Age: 33.0
Sex: F
Vaccine: FLU3
Symptoms: Vaginal haemorrhage, Vision blurred, White blood cell count increased
Clinical narrative: This literature report (initial receipt 15-Dec-2011) concerns a 33-year old female pregnant patient, who had a medical history of seasonal allergies, occasional migraine headaches, and no sexually transmitted disease. She had a previous pregnancy had ended at an unknown gestational age; the reason was not determined. Her only medication was prenatal vitamins. She had no known medication allergies. Her mother had a history of hypertension and headaches, a maternal aunt had hypertension, and her father had died of an unknown cause. The patient did not smoke, drink alcohol, or use illicit drugs. The patient had received routine prenatal care at a hospital. At 5 and 7 weeks of gestation, ultrasonography performed because of intermittent vaginal bleeding was reported to reveal an arcuate uterus with findings suggestive of a corneal ectopic pregnancy. At that time, diagnostic laparoscopy revealed no evidence of an ectopic pregnancy. Repeat ultrasound examinations at 8 and 9 weeks showed a normal uterus and fetus, with a subchorionic hematoma that appeared to be resolving. Ultrasound examination at 18 weeks was normal. Screening for syphilis and the human immunodeficiency virus and a urine culture were negative. At 20 weeks of gestation the patient received a seasonal influenza vaccine. At 28 weeks of gestation she received the H1N1 vaccination (WAVES 2011030575). On an unknown date the patient was admitted to the intensive care unit (ICU) at this hospital 16.5 hours post partum because of leukocytosis and gram-positive rods in the blood. Two weeks before admission, the patient noted increased fatigue and dizziness. One week later, at 36 weeks of gestation, the blood pressure at a routine prenatal examination was 132/80 mm Hg (increased from 108/80 mm Hg 2 weeks earlier); a spot urine sample revealed 2+ protein. One week later, at 37.1 weeks of gestation, the blood pressure was 140/84 mm Hg, with 1+ pedal edema. The fundal height was consistent with the gestational date, fetal activity and heart tones were present, and the fetus was in the cephalic presentation. The remainder of the examination was normal. Urinalysis revealed 4+ proteinuria. The patient was admitted to the hospital for induction of labor. On examination, the blood pressure was 153/98 mm Hg, the pulse 84 beats per minute, and the temperature 37.3 degrees C. The fundus was firm; the height was consistent with the gestational age, and the cervix was 1 cm dilated and 50% effaced. The fetal heart-rate tracing showed a rate of 130 to 139 beats per minute. Screening of the patient for hepatitis B virus surface antigen was negative, and the platelet count, the red-cell indexes, and tests of renal function were normal. Labor was induced with a single dose of misoprostol followed by oxytocin and magnesium sulfate. During labor, the patient's blood pressure ranged from 121 to 159 mm Hg systolic and 69 to 111 mm Hg diastolic, and the temperature from 36.4 to 37.3 degrees C. Rupture of the membranes occurred 28.5 hours after admission. Forty-seven hours after admission, spontaneous vertex vaginal delivery of a healthy boy occurred (weight, 2910 g; 1-minute and 5-minute Apgar scores, 8 and 9, respectively). The patient had received an epidural injection of an anesthetic agent and did not undergo an episiotomy. The amniotic fluid was clear and copious. After induction of labor for pre-eclampsia she underwent a prolonged labor. Approximately 90 minutes post partum, the patient reported blurred vision and appeared fatigued. The temperature was 36.7 degrees C, and the blood pressure 131/85 mm Hg. There was copious vaginal bleeding with clots; misoprostol was administered, and magnesium was continued. Test results from blood drawn 5 hours before delivery were reviewed and postpartum specimens of blood and urine were cultured. Urine output decreased, and crystalloid fluids were administered intravenously. Twelve hours post partum, the temperature was 37.2 degrees C, and the patient reported feeling well. Approximately 15 hours after delivery, gram positive rods were isolated from the anaerobic blood culture; the aerobic culture remained sterile. Clindamycin and penicillin G were administered intravenously. Culture of the urine grew few organisms (1000 to <10,000 colony-forming units [CFU] per milliliter) that were consistent with enterococcus, and very few mixed bacteria (100 to <1000 CFU per milliliter). Computed tomography (CT) of the of the abdomen and pelvis, performed after the administration of contrast material, revealed mild bilateral pleural effusions, basilar atelectasis, an enlarged uterus with increased vascularity (consistent with postpartum status), and hyperdense areas within the endometrial canal, with multiple pockets of air. There is no air in the myometrium, the presence of which would have suggested necrosis. The bowel appears normal, and no intraperitoneal collections are seen. There was a Foley catheter bulb with an air-liquid level in the urinary bladder, ascites in the peritoneal cavity, a few subcentimeter retroperitoneal lymph nodes, and air in the spinal canal (thought to be related to the epidural analgesia). This examination did not indicated a source of infection. The patient was transferred to the surgical ICU 16.5 hours after delivery. On examination, the blood pressure was 161/93 mm Hg, the pulse 98 beats per minute, the temperature 36.9 degrees C, the respiratory rate 16 breaths per minute, and the oxygen saturation 100% while she was breathing ambient air. Examination of the abdomen and pelvis revealed findings that were consistent with her postpartum state, with minimal tenderness to palpation over the uterus and no peritoneal signs. The remainder of the examination was normal. Several gram-positive rods routinely grow in an anaerobic blood-culture bottle. Only two, listeria species (a facultative anaerobe) and clostridium species (an obligate anaerobe), are worthy of consideration in this case. On hospital day 2, the microbiology laboratory received the patient's urine for culture, as well as three sets of blood-culture bottles for aerobic and anaerobic bacterial culture. The anaerobic bottle from the first set of blood cultures, collected 3 hours after delivery, grew gram-positive rods on hospital day 3. The aerobic bottle and the two subsequent sets of blood cultures showed no growth. C. (Clostridium) perfringens (formerly C. welchii), was definitively diagnosed on Gram's staining and the result was reported on hospital day 4. A full histopathological examination of the placenta was performed because of the history of bleeding during the first trimester, preeclampsia, and maternal bacteremia. The placental weight was normal (fresh weight, 500 g; mean weight for a gestational age of 37 weeks, 475 g). The gross appearance was normal except for a simple cyst on the fetal surface. Findings on initial histologic examination included a patchy increase in perivillous fibrin beneath the chorionic plate and a mild acute chorioamnionitis with subchorionitis and with fetal vascular involvement. Abundant gram positive rods were identified in the decidua capsularis, with no associated inflammation. Although the finding of abundant gram-positive rods is unusual, it was thought that the bacteria most likely represented a vaginal contaminant acquired during delivery and did not constitute evidence of placental infection, because findings of severe infection (e.g., villitis, abscess, or severe chorioamnionitis) were all absent. On review, however, a very small number of gram-positive rods that were morphologically similar to those in the decidua capsularis were identified in the intervillous space in the maternal circulation and were absent in the fetal circulation. After the diagnosis of maternal C. Perfringens bacteremia was established, the paraffin block containing the decidua capsularis was sent to the reference laboratory for broad-range polymerasechain-reaction assays targeting 16S ribosomal RNA. The bacteria were confirmed to be C. perfringens. Taken together, these findings are consistent with maternal bacteremia in the context of colonization of the decidua capsularis by C. perfringens. Once the diagnosis of C. perfringens bacteremia is established, the clinical differential diagnosis include intraamniotic infection (also referred to as chorioamnionitis), postpartum endometritis manifested as either an anaerobic cellulitis or a uterine myonecrosis (gas gangrene), and bacteremia with no septic focus. Intraamniotic infection is the result of microorganisms found in the lower genital tract and ascending into the amniotic fluid, usually after rupture of the chorioamnionic membranes. Risk factors associated with this diagnosis include prolonged duration of ruptured membranes, more than the usual number of vaginal examinations, and the use of internal monitors. The clinical diagnosis is based on the presence of fever during labor, fetal and maternal tachycardia, maternal leukocytosis, uterine tenderness, and foul-smelling amniotic fluid. This patient had leukocytosis but no fever or tenderness, and the amniotic fluid was not reported to be foul smelling. The pathophysiology of postpartum endometritis is a similar ascending infection, and the risk factors are similar to those associated with intraamniotic infection; however, cesarean delivery is the greatest risk factor for the development of postpartum endometritis. The diagnosis of postpartum endometritis is based on the presence of fever, leukocytosis, uterine tenderness, and foul smelling lochia. This patient did not have a caesarean delivery and had no apparent criteria other than leukocytosis to support a diagnosis of intraamniotic infection or postpartum endometritis. This left bacteremia without a septic focus as the most likely clinical diagnosis. The patient appeared well after delivery. Her vital signs remained stable, with no evidence of hypotension, tachycardia, or tachypnea. The only laboratory value of concern is the elevated leukocyte count. Notably, her anion gap is normal. The clinician would conclude that the patient is not septic, despite the bacteremia. Appropriate antibiotic therapy was initiated (combination of clindamycin and penicillin). The patient required close follow-up for signs of clinical deterioration, such as a change in the vital signs or a progressive systemic acidosis. The clinician considered if there were no clinical deterioration, antibiotic therapy alone should effectively treat this bacteremia that has no septic focus. Although the clinicians recommended the patient to have a hysterectomy, she declined. She was closely observed in the surgical ICU with intensive hemodynamic monitoring. During the next few days, her white-cell counts continued to improve and her hemodynamics remained stable. She has risk factors for the development of both infection of the intraamniotic fluid and post-partum endometritis but no signs or symptoms of these clinical diagnoses. The blood culture is positive for C. perfringens, but the patient has no signs of sepsis and there is no evidence of uterine necrosis or systemic acidosis. On postpartum day 8, the patient was able to go home. The infant remained well, with negative blood cultures.