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674 CHAPTER 3
VetBooks.ir Clinically apparent infection is usually restricted to 41.1°C [106°F]) with depression and anorexia. There
is serous nasal discharge that becomes mucopurulent
the URT. Limited virus replication does occur in
the LRT and, in a small minority of horses (mainly
ular lymph nodes and occasionally retropharyngeal
foals or immunocompromised animals), clinically (Fig. 3.133), lymphadenopathy (mainly submandib-
apparent pulmonary disease occurs. Virus-induced lymph nodes) and a persistent, dry, harsh, hacking
impairment of mucociliary clearance can allow sec- cough. Complications such as secondary bacterial
ondary bacterial infection to develop, mostly by LRT infections (pneumonia and pleuropneumo-
resident airway microbes (especially Streptococcus nia), vasculitis, myocarditis and chronic post-viral
equi subsp. zooepidemicus and members of the genera fatigue syndromes may be more likely to occur in
Pasteurella, Actinobacillus and Haemophilus). In con- horses that are exercised and/or kept in unhygienic
trast to the equine herpesviruses, orthomyxovirus stable air environments. Clinical disease in horses
replication is restricted to respiratory epithelial cells with incomplete immunity, for example from par-
and the virus does not appear capable of invasion and tially completed or lapsed vaccination programmes,
causing viraemia; persistent infections do not occur, is usually mild and may be difficult to differenti-
and latency is not established. ate clinically from other causes of infectious URT
disease. Disease is generally more severe in foals,
Clinical presentation yearlings, young adult horses and in immune naïve
There is a sudden onset of signs of acute URT infec- populations.
tious disease, with an incubation period of 1–3 days
and duration of less than 3 weeks. Clinical signs are Differential diagnosis
variable, with more obvious disease seen in naïve All other viral and bacterial causes of infectious
animals. The first clinical sign is pyrexia (up to URT disease should be considered, especially equine
herpesviruses, equine viral arteritis (EVA) virus and
Streptococcus equi subsp. equi.
3.133
Diagnosis
Clinical signs are suggestive, but not diagnostic,
of influenza virus infection. Leucopenia from lym-
phopenia and/or neutropenia, and an increase in
serum amyloid A (SAA) are suggestive of viral dis-
ease but are not diagnostic for influenza. A variety
of laboratory methods have been used to confirm
a diagnosis. Detection of virus RNA on nasal or
nasopharyngeal swabs by quantitative (‘real time’)
polymerase chain reaction (qPCR) is the current
diagnostic method of choice, offering rapid results
and very high sensitivity and specificity. Virus iso-
lation is an important part of surveillance because
it allows collection of representative strains for
sequencing, enabling monitoring of genetic drift
in influenza viruses. It is not used for diagno-
sis of clinical cases because it is slow and yields
false-negative results. Virus antigen detection has
Fig. 3.133 Bilateral seromucous nasal discharge in been superseded by qPCR testing, although it is
a horse suffering from an early infection with equine still offered by some laboratories, and patient-side
influenza. The infection was confirmed by polymerase enzyme-linked immunosorbent assay (ELISA)
chain reaction on a nasal swab. tests designed for detection of human influenza