Listeria monocytogenes

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Listeria monocytogenes

NBME

NBME

Amino acid metabolism
Nitrogen and urea cycle
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Gluconeogenesis
Glycogen metabolism
Glycolysis
Pentose phosphate pathway
Physiological changes during exercise
Cholesterol metabolism
Fatty acid oxidation
Fatty acid synthesis
Ketone body metabolism
Alkaptonuria
Cystinuria (NORD)
Hartnup disease
Homocystinuria
Maple syrup urine disease
Ornithine transcarbamylase deficiency
Phenylketonuria (NORD)
Essential fructosuria
Galactosemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hereditary fructose intolerance
Lactose intolerance
Pyruvate dehydrogenase deficiency
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Glycogen storage disease type III
Glycogen storage disease type IV
Glycogen storage disease type V
Mucopolysaccharide storage disease type 1 (Hurler syndrome) (NORD)
Mucopolysaccharide storage disease type 2 (Hunter syndrome) (NORD)
Fabry disease (NORD)
Gaucher disease (NORD)
Krabbe disease
Leukodystrophy
Metachromatic leukodystrophy (NORD)
Niemann-Pick disease type C
Niemann-Pick disease types A and B (NORD)
Tay-Sachs disease (NORD)
Cystinosis
Disorders of amino acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Disorders of fatty acid metabolism: Pathology review
Dyslipidemias: Pathology review
Glycogen storage disorders: Pathology review
Lysosomal storage disorders: Pathology review
Carbohydrates and sugars
Fats and lipids
Proteins
Excess Vitamin A
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Vitamin K deficiency
Kwashiorkor
Marasmus
Iodine deficiency
Zinc deficiency
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Folate (Vitamin B9) deficiency
Niacin (Vitamin B3) deficiency
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Vitamin C deficiency
Wernicke-Korsakoff syndrome
Fat-soluble vitamin deficiency and toxicity: Pathology review
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Zinc deficiency and protein-energy malnutrition: Pathology review
Cell membrane
Cell signaling pathways
Cell-cell junctions
Cellular structure and function
Cytoskeleton and intracellular motility
Endocytosis and exocytosis
Extracellular matrix
Nernst equation
Osmosis
Resting membrane potential
Selective permeability of the cell membrane
Alport syndrome
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Marfan syndrome
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Primary ciliary dyskinesia
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Zellweger spectrum disorders (NORD)
Cytoskeleton and elastin disorders: Pathology review
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DNA cloning
ELISA (Enzyme-linked immunosorbent assay)
Fluorescence in situ hybridization
Gel electrophoresis and genetic testing
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Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)
Amino acids and protein folding
Cell cycle
DNA damage and repair
DNA mutations
DNA replication
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Gene regulation
Lac operon
Mitosis and meiosis
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Transcription of DNA
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Adenosine deaminase deficiency
Lesch-Nyhan syndrome
Orotic aciduria
Bloom syndrome
Fanconi anemia
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McCune-Albright syndrome
Xeroderma pigmentosum
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Human development days 1-4
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Development of the digestive system and body cavities
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Alagille syndrome (NORD)
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Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Cell wall synthesis inhibitors: Cephalosporins
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DNA synthesis inhibitors: Fluoroquinolones
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Introduction to pharmacology
Enzyme function
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Pharmacodynamics: Agonist, partial agonist and antagonist
Pharmacodynamics: Desensitization and tolerance
Pharmacodynamics: Drug-receptor interactions
Pharmacokinetics: Drug absorption and distribution
Pharmacokinetics: Drug elimination and clearance
Pharmacokinetics: Drug metabolism
Adrenergic antagonists: Alpha blockers
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Adrenergic receptors
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Sympatholytics: Alpha-2 agonists
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Nonbenzodiazepine anticonvulsants
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cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
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ACE inhibitors, ARBs and direct renin inhibitors
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Lipid-lowering medications: Fibrates
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Hypoglycemics: Insulin secretagogues
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Assessments

Flashcards

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USMLE® Step 1 questions

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High Yield Notes

6 pages

Flashcards

Listeria monocytogenes

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Questions

USMLE® Step 1 style questions USMLE

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A 23-year-old gravida 1 para 0 woman presents to the obstetrics clinic to discuss pregnancy. Based on the first-trimester ultrasound, the patient is in the 20th week of gestation. As part of pregnancy complication counseling, the patient and physician discuss Listeria monocytogenes infection and how the risk of infection can be decreased. Which of the following measures can be taken to decrease the risk of infection with Listeria monocytogenes?  

External References

First Aid

2024

2023

2022

2021

Ampicillin

Listeria monocytogenes p. , 137

Gastroenteritis

Listeria monocytogenes p. , 137

Granulomatosis infantiseptica p. NaN

Listeria monocytogenes p. , 137

Immunocompromised patients

Listeria monocytogenes p. , 137

Listeria spp.

catalase-positive organism p. 125

Gram-positive algorithm p. 132

intracellular organism p. 125

meningitis p. 177

taxonomy p. 122

Listeria monocytogenes p. , 137

β -hemolysis p. 133

granulomatous diseases p. NaN

neonates p. 181

penicillins for p. 185

Meningitis

Listeria monocytogenes p. , 137

Neonates

Listeria monocytogenes in p. 137

Pregnancy p. 651

Listeria monocytogenes in p. 137

Septicemia

Listeria monocytogenes p. , 137

Spontaneous abortion

Listeria monocytogenes p. , 137

Transcript

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Listeria monocytogenes or just L. monocytogenes, is a gram-positive bacteria that causes listeriosis. Listeria was discovered by a Scottish doctor, J.H.H. Pirie, who named it in honor of British surgeon Joseph Lister,. It’s also called “monocytogenes” because when it was inoculated in rabbits, their monocyte levels increased.

Ok now, L. monocytogenes is a rod-shaped bacteria with a thick peptidoglycan cell wall. So when gram-stained, it takes in purple dye, making it a gram-positive bacteria. It is catalase positive and oxidase negative - which means it produces the enzyme catalase, but not oxidase. L. monocytogenes is a facultative intracellular pathogen, meaning it can live both outside or inside of its host’s cells. It doesn’t form spores and it is facultatively anaerobic, meaning that it can survive in both aerobic and anaerobic environments.

Now, when L. monocytogenes is cultivated on blood agar medium, its colonies cause beta-hemolysis, also called complete hemolysis. That’s because it produces toxins called beta hemolysins, which hydrolyze the hemoglobin within red blood cells to transparent yellow color byproducts.

L. monocytogenes is a motile bacteria, with a very interesting way to move, that depends on both its location, and the temperature. In an extracellular environment, this bacteria moves by beating its flagella creating a characteristic tumbling motility. But this is only possible at 37 degrees Celsius and below. That’s because FlaA, the gene that codes for flagellin, which is the structural protein that makes up the flagella becomes downregulated as the temperature rises up to 37 degree Celsius. So above 37 degrees, there’s reduced production of flagellin proteins, meaning no flagella being made, rendering L. monocytogenes non-motile.

In an intracellular environment, L. monocytogenes moves by an actin-based motility. It start with this bacteria producing a protein called Actin assembly-inducing protein or just ACTA, which recruits small actin filaments at one end. As more and more actin filaments get recruited and polymerized behind the bacteria’s end pole, that propels the bacteria forward, like a rocket.

L. monocytogenes is a foodborne bacteria, meaning people get infected when they eat contaminated food - especially unpasteurized dairy products and cold deli meats, and this bacteria is known to survive even at very low temperatures in the fridge Once this bacteria gets into the gut, it uses its attachment proteins called internalins to attach to the host’s receptor proteins, such as E cadherin located on goblet cells of the intestinal mucosa. After attaching to the host’s cells, this bacteria is slowly engulfed by the cell membrane, which invaginates to form a sac on its inner side. The sac then separates from the actual cell membrane forming what’s referred to a internalization vacuole.

Inside the vacuole, Listeria releases listeriolysin O, and bacterial phospholipases, which are enzymes that degrade the vacuolar membrane. This releases the bacteria in the host’s cell cytoplasm, where it starts using the host’s cell resources and food, and multiply into many identical bacterial cells, by the process of binary fission, which means every bacterial cell splits in two identical copies. On a side note, if this sounds similar to mitosis… well, it is! But the term binary fission is used to describe division of prokaryotic cells, which don’t have a nucleus, and therefore some steps in replication are different from mitosis.

Inside the cell, L. monocytogenes moves around using the actin-propelled motility, and when it reaches the cell’s membrane, it stretches it towards an adjacent cell. When it reaches the adjacent cell membrane, that one invaginates as well, so Listeria ends up wrapped in a double-layered sac. Then, this sac pinches off inside the adjacent cell, as a double membrane vacuole. Inside this vacuole, Listeria releases listeriolysin O and phospholipases to break free into the cytoplasm, repeating the invasion process over and over to invade more adjacent cells and, eventually, get into the bloodstream.

Summary

Listeria monocytogenes is a gram-positive, rod-shaped, facultatively anaerobic bacterium, which can cause an infection known as listeriosis. Although rare, listeriosis can be deadly in immunosuppressed people, pregnant women, newborns, and the elderly.

Listeriosis presents with low-grade fever, diarrhea, and vomiting. It can complicate into a high-grade fever, liver abscess and jaundice, and altered mental status in case of disseminated listeriosis. Listeriosis is diagnosed using cultures, and imaging studies like a CT scan may help identify liver abscesses. Treatment is with antibiotics, such as ampicillin and gentamicin combined, or just meropenem in those who are allergic to ampicillin.