Strangles

GENERAL INTRODUCTION: GRAM-POSITIVE COCCI Streptococcus spp. infections

Introduction

Strangles is an acute contagious disease of horses, mules and donkeys characterized by fever, acute mucopurulent inflammation of the upper respiratory tract, purulent lymphadenitis and abscessation of the submandibular and retropharyngeal lymph nodes.⁶⁰ The disease was first described by Jordanus Rufus in 1251⁵² and the causative agent, Streptococcus equi, was identified in 1888.⁵³ However, genetic analysis dates the common ancestor of contemporary strains of S. equi to the late 19^th or early 20^th Century.²⁶ This period of history was blighted by a series of global conflicts, in which the horse played vital roles. The increased breeding and global transport of horses to replace those killed on the battlefields is thought to have facilitated a population replacement of S. equi, resulting in the emergence and dissemination of the ‘fittest’ strain to horse populations around the world.⁶⁷ The modern day transport of S. equi around the world is now known to be facilitated by the ability of S. equi to persist in the guttural pouches or sinuses of a proportion of carrier horses following their recovery from acute disease.^{23, 45} The transition of S. equi between acute and persistent forms of infection is critical to its success as a pathogen and breaking this cycle through improved biosecurity, diagnostics and vaccines is essential to reducing the global prevalence and impact of strangles.

Strangles is endemic throughout the world with outbreaks in Europe, Australia, New Zealand, India, Malaysia, South Africa, Japan, and North and South America. Indeed, only Iceland remains free of strangles, a situation that is likely due to virtually no importation of horses over the last 1,000 years.¹¹ It is estimated that over 600 outbreaks of strangles occur in the UK each year.³⁰ Information derived from reports submitted annually by 20 countries to the International Collating Centre of the Animal Health Trust, Newmarket, England, indicates that strangles ranks with equine influenza and herpesvirus abortion as one of the three most significant equine infectious diseases.

The outbreaks in 1998 of strangles in the Western Cape Province of South Africa occurred after an interval of 20 years’ freedom from the disease and owe their origin to the introduction of S. equi in breeding stock imported from Australia. Previous outbreaks occurred in Thoroughbred mares and foals during the period November 1977 to February 1978, after the mares had visited the Western Cape for service during the 1977 breeding season. Many contracted the disease during the visit before returning to their home stud farms in the Eastern Cape, Karoo and KwaZulu-Natal.

Theiler⁵⁸ reported on the occurrence in South Africa of sporadic cases and epidemics in the earlier part of the 1900s and considered that aged horses were to a very great extent immune as they had ‘passed through the disease at an earlier age — very few horses escaping it altogether whilst young’. This was before the major decline in equine populations took place throughout the world. During World War II thousands of horses and mules were shipped from South Africa to India to be used as pack animals in the Burma Campaign. Many of these animals were congregated at a military base camp in Pinetown before shipment from Durban harbour. Periodic outbreaks of strangles occurred in this camp.

Aetiology

Streptococcus equi has evolved from an ancestral strain of the opportunistic pathogen S. zooepidemicus through a process of gene loss and gain.^{29, 33, 71} Individual cells are ovoid or spherical, 0.6 to 1.0 µm in diameter, Gram-positive and may form long chains in pus and in recently infected lymph nodes. Excellent aerobic and anaerobic growth occurs in Todd Hewitt broth with 0.2 per cent yeast extract, in chemically defined medium⁶⁴ and in common laboratory media supplemented with serum. The organism produces the β-haemolytic toxin streptolysin S18 and carries a Lancefield Group C carbohydrate typing antigen.

A hyaluronic acid capsule is produced by most strains and is most evident in logarithmic phase cultures. The accumulation of hyaluronic acid capsule is likely due to a mutation in the genome-encoded hyaluronate lyase gene, which is present in all strains of S. equi.²⁹ The capsule shields S. equi from the host immune response³ and its production in some persistent strains is further enhanced by amplification of the biosynthetic has locus, whilst other persistent strains contain deletions, nonsense mutations and non-synonymous mutations in the has locus that can eliminate production of hyaluronic acid.²⁶ Such variability may reflect an increased need for S. equi to evade the immune response of recently recovered animals, but suggests that the production of hyaluronic acid in the guttural pouch is unfavourable in the longer term. The lack of has mutations in populations of S. equi recovered from acute cases of strangles suggests that the decay of the has locus may be an evolutionary dead-end for S. equi and that such strains have a reduced capacity to transmit to naïve animals and cause disease.

The genomes of all strains of S. equi, but no...