Escherichia coli

Last updated: September 12, 2024

Escherichia coli

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
Excess Vitamin D
Vitamin D deficiency
Vitamin K deficiency
Kwashiorkor
Marasmus
Iodine deficiency
Zinc deficiency
Beriberi
Folate (Vitamin B9) deficiency
Niacin (Vitamin B3) deficiency
Vitamin B12 deficiency
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
Ehlers-Danlos syndrome
Marfan syndrome
Osteogenesis imperfecta
Primary ciliary dyskinesia
Adrenoleukodystrophy (NORD)
Zellweger spectrum disorders (NORD)
Cytoskeleton and elastin disorders: Pathology review
Peroxisomal disorders: Pathology review
DNA cloning
ELISA (Enzyme-linked immunosorbent assay)
Fluorescence in situ hybridization
Gel electrophoresis and genetic testing
Karyotyping
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
DNA structure
Epigenetics
Gene regulation
Lac operon
Mitosis and meiosis
Nuclear structure
Nucleotide metabolism
Protein structure and synthesis
Transcription of DNA
Translation of mRNA
Adenosine deaminase deficiency
Lesch-Nyhan syndrome
Orotic aciduria
Bloom syndrome
Fanconi anemia
Li-Fraumeni syndrome
McCune-Albright syndrome
Xeroderma pigmentosum
Acute radiation syndrome
Purine and pyrimidine synthesis and metabolism disorders: Pathology review
Human development days 1-4
Human development days 4-7
Human development week 2
Human development week 3
Development of the digestive system and body cavities
Development of the fetal membranes
Development of the placenta
Development of the umbilical cord
Development of twins
Hedgehog signaling pathway
Ectoderm
Endoderm
Mesoderm
Development of the cardiovascular system
Fetal circulation
Development of the ear
Development of the eye
Development of the face and palate
Pharyngeal arches, pouches, and clefts
Development of the gastrointestinal system
Development of the teeth
Development of the tongue
Development of the axial skeleton
Development of the limbs
Development of the muscular system
Development of the nervous system
Development of the renal system
Development of the reproductive system
Development of the respiratory system
Evolution and natural selection
Hardy-Weinberg equilibrium
Independent assortment of genes and linkage
Inheritance patterns
Mendelian genetics and punnett squares
Achondroplasia
Alagille syndrome (NORD)
Familial adenomatous polyposis
Hereditary spherocytosis
Huntington disease
Multiple endocrine neoplasia
Myotonic dystrophy
Neurofibromatosis
Polycystic kidney disease
Treacher Collins syndrome
Tuberous sclerosis
von Hippel-Lindau disease
Albinism
Alpha-thalassemia
Beta-thalassemia
Cystic fibrosis
Friedreich ataxia
Hemochromatosis
Sickle cell disease (NORD)
Wilson disease
Cri du chat syndrome
Williams syndrome
Angelman syndrome
Prader-Willi syndrome
Beckwith-Wiedemann syndrome
Mitochondrial myopathy
Klinefelter syndrome
Turner syndrome
Fragile X syndrome
Down syndrome (Trisomy 21)
Edwards syndrome (Trisomy 18)
Patau syndrome (Trisomy 13)
Hemophilia
Muscular dystrophy
Wiskott-Aldrich syndrome
X-linked agammaglobulinemia
Autosomal trisomies: Pathology review
Miscellaneous genetic disorders: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Bacterial structure and functions
Bacillus anthracis (Anthrax)
Bacillus cereus (Food poisoning)
Corynebacterium diphtheriae (Diphtheria)
Listeria monocytogenes
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium perfringens
Clostridium tetani (Tetanus)
Actinomyces israelii
Nocardia
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
Streptococcus agalactiae (Group B Strep)
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus viridans
Enterococcus
Bacteroides fragilis
Bartonella henselae (Cat-scratch disease and Bacillary angiomatosis)
Enterobacter
Escherichia coli
Klebsiella pneumoniae
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Proteus mirabilis
Pseudomonas aeruginosa
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Serratia marcescens
Shigella
Yersinia enterocolitica
Yersinia pestis (Plague)
Campylobacter jejuni
Helicobacter pylori
Vibrio cholerae (Cholera)
Moraxella catarrhalis
Neisseria gonorrhoeae
Neisseria meningitidis
Bordetella pertussis (Whooping cough)
Brucella
Francisella tularensis (Tularemia)
Haemophilus ducreyi (Chancroid)
Haemophilus influenzae
Pasteurella multocida
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium avium complex (NORD)
Mycobacterium leprae
Chlamydia pneumoniae
Chlamydia trachomatis
Gardnerella vaginalis (Bacterial vaginosis)
Mycoplasma pneumoniae
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Leptospira
Treponema pallidum (Syphilis)
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Aspergillus fumigatus
Candida
Cryptococcus neoformans
Mucormycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Sporothrix schenckii
Blastomycosis
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Pediculus humanus and Phthirus pubis (Lice)
Sarcoptes scabiei (Scabies)
Acanthamoeba
Naegleria fowleri (Primary amebic meningoencephalitis)
Toxoplasma gondii (Toxoplasmosis)
Cryptosporidium
Entamoeba histolytica (Amebiasis)
Giardia lamblia
Babesia
Plasmodium species (Malaria)
Leishmania
Trichomonas vaginalis
Trypanosoma brucei
Trypanosoma cruzi (Chagas disease)
Diphyllobothrium latum
Echinococcus granulosus (Hydatid disease)
Ancylostoma duodenale and Necator americanus
Angiostrongylus (Eosinophilic meningitis)
Anisakis
Ascaris lumbricoides
Enterobius vermicularis (Pinworm)
Guinea worm (Dracunculiasis)
Loa loa (Eye worm)
Onchocerca volvulus (River blindness)
Strongyloides stercoralis
Toxocara canis (Visceral larva migrans)
Trichinella spiralis
Trichuris trichiura (Whipworm)
Wuchereria bancrofti (Lymphatic filariasis)
Clonorchis sinensis
Paragonimus westermani
Schistosomes
Viral structure and functions
Adenovirus
Hepatitis B and Hepatitis D virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Human herpesvirus 8 (Kaposi sarcoma)
Varicella zoster virus
Human papillomavirus
Parvovirus B19
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Poxvirus (Smallpox and Molluscum contagiosum)
Lymphocytic choriomeningitis virus
Hantavirus
Norovirus
Coronaviruses
Ebola virus
Dengue virus
Hepatitis C virus
West Nile virus
Yellow fever virus
Zika virus
Influenza virus
Human parainfluenza viruses
Measles virus
Mumps virus
Respiratory syncytial virus
Hepatitis A and Hepatitis E virus
Coxsackievirus
Poliovirus
Rhinovirus
Rotavirus
HIV (AIDS)
Human T-lymphotropic virus
Rabies virus
Eastern and Western equine encephalitis virus
Rubella virus
Prions (Spongiform encephalopathy)
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
DNA synthesis inhibitors: Fluoroquinolones
DNA synthesis inhibitors: Metronidazole
Mechanisms of antibiotic resistance
Miscellaneous cell wall synthesis inhibitors
Miscellaneous protein synthesis inhibitors
Protein synthesis inhibitors: Aminoglycosides
Protein synthesis inhibitors: Tetracyclines
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Anti-mite and louse medications
Antimalarials
Hepatitis medications
Herpesvirus medications
Integrase and entry inhibitors
Neuraminidase inhibitors
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Introduction to pharmacology
Enzyme function
Drug administration and dosing regimens
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
Adrenergic antagonists: Beta blockers
Adrenergic antagonists: Presynaptic
Adrenergic receptors
Cholinergic receptors
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympatholytics: Alpha-2 agonists
Sympathomimetics: Direct agonists
Selective serotonin reuptake inhibitors
Atypical antidepressants
Monoamine oxidase inhibitors
Serotonin and norepinephrine reuptake inhibitors
Tricyclic antidepressants
Atypical antipsychotics
Typical antipsychotics
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Lithium
Nonbenzodiazepine anticonvulsants
Psychomotor stimulants
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Lipid-lowering medications: Fibrates
Lipid-lowering medications: Statins
Miscellaneous lipid-lowering medications
Positive inotropic medications
Adrenal hormone synthesis inhibitors
Mineralocorticoids and mineralocorticoid antagonists
Hypoglycemics: Insulin secretagogues
Insulins
Miscellaneous hypoglycemics
Hyperthyroidism medications
Hypothyroidism medications

Transcript

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Escherichia coli or just E. Coli, is a gram-negative rod-shaped bacteria named after Dr. Escherich Theodor, who discovered it in feces, thus concluding that it colonizes the colon.

Alright, now E. Coli is gram-negative because its cell wall has a thin peptidoglycan layer so it cannot retain the crystal violet stain, but instead, it stains pink with Safranin dye used during Gram staining.

So it looks like a little pink rod under the microscope.

Also, E. Coli is a catalase positive bacteria, and that means it produces an enzyme called catalase.

This can be tested by adding a few drops of hydrogen peroxide to a colony of bacteria, and catalase makes hydrogen peroxide dissociate into water and oxygen, making the mixture foam.

E. Coli is also a lactose fermenter, because it can produce an enzyme called beta B-galactosidase that cleaves lactose into glucose and galactose monomers.

To test this, E. Coli can be cultivated on lactose-containing media such as Phenol lactose, and as it ferments it, the fermentation results in the production of acids that turn the red of phenol to yellow.

It is also a facultative anaerobe, meaning it lives in environments with or without oxygen.

Now, taking a closer look to this bacteria, E. Coli is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.

E. Coli is a motile bacteria, because it has helical whip-like threads called flagella that it can use to move around.

When E coli is cultivated on eosin methylene blue agar, it grows into black colonies with a greenish-black metallic sheen.

Alright, most of E. Coli are harmless, and they can peacefully colonize the human gut without causing any trouble.

However, some strains of E. Coli are pathogenic, meaning they can cause illness. It starts with this bacteria using little thread-like extensions called fimbriae to attach to the host cell surface.

E coli has many different strains that can do that, and they cause different diseases. These strains can be classified by two systems.

The first system uses serotypes, and it groups E. Coli strains based on their antigens.

Antigens are elements that the host’s immunity considers foreign and mount an immune reaction as a response.

So, bacteria within a given serotype, trigger a similar immune response.

Alright, E. Coli has a number of antigens, and among them we have somatic antigens located just on the cell membrane, and these ones are abridged with the letter “O”.

There are also capsular – “K” antigens located on the capsule, fimbrial – “F” antigens located on the fimbria, and flagellar – “H” antigens located on the bacterial flagella.

Usually after this letter that tells on what part of the bacteria where the antigen is found, it follows a designation number in case there are more antigens of the same kind, such as K1, K2, and so forth… E. Coli antigens, influence its power to cause diseases, so that’s why they can alternatively be referred to as virulence factors.

For example, E. Coli with capsular antigen one, or K1, are the ones that cause neonatal meningitis, while an E. Coli that has an O157, and an H7 – designated as O157:H7, is associated with hemorrhagic colitis, hemolytic uremic syndrome and diarrheal outbreaks.

Other E. Coli serotypes include E. Coli SE15, E. Coli F11, E. Coli O25:H and so on… but in fact, these serotypes are so numerous and they can go up to 200 serotypes.

Thankfully, there’s a much simpler classification, and that is based on pathotypes.

A pathotype is a group of organisms of the same species, that cause disease in the same way - meaning they use the same virulence factors.

And there are 5 E.Coli pathotypes: Shiga-like toxin-producing E.Coli, or STEC for short, enterotoxigenic E. Coli or ETEC, enteroinvasive E. Coli, or EIEC, enteropathogenic E. Coli, or EPEC, and uropathogenic E. coli or UPEC/

So first, Shiga-like toxin-producing E. Coli, or STEC is called that because it makes a toxin similar to the one called Shiga toxin produced by Shigella.

STEC attaches to the host’s intestinal cells, and then start releasing toxins that cause injury to intestinal epithelium and underlying blood vessels, resulting in inflammation.

This makes fluid and blood leak into the intestinal lumen, resulting in bloody diarrhea.

That’s why some people refer to it as enterohemorrhagic E. Coli, or EHEC.

But STECs can also affect the urinary tract, causing hemolytic uremic syndrome or HUS. Hemolytic uremic syndrome usually develops after STEC have released their toxin into the bloodstream.

From the bloodstream, the toxin can get to the kidneys, and bind to the endothelial cells lining the glomerulus, making them die by apoptosis, or programmed cell death.

Consequently, a dead endothelial cell leaves a gap in the capillary wall, and as more gaps keep forming, it results in holes big enough to allow large molecules such as proteins to start leaking out of the capillaries, resulting in proteinuria.

The destruction of endothelial cells triggers an inflammatory process in which inflammatory molecules such as cytokines and chemokines are released.

Cytokines and chemokines activate blood platelets and initiate the clot formation.

As these platelets are used to form these clots their number in the blood decreases resulting in low platelets or thrombocytopenia.

Also these clots can be big enough to obstruct small arterioles.

So, as red blood cells force to pass through obstructed micro-vessels, they can get sliced into fragments called schistocytes in this process known as microangiopathic hemolysis.

So, as more red blood cells get destroyed in the process, their number reduces, which can cause anemia.

Alternatively, if clots obstruct too many arterioles, organs that depend on high blood flow, like the kidney, may lack blood and die by ischemia.

Now, an ischemic kidney is unable to filter blood. This is how too much of metabolic wastes such as urea, start accumulating in the blood, leading to uremia.

Key Takeaways

Escherichia coli is a gram-negative, rod-shaped, facultative anaerobic bacterium that is commonly found in the lower intestine of warm-blooded animals, and is an important part of the human gut flora. Escherichia coli is also used as a model organism for bacterial genetics and molecular biology. However, It is known to cause food poisoning, urinary tract infections, neonatal meningitis, septicemia, and other diseases in humans.