Actinobacillus equuli

Last updated

Actinobacillus equuli
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Bacteria
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Pasteurellales
Family: Pasteurellaceae
Genus: Actinobacillus
Species:
A. equuli
Binomial name
Actinobacillus equuli
(van Straaten, 1918) Haupt, 1934

Actinobacillus equuli is a gram-negative, non-motile rod bacteria from the family Pasteurellaceae. [1]

Contents

A. equuli is classified as a bio-containment level 2 organism under the U.S. Public Health Service Guidelines. [2] Biochemical differentiation tests with positive results are: catalase, urease and oxidase tests. Actinobacillus equuli subspecies equuli is not hemolytic and is found in equine and porcine hosts. Another subspecies exists and is classified as Actinobacillus equuli subsp. haemolyticus which is positive for hemolysis and is found in horses and very rarely in rabbits. [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. [5]

A. equuli can commonly be isolated from the upper respiratory tract and oral cavity of adult healthy horses and can be important for diseases of foals, adult horses and pigs. [6] It is a commensal bacteria unless it multiplies to overwhelming numbers, at which point it will cause disease. Specifically, A. equuli is known to cause neonatal sepsis in foals, known as Sleepy Foal Disease. Less commonly, A. equuli will cause disease in adult horses, resulting in respiratory infections. [3] A. equuli also has the capability to cause kidney damage, arthritis and septicemia in affected pigs. [7] The subspecies A. equuli subsp. haemolyticus results in similar pathogenesis as A. equuli subsp. equuli in horses. Due to these diseases and conditions, A. equuli can result in great economic losses especially in the equine industry.

Taxonomy and genome

Taxonomy

It was previously thought that this bacteria was limited to the species level, however it is now divided into two subspecies of Actinobacillusequuli which include: A.equuli subsp. equuli, and A.equuli subsp. haemolyticus. [1] [8] Differentiation between these two subspecies can be done via biochemical tests including a CAMP test, and haemolytic properties. A.equuli subsp. equuli is non-haemolytic and CAMP negative, while A. equuli subsp. haemolyticus is haemolytic and CAMP positive. [8]

Actinobacillusequuli Subspecies Differentiation Summary
SubspeciesBiochemical testResult
equuliCAMP

Haemolytic

(−)

(−)

haemolyticusCAMP

Haemolytic

(+)

(+)

Isolation of the subspecies equuli have been found in both horses and pigs, but only subspecies haemolyticus has been isolated from horses. [8]

Genome

Actinobacillusequuli 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. [10] The 16S rRNA gene for A.equuli is AF381186, this helps classification of the bacteria to the species level but not to the subspecies level. [10] This information helped determine that this species is closely related to Actinobacillussuis and Actinobacillushominus. [11] Another 16s rRNA study determined that an A. equuli type strain was 98.3% similar to A. lignieresii but are of different species. [12]

Isolation of the subspecies equuli in the UK and Australia determined that it contained strains NCTC 8529T, and I 5445/4. A.equuli subspecies haemolyticus contain strains: T 355/87, F 92, Ac 7 F 119, F 154T, and F 490. [9] PCR testing that results in the presence of the RTX gene allows differentiation to be made between the two subspecies, as only A. equulisubsp. equuli contains the RTX gene. [13]

To differentiate similar strains of A. equuli from other genera originally thought to be A. equuli, ribotyping can be performed. The characteristic of being L-arabinose positive was thought to be an important taxonomic characteristic to classify A.equuli strains from others. [14] Many different strains of A.equuli were determined through ribotyping, indicating that this species is diverse.

Epidemiology

Horses

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, an mean isolation frequency as low as 37% (n =174) in adult horses and foals was detected in one study. [16] However, the isolation frequency varied from 12 to 88% between farms. [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. [16] An important aspect of the isolation frequency is that a horse or foal will not be culture positive every time it is swabbed, making it hard to determine the correct isolation frequency.

A. equuli is the causative agent in sleepy foal syndrome, which has been documented throughout the world. [4] It is important to note that A. equuli does not only cause sleepy foal syndrome in foals, it is also a causative agent of pneumonia, muscular degeneration and jaundice in foals. On necropsy, foals were found to have the highest distribution of the bacteria in their synovial fluid, followed by the thoracic fluid and the liver. [9] Important risk factors for foals acquiring an infection with A. equuli include failure of passive transfer, unsanitary foaling environments, and the presence of immunosuppressive conditions. [9] Foals can become infected in-utero, during parturition or shortly after birth. [18] Adults horses have similar diseases associated with A. equuli infections, including septicemia, respiratory and bone/joint diseases. [19] Less common forms of infection can manifest as cutaneous abscess, pharyngitis, guttural pouch eustachitis, pericarditis, mastitis, urethritis, and lymphadenitis. [19] Risk factors for developing infections in adult horses differs from that of foals, these factors include: stress, concurrent bacterial and/or viral infections, and discontinuities in the mucosa membranes allowing the bacteria entry into the body's internal compartment. [19]

Swine

Infections in swine are more common in European countries compared to the North American Countries. [13] Infections in the United States are extremely rare with only 2 cases reported prior to 2008 and there was a 30-year period leading up to 2008 in which there were no cases documented. [13] There has only ever been one case reported in Manitoba, Canada in 2010. [7] However, infections may have occurred but were unreported. An infection with A. equuli in swine commonly yields septicemia, metritis, and can result in abortion. It was once thought pigs acquired the infection directly from horses, but there has been reports of swine developing infections on farms that housed horses prior to housing swine, and there has also been one case in which the swine infected had no association with horses. [7] Owing to the fact that the exact source of the infection in swine is not known, the risk factors are also relativity unknown. [7]

Microbiology

Morphology and culture growth

Actinobacillus equuli are rod-shaped bacteria that measure an average of 1 μm in length. [20] According to a study of the complete genome of A. equuli, this microbe can be cultured on blood agar at an optimal temperature of 37 °C, but is able to grow in temperatures ranging from 20 °C to 44 °C. [21] Two studies noted that the colonies of A. equuli are circular, smooth in texture and produce a slimy, viscous material that gives the colonies a gelatinous and glossy appearance. [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. [3] [23] A. equuli is a facultative anaerobe and is moderately fastidious, therefore culture growth in the laboratory may be challenging.

Biochemical tests

Beta hemolysis and gamma hemolysis on sheep blood agar by HansN / CC-BY-SA-3.0 Colonies surrounded by a transparent zone (black in this image) indicate b-hemolysis and represent inoculation with A. equuli subsp. haemolyticus. Absence of a coloured or transparent zone is indicative of g-hemolysis which represents the inability to lyse red blood cells as would be the result of inoculation with A. equuli subsp. equuli. Beta hemolysis and gamma hemolysis on sheep blood agar.jpg
Beta hemolysis and gamma hemolysis on sheep blood agar by HansN / CC-BY-SA-3.0 Colonies surrounded by a transparent zone (black in this image) indicate β-hemolysis and represent inoculation with A. equuli subsp. haemolyticus. Absence of a coloured or transparent zone is indicative of γ-hemolysis which represents the inability to lyse red blood cells as would be the result of inoculation with A. equuli subsp. equuli.

As part of the genus Actinobacillus, Actinobacillus equuli is gram negative. [1] A. equuli displays negative results after inoculation into motility agar indicating a lack of motility. [22] A. equuli is equipped with catalase and urease enzymes and therefore yield positive results for these tests. 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. [3] [24] Differentiation between A. equuli subsp. equuli and A. equuli subsp. haemolyticus can be made using sheep's blood agar or the CAMP test upon the absence or presence of beta-haemolysis, respectively. [3] [25]

A. equuli has varying results for sugar fermentation. A. equuli subsp. equuli is not capable of fermenting cellobiose, whereas the opposite is true for A. equuli subsp. haemolyticus, indicated by a negative and positive result for the cellobiose fermentation test, respectively. However, both subspecies are positive for lactose fermentation, [22] which is indicated by using phenol red lactose broth. Gram negative lactose fermenters typically display positive results on MacConkey agar, however, a study on equine actinobacilli resulted in the lack of growth on MacConkey agar, [22] which may suggest that A. equuli is too fastidious to grow on this medium. 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] [26] Both subspecies yield a positive result for both raffinose and D-galactose fermentation [3] [22] and displays mixed results for D-mannitol fermentation, where only some biovars of A. equuli subsp. haemolyticus displayed a negative result while others were positive for D-mannitol fermentation. [22]

A. equuli is negative for the methyl red test, which indicates that this microbe does not use the mixed acid fermentation pathway. [24] A. equuli also displays a negative Voges-Proskauer test because A. equuli does not use the 2,3-butanediol fermentation pathway resulting in the absence of acetoin production. [20] [24] As demonstrated by a negative Simmon's citrate test result, A. equuli is not able to use citrate as its sole carbon source for energy. [22]

Biochemical Properties of Actinobacillus equuli
Biochemical TestTest Result
Gram Stain-
Motility Agar-
Catalase+
Urease+
Oxidase+
Sheep's Blood AgarA. equuli subsp. equuli: γ-haemolysis

A. equuli subsp. haemolyticus: β-haemolysis

CAMPA. equuli subsp. equuli: -

A. equuli subsp. haemolyticus: +

Cellobiose FermentationA. equuli subsp. equuli: -

A. equuli subsp. haemolyticus: +

Lactose Fermentation+
MacConkey AgarNo growth
Oxidative/Fermentation Glucose+, absent gas production
Raffinose Fermentation+
D-galactose Fermentation+
D-mannitol FermentationA. equuli subsp. equuli: +

A. equuli subsp. haemolyticus: +/-

Methyl Red-
Voges-Proskauer-
Simmon's Citrate-

Pathogenesis

Horses

The major host for A. equuli is horses and under physiological conditions, A. equuli is part of horses' mucosal microbiota and does not normally cause clinical symptoms and/or lesions. [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. A. equuli's penetration into the body's internal environment has been reported to cause septicemia in newborn foals (also called sleepy foal disease) and localized infections in adult horses or in more severe cases acute or chronic peritonitis. [27] It is unknown at this time if there are certain strains of A. equuli that have a greater virulence for adult horses and/or foals.

One study emphasized the contribution of A. equuli to the development of equine valvular endocarditis, where an isolate grown from the bacterial samples of an vegetative equine heart showed stunning resemblance with the phenotypical characteristics of a pure culture of A. equuli subsp. equuli. 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. [28]

The pathogenicity and virulence factors of A. equuli are not well known, but following PCR analysis it has been determined that both subspecies (equuli and haemolyticus) have the RTX toxin gene which is capable of causing host species specific toxicity. [29]

Swine

A. equuli has been found occasionally to cause disease in sows and their piglets however, like in horses, the pathogenicity is not well known. [7] Unlike horses, PCR analysis did not find the aqxA gene and therefore concluded that only subspecies equuli and not subspecies haemolyticus causes disease in pigs. [7] [13] [30] [31] In sows, A. equuli is thought to cause disease as both a primary and a secondary pathogen. [7] [13] In piglets, since they usually show clinical signs within hours up to 4 days after parturition, it is hypothesized that the piglets are infected in utero. [7] [30] Nasal, fecal and vaginal swabs of infected sows were performed and pure cultures of A. equuli were only found in the vaginal swabs, supporting the hypothesis of in utero infection. [30] Navel swabs and blood tests were performed on affected piglets and no A. equuli was cultured and bacteremia was not found. [30] The pathogenicity causing the variation in clinical manifestations between cases of swine affected with A. equuli is not well understood.

The virulence factors of A. equuli in swine is also not well known. [30]

Rabbits

There has been one case that found a rabbit presenting for necropsy, had a secondary infection caused by A. equuli. [4] The rabbit was diagnosed with acute hepatitis characteristic of Tyzzer's disease caused by Clostridium piliforme . However, samples of the lungs and liver of the rabbit also resulted in the culture of A. equuli subspecies haemolyticus. A. equuli was determined to be a secondary opportunistic invader in this rabbit. [4]

Clinical signs

Horses

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. [32]

Sleepy foal syndrome: The acute form of sleepy foal syndrome presents as sepsis that can lead to death. Acutely infected foals appear dull, can have pneumonia and are neutropenic. 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. [21] [33]

Necropsies of horses infected with A. equuli showed consistent diffuse, bilateral, multifocal renal infarcts affecting the renal cortices. Fibrinous exudate and pulmonary edema was also a common finding. [34]

Swine

Acute Signs in sows: Most commonly lethargy, inappetence, sudden death. [7] [13] Less commonly causes recumbency, hyperesthesia, [7] pneumonia, bronchitis, surface wound infections, [35] metritis, and septicemia. [13]

Acute signs in piglets: lethargy, +/- pyrexia, severe arthritis (causing them to be non-weight bearing on that limb), [7] [30] encephalitis (although only neurological signs were lateral recumbency), septicemia and sudden death. [7] [30]

Chronic signs of piglets and sows: Poor doing and weight loss leading to culling or euthanasia [7]

Sow Necropsies: Sows most commonly had dehydration, subcutaneous hemorrhage, embolic infarcts consisting of neutrophils and basophilic bacilli in the renal cortex. [7] [13] Embolic infarcts were also found in liver, lungs spleen, adrenal gland. [7] [13] Sows were concluded to have died of renal infarcts.

Gilt Necropsy: A gilt was found to have liquefactive necrosis in the epicardium of both auricles of the heart, valvular endocarditis of both mitral and tricuspid valves and thrombus of the right atrial wall. [13] She had recently aborted her pregnancy and within the amniotic sacs of the aborted fetuses, a brown serous fluid was found. The gilt was concluded to have died of A. equuli causing valvular endocarditis and metritis with secondary septicemia. [13]

Piglet Necropsies (6 hours to 4 days old belonging to infected sows): Piglets had petechial hemorrhage and multiple bacterial emboli in the renal cortex +/- multifocal purulent nephritis. [7] [30] Piglets were also found to have severe diffuse fibrinopurulent arthritis in one or more joints. [7] [30] Some piglets have additionally had a mild purulent encephalitis and perivasculitis of the vessels in the brain. [30]

Prevention and treatment

Horses

A. equuli causing sleepy foal syndrome in neonatal horses is most often attributed to the mother, as A. equuli is part of the normal microflora of the mare which makes it difficult to prevent exposure of the foal to A. equuli. [36] [37] In a majority of reported cases, sleepy foal syndrome is more than likely a direct result of failure of passive transfer thus, it is important that neonatal foals receive colostrum to reduce the incidence of the disease caused by A. equuli. [38] Reducing environmental contamination when the foal is born has also shown to be effective at reducing the incidence of disease. [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. Ulceration of the GI mucosa can allow A. equuli to set up an opportunistic infection. Limiting the duration or dose of phenylbutazone could reduce the chance of ulceration and thus an infection. [27] Preventative treatments can also include minimizing the risk of infection with other parasites or pathogens that could weaken the immune system or cause physical damage that allows A. equuli to set up an infection. Some studies have found that A. equuli infections have been established after exposure with Strongylus vulgaris as the migrating larvae can transport A. equuli to various parts of the body resulting in infection. [27] Overall, ensuring the health of the horse is maintained has shown to be the best strategy to reduce infection with A. equuli.

Treatment and supportive care of a horses infected with A. equuli has been shown to be very effective when detected early, resulting in low incidence of death associated with infection. [39] One study involving 51 horses with peritonitis associated with A. equuli, found treatment with procaine penicillin or procaine penicillin and gentamicin sulphate to be effective. However, antimicrobial sensitivity testing of 14 cultures showed 1 culture to be resistant to penicillin, 1 resistant to trimethoprim-sulphadimidine and 1 resistant to a combination of penicillin and trimethoprim-sulphadimidine. Thus the study recommended the treatment with procaine penicillin and gentamicin sulphate in cases of antimicrobial resistance. [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. [33] In other cases, treatment of sleepy foal syndrome included antibiotic treatment with amoxicillin-clavulanic acid and amikacin sulfate along with fluid therapy. [40]

Swine

During the outbreak at the swine farm in Canada, both preventative antibiotic therapy in the water and feed of the entire herd and individual therapy of the clinically affected sows was administered. [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. Sow mortality ranged from an average of 8 deaths per day at the beginning of the outbreak, to 2 deaths/day by day 50 of the infection.

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. [7] [30] [31]

Zoonotic potential

A. equuli commonly affects equine hosts. Occasionally, A. equuli has been found to cause disease in sows and their newborn piglets. [7] [30] [13] There was one case describing a rabbit who was infected with A. equuli. [4]

Humans have also been found to have infections caused by A. equuli after being bit by a horse. One case study described a stable hand who had been bitten by a horse 12 hours prior, presenting to the hospital with a red and swollen laceration on the dorsal side of his hand. A. equuli-like species was cultured from the wound and was determined to cause the infection along with A. lignieresii. [41] Additionally, there has been one case of a 13-year-old boy who developed meningitis and sepsis from A. equuli. [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. Prior to the discovery, A. equuli had never been recorded in the blood of a human with septicemia. [42]

Susceptibility and resistance

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. The study also found susceptibility of A. equuli to gentamicin, tetracycline, nitrofurantoin, polymyxin B, sulphonamides, trimethoprim with sulphonamides, carbenicillin, cephalotin, and amoxycillin with clavulanic acid. The study did note it had differing results in susceptibility tests than other studies had reported, which could be a result of regional or strain differences or differences in the methods of the susceptibility testing between studies. [43] Additional reports have found A. equuli resistance to oxacillin and trimethoprim-sulphadimidine along with developed resistance to tetracycline after one month of use in sows. [7] [32] [44]

Related Research Articles

Streptococcus bovis is a species of Gram-positive bacteria that in humans is associated with urinary tract infections, endocarditis, sepsis, and colorectal cancer. S. gallolyticus is commonly found in the alimentary tract of cattle, sheep, and other ruminants, and may cause ruminal acidosis or feedlot bloat. It is also associated with spontaneous bacterial peritonitis, a frequent complication occurring in patients affected by cirrhosis. Equivalence with Streptococcus equinus has been contested.

Betaarterivirus suid 1, commonly Porcine reproductive and respiratory syndrome virus (PRRSV), is a virus that causes a disease of pigs, called porcine reproductive and respiratory syndrome (PRRS), also known as blue-ear pig disease. This economically important, panzootic disease causes reproductive failure in breeding stock and respiratory tract illness in young pigs.

<i>Campylobacter fetus</i> Species of bacterium

Campylobacter fetus is a rod-shaped, gram-negative species of bacteria within the genus Campylobacter of phylum Pseudomonadota. Identification of C. fetus species in infected animals or people is routinely performed by culture on blood or cefoperazone deoxycholate agar. Subspecies of C. fetus commonly causes reproductive disease in ruminants and gastrointestinal disease in humans. Transmission of C. fetus subspecies venerealis occurs mainly through venereal contact while transmission of C. fetus subspecies fetus occurs mainly through ingestion of bacteria in a contaminated environment. Infertility in cattle and abortion in sheep are common outcomes of infection associated with C. fetus subspecies venerealis and C. fetus subspecies fetus, respectively. Disease in humans occurs through zoonotic transmission of C. fetus mainly via ingestion of contaminated food or water sources. C. fetus can be diagnosed with polymerase chain reaction assays, enzyme linked immunosorbent assays and vaginal mucus agglutination testing. As vaccines are typically not efficient in preventing future spread, infected bulls are often culled. Human infections may be treated with erythromycin as antimicrobial resistance has been emerging for the fluoroquinolones.

SMEDI is a reproductive disease of swine caused by Porcine parvovirus (PPV) and Porcine enterovirus. The term SMEDI usually indicates Porcine enterovirus, but it also can indicate Porcine parvovirus, which is a more important cause of the syndrome. SMEDI also causes abortion, neonatal death, and decreased male fertility.

Porcine parvovirus (PPV), a virus in the species Ungulate protoparvovirus 1 of genus Protoparvovirus in the virus family Parvoviridae, causes reproductive failure of swine characterized by embryonic and fetal infection and death, usually in the absence of outward maternal clinical signs. The disease develops mainly when seronegative dams are exposed oronasally to the virus anytime during about the first half of gestation, and conceptuses are subsequently infected transplacentally before they become immunocompetent. There is no definitive evidence that infection of swine other than during gestation is of any clinical or economic significance. The virus is ubiquitous among swine throughout the world and is enzootic in most herds that have been tested. Diagnostic surveys have indicated that PPV is the major infectious cause of embryonic and fetal death. In addition to its direct causal role in reproductive failure, PPV can potentiate the effects of porcine circovirus type II (PCV2) infection in the clinical course of postweaning multisystemic wasting syndrome (PMWS).

Aujeszky's disease, usually called pseudorabies in the United States, is a viral disease in swine that is endemic in most parts of the world. It is caused by Suid herpesvirus 1 (SuHV-1). Aujeszky's disease is considered to be the most economically important viral disease of swine in areas where classical swine fever has been eradicated. Other mammals, such as cattle, sheep, goats, cats, dogs, and raccoons, are also susceptible. The disease is usually fatal in these animal species.

Equid alphaherpesvirus 1, formerly Equine herpesvirus 1 (EHV-1), is a virus of the family Herpesviridae that causes abortion, respiratory disease and occasionally neonatal mortality in horses. Initial spread of EHV-1 by a newly introduced horse through direct and indirect contact can lead to abortion and perinatal infection in up to 70 percent of a previously unexposed herd. Abortion usually occurs in the last four months of gestation, two to four weeks after infection of the mare. Perinatal infection can lead to pneumonia and death. Encephalitis can occur in affected animals, leading to ataxia, paralysis, and death. There is a vaccine available, however its efficacy is questionable. The virus varies in severity from sub-clinical to very severe. Most horses have been infected with EHV-1, but the virus can become latent and persist without ever causing signs of infection. In 2006, an outbreak of EHV-1 among stables in Florida resulted in the institution of quarantine measures. The outbreak was determined to have originated in horses imported from Europe via New York, before being shipped to Florida.

<span class="mw-page-title-main">Equine protozoal myeloencephalitis</span> Central nervous system disease of horses

Equine protozoal myeloencephalitis (EPM) is a disease that affects the central nervous system of horses. It is caused by a protozoal infection that is brought about by the apicomplexan parasites Sarcocystis neurona or Neospora hughesi. Most cases are caused by S. neurona. The lifecycle and transmission of N. hughesi is not well understood. The parasites create lesions in both the brain and spinal cord of the affected horses leading to neurological issues. Most horses infected with S. neurona do not exhibit neurological symptoms consistent with EPM.

<span class="mw-page-title-main">Florfenicol</span> Chemical compound

Florfenicol is a fluorinated synthetic analog of thiamphenicol, mainly used as a antibiotic in veterinary medicine.

Equine viral arteritis (EVA) is a disease of horses caused by a virus of the species Alphaarterivirus equid, an RNA virus. It is the only species in the genus Alphaarterivirus, and that is the only genus in the Equarterivirinae subfamily. The virus which causes EVA was first isolated in 1953, but the disease has afflicted equine animals worldwide for centuries. It has been more common in some breeds of horses in the United States, but there is no breed "immunity". In the UK, it is a notifiable disease. There is no known human hazard.

Taylorella equigenitalis is a Gram-negative, non-motile, microaerophilic bacterium of the genus Taylorella, and the causative agent of contagious equine metritis (CEM) in horses. Phylogeny of T. equigenitalis includes being part of the Alcaligenaceae family.

<i>Rhodococcus equi</i> Species of bacterium

Rhodococcus equi is a Gram-positive coccobacillus bacterium. The organism is commonly found in dry and dusty soil and can be important for diseases of domesticated animals. The frequency of infection can reach near 60%. R. equi is an important pathogen causing pneumonia in foals. Since 2008, R. equi has been known to infect wild boar and domestic pigs. R. equi can infect immunocompromised people, such as HIV-AIDS patients or organ transplant recipients. Rhodococcus equi infection in these populations resemble the clinical and pathological signs of advanced pulmonary tuberculosis. This organism is a facultative intracellular mycobacterial pathogen.

Actinobacillosis is a zoonotic disease caused by Actinobacillus. It is more commonly associated with animals than with humans.

<i>Streptococcus dysgalactiae</i> Species of bacterium

Streptococcus dysgalactiae is a gram positive, beta-haemolytic, coccal bacterium belonging to the family Streptococcaceae. It is capable of infecting both humans and animals, but is most frequently encountered as a commensal of the alimentary tract, genital tract, or less commonly, as a part of the skin flora. The clinical manifestations in human disease range from superficial skin-infections and tonsillitis, to severe necrotising fasciitis and bacteraemia. The incidence of invasive disease has been reported to be rising. Several different animal species are susceptible to infection by S. dysgalactiae, but bovine mastitis and infectious arthritis in lambs have been most frequently reported.

<i>Streptococcus zooepidemicus</i> Species of bacterium

Streptococcus zooepidemicus is a Lancefield group C streptococcus that was first isolated in 1934 by P. R. Edwards, and named Animal pyogens A. It is a mucosal commensal and opportunistic pathogen that infects several animals and humans, but most commonly isolated from the uterus of mares. It is a subspecies of Streptococcus equi, a contagious upper respiratory tract infection of horses, and shares greater than 98% DNA homology, as well as many of the same virulence factors.

Clostridium perfringens beta toxin is one of the four major lethal protein toxins produced by Clostridium perfringens Type B and Type C strains. It is a necrotizing agent and it induces hypertension by release of catecholamine. It has been shown to cause necrotic enteritis in mammals and induces necrotizing intestinal lesions in the rabbit ileal loop model. C. perfringens beta toxin is susceptible to breakdown by proteolytic enzymes, particularly trypsin. Beta toxin is therefore highly lethal to infant mammals because of trypsin inhibitors present in the colostrum.

Porcine epidemic diarrhea is a condition caused by the porcine epidemic diarrhea virus that leads to severe gastrointestinal disease in pigs.

<i>Staphylococcus hyicus</i> Species of bacterium

Staphylococcus hyicus is a Gram-positive, facultatively anaerobic bacterium in the genus Staphylococcus. It consists of clustered cocci and forms white circular colonies when grown on blood agar. S. hyicus is a known animal pathogen. It causes disease in poultry, cattle, horses, and pigs. Most notably, it is the agent that causes porcine exudative epidermitis, also known as greasy pig disease, in piglets. S. hyicus is generally considered to not be zoonotic, however it has been shown to be able to cause bacteremia and sepsis in humans.

<i>Neorickettsia risticii</i> Species of bacterium

Neorickettsia risticii, formerly Ehrlichia risticii, is an obligate intracellular gram negative bacteria that typically lives as an endosymbiont in parasitic flatworms, specifically flukes. N. risticii is the known causative agent of equine neorickettsiosis, which gets its name from its discovery near the Potomac River in Maryland and Virginia. N. risticii was first recovered from horses in this region in 1984 but was not recognized as the causative agent of PHF until 1979. Potomac horse fever is currently endemic in the United States but has also been reported with lower frequency in other regions, including Canada, Brazil, Uruguay, and Europe. PHF is a condition that is clinically important for horses since it can cause serious signs such as fever, diarrhea, colic, and laminitis. PHF has a fatality rate of approximately 30%, making this condition one of the concerns for horse owners in endemic regions N. risticii is typically acquired in the middle to late summer near freshwater streams or rivers, as well as on irrigated pastures. This is a seasonal infection because it relies on the ingestion of an arthropod vector, which is more commonly found on pasture in the summer months. Although N. risticii is a well known causative agent for PHF in horses, it may act as a potential pathogen in cats and dogs as well. Not only has N. risticii been successfully cultured from monocytes of dogs and cats, but cats have become clinically ill after experimental infection with the bacteria. In addition, N. risticii has been isolated and cultured from human histiocytic lymphoma cells.

Actinobacillus pleuropneumoniae, is a Gram-negative, facultative anaerobic, respiratory pathogen found in pigs. It was first reported in 1957, and was formally declared to be the causative agent of porcine pleuropneumonia in 1964. It was reclassified in 1983 after DNA studies showed it was more closely related to A. lignieresii.

References

  1. 1 2 3 Berthoud, H.; Frey, J.; Kuhnert, P. (2002-06-20). "Characterization of Aqx and its operon: the hemolytic RTX determinant of Actinobacillus equuli". Veterinary Microbiology. 87 (2): 159–174. doi:10.1016/S0378-1135(02)00048-2. ISSN   0378-1135. PMID   12034544.
  2. ↑ "Actinobacillus equuli subsp. equuli (van Straaten) Haupt ATCC ® 19". www.atcc.org. Retrieved 2020-11-04.
  3. 1 2 3 4 5 6 7 8 Aalbæk, B.; Østergaard, S.; Buhl, R.; Jensen, H.E.; Christensen, H.; Bigaard, M. (2007). "Actinobacillus equuli subsp. equuli associated with equine valvular endocarditis". APMIS. 115 (12): 1437–1442. doi:10.1111/j.1600-0463.2007.00768.x. PMID   18184417. S2CID   41369747 – via Wiley Online Library.
  4. 1 2 3 4 5 Moyaert, H.; Decostere, A.; Baele, M.; Hermans, K.; Tavernier, P.; Chiers, K.; Haesebrouck, F. (2007-09-20). "An unusual Actinobacillus equuli strain isolated from a rabbit with Tyzzer's disease". Veterinary Microbiology. 124 (1): 184–186. doi:10.1016/j.vetmic.2007.04.013. hdl: 1854/LU-416303 . ISSN   0378-1135. PMID   17482388.
  5. 1 2 3 4 Montagnani, Carlotta; Pecile, Patrizia; Moriondo, Maria; Petricci, Patrizia; Becciani, Sabrina; Chiappini, Elena; Indolfi, Giuseppe; Rossolini, Gian Maria; Azzari, Chiara; de Martino, Maurizio; Galli, Luisa (June 2015). Patel, R. (ed.). "First Human Case of Meningitis and Sepsis in a Child Caused by Actinobacillus suis or Actinobacillus equuli". Journal of Clinical Microbiology. 53 (6): 1990–1992. doi:10.1128/JCM.00339-15. ISSN   0095-1137. PMC   4432038 . PMID   25878346.
  6. ↑ Rycroft, A. N.; Garside, L. H. (January 2000). "Actinobacillus species and their role in animal disease". Veterinary Journal. 159 (1): 18–36. doi:10.1053/tvjl.1999.0403. ISSN   1090-0233. PMID   10640409.
  7. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 Thompson, Amy B.; Postey, Rosemary C.; Snider, Tim; Pasma, Tim (November 2010). "Actinobacillus equuli as a primary pathogen in breeding sows and piglets". The Canadian Veterinary Journal. 51 (11): 1223–1225. ISSN   0008-5286. PMC   2957028 . PMID   21286321.
  8. 1 2 3 Henrik Christensen; Magne Bisgaard; John Elmerdahl Olsen (2002-09-01). "Reclassification of equine isolates previously reported as Actinobacillus equuli, variants of A. equuli, Actinobacillus suis or Bisgaard taxon 11 and proposal of A. equuli subsp. equuli subsp. nov. and A. equuli subsp. haemolyticus subsp. nov". International Journal of Systematic and Evolutionary Microbiology. 52 (5): 1569–1576. doi: 10.1099/00207713-52-5-1569 . ISSN   1466-5026. PMID   12361259.
  9. 1 2 3 4 Kamada M., et al. “Isolation of Actinobacillus Equuli from Neonatal Foals with Death in Colostrum-Deficiency or Failure of Maternal Immunity Transfer.” Bulletin of Equine Research Institute, 1985, pp. 38–42.
  10. 1 2 "Species: Actinobacillus equuli". lpsn.dsmz.de. Retrieved 2020-10-28.
  11. ↑ Huang, Barbara F; Kropinski, Andrew M; Bujold, Adina R; MacInnes, Janet I (2015-06-07). "Complete genome sequence of Actinobacillus equuli subspecies equuli ATCC 19392T". Standards in Genomic Sciences. 10 (1): 32. doi: 10.1186/s40793-015-0009-x . ISSN   1944-3277. PMC   4511653 . PMID   26203343.
  12. ↑ Nørskov-Lauritsen, Niels; Christensen, Henrik; Okkels, Henrik; Kilian, Mogens; Bruun, Brita (2004-05-01). "Delineation of the genus Actinobacillus by comparison of partial infB sequences" (PDF). International Journal of Systematic and Evolutionary Microbiology. 54 (3): 635–644. doi: 10.1099/ijs.0.02785-0 . ISSN   1466-5026. PMID   15143001.
  13. 1 2 3 4 5 6 7 8 9 10 11 12 Ramos-Vara, J. A.; Wu, C. C.; Mitsui, I.; Lin, T. L.; Miller, M. A. (2008-07-01). "Metritis, Valvular Endocarditis, and Septicemia by Actinobacillus equuli in a Gilt in the United States". Veterinary Pathology. 45 (4): 495–499. doi:10.1354/vp.45-4-495. PMID   18587096. S2CID   207268778.
  14. ↑ Blackall, PJ; Christensen, JP; Bisgaard, M (June 1998). "Diversity among isolates of Actinobacillus equuli and related organisms as revealed by ribotyping". Australian Veterinary Journal. 76 (6): 423–425. doi:10.1111/j.1751-0813.1998.tb12394.x. PMID   9673769 . Retrieved November 30, 2020.
  15. ↑ Donahue, James M.; Sells, Stephen F.; Bolin, David C. (2006-08-01). "Classification of Actinobacillus spp isolates from horses involved in mare reproductive loss syndrome". American Journal of Veterinary Research. 67 (8): 1426–1432. doi: 10.2460/ajvr.67.8.1426 . ISSN   0002-9645. PMID   16881857.
  16. 1 2 3 Sternberg, Susanna (1998-01-16). "Isolation of Actinobacillus equuli from the oral cavity of healthy horses and comparison of isolates by restriction enzyme digestion and Pulsed-Field Gel Electrophoresis". Veterinary Microbiology. 59 (2): 147–156. doi:10.1016/S0378-1135(97)00188-0. ISSN   0378-1135. PMID   9549855.
  17. ↑ Borges, Alexandre Secorun; Mair, Tim; Pasval, Israel; Saulez, Montague N.; Tennent-Brown, Brett S.; van Eps, Andrew W. (2014-01-01), Orsini, James A.; Divers, Thomas J. (eds.), "Chapter 40 - Emergency Diseases Outside the Continental United States", Equine Emergencies (Fourth Edition), St. Louis: W.B. Saunders, pp. 656–686, ISBN   978-1-4557-0892-5 , retrieved 2020-10-28
  18. ↑ Higgins, Andrew; Snyder, Jack R. (2006). The Equine Manual. Elsevier Saunders. ISBN   9780702027697 . Retrieved 2020-10-28.
  19. 1 2 3 Layman, Quinci D.; Rezabek, Grant B.; Ramachandran, Akhilesh; Love, Brenda C.; Confer, Anthony W. (2014-04-17). "A retrospective study of equine actinobacillosis cases: 1999–2011". Journal of Veterinary Diagnostic Investigation. 26 (3): 365–375. doi: 10.1177/1040638714531766 . PMID   24742921. S2CID   23285283.
  20. 1 2 Swedish University of Agricultural Sciences- Faculty of Veterinary Medicine and Agricultural Science. Actinobacillus equuli subsp. equuli. Veterinary bacteriology: information about important bacteria. September 21, 2020. Accessed October 2020. https://www.vetbact.org/?artid=107
  21. 1 2 3 Huang, Barbara F; Kropinski, Andrew M; Bujold, Adina R; MacInnes, Janet I (2015). "Complete genome sequence of Actinobacillus equuli subspecies equuli ATCC 19392T". Standards in Genomic Sciences. 10: 32. doi: 10.1186/s40793-015-0009-x . PMC   4511653 . PMID   26203343.
  22. 1 2 3 4 5 6 7 8 Christensen, H. (2002-09-01). "Reclassification of equine isolates previously reported as Actinobacillus equuli, variants of A. equuli, Actinobacillus suis or Bisgaard taxon 11 and proposal of A. equuli subsp. equuli subsp. nov. and A. equuli subsp. haemolyticus subsp. nov". International Journal of Systematic and Evolutionary Microbiology. 52 (5): 1569–1576. doi:10.1099/ijs. PMID   12361259.
  23. ↑ Lauteri, Eleonora; Corsalini, Jacopo; Pepe, Marco; Mandara, Maria Teresa; Passamonti, Fabrizio; Beccati, Francesca (2018-02-01). "EHV-1 Congenital Infection and Concurrent Actinobacillus equuli Septicemia in a Standardbred Neonatal Foal: Clinical, Diagnostic Findings, and Evaluation of Adrenal Gland Function". Journal of Equine Veterinary Science. 61: 7–12. doi:10.1016/j.jevs.2017.10.021. ISSN   0737-0806. S2CID   80442466.
  24. 1 2 3 Watson, Rachel. "General and Medical Microbiology: Summary of Biochemical Tests". General and Medical Microbiology. Retrieved November 3, 2020.
  25. ↑ Aryal, Sagar (June 14, 2019). "CAMP Test- Principle, Uses, Procedure and Result Interpretation". Microbiologyinfo.com. Retrieved November 3, 2020.
  26. ↑ Aryal, Sagar (April 26, 2019). "OF (Oxidation-Fermentation) Test – Principle, Procedure, Uses and Interpretation". Microbiologyinfo.com. Retrieved November 3, 2020.
  27. 1 2 3 4 Patterson-Kane, J C, J M Donahue, and L R Harrison. "Septicemia and Peritonitis Due to Actinobacillus Equuli Infection in an Adult Horse." Veterinary Pathology 38.2 (2001): 230-232. Web
  28. ↑ Nielsen et al., 2008, M.K. Nielsen, D.S. Peterson, J. Monrad, S.T. Thamsborg, S.N. Olsen, R.M.Kaplan, Detection and semi-quantification of Strongylus vulgaris DNA in equine faeces by real-time PCR Int. J. Parasitol., 38 (2008), pp. 443-453
  29. ↑ Kuhnert, P; Berthoud, H; Straub, R; Frey, J (2003-03-20). "Host cell specific activity of RTX toxins from haemolytic Actinobacillus equuli and Actinobacillus suis". Veterinary Microbiology. 92 (1): 161–167. doi:10.1016/S0378-1135(02)00353-X. ISSN   0378-1135. PMID   12488079.
  30. 1 2 3 4 5 6 7 8 9 10 11 12 Maul, Christiane; Suchowski, Marcel; Klose, Kristin; Antov, Vladislav; Pfeffer, Martin; Schwarz, Bernd-Andreas (February 2020). "Detection of Actinobacillus equuli ssp. equuli in piglets with purulent polyarthritis and tendovaginitis". Tierärztliche Praxis Ausgabe G: Großtiere / Nutztiere (in German). 48 (1): 51–58. doi:10.1055/a-1067-3908. ISSN   1434-1220. PMID   32059237. S2CID   211121771.
  31. 1 2 Benavente, C. E., and I. C. Fuentealba. "Actinobacillus Suis and Actinobacillus Equuli, Emergent Pathogens of Septic Embolic Nephritis, a New Challenge for the Swine Industry." Archivos De Medicina Veterinaria 44.2 (2012): 99-107. Web.
  32. 1 2 3 Matthews, S, Dart, Aj, Dowling, Ba, Hodgson, Jl, and Hodgson, Dr. "Peritonitis Associated with Actinobacillus Equuli in Horses: 51 Cases." Australian Veterinary Journal 79.8 (2001): 536-39. Web.
  33. 1 2 3 Lauteri, Eleonora, Jacopo Corsalini, Marco Pepe, Maria Teresa Mandara, Fabrizio Passamonti, and Francesca Beccati. "EHV-1 Congenital Infection and Concurrent Actinobacillus Equuli Septicemia in a Standardbred Neonatal Foal: Clinical, Diagnostic Findings, and Evaluation of Adrenal Gland Function." Journal of Equine Veterinary Science 61 (2018): 7-12. Web.
  34. ↑ Pasma, Tim; Postey, Rosemary C.; Snider, Tim; Thompson, Amy B. (November 2010). "Actinobacillus equuli as a primary pathogen in breeding sows and piglets". Can Vet J. 51 (11): 1223–1225. PMC   2957028 . PMID   21286321 – via PubMed Central.
  35. ↑ Mohan, K.; Muvavarirwa, P.; Pawandiwa, A. (1997). "Strains of Actinobacillus spp. from diseases of animals and ostriches in Zimbabwe". The Onderstepoort Journal of Veterinary Research. hdl:2263/20751. ISSN   0030-2465.
  36. ↑ Berthoud, H., J. Frey, S. Sternberg, R. Straub, and P. Kuhnert. "Antibodies to Aqx Toxin of Actinobacillus Equuli in Horses and Foals." The Veterinary Record 155.8 (2004): 231-233. Web.
  37. ↑ Sternberg, Susanna; Brändström, Boel (1999-03-31). "Biochemical fingerprinting and ribotyping of isolates of Actinobacillus equuli from healthy and diseased horses". Veterinary Microbiology. 66 (1): 53–65. doi:10.1016/S0378-1135(98)00303-4. ISSN   0378-1135. PMID   10223322.
  38. ↑ Rycroft, A., Woldeselassie, Gordon, and Bjomson. "Serum Antibody in Equine Neonatal Septicaemia Due to Actinobacillus Equuli." Veterinary Record 143.9 (1998): 254-255. Web.
  39. ↑ Gay, C.C.; Lording, P.M. (1980). "Peritonitis in Horses Associated with Actinobacillus equuli". Australian Veterinary Journal. 56 (6): 296–300. doi:10.1111/j.1751-0813.1980.tb05727.x. PMID   7425990 . Retrieved November 30, 2020.
  40. ↑ Castagnetti, C., M. Rossi, F. Parmeggiani, R. G. Zanoni, A. Pirrone, and J. Mariella. "Facial Cellulitis Due to Actinobacillus Equuli Infection in a Neonatal Foal." Veterinary Record 162.11 (2008): 347-349. Web.
  41. ↑ Peel, M. M.; Hornidge, K. A.; Luppino, M.; Stacpoole, A. M.; Weaver, R. E. (November 1991). "Actinobacillus spp. and related bacteria in infected wounds of humans bitten by horses and sheep". Journal of Clinical Microbiology. 29 (11): 2535–2538. doi:10.1128/JCM.29.11.2535-2538.1991. ISSN   0095-1137. PMC   270368 . PMID   1774260.
  42. ↑ Ashhurst-Smith, Christopher; Norton, Robert; Thoreau, Wendy; Peel, Margaret M. (1998-09-01). "Actinobacillus equuli Septicemia: an Unusual Zoonotic Infection". Journal of Clinical Microbiology. 36 (9): 2789–2790. doi:10.1128/JCM.36.9.2789-2790.1998. ISSN   0095-1137. PMC   105212 . PMID   9705442.
  43. ↑ Elad, Daniel & Shlomovitz, Sara & Lampert, Meir & Yakobson, Boris & Perl, Samuel & Hermelin, Alon. (1988). Actinobacillus equuli in a foal - first report in Israel. Israel Journal of Veterinary Medicine. 44. 261.
  44. ↑ Weiermayer, Petra. "Wound Healing Disorder in a Horse, Associated With Antimicrobial-Resistant Bacteria, Resolved With a Homeopathic Medicine - A Case Report." Journal of Equine Veterinary Science 67 (2018): 37-43. Web.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.