The Return of Listeria: Difference between revisions

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==structure==
==structure==
<br> L. monocytogenes is a firmicute, which is part of a phylum of bacteria called Bacillota. It is a gram positive bacteria, however it could also be gram negative depending on the age of the culture[5]. The shape of these organisms are rod-like and do not form spores. There is no outer membrane, however, it has a S-layer which is a thick cell wall with layers of peptidoglycan. L. monocytogenes has a cell wall around 200 Å in thickness[5.] L. monocytogenes can thrive in refrigerator temperatures and have an enzyme called RNA helicase which improves activity and replication at low temperatures. This enzyme boosts their ability to survive in harsh climates. This bacteria also has a flagella, which is used to propel itself  and attach it to enterocytes during infection[6]. Enterocytes, found in both the small and large intestines, are predominant epithelial cell lineage which has membranes with tight junctions that form between cells to create a physical barrier for mycobacteria[7].  L. monocytogenes have 4 primary virulence factors that help it infect host cells. It possesses internalins (Inl A and InlB) which are cell-surface galactose residues, lipoteichoic acids, and surface proteins that help L. monocytogenes attach to gastrointestinal epithelial cells using host protein cadherin[6]. This allows them to enter the cell and infect it. After the bacteria has invaded the host cells, it uses listeriolysin (LLO)[6].  Listeriolysin are proteins that form cytotoxic pores on the cell’s vacuole to allow L. monocytogenes to derange cellular processes by going through the cell membrane. Phosphatidylinositol-specific phospholipase C (PI-PLC) aids in the bacteria's evasion from the host cell vacuole and induces membrane disruption[6]. Lastly it  also uses actin polymerization (ActA) to help in move between cells after infection[6].
<br> L. monocytogenes is a firmicute, which is part of a phylum of bacteria called Bacillota. It is a gram positive bacteria, however it could also be gram negative depending on the age of the culture[5]. The shape of these organisms are rod-like and do not form spores. There is no outer membrane, however, it has a S-layer which is a thick cell wall with layers of peptidoglycan. L. monocytogenes has a cell wall around 200 Å in thickness[5.] L. monocytogenes can thrive in refrigerator temperatures and have an enzyme called RNA helicase which improves activity and replication at low temperatures. This enzyme boosts their ability to survive in harsh climates. This bacteria also has a flagella, which is used to propel itself  and attach it to enterocytes during infection[6]. Enterocytes, found in both the small and large intestines, are predominant epithelial cell lineage which has membranes with tight junctions that form between cells to create a physical barrier for mycobacteria[7].  L. monocytogenes have 4 primary virulence factors that help it infect host cells. It possesses internalins (Inl A and InlB) which are cell-surface galactose residues, lipoteichoic acids, and surface proteins that help L. monocytogenes attach to gastrointestinal epithelial cells using host protein cadherin[6]. This allows them to enter the cell and infect it. After the bacteria has invaded the host cells, it uses listeriolysin (LLO)[6].  Listeriolysin are proteins that form cytotoxic pores on the cell’s vacuole to allow L. monocytogenes to derange cellular processes by going through the cell membrane. Phosphatidylinositol-specific phospholipase C (PI-PLC) aids in the bacteria's evasion from the host cell vacuole and induces membrane disruption[6]. Lastly it  also uses actin polymerization (ActA) to help in move between cells after infection[6].
==Symptoms and Treatments==
<br>L. monocytogenes is a worldwide foodborne illness that has a hospitalization and mortality rate. Luckily, the annual cases of Listeria have been declining. 7.7 million per one million cases to 3.1 during the period from 1990 to 2023 in the USA and in Europe the infection rate declined from 4.5 cases per million to 3.4 cases from 1999 to 2003[8]. Annually, there are about 1600 cases of Listeria infections that are reported in the USA[8]. The mortality rate is about 30% while the hospitalization rate is about 99.1%[8]. The Center for Disease Control and Prevention (CDD) estimates that Listeria is the third leading cause of death from food poisoning int the USA[9]. Anyone can have a Listeria infection, however, the ones with the greatest chance of an infection are: people who are pregnant, people who are 65 years and older, and people with a weakened immune system.  Pregnant women are 10 times more likely to have listeriosis which can result in miscarriages, stillbirths, preterm labor, and serious illness to the newborn[9]. The new born could have symptoms of dever, vomiting, little to no interest in feeding, irritability and difficulty breathing[12]. More than half of all infections occurred to people 65 and older[10]. As people age, stomach acid becomes weaker and not able to kill the bacteria, as a result makes people older than 65 four more times to get a Listeria infection [10].
<br>
<br>Symptoms of listeriosis include fever, muscle aches, nausea, vomiting, and diarrhea[11]. More severe symptoms are headaches, stiff neck, loss of balance, convulsions, and death[11]. Patients who are not pregnant most often are diagnosed with bacteremia, meningitis, and meningoencephalitis[29]. Listeriosis is most common during third trimester, however it can occur at any time during pregnancy[29]. Neonatal listeriosis may also occur. This occurs in the first 7 days of life, results from bacteremia or sepsis[29].  These symptoms can last from a few days to several weeks. Michigan State said that Listeria can be even more dangerous and have long term effects. It can compromise the immune system and cause sepsis and meningitis[26]. Meningitis is the infection and inflammation of the fluid and membranes in the brain and spinal cord which results in headaches, fever, and stiff neck[27]. Sepsis is when the body doesn’t respond well to an infection. This leads to organs not working well. Sepsis will lead to septic shock where there are dramatic drops in blood pressure which results in damaging organs such as lungs, kidneys, liver and more[28].

Revision as of 00:37, 15 April 2024

Introduction

By [Chris Chu]

Picture this: It's a scorching summer day, and you're standing in line at your favorite ice cream shop, torn between flavors and toppings. However, what if the seemingly innocent act of choosing your treat was overshadowed by a silent threat?

Enter Listeria monocytogenes, a bacterium lurking in that beloved cold dessert.Listeria monocytogenes, infamous for causing listeriosis, is not limited to ice cream—it can be found in an array of foods, including raw vegetables, meat, and dairy products. While most healthy individuals may experience only mild flu-like symptoms from consuming contaminated food, certain demographics face grave risks.Groups such as the elderly, pregnant women, newborns, and individuals with compromised immune systems are particularly susceptible to severe illness from Listeria monocytogenes. For them, listeriosis can escalate into dangerous conditions like meningitis, posing significant health threats. Symptoms of listeriosis vary but can include fever, muscle aches, nausea, and diarrhea. In severe cases, the infection can progress to affect the nervous system, leading to symptoms such as headache, stiff neck, confusion, and convulsions. Swift diagnosis and treatment, often involving antibiotics, are crucial, especially for high-risk individuals.To combat Listeria monocytogenes contamination, stringent food handling and hygiene practices are imperative. From thorough cooking of raw foods to meticulous washing of produce, proper precautions can significantly reduce the risk of infection.The prevalence of Listeria monocytogenes in the food supply chain can be influenced by environmental conditions and human activities. Understanding these factors is essential for implementing effective prevention strategies and mitigating risks to public health.Delving into the gene expression of Listeria monocytogenes provides valuable insights into its virulence and antibiotic resistance mechanisms. By deciphering its genetic makeup, researchers can better understand how this pathogen interacts with the human body and the environment, aiding in the development of targeted interventions.


Figure 1. Shows image of listeria. monocytogenes which causes Listeria !! Phoro credit: [1]

History


The discovery of Listeria monocytogenes is dated in 1924 where three bacteriologists isolated L. monocytogenes as etiological agents (microorganisms that cause diseases in humans[1]) by injecting rodents in an experiment. One of the microbiologists, E.G.D Murray, isolated the gram-positive rods from the blood of a rodent; however, could not identify the pathogenic microorganism to any genus known resulting in calling it Bacterium monocytogenes[2]. The first recorded case of Listeria monocytogenes in humans dates all the way back to Denmark in 1929. However, the first ever culture of L. monocytogenes was isolated in France from a patient with meningitis[3]. After twenty years of listeriosis discovery, the bacteria was found mostly among livestock, and mostly in small rodents.[4]. Very few cases were found in humans making it very rare and uncommon. This resulted in little to no mention in famous textbooks on bacteriology. It wasn’t until the late 40s that Dr. Stanley extracted monocytosis producing agents from living rabbit cells and described them as lipids[5]. His discovery helped broaden the understanding of how monocytes are distributed throughout the body and contribute to their development in the immune system.

structure


L. monocytogenes is a firmicute, which is part of a phylum of bacteria called Bacillota. It is a gram positive bacteria, however it could also be gram negative depending on the age of the culture[5]. The shape of these organisms are rod-like and do not form spores. There is no outer membrane, however, it has a S-layer which is a thick cell wall with layers of peptidoglycan. L. monocytogenes has a cell wall around 200 Å in thickness[5.] L. monocytogenes can thrive in refrigerator temperatures and have an enzyme called RNA helicase which improves activity and replication at low temperatures. This enzyme boosts their ability to survive in harsh climates. This bacteria also has a flagella, which is used to propel itself and attach it to enterocytes during infection[6]. Enterocytes, found in both the small and large intestines, are predominant epithelial cell lineage which has membranes with tight junctions that form between cells to create a physical barrier for mycobacteria[7]. L. monocytogenes have 4 primary virulence factors that help it infect host cells. It possesses internalins (Inl A and InlB) which are cell-surface galactose residues, lipoteichoic acids, and surface proteins that help L. monocytogenes attach to gastrointestinal epithelial cells using host protein cadherin[6]. This allows them to enter the cell and infect it. After the bacteria has invaded the host cells, it uses listeriolysin (LLO)[6]. Listeriolysin are proteins that form cytotoxic pores on the cell’s vacuole to allow L. monocytogenes to derange cellular processes by going through the cell membrane. Phosphatidylinositol-specific phospholipase C (PI-PLC) aids in the bacteria's evasion from the host cell vacuole and induces membrane disruption[6]. Lastly it also uses actin polymerization (ActA) to help in move between cells after infection[6].

Symptoms and Treatments


L. monocytogenes is a worldwide foodborne illness that has a hospitalization and mortality rate. Luckily, the annual cases of Listeria have been declining. 7.7 million per one million cases to 3.1 during the period from 1990 to 2023 in the USA and in Europe the infection rate declined from 4.5 cases per million to 3.4 cases from 1999 to 2003[8]. Annually, there are about 1600 cases of Listeria infections that are reported in the USA[8]. The mortality rate is about 30% while the hospitalization rate is about 99.1%[8]. The Center for Disease Control and Prevention (CDD) estimates that Listeria is the third leading cause of death from food poisoning int the USA[9]. Anyone can have a Listeria infection, however, the ones with the greatest chance of an infection are: people who are pregnant, people who are 65 years and older, and people with a weakened immune system. Pregnant women are 10 times more likely to have listeriosis which can result in miscarriages, stillbirths, preterm labor, and serious illness to the newborn[9]. The new born could have symptoms of dever, vomiting, little to no interest in feeding, irritability and difficulty breathing[12]. More than half of all infections occurred to people 65 and older[10]. As people age, stomach acid becomes weaker and not able to kill the bacteria, as a result makes people older than 65 four more times to get a Listeria infection [10].

Symptoms of listeriosis include fever, muscle aches, nausea, vomiting, and diarrhea[11]. More severe symptoms are headaches, stiff neck, loss of balance, convulsions, and death[11]. Patients who are not pregnant most often are diagnosed with bacteremia, meningitis, and meningoencephalitis[29]. Listeriosis is most common during third trimester, however it can occur at any time during pregnancy[29]. Neonatal listeriosis may also occur. This occurs in the first 7 days of life, results from bacteremia or sepsis[29]. These symptoms can last from a few days to several weeks. Michigan State said that Listeria can be even more dangerous and have long term effects. It can compromise the immune system and cause sepsis and meningitis[26]. Meningitis is the infection and inflammation of the fluid and membranes in the brain and spinal cord which results in headaches, fever, and stiff neck[27]. Sepsis is when the body doesn’t respond well to an infection. This leads to organs not working well. Sepsis will lead to septic shock where there are dramatic drops in blood pressure which results in damaging organs such as lungs, kidneys, liver and more[28].

  1. Biological Materials Shipping Manual - campus services. (n.d.). https://campus.und.edu/safety/_files/docs/biological-materials-shipping-manual.pdf
  2. H. Hof, History and epidemiology of listeriosis, FEMS Immunology & Medical Microbiology, Volume 35, Issue 3, April 2003, Pages 199–202, https://doi.org/10.1016/S0928-8244(02)00471-6
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88991/#:~:text=The%20first%20cases%20of%20human,meningitis%20(159%2C%20604).
  4. Seeliger HP. Listeriosis--history and actual developments. Infection. 1988;16 Suppl 2:S80-4. doi: 10.1007/BF01639726. PMID: 3138193.
  5. Seeliger HP. Listeriosis--history and actual developments. Infection. 1988;16 Suppl 2:S80-4. doi: 10.1007/BF01639726. PMID: 3138193.