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General infections


Neonatal sepsis


Hypersensitivity reactions

Type I hypersensitivity

Food allergy



Type II hypersensitivity

Immune thrombocytopenic purpura

Autoimmune hemolytic anemia

Hemolytic disease of the newborn

Goodpasture syndrome

Rheumatic heart disease

Myasthenia gravis

Graves disease

Pemphigus vulgaris

Type III hypersensitivity

Serum sickness

Systemic lupus erythematosus

Poststreptococcal glomerulonephritis

Type IV hypersensitivity

Graft-versus-host disease

Contact dermatitis


Transplant rejection

Graft-versus-host disease

Cytomegalovirus infection after transplant (NORD)

Post-transplant lymphoproliferative disorders (NORD)


X-linked agammaglobulinemia

Selective immunoglobulin A deficiency

Common variable immunodeficiency

IgG subclass deficiency

Hyperimmunoglobulin E syndrome

Isolated primary immunoglobulin M deficiency

Thymic aplasia

DiGeorge syndrome

Severe combined immunodeficiency

Adenosine deaminase deficiency


Hyper IgM syndrome

Wiskott-Aldrich syndrome

Leukocyte adhesion deficiency

Chediak-Higashi syndrome

Chronic granulomatous disease

Complement deficiency

Hereditary angioedema


Immune system organ disorders


Ruptured spleen

Immune system pathology review

Blood transfusion reactions and transplant rejection: Pathology review

Immunodeficiencies: T-cell and B-cell disorders: Pathology review

Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review

Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review




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High Yield Notes

4 pages



of complete

External References

First Aid








Abscess p. 491

lung p. NaN

Alcoholism p. 595

lung abscesses and p. 710


brain abscesses p. 177

Bacteroides spp.

lung abscesses p. 710

Bartholin cyst/abscess p. 668

Brain abscesses

HIV-positive adults p. 177

Toxoplasma gondii p. , 174

Chest X-rays

lung abscesses p. 710


lung abscesses p. 710


lung abscesses p. 710

Fusobacterium spp.

lung abscesses p. 710

Lung abscesses p. 710


brain abscesses p. 177

Otitis media

brain abscesses with p. 177

Perinephric abscesses p. 625


brain abscesses p. 177

Staphylococcus aureus p. , 133

brain abscesses p. 177

Viridans streptococci p. 134

brain abscesses p. 177


Content Reviewers

Rishi Desai, MD, MPH


Charles Davis, MD

Tanner Marshall, MS

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.


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  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)

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