Bacterial and viral skin infections: Pathology review

Chapters:

Watch video only

Case studies 0:00–1:14

At the clinic, 10-year-old Quentin is brought by his parents after an episode of dark-colored urine. Upon examination, his blood pressure is high and you notice that the area around his ankles appears swollen.
His parents also mention that last week, Quentin developed multiple vesicles with a honey-colored crusting around his nose and mouth.
You decide to perform a urinalysis test, which reveals there’s blood in the urine with red blood cell casts, as well as higher than normal levels of protein.
Later on that same day, 70-year-old Claudio presents to the emergency department complaining of severe pain in his genital area that started about a week ago.
On examination, you notice severe scrotal swelling, a purplish rash, and palpable crepitus in the perineal area. Claudio also appears lethargic, and has a fever and low blood pressure.
Upon further questioning, Claudio mentions that he had surgery for varicocele about two weeks ago. Past medical history reveals that in his 40s, Claudio was diagnosed with diabetes mellitus, which he has not been controlling properly.
You decide to order a swab culture, which comes back positive for anaerobic bacteria and Streptococcus pyogenes. Based on the initial presentation, both Quentin and Claudio seem to have some form of skin infection.

Physiology 1:14–2:15

Okay, first, let’s go over some physiology. Normally, the skin is divided into three main layers, the hypodermis, dermis, and epidermis.
The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, which contains hair follicles, nerve endings, glands, blood vessels, and lymphatics.
And above the dermis is the epidermis, which contains five layers of developing keratinocytes. Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer.
As keratinocytes in the stratum basale mature, they migrate up into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer.Okay, now skin infections can affect different skin layers, and for your exams, the most relevant bacterial skin infections include impetigo, erysipelas, cellulitis, skin abscess, necrotizing fasciitis, and staphylococcal scalded skin syndrome; while relevant viral skin infections include molluscum contagiosum, herpes, varicella and herpes zoster.

Pathology 2:15–2:37

Let’s begin with bacterial skin infections. These include impetigo, which is an infection of the superficial layers of the epidermis.

Impetigo 2:37–5:05

It is highly contagious, and most commonly affects newborns or children. Now, impetigo can be classified as bullous or non-bullous.
Non-bullous impetigo is usually caused by Staphylococcus aureus or Streptococcus pyogenes. In non-bullous impetigo, lesions usually appear as vesicles or pustules with a characteristic honey-colored, or golden, crusting around an erythematous, moist base.
This can actually be a very important clue in a test question! Remember that these lesions typically appear in the face or limbs, and they often develop on skin that was previously damaged by things like insect bites, minor trauma, eczema, or abrasions, and they usually heal without scarring.
In addition, affected individuals may present with enlargement of the regional lymph nodes. Another very high yield concept is that cases of impetigo caused by Streptococcus pyogenes, if left untreated or treated inadequately, can lead to post-streptococcal glomerulonephritis.
This is caused by a type III hypersensitivity reaction, where there is complement activation and immune complex deposition on the glomerular basement.
In a test question, look for an individual that has an episode of non-bullous impetigo caused by Streptococcus pyogenes, and a few days later presents with signs and symptoms of glomerulonephritis, such as oliguria, hematuria, dark-colored, or coca-cola, urine, proteinuria, RBC casts, hypertension, and edema from fluid retention, often causing swelling around the face or ankles.On the other hand, bullous impetigo is caused by toxin-producing Staphylococcus aureus, and is characterized by painful, flaccid, fluid-filled vesicles and blisters or bullae.
These are typically multiple and develop around the nose, and mouth, but can spread rapidly to the trunk, buttocks, or body folds.
Now, these bullae rupture easily, leaving a rim of dry skin that surrounds a shallow wet erosion. What might help you set these lesions apart from non-bullous impetigo is that they develop on intact skin and there’s usually no surrounding erythema and regional lymphadenopathy.
It’s also important to keep in mind that these lesions are often accompanied by systemic symptoms like fever, chills, and malaise.Moving onto erysipelas, this is an infection of the upper dermis that commonly extends to the superficial lymphatic vessels of the underlying connective tissue.
For your exams, you have to know that the cause is usually Streptococcus pyogenes. Now, erysipelas typically presents as a swollen, red, and tender skin area, most commonly on the face or the lower limbs.

Erysipelas 5:05–5:45

Now, what’s super high yield is that the lesions are sharply defined and well-demarcated, with slightly elevated borders and reddish streaks of lymphangitis.
In more severe cases, there can also be vesicles or bullae. In addition, some individuals may experience systemic symptoms like fever and chills.
Next is cellulitis, which is an infection of the deeper dermis and subcutaneous tissues, and it’s usually caused by Streptococcus pyogenes or Staphylococcus aureus.
Cellulitis typically starts from a cut or break in the skin, often from a recent trauma or another infection. Now, cellulitis typically presents as a swollen, red, and tender skin area that’s warm to the touch, most commonly in the limbs.

Cellulitis 5:45–6:29

What’s important to know is that, unlike erysipelas, with cellulitis, the lesion is poorly demarcated, and has hardly noticeable margins, because the infectious process is deep underneath the skin.
Some individuals may also present with lymphadenopathy and systemic symptoms like fever and chills. Moving on, skin abscesses are walled-off collections of pus that develop within the deeper skin layers.
For the exams, remember that they are almost always caused by Staphylococcus aureus, even the methicillin-resistant strain MRSA.
Now, skin abscesses typically present as a swollen, red, and tender nodule that’s warm to the touch, and if there is a break in the skin, pus can be visually observed.

Skin abscess 6:29–6:58

Some individuals may also present with systemic symptoms like fever and chills. Next there’s necrotizing fasciitis, also known as “flesh-eating disease”.
This is a severe, life-threatening infection of the deeper soft tissues, resulting in the destruction of the subcutaneous fat and underlying skeletal muscle fascia, hence the word “fasciitis.” For your exams, remember that necrotizing fasciitis can be polymicrobial, and is often caused by Streptococcus pyogenes and Staphylococcus aureus, as well as anaerobic bacteria like Clostridium perfringens.

Necrotizing fasciitis 6:58–9:00

Risk factors include diabetes, peripheral vascular disease, along with a history of recent surgery or trauma at the site of the infection.
Now, the most common site of infection is the trunk and limbs, but when necrotizing fasciitis involves the perineum or scrotum, it is also known as Fournier’s gangrene.
And that’s a high yield fact! Clinical presentation of necrotizing fasciitis includes severe pain, erythema, and swelling of the affected area.
The overlying skin can be tense or indurated, or might develop red or violet-colored patches. Another telltale sign upon palpation is crepitus, which is a crackling sound of bubbles beneath the skin that are caused by bacterial production of methane and carbon dioxide.
A characteristic of necrotizing fasciitis is that it progresses rapidly, so over the course of a few days, the skin can break down, giving rise to bullae or ulcers.
This may quickly progress to gangrene, or death of the tissues, which manifests as a hard, dry texture, often with a clear demarcation between viable and black, necrotic tissue.
In addition, the individual might present with signs of systemic toxicity, such as high fever, hypotension, tachycardia, and altered mental status.
Also, bear in mind that necrotizing fasciitis is a surgical emergency, so individuals must be immediately sent for surgical debridement to remove the necrotic tissue; if gangrene has set in, amputation might be required.Alright, now let’s discuss Staphylococcal scalded skin syndrome, or SSSS for short, which most commonly occurs in newborns or individuals with renal insufficiency.
As the name suggests, this skin infection is caused by Staphylococcus aureus, which produces an exfoliative exotoxin that destroys the adhesions between keratinocytes within the stratum granulosum; and that’s a high yield fact that can help you differentiate SSSS from Stevens-Johnson syndrome and toxic epidermal necrolysis, which are acute, severe hypersensitivity reactions in the skin characterized by destruction of the junction between the epidermis and dermis.

Staphylococcal scalded skin syndrome9:00–10:16

Now, SSSS is characterized by systemic symptoms like fever, along with a generalized painful erythematous rash, and sloughing of the superficial epidermal layers above the stratum granulosum.
For your exams, remember that in individuals with SSSS, there’s a positive Nikolsky sign, which means that manually stroking the skin causes sloughing and separation of the epidermis.
In addition, some individuals may develop fluid-filled blisters that rupture easily, leaving erosions, but because these lesions are superficial, they typically heal completely without leaving any scars.
And that’s a high yield fact!Switching gears to viral skin infections, these include molluscum contagiosum, which is a highly contagious infection caused by a poxvirus.
Although it is most commonly seen in children involving the face or limbs, keep in mind that it can also be sexually transmitted in adults, and affect the skin over the genital area.
In a test question, you should think of molluscum contagiosum if they describe a pink, domed-shaped, umbilicated papule, meaning that the papule has a depression in the center.

Molluscum contagiosum 10:16–10:47

Moving onto herpes, which is a highly contagious skin infection caused by the herpes simplex virus, or HSV. There are two types, HSV-1 and HSV-2.
As a rule of thumb, remember that HSV-1 tends to cause infections above the waist, typically affects the lips, and that’s called herpes labialis; while HSV-2 tends to cause infections below the waist, involving the genitals, and that’s herpes genitalis.
There’s a third form of herpes called herpetic whitlow, which appears on the fingers, and can be caused by both HSV-1 and -2.

Herpes 10:47–12:09

Now, regardless of the affected area, herpes typically presents as a localized eruption of painful vesicles or pustules, which tend to burst, ooze, ulcerate, and eventually dry out and crust over.
Primary infections tend to be most severe and can be accompanied by lymphadenopathy and flu-like symptoms. HSV also infects the nearby sensory neurons and travels up their axon to the neuron’s cell body, where it remains latent and is typically asymptomatic.
From time to time, the virus can reactivate and travel back down the axon to the skin or mucosal surfaces. As a result, infected individuals can develop these lesions over and over again throughout their lifetime, with classic triggers including stress, skin damage, and other viral illnesses.
Finally, there’s varicella, also known as chickenpox, and herpes zoster, also known as shingles, which is caused by the varicella zoster virus, or VZV for short.
Primary infection causes varicella, which is a highly contagious disease that most frequently occurs in children. Initially, there’s a prodrome of fever and malaise, followed by the development of an intensely pruritic, generalized maculopapular rash, which then evolves into a vesicular rash, where vesicles come up in groups or crops.
Within a few days, these vesicles begin to crust over and form scabs. Now, as some vesicles heal, new vesicles can pop up.

Varicella and herpes zoster 12:09–13:57

So for your exams, remember that individuals with varicella typically present multiple skin lesions that are in different stages of healing.
Finally, varicella tends to resolve in about one week, providing lifelong immunity. However, bear in mind that varicella zoster virus also infects sensory neurons in the skin, and travels up their axon to the trigeminal ganglion and the dorsal root ganglia, where it can remain dormant in a latent state for many years.
Later on, triggers like aging, stress, or immunosuppressive therapy can cause reactivation of the virus, which travels back down to the skin.
This causes an infection in the innervated skin area, or dermatome, that’s called herpes zoster or shingles. Typically, herpes zoster leads to a rash that looks like a single stripe of vesicles around either the left or right side of the body or on one side of the face, and presents with pain, itching, or tingling of the affected area.
An important fact to keep in mind though is that immunocompromised individuals may develop disseminated zoster, meaning that the lesions are not restricted to a single dermatome.All right, as a quick recap… Bacterial skin infections include impetigo, erysipelas, cellulitis, skin abscess, necrotizing fasciitis, and staphylococcal scalded skin syndrome.
Impetigo is an infection of the superficial layers of the epidermis, most often caused by Staphylococcus aureus or Streptococcus pyogenes.
It usually presents as vesicles or pustules with honey-colored or golden crusting. If left untreated, it can lead to post-streptococcal glomerulonephritis.
Next, erysipelas is an infection that involves the upper dermis and superficial cutaneous lymphatics, caused by Streptococcus pyogenes, and typically presents as a well-demarcated, red, and tender lesion.
On the other hand, cellulitis is an infection of the deeper dermis and subcutaneous tissues, usually caused by Staphylococcus aureus or Streptococcus pyogenes, that presents as a poorly demarcated, red, and tender lesion, and typically starts from a break in the skin.

Review 13:57–16:50

Skin abscesses are walled-off pus collections within the deeper skin layers, typically caused by Staphylococcus aureus, even MRSA, and present as a red, tender nodule.
Necrotizing fasciitis is a severe, life-threatening infection of the deeper tissues that destroys the subcutaneous fat and muscle fascia.
It is most often caused by Staphylococcus aureus, Streptococcus pyogenes, and anaerobic bacteria, and presents with severe pain, as well as red or violet-colored patches that progress rapidly into bullae, ulcers, and gangrene; and a telltale sign is crepitus.
Finally, Staphylococcal scalded skin syndrome is caused by Staphylococcus aureus, which produces an exfoliative exotoxin that destroys the adhesions between keratinocytes in the stratum granulosum; this results in a painful erythematous rash with sloughing, and positive Nikolsky sign.
Switching gears, viral skin infections include molluscum contagiosum, herpes, and varicella and herpes zoster. Molluscum contagiosum is caused by a poxvirus, and has a classical presentation of pink, domed-shaped, umbilicated papules.
Next, herpes is caused by the herpes simplex virus or HSV, and there are two types; HSV-1 typically causes herpes labialis, while HSV-2 tends to cause herpes genitalis.
Lesions typically present as a localized eruption of painful vesicles or pustules that eventually dry out. Finally, varicella and herpes zoster are caused by the varicella zoster virus.
Primary infection causes varicella or chickenpox, with a prodrome of fever, followed by an intensely pruritic maculopapular and vesicular rash.
Reactivation of the virus can cause herpes zoster or shingles, which typically causes a painful vesicular rash in the affected dermatome.Going back to our cases, Quentin is the 10-year-old who was brought in due to dark-colored urine, and urinalysis showed hematuria, RBC casts, and proteinuria.
This, combined with his hypertension and edema, is a classic presentation of glomerulonephritis. But that’s not all there is!
A very important clue here is Quentin’s recent history of honey-colored crusted vesicles around his nose and mouth, which should make you think of impetigo, leading to the final diagnosis of post-streptococcal glomerulonephritis.
Next, Claudio is the 70-year-old who presented with severe pain and swelling in his genital area. He also had symptoms of systemic toxicity, including lethargy, high fever, and hypotension, which is suggestive of a severe infection.
Now, the recent history of surgery in the affected area, combined with a diagnosis of long-standing and poorly controlled diabetes mellitus, should make you think of necrotizing fasciitis, but a very important clue you shouldn’t miss is the presence of crepitus.
A swab culture, which reveals the presence of anaerobic bacteria and Streptococcus pyogenes, confirms the diagnosis of necrotizing fasciitis.

Summary 16:50–17:58

analysis, showed hematuria RBC casts and proteinuria. This combined with his hypertension and edema is a classic presentation of glomerulonephritis, but that's not all.
There is a very important clue. Here is quintin's recent history of Honey colored crested, vesicles around his nose and mouth, which would make you think of impetigo leading to the final diagnosis of post streptococcal glomerulonephritis.
Next Claudia was the 70 year old who presented with severe pain and swelling in his genital area. He also had symptoms of systemic toxicity, including lethargy high fever and hypotension, which is suggestive of a severe infection.
Now, the recent history of surgery in the affected area combined, with a diagnosis of long-standing and poorly controlled, diabetes mellitus should make you think of necrotizing fasciitis, but a very important clue.
You shouldn't. Miss is the presence of crepitus.
A swab culture which revealed the presence of anaerobic bacteria and streptococcus pyogenes confirms the diagnosis of necrotizing fasciitis.
Bacterial and viral skin infections: Video | Osmosis