Microbial Diseases of The Different Organ System SKIN

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Prepared by :

Alex S. Borromeo, RN, MN


 At the end of this chapter, the student should be
able to :

1. Identify the different types of skin rashes or


lesions ;
2. Recognize common skin infections based on
clinical manifestations ;
3. Differentiate the characteristics of the causative
organisms of each skin infection ; and ;
4. Discuss the laboratory diagnosis, treatment,
and prevention of each skin infections.
1. Macules – flat lesion characterized by change in
color of the affected skin

2. Papules – raised lesions, solid in consistency of less


than 5 mm in diameter.

3. Plaques – flat with elevated surface (plateau-like)


with more than 5 mm diameter

4. Nodules – rounded raised lesions more than 5 mm


in diameter.

5. Urticaria – (wheals or hives) – annular or ring-like


papules or plaques with pinkish in color
6. Vesicles – circumscribed fluid-filled lesions less than 5 mm in
diameter.

7. Bullae – circumscribed fluid-filled lesions more than 5mm in


diameter

8. Pustules – circumscribed, exudate-filled lesions

9. Purpura – skin lesions due to bleeding into the skin


a. Petechiae – less than 3 mm diameter
b. Ecchymosis – more than 3 mm diameter

10. Ulcer – crater-like lesion that may involve the deeper layers of
the epidermis and dermis

11. Eschar – Necrotic ulcer covered with a blackened scab or crust.


Macule Papule Plaques Nodules Urticaria

Vesicle Pustules Petechiae Ecchymosis Ulcer


and
Bullae

Eschar
 Staphylococcus aureus
 Streptococcus pyogenes
 Pseudomonas aeruginosa
 Clostridium perfrigens
 Bacillus anthracis
A. Important Properties

- S. aureus is common pathogen in humans.

- They are gram-positive cocci usually


arranged individually, in pairs, short chains,
or in grape-like clusters.

- It is found in the skin and the nasopharynx.


 On culture they produce gray to golden
yellow colonies
- Golden yellow colonies are best produced when
cultured at 20 degree C – 25 degree C.

- It is coagulase positive, which differentiates it


from other species of Staphylococcus.

- Staphylococci also produce catalase which


differentiates it from Streptococci.

- The organism produces enzymes and toxins


responsible for its invasiveness and
pathogenicity.
- Skin infections are transmitted through direct
contact with a person having purulent
lesions, from hands of healthcare or hospital
workers, and through fomites like bed linens
and contaminated clothing.
1. Folliculitis – a pyogenic (pus-producing)
infection involving the hair follicle. It is
characterized by localized painful
inflammation and heals rapidly after
draining the pus.
2. Furuncle – an extension of folliculitis and is
also known as boil. It is characterized by
larger and painful nodules with underlying
collection of dead and necrotic tissue.
3. Carbuncle – represents a coalescence of
furuncles that extends into the
subcutaneous tissue with multiple sinus
tracts.

4. Sty or hordeolum – folliculitis occuring at


the base of the eyelids.
5. Impetigo – infection is common in young
children and primarily involves the face and
the limbs. Initially it starts as a flattened red
spot (macule) which later becomes a pus-
filled vesicle that ruptures and forms crust
(honey-colored crust). It may be caused by
both S. aureus and S. pyogenes
6. Staphylococcal Scalded Skin Syndrome (Ritter’s
disease)

 Primarily a disease found in newborns and young


children.

 It is manifested by sudden onset of perioral


erythema (redness) that covers the whole body
within two days. When slight pressure is applied
over the skin, it causes displacement of the skin.

 This is known as positive Nikolsky sign.


 Bullae and cutaneous blister formation will
soon follow and later underdo desquamation.
> Antibodies against the exfoliative toxin are produced within 7 to
10 days enabling the skin to become intact again.

> The toxin responsible for these manifestation is the exfoliative


toxin.

> Only the outer layer of the epidermis is affected hence there will
be no scarring.
- Laboratory identification includes microscopic
examination of Gram-stained specimen
(gram-positive cocci) and culture (gray to
golden yellow colonies.)

- The qualities of microorganism is catalase


positive and coagulase positive
 The treatment of choice is beta-lactam
antibiotics like penicillin.

 However, S. aureus readily develops resistance to


penicillin and other penicillin derivatives like
methicilin and nafcillin.

 Oxacillin is the only penicillin-derived antibiotic


that has remained active against S. aureus.

 The incision and drainage of localized skin and


soft tissue infection is also necessary
 Staphylococcus aureus
 Streptococcus pyogenes
 Pseudomonas aeruginosa
 Clostridium perfrigens
 Bacillus anthracis
A. Important Properties.

- S. pyogenes are gram positive cocci arranged


in pairs or in chains when seen under the
microscope.
- It belongs to the group A Streptococci based
on Lancefield classification.

- It is beta hemolytic (cause complete


hemolysis of blood).

- Its major virulence factor is M protein which


is anti-phagocytic.
- S. pyogenes also produces enzymes and
toxins responsible for the pathogenesis of
infections caused by the organism.

- Some strains are encapsulated which protect


them from phagocytosis and may be
associated with severe systemic infections.
- Soft tissue infections are acquired through
direct contact with infected persons or
through fomites.
1. Pyoderma (Impetigo) – a purulent skin
infection that is localized and commonly
involves the face, the upper and lower
extremities. It starts as vesicles then
progresses to pustules. The lesions rupture
and form honey-colored crusts. There may
be enlargement of the regional lymph nodes
but no sign of systemic infection
2. Erysipelas (St. Anthony’s Fire) – follows a
respiratory tract or skin infection caused by
S. pyogenes. Patients manifest with
localized areas associated with pain,
erythema, and warmth. It is grossly distinct
from normal skin. There is accompanying
lymphadenopathy and systemic
manifestations.
3. Cellulitis – involves the skin and
subcutaneous tissue. Unlike erysipelas, the
infected and the normal skin are not clearly
differentiated. It is also manifested as local
inflammation with systemic signs.
4. Necrotizing Fasciitis – involves the deep
subcutaneous tissue and is also known as
“flesh-eating” or streptoccocal gangrene.
It starts as cellulitis then becomes bullous
and gangrenous. It spreads to the fascia
then the muscle and fat. It may become
systemic and cause multi-organ failure
leading to death.
 Acute glomerulonephritis and rheumatic fever
are non-suppurative, immune-mediated
complications.

 Acute glomerulonephritis is more commonly


associated with skin infections while
rheumatic fever is usually associated with S.
pyogenes throat infection.
1. Microscopy – Gram stain of samples of
infected tissue will show gram-positive
cocci in pairs and chains associated with
leukocytes.
2. Culture – positive beta hemolysis in blood
agar.

2. Bacitracin test – antibiotic susceptibility test


with (+) zone of inhibition of growth around
the Bacitracin disc.
- The drug of choice is penicillin.

- In case of penicillin allergy, macrolides


(erythromycin, azithromycin) or
cephalosporins are alternate drugs.

- The drainage of pus and through


debridement of infected tissues must also be
done.
 Staphylococcus aureus
 Streptococcus pyogenes
 Pseudomonas aeruginosa
 Clostridium perfrigens
 Bacillus anthracis
- P. aeruginosa are gram-negative bacilli
arranged in pairs that are encapsulated.
- They are capable of producing water-soluble
pigments (e.g., pyocyanin – blue).

- It is an opportunistic pathogen, a common cause


of nosocomial infections (hospital-acquired) and
resistant to most antibiotics.

- The virulence of P. aeruginosa can be attributed


to adhesins (flagella, pili, LPS, alginate), toxins
(exotoxin A, pigments) and enzymes
 A common mode of transmission is through
the colonization of previously injured skin
- P. aeruginosa is commonly associated with
colonization of burn wounds and characterized
by blue-green pus that exudes a sweet grape-
like odor.

- Other skin infections are folliculitis, and


secondary infections in individuals with acne and
nail infections resulting from immersion in
contaminated water.

- It is also the most common cause of


inflammation of the bone and cartilage of the
foot called osteochondritis following a
penetrating injury
 Gram Stain demonstrates gram-negative
bacilli arranged individually or in pairs.

 Culture shows flat colonies with green


pigmentation and characteristic sweet,
grape-like odor.

 Oxidase test is positive.


 P. aeruginosa is resistant to most antibiotics
hence culture and sensitivity must be done.

 Preventive measures for control of P.


aeruginosa should be focused on preventing
contamination of sterile hospital equipments
and instruments, and cross-contamination of
patients by hospital personnel.
 Staphylococcus aureus
 Streptococcus pyogenes
 Pseudomonas aeruginosa
 Clostridium perfrigens
 Bacillus anthracis
 C. perfrigens are gram-positive bacilli that
are anaerobic and rarely produce endospores.
 It produces four lethal toxins namely : alpha,
beta, iota and epsilon toxins.

 Of the four toxins, alpha toxin is the most lethal


because it acts as a lecithinase that cause lysis of
erythrocytes, platelets and leukocytes.

 This toxin also causes massive hemolysis and


bleeding and tissue destruction.

 It is widely distributed in nature and particulary


associated with soil and water contaminated with
feces.
- C. perfrigens is commonly transmitted by the
colonization of the skin following physical
trauma or surgery.
- C. perfrigens causes soft tissue infections like
cellulitis, suppurative myositis, and myonecrosis or
gas gangrene.

- Gas gangrene is a life threatening infection following physical


trauma or surgery characterized by massive tissue necrosis
with gas formation, shock, renal failure, and death within two
days of onset.
- Diagnosis is based on microscopic detection
of gram-positive bacilli in pairs and growth in
culture under anaerobic condition.
 Surgical wound debridement and high-dose
penicillin therapy are the main approaches to
the management of the disease.
 Staphylococcus aureus
 Streptococcus pyogenes
 Pseudomonas aeruginosa
 Clostridium perfrigens
 Bacillus anthracis
- B. anthracis are gram-positive bacilli
arranged individually or in pairs or long
serpentine chains giving them the
characteristic “bamboo fishing rod” or
“Medusa head” appearance.
- It is aerobic, spore-forming and
encapsulated.

- Virulence of the organism is due to its


polypeptide capsule which is responsible for
evading phagocytosis and toxins – edema
toxin and lethal toxin – both of which inhibit
the host’s immune responses.

- B. anthracis can also be used in bioterrorism


 B. anthracis is transmitted through
inoculation into open skin from either the soil
or infected animal products, ingestion of
infected meat or milk and inhalation of
aerosolized spores.
 Anthrax is a disease of herbivores.

 There are three forms of anthrax – cutaneous,


gastrointestinal or pulmonary anthrax.

 The skin infection, cutaneous anthrax, is the


most common form.
 It is characterized by painless papules at the
site of inoculation that become ulcerative,
and later develops necrotic eschar.

 This is associated with painful


lymphadenopathy and edema.
 The peripheral blood contains a larger
number of B. anthracis which is easily seen on
Gram stain.

 Spores are only observed on culture in low


carbon dioxide tension.
 Demonstration of the spores can be done
using Dorner stain or Wirtz Conklin Stain.
 Antibiotics like penicillin or doxycycline are
the drugs of choice.

 In resistant cases, ciprofloxacin is


recommended.

 Prevention is through vaccination of animals


and individuals at risk such as animal
handlers, veterinarians, military personnel
and those working in slaughterhouses.
 Superficial Mycoses - Tinea versicolor
(Pityriasis versicolor)
 Tinea nigra
 CUTANEOUS MYCOSES or DERMATOPHYTOSIS
 Subcutaneous Mycoses
 SUPERFICIAL MYCOSES – Tinea versicolor
(Pityriasis versicolor)

- Tinea versicolor is caused by Malassezia


furfur (Pityrosporum orbiculare).

- M. furfur is a normal flora of the skin particularly in areas rich


in sebaceous glands.

- The infection is worldwide in distribution but more common


in tropical regions.
- The lesions are irregular, discrete hypo – or hyperpigmented
macules depending on the skin color of the affected
individual.

- The lesions are scaly with a dry, chalky appearance, and


usually appear on the face, neck trunk, and arms.

(a) Malassezia furfur spore


(b) Direct microscopy
of skin scrapings
demonstrating
characteristic
clusters of thick-
walled round,
budding yeast-like
cells and short
angular hyphal forms
 Diagnosis is made by microscopic visualization of
“spaghetti and meatballs” appearance of M. furfur
with an alkaline stain (10% KOH or NaOH).

 It can also be demonstrated with Periodic Acid


Schiff Stain (PAS stain) or hematoxyllin-eosin
stain (H & E stain).

 Treatment includes application of keratolytic


agents containing selenium disulfide or salicylic
acid and topical antifungal drugs like
ketoconazole.
 Superficial Mycoses - Tinea versicolor
(Pityriasis versicolor)
 Tinea nigra
 CUTANEOUS MYCOSES or DERMATOPHYTOSIS
 Subcutaneous Mycoses
 The Tinea nigra infection is caused by Hortaea
werneckii (formerly Exophiala werneckii), a
dematiaceous fungus that produces melanin and
grows as mold producing annelids or
annelloconidia.

 The lesions involved the palms and soles and are


described as gray to black, well-demarcated
macules.

 The infection is common in the tropical and


subtropical regions, and is more frequently seen
in adolescents, young adults, and females.
 Diagnosis is made by direct microscopic
examination of skin scrapings with potassium
hydroxide and culture using Sabouraud’s
dextrose agar medium.

Sabouraud’s dextrose agar medium

 Treatment is similar to the treatment for tinea


versicolor.
 Superficial Mycoses - Tinea versicolor
(Pityriasis versicolor)
 Tinea nigra
 CUTANEOUS MYCOSES or
DERMATOPHYTOSIS
 Subcutaneous Mycoses
- Cutaneous mycoses are fungal infections involving the
keratinized structure of the body like the skin, hair and nails.

- The infection is caused by a group of fungi collectively referred


to as Dermatophytes.

- Dermatophytes produce keratinase, an enzyme capable of


breaking down keratin.

- They are keratinophilic and keratinolytic.

- The three genera that cause these infections are :


(1) Microsporum which infect the hair and nails only ; (2)
Trichophyton which infect the skin, hair, and nails, and (3)
Epidermophyton which infect only the skin and nails.
 Microsporum produces both microconidia and
macroconidia with predominance of macroconidia,
while Trichophyton predominantly produces
microconidia.

 Epidermophyton, on the other hand, produces


smooth-walled macroconidia in bundles of two or
three.

 Based on their natural habitat, Dermatophytes are


classified as zoophilic (from animals to humans),
geophilic (from soil to humans or animals), and
antrhopophilic (from humans to humans).
 The infections are referred to as tinea or
ringworm. The name of the infection reflects
the anatomic site involved, namely : (1) tinea
pedis, also known as athlete’s foot (feet) ; (2)
tinea capitis (scalp); (3) tinea corporis (body);
(4) tinea cruris or jock itch (groin); (5) tinea
manus (hands) ; (6) tinea barbae (beard); and
(7) tinea unguium, also known as
onychomycosis (nails)
 Tinea involving the skin usually present with
“ring worm” pattern.

 The lesions have reddish border with central


clearing. There may be inflammatory scaling.

 Hair invasion can be ectothrix (arthroconidia are


outside the hair shaft), endothrix (arthroconidia
are inside the hair shaft), or favic (formed inside
the hair but with “honeycomb” pattern or
resembling a favic chandelier) depeding on the
dermatophyte species causing the infection.
 Cutaneous Mycoses:

A. tinea unguium B. tinea capitis


C. tinea pedis D. tinea corporis
E. tinea cruces or jock itch
 Specimens for diagnosis are skin or nail
scrapings, or hair cuttings from the affected
areas. More fungi can be obtained from the
borders of the lesion rather than the center.

 Diagnosis is based on the clinical appearance of


the lesions, direct microscopic examination and
culture.

 Treatment involves administrating antifungal


drugs such as azoles (miconazole, clotrimazole,
econazole)
 Superficial Mycoses - Tinea versicolor
(Pityriasis versicolor)
 Tinea nigra
 CUTANEOUS MYCOSES or DERMATOPHYTOSIS
 Subcutaneous Mycoses
 The infection initially involves the deeper layers
of the dermis and subcutaneous tissue then later
the bones.

 The mode of transmission is through traumatic


inoculation into the skin.

 The infections are relatively rare with the


exception of sporotrichosis.

 Other infections are chromoblastomycosis,


phaeohyphomycosis, zygormycosis and
mycetoma (Madura foot).
 Sporotrichosis, also known as rose gardener’s
disease, is caused by a dimorphic fungus,
Sporothrix schenckii, that is found in the soil and
decaying vegetation.

- the infection initially presents a small


nodule which may later become ulcerative
and pustular.

- Two weeks later, painless, subcutaneous


nodules along the lymphatic drainage
develops. Sometimes they may present as
verrucous lesions and often misdiagnosed as
malignancy of the skin.
Ulcerated lesion of sporotrichosis following course of draining
lymphatics
 Chromoblastomycosis is characterized by
verrucous nodules or plaques. The infection
is insidious and may become chronic.
- the etiologic agents are all dematiaceous
fungi namely : Exophiala, Fonseca,
Cladosporium, Phialophora, and
Rhinocladiella.
Wart-like lesions of chromomycosis
 Mycetoma or Maruda Foot may be caused by true
fungi (Eumycotic Mycetoma) or Actinomycetes
(Actinomycotic mycetoma).

- the most common cause of eumycotic


mycetoma are Phaeoacremonium, Madurella,
Curvularia, and Furasium.
- it frequently involves the feet and hands.
- The infection is characterized by clinical
triad of tumefaction, granules, and draining sinus.
- Diagnosis is primary based on the
characteristics of the granules.
Madura foot
 Warts
 Herpes Simplex Infections
Etiologic agent

- Warts are caused by a DNA virus, Human


Papillomavirus (Family Papovaviridae).

- There are at least 70 serotypes.

- The virus is capable of causing malignant


transformation of the infected cells
 HPV infection is acquired by (1) direct contact
through mucosal or skin breaks ; (2) sexual
contact ; and (3) upon passage through
infected birth canal
(1) Skin warts (common, plantar, and flat warts) – benign, self-
limiting proliferation of the skin that undergoes spontaneous
resolution.

- these warts may be flat, dome-shaped,


or plantar.
- HPV types 1-4 are the most common
isolates from the lesions. Frequently affected
sites are the hands and feet and common
among children and adolescents.

(2) Genital and anogenital warts – also known as condylomata


acuminata (singular condyloma acuminatum)
a. Dome shaped b. Plantar c. Periungal

d. Flat (plane) e. Filiform


Venereal wart (condyloma acuminate) due to HPV types 6 to 11
- Diagnosis is based on gross appearance of
the lesions and histologic appearance on
microscopic examination that includes
hyperkeratosis.
 Treatment is removal of the lesion by : (1)
surgical excision ; (2) cryosurgery ; (3)
electrocautery ; (4) application of caustic
agents like podophyllin ; and (5) interferon
for genital warts.

 Avoiding contact with infected tissues


prevents spread of the infection
 Warts
 Herpes Simplex Infections
 Etiologic agent :

- the etiologic agents are Herpes simplex


virus types 1 and 2, DNA viruses under
the family of Human Herpesviridae.

- These viruses are capable of latency in


the neurons and are capable of recurrent
infections.
- HSV is present in oral and genital secretions
and vesicle fluid.

- It can be transmitted through (1) oral contact


(kissing); (2) fomites (sharing of glasses,
toothbrushes, and other saliva-contaminated
materials ) ; (3) sexual contact ; (4)
transplacental (during pregnancy); and (5)
during childbirth.
(1) Gingivostomatitis – the primary infection,
primarily caused by HSV-1.

- it presents as vesicles that rupture and


ulcerates.
- lesions are seen in the buccal mucosa,
palate, gingivae, pharynx, and the tongue.
- the most striking feature is gingivitis.
- Gingivostomatitis is common during
childhood.
Herpes simplex infections of the mouth (herpetic gingivostomatitis)
(2) Herpes labialis (Fever Blister or Cold Sore) –
represents recurrent mucocutaneous HSV
infection.
- this is caused by HSV-1 and 2.
- lesions are usually located at the
vermillion borders of the lips.
- Lesions are vesicular, they rupture then
form an ulcer and later form crusts.
- Recurrences are less severe than the
primary infection and often occur on the
same site.
Herpes labialis (Fever Blister or Cold
Sore)
(3) Herpetic whitlow – HSV infection involving
the fingers and caused by both HSV and
types 1 and 2.
4. Eczema herpticum – HSV infection occuring
in children with eczema. This only shows
that HSV can be an opportunistic pathogen.
It can also cause a superimposed infection
in burns.
 Herpes gladiatorum – HSV infection of the
body and is usually acquired during wrestling
or playing rugby.
- Diagnosis is based mainly on the clinical
presentation of the infection.

- Diagnosis can be made based on


hispathologic changes and using the Tzanck
smear to demostrate the characteristic
inclusion bodies known as the Cowdry type A
inclusions.

- Cell culture is also diagnostic but seldowm


requested.
 The recommended drug is acyclovir.

 There is currently no available vaccine for


HSV.

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