Corynebacterium pseudotuberculosis | |
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Scientific classification ![]() | |
Domain: | Bacteria |
Phylum: | Actinomycetota |
Class: | Actinomycetia |
Order: | Mycobacteriales |
Family: | Corynebacteriaceae |
Genus: | Corynebacterium |
Species: | C. pseudotuberculosis |
Binomial name | |
Corynebacterium pseudotuberculosis (Buchanan 1911) Eberson 1918 (Approved Lists 1980) | |
Corynebacterium pseudotuberculosis is a Gram-positive bacterium known to infect ruminants, horses, and rarely people. It is a facultative anaerobic organism that is catalase-positive and capable of beta-hemolysis. In small ruminants, C. pseudotuberculosis causes a disease called caseous lymphadenitis, which is characterized by pyogranulomatous abscess formation. In general, the bacterium causes lesions of the skin, lymph nodes, and internal organs. A disease known as ulcerative lymphagenitis can also result from infection with C. pseudotuberculosis in the distal limbs of horses. This bacterium uses the virulence factors phospholipase D and mycolic acid to damage eukaryotic cell walls and resist phagocytic lysosomal degradation, respectively. Infection with this bacterium is often confirmed by bacterial culture of the purulent exudate. Once the diagnosis has been made, treatment of the infection can begin, but this is difficult due to the nature of the organism and the lesions it forms. Specifically, C. pseudotuberculosis is intrinsically resistant to streptomycin, with varying resistance to penicillin and neomycin depending on the strain. It has been shown to be susceptible to ampicillin, gentamicin, tetracycline, lincomycin, and chloramphenicol. Vaccines have also been produced to develop acquired immunity to this infection.
Development of a vaccine was completed in 1983, and it was added to the recommended clostridial vaccines for sheep. The national average of prevalence in Australia was 5.2% in 2009, although this varies by region. [1] C. pseudotuberculosis also causes disease in horses, and should be considered prevalent in areas where cases of "pigeon fever" and "ulcerative lymphadenitis" have been recorded. [2] [ neutrality is disputed ]
Major bacterial spread occurs when superficial abscesses break open and release discharge that comes into contact by other animals during grooming, or contaminates feed, water, and bedding that other animals consume. In horses, arthropod vectors are considered a significant source of infection. As vector patterns change with warming temperatures, C. pseudotuberculosis in horses is re-emerging in the United States. [2]
This bacterial species has caused occasional cases of infection in people who work closely with infected small ruminants, resulting in similar swellings of the lymph nodes in the neck and groin. [3] [1] The most likely route of infection is direct contact with the infected animal or its raw products. [3]
C. pseudotuberculosis is a Gram-positive bacterium that has been observed as coccoid or filamentous rods, which can be organized into palisades. Metachromatic volutin granules containing phosphate can be seen in the rod form, but not the coccoid form when stained using Albert's or Neisser's methods. Other characteristics of this bacterium include being nonsporulating, noncapsulated, possessing fimbrae, and immobility. [4]
The bacterium is a facultative anaerobe that grows at 37 °C under aerobic or anaerobic conditions. It forms dry, pale yellow colonies measuring 1–2 mm in diameter after incubation on solid media for 48 hours. Media containing serum or whole blood improve bacterial growth, and a band of beta-hemolysis tends to forms around bacterial colonies after 48–72 hours of incubation on blood agar. C. pseudotuberculosis forms clumps in fluid media. [5]
While strains of C. pseudotuberculosis are consistent in their morphology and growth on media, they show greater variation in biochemical properties such as fermenting ability. While they are unable to produce gas, all strains can use glucose, fructose, maltose, mannose, and sucrose to produce acid. Additional biochemical properties of this bacterium include being phospholipase D- and catalase-positive, oxidase-negative, and beta-hemolytic. [4] Generally, two subtypes of C. pseudotuberculosis are known: the equi biovar affects horses and cattle, while the ovis biovar affects small ruminants. [6] Their ability to reduce nitrate can be used to distinguish between the subtypes. The equi biovar can reduce nitrate, while the ovis biovar generally cannot, but some exceptions have been demonstrated. [7] Coryneform bacteria, including C. pseudotuberculosis, can also be differentiated using a biochemical test called the API Coryne system, which involves enzyme and carbohydrate fermentation tests and requires 24–48 hours to perform. [4] Finally, genetic sequence analysis can be used to confirm the identification of C. pseudotuberculosis if biochemical identification is not sufficient. [6] A multiplex polymerase chain reaction assay has been developed using a number of characteristic genes that can differentiate between the closely related species of corynebacteria – C. pseudotuberculosis, C. ulcerans , and C. diphtheriae . [8]
C. pseudotuberculosis causes a disease known as caseous lymphadenitis that most commonly affects small ruminants, such as goats and sheep. [9] [10] The disease often presents with pyogranulomatous abscess formation. [11] Abscessation can occur in numerous areas, but it most commonly affects the cutaneous region and superficial lymph nodes. This is known as the external form of the disease and is the primary form affecting goats, and nodular lesions are often visible. The internal form of the disease is more of a concern for sheep, in which internal organs and lymph nodes are affected. [10] Over time, these abscesses deposit multiple layers of fibrous capsules which gives them a lamellated appearance upon cross section. [11] [10] The contents of the abscess are thick and purulent, and the abscess often ruptures. [11]
The internal manifestation of the disease is harder to recognize, as the clinical signs are not as obvious, but may include a reduction in reproductive ability and diminished body condition. [12] Depending on the location of the lesions, the animal may develop dysphagia and abnormal rumination. [11]
The most common clinical sign for infected cattle is ulcerative lesions of the skin. [13] Mastitis, an infection of the udder that is most commonly caused by species of the Streptococcus and Staphylococcus genera, may also be caused by C. pseudotuberculosis in rare circumstances. [14] [11] [13] Infected cattle may also have a higher frequency of abortions. [13]
C. pseudotuberculosis can also cause disease in horses, which also present with abscessation, but the lesions are most commonly seen on the underside of the abdomenal and pectoral regions. C. pseudotuberculosis can also cause infection of the distal limbs, a manifestation known as ulcerative lymphangitis. It is usually a unilateral lesion and the affected limb is painful, swollen, and contains draining ulcerative and nodular lesions. [13]
Diagnosis of C. pseudotuberculosis can be difficult due to vague clinical signs such as weight loss and general ill thrift[ clarification needed ]. [12] Confirming diagnosis in animals infected with the internal form of the disease is more difficult, but ultrasonography or radiography may be useful. [10] PCR has shown promising results for diagnosis, and a double-antibody sandwich ELISA can be used in sheep and goats. [12]
C. pseudotuberculosis has two well-documented virulence factors: phospholipase D (an endotoxin) [15] [16] [17] and a mycolic acid surface lipid. [15] Both virulence factors are proposed to be independent of plasmids, as no plasmid has been found in C. pseudotuberculosis. [15]
Every isolate of C. pseudotuberculosis in research so far has had the phospholipase D virulence factor. [15] Studies that examine the absence or mutation of the phospholipase D gene in C. pseudotuberculosis-infected mice have been shown to fail to develop chronic abscessation. [16] This phospholipase encoding gene has been isolated to pathogenicity island 1. [18] At least seven pathogenicity islands have been recorded in C. pseudotuberculosis. [18]
Phospholipase D is an ester bond-cleaving exotoxin that provides the bacterium with the ability to cleave sphingomyelin, [15] which is a glycerophospholipid eukaryotic cell-wall component, [19] so by destruction or cleavage of this component, the cell wall becomes damaged. [15] This can cause death or loss of function of eukaryotic cells. This effect may help the invasion of C. pseudotuberculosis. [18]
Phospholipase D also increases vascular permeability, [15] [17] possibly due to sphingomyelinase effects. The increase in permeability may allow increased lymphatic drainage, leading to one of the mechanisms of migration to the lymph nodes, where C. pseudotuberculosis causes chronic abscessation. [17]
Another mechanism of lymphatic transport is facilitated by the presence of a mycolic acid surface lipid that coats C. pseudotuberculosis. [15] Mycolic acid provides a protective barrier that allows the bacterial cell to resist lysosomal degradation by eukaryotic, phagocytic, white blood cells. [17] [15] This allows the bacteria to act as facultative intracellular parasites once they have been phagocytized, where the phagocyte eventually migrates to the lymph node, where chronic infection occurs. The surface lipid is cytotoxic and can cause death to macrophages. [15]
In a prospective study involving 12 Boer goats, inoculation with mycolic acid compared to control animals provided statistically significant evidence of pathological changes in the lung compared to a control group. [20] Groups inoculated with mycolic acid or C. pseudotuberculosis were evaluated through histopathology compared to a control. Both groups showed hemorrhage, congestion, oedema, inflammation, and necrosis. Organs affected by these degenerative changes included the lung, heart, kidney, and spleen, though severity varied within organs and within mycolic-only and C. pseudotuberculosis-infected groups. [20] The importance of this virulence factor has also been highlighted where mice that have been injected with mycolic acid were shown to produce a chronic abscessation that increased with higher doses. [15]
Four different strains of C. pseudotuberculosis are recognized: Cp1002, CpC231, Cp119, and CpFRC41. [18] Comparing genes within these strains, the largest genome was found to be 2,377 genes, of which 1,851 genes were shared among all four strains. [18] In a CpFRC41 strain isolated from a girl, a gene was found to encode for superoxide dismutase among other specific virulence factors. [21] Superoxide dismutase is involved in evading the immune system by deactivating reactive chemicals secreted by the body that would otherwise kill the bacterial cell. [22] When comparing strains Cp1002 and CpC231 in the sixth pathogenicity island (PiCp6), Cp1002 contained the gene pipA1, where CpC231 contained pipB. [18] This island (6) codes for proline iminopeptidase, which is involved with removal of proline from proteins.
Through genomic evaluation, many more possible virulence factors have been found. [18] [21] [22]
Treatment of C. pseudotuberculosis in infected animals has been proven difficult, primarily due to the nature of the lesions and the facultative intracellular nature of the organism. [15] [23] Strains of C. pseudotuberculosis have shown to be susceptible to numerous antimicrobial therapies in vitro, including ampicillin, gentamicin, tetracycline, lincomycin, chloramphenicol, and others. Treatment within live animals (in vivo) is thought to be limited due to the firm capsule and thick, caseous nature of the abscess lesions, which make them a difficult target for antimicrobial therapy. [15] [24] Most strains of C. pseudotuberculosis have been shown to be intrinsically resistant to streptomycin, with varying resistance to penicillin and neomycin depending on the strain. [24]
Several vaccine types are currently available for treatment of C. pseudotuberculosis infections, including bacterin vaccines, toxoid vaccines, combined vaccines, live vaccines, and DNA vaccines. [17] Part of the C. pseudotuberculosis lifecycle being intracellular adds an additional element of difficulty to vaccine treatment, as a vaccine must be able to induce a cell-mediated response rather than a solely humoral antibody response to eliminate the bacteria from the body. [23] A vaccine using a recombinant form of the phospholipase D exotoxin is now in widespread use, and has been shown to decrease the occurrence of lung lesions and amount of tissue damage observed upon infection. Though vaccination does not prevent infection in a flock, it minimizes infection severity, and so it can have positive implications in reducing carcass condemnations for producers. This exotoxin is commonly included in combination vaccines that also protect against clostridial diseases. Good management practices that include the implementation of persistent vaccination protocols with the combination vaccine Glanvac 6 (Zoetis) have demonstrated to be effective and have led to a decrease of caseous lymphadenitis in Australia. [1] Vaccines should be administered as directed by the manufacturer for highest efficacy, ensuring that the vaccines are given to the appropriate animals at the correct ages, and are boosted at the recommended intervals. [17] [ neutrality is disputed ]
With antimicrobial therapy and vaccination protocols being somewhat limited, proper management practices are highly recommended for controlling caseous lymphadenitis. [25] Good husbandry practices can decrease the occurrence and spread of caseous lymphadenitis among small ruminants, thus improving animal health and minimizing economic impacts on the producers. [23] C. pseudotuberculosis is commonly spread through superficial wounds inflicted during shearing, castration, tail docking, and ear tagging, so disinfection of equipment between animals and keeping wound sites clean can help limit spread. The disease can also spread through superficial wounds caused during animal fighting. C. pseudotuberculosis can persist on fomites such as straw bedding, hay, wood, and feces for weeks, and in the soil for up to eight months, making proper disinfection of facilities and pasture management essential to limit spread of disease. [23] Infected animals are recommended to be quarantined, and in some cases the culling of infected animals may be indicated. [23]
Yersinia pestis is a gram-negative, non-motile, coccobacillus bacterium without spores that is related to both Yersinia enterocolitica and Yersinia pseudotuberculosis, the pathogen from which Y. pestis evolved and responsible for the Far East scarlet-like fever. It is a facultative anaerobic organism that can infect humans via the Oriental rat flea. It causes the disease plague, which caused the Plague of Justinian and the Black Death, the deadliest pandemic in recorded history. Plague takes three main forms: pneumonic, septicemic, and bubonic. Yersinia pestis is a parasite of its host, the rat flea, which is also a parasite of rats, hence Y. pestis is a hyperparasite.
Q fever or query fever is a disease caused by infection with Coxiella burnetii, a bacterium that affects humans and other animals. This organism is uncommon, but may be found in cattle, sheep, goats, and other domestic mammals, including cats and dogs. The infection results from inhalation of a spore-like small-cell variant, and from contact with the milk, urine, feces, vaginal mucus, or semen of infected animals. Rarely, the disease is tick-borne. The incubation period can range from 9 to 40 days. Humans are vulnerable to Q fever, and infection can result from even a few organisms. The bacterium is an obligate intracellular pathogenic parasite.
Erysipelothrix rhusiopathiae is a Gram-positive, catalase-negative, rod-shaped, non-spore-forming, nonacid-fast, nonmotile bacterium. Distributed worldwide, E. rhusiopathiae is primarily considered an animal pathogen, causing the disease known as erysipelas that may affect a wide range of animals. Pigs, turkeys and laying hens are most commonly affected, but cases have been reported in other mammals, birds, fish, and reptiles. In pigs, the disease is known as diamond skin disease. The bacterium can also cause zoonotic infections in humans, called erysipeloid. The human disease called erysipelas is not caused by E. rhusiopathiae, but by various members of the genus Streptococcus.
Corynebacterium diphtheriae is the pathogenic bacterium that causes diphtheria. It is also known as the Klebs–Löffler bacillus, because it was discovered in 1884 by German bacteriologists Edwin Klebs (1834–1912) and Friedrich Löffler (1852–1915). The bacteria are usually harmless unless they are infected by a bacteriophage that carries a gene that gives rise to a toxin. This toxin causes the disease. Diphtheria is caused by the adhesion and infiltration of the bacteria into the mucosal layers of the body, primarily affecting the respiratory tract and the subsequent release of an endotoxin. The toxin has a localized effect on skin lesions, as well as a metastatic, proteolytic effects on other organ systems in severe infections. Originally a major cause of childhood mortality, diphtheria has been almost entirely eradicated due to the vigorous administration of the diphtheria vaccination in the 1910s.
Yersinia enterocolitica is a Gram-negative, rod-shaped bacterium, belonging to the family Yersiniaceae. It is motile at temperatures of 22–29°C (72–84°F), but becomes nonmotile at normal human body temperature. Y. enterocolitica infection causes the disease yersiniosis, which is an animal-borne disease occurring in humans, as well as in a wide array of animals such as cattle, deer, pigs, and birds. Many of these animals recover from the disease and become carriers; these are potential sources of contagion despite showing no signs of disease. The bacterium infects the host by sticking to its cells using trimeric autotransporter adhesins.
Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like fever in humans, who occasionally get infected zoonotically, most often through the food-borne route. Animals are also infected by Y. pseudotuberculosis. The bacterium is urease positive.
Bovine malignant catarrhal fever (BMCF) is a fatal lymphoproliferative disease caused by a group of ruminant gamma herpes viruses including Alcelaphine gammaherpesvirus 1 (AlHV-1) and Ovine gammaherpesvirus 2 (OvHV-2) These viruses cause unapparent infection in their reservoir hosts, but are usually fatal in cattle and other ungulates such as deer, antelope, and buffalo. In Southern Africa the disease is known as snotsiekte, from the Afrikaans.
Fusobacterium necrophorum is a species of bacteria responsible for Lemierre's syndrome. It has also been known to cause sinusitis, mastoiditis, and odontogenic infections.
Anaplasmosis is a tick-borne disease affecting ruminants, dogs, and horses, and is caused by Anaplasma bacteria. Anaplasmosis is an infectious but not contagious disease. Anaplasmosis can be transmitted through mechanical and biological vector processes. Anaplasmosis can also be referred to as "yellow bag" or "yellow fever" because the infected animal can develop a jaundiced look. Other signs of infection include weight loss, diarrhea, paleness of the skin, aggressive behavior, and high fever.
Dichelobacter nodosus, formerly Bacteroides nodosus, is a Gram-negative, obligate anaerobe of the family Cardiobacteriaceae. It has polar fimbriae and is the causative agent of ovine foot rot as well as interdigital dermatitis. It is the lone species in the genus Dichelobacter.
Mycoplasma ovipneumoniae is a species of Mycoplasma bacteria that most commonly inhabits and affects ovine animals, first described in 1972. M. ovipneumoniae contributes to harmful pneumonia in sheep and goats. The duration and severity of M. ovipneumoniae varies from region to region.
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 humans. At-risk groups are immunocompromised people, such as HIV-AIDS patients or transplant recipients. Rhodococcus infection in these patients resemble clinical and pathological signs of pulmonary tuberculosis. It is facultative intracellular.
Caseous lymphadenitis (CLA) is an infectious disease caused by the bacterium Corynebacterium pseudotuberculosis, that affects the lymphatic system, resulting in abscesses in the lymph nodes and internal organs. It is found mostly in goats and sheep and at the moment it has no cure.
Edwardsiella tarda is a member of the family Hafniaceae. The bacterium is a facultatively anaerobic, small, motile, gram negative, straight rod with flagella. Infection causes Edwardsiella septicemia in channel catfish, eels, and flounder. Edwardsiella tarda is also found in largemouth bass and freshwater species such as rainbow trout. It is a zoonosis and can infect a variety of animals including fish, amphibians, reptiles, and mammals. Edwardsiella tarda has also been the cause of periodic infections for various animals within zoos. E. tarda has a worldwide distribution and can be found in pond water, mud, and the intestine of fish and other marine animals. It is spread by carrier animal feces.
Pigeon fever is a disease of horses, also known as dryland distemper or equine distemper, caused by the Gram-positive bacteria Corynebacterium pseudotuberculosis biovar equi. Infected horses commonly have swelling in the chest area, making it look similar to a "pigeon chest". This disease is common in dry areas. Pigeon fever is sometimes confused with strangles, another infection that causes abscesses.
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.
Capripoxvirus is a genus of viruses in the subfamily Chordopoxvirinae and the family Poxviridae. Capripoxviruses are among the most serious of all animal poxviruses. All CaPV are notifiable diseases to the OIE. Sheep, goat, and cattle serve as natural hosts. These viruses cause negative economic consequences by damaging hides and wool and forcing the establishment of trade restrictions in response to an outbreak. The genus consists of three species: sheeppox virus (SPPV), goatpox virus (GTPV), and lumpy skin disease virus (LSDV). They share no serological relationship with camel pox, horse pox, or avian poxes. Capripoxviruses for sheeppox and goatpox infect only sheep and goat respectively. However, it is probable that North American relatives, the mountain goat and mountain sheep, may be susceptible to the strains but has not been experimentally proven. Lumpy skin disease virus affects primarily cattle, but studies have been shown that giraffes and impala are also susceptible to LSDV. Humans cannot be infected by Capripoxviruses.
Bordetella avium is a gram negative, nonfermentative, strictly aerobic, motile bacterium from the genus Bordetella which has been isolated from patients with respiratory disease. B. avium has a global distribution, that mainly affects young domesticated turkeys. The disease in birds is called bordetellosis, and is largely associated with confined spaces and multi-aged flocks where management practices are sub optimal. In most infections, mortality is typically low but morbidity is very high.
Actinomyces bovis is a branching, Gram-positive, rod-shaped bacterium of the genus Actinomyces. It is the causative agent of lumpy jaw in cattle, and occasionally causes actinomycosis infections in humans. A. bovis normally populates the gastrointestinal tract of healthy ruminants, but is opportunistic in nature and will move into tissues through ulcerations or abrasions of the mucosa to cause infection. The disease occurs when there is physical damage to the tissue of the mouth, allowing the bacteria to colonize the deep tissue and bone, typically affecting the mandible and maxilla. Actinomycosis is pathognomonic for abscesses containing "sulfur" granules, and its colonies appear basophilic with club-shaped reaction products on a histological preparation. Lumpy jaw is commonly treated with broad-spectrum antibiotics with varying success, and can be a major economic loss for producers in countries where it is endemic. Because this organism is zoonotic, it is a human health concern and can cause granulomas, abscesses, skin lesions, and bronchopneumonia.
Histophilus somni is a non-motile, gram-negative, rod or coccobacillus shaped, facultative anaerobe bacterial species belonging to the family Pasteurellaceae. Prior to 2003, it was thought Haemophilus somnus, Histophilus ovis, and Histophilus agni were three different species, but now are all classified as Histophilus somni. Histophilus somni is a commensal bacteria of mucous membranes of the upper respiratory tract and reproductive tract with a global prevalence and is found in cattle and other small ruminants. Histophilus somni is also a known causative agent that is a part of the Bovine Respiratory Disease (BRD) complex, which typically involves multiple pathogens residing together in biofilm environments. Histophilus somni may also cause Histophilosus symptoms and clinical presentation will depend on the tissue affected. When disease does occur, it can be difficult to catch in time and is often diagnosed on post mortem. This means that treatment often involves metaphylactic mass treatment or no treatment at all. This organism is more fastidious than others and requires knowledge for sample collection, storage and culture. Genomic studies related to this bacteria have enabled scientist to pin point antibiotic resistance genes.
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