FUNUSITIS

Funisitis
Etiology•mostly bacteria •low virulence organisms , normal flora of vagina or •obvious pathogens such as E.Coli, Mycoplasma, Ureaplasma
Pathogenesis• bacteria ascending from vagina, breaching cervical defenses (mucus plug etc.) • bacterial colonization of intrauterine space through intact or ruptured membranes • maternal and fetal acute inflammatory response,
Epidemiology•clinically evident in 0.5-10% of pregnancies
General Gross Description•membranes and chorionic plate appear cloudy and occasionally have a yellow or green tint •in severe cases the umbilical cord may have small yellow round lesions on its surface which represent foci of PMN's (small abscesses)
General Microscopic Description•Chorioamnionitis: membranes (amnion and chorion + parietal decidua) show neutrophilic infiltrate. PMN's originate from maternal vessels in parietal decidua and migrate into chorion and then amnion. •Chorionitis: chorionic plate shows neutrophilic infiltrate. PMN's orginate from maternal intervillous space and migrate into subchorionic fibrin, chorion itself and then amnion •Funisitis: umbilical cord shows neutrophilic infiltrate. PMN's orginate in the fetal vessels of the umbilical cord and migrate sequentially through the muscular layers of the vessel and then into the Wharton's jelly. •Chorionic vasculitis: chorionic vessels show neutrophils in wall. PMN's originate in the fetal vessels of the chorionic plate and migrate through the walls of the fetal vessels toward the amniotic fluid
Clinical Correlation•associated with preterm birth •only 8-25% of mothers have symptoms such as fever, chills •fetus may have decreased biophysical profile score or abnormal heart rate pattern •can lead to congenital pneumonia, gastroenteritis, menigitis, sepsis although most infants do not have sepsis even with umbilical cord inflammation
References•Gibbs and Sweet "Maternal and Fetal Infections" (chapter 42) in Creasy and Resnik, Maternal Fetal Medicine: Principles and Practices 3rd edition; Philadelphia: WB Saunders, 1994, p644-646.
Funisitis


Umbilical Vasculitis - acute 10x


Obstetrics & Gynecology 2007;109:121-127 © 2007 by The American College of Obstetricians and Gynecologists

ORIGINAL RESEARCH
Maternal Serum Cytokines in Preterm Premature Rupture of Membranes
Amy P. Murtha, MD1, Tammy Sinclair, BSN1, Elizabeth R. Hauser, PhD2, Geeta K. Swamy, MD1, William N. P. Herbert, MD3 and R. Phillips Heine, MD1
From the 1Department of Obstetrics and Gynecology and 2Center for Human Genetics, Duke University Medical Center, Durham, North Carolina; and 3Department of Obstetrics and Gynecology, University of Virginia, Charlottesville, Virginia.
OBJECTIVE: To estimate whether maternal serum interleukin (IL)-6 or granulocyte colony-stimulating factor (G-CSF) obtained daily are elevated in women with preterm premature rupture of membranes who develop funisitis.
METHODS: Daily blood samples were obtained from women with preterm premature rupture of membranes and analyzed for IL-6 and G-CSF by enzyme-linked immunosorbent assay. Funisitis was determined by placental examination. Observations were stratified based on the presence or absence of funisitis and analyzed. Proportional hazards models were used to evaluate time-to-delivery on the basis of diagnostic IL-6 and G-CSF levels, determined by receiver operating characteristic curve analysis.
RESULTS: Of the 107 patients available for analysis, 54 (50%) had evidence of funisitis after delivery. Patients with funisitis were more likely to deliver at an earlier gestational age (28.5 weeks compared with 31.5 weeks, P<.001) and have Medicaid insurance (57% compared with 39%, P=.04). Serum IL-6 and G-CSF were elevated 24 to 48 hours before delivery in women with preterm premature rupture of membranes with funisitis compared with those without funisitis (IL-6, 7.5 compared with 2.8 pg/mL, P<.001; G-CSF, 121.7 compared with 56.9 pg/mL, P=.002). Using values identified by the receiver operating characteristic curve, elevated serum IL-6 in the interval 24–72 hours before delivery was significantly associated with funisitis (P<.03), even after controlling for gestational age and insurance status. CONCLUSION: Maternal serum IL-6 and G-CSF appear to be biomarkers in the identification of women with preterm premature rupture of membranes likely to develop funisitis. Immunol Today. 1989 Sep;10(9):299-304.
Links
Comment in:
Immunol Today. 1990 Mar;11(3):74.
The cytokine network.
Balkwill FR, Burke F.
The availability of pure recombinant cytokines and molecular probes for their genes has generated an avalanche of scientific information. These data show that cytokines have a broad and overlapping range of cell regulatory activity both in vitro and in vivo. New factors are added to the cytokine list, and new functions reported for existing cytokines, with such frequency that it is difficult to retain an overall picture. With this problem in mind, a large wallchart was designed and was displayed at the second meeting of the British Cytokine Group* whose members pooled their collective knowledge, to list the known biological activities of these cytokines. This wallchart of cytokine activity, now referenced, is reproduced for Immunology Today. It is not a final list: new information and cytokines are continually reported and space has been left for readers to make their own additions. A neutrophil-activating peptide variously named monocyte-derived neutrophil chemotactic factor (MDNCF), neutrophil-activating factor (NAF), lymphocyte-derived neutrophil-activating peptide (LYNAP), which has been suggested as a candidate for interleukin 8 (IL-8), is included.

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