- Infectious Diseases of Livestock
- Part 3
- Tyzzer's disease
- 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
Tyzzer's disease
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Tyzzer’s disease
J J VAN DER LUGT
Introduction
Tyzzer’s disease was first described in 1977 by Tyzzer 26 in laboratory mice. Since then, naturally occurring disease has been reported in a variety of laboratory and wild rodents, rhesus monkeys, dogs, cats,6, 8, 14 and several species of wildlife.13, 31 In horses, Tyzzer’s disease was first reported in 1973 21 and has subsequently been diagnosed in foals in many countries,2, 10, 22, 23, 25, 30 including South Africa.27 It has also been encountered in two calves.15, 29 The disease in foals and calves is an acute, fatal infection characterized by a multifocal, necrotizing hepatitis. It is caused by the bacterium Clostridium piliforme.
In laboratory animals losses may be extensive,8 but in horses the disease occurs only sporadically in individual foals.
Aetiology
The causative organism was previously classified as Bacillus piliformis although it did not belong to the genus Bacillus, whose members are Gram-positive, spore-forming rods.3, 12, 17 Bacillus piliformis was not listed in Bergey’s Manual of Systemic Bacteriology of 1984.16 Using16S rRNA sequence analysis, the phylogenetic relatedness of the Tyzzer’s bacillus to the genera Clostridium was demonstrated and the causative agent was subsequently reclassified as Clostridium piliforme.5 In their review of Tyzzer’s disease, Ganaway et al.8 described C. piliforme as a Gram negative, spore-forming, pleomorphic rod, 0,5 μm wide and 8 to 10 μm long. It may occasionally be up to 40 μm in length. The bacterium is an obligate, intracellular parasite and is motile, propulsion being by means of peritrichous flagella. In tissue sections, it sometimes appears beaded or banded. This may represent transitional stages in the development of spores.8
The vegetative form of C. piliforme is very labile and is rapidly destroyed in tissues undergoing autolysis. Organisms are also destroyed by freezing, storage at low temperature, heating and centrifugation.8
Spores, on the other hand, survive for as long as a year in soiled bedding of mice,26 and resist repeated cycles of freezing and thawing, heat and certain disinfectants, such as 0,3 per cent sodium hypochlorite solution.7, 8
Epidemiology
Little is known about the epidemiology of Tyzzer’s disease in horses. The disease occurs sporadically in foals between 7 and 42 days of age.25 Seldom is more than one foal from a single farm affected at any one time.22 There appears to be no sex or breed predilection, and predisposing factors incriminated in rodents, such as cortisone administration, poor diet, poor sanitation and sulfonamide treatment,8 have not been identified in foals.22, 25, 30 Horses may be susceptible to at least two distinct strains.12 Although Tyzzer’s disease was diagnosed in two Arabian foals suffering from the combined immunodeficiency (CID) syndrome, the prevalence of the disease in foals with CID is not statistically different from that in foals without CID.25
The isolated and sporadic nature of the disease suggests that it is not highly contagious. Because the vegetative form of C. piliforme is labile and rapidly loses infectivity outside host cells, it is assumed that natural transmission occurs through the ingestion of spores from an environment contaminated by the faeces of infected animals. Many adult horses may be asymptomatic carriers of C. piliforme, and foals can become infected by organisms that are shed in the faeces of such horses.20 Nurse mares may be of particular importance in spreadingthe infection between different farms.20 As foals are naturally coprophagous during the first few days after birth, the most likely route of infection would seem to be per os.2 Rabbits, mice, rats, muskrats and cats, which are all susceptible to natural infections, may also act as reservoirs for environmental contamination.10 Interspecies transmission of Tyzzer’s disease under natural conditions has not been reported.31 Transplacental transmission of C. piliforme has been demonstrated in mice 31 but not in horses.
Pathogenesis
The pathogenesis of Tyzzer’s disease has not been elucidated, but is believed to involve a primary intestinal infection with spread of the organism to the liver and heart.31 Organisms invade hepatocytes, resulting in their death and the formation of necrotic foci. Occasionally, both acute and chronic liver lesions are present in foals, indicating successive cycles of hepatocellular necrosis after initial infection of the liver.27, 30 Foals may suffer from subclinical liver necrosis for some time before death ensues or clinical signs develop.30
Clinical signs
Foals are often found dead having shown no premonitory signs or prior history of illness.20, 25, 30 If clinical signs do occur they usually are of sudden onset and may include fever, listlessness, depression, anorexia, dehydration, and icterus.2, 10, 22, 25, 27 Tachypnoea, tachycardia and diarrhoea are less commonly manifested.4, 19, 24 Terminally affected animals may show convulsions or become comatose before death, which invariably ensues within 48 hours after the first...
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