Actinobacillosis refers to a group of diseases caused by gram-negative coccobacilli in the genus Actinobacillus. Although there are >22 different bacterial species in this genus, only 4 (A pleuropneumoniae, A suis, A equuli, and A lignieresii) are frequently associated with disease in animals.
A pleuropneumoniae causes contagious pleuropneumonia in pigs (see Pleuropneumonia in Pigs). Disease ranges from acute, severe fibrinous pleuropneumonia to subacute or chronic infection with pleuritis and pulmonary abscessation. Immune complexes formed as a result of host response may damage endothelial cells, resulting in vasculitis and thrombosis, with edema, necrosis, infarction, and hemorrhage. Infection is usually restricted to pigs <5 mo of age. A pleuropneumoniae may be normal mucosal flora in pigs, cattle, and sheep. Diagnosis is by culture of the organism from nasal swabs or lung tissue at necropsy. Molecular techniques such as PCR have also been developed to detect the presence of A pleuropneumoniae in tissue samples. Treatment involves use of antibiotics, including penicillin, tetracycline, spectinomycin, cephalosporins, or fluoroquinolones. Control focuses on good management combined with the use of vaccines or eradication of the infection from the herd by depopulation.
A suis is part of the normal flora of the oral cavity of pigs. It causes septicemia in young pigs and arthritis, pneumonia, and pericarditis in older pigs. It may also cause septicemia, arthritis, pneumonia, and purulent nephritis in neonatal and postnatal foals. Disease follows a break in the integrity of the oral mucosa or may be associated with immunosuppression. The organism is typically susceptible to sulfonamides and cephalosporins.
The natural host of A equuli is the horse, and infections are seen in both foals and adult horses. Disease in foals may manifest as diarrhea, followed by meningitis, pneumonia, purulent nephritis, or septic polyarthritis (sleepy foal disease or joint-ill). Infection may be acquired through a contaminated umbilicus, or by inhalation or ingestion. The incidence of foal infection is reduced with greater attention to sanitation in the birthing environment, and maternal antibodies in colostrum are often protective. Abortions, septicemia, nephritis, peritonitis, and endocarditis may result from A equuli infection in adult horses. In both foals and adult horses, several other bacteria can cause the same clinical disease syndromes as A equuli. Therefore, definitive diagnosis of A equuli relies on isolating the bacteria by culture. Infections may be treated with chloramphenicol, gentamicin, or third-generation cephalosporins, depending on the nature of the infection and the ability to achieve therapeutic concentrations at the site of infection. β-Lactam antibiotics and sulfonamides have been recommended, but widespread resistance to both of these antibiotics has been recently reported.
A arthritidis, previously classified as Bisgaard taxon 9, has been isolated from horses with arthritis and septicemia.
A lignieresii causes tumorous abscesses of the tongue, usually referred to as wooden tongue. It is seen primarily in cattle but also in sheep, horses, pigs, and dogs. It is a rare cause of disease in chickens. The organism may also cause pyogranulomatous lesions in soft tissues associated with the head, neck, limbs, and occasionally the lungs, pleura, udder, and subcutaneous tissue. A lignieresii is part of the normal mucosal flora of the upper GI tract and causes disease when it gains access to adjacent soft tissue via penetrating wounds. It causes localized infections and can spread via the lymphatics to other tissues. The primary lesion associated with A lignieresii infection in cattle is a very hard, diffusely swollen, painful tongue. This leads to excessive salivation, the inability to prehend food normally, and sometimes a visibly enlarged tongue that protrudes from the mouth. On palpation, the tongue will feel very hard. Diagnosis requires culture and biopsy of the lesion. Pus from an abscess crushed between 2 glass slides may show clublike spicules of calcium phosphate, giving the appearance of sulfur granules <1 mm diameter. There are no reliable serologic tests available for actinobacillosis, and the hematologic and clinical chemistry findings are generally normal. Gross pathology generally reveals a firm, pale tongue containing multifocal nodules. These nodules are often filled with thick yellow-white pus. Histologically, the primary lesion is a granulomatous abscess.
This form of actinobacillosis is found worldwide, but is sporadic and thus difficult to prevent. Herd outbreaks are possible and are generally associated with the consumption of coarse, abrasive feeds that encourage the formation of lesions in the mouth. Sodium iodide is the treatment of choice in ruminant actinobacillosis. IV sodium iodide (70 mg/kg of a 10–20% solution) is given once and then repeated 1–2 times at 7- to 10-day intervals. If clinical signs of iodine toxicity develop (including dandruff, diarrhea, anorexia, coughing, and excessive lacrimation), iodine administration should be discontinued. Clinical improvement is often seen within 48 hr of therapy, and treatment is usually successful when only the tongue is involved. Systemic antibacterial agents, such as ceftiofur, penicillin, ampicillin, florfenicol, and tetracyclines may be effective and are primarily recommended in severe cases of actinobacillosis or cases refractory to sodium iodide therapy. Surgical debulking of lesions, especially if they interfere with breathing, may be useful. This is particularly true when large granulomatous masses that do not respond to medical therapy are present. Prevention of actinobacillosis in ruminants primarily relies on avoidance of coarse, stemmy feedstuffs and pastures full of hard, penetrating plant awns (ie, foxtails or thistles).
A ureae has caused upper respiratory tract infections in humans and abortions in pigs. In addition, A actinoides has occasionally been associated with suppurative pneumonia in calves and seminal vesiculitis in bulls.
Last full review/revision July 2011 by Geof W. Smith, DVM, MS, PhD, DACVIM