages but varies with conditions, level of immunity, and specific
· Dyspnea or “thumps” as it is
described in pigs is a common sign with more chronic cases.
· Morbidity and Mortality
is highly variable depending on the age, agents involved, and population
· Some respiratory disease
has systemic origins.
· Parasitic (verminous) pneumonia is no longer common but may occur in
back yard operations, pet, or zoo housed pigs.
· Respiratory disease
complex is the most costly disease syndrome in US pig production.
Specific Agents in order of importance:
Porcine Reproductive and
Respiratory Syndrome (PRRS) Virus
is a viral disease of pigs that causes two distinct clinical syndromes. Clinical signs are usually overlapping in
breeding units where pregnant females display both reproductive failure and
respiratory disease during outbreaks.
The reproductive component of this virus has been discussed by Dr. McCaw
and his notes should be used for reference.
The virus affects pigs of all ages but older pigs and adults typically
have shorter and reduced clinical severity when not pregnant.
· The virus causes persistent
infections lasting three to four months or longer. A subset of alveolar macrophages is the only
known tissue infected by the virus. Even
so, this has a paramount effect on the immune system increasing the severity of
many once passive agents present in pig operations.
· This viral agent has become
the most economically significant US swine disease since Classical
Swine Fever (Hog Cholera). There is a
wide range of severity that is believed to be influenced by virus genetics,
management, biosecurity, other pathogens, previous
exposure, vaccine use, possibly pig genetics, and other factors.
· Clinical disease associated with this virus was first described in 1987
although some case reports go back to the winter of 1986. North Carolina,
Iowa, and Minnesota all reported cases. It quickly spread throughout the US
industry over the next few years.
Interestingly a significantly different genetic strain spread through Western Europe almost simultaneously. PRRS has now spread around the world to every
country where pigs are imported.
· To date no other species has been detected that can be infected with this
virus although an early experiment with mallard duck shedding was
reported. Rodents including mice and
prairie dogs, cattle, horses, dogs, cats, goats, sheep, and repeated duck and
other bird studies have been examined.
The virus was originally called Swine Mystery Disease and where it
originated is still a mystery.
· Some scientists believe the virus has been present in the pig for
millennia and evolved into a pathogen as pig industries changed from isolated
rural farms into large production centers.
The virus has tremendous evolutionary potential but to date no other
mammal species or biological vector has been detected.
is caused by an enveloped, single stranded, positive sense RNA virus in the
genus Arterivirus. Other representatives are Simian Hemorrhagic
Fever Virus (SHFV), Equine Arteritis Virus (EAV), and
Lactate Dehydrogenase-elevating Virus (LDV). The original European isolate is known as
virus from where it was identified in the Netherlands. There are significant genetic and antigenic
differences between these early isolates and now there is great variation
within and between strains.
virus survives best in cold wet conditions partially explaining observed
seasonal outbreaks. It is easily
destroyed by drying, most disinfectants, and temperatures above 130˚
F. It is not viable in the
environment. It can survive for 2 weeks
in cool water and 8 days in lagoon slurry.
virus appears to disable or modulate significant macrophage signaling pathways
blocking effective cell and humoral immune
responses. This appears to also disable
important pathways that would normally control other viral and bacterial
pathogens as well.
transmission appears to be non-significant beyond nose to nose contact but
there are numerous reports suggesting airborne transmission is the only
connection between farms during area spread events. This is difficult to document but suggest an
aerial mechanical vector.
virus evades the immune system for extended periods leading to many
persistently infected pigs. These pigs
remain infectious for 150 days or longer but it appears that all eventually
clear the virus.
is shed in the semen and is the only known infectious agent present in the US
virus is highly infectious by less than 10 virions,
and in field conditions highly contagious in an airspace (building). It is often very slow to spread from barn to
barn or pen to pen without direct contact.
Previous recovery from a different strain of PRRS virus appears to slow
the spread of subsequent strains probably by reduced shedding.
flies, stable flies, and mosquitoes carry the virus for short periods and may
contribute to geographic area spread and within sites.
transport vehicles are effective fomites and are
major contributors to virus spread.
· Most infections occur when the virus reaches the tonsil or respiratory
tract where it comes into contact with macrophages. Most virus replication appears to occur in
lymphoid tissues where infected macrophages migrate (tonsil, spleen, thymus, Peyer’s patches, and lymph nodes). Pulmonary and intravascular macrophages are
infected but only a very small percent of total macrophages.
· The resultant immune response is significant with detectable antibodies
at fewer than 10 days to two weeks.
ELISA tests readily pick up infected animals two weeks post
infection. It appears that an effective
neutralizing response takes many weeks longer.
· PRRS virus easily crosses the placental barrier. Early experiments indicated this only
occurred after the 72 day of gestation but recent field experience indicates
this can occur much earlier in gestation with certain stains and
situations. The virus may kill all,
some, or none of the fetuses during outbreaks.
It has been speculated that fetal death may be caused by arteritis leading to hemorrhage in the umbilical
vessels. In outbreaks many pigs are born
alive but are viremic and suffer from interstitial
pneumonia. These pigs often don’t
survive the rigors of early neonatal life.
· Recovered pigs appear to be fully resistant to re-exposure to homologous
challenge but highly susceptible to heterologous
interstitial pneumonia caused by PRRS virus is generally mild. This is usually only observed in research
settings with high health piglets. Pigs
are off feed for less than a week and appear to recover fully after one to two
weeks. Even though there is apparent
recovery pigs remain viremic for weeks with
considerable variation in individual pigs.
the field morbidity always approaches 100% in individual rooms or barns. Nursery mortalities often approach 25% during
virus movement through a system. These health breaks are complicated by a
variety of viral and bacterial opportunists.
Haemophilus parasuis greatly complicates
PRRS and is the major cause of death in nursery situations.
Streptococcus suis and other α
Streptococcal bacteria are enhanced by PRRS virus leading to bacterial
septicemia, pneumonia and meningitis.
(Type A) is normally a secondary invader but with PRRS can cause significant.
signs are lethargy, fever, depression, and subsequent stunting due to secondary
diseases. Pre-weaned pigs born during
outbreaks and nursery pigs often have a characteristic soft cough and “thump”.
or system stability will only develop if the virus is prevented from
evolving. This is difficult to do in
large populations where antigenic change is essential for virus survival. Herds that naturally control the evolutionary
ability of the virus (small herds) typically eliminate it completely. Multi-site production where all growing pigs
move away from the breeding herds at weaning can easily eliminate the virus
through a rollover procedure described in the population health section.
heterologous challenges will often lead to chronic
respiratory disease in finishing pigs.
This is usually complicated with influenza virus.
results in mild to severe lymph node and lung involvement. Large tan colored lymph nodes can be found
associated with every organ system. The
interstitial pneumonia can vary from multifocal to lobular to diffuse. In the field this is often complicated by
bacterial infiltration – nonsuppurative cases are
rare but portions of the lung will have distinct microscopic lesions typical of
PRRS. Mild Myocarditis,
encephalitis, and rhinitis are often secondary lesions.
Other infections that are
commonly found in conjunction with PRRS are as follows: Mycoplasma hyopneumoniae, Haemophilus parasuis, Streptococcus
suis, Actinobacillus suis, Pasteurella multocida, Salmonella choleraesuis,
Influenza virus, porcine circovirus, and porcine
respiratory corona virus. Typically
three or more of these will be present leading to PRDC.
signs and history usually point to a certain diagnosis especially in
reproductive outbreaks. In large growing
pig populations this is usually not as clear.
In many stable systems the virus will be present but may not be the
leading candidate for intervention.
There are characteristic microscopic lesions but they are not pathognomonic and are often complicated by the presence of circovirus.
Today we rely on a number of
testing procedures to support clinical observation. There is no replacement for doing
representative postmortem examinations and laboratory analysis. My rule of thumb is post all the dead pigs
in a barn that are reasonably fresh and euthanize and post at least 5 more with
typical signs. This holds for all
respiratory diseases. Use veterinary
discretion but postmortem examinations should be viewed as a statistical process
and representative numbers of samples must be collected to obtain an accurate
Virus isolation (VI), Immunohistochemistry (IHC), fluorescent antibody test
(FAT), or detection of virus by polymerase chain reaction (PCR) may all be
needed to make an accurate diagnosis.
PCR has become the industry standard for diagnosis especially in naïve
populations. In recent years sequencing
of virus isolates has become popular but often leads to little information
about the virulence of the virus.
Serology (ELISA) is a great population tool but only indicates
exposure. Paired sampling over time may
increase the knowledge of when PRRS is active in a group of growing pigs but
clinical signs are just as accurate when postmortems are also done.
control strategies that attempt to live with the virus have been
unsuccessful. Vaccines provide little
cross protection against heterologous challenge and
have met with limited success.
spread of new virus strains typically keep high risk systems in a constant
state of outbreaks and viral pneumonia in growing pigs.
attempts to replace field virus with vaccine virus by massive sustained
vaccination of all adults and pigs in a system hold some promise but still do
not protect from lateral introductions.
most successful control strategies have been elimination and exclusion through
intensive functional biosecurity implementation. (Review the population health section)
Mycoplasma hyopneumoniae (Enzootic Pneumonia)
Mycoplasmal pneumonia of Swine (MPS) is endemic in
most commercial production systems around the world and the most common cause
of respiratory disease in growing slaughter pigs. Affected pigs typically display a
non-productive “hacking” cough that persists for weeks. Reduced growth rates and lowered feed
conversion are common especially in chronic pigs with secondary infections.
Mycoplasma pneumonia occurs year round but
clinically is at its worst during winter months when poor ventilation and
ammonia levels contribute to the pathology.
Mycoplasma pneumonia appears to make PRRS more
pathogenic. This may be due to the
increased numbers of macrophages attracted to the lung during Mycoplasma infection
pneumonia in swine has been recognized for more than a century. Clinical separation of Mycoplasma
from Influenza occurred in 1948 and the chronic respiratory component was
incorrectly believed to be caused by another undetermined virus. It became known as Virus Pig Pneumonia and
remained so until 1965 when the disease was first experimentally reproduced in
the US and England. The name hung on for many years and only
recently appears to have died away.
Mycoplasma hyopneumoniae is extremely fastidious
and difficult to isolate and grow. Two
other non-pathogens that are normal inhabitants of the respiratory tract, M. hyorhinis
and M. flocculare
are easier to grow and often complicate the isolation of M. hyopneumoniae. These non-pathogens also complicate the
creation of Mycoplasma autogenous
vaccines. This should be avoided since
commercial vaccines are cross protective and effective.
Mycoplasma does not survive once outside the pig even
in moderate environments. It is easily
and quickly killed by most disinfectants.
Transmission is through direct contact with carrier pigs. There have been reports of aerosol
transmission up to a half mile but these were made before molecular identity
was possible and are doubtful. In recent
years breeding stock companies have maintained large populations of M. hyopneumoniae
is plenty of evidence that M. hyopneumoniae is a primary pathogen and also
exacerbates other pathogens specifically PRRS and Influenza viruses. This bacterium is a significant component of
has long been thought that life carriers of M.
hyopneumoniae exist but recent evidence disproves
this notion. It appears that in
multi-site production systems where no growing pigs are housed near the adult
herds, only the gilt replacements have detectable Mycoplasma. Herd rollover elimination strategies have
been very effective and it may be possible to eradicate this agent from modern
Mycoplasma organism does exist in the lungs of
infected pigs for months after recovery but contagiousness to naïve pigs ends
at approximately 10 months post infection.
Transmission from the P-1 females to offspring is the major contributing
factor maintaining this endemic pathogen.
· The organism is
non-evasive and pathogenesis is believed to be the result of the immune
response and disruption of the mucociliary
apparatus. Outer membrane proteins
appear to be the primary virulence factors and this may vary between isolates
but as mentioned above is not a legitimate argument for autogenous
· Poor air quality has
long been known to increase the severity of the disease. Winter ventilation conditions typically
increase the severity of Mycoplasma respiratory
disease and PRDC.
· Gross lung lesions are
typically cranioventral consolidation but this is not
These lesions are usually found in the apical, intermediate and cardiac
lobes but may extend into the diaphragmatic lobe in severe cases.
· Microscopic lesions may
include lymphohistiocytic peribronchiolar
cuffing, mucocellular exudates, and atelectasis. These
findings are not specific and can be present with any bacterial pneumonia.
· Filling of the alveoli
with mucus or mucopurulent material is typical and
this material can be easily squeezed out of bronchi at cut surfaces.
· Secondary bacterial
infections typically follow primary Mycoplasma
pneumonia and are the major cause of Mycoplasma
dry hacking non-productive cough is the primary clinical sign. This cough may persist for weeks in
individuals and months in barns. Pigs
typically do not have elevated temperatures unless secondary or other primary
agents are involved.
incubation period for M. hyopneumoniae is approximately 6 weeks or longer in
modern production systems. Since only a
few carrier pigs are present, pigs usually don’t exhibit clinical signs until
8-10 weeks on the finisher. Influenza
activity often follows this same pattern complicating both diagnosis and
interventions. This natural delay allows
significant time for strategic vaccinations plans.
in diagnosis of Mycoplasmal pneumonia requires
submission of quality samples and laboratory assistance. Isolation of the bacterium is slow and
although confirmatory is insensitive. Immunohistochemical and fluorescent antibody techniques are
the standards for diagnosis today. Emzyme-linked immunosorbent assay
(ELISA) and complement fixation tests are available for herd basis tests but
false positives cloud interpretation in naïve groups. Routine vaccination may also produce many
polymerase chain reaction (PCR) tests are available but are very sensitive,
subject to lab cross contamination, and only indicate the presence of the
microorganism not disease.
checks have been used to diagnose and determine the prevalence of Mycoplasmal pneumonia in pigs but many lesions heal and
results are misleading. Lung examination
at slaughter time only depicts the past six weeks of the pigs life. Gross lesions are not pathognomonic
for Mycoplasma and only indicate bacterial
Mycoplasma vaccines have been on the market since
1980 and have traditionally been the primary control method in the global
appearance of PRRS virus and the evolutionary changes in swine influenza have
significantly changed the efficacy of vaccination programs.
there is an ample supply of replacement breeding stock available in the US, Canada,
Europe and other parts of the world. Stocking with negative females, repopulation,
rollovers, and medicated early weaning (MEW) have been highly successful
methods of elimination.
biosecurity and especially functional isolation
monitoring techniques are essential in maintaining negative statue.
systems tend to control Mycoplasma better than
traditional systems because of greater opportunity to vaccinate during early
incubation after maternal antibodies disappear.
have and continue to be important for control of secondary infections and Mycoplasma. Since
the microorganism is not invasive it is difficult to achieve high levels of
most antimicrobials where it is needed in the mucus with feed and water
tylosin, lincomycin, tiamulin, and enrofloxacin have
claims on efficacy.
Haemophilus parasuis (Glasser’s Disease)(HPS)
is a highly contagious and infectious disease primarily of nursery age pigs in
modern production systems. Both acute
and chronic infections are common. Pigs
exhibit combinations of meningoencephalitis, polyserositis, polyarthritis, and
severe pneumonia. The introduction of
PRRS virus has significantly raised the importance of this agent.
Glasser first reported this disease associated
with a small Gram-negative rod in 1910.
In 1931 it was isolated in association with swine influenza and named Haemophilus influenzae suis. Its name was changed again in 1943 and 1960
becoming Haemophilus parasuis in
1976 which still remains until today.
H. parasuis is a small
Gram-negative rod which is difficult to isolate in many field cases. It will grow on blood agar next to a
Staphylococcus streak or on agar fortified with nicotinamide
adenine dinucleotide (NAD). It is a normal inhabitant of the nasal cavity
and tonsils of normal pigs. Isolates
from systemic sites are considered pathogens while other isolates appear to be
bacterium often grows on serosal surfaces of the
peritoneum, pleura, pericardium, joints and meninges. It is frequently called carpet heart by
production personnel because of the fibrin accumulation and tags.
are at least 21 serotypes but more recently labs have started to genotype the
bacteria. Genotyping is useful but not
often predictive of virulence.
serotypes may be present in the same pig or herd. There are often multiple pathogenic strains
and several non-pathogenic strains present in the same system or farm.
parasuis is found everywhere there are pigs. Most genotypes appear to be non-pathogenic
but dynamics of modern swine production appear to produce both early neonatal
inoculation which is protective and pigs that are not colonized and
susceptible. When these pigs are mixed
outbreaks occur. This can be in the
nursery of different sources of replacement stock mixed during
acclimatization. A complex combination
of colonization and immunity, timing of exposure and PRRS virus activity appear
to play significant rolls in outbreaks.
that trigger onset of disease are poorly understood. The lesions associated with pathogenesis are
associated with vasculitis and leakage of serum and
accumulations of fibrinous exudates over serosal surfaces.
mentioned PRRS virus and also Influenza may lead to increased incidence and
severity of disease.
pigs often become chronic and fail to respond to antimicrobial therapy when
these other viral agents are present.
growing pigs can lead to severe outbreaks without these viruses.
modern production systems bronchopneumonia and pleuritis
are common findings with this bacterium.
of the skin is often in present in pigs that die especially on the “down”
side. More chronic cases will have large
amounts of serofibrinous or fibrinopurulent
exudates in the peritoneal or pleural cavities.
lesions often appear to be embolic in peracute cases
suggesting a hematogenous route.
mixed source pigs onset is generally acute.
“Dog sitting” with posterior paresis is characteristic. Pigs that can rise and are forced to move
often show severe signs of pain.
Occasionally unilateral swelling and pitting edema of the ear are apparent. In acute onset cases typical polyserositis will be absent in most pigs that die during
the first few day of the outbreak.
disease is commonly observed in nurseries on the second week of placement. This is especially apparent if PRRS virus is
circulating in the same age group. This
may be delayed if PRRS seroconversion is later.
is usually easy to find the classic polyserositis
lesions in this age pig especially in hospital pens. Choose non-treated pigs for postmortem
signs will also be present in some pigs in all affected groups when PRRS virus
nursery or wean-to-finish barn situations morbidity may approach 50-75% and
mortality can be as high as 25%. In
these cases pigs do not appear to respond to antimicrobial therapy.
and typical lesions are often all that is needed in nursery situations. Production personnel may call just to inform
that they are treating again.
from systemic sites such as the meninges,
cerebrospinal fluid, joints, peribronchial lymph
nodes, serosal surfaces, and lung lesions are
important because of the presence of non-pathogenic strains in most production
Haemophilus parasuis is typically sensitive
to β-lactam antimicrobials. Preventative administration of oral
(feed/water) antimicrobials is usually of little value. In situations where PRRS virus is circulating
along with H. parasuis,
treatments appear to do little other than reduce mortality.
diagnosis and intervention is critical in all cases. Therapy should always be started prior to
laboratory confirmation. Outbreaks in
breeding age females require whole population injections for several days
unless effective residual antimicrobials are available.
are somewhat effective if outbreaks occur in pigs after they reach 10 weeks
vaccines are very good in these cases.
However, nursery breaks are not prevented by vaccine. This is most likely do to challenge timing
and blocking by maternal immunity.
pigs with on farm virulent isolates while still suckling has been a successful
approach. This makes sure all piglets
are colonized by farm strains prior to loosing maternal antibodies. Management of the live inoculum
is a challenge for most production systems.
Quality control is essential in the lab as well as on farm.
influenza is an acute infectious respiratory disease of pigs.
virus typically moves rapidly through modern pig sites. Pigs are generally off feed for 48
hours. A barking cough is typical with
classic H1N1 virus types but not as apparent with some of
the newer re-assortment strains.
often demonstrate sudden temperature spikes, occulonasal
discharges, prostration, and weakness. A
typical barn will have paroxysmal coughing, thumping, and few if any pigs at
the feeders. This may make a remarkable
change in 48 hours but coughing often remains for a week or more. Mycoplasmal
pneumonia will complicate the severity and rate of recovery.
virus is widespread in the US
and rest of the world. Numerous distinct
genetic types exist along with antigenic drift variants.
classic swine flu is a Type-A H1N1 Influenza virus that
apparently entered pig populations around the world and especially the United States
associated with the human Spanish Flu pandemic of 1918. The actual death toll from this outbreak is
unknown but estimated to be between 20 – 30 million people. It is interesting that the virus quickly
became species adapted and remained remarkably stable for nearly 75 years in
pig populations. Recent isolates in the United States
and elsewhere around the world demonstrate that antigenic drift and shift is in
a new dynamic state. Many re-assortment
strains (shift) are present in the industry along with some more classic viruses.
the Center for Disease Control (CDC), World Health Organization (WHO) and many
other organizations around the world have intense
interest in influenza viruses. The
recent outbreaks in Asia with high pathogenic
avian strains that jumped species to humans has raised
the concern that another world pandemic may soon occur. This is a very interesting virus and one of
the classic zoonosis.
Waterfowl and perhaps other reservoir avian species maintain all genetic
types of influenza viruses without clinical repercussions.
the past 8 years three subtypes of H3N2 viruses, several
subtypes of H1N2 viruses, and numerous H1N1
viruses both drift and shift varieties have widely circulated in the United States
antigenic surface of the influenza virus is primarily composed of glycoprotein
spikes. There are 13 hemagglutinins
(H) and 9 neuraminidases (N). The hemagglutinins are believed to be the more important
antigenic site conferring immune protection.
shift is thought to be a result of concurrent infections with different
influenza’s in the same animal but there is also evidence that the virus
occasionally recombines with its own RNA genetic segments. For example matrix coding RNA incorporated
into hemagglutinin RNA. This is only reported in South American avian
virus survives outside the host for a short time but less than two weeks under
normal production conditions. It is easily destroyed by a wide range of
disinfectants, drying and heat.
virus is traditionally grown in 9-12 day chick embryos and this is still the
source of virus for vaccine production.
It will also grow on a variety of cell culture lines but consistent
titer issues have prevented adoption by the animal health industry.
is a growing body of evidence that indicates swine influenza viruses are moved
by human caretakers and that many of the viruses present in the US swine
population today have genetic components that arrived from widely circulating
human strains. Although the pig has long
been considered a potential mixing vessel for avian and swine strains, there is
little evidence that swine are the source of re-assortment strains that jump to
humans. Humans and pigs share a common
receptor site creating potential for exchange of circulating viruses.
is important to keep swine populations separate from birds especially waterfowl
and the pig water supply must also be protected and purified if
surface/reservoir water in used. “Mixing
vessel” opportunity is especially concerning in Asia
where there are many small farms with pigs, ducks, chickens, and humans living
in close proximity with no existing biosecurity
barriers to separate them.
protection between different strains of virus is generally negligible. Most of the commercial vaccines have
struggled in the field because they are often obsolete by the time they clear
the regulatory process. Likewise
traditional HI tests fail to detect most circulating strains. Many labs now run a battery of HI tests based
on circulating isolates but this will fail to identify future viruses. Isolation of virus and sequencing is the best
method to evaluate and diagnose recurrent influenza like clinical signs.
made and current autogenous vaccines may be necessary
to control influenza in large production systems.
immunological phenomena known as “original antigenic sin” may be important in
pigs just as it is in humans. When
exposed to a virus after prior exposure or vaccination, the rapid immune
response needed to protect is memory B-cell based. Thus the starting immune response and
neutralizing antibodies produced are specific for the previous exposure and not
the invading strain. In this scenario
vaccine may do harm verses prevent illness.
influenza virus has a tropism for bronchial epithelia cells. It enters the pig through nasopharyngeal
is very unusual and transient when it does occur. The incubation period is
often less than 24 hours which explains the rapid onset, high morbidity, and
are typical of most viral pneumonias. Cranioventral involvement is normal but in severe cases
more that 50% of the lung may be involved.
Interlobular edema is usually present and bronchi contain blood stained fibrinous exudate. Affected lung tissue is typically purple and
a clear demarcation zone adjacent to healthy tissue is apparent. Some of the
newer circulating strains are more pathogenic than older isolates and are
associated with large areas of lung consolidation.
sequelae to influenza outbreaks are secondary
bacterial pneumonia and often gastric ulcer outbreaks with acute and chronic
lesions usually include obstruction of airways with fibrinopurlent
or fibrinous exudates with necrosis and degeneration
of airway epithelium.
varies with the different circulating influenza variants and depending on prior
exposure or maternal antibodies levels.
Cross protection between variants will usually be minimal.
can be a challenge when new variants go through a system. HI and newer ELISA tests may not pick up new
variants. Paired serology is always
recommended but it may mistakenly indicate negative results. Directigen Flu-A is
a rapid test that can be run on tissues which picks up the A-antigen on all
type A influenza’s.
is important to recognize that serological tests are unreliable in many systems
and herds today. PCR is another reliable
method but costly. Sequencing is typically
done on the H gene only but some labs are looking at the whole viral
genome. These tests are useful when
relying on autogenous vaccines for control allowing
logical virus switching when new isolates are discovered.
swabs collected from febrile pigs are a good diagnostic tool. Swabs with viral transport media shipped on
ice achieve good results. A drop of
glycerol added to the saline media may improve viral survival in transit.
mentioned, control is becoming more challenging in today’s evolving
environment. A combination of extensive
monitoring and autogenous vaccine has been used
successfully in large systems. Issues
still remain because of the lag time between discovery of a new variant and
getting the vaccine into the field. This
often takes 90 days for the new vaccine to clear USDA hurdles.
has become a year round issue in large systems and clinical signs are often
less pronounced muting the value of history and typical “flu” clinical
observations as reliable observations for making a diagnosis.
Biosecurity is not effective in preventing
influenza. Even so replacements should
be screened and never introduced when exhibiting clinical signs.
herd vaccination is widely used to protect piglets through the nursery
phase. If nursery breaks occur in
vaccinated systems new variants will be present and increasing the number of
vaccinations per year is malpractice.
of growing pigs presents some timing issues.
Pigs typically retain maternal antibodies until 10 weeks of age or
longer. If sow vaccinations protect the
nursery then it will be difficult to protect finishing pigs which suffer
greatest mortality and have added fixed and variable cost attached to them.
programs take time to make substantial differences in large production
systems. They require extensive
monitoring, sequencing of isolates, strategic vaccines (autogenous),
and good timing of administration.
(APP) & A. suis
are two closely related bacteria that can be highly contagious, cause severe
necrotizing pneumonia, high morbidity and high mortality. In naïve populations the onset and spread
will be rapid with many acute deaths in the first 48 hours of the outbreak. A. suis is typically much milder
and less contagious but in mixed source pigs can be clinically very similar
although more responsive to treatment.
bacteria only appear in pigs. Both have
world wide distributions. APP has long
been an issue in Europe and Canada. In the US it has become less common in
modern multi-site systems. This may be
largely due to a few negative breeding stock companies dominating the industry
expansion during the 1980’s. App is still present in some North Carolina production
was first diagnosed in the United
States in 1957. It became widespread by the late 1970’s
though spread by small purebred breeders and small breeding stock
companies. Early serologic tests were
notoriously unreliable but were the basis of many lawsuits. Some cross reacted with A. suis which in
most cases could be managed with occasional antimicrobial therapy in affected
groups. Because of the severe economic
impact of APP many herds were depopulated to eliminate this agent. The pig is the only known reservoir.
Actinobacillus pleuropneumoniae is a hemolytic
Gram-negative, capsulated, coccobacillary rod. There are 12 recognized serotypes in Biotype
I and three in Biotype-II. It is not
uncommon for isolates to also be designed as non-typical or cross reactive to
secretes 4 cytotoxins (exotoxins)
designated as ApxI, (serotypes 1, 5, 9, 10, & 11)
ApxII, (all serotypes except 10), ApxIII,
(2, 4, 6, & 8) and ApxIV. These toxins are the RTX group. Each serotype may secrete some or all of the
toxins. Serotypes 1, 3, 5, and 7 are
reported as the most common in the US but that has changed over the
last several years and is system and geographic dependent.
Actinobacillus suis is closely related to
APP and may contain one or more of the RTX toxins. Hemolysin producing
strains are typically most pathogenic.
The bacterium requires NAD for growth similar to HPS. Outbreaks
typically occur in finishing pigs but occasionally in individual adults, and
that survive APP typically become carriers for a considerable period or perhaps
life. Recent eradication attempts in Europe have been successful in small herds with and
without antimicrobial intervention. Rollover
attempts in the United
States in large herds have not been
is a direct contact disease although clothing, boots, buildings and transport
trailers will remain contaminated and infectious for a period of a few days
under most production conditions. Like
all pathogenic agents cold, wet, and cloudy conditions favor microbial
has a world wide distribution but some serotypes are geographic specific. The bacterium is generally believed to be
species specific and other reservoirs have not been discovered. Short downtimes between infected vs.
non-infected pigs have always been successful in eradication clean-ups
supporting this assumption.
the years most APP outbreaks have been the result of purchased genetic additions. Tests have not been reliable and chronically
infected herds often have few if any clinical indications of disease. Modern breeding stock companies generally
have successfully eliminated APP although most are A.suis positive and a few still
have low virulence strains of APP.
is significant variation in virulence between serotypes but this is also
geographic/country dependent. This may
be because stereotyping is not directly linked to the number and types of RTX
RTX toxin group is generally highly toxic to endothelial cells and alveolar
is followed by thrombosis, infarction, and toxic shock. This can occur in a matter of a few hours
with high virulence strains. Pigs can appear
normal, active, and feeding and within a few hours cyanotic, high fevers,
gasping for air, and struggling for survival.
In these cases treating some pigs is their final stressor.
APP is apparent in naïve pigs but colostral immunity
with gradual exposure appears to be protective.
are generally found in respiratory tract but hemorrhages will be present in
other organs typical of fulminating septicemias especially with A suis. Lungs will be full of blood tinged froth,
feel solid similar to liver, with areas of hemorrhage, necrosis, fibrinous pleuritis. The diaphragmatic lobes will have dorsal
areas of destruction which is not pathognomonic but
classic for this disease. Fibrinous pericarditis and
pleural adhesions are also common.
clinical appearance of this disease can be deceiving between acute outbreaks
and endemic herds with the same agent.
outbreaks acute deaths are common often before the caretakers notice other
clinical signs. These are always some of
the best, fastest growing pigs.
Cyanosis, mouth breathing, severe dyspnea,
bloody foam from the mouth and nostrils, and a shallow dry cough. Generally coughing is not a notable clinical
and mortality are very high when naïve pigs are exposed to highly virulent
strains but may be negligible in chronically infected continuous flow
herds. In these cases pleuritis is apparent on slaughter inspections or
postmortem examination of finishing pigs. Growth rates will be depressed
compared to non-infected herds.
abscesses are common postmortem finding in chronic herds but APP is only rarely
present in these lesions.
a rapidly spreading high mortality respiratory disease is encountered APP
should be suspected. Lung lesions as described above are classic for APP but A.suis must be part of the differential diagnosis.
identification is the gold standard for diagnosis.
can be misleading and has a history of leading veterinarians to mistaken
conclusions. Serological tests developed
by Marcello Gottschalk are the only reliable ones available today. All serology should be evaluated on a
population basis only – never on a single or small group of pigs.
pathogens that must be ruled out are Salmonella
choleraesuis, pneumonic Pasteurella multocida, and PRDC.
of virulent strains of APP has proven challenging. Modern pig flows (multi-site) exacerbate
outbreaks in growing pig populations.
For this reason, APP has been eliminated from the breeding herds in most
is one disease that depopulation is easily justified because of the tremendous
cost of remaining positive.
vaccines in the US
have not proven to be efficacious. They
may reduce mortality but do little to recover the real disease costs which in
endemic herds is rate gain, feed:gain,
morbidity, and slaughter condemnations.
improved vaccines are available in Europe
where the disease is far more prevalent today.
early weaning is a cost effective method of elimination while preserving
may be possible in small breeding herds.
to antimicrobials is typically not an issue but rather timing of
administration. In acute cases the
treatment is nearly too late.
Penicillin’s, ceftiofur, tilmicosin,
tiamulin, and enrofloxacin
are all effective in sub-acute and chronic cases.
Honorable Mention Swine Respiratory Disease
- Pasteurella multocida
bacterial pneumonia of swine that is considered secondary or opportunist to
other viral and bacterial agents, verminous
pneumonia, or poor ventilation and noxious gases/dust.
has worldwide incidence and presence.
occasionally occurs as meningitis in suckling pigs.
bacteria is found in many species of domestic mammals
bacterium was originally studied by Louis Pasteur and later named for him.
Gram-negative coccobacillus which grows well on
enriched media. It is a facultative anaerobe.
bacterium is a normal inhabitant in the nasal passages and respiratory tract of
are 5 capsular serotypes (A, B, D, E, F) and 16 somatic serotypes. Type A and D are found in swine and typically
type A’s are pneumonic.
is ubiquitous in swine and swine strains are fully species adapted.
only occurs when normal resistance has been lowered by other primary pathogens
or extremely bad environmental and stressful conditions.
PM enters deeper portions of the lung abscesses form in areas of
chronic pneumonia pigs (“thumpers”) PM is often isolated but it is doubtful
that it acted as the lone infectious agent
is dependent on good husbandry, avoiding mix sourcing, control of other
infectious pneumonic agents, and preventative antimicrobial therapies.
feed and water antimicrobial medications have PM claims but it is doubtful that
they are useful in the field as strictly PM interventions.
PM causes damage in the lung it is not economically reasonable to treat. Long term parenteral
antimicrobial treatments may be effective but impractical.
all cases of tuberculosis in US swine are caused by Mycobacterium avian. There
are numerous serovars including M. intracellulare which are all
considered part of the same complex.
TB is still a significantly costly problem in the US industry.
condemnations account for most of the cost but losses in route and prior to
slaughter also occur. Caseous lymphadenitis is the main postmortem finding.
birds, weathered sawdust, and water are the main sources of exposure. In large systems that use surface water,
condemnations will be greater than pigs from other sources. Humans are most often exposed to this agent
by frequenting outdoor hot tubs.
disease is self-limiting in pigs and believed to be non-contagious.
pigs in the US
are exposed to birds or chickens today.
In slaughter pigs that can be tracked back to their source farms
(Integrators) drinking water is the most likely source of infection.
Bordetella bronchiseptica (BB)
bacteria is a normal inhabitant and colonizer of the
upper respiratory track of pigs. It is
associated with sneezing in nursery age piglets especially where air quality is
questionable and when concurrent infections with Inclusion Body Rhinitis virus
can occasionally be recovered in pure culture from bronchopneumonia cases of
young pigs. Clinical signs are a
“whooping” cough and dyspnea.
may be important for normal colonization with H. parasuis preventing systemic
is a motile Gram-negative aerobic rod or coccobacillus.
is ubiquitous in pig populations. It was
once believed to be the causative agent associated with progressive atrophic
rhinitis but this is not valid. Rhinitis
caused by BB is regenerative.
this bacteria is usually associated with the GI tract
it can cause severe necrotizing pneumonia.
choleraesuis is a highly
host-adapted salmonella. There have been
a few rare cases of human infections, which almost always end in mortality.
There are no associated risk factors between pig exposure and human disease.
var. kuzendorf is most frequently isolated in pneumonic
cases. The bacterium appears to be
filtered out in the diaphragmatic lobes and can be confused with APP or A. suis
on gross examination.
highly efficacious modified live vaccines are available in the US and
provide excellent control in pigs from positive breeding farms.
that become infected will have high temperatures, lethargy, remain off feed and
thus quickly have an empty appearance (“slab sided”). Cyanosis and dyspnea
may occur before death. Dead pigs will
usually be purple on the down side.
mortality rates are high but morbidity levels in affected groups will usually
be less than 10%.
Pseudorabies virus (Aujeszky’s disease)
virus is covered in another section but when present in the United States was a major
contributor to winter PRDC in growing pigs.
first published report of the disease was in 1813 in cattle. The virus was
discovered in 1910. It became a major
problem in US
swine production during the 1970’s.
Eradication at a national level began in 1989 and this was completed in
virus is in the herpes group and different isolates often had wide variation in
Carriers and latent infections/contagiousness are a common component of
virus is easily spread by direct contact, nasal secretions, transport
vehicles/trailers, clothing, airborne and other routes.
virus is associated with bronchitis, bronchiolitis, alveolitis, inclusion bodies, and hemorrhagic foci of
necrosis. Uncomplicated cases are mild.
Porcine Respiratory Corona Virus (PRCV)
is a highly contagious and infectious respiratory virus of pigs.
first appeared in Europe in the mid 1980’s.
virus is a TGE mutant with a large deletion of 621 to 681 nucleotides from the
S glycoprotein gene which is thought to have changed the tissue tropism from
gut to respiratory epithelial cells.
from PRCV infected pigs cross reacts with the TGE serum neutralization test
which may be the most important concern.
the virus spread across Europe cases of TGE
disappeared. That has not been the case
in the US
where it has complicated TGE diagnosis and increased the number of TGE endemic
a respiratory agent it is not of any clinical significance. Early investigators incriminated the virus as
part of the PRDC syndrome but that does not appear to be a reality in field
Ascaris suum (porcine round worm)
is the large round worm of swine and their most common gastrointestinal
life cycle of this worm is direct. Eggs
survive in the environment for many years contaminating buildings and
surrounding grounds. These eggs are
resistant to all disinfectants, environmental, and weather conditions.
the eggs hatch in the gut the larvae go through a hepatotracheal
migration. Liver and lung damage
followed by death can occur with massive exposure. This was common in the days when new genetic
stock usually boars were housed in dirt isolation lots. After repeated use a build up of infective embryonated eggs would lead to massive exposure.
with heavy infestation have a productive asthmatic cough, dyspnea,
all-in, all-out production has greatly reduced the significance of this
parasite. Although the eggs are
extremely resistant they can be washed out of buildings over time all but
eliminating exposure. Adults mount an
effective immune response and clear infestations over time. The egg only becomes infective after a 30 to
60 day period which is greater than the suckling period. These factors have created a natural
unexpected control mechanism through modern production practices.
is extremely rare to find round worms or pathology in nursery pigs but they do
survive in continuous flow finisher sites and farms.
number of effective anthelmintics are available for
feed, water, or individual per os treatment. Cost effective use is doubtful in true
all-in, all-out and multi-site production systems. Individual treatment is practiced in many
breeding herds but is not cost effective or warranted.