Table 1601

Properties Conferred by Naturally Occurring Plasmids

Resistance and Defense

Antibiotic resistance against aminoglycosides, p-lactams, chloramphenicol, sulfonamides, trimethoprim, fusidic acid, tetracyclines, macrolides, fosfomycin Resistance to many heavy metal ions including Ni, Co, Pb, Cd, Cr, Bi, Sb, Zn, Cu and Ag Resistance to mercury and organomercury compounds

Resistance to toxic anions such as arsenate, arsenite, borate, chromate, selenate, tellurite, etc

Resistance to intercalating agents such as acridines and ethidium bromide

Protection against radiation damage by UV and X-rays

Restriction systems that degrade bacteriophage DNA

Resistance to certain bacteriophages

Aggression and Virulence

Synthesis of bacteriocins

Synthesis of antibiotics

Crown gall tumors and hairy root disease in plants caused by Agrobacterium Nodule formation by Rhizobium on roots of legumes

R-body synthesis due to plasmids of Caedibacter symbionts in killer Paramecium Virulence factors of many pathogenic bacteria, including toxin synthesis, protection against immune system and attachment proteins Metabolic Pathways

Degradation of sugars e.g. lactose (in Salmonella), raffinose, sucrose

Degradation of aliphatic and aromatic hydrocarbons and their derivatives such as octane, toluene, benzoic acid, camphor Degradation of halogenated hydrocarbons such as polychlorinated biphenyls Degradation of proteins Synthesis of hydrogen sulfide Denitrification in Alcaligenes Pigment synthesis in Erwinia Miscellaneous

Transport of citrate in E. coli Transport of iron

Gas vacuole production in Halobacterium

FIGURE 16.10 Antibiotic Resistance Plasmids

Plasmids carry genes for replicating their DNA, transferring themselves from one host cell to another, and genes for a variety of phenotypes. Many plasmids carry genes that confer antibiotic resistance on the host cell when the genes are expressed.

FIGURE 16.10 Antibiotic Resistance Plasmids

Plasmids carry genes for replicating their DNA, transferring themselves from one host cell to another, and genes for a variety of phenotypes. Many plasmids carry genes that confer antibiotic resistance on the host cell when the genes are expressed.

by 1970 this had risen to over 30%. These strains often carry resistance genes for different antibiotics on one single plasmid. Today, the transfer of multiple antibiotic resistance plasmids between bacteria has become a major clinical problem. Patients with infections after surgery, with severe burns, or with immuno-compromised systems are at highest risk to antibiotic resistant infections.

Soil bacteria (e.g. Streptomyces) or fungi (e.g. Penicillium) produce antibiotics as a natural part of there physiology. Consequently, R-plasmids were in existence before the clinical use of antibiotics by humans, but they have spread far and wide since wide scale use of antibiotics started. A major factor in R-plasmid spread is the practice of feeding animals (e.g. pigs and chickens) antibiotics to prevent illnesses that reduce yield. Recently, some countries have banned the use of human antibiotics in animal feed and there has been a major decline in the frequency of R+ bacteria carried by farm animals.

Most R-plasmids are of moderate to large size and present in 1-2 copies per host cell. Most are self-transmissible at a low frequency, although de-repressed mutants showing high transfer frequency are sometimes found. The original F-plasmid is such a "naturally-occurring mutant". R-plasmids belong to a wide range of incompatibility groups. Many carry resistances to one or more antibiotics and/or toxic heavy metals and may also carry genes for colicins, virulence factors etc.

Plasmid borne resistance mechanisms usually inactivate or expel the antibiotic, rather than altering vital cell components.

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