HERD HEALTH                                       PIH-50


                          Atrophic Rhinitis

Barbara Straw, University of Nebraska
G. Michael Daniel, Sioux Center, Iowa

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

     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

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

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

     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-

     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)

Cooperative Extension Work in  Agriculture  and  Home  Economics,
State  of Indiana, Purdue University and U.S. Department of Agri-
culture Cooperating. H.A. Wadsworth,  Director,  West  Lafayette,
IN. Issued in furtherance of the Acts of May 8 and June 30, 1914.
It is the policy of the Cooperative Extension Service  of  Purdue
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