Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “funisitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1992

Necrotizing funisitis.

Necrotizing funisitis is an umbilical cord lesion characterized by perivascular bands of necrotic Wharton jelly containing inflammatory cells in various stages of degeneration. Sixty cases were reviewed histologically. Clinical information was available in 45. Forty-five age-matched infants with acute (nonspecific) funisitis only were used as controls. Infants with necrotizing funisitis had more stillbirths, birth weights below the tenth percentile (small for gestational age [SGA]), infectious complications, and necrotizing enterocolitis. No consistent infectious agents or predisposing maternal factors were found. Cord neovascularization correlated with SGA infants. Necrotizing funisitis occurred in 0.1% of deliveries greater than 20 weeks' gestation. The perivascular bands, likened to the pattern of an Ouchterlony diffusion plate, suggest the presence of a diffusible toxin in the amniotic fluid. The stillbirths and SGA infants may represent the toxin's effect on the fetus. The lack of perivascular necrotic bands around vessels on the placental surface suggests neutralization or more effective clearing of the agent in this region, for reasons as yet undetermined. The factors underlying the cord lesion may contribute to superimposed acute nonspecific vasculitis and chorioamnionitis.

Acute Disease↗
PubMedDate not supplied

Congenital syphilis and necrotizing funisitis.

During the past 5 years we encountered 16 cases of necrotizing funisitis, a deeply seated inflammatory process within the matrix of the umbilical cord, and established that all of them were associated with maternal and congenital syphilis. During that time necrotizing funisitis was not found to be associated with any other infection. The relationship was unexpected on the basis of current knowledge of the condition, but we found the older medical literature documents syphilis as the virtually specific cause of deep funisitis with angiophlebitis. Necrotizing funisitis has a characteristic macroscopic appearance, the "barberpole" cord, that permits the presumptive diagnosis of congenital syphilis at the time of birth.

Autopsy↗
PubMed1977

Chronic viral funisitis.

Four cases chronic funisitis, a rare variant of umbilical cord inflammation, are presented and compared with the acute and subacute forms. The distinctive findings are a predominantly lymphoplasmocytic infiltration, coagulative necorsis of the vascular media with secondary calcification, and the unusual association of chronic funisitis with chronic chorioamnionitis and chronic villitis. One fetus was stillborn, another was aborted, and two were live-born. Two fetuses were growth retarded and three had evidence of infection. Viral inclusions were identified in three placentas. The data strongly suggest that lymphoplasmocytic funisitis in these cases is the result of chronic intrauterine viral infection.

Amnion↗
PubMed1992

Necrotizing funisitis: a study of 45 cases.

Necrotizing funisitis (NF) is a distinctive inflammatory condition of the umbilical cord, characterized by perivascular concentric rings of inflammatory cells, necrotic debris, or calcium deposits. Necrotizing funisitis has been strongly associated with syphilis by some investigators, while others have failed to link NF with any consistent infectious agents. We examined 45 cases of NF to determine its relationship with syphilis. Five (11%) mothers had syphilis as confirmed by a positive rapid plasma reagin test and a positive fluorescent antibody absorbed test, 31 (69%) had a negative rapid plasma reagin test or venereal disease research laboratory test, and test results were not available for the remaining nine (20%). There was no record of syphilis in those babies born to mothers without confirmed syphilis. Estimated gestational age at the time of delivery ranged from 18 to 40 weeks (mean, 28 weeks). Prolonged rupture of membranes was present in 28 (62%) of the mothers, and ranged from 1 to 51 days (mean, 9 days); this was the most frequently seen maternal factor in connection with NF. Fourteen (31%) of the babies were stillborn or nonviable, including three (60%) of the five born to mothers with syphilis. Maternal and fetal cultures revealed no consistent microorganisms. Placental histology was significant for chronic villitis in 26 (58%) cases, including all five (100%) with maternal syphilis. Acute chorioamnionitis was present in each case (100%) and varied from mild to severe. We conclude that (1) NF has a polymicrobial etiology, (2) in the absence of other placental findings associated with syphilis NF should not be considered presumptive of this disease, and (3) factors leading to NF may also contribute to acute chorioamnionitis, premature rupture of membranes, and stillbirth.

Female↗
PubMed1979

Chorioamnionitis and funisitis due to Corynebacterium kutscheri.

When isolated from the female genital tract, diphtheroids are usually regarded as commensal organisms. Corynebacterium kutscheri however is a pathogen in laboratory rodents. We report a case in which C. kutscheri was isolated as a pure culture from the umbilical cord and from other surface sites in an infant. Histological examination of the cord and membranes demonstrated the organisms within these fetal tissues. The organisms evoked a fetal cellular response. The importance of recognising commensals as potential pathogens in states of altered host resistance in stressed.

Corynebacterium↗
PubMed1978

The significance of different forms of placentitis.

A blind histological examination of placentae, with regard to placentitis, was carried out of 2 prospective, selected materials. The first consisted of 283 placentae, which were selected with regard to optimal obstetric outcome. The second consisted of 160 placentae, randomized from all premature and low birth weight infants in the local area. Placentitis was sub-divided into: funisitis, chorionitis, villitis and hypercellular villi. Funisitis was found in premature infants only. Villitis resulted in the birth of significantly smaller infants and placentae, and must therefore, in contrast to funisitis and chorionitis, be considered chronic. Hypercellular villi are found to have no importance. Funisitis, chorionitis and villitis could possibly be explained by an infection in 10 of a total of 15 cases of placentitis.

Birth Weight↗
PubMed1979

Pathology of the placenta and cord in ascending and in haematogenous infection.

The two main patterns of inflammatory response in the placenta and its adnexae are: (1) amniotic infection, usually bacterial ascending, with acute chorioamnionitis and funisitis; (2) haematogenous villitis, usually viral, with early necrotizing lesions and vasculitis and, later, chronic infiltrates and obliterative vasculitis. In amniotic infection most cells in the exudate are maternal. These leucocytes participate in antibacterial defence of the amniotic cavity in conjunction with substances such as zinc polypeptide and lysozyme and may contribute directly to fetal defence. Immunoglobulins may be produced in the cord of placenta only in protracted lesions such as 'healed' funisitis. Individual variations in the resistance of the membranes to bacterial penetration are possible. In viral infections a massive multifocal production by plasmacytes of immunoglobulins M, G and A is seen in affected villi. The secretion of non-specific antiviral substances in the infected placenta is possible. In all affected villi there is an activation of fixed macrophages (Hofbauer cells) that remain partly 'immature', i.e. are lysozyme-negative. Multifocal lymphoplasmacytic villitis is uncommon and has helped to focus the diagnosis on prenatal infection. In contrast, non-specific lymphocytic villitis is common; since there is no morphological difference between cases known to be associated with an infection, e.g. varicella, and the others, many cases may well be due to silent infection, although a graft-versus-host reactions remains a distinct possibility.

Amnion↗
PubMed1977

Placental abnormalities in victims of the sudden infant death syndrome.

Placentas from 79 victims of the sudden infant death syndrome (SIDS) were compared with placentas from 30,640 controls who survived in a search for evidences of infections or other disorders that might have damaged the SIDS victims before birth. Placentas from the SIDS victims had an increased frequency of acute funisitis, acute chorioamnionitis, lymphocytic infiltration of the decidua and macrophages in the fetal membranes. The acute funisitis and chorioamnionitis were associated with preterm deliveries and were probably related to amniotic fluid bacterial infections which are a common cause of premature delivery.

Bacterial Infections↗
PubMed1975

Congenital cutaneous candidiasis.

Two cases of congenital cutaneous candidiasis are presented in order to call attention to this rarely recognized and infrequently reported condition. Clinical features and appropriate cultures are useful in differentiating the lesions from other more common dermatoses of the neonatal period. Microscopic examination of the placenta may disclose fungal funisitis or chorioamnionitis, thus defining the congenital nature of the disease. Topical antifungal therapy is sufficient unless systemic candidiasis is present. No evidence of impaired immunological responsiveness was found in the two infants.

Candidiasis, Cutaneous↗
PubMed1992

The relationship between acute inflammatory lesions of the preterm placenta and amniotic fluid microbiology.

OBJECTIVE: Our objective was to determine the relationship between microbial invasion of the amniotic cavity and the presence and severity of acute inflammatory lesions in the placenta. STUDY DESIGN: Placental histologic and amniotic fluid microbiologic studies were performed in 92 consecutive patients who were admitted with preterm labor and intact membranes and delivered within 48 hours after amniocentesis. RESULTS: The prevalence of a positive amniotic fluid culture was 38% (35 of 92). There was a strong association between the presence and severity of inflammation in the amnion, chorion-decidua, umbilical cord, and chorionic plate and the results of the amniotic fluid culture (p less than 0.0001 for each tissue section). Three patterns of inflammation of the chorion-decidua were identified: marginating, nonmarginating, and a mixed pattern. The marginating and the mixed patterns of inflammation were strongly associated with the presence of a positive amniotic fluid culture. Acute inflammation of the chorionic plate was the most sensitive indicator of a microbial invasion of the amniotic cavity (sensitivity 96.6%), and funisitis and umbilical vasculitis had the highest specificity (85.7%). CONCLUSION: The presence of acute inflammatory lesions of the chorioamniotic membranes can serve as a marker of microbial invasion of the amniotic cavity.

Amnion↗
PubMed1988

Antenatal origin of neurologic damage in newborn infants. I. Preterm infants.

Currently, the diagnosis of white matter necrosis may be performed with echoencephalography when cysts are observed in the white matter adjacent to the lateral ventricles. One hundred twenty-seven infants with a gestational age less than 36 weeks (mean [+/- SE] gestational age = 31 +/- 3.2 weeks) were studied in the neonatal period with echoencephalography to determine the incidence of white matter necrosis and the perinatal variables associated with this complication. Twenty-three infants (18.3%) had white matter necrosis. Thirteen (10.3%) had cysts by day 3 (11 on day 1), indicating that the onset of white matter necrosis occurred antenatally. The incidence of antenatal white matter necrosis was inversely related to birth weight and was more frequent in infants weighing less than 1000 gm (19%). Stepwise logistic regression analysis of 31 antenatal variables showed that placental vascular anastomoses in multiple pregnancies, funisitis, and purulent amniotic fluid were the only complications associated with antenatal white matter necrosis. Follow-up neurologic evaluations were abnormal in four of six patients with antenatal white matter necrosis. The findings in this study focus attention on prenatal, rather than intrapartum and postnatal, factors as causative agents of neurologic morbidity and emphasize the importance of early and sequential evaluation of neonatal brain structures.

Cerebral Hemorrhage↗
PubMed1986

Intrauterine latent herpes simplex virus infection: II. Latent neonatal infection.

Herpes simplex virus (HSV, probably type 2) antigen has been detected in endometria and abortion tissue (companion paper) and in placentae, umbilical cords, and fetal and neonatal organs by avidin-biotin complex immunohistochemical studies. HSV cytologic abnormalities were not detected in any of the 12 normal and 64 abnormal cases analyzed, nor was HSV detected by culture or electron microscopy in selected cases. Antigen was present in single epithelial and, rarely, mesenchymal cells of various organs. Clinically unexplained fetal or neonatal problems associated with HSV antigen positivity included intrauterine death, fetal growth retardation, cystic brain degeneration, hydrops, interstitial pneumonitis, necrotizing enterocolitis, hepatitis, encephalitis, myocarditis, and renal failure. Maternal floor infarct of placenta and calcifying funisitis are the manifestations of intrauterine HSV infection in most cases. Maternal history of HSV infection was uncommon. It is concluded that intrauterine HSV infection may persist in the fetus and neonate in a latent fashion without cytologic abnormalities or detectable virus. This latent infection may be associated with intrauterine and neonatal death, organ damage, and neonatal disease.

Antigens, Viral↗
PubMed1991

Pathology and human immunodeficiency virus expression in placentas of seropositive women.

The pathology of term placentas from seropositive human immunodeficiency virus (HIV)-infected and seronegative women was investigated by routine histologic, immunocytochemical, and in situ hybridization techniques. Placentas were evaluated for evidence of villitis, chorioamnionitis, and funisitis. Membranes, trophoblast, and decidua were also examined by immunohistochemistry using monoclonal HIV p24 antibody. Twenty placentas were evaluated by combined immunochemical and in situ hybridization techniques, using a 35S-labeled RNA probe complementary to the 3' long terminal repeat and envelope region of HIV-1. HIV-seropositive placentas did not show significant villitis; however, the incidence of chorioamnionitis increased (P less than .01). HIV antigens and nucleic acids were identified in the trophoblast of 10% of the placentas that also showed chorionitis. Term HIV-positive placentas may show histologic changes that may or may not be directly related to the virus. Analysis of tissues from earlier gestational placentas may prove more informative in clarifying the mechanism of maternal-fetal HIV transmission.

Chorion↗
PubMed1990

Congenital candidiasis limited to the nail plates.

Numerous case reports have been published of patients with cutaneous congenital candidiasis and neonatal candidiasis; however, this is the first reported case of congenital candidiasis confined to the nail plates. A subplacental candidal abscess, funisitis, and demonstration of hyphal invasion of fetal nail plates supported the diagnosis.

Candida albicans↗
PubMed1989

Umbilical cord sclerosis as an indicator of congenital syphilis.

In two cases of congenital syphilis examination of the umbilical cord showed a distinctive picture of perivascular sclerosis and inflammation. Large numbers of spirochaetes were shown in the sclerotic zone in both cases. No organisms were demonstrable in the placental disc and there were no morphological changes suggestive of syphilis. It is concluded that the finding of sclerosing funisitis, together with the clinical circumstances, should raise the possibility of congenital syphilis.

Adolescent↗