Abscesses

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Abscesses

I&D Part 1

I&D Part 1

Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Abscesses
Anaphylaxis
Rheumatic heart disease
Poststreptococcal glomerulonephritis
Contact dermatitis
X-linked agammaglobulinemia
Thymic aplasia
DiGeorge syndrome
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Bacillus anthracis (Anthrax)
Nocardia
Escherichia coli
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Pseudomonas aeruginosa
Enterobacter
Klebsiella pneumoniae
Shigella
Yersinia enterocolitica
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Bacteroides fragilis
Yersinia pestis (Plague)
Vibrio cholerae (Cholera)
Helicobacter pylori
Campylobacter jejuni
Neisseria meningitidis
Neisseria gonorrhoeae
Moraxella catarrhalis
Francisella tularensis (Tularemia)
Bordetella pertussis (Whooping cough)
Brucella
Haemophilus influenzae
Haemophilus ducreyi (Chancroid)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Mechanisms of antibiotic resistance
Viral structure and functions
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Human papillomavirus
Poxvirus (Smallpox and Molluscum contagiosum)
HIV (AIDS)
Poliovirus
Coxsackievirus
Rhinovirus
Influenza virus
Respiratory syncytial virus
Human parainfluenza viruses
Dengue virus
Yellow fever virus
Zika virus
West Nile virus
Norovirus
Rotavirus
Coronaviruses
Ebola virus
Rabies virus
Rubella virus
Eastern and Western equine encephalitis virus
Candida
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications

Flashcards

Abscesses

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Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses.

An abscess forms when normal tissue, like skin for example, is split apart and that new space is invaded by nearby pathogens like bacteria.

And there are roughly ten bacterial cells for every one human cell and they cover every surface of the human body.

So any cut or break in the skin or closed off area within the body is an invitation for bacteria to dive in and multiply.

When that happens the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.

So, in response to an injury, the tissue releases small chemicals in the local area called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6 and interleukin-17, and chemokines which attract nearby white blood cells which are part of the immune system. It’s kinda like yelling for help and being heard by the nearby police.

In addition to attracting immune cells, the cytokines also dilate nearby capillaries - which brings more blood to the site, and make the capillaries more leaky, so that the white blood cells that do show up, can slip out of the blood and get into the tissue more easily.

Often times, the first immune cells at the scene are neutrophils, which release chemicals and enzymes that kill bacteria and dissolve pieces of of dead cells, creating a pool of dead material.

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.

From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid.

As those immune cells get to a point where they can’t withstand the environment, they die too, and become part of that pool.

Initially the debris might be intermixed with healthy tissue, but over time it can coalesce into a single area - a process that is often sped up when more immune cells get involved.

Around this pool of pus, a wall of fibrinogen - which is the same protein that holds together blood clots - starts to harden into a barrier.

Occasionally sheets of fibrin form septations, creating loculations or pockets of pus within the abscess itself...kinda like an abscess within an abscess.

Even though the pus is largely dead material, there are still plenty of live bacteria within the pus, which makes it highly infectious if it gets spread from one place to another.

One of the most common bacteria found in abscesses, especially in the skin or underlying soft tissue, is Staphylococcus aureus.

In fact, Staphylococcus aureus releases the enzyme coagulase, which helps speed up the process of building the fibrinogen wall.

In contrast to an abscess near the skin, ones that originate deeper in the body often occur in spaces that are already relatively walled off.

For example, in the gallbladder, if a stone blocks bile from flowing out, it essentially becomes a new home for bacteria.

Bacteria from the nearby small intestine can easily sneak past the stone, crawl into the gallbladder, and multiply, which causes an inflammatory response, and eventually an abscess might form.

Typically these deep infections are a mix of aerobic bacteria that use up all of the available oxygen, and anaerobic bacteria that can only live in its absence.

Sources

  1. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  2. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  3. "Yen & Jaffe's Reproductive Endocrinology" Saunders W.B. (2018)
  4. "Bates' Guide to Physical Examination and History Taking" LWW (2016)
  5. "Robbins Basic Pathology" Elsevier (2017)
  6. "Etymologia:<i>Staphylococcus</i>" Emerging Infectious Diseases (2013)
  7. "Patterns of Contrast Enhancement in the Brain and Meninges" RadioGraphics (2007)
  8. "A play in four acts: Staphylococcus aureus abscess formation" Trends in Microbiology (2011)