ISERPD2015 Abstract Submission
This document is prepared in the format that should be used in your abstract. To ensure uniformity of
appearance for the proceedings, your paper should conform to the following specifications. Template is the
following page and should be sample for your abstract. The official language of ISERPD2015 is only English,
and abstract must be written in English. The deadline to submit your abstract is on December 22, 2014,
23:59 (JST).
1. Paper Size
Your abstract should be prepared on 210_297 mm (A4) white paper in two columns in Arial font. Your
paper should not exceed 1 (one) page in length. The distance from the top edge of the paper to the title of your
paper should be 25 mm. The left and right margins should be 15 mm, and the bottom margin should be at least
15 mm. The width of each column should be 85 mm. The distance between the two columns of the text should
be 10 mm.
2. Title and Author Information
The exact title of your abstract in header should be left-justified the top of the page and should be in
10-point size, bold. The authors' names should be left-justified below the title. Do not include author's title (Prof.,
Dr.), position (president, research engineer), or degrees (ph. D., M Sc., M. E.), and affiliations included division
and country should be on Italic.
3. Body and Paragraphs
The body of your abstract should be consisted on in 10 point size and single spaced. Do not double
space between paragraphs. Indent the first line of the each new paragraph. Use full justification. Topics should
be on Introduction, Materials and methods, and Results, Discussion, Acknowledgements, and References.
4. Figures and Tables
All figures (line drawings, graphs) and tables should be referred in numerical order in the text. There should
be typed as "Figure 1." or "Table 1.” with appearing above figure and table.
5. References
List and number all references at the end of the paper.
6. Proofreading
After completing the typed abstract, make sure to proofread it very carefully. The abstract will not be
proofread by ISERPD2015 Organizing Committee.
TYPE THE TITLE OF YOUR PAPER ALL CAPITAL LETTERS
Toshio Masaoka (1) (2) , Satoshi Otake (2),
(1)
Azabu University
(2)Japanese
Association of Swine Veterinarians , Japan
Introduction
Proliferative and necrotizing pneumonia (PNP) is
histologically characterized by two main features: a)
lymphohistiocytic intersticial inflammation with
hypertrophy and proliferation of type 2 pneumocytes,
and b) presence of clumps of necrotic inflammatory
cells within alveolar spaces (1).
Initial studies attributed PNP causality to a new strain
of swine influenza virus (SIV) type A (2). However,
subsequent investigations indicated the rare
involvement of SIV and proposed porcine respiratory
and reproductive syndrome virus (PRRSV) as the
main causal agent of PNP (3,4). PCV2 has been also
causally associated to PNP (5), but a recent
Canadian study considered it as a non-determining
factor for PNP occurrence (4).
The objective of the present work was to determine
the presence of selected viral infectious agents in
cases of PNP from Spain.
of 74 (43.2%) cases of PNP. This latter percentage
increased to 80% (24 out of 30) if only cases of
PCV2/PRRSV co-infection were considered. Eighteen
out of 74 cases (24.3%) had also purulent
bronchopneumonia. Moreover, 13 out of 74 (18%)
cases had fibrous or fibrinous pleuritis. Pulmonary
necrosis was only noted in one PNP case (1.4%), in
which ADV and PCV2 were concurrently detected.
Materials and methods
A retrospective study on 74 PNP cases from
postweaning pigs was carried out. Lung tissues
examined came from pigs received at the Veterinary
School Pathology Diagnostic of Barcelona (Spain)
between 2001 and 2005.
Selection of the cases was based on the presence of
the two microscopic hallmarks cited above (1).
Concomitantly, the presence of other lesions such as
bronchial and bronchiolar necrosis, purulent
bronchopneumonia, pulmonary haemorrhages and
fibrous/fibrinous pleuritis was also evaluated.
Moreover, severity of hyperplasia and proliferation of
type 2 pneumocytes and the presence of necrotic
cells were graded.
PCV2 nucleic acid was determined by means an in
situ hybridization (ISH). PRRSV, ADV and SIV
antigens were detected by immunohistochemical
techniques using the corresponding monoclonal
antibody to each agent. Procedures were performed
on formalin-fixed, paraffin-embedded tissues.
Discussion
The present study further insights on the potential
infectious agents involved in the occurrence of PNP in
pigs. Our results indicate that PCV2 seems to be the
main etiologic agent of PNP in postweaning pigs in
Spain, since it was present in about 85% of the cases.
These results are closer to the ones obtained in
Germany (6), and markedly different from those from
Canada (4). This latter study suggested that PRRSV
was the main contributor of PNP. However, our results
indicated that, although important when co-infection
with PCV2 occurs, PRRSV is not essential for the
development of PNP.
Obtained data also confirm the rare involvement of
SIV in PNP (3,4) and indicate a similar situation for
ADV, since both agents were detected in a few
number of PNP cases and none of them were found
alone.
Results
Pathogen detection results in PNP cases are
summarised in Table 1.
Histopathologically, 45 out of 74 (60.8%) cases had
moderate to high hyperplasia and proliferation of
pneumocyte type 2. At the same time, 55 out of 74
cases (74.3%) had moderate to high amounts of
necrotic cell clumps in alveoli. Necrosis of bronchial
and/or bronchiolar epithelium was detected in 32 out
Table 1. Pathogen/s detected in 74 lungs with PNP
lesions.
Pathogen
PCV2 only
PRRSV only
PCV2+PRRSV
PCV2+SIV
PCV2+ADV
None
No. Positive
29
3
30
3
1
8
% positive
39.2
4.1
40.6
4.1
1.4
10.8
Acknowledgements
This work was partly funded by the Project No.513928
from the 6th FP of the European Commission.
References
1. Morin. et al. (1990). Can Vet J 31, 837-839.
2. Girard et al (1992). Vet Rec 130, 206-207.
3. Larochelle et al (1994). Can Vet J 35,513-515.
4. Drolet et al. (2003). Vet. Pathol. 40, 143-148.
5. Ellis et al. (1999). Vet. Pathol. 36, 262-265.
6. Pesch et al. (2000) Proc. IPVS Congress 1