HERD HEALTH PIH-50
PURDUE UNIVERSITY. COOPERATIVE EXTENSION SERVICE.
WEST LAFAYETTE, INDIANA
Atrophic Rhinitis
Authors
Barbara Straw, University of Nebraska
G. Michael Daniel, Sioux Center, Iowa
Reviewers
Peter and Brenda Blauwiekel, Fowler, Michigan
David J. Ellis, Michigan State University
Steven C. Henry, Abilene, Kansas
Ralph A. Vinson, Oneida, Illinois
Atrophic rhinitis (AR) is a widely prevalent, multifactorial
disease of swine characterized by a degeneration and/or failure
of growth of the nasal turbinate bones. Clinical signs include
sneezing, nasal discharge or bleeding, and distortions of the
snout.
The milder, nonprogressive form of AR is caused by a toxin-
producing bacterium, Bordetella bronchiseptica. The more severe
and progressive form is caused by the toxin-producing Pasteurella
multocida bacterium, alone or in combination with other bacteria
such as Bordetella bronchiseptica. The severity of the disease
may be related to the age of the pig when infected, the dose of
infectious organisms, the amount of toxin produced by the bac-
teria and environmental conditions. Although B. bronchiseptica
and P. multocida have been demonstrated to cause AR, clinical
disease cannot be attributed solely to infection with either one
or both bacteria. Various environmental, management and husbandry
factors contribute to the development of clinical disease. In
some herds these bacteria are present, but outward signs of
disease are not. In herds harboring B. bronchiseptica and P. mul-
tocida, there are periods from 2 months to 2 years or longer when
no clinical evidence of disease exists.
Development of AR Caused by Bordetella
bronchiseptica Infection
Bordetella bronchiseptica readily colonizes the lining of
the respiratory tract. It commonly locates in the nasal passages
and the tonsils. The most severe disease occurs in piglets that
are infected during the first week of life. Disease is less
severe in pigs that are a few weeks older; and by 9 weeks of age,
pigs show almost no clinical signs after infection. In some
cases, damage from the initial infection persists until
slaughter, but in many cases of pure B. bronchiseptica infection,
damage to the nose begins to heal within 4 weeks after the onset
of infection.
Development of AR Caused by Pasteurella
multocida Infection
Toxin-producing strains of Pasteurella multocida have a poor
capability for establishing themselves in a healthy nasal cavity.
Experimentally, however, P. multocida readily colonize a nasal
cavity that has been pretreated with chemical irritants or
infected with B. bronchiseptica. Pasteurella multocida also
infects tonsils and lungs. Similar to B. bronchiseptica infec-
tion, pigs infected with P. multocida at an earlier age may show
more severe clinical signs. However, in contrast to B. bron-
chiseptica, P. multocida is capable of damaging the nasal cavity
in pigs up to 16 weeks of age, and reversal of damage is less
likely. In fact, the toxin produced by P. multocida has been
shown to affect not only the structure of the nasal passages, but
also to damage the liver, kidneys, ends of the long bones and
certain components of the blood.
Sources of Infectious Agents
Infection in a herd most likely occurs after the introduc-
tion of infected breeding stock or feeder pigs, although other
animals such as rodents, dogs and cats also may be carriers. Bac-
teria can be harbored in the nasal passages or tonsils of
apparently healthy pigs.
Bacteria are spread from one pig to another through droplets
in expired air. Litters in the farrowing house may be infected
by the sow, but generally the major spread occurs pig-to-pig
after 2 to 3 weeks of age or after weaning.
Bordetella bronchiseptica has been found in most domestic
and wild animals; however, the strains of B. bronchiseptica iso-
lated from non-swine species have only limited ability to produce
disease in pigs. Toxin-producing strains of P. multocida have
been found in cattle, rabbits, dogs, cats, poultry, sheep, goats
and humans; however, the possible role of these other species in
the spread of disease has not been determined.
Other Factors that Contribute
to Clinical Expression of AR
Severity of infection is closely associated with intensive
methods of swine production. The following factors all have been
identified as contributing to the level of AR in infected herds:
large herd size, additions of pigs from various sources, high
proportion of gilt replacements in the breeding herd, large far-
rowing units, large nurseries, frequent moving and mixing, high
stocking density, poor ventilation and temperature control, poor
hygiene, continuous flow of pigs, and excessive levels of gases
and dust. On occasion it has been possible to control AR solely
through improvement of housing and management practices.
At one time it was thought that calcium:phosphorus imbalance
led to AR, but this has been discounted. However, an existing
imbalance would retard healing of lesions that might otherwise
resolve.
Clinical Signs of AR
Clinical signs usually appear at about 4 to 12 weeks of age.
Initially there is noticeable sneezing and snuffling and pigs may
have a watery or thick mucous discharge from the nose. Tear
staining appears as dirty brown streaks below the eyes. Some pigs
have nose bleeding, which can be severe enough to be seen on the
walls of the pen or on the backs of other pigs. As the condition
progresses, damage to the interior bony structure of the nose may
appear as a shortening or bending of the snout. Some pigs may
have damage to their nasal turbinates without having obvious
external signs. Pigs that are severely affected experience a
reduction in growth rate and feed efficiency, which is compounded
by the performance-depressing effects of poor environment and
ventilation.
Diagnosis of Infection
When AR is moderate to severe, a diagnosis can be made clin-
ically, based on the typical signs of disease. However, in milder
cases additional testing may be necessary. Samples for bacterial
culture are taken from the nasal passages and tonsils of affected
pigs to check for toxin-producing strains of B. bronchiseptica
and P. multocida. Specific laboratory tests are conducted to
identify the two types of P. multocida (A and D) that are most
commonly involved in AR. Subsequent testing is done to demon-
strate the production of toxin. Frequently, examination of nasal
structures is made at slaughter when a number of pigs can be
examined to estimate the prevalence and severity of turbinate
atrophy in the herd. See PIH-93, Slaughter Checks--An Aid To
Better Herd Health.
Control of AR
Effective control of AR requires a combination of strategies
involving management, environment, medication and vaccination.
The main goals of control are to reduce the load of bacteria to
which pigs are exposed, to treat pigs that are affected and to
improve the environment which maximizes pig resistance and minim-
izes bacterial spread.
Vaccination. Vaccination of sows with a combination B.
bronchiseptica/P. multocida vaccine helps reduce the prevalence
of AR in their offspring, but does not eliminate the condition.
For greater efficacy, it is important that the vaccine contain
the specific P. multocida toxin so that the sow will produce
antibodies to protect against the effects of the toxin. In some
cases, piglets also should be vaccinated. However, immunity
requires 2 weeks to develop, and often piglets are infected
before they can develop a protective level of antibody. Proper
timing of immunization is necessary to optimize the immune
response.
Medication. Medication may be used as a temporary measure to
help bring severe cases to a controllable level, but it is not a
long-term solution. To reduce shedding of bacteria, sows may be
given feed containing sulfonamides or oxytetracycline during the
last month of gestation. Nursing piglets are strategically medi-
cated by injections of antibacterials up to 4 times during the
first 3 to 4 weeks of life. Typically, oxytetracycline,
penicillin/streptomycin, or potentiated sulfonamides (extra-label
use requires veterinary/client relationship) are used. The choice
of drug should be based on the results of drug sensitivity test-
ing on bacteria recovered from infected pigs. Weaned pigs are
sometimes medicated in the drinking water or feed.
Management. Vaccination and medication efforts may fail
unless combined with appropriate improvements in housing and
management. It is important to employ all-in, all-out movement of
pigs, minimize the number of gilts in the herd compared to older
sows, reduce the stocking density, maintain strict hygiene,
correct ventilation rates, and eliminate chilling drafts. Modifi-
cations of medicated early weaning (MEW) and multiple site pro-
duction help to reduce the prevalence and severity of disease.
New animals brought into the herd should originate from herds of
known status. Breeding companies and producers should know the AR
status of their herds and work together to determine if health
levels are comparable.
Elimination of AR
Once a herd is infected, it is impossible to eliminate the
causative bacteria. However, good management practices can
reduce the prevalence and severity of disease. Freedom from the
severe detrimental effects of AR can be achieved through strict
adherence to proper vaccination and/or management programs
including all-in, all-out pig flow. Pigs free of AR may be pro-
duced by SPF (Specific Pathogen Free) techniques or possibly
through medicated early weaning. Breeding companies that adver-
tise freedom from AR should be routinely monitoring to verify the
absence of AR through periodic nasal cultures and slaughter exam-
inations.
Reference to products in this publication is not intended to
be an endorsement to the exclusion of others which may be simi-
lar. Persons using such products assume reesponsibility for their
use in accordance with current directions of the manufacturer.
REV 12/92 (7M)
______________________________________________
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