It frequently includes organisms such as Ureaplasma, Streptococcus, Mycoplasma, and Bacteroides, and may also include organisms such as Gardnerella, Chlamydia, Lactobacillus, Escherichia, and Staphylococcus. Differential diagnosis
A number of other conditions can cause fevers following delivery including: urinary tract infections, breast engorgement, atelectasis and surgical incisions, among others. Management
Antibiotics have been used to prevent and treat these infections—however, the misuse of antibiotics is a serious problem for global health. It is recommended that guidelines be followed that outline when it is appropriate to give antibiotics and which antibiotics are most effective.Atelectasis: mild to moderate fever, no changes or mild rales on chest auscultation.Management: pulmonary exercises, ambulation (deep breathing and walking). Urinary tract infection: high fever, malaise, costovertebral tenderness, positive urine culture.Management: antibiotics as per culture sensitivity (cephalosporine). Endometritis: moderate fever, exquisite uterine tenderness, minimal abdominal findings.Management: multiple agent IV antibiotics to cover polymicrobial organisms: clindamycin, gentamicin, addition of ampicillin if no response, no cultures are necessary. Wound infection: persistent spiking fever despite antibiotics, wound erythema or fluctuance, wound drainage.Management: antibiotics for cellulitis, open and drain wound, saline-soaked packing twice a day, secondary closure. Septic pelvic thrombophlebitis: persistent wide fever swings despite antibiotics, usually normal abdominal or pelvic exams.Management: IV heparin for 7–10 days at rates sufficient to prolong the PTT to double the baseline values. Mastitis: unilateral, localized erythema, edema, tenderness.Management: antibiotics for cellulitis, open and drain abscess if present. Epidemiology
The number of cases of puerperal sepsis per year shows wide variations among published literature—this may be related to different definitions, recordings etc.
When this mutant subunit is expressed in cells with wild-type α and β subunits it produces non-functional receptors. Since wild-type α and β subunits expressed alone are able to produce GABA inducible current this indicates that the mutation either prevents both coassembly of the mutant and wild-type subunits but also coassembly of the wild-type α and β subunits or prevents proper trafficking of the formed receptor to the membrane. Fusion of GFP onto this mutated subunit has indicated that it is localized to the endoplasmic reticulum instead of the cell membrane. As with other known GEFS+ type 3 mutation, Q351X likely results in neuronal hyperexcitability. SCN2A mutations
The final type of GEFS+ is caused by mutations in the SCN2A gene, which encodes a sodium channel α subunit. The first associated mutation in this gene is R187W, located on the intracellular region linking membrane spanning units two and three in the first domain (D1S2-S3, figure 3). Patients with this mutation have both febrile and afebrile seizures. Electrophysiological examination of this mutant revealed that it increases the time constant for inactivation, presumably increasing sodium current and leading to hyperexcitability. However, this mutation also yields channels that inactivate at more hyperpolarized potentials relative to wild-type channels, indicative of hypoexcitability. Whether the result on membrane excitability of this mutation is hyperexcitability or hypoexcitability is, as yet, unclear.The second known mutation in SCN2A associated with GEFS+ is R102X. This mutation is located in the intracellular N-terminus (figure 3) and results in SMEI in patients.