[Pork Producer's Viewpoint-](../02N-0027_ts00011_02_vol2.ppt)

[Economic Impact of Mycoplasmal
Pneumonia](../02N-0027_ts00011_02_vol2.ppt)

[On Pork Production and](../02N-0027_ts00011_02_vol2.ppt)

[What is Needed to Treat and Prevent the
Disease](../02N-0027_ts00011_02_vol2.ppt)

[**John A. Korslund DVM**](../02N-0027_ts00011_02_vol2.ppt)

**Korn-Land Hog Farm**

**3335 230^th^ St.**

**Eagle Grove IA 50533-8714**

**515-825-3630**

[**korslund@goldfieldaccess.net**](mailto:korslund@goldfieldaccess.net)

**[Introduction:]{.underline}**

I have been involved in hog production for 40 years, first in 4-H
projects, in college as a veterinary student, 2 years in practice, and
since 1979 in production on a family-sized commercial production farm.
During that entire period Mycoplasmal pneumonia has been recognized as a
pathogen in the lungs of pigs with economic impact on finishing pigs.
This paper will lay out some of changes that have occurred in the pork
industry over those 40 years. These changes have in turn modified the
expression, course, treatment, and economics of Mycoplasmal pneumonia
prevention and control. This will not be a reference-based scientific
discourse, but rather an overview of the environment-disease-pig
interaction regarding *[M. hyopneumoniae]{.underline}* over time in
commercial production in the United States.

**[1960-1980- Continuous Flow/Continuous Antibiotics:]{.underline}**

During the 1960-1980 time period the concepts of all-in all-out
production had not yet taken hold in commercial pork production.
Although the Nebraska SPF program had some success in producing
[M.]{.underline} [hyo.]{.underline}-free herds, the concept was never
widely adopted in the industry, and setbacks were common due to
re-infections and lack of knowledge of how to maintain [M.
Hyo]{.underline}.-free herds (knowledge we may *still* lack in hog-dense
areas). Because most pigs were raised with contact between age groups
and with older weaning ages (4-6 weeks) essentially all pigs were
exposed to the organism at a relatively young age in tandem with waning
colostral immunity at the time of exposure. Disease expression was
highly variable, depending on infectious dose, and co-infections were
common with atrophic rhinitis, verminous pneumonia, swine influenza, hog
cholera, and pseudorabies being several common examples. Outbreaks could
be quite severe, but what was often seen was a chronic dry cough, rough
hair coat, and poor doing pigs. Disease occurred at variable weights,
depending upon when all the immune and disease conditions came together
to allow disease expression.

Because the timing of disease expression was uncertain, so was the
timing of treatment. Vaccine was not available during this time; however
use of antibiotics, especially feed-grade, was a wide-open option.
Tetracycline was the drug of choice for Mycoplasma control and
sulfonamides the drug of choice for atrophic rhinitis control.
Combination drugs containing these 2 antimicrobials (plus penicillin)
were commonly used, sometimes at doubled doses. While economics was a
factor, producers were less concerned about the costs of continuous
supplementation with antibiotics than with the potential health problems
and difficulties in managing finishing pigs without suppression of
Mycoplasmal and other pneumonias in finishing.

In general the tetracyclines worked pretty well as a suppressant, and
good producers sensed when to increase doses during particularly
susceptible times in the pigs' lives (e.g. weather extremes, animal
movements, crowding, secondary disease, etc.). With continuous
medication there was no guesswork needed regarding immune status or
disease susceptibility. The pigs had it or were going to get it
(actually both), and the treatment would be there when the bug arrived.

If Mycoplasmal pneumonia developed clinically, treatment choices were
usually tetracyclines in the water, lincomycin or tetracycline
injections, and increased levels of in-feed tetracyclines. If influenza
was also involved, sulfonamides with expectorants in the water were the
treatment of choice. Amazingly, the hogs miraculously recovered in about
5 days as immunity to the virus built, and "Doc" was a hero.

**[1980-2002- Age Segregation, Economies of Scale, and
Industrialization]{.underline}**

The *[Mycoplasma hyopneumoniae]{.underline}* organism perhaps hasn't
changed in the last 20 years, but everything else affecting the pig
seems to have been transformed. Even the pig itself is quite different
in composition and lean growth potential than its 20-year-earlier
counterpart. All these changes have drastically changed the
host/microbial/immunity interface regarding not only [*M.
hyo*.]{.underline}, but also the current secondary infections that
accompany it.

Excellent profits in hog production drew new participants, capital, and
geographical areas into pork production during this time. Production
units were sized much larger than had been traditional in the upper
Midwest. It was an exciting time in the industry, with little consensus
on production methods. Lots of changes were occurring under the radar
screen of the industry as new entrants quietly gained a very profitable
foothold in the Southeastern U.S.

As economies of scale developed in pork production and units got larger,
bacterial infections got ugly and very uneconomical. Swine dysentery,
atrophic rhinitis, and *[Actinobacillis pleuropneumoniae]{.underline}*
(APP) were all quite costly finishing pig diseases early in this period
for many expanding operations. Mycoplasmal pneumonia was there, but it
wasn't killing pigs, so it wasn't seen as a big threat.

The concept of segregated rearing as a method of disease control began
to develop early in this period. With larger group sizes brought about
by larger farrowing units it became possible to assemble relatively
large groups of pigs, weaned early on improved rations, into
geographically separated facilities. Over the years it was shown that
this system could effectively remove many of the bacterial pathogens
from the production systems.

Improved nursery diets and facilities led producers to continually lower
average weaning age over the past 20 years. The biggest driver of the
trend has been the need for intensive use of expensive farrowing
facilities and sow herds. A secondary reason, especially in recent years
has been the desire to wean at ages below which it is thought that
transmission of certain pathogens (including *[Mycoplasma]{.underline}
[hyopneumoniae]{.underline}*) would be prevented. Weaning age has
dropped from 28-35 days to as low as 12-16 days currently in some herds.

Economic analysis and tighter margins both drove the industry to embrace
all-in all-out production, then separate-site production for
nursery-finishing pigs as it became apparent that bacterial disease
loads would not allow consistently economical performance. In addition
antibiotic usage continued to look more and more problematic each year
from a public policy standpoint. The industry briefly believed that
respiratory disease might soon be a thing of the past in properly
designed production systems, via elimination of pathogens with
segregated/medicated-type early weaning programs of one type or another.

In general segregated production methods *have* done a good job of
eliminating several bacterial pathogens as economically important swine
diseases in commercial finishers. However, other pathogens have replaced
them, and through it all, *[Mycoplasma]{.underline} [hyopneumoniae
]{.underline}*is still in most finishing pig populations in the U.S.

As some bacteria bowed out, new viruses stepped in with a vengeance.
Porcine Respiratory and Reproductive Syndrome Virus (PRRS) first
appeared in North America in 1986, although not characterized until
later. Influenza has appeared to be more virulent in some cases and in
addition to the old H1N1 strain, the H3N2 strain is now endemic, with
the possibility of further reassortments. The latest viral pathogen to
assert itself is Porcine Circovirus type II (PCV II) which appears to
manifest itself in Postweaning Multisystemic Wasting Syndrome (PMWS) and
possibly Porcine Dermatitis and Nephropathy Syndrome (PDNS). These viral
infections have become more devastating and refractory to treatment at
times than the old bacterial infections.

Changes in the metabolic makeup and environment of the finishing pig
population have also been huge in the last 20 years. Pigs are now bred
to be marketed at 260-300 lb at 53-58% lean versus 220-240 lb. at 46-48%
lean 20 years ago. Barrows and gilts now carry much less fat reserves
than 20 years ago, with a much higher percentage of feed intake going to
protein accretion. Rates of gain are equal or greater over this time
period. The average finishing pig is now housed in a thermo-neutral
environment, except during summer heat stress. Bedded housing is less
commonly used, so any malfunctions in environmental control equipment
can lead to greater relative discomfort to the animals due to lack of
bedding and little fat cover on the animals.

A final factor to consider has been a big increase in animal density,
not only within barns, but also between barns in many areas. Huge
numbers of finishing animals now reside in close proximity, making area
spread of pathogens more of a possibility. When sites become infectious
the pathogen "clouds" are much larger than ever experienced in the past.

**[(Lack of) Exposure, Immunity and Changes in Mycoplasmal
Pneumonia]{.underline}**

The changes in pig flow and exposure brought about by separate site
production and early weaning have drastically changed the immune status
of the animals in the finishing units. Early weaned pigs lack immune
stimulation from pathogen seeding via dam exposure. Early weaned pigs
also carry fairly high levels of maternal antibodies to many pathogens,
so that any microbes from the sows that do bleed through to a few pigs
are suppressed for a period of time.

However, as maternal protection wanes the opportunity develops for
problems to develop. A large group of naïve animals housed in close
proximity is very susceptible to either small populations of surviving
pathogens from the weaning process, or infections introduced by other
means to the group (aerosol, fomites, carrier animals, etc.). When the
"tipping point" is reached, an explosive outbreak of disease can occur.
This phenomenon in respiratory disease came to be called Porcine
Respiratory Disease Complex (PRDC) in finishing pigs in the 1990's. The
common pathogenic culprits were *[Mycoplasma]{.underline}
[hyopneumoniae]{.underline}*, PRRS virus, and swine influenza virus in
one or more combinations, with various secondary bacterial invaders
thrown in for good measure. While it initially appeared to be more
virulent forms of disease, an alternate explanation is that the
populations of pigs were set up for a big problem by almost total
naïveté to the pathogens that struck them.

Since the explosion of PRDC in the past few years, veterinarians have
scrambled to develop protocols to manage the problem. Solutions have
included vaccination, especially for *[M. hyopneumoniae]{.underline}*,
sow herd stabilization schemes for PRRS and influenza, and pulse
medication programs for suspected likely periods of PRDC outbreaks. Feed
medication in the nursery period has also been used to retard
development of the *[M.]{.underline} [hyopneumoniae]{.underline}*
population. Programs have become very herd and system-specific. Standard
recommendations currently don't exist due to all the variables that
affect how the disease presents itself across the industry.

**[How We Control Mycoplasmal Pneumonia]{.underline}**

Part of my charge is to bring the discussion to a personal level
regarding my experiences with handling Mycoplasmal-associated pneumonias
in our production units. Our history very much mirrors that of the
industry as a whole regarding this disease. We now have a 700 sow
farrowing unit on one site with nurseries and finishers all located
off-site and managed as all-in all-out production units. Due to our
smaller herd size, age spread is a little wider than desired on each
site, especially the nursery. The sow herd is PRRS-positive but
"stable", and *[Mycoplasma hyopneumoniae]{.underline}*-positive. Titers
to both common strains of influenza have been found in the sow herd and
in finishing groups. Pigs are weaned at 12-24 days depending on
farrowing pressure, with 14-18 days the preferred weaning age.

Replacement gilts are purchased as weaned animals from as PRRS negative
source and exposed to our PRRS strain in a continuous flow
nursery-grower located in isolated facilities on the farrowing site.
They are vaccinated for *[M.]{.underline} [hyo]{.underline}*.,
erysipelas, and both influenza strains as feeder pigs and again at
selection. All parity 3 and younger sows are revaccinated for flu, *[M.
hyo.]{.underline}*, and erysipelas 3 weeks prior to farrowing. We want
to maximize maternal antibodies in the piglets at weaning with this
program.

Pigs receive 5000 I.U. penicillin at tail docking, 16 mg ceftiofur at 1
week of age and 16 mg ceftiofur at weaning. Weaning feed contains 400
gm/ton of chlortetracycline and 35 gm/ton of tiamulin for approximately
2 weeks, followed by 200 gm/ton of lincomycin for another 2 weeks. No
vaccine is currently used in piglets in our Mycoplasma control program.

**[Clinical Results to Date]{.underline}**

This program has been quite successful in avoiding clinical respiratory
disease. Except during influenza outbreaks, coughing has been minimal
throughout the finishing period. Mortality has been low, unless PRRS has
developed in conjunction with other infections in individual groups.
PRDC has not been a significant problem for 18 months.

Seven finishing groups were recently sampled serologically for
*[M.]{.underline}* *[hyopneumoniae]{.underline}* (ELISA), PRRS (ELISA),
and 2 strains of influenza (HI). Five of the seven groups had one or
more positive Mycoplasma ELISA titers from ten pigs sampled. However, 3
groups had **only** one positive animal (10% incidence), with 2 other
groups completely negative. The program we use has not completely
prevented *[M.]{.underline} [hyo]{.underline}*. transmission and
infection of offspring from the sow herd. However, it appears that
buildup to clinical levels has been suppressed and delayed to a point
near or after marketing weight for most of the population. See the
Appendix for serological data. The serological data will be further
presented and discussed in the oral presentation.

**[Economic Cost of Mycoplasmal Control]{.underline}**

The cost of this program is limited to sow vaccination and the
difference in cost between feed medications used for Mycoplasmal
suppression versus medications that would have been used otherwise.
Early-weaned pigs will usually be fed a feed antibiotic regardless of
Mycoplasma control strategies. All other housing and management
strategies remain unchanged.

The bulk of the expense is in the Phase I feeding period, when
consumption starts to pick up; however uniform feed consumption during
the first 10 days after weaning is unlikely. One advantage of the 3-4
week feeding period is the length of time that all pigs are exposed to
therapeutic doses of antimicrobials in their diets.

This program does not totally eliminate *[M.]{.underline}
[hyo.]{.underline}* from the respiratory tract of the young pigs. My
theory is that the combination of relatively early weaning, high
maternal antibody titers, and organism-suppressing antimicrobials in the
early nursery feed work synergistically to drop Mycoplasmal population
levels to extremely low levels early in the life of the group. Then it
becomes a question of whether or not levels build and interact with
other pathogens to cause clinical illness prior to slaughter.
Serological and clinical evidence to date indicate that the program has
successfully kept Mycoplasmal buildup at bay until slaughter.

**[Costs of Alternative Programs and Treatment]{.underline}**

The most common alternative and/or addition to the program we use for
Mycoplasmal control is vaccination of the piglets. In stubborn cases of
PRDC or where piglet immunity and exposure is unstable I feel it gives
quite a bit of added protection. There are many people much more
qualified than me to address many of the vaccine issues. However, I
would be remiss to not address labor and quality control as 2 issues
that are easily glossed over when planning vaccine strategies. I'm
relatively close to both the pigs and my people who do the work in my
modest operation. Vaccination can be a detriment to the pigs and the
employees if it can't be done easily and cleanly. Good injection
technique on 6-10 week old pigs is really tough; they're too big to pick
up, too quick to hit on the run, and hard to work in a pile. It may well
be cost-effective to vaccinate for Mycoplasma and other diseases at this
age, but one must carefully estimate what the true cost of handling the
pigs really is and have empathy for the people doing the work and the
pigs receiving the injection.

When respiratory disease does strike in grow-finish pigs in our barns,
we initially try to treat with injectable antibiotics. I usually
recommend ceftiofur, due its broad spectrum and short withdrawal,
despite its high cost. If we are lucky enough to have the feed bin
empty, we will medicate the feed with chlortetracycline (400 gm/ton) and
tiamulin (35 gm/ton) for 7-10 days if the group's weight averages under
220 pounds (we sell at 280 lb.). I have pretty much quit using water
medication due to lack of cleared efficacious products that work well in
medicators.

Any program that requires much use of feed grade antibiotics in heavier
pigs for control becomes quite expensive. 7 days of feed medication at
\$30 per ton for a pig eating 5 pounds per day will cost just over \$.50
per pig. This is a cost that can be justified on a short-term or
emergency basis, but it is not an expense that one would want often
repeated or as a routine part of a finishing program. There are also the
longer-term issues of drug availability and residue avoidance,
especially with tetracyclines.

**[What Do We Still Need for Treatment and Control of *M.
hyo*.?]{.underline}**

In an ideal world we would be able to eradicate the organism from the
breeding herd, preferably with a non-antibiotic feed additive or water
medication, so that there would be no transmission to offspring. Given
that this is unlikely to happen in the near future, we still need to
work towards these concepts: 1) Minimize or stop spread from dam to
offspring; 2) Eliminate or minimize the population of the organism in
the young nursery pig; 3) Induce active immunity in young pigs in a
non-invasive pig-friendly and labor-friendly way; and 4) Develop
treatment products that have no human counterparts ("smart bombs") and
that can be delivered orally or via aerosol.

This "wish list" is in order of preference. If *[Mycoplasma]{.underline}
[hyopneumoniae]{.underline}* can be eradicated, there is no need for
steps 1-4. Likewise if the population could be eliminated in the nursery
stage, treatment would not be necessary later.

The bottom line is that the pork industry can't live with a chronic
debilitating disease condition like Mycoplasmosis and associated PRDC in
finishing pigs in the future. Every product in the world is now required
to be ***"Faster, Better, Cheaper!"***, just to stay in business in
today's economic climate. If the industry limits its thinking to just
***treating*** this disease, we'll be hard-pressed to improve pork's
competitive position in the nutritional protein industry.