STRUCTURE AND FUNCTION OF THE SKIN

Anatomy of the Skin

The Epidermis

The Dermis

The Subcutaneous Tissue

11

Blood Supply of the Skin

11

Lymphatics of the Skin

12

Enervation of the skin

17

PHYSIOLOGY OF THE SKIN

18

ERYSIPELAS

20

Pathophysiology

23

Structure and Function of the Skin

Anatomy of the Skin

The skin is an ever-changing organ that contains many specialized cells
and structures. The skin had lots of function and in order to understand how it
functions we should start with the 3 layers of the skin- the epidermis, dermis and
the subcutaneous tissue.

Structure of skin (5)

The Epidermis
The epidermis is the outer layer of skin and it is derived from the
embryonic ectoderm. The thickness of the epidermis varies in different types of
skin. It is the thinnest on the eyelids at 0.5 mm and the thickest on the palms and
soles at 1.5 mm.

The epidermis consists of stratified epithelium which is

arranged in four layers from within outward as follows:

(a) Stratum mucosum,
(b) Stratum granulosum,
(c) Stratum lucidum, and
(d) Stratum corneum.

The Stratum Mucosum

The stratum mucosum (mucous layer) is composed of several layers of

cells; those of the deepest layer are columnar in shape and placed
2

perpendicularly on the surface of the basement membrane, to which they are

attached by toothed extremities; this deepest layer is sometimes termed the
stratum germinativum; the succeeding strata consist of cells of a more rounded
or polyhedral form, the contents of which are soft, opaque, granular, and soluble
in acetic acid. These are known as prickle cells because of the bridges by which
they are connected to one another. They contain fine fibrils which are continuous
across the connecting processes with corresponding fibrils in adjacent cells.
Between the bridges are fine inter-cellular clefts serving for the passage of
lymph, and in these lymph corpuscles or pigment granules may be found.

The Stratum Granulosum

The stratum granulosum comprises two or three layers of flattened cells

which contain granules of eleidin, a substance readily stained by hematoxylin or
carmine, and probably an intermediate substance in the formation of keratin.
They are supposed to be cells in a transitional stage between the protoplasmic
cells of the stratum mucosum and the horny cells of the superficial layers.

The Stratum Lucidum

The stratum lucidum appears in section as a homogeneous or dimly

striated membrane, composed of closely packed cells in which traces of flattened
nuclei may be found, and in which minute granules of a substance named
keratohyalin are present.

The Stratum Corneum

The stratum corneum (horny layer) consists of several layers of horny

epithelial scales in which no nuclei are discernible, and which are unaffected by
acetic acid, the protoplasm having become changed into horny material or
keratin. According to Ranvier they contain granules of a material which has the
characteristics of beeswax.
The black color of the skin in the Negro, and the tawny color among
some of the white races, is due to the presence of pigment in the cells of the
epidermis. This pigment is more especially distinct in the cells of the stratum

mucosum, and is similar to that found in the cells of the pigmentary layer of the
retina. As the cells approach the surface and desiccate, the color becomes

partially lost; the disappearance of the pigment from the superficial layers of the
epidermis is, however, difficult to explain.
The pigment (melanin) consists of dark brown or black granules of very
small size, closely packed together within the cells, but not involving the nucleus.
The main purpose served by the epidermis is that of protection, as the
surface is worn away new cells are supplied and thus the true skin, the vessels
and nerves which it contains are defended from damageThe skin is an everchanging organ that contains many specialized cells and structures. The skin had
lots of function and in order to understand how it functions we should start with
the 3 layers of the skin- the epidermis, dermis and the subcutaneous tissue.
The epidermis is the outer layer of skin and it is derived from the
embryonic ectoderm. The thickness of the epidermis varies in different types of
skin. It is the thinnest on the eyelids at 0.5 mm and the thickest on the palms and
soles at 1.5 mm.

The epidermis consists of stratified epithelium which is

arranged in four layers from within outward as follows:

(a) Stratum mucosum,
(b) Stratum granulosum,
(c) Stratum lucidum, and
(d) Stratum corneum.
The stratum mucosum (mucous layer) is composed of several layers of
cells; those of the deepest layer are columnar in shape and placed
perpendicularly on the surface of the basement membrane, to which they are
attached by toothed extremities; this deepest layer is sometimes termed the

stratum germinativum; the succeeding strata consist of cells of a more rounded

or polyhedral form, the contents of which are soft, opaque, granular, and soluble
in acetic acid. These are known as prickle cells because of the bridges by which
they are connected to one another. They contain fine fibrils which are continuous
across the connecting processes with corresponding fibrils in adjacent cells.
Between the bridges are fine inter-cellular clefts serving for the passage of
lymph, and in these lymph corpuscles or pigment granules may be found.
The stratum granulosum comprises two or three layers of flattened cells
which contain granules of eleidin, a substance readily stained by hematoxylin or
carmine, and probably an intermediate substance in the formation of keratin.
They are supposed to be cells in a transitional stage between the protoplasmic
cells of the stratum mucosum and the horny cells of the superficial layers.
The stratum lucidum appears in section as a homogeneous or dimly
striated membrane, composed of closely packed cells in which traces of flattened
nuclei may be found, and in which minute granules of a substance named
keratohyalin are present.
The stratum corneum (horny layer) consists of several layers of horny
epithelial scales in which no nuclei are discernible, and which are unaffected by
acetic acid, the protoplasm having become changed into horny material or
keratin.
According to Ranvier they contain granules of a material which has the
characteristics of beeswax.
The black color of the skin in the Negro, and the tawny color among
some of the white races, is due to the presence of pigment in the cells of the

epidermis. This pigment is more especially distinct in the cells of the stratum
mucosum, and is similar to that found in the cells of the pigmentary layer of the
retina. As the cells approach the surface and desiccate, the color becomes
partially lost; the disappearance of the pigment from the superficial layers of the
epidermis is, however, difficult to explain.
The pigment (melanin) consists of dark brown or black granules of very
small size, closely packed together within the cells, but not involving the nucleus.
The main purpose served by the epidermis is that of protection, as the
surface is worn away new cells are supplied and thus the true skin, the vessels
and nerves which it contains are defended.

The Dermis
The dermis also varies in thickness depending on the location of the skin.
It is 0.3 mm on the eyelid and 3.0 mm on the back. The dermis is composed of
three types of tissue that are present throughout - not in layers. The types of
tissue are collagen, elastic tissue, and reticular fibers.
It consists of felted connective tissue, with a varying amount of elastic
fibers and numerous bloodvessels, lymphatics, and nerves. The connective
tissue is arranged in two layers: a deeper or reticular, and a superficial or
papillary. Unstriped muscular fibers are found in the superficial layers of the
corium, wherever hairs are present, and in the subcutaneous areolar tissue of the
scrotum, penis, labia majora, and nipples. In the nipples the fibers are disposed
in bands, closely reticulated and arranged in superimposed laminae.

The Stratum reticulare

The reticular layer (stratum reticulare; deep layer) consists of strong

interlacing bands, composed chiefly of white fibrous tissue, but containing some
fibers of yellow elastic tissue, which vary in number in different parts; and
connective-tissue corpuscles, which are often to be found flattened against the
white fibrous tissue bundles. Toward the attached surface the fasciculi are large
and coarse, and the areol left by their interlacement are large, and occupied by
adipose tissue and sweat glands. Below the reticular layer is the subcutaneous
areolar tissue, which, except in a few situations, contains fat.

10

13

The Stratum Papillare

The papillary layer (stratum papillare; superficial layer; corpus papillare of

the corium) consists of numerous small, highly sensitive, and vascular
eminences, the papill, which rise perpendicularly from its surface. The papill
are minute conical eminences, having rounded or blunted extremities,
occasionally divided into two or more parts, and are received into corresponding
pits on the under surface of the cuticle.
On the general surface of the body, more especially in parts endowed with
slight sensibility, they are few in number, and exceedingly minute; but in some
situations, as upon the palmar surfaces of the hands and fingers, and upon the
plantar surfaces of the feet and toes, they are long, of large size, closely
aggregated together, and arranged in parallel curved lines, forming the elevated
ridges seen on the free surface of the epidermis.
Each ridge contains two rows of papill, between which the ducts of the
sudoriferous glands pass outward to open on the summit of the ridge.
Each papilla consists of very small and closely interlacing bundles of finely
fibrillated tissue, with a few elastic fibers; within this tissue is a capillary loop, and
in some papill, especially in the palms of the hands and the fingers, there are
tactile corpuscles.

11

The Subcutaneous Tissue

The subcutaneous tissue is a layer of fat and connective tissue that
houses larger blood vessels and nerves. This layer is important is the regulation
of temperature of the skin itself and the body. The size of this layer varies
throughout the body and from person to person.

Blood Supply of the Skin

Cutaneous vessels ultimately arise from underlying named source

vessels. Each source vessel supplies a 3-dimensional vascular territory from
bone to skin termed an angiosome. Adjacent angiosomes have vascular

12

connections via reduced caliber (choke) vessels or similar caliber (true)

anastomotic vessels. The cutaneous vessels originate either directly from the
source arteries (septocutaneous or fasciocutaneous perforators) or as terminal
branches of muscular vessels (musculocutaneous perforators).
During their course to the skin, they travel within or adjacent to the
connective tissue framework and supply branches to each tissue with which they
come into close contact (bone, muscle, fascia,nerve, fat). They emerge from the
deep fascia in the vicinity of the intermuscular or intramuscular septa or near
tendons and travel toward the skin, where they form extensive subdermal and
dermal plexuses. The dermis contains horizontally arranged superficial and deep
plexuses, which are interconnected via communicating vessels oriented
perpendicular to the skin surface. Cutaneous vessels ultimately anastomose with
other cutaneous vessels to form a continuous vascular network within the skin.
Clinically, this extensive horizontal network of vessels allows for random skin flap
survival.
In addition to the skin's natural heat conductivity and loss of heat from the
evaporation of sweat, convection from cutaneous vessels is a vital component of
thermoregulation. Cutaneous blood flow is 10-20 times that required for essential
oxygenation and metabolism, and large amounts of heat can be exchanged
through the regulation of cutaneous blood flow. The thermoregulatory center in
the hypothalamus controls vasoconstriction and vasodilatation of cutaneous
vessels through the sympathetic nervous system

Lymphatics of the Skin

Skin lymphatics parallel the blood supply and function to conserve plasma
proteins and scavenge foreign material, antigenic substances, and bacteria.

13

Blind-ended lymphatic capillaries arise within According to Ranvier they contain

granules of a material which has the characteristics of beeswax.
The black color of the skin in the Negro, and the tawny color among
some of the white races, is due to the presence of pigment in the cells of the
epidermis. This pigment is more especially distinct in the cells of the stratum
mucosum, and is similar to that found in the cells of the pigmentary layer of the
retina. As the cells approach the surface and desiccate, the color becomes
partially lost; the disappearance of the pigment from the superficial layers of the
epidermis is, however, difficult to explain.
The pigment (melanin) consists of dark brown or black granules of very
small size, closely packed together within the cells, but not involving the nucleus.
The main purpose served by the epidermis is that of protection, as the
surface is worn away new cells are supplied and thus the true skin, the vessels
and nerves which it contains are defended from damageThe skin is an everchanging organ that contains many specialized cells and structures. The skin had
lots of function and in order to understand how it functions we should start with
the 3 layers of the skin- the epidermis, dermis and the subcutaneous tissue.
The epidermis is the outer layer of skin and it is derived from the
embryonic ectoderm. The thickness of the epidermis varies in different types of
skin. It is the thinnest on the eyelids at 0.5 mm and the thickest on the palms and
soles at 1.5 mm.

The epidermis consists of stratified epithelium which is

arranged in four layers from within outward as follows:

(a) Stratum mucosum,
(b) Stratum granulosum,
(c) Stratum lucidum, and
(d) Stratum corneum.
The stratum mucosum (mucous layer) is composed of several layers of
cells; those of the deepest layer are columnar in shape and placed

14

perpendicularly on the surface of the basement membrane, to which they are

attached by toothed extremities; this deepest layer is sometimes termed the
stratum germinativum; the succeeding strata consist of cells of a more rounded
or polyhedral form, the contents of which are soft, opaque, granular, and soluble
in acetic acid. These are known as prickle cells because of the bridges by which
they are connected to one another. They contain fine fibrils which are continuous
across the connecting processes with corresponding fibrils in adjacent cells.
Between the bridges are fine inter-cellular clefts serving for the passage of
lymph, and in these lymph corpuscles or pigment granules may be found.
The stratum granulosum comprises two or three layers of flattened cells
which contain granules of eleidin, a substance readily stained by hematoxylin or
carmine, and probably an intermediate substance in the formation of keratin.
They are supposed to be cells in a transitional stage between the protoplasmic
cells of the stratum mucosum and the horny cells of the superficial layers.
The stratum lucidum appears in section as a homogeneous or dimly
striated membrane, composed of closely packed cells in which traces of flattened
nuclei may be found, and in which minute granules of a substance named
keratohyalin are present.
The stratum corneum (horny layer) consists of several layers of horny
epithelial scales in which no nuclei are discernible, and which are unaffected by
acetic acid, the protoplasm having become changed into horny material or
keratin.
According to Ranvier they contain granules of a material which has the
characteristics of beeswax.
The black color of the skin in the Negro, and the tawny color among
some of the white races, is due to the presence of pigment in the cells of the
epidermis. This pigment is more especially distinct in the cells of the stratum
mucosum, and is similar to that found in the cells of the pigmentary layer of the
retina. As the cells approach the surface and desiccate, the color becomes

15

partially lost; the disappearance of the pigment from the superficial layers of the
epidermis is, however, difficult to explain.
The pigment (melanin) consists of dark brown or black granules of very
small size, closely packed together within the cells, but not involving the nucleus.
The main purpose served by the epidermis is that of protection, as the
surface is worn away new cells are supplied and thus the true skin, the vessels
and nerves which it contains are defended
The dermis also varies in thickness depending on the location of the skin.
It is 0.3 mm on the eyelid and 3.0 mm on the back. The dermis is composed of
three types of tissue that are present throughout - not in layers. The types of
tissue are collagen, elastic tissue, and reticular fibers.
It consists of felted connective tissue, with a varying amount of elastic
fibers and numerous bloodvessels, lymphatics, and nerves. The connective
tissue is arranged in two layers: a deeper or reticular, and a superficial or
papillary. Unstriped muscular fibers are found in the superficial layers of the
corium, wherever hairs are present, and in the subcutaneous areolar tissue of the
scrotum, penis, labia majora, and nipples. In the nipples the fibers are disposed
in bands, closely reticulated and arranged in superimposed laminae.
The reticular layer (stratum reticulare; deep layer) consists of strong
interlacing bands, composed chiefly of white fibrous tissue, but containing some
fibers of yellow elastic tissue, which vary in number in different parts; and
connective-tissue corpuscles, which are often to be found flattened against the
white fibrous tissue bundles. Toward the attached surface the fasciculi are large
and coarse, and the areol left by their interlacement are large, and occupied by
adipose tissue and sweat glands. Below the reticular layer is the subcutaneous
areolar tissue, which, except in a few situations, contains fat.

16

13

The papillary layer (stratum papillare; superficial layer; corpus papillare of

the corium) consists of numerous small, highly sensitive, and vascular
eminences, the papill, which rise perpendicularly from its surface. The papill
are minute conical eminences, having rounded or blunted extremities,
occasionally divided into two or more parts, and are received into corresponding
pits on the under surface of the cuticle.
On the general surface of the body, more especially in parts endowed
with slight sensibility, they are few in number, and exceedingly minute; but in
some situations, as upon the palmar surfaces of the hands and fingers, and upon
the plantar surfaces of the feet and toes, they are long, of large size, closely
aggregated together, and arranged in parallel curved lines, forming
the elevated ridges seen on the free surface of the epidermis. Each ridge
contains two rows of papill, between which the ducts of the sudoriferous glands
pass outward to open on the summit of the ridge. Each papilla consists of very
small and closely interlacing bundles of finely fibrillated tissue, with a few elastic
fibers; within this tissue is a capillary loop, and in some papill, especially in the
palms of the hands and the fingers, there are tactile corpuscles.
The subcutaneous tissue is a layer of fat and connective tissue that
houses larger blood vessels and nerves. This layer is important is the regulation
of temperature of the skin itself and the body. The size of this layer varies
throughout the body and from person to person
Cutaneous vessels ultimately arise from underlying named source
vessels. Each source vessel supplies a 3-dimensional vascular territory from
bone to skin termed an angiosome. Adjacent angiosomes have vascular
connections via reduced caliber (choke) vessels or similar caliber (true)
anastomotic vessels. The cutaneous vessels originate either directly from the
source arteries (septocutaneous or fasciocutaneous perforators) or as terminal
branches of muscular vessels (musculocutaneous perforators).
During their course to the skin, they travel within or adjacent to the
connective tissue framework and supply branches to each tissue with which they

17

come into close contact (bone, muscle, fascia,nerve, fat). They emerge from the
deep fascia in the vicinity of the intermuscular or intramuscular septa or near
tendons and travel toward the skin, where they form extensive subdermal and
dermal plexuses. The dermis contains horizontally arranged superficial and deep
plexuses, which are interconnected via communicating vessels oriented
perpendicular to the skin surface. Cutaneous vessels ultimately anastomose with
other cutaneous vessels to form a continuous vascular network within the skin.
Clinically, this extensive horizontal network of vessels allows for random skin flap
survival.
In addition to the skin's natural heat conductivity and loss of heat from the
evaporation of sweat, convection from cutaneous vessels is a vital component of
thermoregulation. Cutaneous blood flow is 10-20 times that required for essential
oxygenation and metabolism, and large amounts of heat can be exchanged
through the regulation of cutaneous blood flow. The thermoregulatory center in
the hypothalamus controls vasoconstriction and vasodilatation of cutaneous
vessels through the sympathetic nervous system
Skin lymphatics parallel the blood supply and function to conserve plasma
the interstitial spaces of the dermal papillae. These unvalved superficial
dermal vessels drain into valved deep dermal and subdermal plexuses. These
then coalesce to form larger lymphatic channels, which course through numerous
filtering lymph nodes on their way to join the venous circulation near the
subclavian vein-internal jugular vein junction bilaterally.

Enervation of the skin

Sensory perception is critically important in the avoidance of pressure,

mechanical or traumatic forces, and extremes of temperature. Numerous

18

specialized structures are present in the skin to detect various stimuli. As

previously mentioned, Merkel cells of the epidermis detect light touch. Meissner
corpuscles also detect light touch. These are found in the dermal papillae and
are most concentrated in the fingertips. Pacini corpuscles are found deep within
the dermis or even in the subcutaneous tissue. These structures are specialized
to detect pressure.
Pain is transmitted through naked nerve endings located in the basal layer
of the epidermis. Krause bulbs detect cold, whereas Raffini corpuscles detect
heat. Heat, cold, and proprioception also are located in the superficial dermis.
Cutaneous nerves follow the route of blood vessels to the skin. The area
supplied by a single spinal nerve, or single segment of the spinal cord, is termed
a dermatome. Adjacent dermatomes may overlap considerably, of importance to
note when performing field blocks with local anesthesia.

Structure of the skin ( 5)

Physiology of the skin

Skin serves several functions, which are introduced here.

19

1. Regulation of body temperature.

In response to high environmental temperature or strenuous exercise, the
evaporation of sweat from the skin surface helps lower an elevated body
temperature to normal. In response to low environmental temperature, production
of sweat is decreased, which helps conserve heat. Changes in the flow of blood
to the skin also help regulate body temperature.
2. Protection.
The skin covers the body and provides a physical barrier that protects underlying
tissues from physical abrasion, bacterial invasion, dehydration, and ultraviolet
(UV) radiation. Hair and nails also have protective functions.
3. Sensation.
The skin contains abundant nerve endings and receptors that detect stimuli
related to temperature, touch, pressure, and pain.
4. Excretion.
Besides removing heat and some water from the body, sweat also is the vehicle
for excretion of a small amount of salts and several organic compounds.
5. Immunity.
Certain cells of the epidermis are important components of the immune system,
which fends off foreign invaders.
6. Blood reservoir.

20

The dermis of the skin houses extensive networks of blood vessels that carry 8 to
10% of the total blood flow in a resting adult. In moderate exercise, skin blood
flow may increase, which helps dissipate heat from the body. During hard
exercise, however, skin blood vessels constrict (narrow) somewhat, and more
blood is able to circulate to contracting muscles.

7. Synthesis of Vitamin D.
Vitamin D is a group of closely related compounds.

Synthesis of vitamin D

begins with activation of a precursor molecule in the skin by ultraviolet (UV) rays
in sunlight. Enzymes in the liver and kidneys then modify the molecule, finally
producing calcitriol, the most active form of vitamin D. Calcitriol contributes to the
homeostasis of body fluids by aiding absorption of calcium in foods. According to
the synthesis sequence just described, vitamin D is a hormone, since it is
produced in one location in the body, transported by the blood, and then exerts
its effect in another location. In this respect, the skin may be considered an
endocrine organ.

21

Chapter

2.

ERYSIPELAS

GENERAL

INFORMATION
1. History
Erysipelas has three patron saints - Anthony the Abbott, Benedict and Ida
of Nivelles - who date back to the early days of Christianity, indicating that this
condition has afflicted mankind since antiquity. It was originally known (as was
ergotism) as St Anthony's Fire, the said saint having a reputation for reducing the
inflammation and itching of skin diseases. According to Steven Lehrer's book
'Explorers of the Body', the term erysipelas was originally coined by the Ancient
Greeks from the redness which developed around an infected wound. It is worth
reading the chapter that mentions this, available online, for the chilling account of
the lightning-fast surgeon Robert Liston, who, in a moment of regrettable over-

22

exuberance during a leg amputation, accidentally removed one of his patient's

testicles and two of his assistant's fingers.
Awareness of erysipelas rose sharply in the mid-19th century, when it was
recognised that the disease could be caused by smallpox vaccination. A report at
the time used the Registrar-General's figures to demonstrate that from 1859 to
1880 almost 400 people died from erysipelas following vaccination, and that the
annual death rate from this cause had increased almost eight-fold over the
period.

2. Definition
Erysipelas is an infectious disease, characterized by an acute and specific
inflammation of the skin and subcutaneous tissues, attended by a shining
redness, which spreads rapidly; marked swelling and pain, and which finally
terminates in desquamation. A fever of variable intensity, moderate prostration,
and supposed to be caused by the streptococcus erysipelatis.
The toxic effect of the streptococci cause a vasodilation and the red blood
cells can easily get to the affected region causing the erythema ( redness) .All
the signs of inflammation ( Rubor- redness, Dolor- pain, Calor- warmth) are
present. The inflammation also causes movement fluids in the different
compartments of the organism hence causing swelling or oedema. Initially, the
fluid is less in protein content ( transudate) but eventually it turns into transudate
due to the effect of polymorphonuclear cells, macrophages and fibrinogen.

23

Erysipelas is caused by Beta Hemolytic Streptococci after an incubation

period of minimum three days. Usually it is caused by Group A Beta hemolytic
Streptococci or Streptococcus Pyogenes. Rarely, it is due to Streptococci of
Group C and G.
Erysipelas is more common in elderly and immunocompromised patients.
In the new born it is caused by Group B Streptococci.

3. Etiopathogenesis

In 1991, Iushchuuk and his colleagues made a study on a group of 517

patients who were presenting with symptoms of Erysipelas. They found that there
is genetic predisposition to Erysipelas and its different forms.
This is polygenic and is associated with the antigens HLA-A2, B5, B12,
B12 and BW35. On the other hand, Histocompatibility complex HLA-A10, AW12,
B7 and B8 have a protective role.

Etiology
Streptococcus pyogenes (Group A streptococcus) is a Gram-positive,
non-motile, non-spore-forming cocci that occurs in chains or in pairs of cells.

24

Individual cells are round-to-ovoid cocci, 0.6-1.0 micrometer in diameter (Figure

1). Streptococci divide in one plane and thus occur in pairs or (especially in liquid
media or clinical material) in chains of varying lengths.
The metabolism of S. pyogenes is fermentative; the organism is a
catalase-negative aerotolerant anaerobe (facultative anaerobe), and requires
enriched medium containing blood in order to grow. Group A streptococci
typically have a capsule composed of hyaluronic acid and exhibit beta (clear)
hemolysis on blood agar.

Figure 1. Streptococcus pyogenes. Left. Gram stain of Streptococcus pyogenes in a

clinical specimen. Right. Colonies of Streptococcus pyogenes on blood agar
exhibiting beta (clear) hemolysis

Classification of Streptococci
The type of hemolytic reaction displayed on blood agar has long been
used to classify the streptococci.

Beta -hemolysis is associated with complete lysis of red cells

surrounding the colony, whereas

25

alpha-hemolysis is a partial or "green" hemolysis associated with

reduction of red cell hemoglobin.

Nonhemolytic colonies have been termed gamma-hemolytic.

Hemolysis is affected by the species and age of red cells, as well
as by other properties of the base medium.

Group A streptococci are nearly always beta-hemolytic

Group B can manifest alpha, beta or gamma hemolysis.

Most strains of S. pneumoniae are alpha-hemolytic but can cause hemolysis during anaerobic incubation. Most of the oral streptococci and
enterococci are non hemolytic. The property of hemolysis is not very reliable for
the absolute identification of streptococci, but it is widely used in rapid screens
for identification of S. pyogenes and S. pneumoniae

Antigenic types
The cell surface structure of Group A streptococci is among the most
studied of any bacteria (Figure 2). The cell wall is composed of repeating units of
N-acetylglucosamine and N-acetylmuramic acid, the standard peptidoglycan.
Historically , the definitive identification of streptococci has rested on the
serologic reactivity of "cell wall" polysaccharide antigens as originally described
by Rebecca Lancefield. Eighteen group-specific antigens (Lancefield
groups) were established. The Group A polysaccharide is a polymer of Nacetylglucosamine and rhamnose. Some group antigens are shared by more
than one species. This polysaccharide is also called the C substance or group
carbohydrate antigen.
Pathogenesis
Streptococcus pyogenes is one of the most frequent pathogens of
humans. It is estimated that between 5-15% of normal individuals harbor the

26

bacterium, usually in the respiratory tract, without signs of disease. As normal

flora, S. pyogenes can infect when defenses are compromised or when the
organisms are able to penetrate the constitutive defenses. When the bacteria are
introduced or transmitted to vulnerable tissues, a variety of types of suppurative
infections can occur.
Streptococcus pyogenes owes its major success as a pathogen to its
ability to colonize and rapidly multiply and spread in its host while evading
phagocytosis and confusing the immune system
S. pyogenes is the leading cause of uncomplicated bacterial pharyngitis
and tonsillitis commonly referred to a strep throat. Other respiratory infections
include sinusitis and pneumonia. Infections of the skin can be superficial
(impetigo) or deep (cellulitis). Invasive streptococci cause joint or bone
infections, destructive wound infections (necrotizing fasciitis) and myositis,
meningitis and endocarditis. Two post streptococcal sequelae, rheumatic
fever and glomerulonephritis, may follow streptococcal disease, and occur in
1-3% of untreated infections. These conditions and their pathology are not
attributable to dissemination of bacteria, but to aberrant immunological reactions
to Group A streptococcal antigens. Scarlet fever and streptococcal toxic
shock syndrome are systemic responses to circulating bacterial toxins.

27

Figure 2. Cell surface structure of Streptococcus pyogenes and

secreted products involved in virulence

The cell surface of Streptococcus pyogenes accounts for many of the

bacterium's

determinants

of

virulence,especially

those

concerned

with

colonization and evasion of phagocytosis and the host immune responses. The
surface of Streptococcus pyogenes is incredibly complex and chemically-diverse.
Antigenic component s include capsular polysaccharide (C-substance),
cell wall peptidoglycan and lipoteichoic acid (LTA), and a variety of surface
proteins, including M protein, fimbrial proteins, fibronectin-binding proteins,
(e.g. Protein F) and cell-bound streptokinase
The cytoplasmic membrane of S. pyogenes contains some antigens
similar to those of human cardiac, skeletal, and smooth muscle, heart valve
fibroblasts, and neuronal tissues, resulting in molecular mimicry and a tolerant
or suppressed immune response by the host.

28

In Group A streptococci, the R and T proteins are used as epidemiologic

markers and have no known role in virulence. The group carbohydrate antigen
(composed of N-acetylglucosamine and rhamnose) has been thought to have no
role in virulence, but emerging strains with increased invasive capacity produce a
very mucoid colony, suggesting a role of the capsule in virulence.
The M proteins are clearly virulence factors associated with both
colonization and resistance to phagocytosis. More than 50 types of S. pyogenes
M proteins have been identified on the basis of antigenic specificity, and it is the
M protein that is the major cause of antigenic shift and antigenic drift in the Group
A streptococci. The M protein (found in fimbriae) also binds fibrinogen from
serum and blocks the binding of complement to the underlying peptidoglycan.
This allows survival of the organism by inhibiting phagocytosis.
The

streptococcal

protein,

as

well

as

peptidoglycan,

N-

acetylglucosamine, and group-specific carbohydrate, contain antigenic epitopes

that mimic those of mammalian muscle and connective tissue. As mentioned
above, the cell surface of recently emerging strains of streptococci is distinctly
mucoid (indicating that they are highly encapsulated). These strains are also rich
in surface M protein. The M proteins of certain M-types are considered
rheumatogenic since they contain antigenic epitopes related to heart muscle,
and they therefore may lead to autoimmune rheumatic carditis (rheumatic fever)
following an acute infection.
The capsule of S. pyogenes is non antigenic since it is composed of
hyaluronic acid, which is chemically similar to that of host connective tissue.
This allows the bacterium to hide its own antigens and to go unrecognized as
antigenic by its host. The Hyaluronic acid capsule also prevents opsonized
phagocytosis by neutrophils or mancrophages
Colonization of tissues by S. pyogenes is thought to result from a failure in
the constitutive defenses (normal flora and other nonspecific defense

29

mechanisms) which allows establishment of the bacterium at a portal of entry

(often the upper respiratory tract or the skin) where the organism multiplies and
causes an inflammatory purulent lesion.
It is now realized that S. pyogenes (like many other bacterial pathogens)
produces multiple adhesins with varied specificities. There is evidence that
Streptococcus pyogenes utilizes lipoteichoic acids (LTA), M protein, and
multiple fibronectin-binding proteins in its repertoire of adhesins. LTA is
anchored to proteins on the bacterial surface, including the M protein. Both the M
proteins and lipoteichoic acid are supported externally to the cell wall on fimbriae
and appear to mediate bacterial adherence to host epithelial cells.

The

fibronectin-binding protein,
Protein F , has also been shown to mediate streptococcal adherence to
the amino terminus of fibronectin on mucosal surfaces.
Identification of Streptococcus pyogenes adhesins has long been a
subject of conflict and debate. Most of the debate was between proponents of the
LTA model and those of the M protein model. In 1972, Gibbons and his
colleagues proposed that attachment of streptococci to the oral mucosa of mice
is dependent on M protein.
However, Olfek and Beachey argued that lipoteichoic acid (LTA), rather
than M protein, was responsible for streptococcal adherence to buccal epithelial
cells. In 1996, Hasty and Courtney proposed a two-step model of attachment that
involved both M protein and teichoic acids. They suggested that LTA loosely
tethers streptococci to epithelial cells, and then M protein and/or other fibronectin
(Fn)-binding proteins secure a firmer, irreversible association. The first
streptococcal fibronectin-binding protein (Sfb) was demonstrated in 1992. Shortly
thereafter, protein F was discovered. Most recently (1998), the M1 and M3
proteins were shown to bind fibronectin.

30

Streptococcal invasins and protein toxins interact with mammalian blood

and tissue components in ways that kill host cells and provoke a damaging
inflammatory response. The soluble extracellular growth products and toxins of
Streptococcus pyogenes (see Figure 2, above), have been studied intensely.

Streptolysin S is an oxygen-stable leukocidin;

Streptolysin O is an oxygen-labile leukocidin.

NADase is also leukotoxic.

Hyaluronidase (the original "spreading factor") can digest host

connective tissue hyaluronic acid, as well as the organism's own
capsule.

Streptokinases participate in fibrin lysis.

Streptodornases A-D possess deoxyribonuclease activity;

Streptodornases B and D possess ribonuclease activity as well.

Protease activity similar to that in Staphylococcus aureus has been

shown in strains causing soft tissue necrosis or toxic shock
syndrome.

This large repertoire of products is important in the pathogenesis of S.

pyogenes infections. Even so, antibodies to these products are relatively
insignificant in protection of the host.
The streptococcal invasins act in a variety of ways summarized in Table 1
at the end of this article. Streptococcal invasins lyse eukaryotic cells, including
red blood cells and phagocytes; they lyse other host macromolecules, including
enzymes and informational molecules; they allow the bacteria to spread among
tissues by dissolving host fibrin and intercellular ground substances

31

Three streptococcal pyrogenic exotoxins (SPE), formerly known as

Erythrogenic toxin, are recognized: types A, B, C. These toxins act as
superantigens by a mechanism similar to those described for staphylococci.
As antigens, they do not requiring processing by antigen presenting cells.
Rather, they stimulate T cells by binding class II MHC molecules directly and
nonspecifically. With superantigens about 20% of T cells may be stimulated (vs
1/10,000 T cells stimulated by conventional antigens) resulting in massive
detrimental cytokine release. SPE A and SPE C are encoded by lysogenic
phages; the gene for SPE B is located on the bacterial chromosome.
The erythrogenic toxin is so-named for its association with scarlet fever
which occurs when the toxin is disseminated in the blood. Re-emergence in the
late 1980's of exotoxin-producing strains of S. pyogenes has been associated
with a toxic shock-like syndrome similar in pathogenesis and manifestation to
staphylococcal toxic shock syndrome, and with other forms of invasive disease
associated with severe tissue destruction. The latter condition is termed
necrotizing fasciitis. Outbreaks of sepsis, toxic shock and necrotizing fasciitis
have been reported at increasing frequency.
The destructive nature of wound infections prompted the popular press to
refer to S. pyogenes as "flesh-eating bacteria" and "ski-eating streptococci". The
increase in invasive streptococcal disease was associated with emergence of a
highly virulent serotype M1 which is disseminated world-wide. The M1 strain
produces the erythrogenic toxin (Spe A), thought to be responsible for toxic
shock, and the enzyme cysteine protease which is involved in tissue destruction.
Because clusters of toxic shock were also associated with other serotypes,
particularly M3 strains, it is believed that unidentified host factors may also have
played an important role in the resurgence of these dangerous infections.

32

Erysipelas may be caused by other pathogens also and some are listed in
the table below. It is to be noted that the pathogens can be different in people
with decreased immunity and normal people from the general population.

Cellulitis

Indigenous
skincolonizing
bacteria

Exogenous
bacteria

Typical Pathogens Causing Erysipelas and Cellulitis

In immunocompromised
In the general population
individuals
Streptococcus
S. pyogenesc (group A
agalactiaeb(group B
streptococci), Staphylococcus
streptococci)
aureus
Vibrio vulnificus,V.
Haemophilus influenzae,
alginolyticus,Streptococcus Aeromonas
pneumoniae, Pseudomonas hydrophila,Erysipelothrix
aeruginosa
rhusiopathiae, Pasteurella
multocidad, Staphylococcus
intermediusd, Capnocytophaga
canimorsusd, Mycobacterium
marinum, anaerobes (e.g.,
Clostridium perfringens), facultative
anaerobes
P. aeruginosa; opportunistic S. pyogenes (often in synergy with
fungi (e.g., Mucor or
S. aureus and other organisms);
Rhizopus); Cryptococcus
Mycobacterium fortuitum; Vibrio
neoformans
spp., Aeromonas spp., Clostridium
spp.

Necrotizing
infections
In addition to those affecting the general population.
Primarily in patients with diabetes mellitus or peripheral vascular disease. Also
the agent of puerperal sepsis.
C Also (along with group B, C, and G streptococci) the causative agent of
erysipelas
d Especially following cat and dog bites.

33

Pathophysiology
Bacterial inoculation into an area of skin trauma is the initial event in
developing erysipelas. Usually, the bacterium needs an access to the body. This
can be anything from a break of the skin or conditions which makes the organism
susceptible to attack by the bacteria.

Portals of Entry for Pathogens Causing Erysipelas

Category

Examples

Underlying

Inflammatory dermatoses: atopic dermatitis, contact dermatitis,

dermatoses

stasis

dermatitis,

psoriasis,

chronic

cutaneous

lupus

Bullous disease

erythematosus, pyoderma gangrenosum

Pemphigus vulgaris, bullous pemphigoid, sunburn, porphyria

Ulcers
Umbilical stump
Superficial

cutanea tarda
Pressure, stasis
Newborn
Impetigo, folliculitis , furuncle, carbuncle, ecthyma

pyoderma
Viral infection
Dermatophytosis
Injury

Herpes simplex, varicella, herpes zoster

Tinea pedis, tinea capitis, tinea barbae
Trauma, abrasion, laceration, puncture, burn, bite (human,

Surgical wound

animal, or insect)
Venous access device, arterial monitoring device, surgical

Adjacent localized

incision
Otitis , sinusitis and other infections

Risk factors

34

Streptococci are a saprophyte of the mouth, pharynx, digestive tract and

skin. Some of the species are pathogenic. The contact with pathogen can be
direct of indirect. The Human being is the sole reservoir of contamination in
cases of direct contamination. Not all the persons infected with streptococci have
clinical manifestations. Most of them are carriers.
The incidence of carriers for streptococci is very large (4-25 %)
predominant in the cold n humid environment. It is also frequent in winter as
there is an increased risk of upper respiratory tract infections. In some cases, the
incubation period is very short but it can last up to three months. The more recent
the infection/contact, or the infection massive, the more is the risk of
contamination. Old carriers are less dangerous and the pathogenicity may even
decrease depending on the virulence of the organism.
The clinical manifestation and the severity depend on the age group,
gender and the level of immunity. As such, streptococcal infections of the skin are
more common in young person and are increased in infancy due to the
decreased or underdeveloped defense mechanism.
Some infants between 4 and 6 months are affected by hypoglobulinemia
due to an inability to synthesize IgA and IgM, and the decrease the IgG acquired
transplacentally. There are also other conditions when there is a decrease in
immunity. They may be congenital or some are acquired.

Brutons

Agammaglobulinemia which is an inherited disorder acquired by X-linked is

among the first to be described.
In infants, the local defense is decreased due to the immaturity of the skin.
The stratum corneum is immature, the desmosomes and hemidesmosomes hold

weakly to each other, the hydrolipidic film of the skin is not functioning
properly and the sweat and secretary glands are not developed.

35

Decrease in immunity is also common in many disease and some of the

risk factors and diseases which can cause erysipelas are listed in the tables
below.
Conditions and Characteristics That May Predispose to Erysipelas
Systemic
Diabetes mellitus
Cancer and cancer chemotherapy
Neutropenia (e.g., following cancer chemotherapy)
Renal failure
Cirrhosis
Alcohol and drug abuse
Malnourishment
Immunodeficiency syndromes
Iatrogenic immunosuppression
Long-term systemic steroid treatment
Systemic atherosclerosis
Peripheral vascular disease
Infancy
Advanced age
Local
Exposure to marine organisms
Puncture wound of foot
Hot-tub bathing
Chronic lymphedema
Venous insufficiency
Toe-web intertrigo
Tinea infection
Age groups with increased risk of erysipelas.

36

Erysipelas is a true dermatitis, involving the skin, subcutaneous, and

mucous surfaces. The blood-vessels are dilated and distended with blood, and
cell-infiltration may extend into the deeper tissues, where suppuration is apt to
take place. The cocci are found in the lymph spaces of the affected area, while
beyond this they are found in the lymph vessels, where the battle is fought and
won by the leukocytes (phagocytes).

Common localizations of erysipelas

Erysipelas was previously found mainly on the face. However, now it is
seen most commonly on the lower extremities. Erysipelas tends to occur in areas
where the lymphatic system is obstructed (A). Erysipelas occurs mostly where
the skin is thin or the connective tissue lax (eye lids, scrotum, perianal region).
The face forms part of approximately 35 % of all cases of erysipelas. The
eyelids are oedematous and erysipelas of the helix and antehelix region is also
associated with lots of pain. Sometimes, the nose may also be affected and one
of the commonly described forms here is erysipelas vespertilio.
Bastion (B) described two varieties of erysipelas of the face. The first one
is seasonal and appears mostly in spring or winter. It is preceded by coryza and
is due to streptococci. Herpes simplex infections or the common cold may
activate the streptococci found as commensals in the nasal cavity.
The other form of erysipelas of the face is the one which needs a port of
entry for the streptococci. It can be a fissure, erosion, or ulceration of the nasal

37

mucosa or a trauma of the face. Fissures of the lips and other lesions may also
give the same result.
When there is an absence of an upper respiratory tract infection in a
patient, we should look for the portal of entry and treat the latter.
Erysipelas also occurs in the lower limbs. 50% of cases of erysipelas
occur at the level of the lower limbs. Other places which can be affected are the
forehead, and the trunk. In the new born, erysipelas usually occurs at the level of
the umbilicus and in kids in the perianal region.

Evolution and complications

Erysipelas of the lower limbs is an acute infection which usually heals in
about 10-12 days without any sequelae. However, some patients may face the
post erysipelas syndrome which is made up of dermic lesions and obstructive
lesions. If left untreated, this leads to chronisization and recurrence. It can cause
lymphatic obstruction, edema and even elephantiasis. These are the factors
which lead to recurrence.
The causes of post erysipelas syndrome are numerous:
Severe erysipelas ( phlegmonos, bullous or necrotic )
Late treatment
Incorrect treatment
Persistence of portal of entry

38

The streptococcal infections cause an inflammation which can damage the

vessels and the tissue. Firstly, the lymphatic system is affected.

Both the

intercellular lymphatic spaces and the lymph tracts are affected. At the level of
the capillaries, there is increased permeability and fragility while at the level of
the veins thrombosis. Once the vascular disturbances have started, stasis occurs
and its consequences are edema, anoxia, acidosis and metabolic disturbances.
Also, there is the release of kinin, bradykinin, histamine, serotonine which further
act on the tissues and cause destruction. This worsens the stasis and a vicious
cycle may occur which can not be treated by penicillin. As prophylaxis,
corticotherapy is used.
The complications of stasis and lesions after erysipelas are:
Edema of the lower limbs. This is due to the lymphatic obstruction.
Elephentiasis. This is a more severe form of post erysipelas edema.
Thrombophlebitis
Dermatitis
Ulcerations
Purpura
Sclerosis of the skin
Cervical sinus thrombophlebitis
Meningitis
Cerebral Abscess
Cellulitis
Cutaneous Abscess
Septicaemia
Visceral Metastatic infections
Acute Glomerular nephritis
Hypersensitivity due to streptococci makes the organism more susceptible
to recurrence of erysipelas. The lymphedema which is rare in the first episode

39

increases after each recurrence and may result in fibrosis and permanent
lymphedema. This is manifested as macrocheilitis or elephantiasis of the legs. (I)

Prognosis
The prognosis for patients with erysipelas is excellent. Complications of
the infection usually are not life threatening, and most cases resolve after
antibiotic therapy without sequelae. However, local recurrence has been reported
in up to 20% of patients with predisposing conditions(C). In old and impoverished
subjects, the prognosis must be guarded, and also in infants and in puerperal
women (D).

40

Chap

3.

CLINICAL

FORMS

OF

ERYSIPELAS
Clinical Manifestations
Erysipelas

is an

acute

infectious disease

caused

by Pyogenic

Streptococci. The incubation period is 2-5 days (E).

The onset is abrupt and is accompanied by chills and fever, head ache,
nausea and vomiting, malaise and even convulsions in children (F). On the
second day, an erythemato-edematous lesion may appear on the face or on the
lower limbs.

Symptoms
Abrupt onset with rapid course
Influenza-like prodrome
Fever,
Chills,
Malaise
Headache
Vomiting
Red rash with feeling of tightness and warmth

41

Signs
Lesion indurated with elevated margins
Irregular border that is sharply demarcated
Lesions show staged progression
Spreading erythema over 3-6 days
Shiny, bright red erythema
Painful, hot, edematous lesion
Vesicles and bullae may develop and then crust
Central clearing may then develop within 7-10 days
Areas of involved skin may exfoliate
Post-inflammatory Hyperpigmentation may occur
Marked lymphangitis
Hypotension may be first sign before erythema (G)
The lesion is extremely painful and extends rapidly on the surface,
reaching a diameter of 15-20 cm in the first days. It is also associated with
regional inflammatory lymphadenopathy. Usually, there is only one lesion; rarely
multiple and most frequently localized on the face and lower limbs. Less
frequently, it can be localized at the level of the hands, scalp, genitals, and
breasts and in new-born peri-umbilical region.
In cases involving the lower limbs, the ports of entry are tinea pedis,
varices, and venous insufficiency and stasis, and leg ulcers. For facial
involvement (perinasal/periocular), the port of entry is nasal, ocular, pharyngeal
and auditory. The disease can heal by itself within weeks with desquamation and
descrete pigmentation or can be complicated by cellulitis, cutaneous abscess,
septicaemia, emboli or acute glomerular nephritis.
At the level of the face, it may be complicated by cervical sinus
thrombophlebitis, meningitis, cerebral abscess. (I)

42

43