Chorioamnionitis Causes Perinatal Illnesses Blamed on Smoking

The anti-smokers have concealed an enormous, gold-standard NINDS study because it proves their claims are fallacious

"Acute chorioamnionitis is the largest contributor to the poor pregnancy outcomes of black women and women who have low socioeconomic status," and it is "the most common cause of preterm labor wherever it has been studied" (RL Naeye. Acute chorioamnionitis and the disorders that produce placental insufficiency. In: Monographs in Pathology No. 33, Pathology of Reproductive Failure. FT Krause et al., eds.Williams and Wilkins, 1991, Ch 10, pp 286-307).

Chorioamnionitis is the general term for infection of the amniotic membranes (the chorion, amnion, and placenta, and sometimes also the umbilical cord) by bacteria, mycoplasmas, and ureaplasmas during pregnancy. The infection weakens the membranes which results in their premature rupture. Inflammation causes swelling around the placental villa which reduces the flow of blood and causes hypoxia in the fetus, and by-products of bacteria and/or of fetal distress initiate preterm labor.

"Infants who are born preterm as the result of acute chorioamnionitis are often ill because their lungs, brains, and intestinal tracts are immature and because placental edema made them hypoxic before birth. Most of the morbidity associated with acute chorioamnionitis in preterm-born infants presents with signs of acute antenatal hypoxia (i.e., low Apgar scores, the need to resuscitate vigorously at birth, neonatal respiratory distress syndrome, and recurrent apneic episodes). These findings usually correlate much more strongly with the severity and extent of placental villous edema that is present than with the severity and stage of chorioamnionitis." (RL Naeye. Acute chorioamnionitis and the disorders that produce placental insufficiency. In: Pathology of Reproductive Failure. FT Krause et al., eds. Williams & Wilkins, 1991, Ch 10, pp 286-307.)

The bacteria can also make the baby ill. Pneumonia in newborns is nearly always caused by chorioamnionitis. Exposed neonates are also at greater risk of septicemia, and more rarely, of neonatal otitis media, meningitis, and septic arthritis.

Pathological examination of the placenta is necessary to determine the presence of chorioamnionitis in epidemiological studies, because there is sufficient clinical evidence to diagnose the infection in only about 10% of affected pregnancies. Even in cases that turned out to be fatal, there was sufficient clinical evidence for a diagnosis in only one fourth of them. (RL Naeye. Editorial. The investigation of perinatal deaths. NEJM 1983;309(10):611-612.)

The anti-smokers have falsely blamed smoking for all the ills caused by chorioamnionitis (preterm birth, premature rupture of membranes, stillbirth, septicemia and the other neonatal infections) by using defective studies which did not include pathological examinations of the placenta. Because chorioamnionitis is more common in women of lower socioeconomic status, and smokers are more likely to be of lower socioeconomic status, smoking got the blame instead.

"We recently found no significant association between maternal smoking and either stillbirths or neonatal deaths when information about the underlying disorders, obtained from placental examinations, was incorporated into the analysis. Similar analyses found no correlation between maternal smoking and preterm birth. The most frequent initiating causes of preterm birth, stillbirth, and neonatal death are acute chorioamnionitis, disorders that produce chronic low blood flow from the uterus to the placenta, and major congenital malformations. There is no credible evidence that cigarette smoking plays a role in the genesis of any of these disorders." (RL Naeye. Disorders of the placenta, fetus and neonate, diagnosis and clinical significance. CV Mosby Co., 1992.)

Naeye's study population was the 56,000 pregnancies of the Collaborative Perinatal Project, sponsored by the National Institutes of Neurological Diseases and Stroke of the National Institutes of Health, in which nearly 45,000 placentas were painstakingly examined. This is an enormous, gold-standard study with no equivalent in either size or quality, and the anti-smoking conspirators have purposely covered it up.

The anti-smokers refuse to even mention the subject of infection in their studies and reviews, let alone discuss its importance in the diseases for which they blame smoking. And if they mention Naeye's work, it is only his earlier, not his later publications. I personally brought this issue to the attention of the authors of the California EPA ETS report chapter on "Developmental Toxicity I: Perinatal Manifestations," Gayle Windham and Mari Golub. But there was no mention of this in the published "Summary of Public Comments and Responses."

And, they go right on repeating their false claims that maternal smoking is harmul to the babies even when the data make a mockery of this claim. In a masterpiece of pretense, last year HHS Secretary Donna Shalala spent 12 paragraphs gushing exuberantly about declines in teen pregnancy and rates of maternal smoking, and increases in prenatal care, all of which should supposedly be expected to improve birth outcomes, before reluctantly admitting the sorry truth in the second to last paragraph of her press release.

"In contrast to improvements in prenatal care and a reduction in maternal smoking, the rate of preterm births increased sharply in 1997 to 11.4 percent (437,000) and the proportion of infants born low birthweight (291,000) reached the highest level in over two decades, 7.5 percent." A lame excuse was attempted that this was "due in part to a remarkable rise in multiple births," before conceding that low birthweight has also risen among single births.

As Naeye observed in 1991, "Because the frequency of preterm births has hardly changed in the United States during the past three decades, it is unlikely that anything currently being done in the health care system is preventing these infections." For starters, the health establishment ought to stop deceiving the public and laying guilt trips on pregnant smokers. They should stop shoveling out money for medically worthless social engineering projects aimed at making them quit, and redirect the money to preventing and treating infection instead. Nonsmokers would benefit from this as well.

Cervical cultures and amniocentesis have been of negligible value in predicting outcome. Even in cases of preterm premature rupture of membranes, positive cultures of amniotic fluid were found in only 27.9%, and it was conceded that "This figure probably underestimates the true prevalence of intraamniotic infection" (R Romero et al. Infection in the pathogenesis of preterm labor. Semin Perinatol 1988;12(4):262-279). Besides, amniocentesis is an invasive procedure which introduces additional risks. Not even the recent directive to treat pregnant women with antibiotics to prevent complications from group B streptococcus appears to have made a dent in the problem, so perhaps treatment would have to be attempted earlier, before pregnancy occurs.

An example of the CDC's scientific fraud of deliberately using defective studies to falsely blame smoking for perinatal illness caused by chorioamnionitis: Medical-Care Expenditures Attributable to Cigarette Smoking During Pregnancy -- United States, 1995. MMWR 1997 Nov 7;46(44):1048-1050 (pages 12-14 of pdf document).

MMWR 1997 / Centers for Disease Control (pdf)

New studies

The contribution of pathological examination of the placenta in the investigation of the causes of foetal mortality. E Agapitos, C Papadopoulou, N Kavantzas, J Papoulias, V Antonaki, P Davaris. Arch Anat Cytol Pathol 1996;44(1):5-11. "Three hundred (300) placentas were examinated over a period of three years (1988-1991). The clinical history, autopsy examination and placental histological examination were taken into account to determine the cause of death. Autopsy findings revealed the cause of death in only 33 cases (12.9%). In contrast, placental examination allowed us to determine the cause of death in 123 cases (48.4%) especially in abortions (54.4%). The most frequent abnormalities found were vascular insufficiency in intrauterine deaths (16.47%) and acute chorioamnionitis with foetal involvement in abortions (31.4%). Fifty six (56) cases with diagnoses of acute chorioamnionitis, chronic villitis of unknown aetiology and erythroblastosis were classified in the highrisk group for a subsequent pregnancy."

Agapitos - Arch Anat Cytol Pathol 1996 abstract / PubMed

"Preterm delivery is the chief problem in obstetrics today, accounting for 70 percent of perinatal mortality and nearly half of long-term neurologic morbidity. Approximately 10 percent of all births are preterm, but most of the serious illness and death is concentrated in the 1 to 2 percent of infants who are born at less than 32 weeks of gestation and who weigh less than 1500 g. Approximately 20 percent of preterm births are the result of a physician's decision to bring about delivery for maternal or fetal indications, and the remainder follow the spontaneous onset of labor or rupture of the membranes." Intrauterine Infection and Preterm Delivery. RL Goldenberg, JC Hauth, WW Andrews. NEJM 2000 May 18;342(20):1500-1507.) Review.

Goldenberg / NEJM 2000 full article

Adeno-associated virus DNA in human gestational trophoblastic disease. K Kiehl, JR Schlehofer, R Schultz, M Zugalb, E Armbruster-Moraes. Placenta 2002 May;23(5):410-415. "AAV DNA was found in 43 samples (28/49 hydatiform moles, 4/14 choriocarcinomas, 11/15 miscarriage material material)."

Kiehl - Placenta 2002 abstract / PubMed

Patterns of colonization with Ureaplasma urealyticum during neonatal intensive care unit hospitalizations of very low birth weight infants and the development of chronic lung disease. S Castro-Alcaraz, EM Greenberg, DA Bateman, JA Regan. Pediatrics 2002 Oct;110(4):e45. "We found a significantly higher rate of CLD at 28 days of age (odds ratio: 8.7; 95% confidence interval: 3.3, 23) and at 36 weeks' postconceptional age."

Castro-Alcaraz / Pediatrics 2002 abstract

Correlation of in situ detection of infectious agents in the placenta with neonatal outcome. L Genen, GJ Nuovo, L Krilov, JM Davis. J Pediatr 2004 Mar;144(3):316-320. "Placental tissue from 33 newborn infants with systemic illness and poor neonatal outcome [death or significant neurodevelopmental abnormalities] were tested by in situ hybridization or reverse transcriptase-polymerase chain reaction for infectious pathogens. Control placentas came from mothers delivering infants with poor neonatal outcome of known cause (ie, cord prolapse, uterine rupture), mothers with known infections, and normal births (n=21). RESULTS: There were 5 deaths among the newborn infants, and all survivors had poor neonatal outcome. Placentas from 24 of 33 cases (73%) had positive test results for Coxsackie virus (46%), bacteria (38%), herpes (8%), and parvovirus (4%) and picornavirus (4%). At autopsy, multiple organs from the newborn infant had positive test results for the same organism isolated from the placenta."

Genen - J Pediatr 2004 abstract / PubMed

Histologic correlates of viral and bacterial infection of the placenta associated with severe morbidity and mortality in the newborn. A Satosar, NC Ramirez, D Bartholomew, J Davis, GJ Nuovo. Hum Pathol 2004 May;35(5):536-545. 77 cases, "either fetal or neonatal death (11 cases with autopsy material available in 8 cases) or idiopathic severe respiratory distress or central nervous system-related symptoms at birth (49 cases). Controls included 11 placentas from births with no morbidity and 6 placentas that were associated with severe neonatal morbidity of known etiology (trisomy, ruptured uterus, prolapsed cord)... An infectious cause was found in 46/60 (76%) of cases; these were distributed as follows: enterovirus, 23 cases (22 were coxsackie virus); bacterial (consensus probe), 15 cases; cytomegalovirus (CMV), 4 cases; herpes simplex virus (HSV), 2 cases; parvovirus, 2 cases. The infectious agents localized primarily to Hofbauer cells and trophoblasts. In each of the 8 cases for which autopsy material was available, the same infectious agent that was detected in the placenta was also detected in the autopsy material (spleen, heart, central nervous system, or lungs). No infectious agent was detected in any of the 17 controls."

Satosar - Hum Pathol 2004 abstract / PubMed

Histologic, infectious, and molecular correlates of idiopathic spontaneous abortion and perinatal mortality. GJ Nuovo, LD Cooper, D Bartholomew. Diagn Mol Pathol 2005 Sep;14(3):152-158. "Placentas and corresponding neonatal tissues in 21 consecutive cases of idiopathic spontaneous abortion or perinatal death, before or within 2 days of birth, were tested for an infectious agent. The controls included 10 consecutive cases of fetal and placental tissues from therapeutic abortions, 5 placentas from unremarkable childbirths, and 11 placentas from cases of spontaneous abortion or perinatal death of known cause (ruptured uterus, placenta abruption, prolapsed cord). An intrauterine infection was noted in 16 of 21 (76%) of the placentas associated with neonatal mortality; in each case, the same infectious agent was found in the neonatal tissues, primarily the spleen. The most common infectious agent was enterovirus/coxsackie virus (10 cases); the histologic findings in the placenta were nonspecific. There was strong expression of TNF-alpha in the placenta and spleen of each of the cases of intrauterine infection and in none of the 26 controls."

Nuovo - Diagn Mol Pathol 2005 abstract / PubMed

Mycoplasmas and Ureaplasmas as Neonatal Pathogens. KB Waites, B Katz, RL Schelonka. Clin Microbiol Rev 2005 Oct;18(4):757-789. Review. "Isolation of Ureaplasma spp. but not M. hominis from the chorioamnion has been consistently associated with histological chorioamnionitis and is inversely related to birth weight, even when adjusting for duration of labor, rupture of fetal membranes, and presence of other bacteria..."

Waites / Clin Microbiol Rev 2005 full article

Universal DNA primers amplify bacterial DNA from human fetal membranes and link Fusobacterium nucleatum with prolonged preterm membrane rupture. RJ Cahill, S Tan, G Dougan, P O'Gaora, D Pickard, N Kennea, MH Sullivan, RG Feldman, AD Edwards. Mol Hum Reprod 2005 Oct;11(10):761-766. "The commonest organism Fusobacterium nucleatum was found in 9/15 (60%) of samples. Ten of the 12 samples obtained after prolonged membrane rupture were positive for bacterial DNA, and 7 of these (70%) contained DNA from F. nucleatum."

Cahill - Mol Hum Reprod 2005 abstract / PubMed

Proteomic profiling of the amniotic fluid to detect inflammation, infection, and neonatal sepsis. CS Buhimschi, V Bhandari, BD Hamar, MO Bahtiyar, G Zhao, AK Sfakianaki, CM Pettker, L Magloire, E Funai, ER Norwitz, M Paidas, JA Copel, CP Weiner, CJ Lockwood, IA Buhimschi. PLoS Med 2007 Jan 16;4(1):e18. In 169 consecutive women with singleton pregnancy following admission at Yale-New Haven Hospital with symptoms of premature labor (PTL), advanced cervical dilatation, and/or preterm premature rupture of membranes (PPROM). All degrees of inflammation were associated with preterm birth, regardless of membrane status. "There was a significant association between the MR score and severity of histological chorioamnionitis (r = 0.599, p < 0.001)." "When compared with other laboratory tests routinely used to diagnose amniotic fluid inflammation and infection, the MR score had the highest accuracy to detect inflammation." "Premature birth is fairly common, with around 12% of births in the US fitting this definition. However, it has serious consequences, being responsible for around 70% of infant deaths and other adverse outcomes for the baby. It is not clear in all cases what directly causes premature birth or how to identify cases in which mother and child are at greater risk of serious outcomes. Evidence from case-control and other studies strongly suggests that infections of the uterus, placenta, or genital tract are associated with, and are likely to directly cause, premature deliveries. Such infections, even if they are “subclinical” (that is, they do not directly cause signs or symptoms that the doctor or patient would notice) cause inflammation in the affected tissues... This study showed that the MR score was closely associated with a number of different indicators of poor outcome in preterm birth. These outcomes included sooner deliveries, sepsis in the baby, and inflammation in the placenta." Among those with positive microbial culture results, the most common isolates were Ureaplasma urealyticum (17/44), Streptococcus species (9/44), and Bacteroides species (5/44).

Buhimschi / PLoS Med 2007 full article
Buhimschi - PLoS Med 2007 / PubMed Central full article

"Of 459 stillbirths, 428 stillbirths were included. The incidence of chorioamnionitis was 36.9%, with higher rates evident in early and late gestation. A fetal inflammatory response was present in 13.3% and correlated with spontaneous labor and very early spontaneous preterm death. The absence of a fetal response was associated with unexplained antepartum death." (Chorioamnionitis and fetal response in stillbirth. MM Lahra, A Gordon, HE Jeffery. Am J Obstet Gynecol 2007 Mar;196(3):229.e1-4; Chorioamnionitis and Fetal Response Tied to Stillbirth. Reuters Health 2007 Mar 30.)

Lahra Am J Obstet Gynecol 2007 abstract / PubMed
Chorioamnionitis and fetal response in stillbirth / Medscape

Waddlia chondrophila, a Potential Agent of Human Fetal Death. D Baud, V Thomas, L Regan, G Greub. EID 2007 Aug;13(8):1239. In 69 women with sporadic miscarriages, 200 women with recurrent miscarriages, and 169 control women who had had uneventful pregnancies, seroprevalence of Waddlia chondrophila, a type of Chlamydia, was higher in women who had had sporadic and recurrent miscarriages than in control women (p<0.001). "In a multivariate logistic regression adjusted for age, ethnicity, contact with animals and C. trachomatis serostatus (Figure 2), miscarriage (SM/RM) remained strongly associated with Waddlia seropositivity (odds ratio [OR] 4.9, 95% confidence interval [CI] 2.5–9.4). In this model, miscarriage was also independently associated with age (OR 2.9, 95% CI 2.0–4.1) and C. trachomatis seropositivity (OR 2.3, 95% CI 1.2–4.5). Additional multivariate models confirmed the association between Waddlia IgG seropositivity and miscarriage, with ORs ranging from 4.9 to 6.2... Waddlia seropositivity was associated with early miscarriage (p<0.001."

Baud / EID 2007 full article

Microbial prevalence, diversity and abundance in amniotic fluid during preterm labor: a molecular and culture-based investigation. DB DiGiulio, R Romero, HP Amogan, JP Kusanovic, EM Bik, F Gotsch, CJ Kim, O Erez, S Edwin, DA Relman. PLoS One 2008 Aug 26;3(8):e3056. 166 women in preterm labor with intact membranes. "A positive PCR was associated with histologic chorioamnionitis (adjusted odds ratio [OR] 20; 95% CI, 2.4 to 172), and funisitis (adjusted OR 18; 95% CI, 3.1 to 99). The positive predictive value of PCR for preterm delivery was 100 percent. A temporal association between a positive PCR and delivery was supported by a shortened amniocentesis-to-delivery interval (adjusted hazard ratio 4.6; 95% CI, 2.2 to 9.5). A dose-response association was demonstrated between bacterial rDNA abundance and gestational age at delivery (r(2) = 0.42; P<0.002)." "Importantly, compared to both methods combined, culture exhibited a false negative rate of 27% (3/11) in subjects delivering before 25 weeks (Figure 4A), a cohort with a neonatal mortality rate exceeding 70% in meta-analyses [25]. This underscores the need for improved diagnostic assays in this setting."

DiGiulio - PLoS One 2008 full article / PubMed Central
DiGiulio / PLoS One 2008 full article

Can placental pathology explain second-trimester pregnancy loss and subsequent pregnancy outcomes? SK Srinivas, LM Ernst, AG Edlow, MA Elovitz. Am J Obstet Gynecol 2008 Oct;199(4):402.e1-5. "A blinded pathologist examined placentas from 90 patients with spontaneous second-trimester pregnancy loss and 17 controls who presented for induction of labor for fetal indications... Acute inflammation was more prevalent in cases than controls (P < .001). Sixty-seven percent of all cases and none of the controls showed a stage 2-3 inflammatory response. Histologic abruption was also more prevalent in cases than controls (P = .05)."

Srinivas - Am J Obstet Gynecol 2008 abstract / PubMed

Uncultivated Bacteria as Etiologic Agents of Intra-Amniotic Inflammation Leading to Preterm Birth. YW Han, T Shen, P Chung, IA Buhimschi, CS Buhimschi. J Clin Microbiol 2009 Jan;47(1):38-47. "Amniotic fluids (AF) from 46 pregnancies complicated with PTB and 16 asymptomatic women were analyzed. No bacterial DNA was amplified in AF collected from the asymptomatic women. Among the 46 samples associated with PTB, bacterial DNA was amplified from all (16/16) which were culture positive and 17% (5/30) which were culture negative. In the culture positive group, additional species were detected in more than half (9/16) of the cases by PCR and clone analysis. Altogether, approximately 60% of the species detected by the culture-independent methods were not isolated by culture. They include both uncultivated and difficult-to-cultivate species such as Fusobacterium nucleatum, Leptotrichia/Sneathia spp. Bergeyella sp., Peptostreptococcus sp., Bacteroides spp., and Clostridiales sp. To examine intra-amniotic inflammation, AF proteomic fingerprint (Mass Restricted (MR) score) was determined using mass spectrometry SELDI-TOF. Inflammation was detected in all five samples which were culture negative but PCR positive. Women who were PCR positive more often had elevated interleukin-6 in AF, histological chorioamnionitis, funisitis, and delivered neonates with early-onset neonatal sepsis. Previously unrecognized, uncultivated or difficult-to-cultivate species may play a key role in initiating PTB."

Han - J Clin Microbiol 2009 abstract / PubMed

Intrauterine inflammation, neonatal sepsis, and chronic lung disease: A 13-year hospital cohort study. M Lahra, PJ Beeby, HE Jeffery. Pediatricts 2009 May;123(5):1314-1319. 761 births <30 weeks gestation, with placental examinations. "Regression analysis showed that chorioamnionitis with umbilical vasculitis and increasing gestation were associated with reduced odds of chronic lung disease. Chorioamnionitis without umbilical vasculitis showed a trend to reduced odds of chronic lung disease. Birth weight at <3rd percentile and neonatal sepsis were associated with increased odds of chronic lung disease... A fetal inflammatory response is protective for chronic lung disease. Neonatal sepsis is strongly associated with chronic lung disease, and the infecting organism is important. Coagulase-negative staphylococcal infection confers a risk for chronic lung disease similar to that of other bacteremias. Candidemia confers the greatest risk of chronic lung disease."

Lahra / Pediatrics 2009 abstract

Perinatal correlates of Ureaplasma urealyticum in placenta parenchyma of singleton pregnancies that end before 28 weeks of gestation. IN Olomu, JL Hecht, AO Onderdonk, EN Allred, A Leviton, for the Extremely Low Gestational Age Newborn Study Investigators. Pediatrics 2009 May;123(5):1329-1336. Culture of chorion samples from 866 singleton deliveries <28 weeks. "U urealyticum was recovered from 6% and bacteria from 47%; 47% of placentas had no bacteria detectable. Sixty-seven percent of Ureaplasma-positive placentas also harbored bacteria. Placentas that harbored U urealyticum only were more likely than sterile placentas to be associated with a higher prevalence of preterm labor and preterm premature rupture of membranes, as well as umbilical cord, fetal vessel, membrane, and parenchymal inflammation and to predict intraventricular hemorrhage and echolucent brain lesions. Placentas that harbored U urealyticum only were similar to placentas that harbored bacteria only."

Olomu / Pediatrics 2009 abstract

Parachlamydia and Rhabdochlamydia in Premature Neonates. F Lamoth, S Aeby, A Schneider, K Jaton-Ogay, B Vaudaux, G Greub. EID 2009 Dec;15(12):2072. Respiratory samples from 29 neonates admitted to the neonatology unit, all but one with a gestational age of less than or equal to 36 weeks; 25 (86%) had respiratory distress. 12 were PCR positive for Parachlamydia and/or Rhabdochlamydia. "Newborns with a Chlamydia-related organism documented in the respiratory tract had a significantly worse primary adaptation score (Apgar). These patients experienced more resuscitation maneuvers at birth. Durations of invasive mechanical ventilation and hospital stay were also longer among them. Three newborns died, compared with no deaths among the 17 with negative PCR results (p = 0.06). Pneumonia was documented in 5 of the 12 patients with positive Parachlamydia and/or Rhabdochlamydia PCR results but was concomitant to PCR positivity for only 3 of them. An alternative etiology was documented in all 3."

Lamoth / EID 2009 full article

Activation of Peroxisome Proliferator-Activated Receptor Gamma by Human Cytomegalovirus for De Novo Replication Impairs Migration and Invasiveness of Cytotrophoblasts from Early Placentas. B Rauwel, B Mariamé, H Martin, R Nielsen, S Allart, B Pipy, S Mandrup, MD Devignes, D Evain-Brion, T Fournier, C Davrinche. J Virol 2010 Mar;84(6):2946-2954. "In the present report, by using reporter gene activation assays and confocal microscopy in the presence of a specific antagonist, we show for the first time that HCMV infection induces peroxisome proliferator-activated receptor gamma (PPAR) transcriptional activity in infected cells... we then provided evidence that by activating PPAR human cytomegalovirus dramatically impaired early human trophoblast migration and invasiveness, as assessed by using well-established in vitro models of invasive trophoblast, i.e., primary cultures of extravillous cytotrophoblasts (EVCT) isolated from first-trimester placentas and the EVCT-derived cell line HIPEC. Our data provide new clues to explain how early infection during pregnancy could impair implantation and placentation and therefore embryonic development."

Rauwel / J Virol 2010 abstract

Antibody treatment promotes compensation for human cytomegalovirus-induced pathogenesis and a hypoxia-like condition in placentas with congenital infection. E Maidji, G Nigro, T Tabata, S McDonagh, N Nozawa, S Shiboski, S Muci, MM Anceschi, N Aziz, SP Adler, L Pereira. Am J Pathol 2010 Sep;177(3):1298-1310. "In untreated infection, viral replication proteins were found in trophoblasts and endothelial cells of chorionic villi and uterine arteries. Associated damage included extensive fibrinoid deposits, fibrosis, avascular villi, and edema, which could impair placental functions. Vascular endothelial growth factor and its receptor fms-like tyrosine kinase 1 (Flt1) were up-regulated, and amniotic fluid contained elevated levels of soluble Flt1 (sFlt1), an antiangiogenic protein, relative to placental growth factor. With hyperimmune globulin treatment, placentas appeared uninfected, vascular endothelial growth factor and Flt1 expression was reduced, and sFlt1 levels in amniotic fluid were lower. An increase in the number of chorionic villi and blood vessels over that in controls suggested compensatory development for a hypoxia-like condition."

Maidji - Am J Pathol 2010 full article / PubMed Central

Human cytomegalovirus infection inhibits CXCL12- mediated migration and invasion of human extravillous cytotrophoblasts. JA Warner, KJ Zwezdaryk, B Day, DE Sullivan, G Pridjian, CA Morris. Virol J 2012 Nov 1;9:255. "Infection with HCMV significantly decreased secretion of CXCL12 by SGHPL-4 cells, and induced a striking perinuclear accumulation of the chemokine. HCMV infection significantly increased mRNA and total cell surface expression of the two known receptors for CXCL12: CXCR4 and CXCR7. Functionally, HCMV-infected SGHPL-4 cells were unable to migrate or invade in response to a gradient of soluble CXCL12 in transwell assays. Collectively, these studies demonstrate that HCMV impairs EVT migration and invasion induced by CXCL12. As HCMV has the ability to inhibit EVT migration and invasion through dysregulation of other relevant signaling pathways, it is likely that the virus affects multiple signaling pathways to impair placentation and contribute to some of the placental defects seen in HCMV-positive pregnancies."

Warner - Virol J 2012 full article / PubMed Central
Warner - Virol J 2012 full article

BECAUSE OF THIS VICIOUS LIE THAT SMOKING HARMS THE FETUS, AN ANTI-SMOKER SHOT A PREGNANT WOMAN!

"Most people cringe at the sight of a pregnant woman smoking. Some people feel strongly enough to say something in protest. But one local man took matters into his own hands early Friday when, according to police, he shot an expectant mother who refused to put out her cigarette..." (Pregnant woman shot over cigarette 18-year-old refused to stop smoking. By Michael Perlstein Staff writer/The Times Picayune Oct. 5, 2002.)

Perlstein / The Times Picayune 2002

Premature births in the US have increased for over two decades, despite persecution of smokers

"Premature births have hit their highest level in two decades, making up roughly 12 percent of the 4,025,933 newborns in 2001. Premature babies - those born earlier than 37 weeks of gestation - are often underweight. Not surprisingly, the incidence of low birth weight infants - defined as weighing less than about 5.5 pounds - rose to 7.7 percent of deliveries, up more than 13 percent since the mid-1980s." This was despite the persecution of pregnant smokers to make them quit, the workplace and public smoking bans, and smokers intimidated out of smoking in their own homes by the false and reckless accusations of the "health authorities." It was also despite increased rates of prenatal care, and a decrease in the number of births to teenagers. Experts lamely attempted to blame an increase in induced labor and multiple births, which make up only a small percentage of the total. (More Women Receiving Prenatal Care. By Adam Marcus, HealthScoutNews Reporter, Dec. 18, 2002. Source: Joyce Martin, MPH, statistician, National Center for Health Statistics; Health and Human Services Report, "Births: Final Data For 2001," Dec. 18, 2002.)

HealthScoutNews Dec. 18, 2002 / Health on the Net, 2002

The truth: "The rate of premature births jumped from 9.4 percent of live births in 1981 to 11.9 percent in 2001, [Dr. Nancy S.] Green says, and the March of Dimes would like to see the rate lowered to no more than 10.1 percent of live births. The public is largely misinformed about what causes premature delivery, two March of Dimes surveys found. One survey of 600 pregnant women and a second of 2,000 men and women found that two-thirds of both groups felt that premature births were due to a mother not taking care of herself -- smoking, abusing drugs or not getting prenatal care. That's because doctors thought so, too, says Dr. Ian Holzman, chief of newborn medicine at New York City's Mount Sinai School of Medicine. 'It has been medicine's perception that if we can just get everybody into prenatal care, we'll stamp out prematurity, but it isn't that simple,' he says. 'Premature deliveries continue to be a major health issue, and what is disturbing is that the rates haven't come down even though other areas of health care have improved. This campaign is important.'" (Premature Births on the Rise. By Janice Billingsley. HealthScoutNews, Jan. 30, 2003.)

Premature Births on the Rise / Health on the Net, 2003

"Nationwide, the rate of premature births jumped 13% between 1992 and 2002, with seven states showing increases of 30 percent or more... 'This is alarming news,' says Dr. Jennifer L. Howse, president of the March of Dimes. 'Premature birth is now the most common, serious and costly infant health problem facing our nation. Last year annual hospitalization of these infants cost $13.6 billion. As a nation we must address this growing crisis in infant health and make it a priority...' Other data from the new report from the National Center for Health Statistics: The premature birth rate in 2002 rose to 12.1 percent of live births, up from 11.9 percent in 2001." (Premature Birth Rate in U.S. Reaches Historic High; Now Up 29 Percent Since 1981. March of Dimes Press Release, Feb. 3, 2004.)

Premature Birth Rate in U.S. Reaches Historic High, 2004 / March of Dimes

"Some 12.3 percent of all babies – 499,008 infants -- were born prematurely (less than 37 weeks gestation) in 2003, according to the report released by the National Center for Health Statistics (NCHS). That’s up from 12.1 percent (or about 480,000 babies) in 2002 – and an increase of more than 30 percent since the government began tracking premature births in 1981. The prematurity rate was 9.4 in 1981; it has increased every year since then except for slight dips in 1992 and 2000... The NCHS report, entitled “Births Final Data for 2003” appeared in the National Vital Statistics Report, volume 54, number 2." (Number of Babies Born Prematurely Nears Historic Half Million Mark in U.S. March of Dimes Press Release, Sep. 8, 2005.)

Number of Babies Born Prematurely Nears Historic Half Million Mark in U.S., 2005 / Science Daily

"The preterm birth rate, the percentage of babies born at less than 37 completed weeks gestation, now is 12.5 percent and has increased more than 30 percent since 1981, when the government began tracking premature birth. More than 71% of preterm infants were born between 34 and 36 weeks gestation and are considered “late preterm.” The NCHS report confirms a March of Dimes finding that those born late preterm are the fastest growing subgroup of premature babies... The NCHS report confirmed an increase in the percent of babies born with low birthweight from 7.9 percent in 2003 to 8.1 percent in 2004..." (Government Data Confirms Rise in Preterm Birth Rate. March of Dimes Press Release, October 2, 2006.)

Government Data Confirms Rise in Preterm Birth Rate, 2006 / March of Dimes

Trends in Birth Weight and Gestational Length Among Singleton Term Births in the United States: 1990-2005. SM Donahue, KP Kleinman, MW Gillman, E Oken. Obstet Gynecol 2010 Feb;115(2):357-364. Data from the U.S. National Center for Health Statistics for 36,827,828 singleton neonates born at 37–41 weeks of gestation, 1990–2005. "We examined trends in birth weight, birth weight for gestational age, large and small for gestational age, and gestational length in the overall population and in a low-risk subgroup defined by maternal age, race or ethnicity, education, marital status, smoking, gestational weight gain, delivery route, and obstetric care characteristics. RESULTS: In 2005, compared with 1990, we observed decreases in birth weight (−52 g in the overall population, −79 g in a homogenous low-risk subgroup) and large for gestational age birth (−1.4% overall, −2.2% in the homogenous subgroup) that were steeper after 1999 and persisted in regression analyses adjusted for maternal and neonate characteristics, gestational length, cesarean delivery, and induction of labor. Decreases in mean gestational length (−0.34 weeks overall) were similar regardless of route of delivery or induction of labor."

Donahue - Obstet Gynecol 2010 abstract / PubMed
Donahue - Obstet Gynecol 2010 full article / PubMed Central

No Explanation for Smaller Babies. By Crystal Phend, Senior Staff Writer, MedPage Today, Jan. 22, 2010. Re: Donahue 2010. "Gestational duration dropped by an average of 2.4 days overall, by 2.31 days in the low-risk subgroup, and for those born after induction of labor, cesarean delivery, or both."

No Explanation for Smaller Babies / MedPage Today

Anti-Smoker Scientific Fraud: "A new study revealed that strong smoke-free policies can improve foetal outcomes by significantly reducing the prevalence of maternal smoking. Researchers from the University of Colorado School of Pharmacy collected data from mothers residing in Pueblo, Colo., before and after a citywide smoking ban took effect. Results show a 23 percent decrease in the odds of preterm births and a 37 percent decrease in the odds of maternal smoking in Pueblo following the ban, while El Paso County, Colo, showed no such drop during the same time period... “This research proves that smoking is an irrefutable risk factor for expectant mothers who are acutely more affected,” said Professor Robert Page." This study hasn't even been published. (Smoking ban leads to major decrease in maternal smoking, pre-term births. Press release, American Public Health Association, Nov. 9, 2010.) If this claim were true, it would have shown up in national statistics long ago. This propaganda proves (again) the utter reckless disregard that these criminals have for science and truth. It was presumably inspired by the same cabal who concocted the fraudulent Pueblo heart attack study, which cherry-picked seasonal periods to falsely pretend that heart attack death rates declined after the ban, when they actually increased.

Fraudulent claims of "smoking costs"

Estimation of the break-even point for smoking cessation programs in pregnancy. M Shipp, MS Croughan-Minihane, DB Petiti, AE Washington. American Journal of Public Health 1992 Mar;82(3):383-390. Preterm low birth had the most impact on the cost: "For instance, in a population studied recently with a high incidence of and high relative risk for preterm LBW, the break-even cost was $237." The study was intended to justify the cost of quit-smoking programs for pregnant smokers, with imaginary "savings" supposedly to result from the decreased rates of preterm low birthweight which have never materialized. The authors were all at the School of Medicine of the University of California at San Francisco, the home of anti-smoker Stanton A. Glantz. It was funded by a fellowship grant from the Pew Charitable Trusts, and with money from the California cigarette and tobacco surtax from the Tobacco-Related Disease Research Program of the University of California.

Shipp - AJPH 1992 full article / tobacco document

The Department of Health and Human Services LIES through their teeth.

(From Healthy People 2010): "The general category of LBW infants includes both those born too early (preterm infants) and those who are born at full term but who are too small, a condition known as intrauterine growth retardation (IUGR). Maternal characteristics that are risk factors associated with IUGR include maternal LBW, prior LBW birth history, low prepregnancy weight, cigarette smoking, multiple births, and low pregnancy weight gain. Cigarette smoking is the greatest known risk factor." This claim, that "Cigarette smoking is the greatest known risk factor" for low birth weight is a deliberate, conscious lie, created by ignoring the role of chorioamnionitis in preterm birth and its greater prevalence among the lower socioeconomic classes, in which smokers are more likely to be found; and lumping healthy births of lower weight together with low birth weights caused by disease, in order to create the false impression that increasing birth weight alone would improve health - which it does not.

"VLBW usually is associated with preterm birth. Relatively little is known about risk factors for preterm birth, but the primary risk factors are prior preterm birth and spontaneous abortion, low prepregnancy weight, and cigarette smoking. These risk factors account for only one-third of all preterm births." This is the same lie again, plus that outrageous weasel that "Relatively little is known" as a pretext for ignoring what IS known - namely, that chorioamnionitis is the most important cause of preterm birth, and their list of so-called "risk factors" is a lie by omission.

The Big Lie of "Smoking-attributable costs of complicated births"

"Smoking-attributable costs of complicated births in 1995 were estimated at $1.4 billion (11 percent of costs for all complicated births, based on smoking prevalence during pregnancy of 19 percent) and $2.0 billion (15 percent for all complicated births, based on smoking prevalence during pregnancy of 27 percent)." This is based on a claim that complicated births in smokers cost more than complicated births in non-smokers, which is based, not upon direct comparison, as most readers presume, but on using multivariate analysis to concoct fictitious costs of smokers versus non-smokers. [A hint to the clueless: direct comparison of costs does NOT involve multivariate analysis!] Their statistical fraud falsely presumes that smokers' costs are higher than they 'should have been' based on the amount of prenatal care they received. But the established ineffectuality of prenatal care to prevent the leading complication, preterm birth, makes their ritual adjustment for prenatal care a means of creating confounding, not preventing it. Then, they use the phony excess plus the rates of smoking during pregnancy to concoct a bogus "smoking-attributable fraction" and "smoking-attributable cost," as per the CDC's infamous SAMMEC (Smoking-Attributable Mortality, Morbidity and Economic Costs) computer program. This is the fraudulent source article: Medical-Care Expenditures Attributable to Cigarette Smoking During Pregnancy -- United States, 1995. MMWR November 07, 1997 / 46(44);1048-1050.

MMWR Nov. 7, 1997 / Centers for Disease Control

Healthy People 2010 Lies

"Smoking accounts for 20 to 30 percent of all LBW births in the United States. The effect of smoking on LBW rates appears to be attributable to intrauterine growth retardation rather than to preterm delivery." They are deliberately misusing words to confuse mere smaller size in healthy term infants, with a distinct and serious medical condition called intrauterine growth retardation (IUGR), which is associated with pre-eclampsia and chronic maternal hypertension, that cause low uteroplacental blood flow and markedly reduce fetal growth.

Healthy People 2010. 16. Maternal, Infant, and Child Health. Co-Lead Agencies: Centers for Disease Control and Prevention, Health Resources and Services Administration.

16. Maternal, Infant, and Child Health / Healthy People 2010

RWJF Funded the SAMMEC Maternal Smoking Costs Fraud

The lying scum simply proclaim grandiosely that "The causal association between maternal smoking and maternal morbidity, infant mortality, and infant morbidity is well established" - ignoring the fact that this phony "causal association" was manufactured with the use of studies which had no placental examinations for chorioamnionitis. (Costs of smoking during pregnancy: development of the Maternal and Child Health Smoking Attributable Mortality, Morbidity and Economic Costs (MCHSAMMEC) software. Cathy L Melvin, E Kathleen Adams, Vince Miller. Tob Control 2000;9(Suppl 3):iii12-iii15(Autumn).) The development of this fraudulent computer program was funded by The Robert Wood Johnson Foundation. (Adams EK. Development of the Maternal and Child Health (MCH) Smoking Attributable Morbidity, Mortality, and Economic Cost (SAMMEC) Model: Final Report to the Robert Wood Johnson Foundation (under grant 022247); 1999. In: Prenatal Smoking Book Data: References. Centers for Disease Control and Prevention. Date last reviewed: 03/29/2006.) Melvin was one of the co-authors of this book.

Melvin / Tobacco Control 2000 full article
Index, Prenatal Smoking Book / Centers for Disease Control and Prevention
References, Prenatal Smoking Book / Centers for Disease Control and Prevention

Cathy L. Melvin is the Project Director of a $1,399,902 grant from the Robert Wood Johnson Foundation running from May 1, 2002 to Jun 30, 2007 (ID# 045257 ) to the Cecil G. Sheps Center for Health Services Research at the University of North Carolina - Chapel Hill, for "Marketing and communications support for the Smoke-Free Families National Partnership to Help Pregnant Smokers Quit." The Sheps Center was designated the National Dissemination Office of RWJF's Smoke-Free Families project and has been funded by them since 1994. Melvin is also the author of fraudulent claims about “Smoking and Reproductive Health” in the Surgeon General’s Report on Smoking and Women’s Health, 2001, and other anti-smoking dreck.

ID# 045257 / Robert Wood Johnson Foundation
Child Health Services / Sheps Center for Health Services Research
Melvin CV / University of North Carolina School of Public Health
Search: Melvin CL / PubMed

"Last year, Carolina received more than $7.6 million in research funding from the foundation... A $5 million gift in 2000 established the NDO at UNC-Chapel Hill." Cathy L. Melvin, research associate professor of maternal and child health and director of NDO, lies that "[Smoking] causes over 1,000 infant deaths per year and is the single biggest preventable cause of premature and low birth weight babies." (Robert Wood Johnson Foundation grants to help pregnant women quit smoking, dentist shortage. Carolina Connections, Spring 2003.)

Robert Wood Johnson Foundation grants, 2003 / University of North Carolina

March of Dimes Collusion with the Anti-Smokers

The March of Dimes lies that "Smokers have smaller babies than nonsmokers, on average, and maternal exposure to another person's smoking may also decrease the baby's birthweight," and falsely pretends that therefore, elimating these factors would eliminate the adverse health conditions that are the real cause of low birthweight.

Low Birthweight / March of Dimes

Bonnie Dobrowolski, Assistant Director of Public Health Education of the March of Dimes, participated in Work Group 1, "Prevention of Smoking Through Comprehensive School Health Education," of the National Conference on Smoking or Health, Nov. 18, 1981.

Work Group 1, NCSH 1981 / tobacco document

Irwin Tobin, Director of Public Education, Greater New York Chapter of the March of Dimes, participated in Work Group 2, "Use of 'High Risk' Concept in Smoking Control." Its Group Leader was Lester Breslow.

Work Group 2, NCSH 1981 / tobacco document

Edward A. Franck, Vice President for Public Information of the March of Dimes, participated in Work Group 8, "Countering Cigarette Advertising and Supporting the Rights of Nonsmokers Through the Media" (this is how these subhuman vermin mischaracterize a systematic campaign of deliberate psychopathic lies and defamations against smokers) of the 1981 National Conference on Smoking or Health.Edward L. Bernays was also a participant.

Work Group 8, NCSH, 1981 / tobacco document

The March of Dimes Still Lies

"Smoking is a known cause of some cases of preterm birth, low-birthweight and very low-birthweight, resulting in increased neonatal deaths and increased health care costs." LIE. Those studies are based on deliberately fraudulent studies that ignore the role of chorioamnionitis. "Nearly 13% of low birthweight deaths are due to smoking. About 18% of Sudden Infant Deaths are attributable to smoking. (WI Burden of Tobacco Report, DHFS)" The SIDS studies ignore infection as well, and the Wisconsin Burden of Tobacco Report is nothing but a mini version of the SAMMEC, which uses the same fraudulent methods. "Prematurity/low birthweight is one of the costliest reasons for a hospital stay. Charges averaged $58,000 for these stays. Of these babies 10% had charges of at least $146,000. By contrast, stays for newborns typically average $4,300. (March of Dimes Data Book for Policy Makers, 2003)" And, as the March of Dimes is fully aware, the rates of preterm birth have steadily risen, despite persecution of smoking. (Pregnancy and Smoking in Wisconsin. March of Dimes, Wisconsin Chapter. Accessed Mar. 3, 2006.)

Smoking and Pregnancy in Wisconsin / March of Dimes

"Scheduling a preconception check-up is the most important New Year’s resolution a woman planning to have a baby can make." [Then why have the rates of preterm birth steadily increased despite higher rates of prenatal care? Perhaps these people ought to read their own press releases before they babble.] "Don’t smoke and avoid second hand smoke. Smoking increases the risk of premature birth." [LIAR! Then why why have the rates of preterm birth steadily increased despite lower rates of smoking?] (March of Dimes New Years' Resolutions for a Healthy Baby. March of Dimes Press Release, Dec. 22, 2006.)

March of Dimes New Years' Resolutions for a Healthy Baby / March of Dimes

Don't Give to the March of Dimes

The March of Dimes actively lobbied for SF 128, the extortionate 2007 state cigarette tax increase in Iowa (lobbyists - Erika Anderson, John Pederson, Lorelei Heisinger).

Sepsis, Pneumonia, and Meningitis

Epidemiology of group B streptococcal disease in the United States: shifting paradigms. A. Schuchat. Clin Microbiol Rev 1998 Jul;11(3):497-513. (Review) Group B streptococci (GBS) are the leading cause of sepsis and meningitis in newborns.

Schuchat / Clin Microbiol Rev 1998 full article

Prevention of Perinatal Group B Streptococcal Disease. Revised Guidelines from CDC. S Schrag, R Gorwitz, K Fultz-Butts, A Schuchat. MMWR August 16, 2002;51(RR11):1-22. "The majority of infections in newborns occur within the first week of life and are designated early-onset disease. Late-onset infections occur in infants aged >1 week, with most infections evident in the first 3 months of life. Young infants with invasive GBS disease usually present with sepsis or pneumonia, and less often contract meningitis, osteomyelitis, or septic arthritis. The proportion of infants with meningitis is higher among those with late-onset infections... In addition to colonization with GBS, other factors increase the risk for early-onset disease. These include gestational age <37 completed weeks, longer duration of membrane rupture, intraamniotic infection, young maternal age, black race, Hispanic ethnicity, and low maternal levels of anticapsular antibody."

Schrag / MMWR 2002 full article

Hyperinvasive neonatal Group B Streptococcus has arisen from a bovine ancestor. N Bisharat, DW Crook, J Leigh, RM Harding, PN Ward, TJ Coffey, MC Maiden, T Peto, N Jones. J Clin Microbiol 2004 May;42(5):2161-2167. "Streptococcus agalactiae, the species designation of GBS, was initially described in 1887 as an animal pathogen causing bovine mastitis. Human infections caused by this bacterium were only reported 50 years later, in the 1930s. Neonatal disease, though, was rarely reported. However, during the 1960s numerous reports linked neonatal infections with this organism, and by the 1970s, GBS had become the leading neonatal pathogen in much of the developed world and has remained so ever since... The phylogenetic evidence indicates that the human isolate ST-17 complex, the major hyperinvasive neonatal clone (which accounts for 30% of neonatal infections [N. Jones, unpublished data]), has arisen from a bovine lineage... The finding that the ST-17 complex accounts for a proportion of strains carried by adults (Table 1) suggests that it is now autonomously circulating within the human population."

Bisharat / J Clin Microbiol 2004 full article

Perinatal infections due to group B streptococci. RS Gibbs, S Schrag, A Schuchat. Obstet Gynecol 2004 Nov;104(5 Pt 1):1062-1076. "Group B streptococci (GBS) emerged dramatically in the 1970s as the leading cause of neonatal infection and as an important cause of maternal uterine infection... In 1996, the first national consensus guidelines were released. Since then, there has been a 70% reduction in early-onset neonatal GBS infection, but no decrease in late-onset neonatal GBS disease."

Gibbs - Obstet Gynecol 2004 abstract / PubMed

Genome sequence of a serotype M28 strain of group a streptococcus: potential new insights into puerperal sepsis and bacterial disease specificity. NM Green, S Zhang, SF Porcella, MJ Nagiec, KD Barbian, SB Beres, RB LeFebvre, JM Musser. J Infect Dis 2005 Sep 1;192(5):760-770. "Puerperal sepsis, a major cause of death of young women in Europe in the 1800s, was due predominantly to the gram-positive pathogen group A Streptococcus... Importantly, genes for 7 inferred extracellular proteins are encoded by a 37.4-kb foreign DNA element that is shared with group B Streptococcus and is present in all serotype M28 strains. Proteins encoded by the 37.4-kb element were expressed extracellularly and in human infections. Acquisition of foreign genes has helped create a disease-specialist clone of this pathogen."

Green - J Infect Dis 2005 abstract / PubMed

Early-Onset and Late-Onset Neonatal Group B Streptococcal Disease --- United States, 1996--2004. [Many contributors]. MMWR December 2, 2005;54(47):1205-1208. Note the rapid decline in early-onset disease, which is attributable to intrapartum antimicrobial prophylaxis to carriers of GBS, versus the lack of change in late-onset disease, despite decreases in rates of smoking during 1996 to 2004.

CDC / MMWR 2005 full article

Neonatal Bacterial Meningitis: 444 Cases in 7 Years. J Gaschignard, C Levy, O Romain, R Cohen, E Bingen, Y Aujard, P Boileau. Pediatr Infect Dis J 2011 Mar;30(3):212-217. "Group B streptococci (GBS) and Escherichia coli accounted respectively for 59% and 28% of the cases, followed by Gram-negative bacilli other than E. coli (4%), other streptococci (4%), Neisseria meningitidis (3%), and Listeria monocytogenes (1.5%). GBS was the most common pathogen both in early-onset (77% vs. 18% for E. coli) and in late-onset meningitis (50% vs. 33% for E. coli). Among preterm infants, E. coli was more commonly isolated (45% vs. 32% for GBS), especially in very preterm infants (54%). GBS was more often involved in seizures than E. coli (41% vs. 25%). The overall mortality rate was 13% but reached 25% in preterm or small for gestational age infants, regardless of the etiology."

Gaschignard - Pediatr Infect Dis J 2011 abstract / PubMed

Early onset neonatal sepsis: the burden of group B Streptococcal and E. coli disease continues. BJ Stoll, NI Hansen, PJ Sánchez, RG Faix, BB Poindexter, KP Van Meurs, MJ Bizzarro, RN Goldberg, ID Frantz 3rd, EC Hale, S Shankaran, K Kennedy, WA Carlo, KL Watterberg, EF Bell, MC Walsh, K Schibler, AR Laptook, AL Shane, SJ Schrag, A Das, RD Higgins; Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Pediatrics 2011 May;127(5):817-826. 389 cases. "GBS (43%, 0.41 per 1000 LBs) and E coli (29%, 0.28 per 1000 LBs) were most frequently isolated. Most infants with GBS were term (73%); 81% with E coli were preterm. Mothers of 67% of infected term and 58% of infected preterm infants were screened for GBS, and results were positive for 25% of those mothers. Only 76% of mothers with GBS colonization received intrapartum chemoprophylaxis. Although 77% of infected infants required intensive care, 20% of term infants were treated in the normal newborn nursery. Sixteen percent of infected infants died, most commonly with E coli infection (33%)."

Stoll - Pediatrics 2011 abstract / PubMed

Intrapartum evidence of early-onset group B streptococcus. CM Tudela, RD Stewart, SW Roberts, GD Wendel Jr, IA Stafford, DD McIntire, JS Sheffield. Obstet Gynecol 2012 Mar;119(3):626-629. 94 cases, 93 of whom were diagnosed within the first hour of life. "Neonates with early-onset GBS sepsis had a significant increase in preterm delivery, cesarean delivery (total and for fetal distress), 1- and 5-minute Apgar scores of 3 or lower, umbilical cord pH less than 7.0, and a base deficit of 12 mmol/L or higher. In addition, nulliparity differed between those with early-onset GBS and those without (74% compared with 33%, P<.001) as did chorioamnionitis rates (62% compared with 8%, P<.001)."

Tudela - Obstet Gynecol 2012 abstract - PubMed

Risk of Early-Onset Neonatal Infection with Maternal Infection or Colonization: A Global Systematic Review and Meta-Analysis. GJ Chan, AC Lee, AH Baqui, J Tan, RE Black. PLoS Med 2013 Aug;10(8):e1001502. 83 studies. The odds ratio for neonatal lab-confirmed infection among newborns of mothers with lab-confirmed infection was 6.6 (95% CI 3.9–11.2). Newborns of mothers with colonization had a 9.4 (95% CI 3.1–28.5) times higher odds of lab-confirmed infection than newborns of non-colonized mothers. Newborns of mothers with risk factors for infection (defined as prelabour rupture of membranes [PROM], preterm <37 weeks PROM, and prolonged ROM) had a 2.3 (95% CI 1.0–5.4) times higher odds of infection than newborns of mothers without risk factors."

Chan / PLoS Med 2013 full article

Group B Streptococcal Infection of the Choriodecidua Induces Dysfunction of the Cytokeratin Network in Amniotic Epithelium: A Pathway to Membrane Weakening. JP Vanderhoeven, CJ Bierle, RP Kapur, RM McAdams, RP Beyer, TK Bammler, FM Farin, A Bansal, M Spencer, M Deng, MG Gravett, CE Rubens, L Rajagopal, KM Adams Waldorf. PLoS Pathog 2014;10(3):e1003920. 10 macaques, plus human placental samples. "Despite uterine quiescence in most cases, significant elevations of AF cytokines (TNF-α, IL-8, IL-1β, IL-6) were detected in GBS versus controls (p<0.05). Choriodecidual infection resolved by the time of cesarean section in 3 of 5 cases and GBS was undetectable by culture and PCR in the AF. A total of 331 genes were differentially expressed (>2-fold change, p<0.05). Remarkably, GBS exposure was associated with significantly downregulated expression of multiple cytokeratin (CK) and other cytoskeletal genes critical for maintenance of tissue tensile strength... In human pregnancies affected by PPROM, there was further evidence of CK network retraction with significantly shorter amniocyte foot processes (p = 0.002)."

Vanderhoeven / PLoS Pathog 2014 full article

Coxsackie Viruses and Developmental Delays

A study of school children who had identified virus infections of the central nervous system during infancy. RN Chamberlain, PN Christie, KS Holt, RM Huntley, R Pollard, MC Roche. Child Care Health Dev 1983 Jan-Feb;9(1):29-47. "Forty-nine children who had a virus infection of the central nervous system (CNS) when under 1 year of age were studied. One child had died during the initial illness and three of the survivors were severely disabled. The other survivors, more than 5 years after the initial illness, were all attending normal schools... We confirm the findings of other studies that virus infections of the CNS in infancy may cause severe disabilities in some cases, and may depress intellectual abilities in others, even though they appear to have recovered fully. Many of the children who had a virus infection of the CNS in infancy had adverse birth and social histories and so were exceptionally vulnerable, but these factors did not account fully for the findings, and when their influence was included in the analysis, the index children still had a mean performance IQ (WISC) 6 points lower than the control children (P less than 0.05), whereas there was less than 1 point difference between the verbal IQs.

Chamberlain - Child Care Health Dev 1983 abstract / PubMed

Coxsackie virus infection of the placenta associated with neurodevelopmental delays in the newborn. E Euscher, J Davis, I Holzman, GJ Nuovo. Obstet Gynecol 2001 Dec;98(6):1019-1026. "Coxsackie virus RNA was detected in six of the seven cases, and in none of the ten normal controls or five cases with known viral infection. Viral RNA localized primarily to the Hofbauer cells and trophoblasts of the terminal villi. Immunohistochemical analysis for the coxsackie virus antigen VP1 yielded equivalent results." "Six of the seven children ranged in age from 4 to 15-years-old, and included five boys. One child died 1 day after birth. Each of the six living children experienced marked, global cognitive defects evident soon after birth, which required intensive physical therapy, occupational therapy, and, occasionally, antiseizure therapy, and institutional therapy. All children (except for case 4 below) have not shown evidence of cerebral palsy because there have been minimal motor-related symptoms." "The most common histologic finding in the 12 placental cases (five known viral infections and the seven cases included in this report) was Hofbauer cell hyperplasia, which was seen in all cases except one with herpes simplex virus infection; this was not evident in the ten normal control tissues. Four of the five cases of known viral infection showed focal calcification, and each showed focal chronic villitis as well as focal hemorrhagic vasculitis. In comparison, of the seven cases associated with profound neurologic sequela, three showed focal chronic villitis, two showed focal hemorrhagic endovasculitis, and one showed focal calcifications."

Euscher - Obstet Gynecol 2001 abstract / PubMed
Euscher / Obstet Gynecol 2001 full article

See Also:

Parvovirus B19 Causes Fetal Loss
Meningococcal Disease and the fraudulent "science" blaming smoking and secondhand smoke
Infections are implicated in SIDS
AAV Infection During Pregancy Causes Spontaneous Abortions and Trophoblastic Disease
Infection is Implicated in Early Childhood Asthma - New Views About Asthma Causes
Infections Cause Hearing Loss - CMV and otitis media pathogens

<= HOME

cast 03-07-14