Page 706 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Respir atory system: 3.3 Medical conditions of the upper respir atory tr act 681

VetBooks.ir greater than the number of severe ‘classical’ cases. airway, causing dyspnoea (hence the term ‘strangles’)
before rupturing either externally or internally into
Strangles affects naïve horses and ponies of all ages
and types, although younger animals kept in large
tion and empyema.
open populations are generally most likely to become the guttural pouch, causing guttural pouch infec-
affected. Some horses develop chronic infections of Chondroids (balls of inspissated pus that contain
the guttural pouch and become carriers, acting as viable bacteria) may develop in chronic cases of gut-
reservoirs of infection and a source of contagion to tural pouch empyema. Persistent (months to years)
other horses. Strangles is a reportable disease in the guttural pouch infection may develop in a small pro-
USA and many other countries. portion (<10%) of recovered horses. These animals
are carriers, are often asymptomatically infected
Aetiology/pathophysiology and shed bacteria intermittently in respiratory-tract
Strangles is caused by the Lancefield Group C secretions.
organism Streptococcus equi subsp. equi. It is closely In most cases, bacteria do not disseminate beyond
related to the other common equine Group C strep- the head, but in a small proportion of horses bacte-
tococcus, Streptococcus equi subsp. zooepidemicus, but ria disseminate widely via the blood and lymph cir-
can be differentiated by sugar fermentation tests, culations, causing metastatic abscessation (‘bastard
PCR and multilocus sequence typing. S. equi pos- strangles’) in the abdomen (abdominal viscera and
sesses a variety of virulence determinants, of which peritoneum), thorax (lungs, pleura and mediasti-
the surface M protein (the major immunogenic and num), central nervous system, eye, skeletal and car-
antiopsonic protein) and its antiphagocytic hyal- diac muscle and tendon and joint sheaths. S. equi
uronic acid capsule are best characterised. Most antigens in the circulation can trigger purpura
pathogenic isolates are capsulated and possess full- haemorrhagica, an immune-mediated vasculitis
length M proteins; isolates with less capsule or causing petechial haemorrhages, subcutaneous and
truncated M proteins are less pathogenic, possibly visceral oedema and sometimes skin sloughs of the
because of reduced resistance to phagocytosis. extremities.
Infection is acquired by direct horse-to-horse The milder form of the disease, known as atypical
transmission of infected respiratory tract secretions strangles, causes transient URT disease with lymph-
or indirectly via infected droplets on water troughs adenopathy but no abscessation or other complica-
and buckets, feeding utensils, hands, veterinary tions. It is not entirely clear why there are two forms
equipment and tack. In contrast to the respiratory of the disease, but infectious dose and frequency,
viruses, aerosol transmission does not appear to be bacterial strain differences, horse genetic differ-
important. Bacterial survival in the environment ences and previous immune exposure of the horse
is short-lived (<1 week if cultures are dessicated or are probably all factors. Bacteria isolated from atypi-
exposed to UV light). Bacteria can survive for a few cal cases retain their virulence and are capable of
weeks (possibly up to 2 months) in water troughs or causing more severe disease in other horses.
in droplets of water or pus on wood and tack.
Bacteria colonise the nasopharynx (and other Clinical presentation
regions of the URT including the paranasal sinuses Severe ‘classical’ disease
and guttural pouches), producing typical clini- The incubation period is variable (1–14 days),
cal signs of URT infectious disease. Bacteria may even following experimental challenge. Pyrexia
cross the respiratory epithelium and reach drainage (up to 42°C [107.6°F]) is the earliest clinical sign
lymph nodes (mainly the submandibular and retro- and persists for up to 2 weeks. Affected horses are
pharyngeal lymph nodes) where they persist despite depressed and anorexic for 1–2 weeks. Nasal dis-
efficient neutrophil recruitment to the site, and charge (Fig. 3.135) becomes increasingly purulent
cause abscesses. Occasionally, parotid lymph node and persists for 2–3 weeks. Lymph node enlarge-
abscesses develop. Retropharyngeal lymph node ment is palpable from 2–3 days after infection but
abscesses may become very large and compress the abscesses usually develop 2–3 weeks later (Fig. 3.136).