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Rhodococcus equi ist ein grampositives, kokkoides Stäbchen. Das Bakterium kommt als Umweltkeim gewöhnlich in staubigen, trockenen Böden vor und kann in Aufzuchtbetrieben (von Pferden und Ziegen) bis zu 60 Prozent infizieren.[1] Die früher hohe Letalität der Infektion ist bis 2009 auf etwa 12 Prozent zurückgegangen, vermutlich durch besseres Monitoring der Fohlen und Antibiotika-Behandlung. Häufigste Symptome heute sind eine milde neutrophile Leukozytose und Hyperfibrinogenämie mit übermäßiger Fibrinogenbildung[2]. Seit 2008 ist bekannt, dass R. equi neben Hausschweinen auch Wildschweine befallen kann.[3] Bei Fohlen ist R. equi der häufigste Verursacher von Atemwegserkrankungen. Zudem kann der Erreger auch auf Menschen übertragen werden. Vor allem bei stark immungeschwächten Menschen wie AIDS-Patienten kann es so tödliche Lungenentzündungen (Pneumonien) verursachen. Auch Wundinfektionen, Osteomyelitis und Abszesse können beim Menschen durch Rhodococcus equi hervorgerufen werden.[4]
Rhodococcus equi gehört zur Gruppe der fakultativ intrazellulären Pathogene, kann sich also sowohl auf Nährmedien (z. B. Brain Heart Infusion) als auch in Immunfresszellen (Makrophagen) des Wirtes vermehren[5]. Ein zentraler Virulenzfaktor ist dabei das bakterielle Virulenz-assoziierte Protein A (VapA)[6], welches zusammen mit langen, mykolsäurehaltigen Oberflächenglykolipiden die Phagosomenreifung blockiert[7][8]. So bleibt die Verschmelzung von Bakterien-enthaltenden Phagosomen mit den Lysosomen als Verdauungskompartimenten der Immunfresszellen aus und die Bakterien können sich vermehren.
Zur antibiotischen Therapie bei Infektionen mit Rhodococcus equi kann Vancomycin kombiniert mit Rifampicin, alternativ auch Imipenem mit Rifampicin, über vier bis acht Wochen eingesetzt werden, wenn möglich gefolgt von oraler Gabe von Ciprofloxacin oder Levofloxacin.[9]
Fälschlicherweise werden für Rhodococcus equi auch andere Artbezeichnungen verwendet. Neben Corynebacterium equi sind Synonyme wie Bacillus hoagii, Corynebacterium purulentus, Mycobacterium equi, Mycobacterium restrictum, Nocardia restricta und Proactinomyces restrictus gebräuchlich.
Rhodococcus equi ist ein grampositives, kokkoides Stäbchen. Das Bakterium kommt als Umweltkeim gewöhnlich in staubigen, trockenen Böden vor und kann in Aufzuchtbetrieben (von Pferden und Ziegen) bis zu 60 Prozent infizieren. Die früher hohe Letalität der Infektion ist bis 2009 auf etwa 12 Prozent zurückgegangen, vermutlich durch besseres Monitoring der Fohlen und Antibiotika-Behandlung. Häufigste Symptome heute sind eine milde neutrophile Leukozytose und Hyperfibrinogenämie mit übermäßiger Fibrinogenbildung. Seit 2008 ist bekannt, dass R. equi neben Hausschweinen auch Wildschweine befallen kann. Bei Fohlen ist R. equi der häufigste Verursacher von Atemwegserkrankungen. Zudem kann der Erreger auch auf Menschen übertragen werden. Vor allem bei stark immungeschwächten Menschen wie AIDS-Patienten kann es so tödliche Lungenentzündungen (Pneumonien) verursachen. Auch Wundinfektionen, Osteomyelitis und Abszesse können beim Menschen durch Rhodococcus equi hervorgerufen werden.
Rhodococcus equi gehört zur Gruppe der fakultativ intrazellulären Pathogene, kann sich also sowohl auf Nährmedien (z. B. Brain Heart Infusion) als auch in Immunfresszellen (Makrophagen) des Wirtes vermehren. Ein zentraler Virulenzfaktor ist dabei das bakterielle Virulenz-assoziierte Protein A (VapA), welches zusammen mit langen, mykolsäurehaltigen Oberflächenglykolipiden die Phagosomenreifung blockiert. So bleibt die Verschmelzung von Bakterien-enthaltenden Phagosomen mit den Lysosomen als Verdauungskompartimenten der Immunfresszellen aus und die Bakterien können sich vermehren.
Zur antibiotischen Therapie bei Infektionen mit Rhodococcus equi kann Vancomycin kombiniert mit Rifampicin, alternativ auch Imipenem mit Rifampicin, über vier bis acht Wochen eingesetzt werden, wenn möglich gefolgt von oraler Gabe von Ciprofloxacin oder Levofloxacin.
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 (horses and goats). The frequency of infection can reach near 60%.[1] R. equi is an important pathogen causing pneumonia in foals. Since 2008, R. equi has been known to infect wild boar and domestic pigs.[2] 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.[3]
The most common route of infection in horses is likely via inhalation of contaminated dust particles. Inhaled virulent strains of R. equi are phagocytosed by alveolar macrophages. During normal phagocytosis, bacteria are enclosed by the phagosome, which fuses with the lysosome to become a phagolysosome. The internal environment of the phagolysosome contains nucleases and proteases, which are activated by the low pH of the compartment. The macrophage produces bacteriocidal compounds (e.g., oxygen radicals) following the respiratory burst. However, like its close relative Mycobacterium tuberculosis, R. equi prevents the fusion of the phagosome with the lysosome and acidification of the phagosome.[4][5][6] Additionally, the respiratory burst is inhibited. This allows R. equi to multiply within the phagosome where it is shielded from the immune system by the very cell that was supposed to kill it.[7] After about 48 hours, the macrophage is killed by necrosis, not apoptosis.[8] Necrosis is pro-inflammatory, attracting additional phagocytic cells to the site of infection, eventually resulting in massive tissue damage.
All strains isolated from foals and the majority of human, cattle, and pig isolates contain a large plasmid. This plasmid has been shown to be essential for infection of foals, and presumably plays a similar role for infection of other hosts, although this has not been established yet. Strains that lack the virulence plasmid are unable to proliferate in macrophages. This virulence plasmid has been characterised in detail from equine and porcine strains, although only the former has been functionally characterised.[9][10] These circular plasmids consist of a conserved backbone responsible for replication and bacterial conjugation of the plasmid. This portion of the plasmid is highly conserved and found in nonpathogenic Rhodococci plasmids. In addition to the conserved region, the virulence plasmids contain a highly variable region that has undergone substantial genetic rearrangements, including inversion and deletions. This region has a different GC-content from the rest of the plasmid, and is flanked by genes associated with mobile genetic elements. It is therefore assumed to be derived from a different bacterial species than the backbone of the plasmid via lateral gene transfer.
The variable region of the virulence plasmid contain genes that are highly expressed following phagocytosis of R. equi by macrophages.[11] This variable region is believed to be a pathogenicity island that contains genes essential for virulence.
A hallmark of the pathogenicity island (PAI) is that many genes within it do not have homologues in other species. The most notable of these are the virulence-associated protein (vap) genes. All foals infected with R. equi produce high levels of antibodies specific for vapA, the first vap gene to be characterised. Deletion of vapA renders the resulting strain avirulent.[12] In addition to vapA, the PAI encodes a further five full-length vap homologues, one truncated vap gene, and two vap pseudogenes. The porcine PAI contains five full-length vap genes, including the vapA homologue, vapB. In addition to these unique genes, the PAI contains genes that have a known function, in particular two regulatory genes encoding the LysR-type regulator VirR and the response regulator Orf8. These two proteins have been shown to control expression of a number of PAI genes including vapA.[13] Other genes have homology to transport proteins and enzymes. However, the functionality of these genes or how the proteins encoded within PAI subvert the macrophage has not yet been established.
While this organism is generally known as Rhodococcus equi, there has been taxonomic debate since the 1980s[14] about whether this name is the valid name, with Rhodococcus hoagii and Prescottella equi both proposed as official alternative names.[15] Other names used include Nocardia restricta,[14] Corynebacterium equi,[16] Bacillus hoagii,[16] Corynebacterium purulentus,[16] Mycobacterium equi,[16] Mycobacterium restrictum,[16] and Proactinomyces restrictus.[16]
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 (horses and goats). 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.
Rhodococcus equi (do grego, esferas rosadas de equinos) é uma espécie de bactérias patogênicas intracelulares facultativas, cocobacilares, gram-positivas, aeróbicas, não esporulantes, imóveis, com grandes plasmídeos, pouco virulentos, crescimento rápido, que formam colônias arredondadas e produzem um pigmento rosa (origem de seu nome) e causam infecção respiratória em equinos, suínos, caprinos, ovinos e humanos com imunidade deprimida.
É similar a muitas outras espécies, de modo que já foi categorizada como Corynebacterium equi, Bacillus hoagii, Corynebacterium purulentus, Mycobacterium equi, Mycobacterium restrictum, Nocardia restricta e Proactinomyces restrictus.
Sua manifestação mais comum é na forma em humanos é de uma pneumonia necrotizante em imunodeprimidos e seus sintomas são parecidos aos da tuberculose. Também pode causar infeccionar feridas, formar abscessos subcutâneos, abscesso cerebral, abscesso tireóideo, abscesso retroperitoneal, peritonite, meningite, pericardite, osteomielite, endoftalmite, linfadenite, linfangite, artrite séptica, osteíte, diarreia com sangue e febre. Bacteremia pode ocorrer com a disseminação da infecção a partir do local da infecção primária, que geralmente é o pulmão ou a pele.[1]
É três vezes mais comum em homens, em ambientes rurais e afeta todas as idades (média 34-36 anos), um terço dos casos é em crianças. Quando a imunidade boa a melhora é excelente, mas em imunodeprimidos a mortalidade é de 25%. Pode ser transmitida pelo consumo de carnes mal cozidas ou aspiração da poeira (aerossol) de fazendas com animais contaminados.[2]
R equi é normalmente resistente a penicilina G, ampicilina, carbenicilina e cefazolina. Pode ser tratada com eritromicina, vancomicina, ciprofloxacino, aminoglicosídeos e outros.[3]
Rhodococcus equi (do grego, esferas rosadas de equinos) é uma espécie de bactérias patogênicas intracelulares facultativas, cocobacilares, gram-positivas, aeróbicas, não esporulantes, imóveis, com grandes plasmídeos, pouco virulentos, crescimento rápido, que formam colônias arredondadas e produzem um pigmento rosa (origem de seu nome) e causam infecção respiratória em equinos, suínos, caprinos, ovinos e humanos com imunidade deprimida.
