Talk:Abnormal Development - Bacterial Infection

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Cite this page: Hill, M.A. (2021, April 10) Embryology Abnormal Development - Bacterial Infection. Retrieved from


The Safety of Influenza and Pertussis Vaccination in Pregnancy in a Cohort of Australian Mother-Infant Pairs, 2012-2015: The FluMum Study

Clin Infect Dis. 2019 Jan 18;68(3):402-408. doi: 10.1093/cid/ciy517.

McHugh L1, Marshall HS2, Perrett KP3, Nolan T3, Wood N4, Lambert SB5, Richmond P6, Ware RS7, Binks P1, Binks MJ1, Andrews RM1,8. Author information Abstract BACKGROUND: Inactivated influenza vaccine (IIV) and pertussis vaccination are recommended in pregnancy. Limited safety data exist for women who received IIV vaccine during the first trimester of pregnancy or received both vaccines in pregnancy. We assessed adverse birth outcomes between vaccinated and unvaccinated pregnancies. METHODS: Among prospectively enrolled Australian "FluMum" participants (2012-2015), primary exposure was receipt and timing of IIV during pregnancy. Primary outcomes included preterm birth, low birthweight at term (LBWT), and small for gestational age (SGA). We compared birth outcomes for IIV in pregnancy with women unvaccinated in pregnancy using Cox proportional hazard ratios (HRs) with 95% confidence intervals (CIs). Adjusted HRs (aHRs) controlled for potential confounding variables. Sensitivity analyses were conducted in a subgroup of women who received pertussis vaccination during pregnancy to assess whether associations between IIV and adverse outcomes were maintained after adjusting for pertussis vaccination. RESULTS: Among 8827 participants in our study, women who received IIV in pregnancy did not have an elevated risk of an adverse birth outcome compared with unvaccinated pregnant women: preterm births (HR, 1.10 [95% CI, .92-1.31]; P = .28); LBWT (HR, 1.05 [95% CI, .76-1.44]; P = .77); or SGA (HR, 0.99 [95% CI, .86-1.15]; P = .94). Adjustment for pertussis vaccination during pregnancy yielded similar results: preterm births (aHR, 1.05 [95% CI, .82-1.34]; P = .69); LBWT (aHR, 0.81 [95% CI, .50-1.29]; P = .37); SGA (aHR, 0.92 [95% CI, .74-1.14]; P = .43). There was no evidence of elevated risk by trimester of IIV. CONCLUSIONS: No significant associations were found between maternal IIV or pertussis vaccination in pregnancy and adverse birth outcomes, regardless of the trimester of pregnancy a vaccination was given compared to unvaccinated pregnancies. PMID: 30475988 DOI: 10.1093/cid/ciy517


Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Am J Reprod Immunol. 2018 May;79(5):e12816. doi: 10.1111/aji.12816. Epub 2018 Jan 25.

Fricke EM1, Elgin TG1, Gong H1, Reese J2, Gibson-Corley KN1, Weiss RM1, Zimmerman K1, Bowdler NC1, Kalantera KM3, Mills DA3, Underwood MA3, McElroy SJ1.


PROBLEM: Premature birth complicates 10%-12% of deliveries. Infection and inflammation are the most common etiologies and are associated with increased offspring morbidity and mortality. We hypothesize that lipopolysaccharide (LPS)-induced maternal inflammation causes direct placenta injury and subsequent injury to the fetal intestine. METHOD OF STUDY: Pregnant C57Bl6 mice were injected intraperitoneally on day 15.5 with 100 μg/kg LPS or saline. Maternal serum, amniotic fluid, placental samples, and ileal samples of offspring were obtained assessed for inflammation and/or injury. Maternal placental ultrasounds were performed. Placental DNA was isolated for microbiome analysis. RESULTS: Maternal injection with LPS caused elevated IL-1β, IL-10, IL-6, KC-GRO, and TNF. Placental tissue showed increased IL-1β, IL-6, and KC-GRO and decreased IL-10, but no changes were observed in amniotic fluid. Placental histology demonstrated LPS-induced increases in mineralization and necrosis, but no difference in placental blood flow. Most placentas had no detectable microbiome. Exposure to maternal LPS induced significant injury to the ilea of the offspring. CONCLUSION: Lipopolysaccharide causes a maternal inflammatory response that is mirrored in the placenta. Placental histology demonstrates structural changes; however, placental blood flow is preserved. LPS also induces an indirect intestinal injury in the offspring that lasts beyond the neonatal period. © 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. KEYWORDS: cytokines; lipopolysaccharide; microbiome; mouse; placenta PMID: 29369434 PMCID: PMC5908742 DOI: 10.1111/aji.12816


Prenatal exposure to bacterial endotoxin reduces the number of GAD67- and reelin-immunoreactive neurons in the hippocampus of rat offspring

Eur Neuropsychopharmacol. 2011 Aug 31. [Epub ahead of print]

Nouel D, Burt M, Zhang Y, Harvey L, Boksa P.


Epidemiological studies implicate prenatal infection as a risk factor for the development of schizophrenia and autism. Subjects with schizophrenia and autism are reported to exhibit reduced levels of glutamic acid decarboxylase 67 (GAD67), a marker for GABA neurons, in various brain regions. Reduced levels of reelin, a secretory glycoprotein present in a subpopulation of GABA neurons, have also been found in these disorders. To test if prenatal infection can cause abnormalities in GAD67 and reelin in the brains of offspring, this study used a rat model ofprenatal exposure to the bacterial endotoxin, lipopolysaccharide (LPS), and assessed numbers of GAD67-immunoreactive (GAD67+) and reelin-immunoreactive (reelin+) neurons in the hippocampus of offspring. In offspring at postnatal day 14 (PD14), GAD67+ cell counts were reduced in the dentate gyrus of the prenatal LPS group compared to prenatal saline controls, while at PD28, GAD67+ cells counts were reduced in the prenatal LPS group in both the dentate gyrus and the CA1. There was a decrease in the number of reelin+ cells in the prenatal LPS offspring compared to controls in the dentate gyrus at PD14. However using Western blotting, no significant effects of prenatal LPS on levels of GAD67 or reelin protein were observed in various brain regions at PD14. These findings support the idea that prenatal infection can cause reductions in postnatal expression of GAD67 and reelin, and in this way, possibly contribute to the pathophysiology of schizophrenia or autism.Copyright © 2011 Elsevier B.V. All rights reserved.

PMID 21889316

President's commission considers how to protect human rights after Guatemala experiment

BMJ. 2011 May 23;342:d3232. doi: 10.1136/bmj.d3232.

Tanne JH. Source New York. PMID: 21606141

"The US Presidential Commission for the Study of Bioethical Issues was established in 2009. Since Susan Reverby, a historian from Wellesley College, near Boston, discovered last year that the US Public Health Service had conducted unethical research in Guatemala from 1946 to 1948, the commission has concentrated on protecting the human rights of people in such studies. The commission held its fifth public session in New York on 18 and 19 May and plans to present its report this summer."
"In the Guatemala studies nearly 700 people were deliberately infected with syphilis and other sexually transmitted diseases in hopes of showing that the new drug penicillin could be used immediately after sex to prevent infection. Among those included in the studies were female sex workers, soldiers, prison inmates, and mental hospital patients. They were not told the study’s purpose and did not give informed consent. The studies were never published. Guatemalan authorities are also conducting their own investigation into what happened."

President Obama apologises to Guatemala over 1940s syphilis study BMJ 2010; 341:c5494 doi: 10.1136/bmj.c5494 (Published 4 October 2010)

Tuberculosis in pregnancy--a major maternal and perinatal challenge

BJOG. 2011 Aug;118(9):1145-6; author reply 1146. doi: 10.1111/j.1471-0528.2011.03012.x.

Jana N, Barik S, Arora N. Comment on BJOG. 2011 Jan;118(2):226-31. PMID 21749618


Chorioamnionitis: a multiorgan disease of the fetus?

J Perinatol. 2010 Oct;30 Suppl:S21-30. Gantert M, Been JV, Gavilanes AW, Garnier Y, Zimmermann LJ, Kramer BW. Source Department of Obstetrics and Gynecology, Klinikum Osnabrück, Osnabrück, Germany.


The bacterial infection of chorion and amnion is a common finding in premature delivery and is referred to as chorioamnionitis. As the mother rarely shows symptoms of a systemic inflammation, the course of chorioamnionitis is frequently asymptomatic and chronic. In contrast, the fetal inflammatory response syndrome represents a separate phenomenon, including umbilical inflammation and increased serum levels of proinflammatory cytokines in the fetus. Ascending maternal infections frequently lead to systemic fetal inflammatory reaction. Clinical studies have shown that antenatal exposure to inflammation puts the extremely immature neonates at a high risk for worsening pulmonary, neurological and other organ development. Interestingly, the presence of chorioamnionitis is associated with a lower rate of neonatal mortality in extremely immature newborns. In the following review, the pathogeneses of inflammation-associated perinatal morbidity are outlined. The concept of fetal multiorganic disease during intrauterine infection is introduced and discussed.

PMID 20877404

A safe vaccine (DV-STM-07) against Salmonella infection prevents abortion and confers protective immunity to the pregnant and new born mice

PLoS One. 2010 Feb 10;5(2):e9139.

Negi VD, Nagarajan AG, Chakravortty D. Source Department of Microbiology and Cell Biology, Centre for Infectious Disease Research and Biosafety Laboratories, Indian Institute of Science, Bangalore, India.


Pregnancy is a transient immuno-compromised condition which has evolved to avoid the immune rejection of the fetus by the maternal immune system. The altered immune response of the pregnant female leads to increased susceptibility to invading pathogens, resulting in abortion and congenital defects of the fetus and a subnormal response to vaccination. Active vaccination during pregnancy may lead to abortion induced by heightened cell mediated immune response. In this study, we have administered the highly attenuated vaccine strain DeltapmrG-HM-D (DV-STM-07) in female mice before the onset of pregnancy and followed the immune reaction against challenge with virulent S. Typhimurium in pregnant mice. Here we demonstrate that DV-STM-07 vaccine gives protection against Salmonella in pregnant mice and also prevents Salmonella induced abortion. This protection is conferred by directing the immune response towards Th2 activation and Th1 suppression. The low Th1 response prevents abortion. The use of live attenuated vaccine just before pregnancy carries the risk of transmission to the fetus. We have shown that this vaccine is safe as the vaccine strain is quickly eliminated from the mother and is not transmitted to the fetus. This vaccine also confers immunity to the new born mice of vaccinated mothers. Since there is no evidence of the vaccine candidate reaching the new born mice, we hypothesize that it may be due to trans-colostral transfer of protective anti-Salmonella antibodies. These results suggest that our vaccine DV-STM-07 can be very useful in preventing abortion in the pregnant individuals and confer immunity to the new born. Since there are no such vaccine candidates which can be given to the new born and to the pregnant women, this vaccine holds a very bright future to combat Salmonella induced pregnancy loss.

PMID 20161765


Trophoblast infection with Chlamydia pneumoniae and adverse pregnancy outcomes associated with placental dysfunction

Am J Obstet Gynecol. 2009 May;200(5):526.e1-7.

Gomez LM, Parry S.

Maternal and Child Research Program, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA. Abstract OBJECTIVE: We sought to determine whether Chlamydia pneumoniae impairs invasive trophoblast function and is associated with preeclampsia.

STUDY DESIGN: We conducted cell viability and invasion assays using primary extravillous trophoblast cells isolated from first-trimester placentas. We performed a case-control study to identify C pneumoniae in trophoblast cells dissected by laser capture microscopy from placentas in women with severe preeclampsia and control subjects who delivered at term.

RESULTS: Trophoblast cell viability and invasion through extracellular matrices were decreased after infection with C pneumoniae (both P < .05). C pneumoniae DNA was detected in trophoblast cells in 15/48 cases but only 3/30 controls (odds ratio, 4.1; P = .02). Positive and negative controls yielded expected results.

CONCLUSION: C pneumoniae infection can reduce trophoblast invasion into the uterine wall and is associated with preeclampsia. Further investigation of the mechanisms by which C pneumoniae induces trophoblast dysfunction, and the identification of therapies to prevent adverse outcomes attributed to trophoblast dysfunction, are warranted.

PMID 19375572


Induced biliary excretion of Listeria monocytogenes

Infect Immun. 2006 Mar;74(3):1819-27.

Hardy J, Margolis JJ, Contag CH.

SourceDepartment of Pediatrics, E150 Clark Center MC 5427, Stanford University School of Medicine, Stanford, CA 94305, USA. AbstractListeria monocytogenes is a ubiquitous gram-positive bacterium that can cause systemic and often life-threatening disease in immunocompromised hosts. This organism is largely an intracellular pathogen; however, we have determined that it can also grow extracellularly in animals, in the lumen of the gallbladder. The significance of growth in the gallbladder with respect to the pathogenesis and spread of listeriosis depends on the ability of the bacterium to leave this organ and be disseminated to other tissues and into the environment. Should this process be highly inefficient, growth in the gallbladder would have no impact on pathogenesis or spread, but if it occurs efficiently, bacterial growth in this organ may contribute to listeriosis and dissemination of this organism. Here, we use whole-body imaging to determine the efficacy and kinetics of food- and hormone-induced biliary excretion of L. monocytogenes from the murinegallbladder, demonstrating that transit through the bile duct into the intestine can occur within 5 min of induction of gallbladder contraction by food or cholecystokinin and that movement of bacteria through the intestinal lumen can occur very rapidly in the absence of fecal material. These studies demonstrate that L. monocytogenes bacteria replicating in the gallbladder can be expelled from the organ efficiently and that the released bacteria move into the intestinal tract, where they pass into the environment and may possibly reinfect the animal.

PMID 16495556

Previous References


Donders GG. Management of genital infections in pregnant women. Curr Opin Infect Dis. 2006 Feb;19(1):55-61.

Goodnight WH, Soper DE. Pneumonia in pregnancy. Crit Care Med. 2005 Oct;33(10 Suppl):S390-7.

Boggess KA. Pathophysiology of preterm birth: emerging concepts of maternal infection. Clin Perinatol. 2005 Sep;32(3):561-9.

Hirsch E, Wang H. The molecular pathophysiology of bacterially induced preterm labor: insights from the murine model. J Soc Gynecol Investig. 2005 Apr;12(3):145-55.

Berman SM. Maternal syphilis: pathophysiology and treatment. Bull World Health Organ. 2004 Jun;82(6):433-8.

Doganay M. Listeriosis: clinical presentation. FEMS Immunol Med Microbiol. 2003 Apr 1;35(3):173-5.

Goldenberg RL, Hauth JC, Andrews WW. Intrauterine infection and preterm delivery. N Engl J Med. 2000 May 18;342(20):1500-7.

Ross SM. Sexually transmitted diseases in pregnancy. Clin Obstet Gynaecol. 1982 Dec;9(3):565-92.


Guerra B, Ghi T, Quarta S, Morselli-Labate AM, Lazzarotto T, Pilu G, Rizzo N. Pregnancy outcome after early detection of bacterial vaginosis. Eur J Obstet Gynecol Reprod Biol. 2006 Sep-Oct;128(1-2):40-5. Epub 2006 Feb 3.

Giuliani MM, Adu-Bobie J, Comanducci M, Arico B, Savino S, Santini L, Brunelli B, Bambini S, Biolchi A, Capecchi B, Cartocci E, Ciucchi L, Di Marcello F, Ferlicca F, Galli B, Luzzi E, Masignani V, Serruto D, Veggi D, Contorni M, Morandi M, Bartalesi A, Cinotti V, Mannucci D, Titta F, Ovidi E, Welsch JA, Granoff D, Rappuoli R, Pizza M. A universal vaccine for serogroup B meningococcus. Proc Natl Acad Sci U S A. 2006 Jul 6; [Epub ahead of print]

Colombo DF, Lew JL, Pedersen CA, Johnson JR, Fan-Havard P. Optimal timing of ampicillin administration to pregnant women for establishing bactericidal levels in the prophylaxis of Group B Streptococcus. Am J Obstet Gynecol. 2006 Feb;194(2):466-70.

Bakardjiev AI, Stacy BA, Portnoy DA. Growth of Listeria monocytogenes in the guinea pig placenta and role of cell-to-cell spread in fetal infection. J Infect Dis. 2005 Jun 1;191(11):1889-97.

Goffinet F, Maillard F, Mihoubi N, Kayem G, Papiernik E, Cabrol D, Paul G. Bacterial vaginosis: prevalence and predictive value for premature delivery and neonatal infection in women with preterm labour and intact membranes. Eur J Obstet Gynecol Reprod Biol. 2003 Jun 10;108(2):146-51.

Morley SL, Cole MJ, Ison CA, Camaraza MA, Sotolongo F, Anwar N, Cuevas I, Carbonero M, Campa HC, Sierra G, Levin M. Immunogenicity of a serogroup B meningococcal vaccine against multiple Neisseria meningitidis strains in infants. Pediatr Infect Dis J. 2001 Nov;20(11):1054-61.

Nowicki S, Selvarangan R, Anderson G. Experimental transmission of Neisseria gonorrhoeae from pregnant rat to fetus. Infect Immun. 1999 Sep;67(9):4974-6.

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WWW Links


Public Health Training Network Epidemiology and Prevention of Vaccine-Preventable Diseases (viewable Webcasts requires Media Player) |

Advisory Committee on Immunization Practices (ACIP) Recommendations

Royal College of Obstetricians and Gynaecologists (UK)

Infection and Pregnancy - study group recommendations (Jun 2001)