Thus, protecting piperacillin from hydrolysis.The inclusion of a β-lactamase inhibitor does not always increase drug efficacy. Some bacteria may produce certain types of β-lactamase such as AmpC, which are intrinsically resistant to tazobactam. Mechanisms of resistance
A major mechanism of resistance against piperacillin-tazobactam is Gram-negative bacteria producing β-lactamases. Other currently known mechanisms include mutations in the active site of penicillin-binding proteins, changes in membrane efflux, or bacteria permeability. Some enzymes, such as extended-spectrum β-lactamase (ESBL) have evolved from narrow-spectrum β-lactamases due to genetic mutations, increasing their capabilities to hydrolyze much broader spectrum penicillin. Due to prior conflicting reports on the drugs affinity with ESBL-producing bacteria, piperacillin-tazobactam treatment for such is not recommended. Antibiotic resistance occurs sporadically, conferred by the continuous use of piperacillin-tazobactam in situations where it may prove to be ineffective, leading to cases where plasmid-mediated β-lactamases are being produced in bacteria that do not naturally produce it.Some Gram-positive bacteria penicillin-binding proteins such as Enterococcus faecium (PBP-5) or Staphylococcus aureus (PBP-2a) are intrinsically antibiotic resistant, consisting of relatively low affinity with piperacillin and therefore high resistance to piperacillin-tazobactam. Furthermore, mutations in penicillin-binding proteins cause fluctuations in piperacillin affinity, whereas Streptococcus pneumoniae (PBP-2b) autolytic response is significantly reduced due to decreased affinity with piperacillin. Although membrane permeability changes are less common as a mechanism of resistance, studies investigating Klebsiella pneumoniae have reported a correlation between decreased permeability of piperacillin and increased SHV-1 β-lactamase production.
The organisms most often isolated are believed to be because of compromised abortions, delivery, medical instrumentation, and retention of placental fragments. There is not enough evidence for the use of prophylactic antibiotics to prevent endometritis after manual removal of placental in vaginal birth. Histologically, neutrophilic infiltration of the endometrial tissue is present during acute endometritis. The clinical presentation is typically high fever and purulent vaginal discharge. Menstruation after acute endometritis is excessive and in uncomplicated cases can resolve after 2 weeks of clindamycin and gentamicin IV antibiotic treatment. In certain populations, it has been associated with Mycoplasma genitalium and pelvic inflammatory disease. Chronic endometritis
Chronic endometritis is characterized by the presence of plasma cells in the stroma. Lymphocytes, eosinophils, and even lymphoid follicles may be seen, but in the absence of plasma cells, are not enough to warrant a histologic diagnosis. It may be seen in up to 10% of all endometrial biopsies performed for irregular bleeding. The most common organisms are Chlamydia trachomatis (chlamydia), Neisseria gonorrhoeae (gonorrhea), Streptococcus agalactiae (Group B Streptococcus), Mycoplasma hominis, tuberculosis, and various viruses. Most of these agents are capable of causing chronic pelvic inflammatory disease (PID). Patients with chronic endometritis may have an underlying cancer of the cervix or endometrium (although infectious cause is more common). Antibiotic therapy is curative in most cases (depending on underlying cause), with fairly rapid alleviation of symptoms after only 2 to 3 days.