Strangles: clinical disease and practical steps to its control Josh - PDF document

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London Strangles: clinical disease and practical steps to its control Josh Slater Royal Veterinary College University of London Strangles • clinical disease – pathogenesis – ‘classical’ strangles – complications – ‘atypical’ strangles – treatment • diagnosis and control – carriers, control measures • strangles research – vaccines Strangles in medieval times • accurate descriptions of strangles in 13thC veterinary literature • Giordano Ruffo (1251) – De medicina equorum • Albertus Magnus (1258) – De animalibus 1

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London Strangles in more modern times • clinical disease thoroughly understood, including carriers • strangles an increasing problem in military horses, especially at the end of the 19thC and WW1 Strangles today • clinical disease has changed little over the last 800 years – endemic infection cycles in herds – ‘atypical’ disease may be more prevalent – carrier horses are the main reservoir of infection • the first purely veterinary pathogen to be sequenced (WT Sanger Institute & Home of Rest for Horses) Strangles bacterium • Streptococcus equi subsp equi ( S. equi ) - Gram positive, Lancefield group C, chain forming cocci (shorter chains in abscesses, longer in culture) • wide zones of beta haemolysis on blood agar • most isolates are capsulated (mucoid colonies); some are less capsulated or acapsular (matt) 2

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London S.equi structure lipoprotein cytoplasm cell wall hyaluronic acid M protein capsule Strangles disease profile • highly contagious – infects up to 100% of horses in a yard – deaths uncommon (typically 1-3%) but can reach 10% – disease mainly in young or naïve horses • transmission via droplets – direct horse to horse – indirect via food/water troughs, personnel • respiratory disease followed by dissemination of bacteria causing abscesses (‘classical strangles’) • often have mild disease without abscesses (‘atypical strangles’) Key stages in pathogenesis colonisation of URT epithelium epithelial invasion and entry to lamina propria entry into lymphatics ± circulation persistence despite neutrophil chemotaxis and phagocytosis abscessation (LN and other organs) 3

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London Virulence mechanisms • colonisation – surface proteins adhere to epithelium – bacterial metabolic pathways use host nutrients for biosynthesis and growth • epithelial invasion – cytolytic and proteolytic enzymes (toxins) degrade epithelial integrity and allow entry • evasion of phagocytosis – capsule and M protein prevent opsonisation Classical strangles • highly contagious, attack rates >80% – susceptibility and disease severity mainly relate to previous exposure • associated with capsulated bacteria – isolates with less or no capsule are less pathogenic (Anzai, 1999) • apparent decrease in prevalence (compared to ‘atypical’ strangles) noted in UK since 1960’s (Mafferty, 1962; Woolcock, 1975 ) Clinical signs 0 2 4 6 8 10 12 14 16 18 20 22 4 weeks 5 weeks 6 weeks 7 weeks bacteria pyrexia discharge abscesses leucocytosis neutrophilia 4

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London ‘Classical strangles’ abscesses • mainly SMLN and RPLN • occasionally parotid LN Other strangles complications: 2. Metastatic abscessation • haematogenous and lymphatic spread to lymph nodes and other organs (Bartlett, 1777; Haycock, 1838; Blakeway, 1881; Ford, 1980; Sweeney, 1987) – abdomen: mesenteric LN abscess, abscesses in abdominal viscera (liver, spleen, kidney), peritonitis – thorax: mesenteric and tracheobronchial LN, lung – CNS: brain and spinal cord – eye: panophthalmitis – joints and tendon sheaths – heart: myocarditis and endocarditis – skeletal muscle: rhabdomyolysis Other strangles complications • laryngeal paralysis • purpura haemorrhagica • death (<10%) 5

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London ‘Atypical’ strangles • most common clinical presentation? – under-diagnosed because not investigated • mild disease (Woolcock, 1975; Prescott, 1982; Timoney, 1993) – pyrexia, depression, cough, purulent nasal discharge, self-limiting lymphadenopathy – no abscesses or associated complications • genetic basis of virulence poorly understood – some cases associated with non-capsulated or less- capsulated isolates (Prescott, 1982; Anzai, 1999 ) or M protein attenuations (Chanter, 2001) • role of ‘atypical’ isolates in epidemiology unclear Importance of atypical strangles • atypical disease is dangerous because it does not look like strangles – looks just like any other respiratory infection – samples not taken for bacterial culture – control and prevention not implemented • ‘atypical’ isolates important in disease spread – bacteria from atypical cases can cause classical strangles in others – strangles outbreaks with atypical cases often go un-recognised until classical cases appear later Your opinions: Management & Treatment • hygiene precautions • housing • nursing • antibiotics – to use or not to use? – which antibiotic? – which animals? • other medical treatments • surgical treatments 6

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London Treatment • no consensus but deeply held beliefs • long-standing concern that antibiotic treatment may: – impair development of immunity (Piche, 1983) – prolong the course of disease (Timoney, 1993) – encourage metastatic abscessation (Fitzwygram, 1886) • isolates generally sensitive to the pencillins • also tetracyclines and TMS but penicillin is the antibiotic of choice Recommendations for antibiotic treatment • early cases showing pyrexia only • sick horse, especially foals, with marked anorexia, depression ± persistent pyrexia • horses with complications – airway compression – suspected metastatic disease – purpura haemorrhagica • in contacts - treat and move or continue treatment until the outbreak ends • NOT be used cases with abscesses Transmission of S.equi • environment reservoir less important than carriers: – S.equi survives for < 1 week if dessicated, but – survives at least 4 weeks in drinking water – survives up to 8 weeks in water, pus or blood droplets on wood or tack (Jorm, 1991) – easily killed by pevidine, chlorhexidine, Virkon and glutaraldehyde • no evidence for wind-borne aerosol transmission • direct and indirect (via personnel) horse-horse droplet transmission important • main reservoir of infection clinical cases and carriers 7

Intervet symposium om Kvarka. Lund 2005-03-16. Stockholm 2005-03-17. Föreläsare: Josh Slater, Royal Veterinary College, University of London Risk factors • attack rates increase with (Jorm, 1990) : – increasing group size – increased movement of horses – increased mixing of horses – communal feeders and drinkers – younger horses • but apparent age-related immunity is almost certainly due to previous exposure: older naïve horses are susceptible (Sweeney, 1987) Low and medium risk groups • Closed populations – individual horses and small groups kept at in private yards and fields – horses that don’t travel or mix with others • Race horses in training – closed populations - mixing within the population but not with other groups • Closed populations that travel and mix – events, shows, competitions High risk groups • Livery yards and studs, ‘feral’ herds – open populations – mixing of age groups – frequent mixing of new horses, often with wide geographical distribution – background of new arrivals often uncertain – disease status of new arrivals uncertain – housing allows contact between horses – communal feeding and drinking areas 8