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| − | <big><center>[[Infectious agents and parasites|'''BACK TO INFECTIOUS AGENTS AND PARASITES''']]</center></big>
| + | #REDIRECT[[:Category:Actinobacillus species]] |
| − | <big><center>[[Bacteria|'''BACK TO BACTERIA''']]</center></big>
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| − | * Cause [[Peritoneal cavity - inflammatory#In horses|peritonitis in horses]]
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| − | * ''A. pleuropneumoniae'' causes [[Bacterial infections#Actinobacillus pleuropneumoniae|pneumonia]] in pigs
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| − | * Cause [[General Pathology - Chronic Inflammation#Granulomatous Inflammation|granulomatous inflammation]].
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| − | ** E.g. ''Actinobacillus lignieresii'' causes wooden tongue in cattle -> [[Muscles - inflammatory#Wooden tongue|myositis]]
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| − | *''A. equuli'' in [[Joints - inflammatory#In Horses|arthritis of horses]]
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| − | ===Overview===
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| − | ===''Actinobacillus'' characteristics===
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| − | *Small Gram negative coccobacilli
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| − | *Oxidase negative
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| − | *Do not grow on MacConkey
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| − | ===''Actinobacillus lignieresii''===
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| − | *Commensal in the mouth of sheep and cattle
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| − | *Penetrates damaged mucosa to cause a granuloma, a condition known as Actinobacillosis
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| − | *Enodogenous, sporadic and chronic infection
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| − | *Lesions in the tongue, cheek, lips and sometimes in the lower gut and lungs from aspiration
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| − | *Often spreads from the site of infection to lymphatics
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| − | *Formation of fibrous tissue in the lesions lead to hardening of the tissue, hence the condition is known as 'wooden tongue' in cattle
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| − | *In sheep abscesses with thick walls are produced
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| − | *Feeding is impaired, causing loss of condition
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| − | *Recovery with antibiotics
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| − | ===''Actinobacillus equuli''===
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| − | *Commensal of the equine intestinal mucosa
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| − | *Infection at birth causes severe enteritis and septicaemia within 24 hours, known as sleepy foal disease
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| − | *In foals that survive neonatal infection the condition progresses to cause joint infections and purulent nephritis
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| − | *RTX group cytotoxin present
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| − | ===''Actinobacillus suis''===
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| − | *Fatal septicaemia in pigs 1-8 weeks old
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| − | *Causes abscesses in joints and lungs of older pigs
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| − | *Carried in the nasopharynx of pigs and nose of horses
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| − | *Carriage may confer immunity to the more severe pleuropneumonia
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| − | ===''Actinobacillus pleuropneumoniae''===
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| − | *Contagious porcine pleuropneumonia
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| − | *Endemic in UK
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| − | *Most strains are NAD-dependent (grow on Heated Blood agar)
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| − | *Positive CAMP reaction
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| − | *12 serotypes causing the same disease
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| − | *Different serotypes in different regions, with serotypes 3,6 and 8 the most common in the UK
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| − | *Acute disease in susceptible herds with high morbidity and mortality
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| − | *Carrier herds have some immunity, protecting from acute disease, where lesions are often subclinical, and deaths sporadic
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| − | *Lung scarring and pleural adhesions in many recovered animals
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| − | *Solid immunity develops in recovered animals to all serotypes
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| − | *The disease is spread between herds by carrier pigs
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| − | *The bacteria on the palatine tonsil are undetected by serologucal tests and swabbing, and can therefore cause an outbreak in naive pigs
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| − | *Killed and bacterin vaccines are available
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| − | *Produce one or two RTX group cytolytic toxins
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| − | *RTX toxins:
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| − | **'Repeat in ToXin' - named because there are several peptide repeats within the molecules
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| − | **Produced by various Gram-negative bacteria, including [[Escherichia coli|''E. coli'']], [[Bordetella|''Bordetella sp.'']] and [[''Pasteurella haemolytica#Pasterurella''|''Pasteurella haemolytica'']]
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| − | **Possess four contiguous genes, C, A, B and D
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| − | **A is the structural gene; B and D are required for secretion; C is required for post-translational activation of the gene product of A to produce a functional product
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| − | **ApxI is a strong haemolysin with cytolytic activity
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| − | **ApxII is a weak haemolysin
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| − | **ApxIII is a cytotoxin
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| − | **Different ''Actinobacillus pleuropneumonia'' serotypes secrete a particular combination of toxins; American serotypes secrete ApxI and II; European serotypes secrete ApxII and III
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