Antimicrobial resistance developed in several pathogens poses an increasing threat to human health across the world. No country can escape from the medical and economic impacts from this serious problem. Although the antibiotic resistance is not a new phenomenon, the current magnitude and speed with which it is developing is a cause for the global concern including in India. There are so many common diseases resulting from the microorganisms such as blood stream infections, urinary tract infections, post-operative wound infections and intra-abdominal infections. In this review the antimicrobial susceptibility or resistance of Enterobacter towards antimicrobial agents and heavy metals, viz. ceftazidime, moxifloxacin, nalidixic acid, sulfamethaxazole, and nickel and lead is discussed briefly along with other antimicrobials and heavy metals. The mechanisms behind the resistance by Enterobacter was analyzed and evaluated by many workers after using currently employed susceptibility testing methods for Enterobacter spp. There are some factors influencing mode of action of fluoroquinolones, quinolones and sulfamethaxazole. History, classification, identification, clinical features and treatment of infections and the epidemiology of antimicrobials (drugs and heavy metals) resistance by the Enterobacter spp. is included in this review. Now a day, antimicrobial resistance is common in hospitals where acquired infections can be perilous. This situation compels scientists to synthesize new antibiotics and treatment modalities. Enterobacter causes nosocomial infections. It is ubiquitous and can survive on skin and dry surfaces and replicate in contaminated fluids. Numerous outbreaks have been described. Various mechanisms have been adapted by microorganisms to resist toxicity of antimicrobials. Antimicrobial drugs may be rendered inactive or ineffective by the major ways such as barrier to antibiotic entry into the bacterial cell, prevention of the antibiotic from reaching the target, often by extrusion, alteration of the target of the drug and inactivation of the antibiotic by modification or destruction. In addition, bacteria may be able to bypass the metabolic pathway affected by a particular drug or may be able to overproduce an enzyme that is inhibited by the drug action, more than one mechanism may operate at any given time