The effect of coumermycin on experimental listeriosis

Hof, Herbert

doi:10.1016/s0163-4453(86)92141-9

Cited by 7 publications

(6 citation statements)

References 15 publications

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“…Killing occurs rather late, i.e., several hours after exposure to the antimicrobial agent, whereas with gram-negative bacteria, killing occurs rapidly, often within an hour. Coumermycin, another gyrase inhibitor, also is not bactericidal for listeriae (44).…”

Section: Bactericidal Activities Of Antibioticsmentioning

confidence: 99%

Management of listeriosis

1997

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Determination of the MIC in vitro is often used as the basis for predicting the clinical efficacy of antibiotics. Listeriae are uniformly susceptible in vitro to most common antibiotics except cephalosporins and fosfomycin. However, the clinical outcome is poor. This is partially because listeriae are refractory to the bactericidal mechanisms of many antibiotics, especially to ampicillin-amoxicillin, which still is regarded as the drug of choice. A true synergism can be achieved by adding gentamicin. Another point is that listeriae are able to reside and multiply within host cells, e.g., macrophages, hepatocytes, and neurons, where they are protected from antibiotics in the extracellular fluid. Only a few agents penetrate, accumulate, and reach the cytosol of host cells, where the listeriae are found. Furthermore, certain host cells may exclude antibiotics from any intracellular compartment. Thus, determination of the antibacterial efficacy of a drug against listeriae in cell cultures may be a better approximation of potential therapeutic value. Certain host cells may have acquired the property of excluding certain antibiotics, for example macrolides, from intracellular spaces, which might explain therapeutic failures of antibiotic therapy in spite of low MICs. Animal models do not completely imitate human listeriosis, which is characterized by meningitis, encephalitis, soft tissue and parenchymal infections, and bacteremia. Meningitis produced in rabbits is a hyperacute disease, whereby most listeriae lie extracellularly, fairly accessible to antibiotics that can cross the blood-cerebrospinal fluid barrier. In the murine model of systemic infection, Listeria monocytogenes is located mainly within macrophages and parenchymal cells of the spleen and liver, hardly accessible to certain drugs, such as ampicillin and gentimicin. The therapeutic efficacy of drugs clearly depends on the model used. Thus, for example, the combination of ampicillin with gentamicin acts synergistically in the rabbit meningitis model but not in the mouse model. Since conventional antimicrobial therapy with antibiotics is not satisfactory, particularly in the immunocompromised host (about 30% of patients with listeriosis die in spite of a rational choice of antibiotics), other possibilities must be considered for therapy as well as prevention. Indeed, listeriae are highly susceptible to several endogenous antibiotics, such as defensins. Bacteriocins produced by related bacterial species, e.g., lactobacilli and enterococci, are rapidly bactericidal. However, unfortunately, the use of such alternative measures along with immunization and immunmodulation is not yet feasible.

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Section: Bactericidal Activities Of Antibioticsmentioning

confidence: 99%

Management of listeriosis

1997

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“…Using the bacterial immunomodifier Propionibacterium avidum KP-40 the importance of an activated mononuclear phagocyte system in the early stage of Listeria infection could be demonstrated.Listeria monocytogenes is a facultative intracellular bacterium which parasitizes host phagocytes [3,4,8]. Virulent strains induce in mice acute systemic infections which primarily affect reticulo-endothelial organs [4,8,9].…”

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confidence: 99%

“…The mononuclear phagocyte system (MPS) is surely the major mediator of natural antilisterial resistance [2,8,10,12]. The role of NK cells, granulocytes and hepatocyte membrane receptors (hepatic lectins) in Listeria infection is not yet clear [1,2,8,10].In this report we discuss the blocking of hepatic lectins by systemic D-galactose treatment as well as the effect of activated MPS in the very early stage of systemic Listeria infection using a murine model [4,5,6] and Propionibacterium avidum KP-40, a very potent MPS activator. To initiate acute systemic infection the highly Listeria-…”

mentioning

confidence: 99%

“…Virulent strains induce in mice acute systemic infections which primarily affect reticulo-endothelial organs [4,8,9]. The mononuclear phagocyte system (MPS) is surely the major mediator of natural antilisterial resistance [2,8,10,12].…”

mentioning

confidence: 99%

“…In this report we discuss the blocking of hepatic lectins by systemic D-galactose treatment as well as the effect of activated MPS in the very early stage of systemic Listeria infection using a murine model [4,5,6] and Propionibacterium avidum KP-40, a very potent MPS activator. To initiate acute systemic infection the highly Listeriasensitive Balb/c mouse strain [2,8,12] is used as well as a rather high challenge dose (5 x 106 cells i.v.)…”

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confidence: 99%

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The role of hepatic lectins and the activity of the mononuclear phagocyte system in systemic Listeria monocytogenes infection in Balb/c mice

Beuth¹,

Ko²,

Pulverer³

1987

Med Microbiol Immunol

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Hepatic lectin blocking experiments with D-galactose in Balb/c mice showed that parenchymal liver cells are obviously not involved in Listeria monocytogenes infection (strain SLCC 4013, 5 x 104 cells i.v.). Using the bacterial immunomodifier Propionibacterium avidum KP-40 the importance of an activated mononuclear phagocyte system in the early stage of Listeria infection could be demonstrated.Listeria monocytogenes is a facultative intracellular bacterium which parasitizes host phagocytes [3,4,8]. Virulent strains induce in mice acute systemic infections which primarily affect reticulo-endothelial organs [4,8,9]. The mononuclear phagocyte system (MPS) is surely the major mediator of natural antilisterial resistance [2,8,10,12]. The role of NK cells, granulocytes and hepatocyte membrane receptors (hepatic lectins) in Listeria infection is not yet clear [1,2,8,10].In this report we discuss the blocking of hepatic lectins by systemic D-galactose treatment as well as the effect of activated MPS in the very early stage of systemic Listeria infection using a murine model [4,5,6] and Propionibacterium avidum KP-40, a very potent MPS activator. To initiate acute systemic infection the highly Listeria-

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Wertung der therapeutischen Wirksamkeit verschiedener Antibiotika auf die experimentelle Listeriose

Waldenmeier

1988

Infection

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The therapeutic activities of various antibiotics were evaluated in two murine models, i.e. the infection of normal mice as well as of nude mice. Coumermycin and rifampicin were the most active drugs, since not only inhibition of multiplication but also rapid elimination of Listeria monocytogenes could be achieved in normal and immunocompromised animals. Ampicillin was the most active beta-lactam antibiotic followed by azlocillin. The other beta-lactam antibiotics were definitely less active. The combination of ampicillin with gentamicin expressed no synergistic effect in vivo. Co-trimoxazole as well as ciprofloxacin were of moderate therapeutic value. The bacteriostatic drugs such as tetracycline and erythromycin were able to inhibit the bacterial multiplication in the normal mouse but not in the immunocompromised host. Thus an optimal drug for therapy of listeriosis does not yet exist.

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The effect of coumermycin on experimental listeriosis

Cited by 7 publications

References 15 publications

Management of listeriosis

Management of listeriosis

The role of hepatic lectins and the activity of the mononuclear phagocyte system in systemic Listeria monocytogenes infection in Balb/c mice

Wertung der therapeutischen Wirksamkeit verschiedener Antibiotika auf die experimentelle Listeriose

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