Abnormal Development - Listeria

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Introduction

Listeria monocytogenes bacteria (Image CDC)

The bacterium Listeria monocytogenes is the pathogenic form of the 7 listeria species. Infection is generally through ingestion of organisms in contaminated food. Maternal symptoms may be mild, fetal effects can range from insignificant through to major abnormalities. Maternal treatment relates to potential developmental effects. Pregnancy greatly increases the risk of listeriosis, with pregnant women about 60% of all cases (male and female) aged 10 to 40 years. Similar effects are seem in other mammalian species.[1] See also the listeriosis review article[2] and the Guinea pig placenta listeria model[3] Generalized suppression of immunity during pregnancy is suggest to have a role in susceptibility, though recent results in a mouse model suggest that susceptibility can occur very early in a pregnancy and may relate to enteric carriage rate.[1]


Bacterial Links: bacterial infection | syphilis | gonorrhea | tuberculosis | listeria | salmonella | TORCH | Environmental | Category:Bacteria

Some Recent Findings

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Search term: Listeria Infections

<pubmed limit=5>Listeria Pregnancy</pubmed>

Listeria Infection

  1. ingestion of contaminated food
  2. colonization of the intestine
  3. intestinal translocation
  4. replication in the liver and spleen
  5. either the resolution of infection or spread to other organs resulting in a systemic infection


Lineage

Placental Infection

Model of L. monocytogenes mechanisms for breaching the maternal-fetal barrier[5] (text below modified from original reference)

L. monocytogenes is subjected to multiple bottlenecks when infecting the placenta. Our data support extravillous cytotrophoblasts (EVT) as the primary portal of entry.

  1. Relatively few L. monocytogenes reach the maternal decidua, carried by phagocytes. These can infect extravillous cytotrophoblasts by cell-to-cell spread, or by lysing the leukocyte and subsequently infecting extravillous cytotrophoblasts via InlA-E-cadherin interactions.
  2. Extravillous cytotrophoblasts further winnow bacterial numbers by delaying the L. monocytogenes intracellular life cycle. If infection progresses, bacteria spread through subsyncytial cytotrophoblasts.
  3. The basement membrane underlying these cells presents a third barrier, which few bacteria cross to invade the fetal stroma (STR). On the other hand, L. monocytogenes in the blood contacts only the syncytiotrophoblast (SYN), which is highly resistant to both internalin-mediated infection and intercellular spread. However, it is possible that sites of syncytial damage provide access to subsyncytial cytotrophoblasts. In vivo, such sites are rapidly covered by fibrinoid clots that may present yet another physical barrier to infection.
Listeria maternal-fetal barrier.jpg

Gram Stain

Bacterial staining procedure named after Hans Christian Gram (1853 - 1938). Generally divides bacteria into either:

  • Gram-positive bacteria purple crystal violet stain is trapped by layer of peptidoglycan (forms outer layer of the cell).
  • Gram-negative bacteria outer membrane prevents stain from reaching peptidoglycan layer in the periplasm, outer membrane then permeabilized and pink safranin counterstain is trapped by peptidoglycan layer.


Links: Histology Stains

Australian NHMRC Recommendations

The Australian NHMRC (1988) recommends neonates be assessed for follow-up care under the following conditions.

  • Birthweight less than 1500g or gestational age less than 32 weeks
  • Small-for-gestational-age neonates
  • Perinatal asphyxia
  • Apgar score less than 3 at 5 minutes
  • clinical evidence of neurological dysfunction
  • delay in onset of spontaneous respiration for more than 5 minutes and requiring mechanical ventilation
  • Clinical evidence of central nervous system abnormalities ie., seizures, hypotonia
  • Hyperbilirubinaemia of greater than 350umol/l in full term neonates
  • Genetic, dysmorphic or metabolic disorders or a family history of serious genetic disorder
  • Perinatal or serious neonatal infection including children of mothers who are HIV positive
  • Psychosocial problems eg., infants of drug-addicted or alcoholic mothers.


Links: NHMRC WWW Page

References

  1. 1.0 1.1 Suyemoto MM, Spears PA, Hamrick TS, Barnes JA, Havell EA & Orndorff PE. (2010). Factors associated with the acquisition and severity of gestational listeriosis. PLoS ONE , 5, e13000. PMID: 20885996 DOI.
  2. Doganay M. (2003). Listeriosis: clinical presentation. FEMS Immunol. Med. Microbiol. , 35, 173-5. PMID: 12648833
  3. Bakardjiev AI, Stacy BA & Portnoy DA. (2005). Growth of Listeria monocytogenes in the guinea pig placenta and role of cell-to-cell spread in fetal infection. J. Infect. Dis. , 191, 1889-97. PMID: 15871123 DOI.
  4. Blencowe H, Cousens S, Kamb M, Berman S & Lawn JE. (2011). Lives Saved Tool supplement detection and treatment of syphilis in pregnancy to reduce syphilis related stillbirths and neonatal mortality. BMC Public Health , 11 Suppl 3, S9. PMID: 21501460 DOI.
  5. <pubmed>20107601</pubmed>| PLoS

Reviews

Lamont RF, Sobel J, Mazaki-Tovi S, Kusanovic JP, Vaisbuch E, Kim SK, Uldbjerg N & Romero R. (2011). Listeriosis in human pregnancy: a systematic review. J Perinat Med , 39, 227-36. PMID: 21517700 DOI.

Posfay-Barbe KM & Wald ER. (2009). Listeriosis. Semin Fetal Neonatal Med , 14, 228-33. PMID: 19231307 DOI.

Goldenberg RL & Thompson C. (2003). The infectious origins of stillbirth. Am. J. Obstet. Gynecol. , 189, 861-73. PMID: 14526331

Albritton WL, Cochi SL & Feeley JC. (1984). Overview of neonatal listeriosis. Clin Invest Med , 7, 311-4. PMID: 6398177

Articles

Jackson KA, Iwamoto M & Swerdlow D. (2010). Pregnancy-associated listeriosis. Epidemiol. Infect. , 138, 1503-9. PMID: 20158931 DOI.

Bakardjiev AI, Stacy BA, Fisher SJ & Portnoy DA. (2004). Listeriosis in the pregnant guinea pig: a model of vertical transmission. Infect. Immun. , 72, 489-97. PMID: 14688130

Topalovski M, Yang SS & Boonpasat Y. (1993). Listeriosis of the placenta: clinicopathologic study of seven cases. Am. J. Obstet. Gynecol. , 169, 616-20. PMID: 8372871

Storrs CN & Partridge JW. (1980). Listeria infections in the newborn. Arch. Dis. Child. , 55, 246. PMID: 7387172

Luft BJ & Remington JS. (1982). Effect of pregnancy on resistance to Listeria monocytogenes and Toxoplasma gondii infections in mice. Infect. Immun. , 38, 1164-71. PMID: 6818146

Scott JM & Henderson A. (1968). A case of listeriosis of the newborn. J. Med. Microbiol. , 1, 97-104. PMID: 4990031 DOI.

Textbooks

Medical Microbiology - Listeria | Listeria Search


Search Pubmed

Search PubMed: Congenital Listeria | Abnormal Embryology Listeria | Abnormal Development Listeria

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Cite this page: Hill, M.A. (2019, October 20) Embryology Abnormal Development - Listeria. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Listeria

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© Dr Mark Hill 2019, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G