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EQUINE VETERINARY JOURNAL

Equine vet. J. (2008) 40 (3) 199-203
doi: 10.2746/042516408X292214

199

General Articles
The pathology of bronchointerstitial pneumonia in young
foals associated with the first outbreak of equine influenza in
Australia
J. C. PATTERSON-KANE*, J. B. CARRICK, J. E. AXON, I. WILKIE and A. P. BEGG
School of Veterinary Science, The University of Queensland, St. Lucia, Queensland 4072; Symbion Health Vetnostics, 60 Waterloo Road,
North Ryde, Sydney, New South Wales 2113; and Scone Veterinary Hospital, 106 Liverpool Street, Scone, New South Wales 2337, Australia.

Keywords: horse; horse disease; foal; influenza A virus; H3N8 serotype; pneumonia; pathology

Summary

Introduction

Reasons for performing study: The first outbreak of equine

influenza virus (EIV) infection was confirmed in Australia in
2007. Some EIV-positive young foals died with bronchointerstitial pneumonia, a rare disease process in this age
group that is often postulated to be caused by viral infection.
Objectives: The aim of this study was to describe post mortem
lesions in EIV-infected foals.
Methods: Post mortem examinations were conducted on
11 young foals (age 212 days) submitted to the Scone
Veterinary Hospital, New South Wales, Australia over a
2-month period in 2007. The foals had presented with or
developed fatal pneumonia, and were known or suspected to
be EIV-positive. Equine influenza virus nucleic acid was
detected in tissue specimens using an influenza A group
reactive real-time reverse transcriptase PCR assay.
Results: Grossly there was diffuse or extensive pulmonary
consolidation. Histological changes included: bronchiolar and
alveolar necrosis; neutrophilic infiltration; hyaline membrane
formation; and hyperplasia and squamous metaplasia of
airway epithelium. Tissues for 10 foals were EIV-positive,
with a positive nasal swab from the remaining animal.
Conclusions: This is the first detailed pathological description
of bronchointerstitial pneumonia associated with EIV
infection in young foals. It is also the first series of such cases
in which a causative agent has consistently been detected.
Potential relevance: Given the findings in this outbreak, and a
previous outbreak in the UK in 1965 involving a similarly
nave population, veterinary clinicians and pathologists should
be aware that EIV can cause fatal bronchointerstitial
pneumonia in young foals that do not have maternal immunity.
The lesions did not differ from those previously reported in
foals of various ages with bronchointerstitial pneumonia of
other or undefined causes, indicating that this is most likely to
be a stereotypical response to a variety of insults. Therefore,
tissue specimens should be obtained from cases of pneumonia
in young foals for virological and bacteriological testing.

Internationally, equine influenza is the most commonly diagnosed

respiratory viral disease of the horse (Townsend 2003). The
disease is enzootic in many parts of the world with localised or,
sometimes, extensive and pandemic outbreaks in horses of all ages
(Wilson 1993). There are 2 subtypes of this influenza A virus
based on antigenic differences in haemagglutinin (HA) and
neuraminidase (N) proteins: H7N7, which has not been isolated
since 1979; and H3N8, which is circulating worldwide with the
exception of a small number of countries that, until 2007, included
Australia (van Maanen and Cullinane 2002). The H3N8 subtype
has not been successfully controlled by vaccination and causes
significant ongoing economic loss to the equine industries (Paillot
et al. 2006). Morbidity can be up to 100% in nonendemic areas
but, typically, the mortality rate is low in mature horses, unless
overwhelming secondary bacterial pneumonia develops.
On 24th August 2007, the first outbreak of equine influenza
virus (H3N8) in Australia was confirmed by the New South Wales
(NSW) Department of Primary Industries (DPI). The source
appears to have been one or more horses imported by air from
areas where the virus is endemic. The first positive finding was
from a stallion at Sydneys Eastern Creek Quarantine Centre.
There was rapid spread of the disease through areas of NSW and
Queensland as had been seen previously in immunologically nave
populations including those in South Africa and India in 1986 and
1987, respectively (Guthrie et al. 1999). New Zealand and Iceland
are now the only countries free of EIV.
Equine influenza virus is highly contagious by inhalation and
replicates extensively in epithelial cells of the upper and lower
respiratory tract if it is not neutralised by mucus glycoprotein or
local antibody directed against the haemagglutinin (HA)
glycoprotein (Wilson 1993). The virus causes impaired ciliary
beating and epithelial necrosis, detachment and erosion, and may
impair macrophage function (Caswell and Williams 2007).
Clinically, the severity of the infection is dependent on viral strain
and the immune status of the individual. Mature horses generally

*Author to whom correspondence should be addressed.

[Paper received for publication 26.12.07; Accepted 18.01.08]

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200

present with pyrexia, depression, anorexia, a harsh dry cough and

nasal discharge after an incubation period of 25 days. However,
the infection can also be subclinical, particularly in vaccinated
animals. It is recognised that there can be mortality in foals, who
only have defence against the virus if maternal antibodies have
been acquired through ingestion of colostrum (Miller 1965a,b;
Paillot et al. 2006). In the nave Australian equine population,
foals were unlikely to have been born to vaccinated mares unless
the mares had been imported.
There are few previous descriptions of lesions in foals
specifically due to EIV, although it has been noted that pulmonary
lesions can be extensive and involve necrosis of bronchiolar
epithelium (Britton and Robinson 2002; Peek et al. 2004; Caswell
and Williams 2007). In the 1965 outbreak of EIV in the UK, severe
and sometimes fatal pneumonia was also reported in young foals
born to unvaccinated infected mares (Miller 1965a,b). However, no
detailed pathological descriptions appear to have been published.
In September and October 2007 during the spread of equine
influenza in the nave NSW horse population, a number of deaths
of young foals occurred due to EIV. The present report describes 11
cases of fatal bronchointerstitial pneumonia in EIV-positive foals.
Methods
Case details
Post mortem samples were submitted over a 2 month period
(September to October 2007) from 11 young foals (age 212
days) presented to the Scone Veterinary Hospital, NSW,
Australia. The post mortem examinations were conducted or
supervised at the hospital by an equine veterinarian (J.B.C.) with
over 20 years of experience in post mortem examination of
young foals. Some of the foals presented with severe acute
respiratory distress (n = 6), one foal died on the farm and was
presented for post mortem examination, while 4 were critically
ill foals recovering from other diseases that then developed signs
of pneumonia prior to death.
Results
Gross pathology
In some foals (n = 3) the lungs were diffusely consolidated and
pale to dark red, while in the remainder there were extensive,
coalescing areas of dark red consolidated tissue with intervening
normal or slightly hyperinflated parenchyma (Fig 1). There was
no notable lobar variation in the distribution of these pulmonary
lesions. Lymph nodes associated with the respiratory tract were
slightly enlarged. Gross lesions were not noted in other tissues or
organs. Tissue specimens from multiple organs (Table 1) were
submitted in 10% neutral buffered formalin to Symbion Health
Vetnostics, Sydney, NSW, Australia for histological examination.
Because none of the foals had clinical signs of neurological
dysfunction, this did not include brain tissue. The specimens were
processed routinely and embedded in paraffin wax; sections were
stained with haematoxylin and eosin (H&E).
Histopathology
No consistent differences were noted between foals presented
with acute respiratory distress syndrome and critically ill foals

Bronchointerstitial pneumonia in foals associated with equine influenza

Fig 1: View of the left lung of a 12-day-old foal with bronchointerstitial

pneumonia, from which equine influenza virus was isolated. There are
numerous interconnecting, depressed areas of dark consolidated
parenchyma (arrows).

initially treated for other diseases. In extensive areas, there was

mild to marked hyperplasia and squamous metaplasia of the
bronchial and bronchiolar epithelium with small foci of necrosis
and erosion, and multifocal neutrophil infiltration (Figs 2 and 3).
Airway epithelial cells were enlarged and arranged in multiple
layers (Fig 2) with large nuclei containing 14 prominent, central,
deeply eosinophilic nucleoli; small numbers of mitotic figures
were noted and were not confined to basal layers. Squamous
metaplasia always involved the bronchi and larger bronchioles
but, in some cases (n = 2/11), it extended into the terminal
bronchioles. Many of the airway lumina in inflamed areas were
filled with degenerate neutrophils, mucus and necrotic cellular
debris often including strands of nuclear material, with
infiltration of the airway walls by small numbers of lymphocytes,
plasma cells and neutrophils. Occasionally, excess mucus spilled
into adjacent alveolar spaces. Alveolar lesions were variable in
severity and extent. In the least severe cases, peribronchiolar
alveolar spaces were collapsed with mild infiltration of
neutrophils and multifocal mild necrosis (n = 2/12); these lesions
were patchy with some unaffected lobules. In the remaining foals
TABLE 1: Tissue specimens submitted for histological examination
from foals with fatal interstitial pneumonia that had presented with
acute respiratory distress syndrome (ARDS) or were initially treated for
other diseases (critical)
Foals

Lung Trachea Thymus Spleen

Liver

Kidney

Heart Intestine

ARDS
1
2
3
4
5
6
7

+
+
+
+
+
+
+

+
+
+
+
+
+

+
+
+
+
+
+

+
+
+
+
+
+

+
+
+
+
+

+
+
+
+
+
+

+
+

Critical
1
2
3
4

+
+
+
+

+
+

+
+
+
+

+
+
+
+

+
+
+
+

+
+
+
+

+
-

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TABLE 2: Equine influenza virology results for foals presented with

acute respiratory distress syndrome (ARDS) and foals that were
critically ill and initially treated for other diseases (critical)

Fig 2: Photomicrograph of lung tissue from a 7-day-old foal with

bronchointerstitial pneumonia that died following 18 h hospitalisation.
There is marked hyperplasia of bronchiolar epithelium, with enlarged
epithelial cells arranged in multiple layers (arrowheads). The airway
lumen is filled with cellular debris including strands of nuclear material
(arrow). H&E; bar = 100 m.

there was multifocal (n = 4/9) or diffuse alveolar epithelial

necrosis (n = 5/9) with multifocal mild to moderate infiltration of
neutrophils into alveolar spaces, increased numbers of
macrophages, haemorrhage, fibrinous exudation and variably
extensive formation of hyaline membranes (Fig 3).
In some fields in all of the foals with multifocal or diffuse
necrosis (n = 9/11) there was marked type 2 pneumocyte
hyperplasia and hypertrophy and, in 2 foals, occasional intraalveolar syncytial cells. In foals from which tracheal tissue was
submitted (n = 8/11), there was diffuse moderate epithelial
hyperplasia and often extensive squamous metaplasia;
inflammatory changes, when present, were limited to small
numbers of scattered neutrophils and occasional lymphocytes in
the lamina propria.

Foals

Nasal
swab

ARDS
1
2
3
4
5
6
7

+
nd
+
+
+
+
+

+
+
+
+

Critical
1
2
3
4

+
+
nd

+ (p)
+
+
+

Trachea

(p)
(p)
(p)
(p)
+
+

Lung

+
+
+
+

(p)
(p)
(p)
(p)
+
+

+ (p)
+
+
+

Thymus

+
+
+
+

(p)
(p)
(p)
(p)
+
-

+ (p)
+
+
+

Liver

+
+
+
+

(p)
(p)
(p)
(p)
+
-

+ (p)
+
+
+

Spleen

+
+
+
+

(p)
(p)
(p)
(p)
+
-

+ (p)
+
+
+

Kidney

+
+
+
+

(p)
(p)
(p)
(p)
+
-

+ (p)
+
+
+

+ = positive PCR test for equine influenza virus; - = negative PCR test;
nd = not done; p = pooled tissue specimens.

There was moderate to marked depletion of lymphoid tissue in

the thymus and spleen in all foals from which those tissue
specimens were submitted (n = 10). In some cases (n = 5) there
were increased numbers of neutrophils in hepatic sinusoids
with occasional small clusters between hepatocytes. Other
nonpulmonary histological lesions included: necrotising
tubulointerstitial nephritis (n = 1); suppurative colitis (n = 1); and
mineralisation of thymic blood vessel walls (n = 1).
Virology (Table 2)
Pooled tissue specimens from the trachea, lung, thymus, liver,
spleen and kidney of 5 foals were submitted to the NSW DPI,
Elizabeth Macarthur Agricultural Institute Virology Laboratory,
Menangle, NSW for detection of EIV nucleic acid by influenza
A group reactive real time reverse transcriptase PCR (qRTPCR)
assay. Separately labelled specimens were submitted to the
same laboratory for the remainder. Equine influenza virus
infection was confirmed for 10 foals; for the 4 of 6 foals for
which individually labelled tissue specimens were submitted,
all were EIV-positive. Trachea and lung only were positive in
one foal, and all tissue specimens were negative in a second
foal. PCR testing of a nasal swab taken ante mortem at
presentation for the latter foal confirmed EIV infection. Nasal
swabs were submitted for 9 foals including the latter animal,
8 of which were positive; the foal with a negative nasal swab
result had a positive EIV PCR test for all submitted tissue
specimens.
Bacteriology

Fig 3: Photomicrograph of lung tissue from a 2-day-old foal with

bronchointerstitial pneumonia that died 10 h after presentation. Many
alveolar spaces are lined by hyaline membranes (arrows), with mild
infiltrates of neutrophils (arrowhead) and macrophages. H&E; bar = 30 m.

Samples for bacterial culture were obtained from the lungs of 4 of

the 7 foals that presented with severe respiratory distress. No
bacteria were isolated from 3 of these foals and E. coli was
isolated from the lungs of the other foal. Citrobacter fruendii and
a group D Streptococcus sp. were isolated from the lungs of one
of the critically-ill foals. There was a heavy growth of mixed
bacteria from the lungs of all other critically ill foals (n = 3); this
was considered to be due to post mortem invasion because of
delayed examination.

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Discussion
Bronchointerstitial pneumonia of postulated viral origin is most
common in foals age 23 months of age (Lakritz et al. 1993).
This has been related to declining maternal antibody levels and
various other factors that may compromise the effectiveness of
respiratory defence mechanisms, including environmental
irritants, high environmental temperatures, overcrowding and
parasitism (Rush and Mair 2004). In contrast, this disease process
is rare in neonates/young foals; in one report of 19 cases of
bronchointerstitial pneumonia in foals submitted over a 10 year
period to a diagnostic centre in Ontario, Canada, only 2 of the
animals were 7 days old (Prescott et al. 1991). In a report from
a diagnostic centre in British Columbia only 2 of 7 foals with this
diagnosis over a 9 year period were <7 days of age (Britton and
Robinson 2002). Similarly only 3 of 14 cases of interstitial lung
disease in foals submitted to the University of Florida
from 19821985 involved animals 9 days of age (Buergelt
et al. 1986). The current report of 11 young foals with
bronchointerstitial pneumonia, from which tissues were
submitted to a single diagnostic laboratory within a 2 month
period is therefore a highly unusual occurrence.
The microscopic lesions described in the lungs of foals in the
current report are identical to those previously noted in suckling
and weanling foals (and rarely in neonates) including: bronchiolar
and alveolar septal necrosis; neutrophilic infiltration; intraluminal
necrotic debris in airways; significant bronchiolar epithelial and
alveolar type II pneumocyte hyperplasia in animals surviving the
acute stage; hyaline membrane formation; and occasional syncytial
cell formation (Prescott et al. 1991; Lakritz et al. 1993; Rush and
Mair 2004). All 11 foals had survived for a sufficient period for
pronounced hyperplasia of airway epithelium to occur, inclusive of
the trachea. Lesions were noted in other tissues in some foals and
EIV is thought to cause damage to parenchymal organs other than
the lungs in some cases (Caswell and Williams 2007). The most
common extrapulmonary lesion in these foals (n = 5) was mild
neutrophilic infiltration of the liver, which could be due to bacterial
infection. No liver specimens were submitted for bacterial culture
and, in 2 of these foals, the liver tissue was not positive for EIV;
for the other 3 animals tissue specimens for EIV testing were
pooled. The uniformity of the respiratory system histopathology in
current and previous cases indicates a stereotypical response of
lung tissue in this age group, as no common denominator in terms
of inciting cause has previously been found. Primary viral infection
is usually suspected to be responsible with variable bacterial
isolates considered to be opportunistic invaders (Buergelt et al.
1986; Prescott et al. 1991). This appears to be the first report of
pneumonia in young foals in which one virus has been consistently
isolated from a number of animals.
Isolation of EIV from the lung tissue of foals with
bronchointerstitial pneumonia has been reported infrequently in
young and older foals in countries where this viral infection is
endemic (Britton and Robinson 2002; Peek et al. 2004; Dunkel
et al. 2005). It has been suggested that EIV is difficult to isolate
when lesions reach the stage of sloughing of necrotic epithelium
as that may remove the virus (Britton and Robinson 2002). The
detection of EIV RNA in the tissues of 10 of the 11 foals may be
related to the use of a very sensitive qRTPCR or a lack of
maternally-derived immunity, which normally persists at
protective levels for up to 6 months (van Maanen et al. 1992;
Cullinane et al. 2001) or both. Horses without immunity through

Bronchointerstitial pneumonia in foals associated with equine influenza

previous exposure or vaccination shed EIV for a more prolonged

period and virus isolation is more consistent (Wilson 1993).
On 29th September 2007, vaccination of horses against EIV
was commenced in NSW and Queensland in buffer zones and for
other animals considered to be at risk of exposure using a live
recombinant canarypox viral vaccine (Proteq Flu)1 with the aim of
confining and eradicating the disease. In the next foaling season,
it is therefore unlikely that in these States there will be such a large
immunologically nave population of young foals.
Usually the most likely viral cause of neonatal pneumonia in
Australia would be equine herpesvirus-1, although uncommon.
Outbreaks of herpesvirus in that age group have not frequently
been reported (Hartley and Dixon 1979; McCartan et al. 1995;
Murray et al. 1998). Histological lesions in the lungs and other
tissues of these foals did not indicate herpesvirus infection and
inclusion bodies were not noted. Specimens from these foals could
not be submitted for EHV-1 PCR detection as transportation of
known EIV-positive specimens to an EIV-free state (Victoria) was
not possible. Equine herpesvirus-2 infection has been associated
with outbreaks of pneumonia in foals in a number of countries
including Australia and New Zealand; however, EHV-2 is
ubiquitous in all age groups and its exact role as a primary agent
is controversial (Ames et al. 1986; Fu et al. 1986).
It has been proposed that there is a normal, general cellular
immunodeficiency state focused on the respiratory tract in foals,
that is unmasked at age 23 months by the reductions in
maternally-derived antibody. There has not been another
satisfactory explanation as to why there is such a common
occurrence of infections including Rhodococcus equi and
Pneumocystis carinii that, in other species, are usually only
diagnosed in immunosuppressed individuals (Ainsworth et al.
1993; Prescott 1993). In these foals, there has probably been an
acceleration of this process due to lack of specific antibodies to
EIV in a situation where an exotic disease has been introduced,
but possibly also due to detrimental viral effects on alveolar
macrophage function, i.e. the key players in the cell-mediated
immune response (Seo et al. 2004; Caswell and Williams 2007).
In summary, during the EIV outbreak in NSW in 2007 there
were a number of cases of bronchointerstitial pneumonia in young
foals. This is usually a rare pathological process in that age group.
Variably fatal pneumonia was reported previously in young foals
in the 1965 outbreak of EIV in the UK. The situation in the UK at
that time was similar, in that unvaccinated mares were infected
with EIV in the periparturient period (Miller 1965b).
All cases in the current series were positive for EIV by virus
isolation from tissues and/or nasal swabs, which probably reflects
the lack of transfer of passive immunity. Gross and histological
lesions were not specific based on previous reports of
bronchointerstitial pneumonia of various possible causes in foals
in other countries. Virus isolation is therefore required to confirm
the diagnosis. Given the initiation of vaccination to control the
spread of EIV in Australia and presence of maternal immunity this
situation is unlikely to arise in the next foaling season, unless there
are further outbreaks in previously unexposed areas where horses
have not been vaccinated.
Acknowledgement
The authors would like to acknowledge the contribution of the
staff of the EMAI Virology Laboratory who performed all of the
virology assays.

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Manufacturers address
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Parramatta, New South Wales, Australia.

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Author contributions All authors contributed to all aspects of this

study.