[3][4] Occasionally, humans can become infected with A. equuli, more commonly as a result from destruction to the skin barrier, such as a horse bite.
[8] Actinobacillus equuli genome's size is approximately 1.7 GDa and contains 40% guanine and cytosine in its genetic makeup.
[9] A. equuli type strains include: ATCC 19392, CCUG 2041, GIP 103284, DSM 19655, JCM 2432, LMG 3736, and NCTC 8529.
[11] Another 16s rRNA study determined that an A. equuli type strain was 98.3% similar to A. lignieresii but are of different species.
[9] PCR testing that results in the presence of the RTX gene allows differentiation to be made between the two subspecies, as only A. equuli subsp.
A. equuli is found on a variety of mucosal surfaces in the horse; it is considered to be part of the normal flora and an opportunistic pathogen.
[15] Despite it being a component of the normal flora, a mean isolation frequency as low as 37% (n =174) in adult horses and foals was detected in one study.
[16] A. equuli does not have a preference for age, breed or gender,[17] suggesting that husbandry practices may play a role in isolation frequency.
[19] Less common forms of infection can manifest as cutaneous abscess, pharyngitis, guttural pouch eustachitis, pericarditis, mastitis, urethritis, and lymphadenitis.
[21][22] In addition to its mesophilic properties, A. equuli can grow at a pH of 6.0 to 8.4 which allows the organism to inhabit the intestine and survive in various structures such as the heart and adrenal gland.
Although facultatively anaerobic, A. equuli can survive in environments exposed to oxygen as it contains the enzyme cytochrome oxidase for use in the electron transport chain.
To add, A. equuli ferments D-glucose as indicated by a positive result for the oxidative-fermentation glucose test performed using Hugh-Leifson medium.
[22] A. equuli is negative for the methyl red test, which indicates that this microbe does not use the mixed acid fermentation pathway.
[3] However, when mucous membranes become compromised (wound penetration, ulcers/erosions) it allows for resident A. equuli to establish infection in the horses' internal environment.
Although the exact source of infection is not yet known for horses with valvular endocarditis, it has been suggested that this microbe may be distributed through the body by the migration of Strongylus vulgaris,[3] a common pasture parasite that inhabits the intestinal mucosa of horses and can migrate intravascularly to various organs of the body.
[30] Navel swabs and blood tests were performed on affected piglets and no A. equuli was cultured and bacteremia was not found.
[4] Acute signs: moderate to severe abdominal pain (colic), inappetence, intestinal stasis, lethargy.
[27] Chronic signs: weight loss Less frequently A. equuli has also been known to cause respiratory tract disease, abortion, haemorrhagic diatheses, pericarditis, periorchitis, enteritis, and peritonitis.
However, in some cases a chronic form of the disease can manifest in the kidneys, lungs, and joints resulting in lesions to the affected areas.
[7][13] Less commonly causes recumbency, hyperesthesia,[7] pneumonia, bronchitis, surface wound infections,[35] metritis, and septicemia.
[33] In adult horses, there has been a reported case of infection caused by A. equuli associated with gastrointestinal ulceration possibly due to the use of phenylbutazone for extended periods of time.
[32] In neonatal foals with sleepy foal syndrome, treatment failure resulting in fatal outcome has been recorded because of the severity of the condition and an inability of the neonate to successfully mount an immune response against the pathogen due to failure of passive transfer.
[7] Susceptibility testing showed that A. equuli was sensitive to ampicillin, tetracycline, trimethoprim, ceftiofur, neomycin and spectinomycin.
Clinically affected sows were determined by failure to rise when stimulated and temperature, and were additionally treated with antibiotics and anti-inflammatories.
[7] Some of the clinically affected sows who survived the initial infection were euthanized or culled due to wasting and poor-doing.
Prevention of A. equuli spread in swine operations with herd outbreak from the infected to the non-infected sows or newly introduced gilts was mitigated by the development of a herd-specific killed vaccine.
[5] The boy had visited a farm 3 days prior but denied coming into direct contact with horses or pigs.
[5] Furthermore, a blood sample from a 53 year old butcher with septicemia was found to contain A. equuli after the individual had lacerated his left thumb.
[42] Susceptibility testing performed found that A. equuli was sensitive to ampicillin, tetracycline, trimethorprin, ceftiofur, neomycin, cefotaxime, ceftazidime, imipenem, meropenem, ciprofloxacin, levofloxacin, piperacillin-tazobactam, tigecycline and spectinomycin.
[5][7] However, after conducting susceptibility testing, one study found A. equuli resistance to penicillin, ampicillin, streptomycin, neomycin, chloramphenicol, methicillin, and nalidixic acid.