Discussion
Though, it was suspected preoperatively, the diagnosis of clinical chorioamnionitis was made at surgery as the liquor was very foul smelling. The risk factors were preterm pre-labour rupture of membranes (PROM) and gestational diabetes. There was initially no maternal fever which is present in most cases. This confirmed that knowing the risk factors can add to the diagnostic accuracy, as in all situation treatment needs to be initiated based on clinical diagnosis. Hence the definition of chorioamnionitis varies according to the key diagnostic criteria which can be clinical based on the presence of typical findings like maternal fever and tachycardia and foul-smelling liquor or vaginal discharge; microbiologic based on the culture of microbes from properly collected amniotic fluid or chorioamnion histo-pathologic based on microscopic evidence of infection or inflammation on examination of placenta or chorioamnionic specimen. Histologic chorioamnionitis is a more common diagnosis as it includes both subclinical and clinical chorioamnionitis. Funisitis occurs when infection/inflammation extends to the umbilical cord1,2-4.
When chorioamnionitis is suspected in the absence typical clinical signs, biochemical, serum or amniotic fluid tests may be used to diagnose subclinical chorioamnionitis. Amniocentesis for amniotic fluid culture is the best method for diagnosis of subclinical chorioamnionitis in preterm gestations. Other tests that can be obtained rapidly include white cell count, c-Reactive Protein (CRP) level, leukocyte esterase level, gram stain and glucose concentration and cytokine level (IL-6)1,5-7. Blood culture was not done in our patient as she initially did not have fever. Ideally this should be done prior to administration of antibiotics which should be done within an hour of recognition of severe sepsis and sepsis bundle protocol should be implemented. Critical care outreach team should be contacted if indicated8.
The maternal complications of chorioamnionitis are postpartum haemorhage, endometritis, wound infection, sepsis and death. The neonatal complications include premature birth, stillbirth, neonatal sepsis, chronic lung disease and brain injury causing cerebral palsy and other neuro-developmental disabilities1,5-6.
Route of infection is ascending infection in 96% of cases. The remainder are from haematogenous spread due to maternal septiaemia, iatrogenic from procedures like amniocentensis and CVS. Infection from the peritoneum via the fallopian tubes have been postulated1,2.
The most common organisms identified in pregnant women dying from sepsis are genital mycoplasmas, Lancefield group A beta haemolytic streptococcus and Escherichia Coli9. E. Coli belongs to the family of Enterobacteriaceae - a large order of different types of bacteria that commonly cause infections both in healthcare settings and in communities. To survive the effects of antibiotics, some Enterobacteriaceae produce extended-spectrum beta-lactamase (ESBL) enzyme that destroy and render ineffective commonly used antibiotics like penicillins and 1st, 2nd and 3rd generation cephalosporins, but not cephamycin and carbapenems. This resistance means fewer antibiotic options available to treat ESBL producing bacterial infection and even more common infection caused by such organism may require more complex treatment requiring prolonged hospitalization and intravenous carbapenem antibiotics - a class of highly effective antibiotic agents commonly used for the treatment of severe or high-risk bacterial infections9-11. This class of antibiotics is usually reserved for known or suspected multidrug-resistant bacterial infections. Resistance that render these antibiotics ineffective are on the rise too. Therefore, appropriate and justified use of this important class of antibiotics is necessary to decrease the risk of emergence of resistance. Our patient’s specimen from placental tissue and wound pus culture was resistant to commonly used antibiotics and was sensitive only to Meropenem, Ertapenem and Gentamicin. Resistance that destroys these antibiotics are on the rise too. The more we rely on this important class of antibiotics, the greater the risk of spreading resistance to them. This mandates the practice of sending appropriate specimens for culture before initiating antimicrobials as well as implementation of stewardship programs to regulate the appropriate use of antimicrobials to reduce emergence of resistance. As well as, robust infection control practices that help to prevent cross transmission of infection11.
ESBL- producing organisms were first found in Europe and the earliest cases were identified in the USA in 198810. A pooled prevalence of faecal colonization of 14% globally was estimated by a systematic review9 and Villa HE10 et al in Argentina quoted 5.4% of pregnant women in their study had ESBL-producing E coli vaginal colonization revealing that colonization with resistant Enterobacteriaceae is significant in pregnancy. A higher prevalence of 22% was reported in South-Asia9 where our patient came from.
According to CDC, ESBL-producing Enterobacteriaceae pose challenging infection control issues and are a serious global threat that requires prompt and sustained action12. Appropriate use of antibiotic therapy under the guidance of infectious disease team is imperative. Prophylactic use of antibiotics during conservative management of PROM and prompt delivery after 34 weeks will help reduce the risk of infection. Screening strategies designed to monitor for ESBL-producing E. coli could be useful in women from endemic areas to prevent perinatal transmission and the introduction of multi-resistant strains to the maternity ward.