- Infectious Diseases of Livestock
- Part 3
- Strangles
- GENERAL INTRODUCTION: SPIROCHAETES
- Swine dysentery
- Borrelia theileri infection
- Borrelia suilla infection
- Lyme disease in livestock
- Leptospirosis
- GENERAL INTRODUCTION: AEROBIC ⁄ MICRO-AEROPHILIC, MOTILE, HELICAL ⁄ VIBROID GRAM-NEGATIVE BACTERIA
- Genital campylobacteriosis in cattle
- Proliferative enteropathies of pigs
- Campylobacter jejuni infection
- GENERAL INTRODUCTION: GRAM-NEGATIVE AEROBIC OR CAPNOPHILIC RODS AND COCCI
- Moraxella spp. infections
- Bordetella bronchiseptica infections
- Pseudomonas spp. infections
- Glanders
- Melioidosis
- Brucella spp. infections
- Bovine brucellosis
- Brucella ovis infection
- Brucella melitensis infection
- Brucella suis infection
- Brucella infections in terrestrial wildlife
- GENERAL INTRODUCTION: FACULTATIVELY ANAEROBIC GRAM NEGATIVE RODS
- Klebsiella spp. infections
- Escherichia coli infections
- Salmonella spp. infections
- Bovine salmonellosis
- Ovine and caprine salmonellosis
- Porcine salmonellosis
- Equine salmonellosis
- Yersinia spp. infections
- Haemophilus and Histophilus spp. infections
- Haemophilus parasuis infection
- Histophilus somni disease complex in cattle
- Actinobacillus spp. infections
- infections
- Actinobacillus equuli infections
- Gram-negative pleomorphic infections: Actinobacillus seminis, Histophilus ovis and Histophilus somni
- Porcine pleuropneumonia
- Actinobacillus suis infections
- Pasteurella and Mannheimia spp. infections
- Pneumonic mannheimiosis and pasteurellosis of cattle
- Haemorrhagic septicaemia
- Pasteurellosis in sheep and goats
- Porcine pasteurellosis
- Progressive atrophic rhinitis
- GENERAL INTRODUCTION: ANAEROBIC GRAM-NEGATIVE, IRREGULAR RODS
- Fusobacterium necrophorum, Dichelobacter (Bacteroides) nodosus and Bacteroides spp. infections
- GENERAL INTRODUCTION: GRAM-POSITIVE COCCI
- Staphylococcus spp. infections
- Staphylococcus aureus infections
- Exudative epidermitis
- Other Staphylococcus spp. infections
- Streptococcus spp. infections
- Strangles
- Streptococcus suis infections
- Streptococcus porcinus infections
- Other Streptococcus spp. infections
- GENERAL INTRODUCTION: ENDOSPORE-FORMING GRAM-POSITIVE RODS AND COCCI
- Anthrax
- Clostridium perfringens group infections
- Clostridium perfringens type A infections
- Clostridium perfringens type B infections
- Clostridium perfringens type C infections
- Clostridium perfringens type D infections
- Malignant oedema⁄gas gangrene group of Clostridium spp.
- Clostridium chauvoei infections
- Clostridium novyi infections
- Clostridium septicum infections
- Other clostridial infections
- Tetanus
- Botulism
- GENERAL INTRODUCTION: REGULAR, NON-SPORING, GRAM-POSITIVE RODS
- Listeriosis
- Erysipelothrix rhusiopathiae infections
- GENERAL INTRODUCTION: IRREGULAR, NON-SPORING, GRAM-POSITIVE RODS
- Corynebacterium pseudotuberculosis infections
- Corynebacterium renale group infections
- Bolo disease
- Actinomyces bovis infections
- Trueperella pyogenes infections
- Actinobaculum suis infections
- Actinomyces hyovaginalis infections
- GENERAL INTRODUCTION: MYCOBACTERIA
- Tuberculosis
- Paratuberculosis
- GENERAL INTRODUCTION: ACTINOMYCETES
- Nocardiosis
- Rhodococcus equi infections
- Dermatophilosis
- GENERAL INTRODUCTION: MOLLICUTES
- Contagious bovine pleuropneumonia
- Contagious caprine pleuropneumonia
- Mycoplasmal pneumonia of pigs
- Mycoplasmal polyserositis and arthritis of pigs
- Mycoplasmal arthritis of pigs
- Bovine genital mycoplasmosis
- Neurotoxin-producing group of Clostridium spp.
- Contagious equine metritis
- Tyzzer's disease
- MYCOTIC AND ALGAL DISEASES: Mycoses
- MYCOTIC AND ALGAL DISEASES: Pneumocystosis
- MYCOTIC AND ALGAL DISEASES: Protothecosis and other algal diseases
- DISEASE COMPLEXES / UNKNOWN AETIOLOGY: Epivag
- DISEASE COMPLEXES / UNKNOWN AETIOLOGY: Ulcerative balanoposthitis and vulvovaginitis of sheep
- DISEASE COMPLEXES / UNKNOWN AETIOLOGY: Ill thrift
- Eperythrozoonosis
- Bovine haemobartonellosis
Strangles
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Strangles
Previous Author: J F TIMONEY
Current Authors:
A S WALLER - Head of Bacteriology, BSc, PhD, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU, United Kingdom
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 19th or early 20th 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 a 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...
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