DERMATITIS GANGRENOSA
Gangrene of the skin is a
serious skin problem.
Predisposing factors
Devitalization of tissues
due to loss of blood supply
Trauma or lacerations to
the skin.
Certain viral skin
disease in infants or children that are followed by bacterial invasion.
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Fig. 35b. Skin Gangrene
|
Etiology
Different bacterial
strains can cause skin gangrene. These include hemolytic streptococci,
non-hemolytic and clostridium species causing gas gangrene.
|
Fig. 36a. Dermatitis Gangrenosa
Fig. 35a. Skin gangrene
|
Clinical manifestations
General manifestations:
Severe constitutional
symptoms, which may lead to a fulminating course endangering life
especially in young children.
Skin manifestations
Skin lesions may show
bullae, pustules or abscesses followed by lymphangitis and lymphadenitis.
After few days the skin at the inflamed site becomes dark in color,
necrotic and may show extensive ulceration.
DERMATITIS GANGRENOSA
INFANTUM
Dermatitis gangrenosa
infantum is a special type of skin gangrene that occurs in infants and
young children.
Two types of skin
gangrene may occur in infants:
-
Primary skin gangrene
- this begins as an ulcerating skin lesion surrounded by an inflammatory
zone due to invasion of bacteria such as Staph. Pyogenes or hemolytic
streptococci.
-
Secondary skin
gangrene - this begins following varicella or measles infections.
Fig.35 b,c,d,e Skin gangrene due to Chicken pox
Treatment
Surgical debridement and
cleaning of the lesion.
Cases due to Clostridium
species are given gas gangrene anti serum.
Wet oozing lesions can be
dried by using Potassium permanganate compresses 1: 9000 followed by
topical antibacterial cream as Mupricine (Bactropan).
High doses of antibiotics
may be needed in the beginning to control severe infection.
ERYTHRASMA
Erythrasma is bacterial
skin infection of the intertriginous areas caused by Mycobacterium
minutismus.
Clinical
features
The crural and intertriginous areas are
the most common sites involved. The lesions are sharply defined erythematous
patches and are usually unilateral with minimal scaling. Itching is not a
prominent feature while excessive sweating and irritation of the crural
area may cause mild itching. |
Fig. 39. Erythrasma |
Fig. 38. Erythrasma |
Fig. 37. Erythrasma
|
Characteristically,
erythrasma gives a coral red fluorescence as seen under Wood‘s Light.
That differentiates the condition from other crural skin diseases such as
T. cruris.
Treatment
Mild cases can be treated
by topical erythrocin lotion (Eryderm), Tolniftate, and antibacterial soap
as Cidal soap. These usually can help in rapid clearance of the skin
lesion.
Erythrocin may be given
orally for two weeks in extensive cases.
ANGULAR
CHEILITIS
(Perleche)
Perleche or angular
cheilitis is a low-grade inflammation at the angles of the mouth.
Predisposing
Factors
Angular stomatitis has
been attributed to different factors:
-
Staphylococcal
infection or Candidiasis.
-
Avitaminosis of the B
complex group.
-
The condition is
usually aggravated and perpetuated by constant licking of the lips
especially in children.
-
Bottle-feeding may
lead to accumulation of remnants of irritating debris and sugar on the
angle of the mouth predisposing to infection.
-
Certain food or
beverages such as orange juice may increase the inflammatory changes.
Fig. 41. Angular cheilitis
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Fig. 40. Angular cheilitis
|
-
Problems of the
teeth as malocclusion may play also an important role.
Clinical features
The lips become macerated
and fissured, and may bleed in severe cases. The condition may become
exceedingly chronic, and in many patients all local treatments may be of
no value.
|
Fig. 42. Chronic Actinic Cheilitis
|
Treatment
Treatment of angular
cheilitis is directed to the causative factor.
Topical antifungal or
anti bacterial preparations may cure some cases.
Correction of the
avitaminosis.
Mothers should be
instructed to prevent their children from licking their lips.
Perfumes and perfumed
soaps should be avoided.
Proper mouth hygiene of
the child.
Pufexamac Cream or
Ointment (Flogocid, Parfenac) may give good results.
Erythema Neonatorum
Exfoliativa
(Ritter‘s Disease)
This is a rare
staphylococcal and streptococcal infection of the breast-fed infants. The
disease occurs during the first weeks of life and is characterized by a
fulminating course.
The lesions show
extensive bullous eruption with easily detached epidermis leaving red
oozing areas. The condition is caused by the bacterial exotoxins.
A similar condition
occurs in adults known as "Lylle Disease" or epidermolysis acuta
toxica.
Clinical features
Skin lesion presents with
red macules that begin around the mouth. These change into vesicles and
pustules that rupture leaving a yellowish crust. The condition may spread
eccentrically to the face and other parts of the body. The skin later
becomes scalded, scarlet red empetiginized, covered by vesicles and
bullae.
Complications
Stomatitis, rhinitis and
corneal ulceration.
Differential diagnosis
Toxic epidermal
necrolysis: may simulate Ritter‘s disease.
Leiner‘s disease:
Leiner‘s disease shows branny greasy scales while in Ritter‘s disease
there are large bullae, which peel off, in large sheets.
Treatment
-
Improving the general
condition of the infant is very important.
-
Proper hygiene of
both the
mouth and nose.
-
Mild antiseptic soaks
as potassium permanganate 1:10000.
-
Topical anti bacterial
cream and a septic sterile dressings.
-
Systemic antibiotics
according to the culture and sensitivity results.
-
Treatment of the
complications such as corneal ulcers and others.
TOXIC
SHOCK SYNDROME
Toxic shock syndrome is a
serious problem affecting infants and other age groups due to
staphylococcal toxins.
The disease is
characterized by fever, multisystem involvement, circulatory shock,
widespread erythema and desquamation.
Clinical features
The onset of the disease
is acute with fever and skin rash.
Constitutional
manifestations: fever, vomiting, diarrhea, purpura, thrombocytopenia,
alopecia and nail destruction.
Systemic manifestations
Involvement of muscles,
liver, kidneys and central nervous system may follow. Dizziness and shock
are important manifestations of the syndrome.
Skin manifestations
The rash may develop
within the first day in the form of widespread macular erythema,
papulopustular eruption or scarlatiniform that may clear within 3 days.
Desquamation of the
affected skin is highly characteristic.
Edema of hands and feet
may be marked.
Towards the end of the
second week the majority of patients develop a widespread, itchy,
maculopapular or urticarial rash, which simulate drug reaction.
Occasionally vesicles and
bullae may be formed.
Purpura due to
thrombocytopenia may be another manifestation.
Alopecia and nail changes
as transverse ridging and nail loss.
Mucous membrane manifestations:
There is generalized
mucous membrane erythema, especially intense in the conjunctiva under
which there may be hemorrhage.
Oral, esophageal, vaginal
and bladder mucosa may ulcerate.
Diagnosis
The diagnosis is
primarily clinical. Fever, rash, and later desquamation.
Staphylococcal organisms
detection from the skin or mucous membrane lesions.
Bacterial culture from
the primary site, not from the scalded skin, and frozen section of peeled
skin may show the causative organism.
Shock is a marked feature
in the fully developed disease, but postural dizziness may be sufficient
for the diagnosis in mild cases.
Differential diagnosis
-
Erythema multiform.
-
Drug reaction.
-
Kawasaki disease may
simulate toxic shock syndrome. The diseases have features in common but
prolonged fever, cardiac involvement, generalized lymphadenopathy and
absence of peripheral shock can usually differentiate Kawasaki disease.
-
Staphylococcal
Scarlatina may represent milder cases of toxic shock syndrome.
Treatment
-
Hospitalization of
severe cases and intensive care may be needed especially in young age
groups.
-
Appropriate systemic
antibiotic therapy should be given.
-
Intensive general
supportive measures are essential.
-
Treatment and care of
skin lesions.
TOXIC
EPIDERMAL NECROLYSIS
This is a serious skin
problem that may be fatal especially in infants and young children.
Etiology
-
Staphylococcal
infection toxins:
The skin of children may
be more susceptible to staphylococcal toxins or the renal clearance of the
toxin is slower in children.
-
Drug reaction:
Different drugs that
can cause this syndrome are: Tetracycline, Sulfa, Penicillin,
antihistamines, Phenolphthalein, antipyretics, Boric acid powder,
Salicylates, Phenylbutazone, Barbiturates, Aminopyrine and others.
Fig. 43. Toxic Epidermal Necrolysis
|
Fig. 44. Toxic Epidermal Necrolysis |
Fig. 45. Toxic
Epidermal Necrolysis
(Drug Reaction)
|
-
Vaccines:
Such as polio vaccine and diphtheria
inoculation.
Clinical
features
Generalized skin eruption
appears suddenly in infants and children following Staphylococcal
infections of the upper respiratory tract.
The skin shows flaccid
blistering which later becomes red, scalded, tender mainly on the trunk,
perioral and the peri-genital areas .The tender skin becomes gathered into
folds and may separate into sheets leaving raw areas which are extremely
painful.
Differential diagnosis
Toxic shock syndrome.
Staphylococcal scalded
skin syndrome.
Erythema multiform and
Stevens-Johnson‘s syndrome have the same clinical manifestations.
Treatment
Symptomatic to relieve
pain and discomfort by using analgesic. Care should be taken to select an
analgesic not causing drug reaction.
Care of the scalded areas
of skin: Potassium permanganate compresses 1:9000 and topical anti
bacterial cream.
Topical and systemic
steroids for cases due to drug reaction.
Antibiotics - culture and
sensitivity to detect any causative bacteria and to be treated by the
proper antibiotic (Tetracycline, Sulfa and Penicillin should be avoided
because of the possibility of drug reaction.
SCARET FEVER
(Scarlatina)
Scarlet fever is an acute
infection affecting mainly children, caused by strains of Strep. Pyogenes.
Modes of Infection
Droplet infection from
the infected upper respiratory tract.
Infected belongings of
patients.
From infected milk.
Clinical features
The incubation period is
usually from 2-5 days.
Constitutional symptoms
Fever, which may be high,
anorexia, vomiting, and sore throat.
The patient is delirious
or comatosed.
Other serious
manifestations such as myocarditis may complicate certain cases.
Skin manifestations:
The skin lesion appears
on the second day on the upper trunk in the form of punctate erythema that
becomes generalized.
There is flushing of the
face with pallor around the mouth, which is one of the characteristic
signs of scarlet fever.
Desquamation of the rash,
with branny lamellar scales mainly on palms and soles.
In its severe toxic form,
the eruption is very intense and may be purpuric.
Pastia‘s lines -
Transverse red streaks appear on the skin folds due to capillary
fragility.
Mucous membrane
manifestations:
The oral mucous membranes
are bright red and there may be deeper red puncta on the palate.
Strawberry tongue
First, the tongue becomes
heavily coated. By the second or third day scattered, swollen, red
papillae give the "white strawberry tongue" appearance. As the
epithelium is shed the tongue becomes smooth and dark red ("red
strawberry tongue").
In the septic forms the local pharyngeal
lesions are severe and there may be extensive edema. Otitis media and
peritonsillar abscesses are frequent. The rash may be slight.
Diagnosis
-
Typical clinical
picture associated with tonsillitis.
-
Culture and detection
of hemolytic streptococcus.
-
Antistreptolysin-O
titter is high.
-
Schultz-Charlton test
is positive.
-
Polymorphonuclear
leukocytosis.
Differential diagnosis
Treatment
Penicillin should be
given in full dose as soon as the diagnosis is suspected. Management of
the complications and renal damage should be taken into consideration.
MENINGOCOCCAL
INFECTIONS
Meningococcal infection
is an acute inflammation of the meninges accompanied by other systemic
manifestations and skin rash.
Clinical features
Acute meningococcal
septicemia and meningitis may present with fulminating course.
Purpura follows in nearly
all cases.
Skin manifestations
The skin eruption may be
very helpful for the early diagnosis.
Early skin lesions are
discrete pink macules or small papular lesions that may be hemorrhagic,
appearing on palms and soles. Some lesions are erythematous, morbilliform
or urticarial.
A purpuric eruption is
characteristic, and occurs mainly on trunk and limbs. The petechiae are
usually small and scanty, but vary in size and number.
In severe cases larger
purpuric lesions may occur including extensive ecchymoses and necrotic
ulceration. The condition may be associated with a high mortality.
Vasculitis may occur
during the acute illness, beginning 5 -9 days after the onset even if
adequate antibiotic treatment has been given. Arteritis and episcleritis
may be associated with some cases.
PSEUDOMONAS INFECTIONS
This is a serious skin
infection caused by Pseudomonas aeruginosa organisms, which is common in
infants.
Clinical features
Skin lesions may be
localized or extensive.
-
Localized lesions
Local infections in
infants or patients with debilitating illnesses should be regarded as
potentially dangerous.
Periumbilical lesions:
The lesions may manifest with spreading erythema, a foul-smelling and
bluish-green discharge. Necrotic ulcers may develop.
Nail involvement -
paronychial pustules may be accompanied by green discoloration of the
nails.
Lips and cheeks may
become gangrenous.
Superficial wounds and
burns may be secondarily infected. Secondarily infected burns show
discoloration of the sloughs with extensive surrounding edema.
-
Extensive lesions
Extensive lesions may
present as:
-
Extensive necrosis
develops around a local erosion.
-
Non-specific tender
erythema, purpura, or a cellulitis-like picture. Bullae may form,
particularly in moist areas, such as the axillae, perineum and the
buttocks. These may rupture rapidly to give necrotic ulcers.
Complications
The prognosis of systemic
infections is always grave, even with early treatment.
Fever and shock may
supervene.
High mortality rate
especially in infants and young age due to septicemia is common.
SWIMMING POOL RASH
This type of skin
infection may be due to Pseudomonas aerogynosa organisms. Pseudomonas
usually of serotype O type II, which may be cultured from the skin and the
infected water.
Clinical features
Skin manifestations
include macular, papular or pustular lesions. Some are urticarial
suggesting insect bites. Any part of the body that has been immersed in
water may be affected but often the worst areas are those in contact with
bathing costumes. Hot tubs and whirlpools even if chlorinated may act as a
source of infection.
TROPICAL IMMERSION FOOT
This is a distinctive
infection of the toe webs caused by pseudomonas organisms. Sharply
demarcated macerated areas, sometimes tinged with green patches,
characterize the lesions. The devitalized tissues are invaded by Candida
albicans.
PERIPORITIS
Periporitis is the term
applied to pustular lesions appearing in the neonatal skin as a result of
secondary infection of sweat glands by staphylococcus aureus.
The commonest sites
involved are the buttocks, upper part of the trunk and the scalp. The
lesion affects mainly malnourished infants and young children. Skin
lesions may progress to sweat gland abscesses.
Sweat gland abscesses are
clinically distinguished from furuncles by a lack of any tendency to
"point", "coldness" and absence of tenderness.
Clinical manifestations
Erythematous deep seated
infiltrating nodules, which may be single or multiple, small or big size.
The inflammation becomes localized and soften where it ruptures exuding
thick, creamy pus and later on heals leaving a scar.
Differential diagnosis
from furuncles can be confirmed by that furuncles arise in relation to
hair follicles and have yellow center, where it points to the surface and
ruptures later.
Treatment
Treatment is directed
towards improving the nutrition and general condition of infants as well
as young children.
Preventing sweat
retention by aeration of the crural area and minimizing sweating.
Appropriate topical
antibiotic may be enough to control periporitis.
Oral antibiotics may be
needed, especially when there are multiple abscesses.
NECROTIZING FASCITIS
Etiology
-
In neonates:
narcotizing fascitis may arise spontaneously.
-
Following complication
of physical birth trauma, omphalitis or circumcision.
-
Secondary infection
from infected genital tract of the mother.
The organisms responsible
for the infection are Streptococci group A, but also group B Streptococci,
Staphylococcus aureus and Escherichia coli can cause the infection.
Clinical features
Skin manifestations
The early skin
manifestations are cellulitis, which become very indurated and extend
progressively. Purpura, and occasionally bullae, may appear in the center
of the indurated area, often followed by frank necrosis.
Systemic manifestations
The child becomes toxic.
Local cutaneous
anesthesia due to destruction of superficial nerves.
Pneumonia.
Treatment
Antibiotic therapy
appears to be of limited value in this potentially lethal situation.
Early surgical excision
of necrotic tissue is the most important aspect of treatment.
OMPHALITIS
The umbilical cord may
become colonized by a variety of potentially pathogenic bacteria mainly
Staph, Streptococci and E. coli. Occasionally infection of the umbilical
cord becomes disseminated, either by blood stream or by direct spread via
the umbilical vessels to the peritoneal cavity. Tetanus, diphtheria and
necrotizing fasciitis may also occur as complications of umbilical
infection.
Such infections are still
responsible for a high proportion of deaths in the neonatal period in
developing countries.
CLINICAL FEATURES
Skin manifestations
The skin lesion presents
with cellulitis where the skin around the umbilical area becomes
indurated.
Bullae may appear in the
center of the indurated area followed by necrosis.
Purpura: Purpuric
reactions are common manifestations of omphalitis and may be related to
bacterial toxins.
TREATMENT
The most important aspect
of treatment is early surgical excision of necrotic tissue.
The use of
Hexachlorophene as an antiseptic was popular until it became apparent that
this could lead to serious neurotoxicity, particularly in the preterm
infant. The best substitute may be Chlorhexidine that can be applied as a
dusting powder rather than as an alcoholic solution.
Antibiotics are of
limited value.
PARONYCHIA
Paronychia is an
inflammation of the folds of the skin surrounding the nail. Infection
usually extends to the adjacent soft tissue causing painful tender
swelling around the nail.
Paronychia may be
bacterial or fungal.
Pyogenic paronychia
Infection is due to
Staphylococci, pseudomonas aeruginosa and less frequently to streptococci.
Fungal paronychia
Candida albicans is the
commonest fungi causing paronychia. Dermatophytes and saprophytic fungi
may be responsible for some cases of paronychia.
Predisposing Factors
CLINICAL MANIFESTATIONS
The infection is
characterized by an acute or chronic purulent, tender and painful swelling
of the tissue around the nail. Horizontal ridges appear at the base of the
nail in chronic conditions. The moist groove of the nail and the nail fold
becomes inflamed.
Fig. 47b.Bacterial paronychia & Ingrowing nail
Fig.47c Bacterial Paronychia
Fig. 46. Candidal paronychia
|
Fig. 47. Bacterial paronychia
|
Candidal paronychia
The manifestations are
less severe than the bacterial paronychia. Candida paronychia is usually
chronic. The finger becomes swollen, tender and beads of pus
characteristically can be squeezed from the lesion.
TREATMENT
This is directed to
correct the predisposing factors as preventing trauma to the fingers or
toes and to keep these areas in normal dry conditions.
Pyogenic paronychia
Topical antibacterial and
oral antibiotic besides dressing of the inflamed areas. If an abscess is
formed incision and drainage is indicated.
Fungal paronychia
Topical and oral anti
fungal medications such as Itraconazole, Ketoconazole or Fluconazole are
effective. These medications should be used for a long period extending
from 3-6 months.
ACTINOMYCOSIS
Actinomycosis is a
chronic bacterial skin infection caused by Actinomyces Israeli,
characterized by suppurative granulomatous lesions with draining sinuses.
CLINICAL FEATURES
The commonest sites
involved are the jaw and to less extent the trunk.
The lesions present with
dusky red, firm, fluctuating swellings with multiple sinuses exuding
yellowish granules known as "sulfur granules" which are
pathogonomonic for Actinomycosis. The underlying jaw shows periosteitis
and even osteomylitis.
Actinomycosis is usually
classified into three main types according to the areas involved.
DIAGNOSIS
Examination of the
granules from the draining sinuses is a characteristic of the disease.
These show lobulated bodies consisting of delicate branching and
intertwining filaments resembling sunrays.
Gram stain of the crushed
sulfur granules will show gram-positive mycelia.
TREATMENT
High doses of penicillin
are effective.
Erythromycin and tetracycline are also
effective medications.
CUTANEOUS DIPHTHERIA
Cutaneous diphtheria is a
skin infection caused by "Corynebacterium Diphtheria." Carriers
have the organism in the throat. The disease occurs in non-immunized
persons with the diphtheria toxoid mainly in the tropical areas or in poor
communities with poor hygiene.
CLINICAL FEATURES
Different clinical
pictures may be seen during the course of the disease:
-
Diphtheric Ulcer -
occur mainly on the extremities but other sites may be involved. It
leaves a scar after healing.
Clinically the ulcer is
shallow, well demarcated with rolled firm borders. There is a brownish
gray or gray membrane covering the ulcer that can be easily removed
leaving a clean surface. Later on a black brownish adherent leathery
sloughs or eschar appears on the ulcer surface. The eschar is removed
with difficulty leaving an unhealthy base.
-
Bulla - this is very
characteristic to cutaneous diphtheria when present. The bulla extends
about 2 cm beyond the ulcer. Repeated formation of bulla on the scar is
an important sign for diagnosis.
-
Anesthesia around
the ulcer, 2-5 weeks after infection. This sign is diagnostic to
diphtheria ulcer. This is due to destruction of cutaneous nerves by
diphtheria bacilli toxins.
-
Non-specific lesions
- sometimes the cutaneous diphtheria lesion is non-specific simulating
skin abrasion, insect bite or eczematous lesion where the lesion can‘t
be easily diagnosed.
DIAGNOSIS
Diagnosis depends on the
following:
TREATMENT
Combination of diphtheria
antitoxin and appropriate antibiotic.
Intramuscular injection
of 20,000-40,000 units of anti toxin.
General measures as good
supportive care, bed rest, immunization of the contacts.
It should be noted that
immunity requires several weeks to develop after the injection of
diphtheria toxoid
RAT BITE FEVER
Rats or other animals
such as cats, or squirrels may cause cutaneous and systemic manifestations
after biting human beings.
Different organisms may
cause different syndromes
Sodoku is a clinical type
caused by Spirillium minus.
Haverhill Fever
Septicemia caused by Sterptobacillus moniliformis due to rat bite or in
some cases due to contaminated milk by the Sterptobacillus moniliformis.
CLINICAL FEATURES
The clinical picture of
Sodoku and Haverhill are the same and differentiation is only by the
different isolated microorganism.
-
The skin lesion is a
wound at the site of biting. After healing of the wound, an inflamed
edematous lesion appears associated by lymphangitis and constitutional
symptoms such as fever, malaise, pain in the joints and relapsing fever.
-
Rose spot macular
eruption develops on the abdomen and spreads to the face. The lesions
enlarge and form purplish red indurated plaques.
DIAGNOSIS
Blood culture or fluid
aspirated from the joints has the characteristic causative organism.
Animal inoculation:
Spirillium minus can be demonstrated.
Blood picture - the disease is
accompanied by leucocytosis and sometimes eosinophilia.
TREATMENT
Penicillin is an
effective antibiotic for treatment of rat bite fever.
Cauterization of the
wound by nitric acid may prevent spread of the disease when this is
applied early after the bite.
CAT SCRATCH DISEASE
Cat scratch disease is
caused by Gram-negative rods, which are part of the normal bacterial flora
of cats, dogs and some other animals.
Most of the patients are
children playing with cats, dogs that are a vector for the organism.
Infection reaches the skin through traumatization of the skin by the cat
scratch or by cat biting.
General manifestations
Fever, malaise and
anorexia are not uncommon following the cat scratch. Central nervous
system involvement. Purpura, thrombocytopenia and eye involvement are rare
complications of the disease.
Skin manifestations
Scratch marks or bite are
apparent at the site of injured skin .A red papule appears after 1-2
weeks. The papule enlarges into a nodule where the draining lymph node
become enlarged, tender, suppurate and are accompanied by lymphangitis.
The lesions usually heal within two weeks leaving no scarring.
DIFFERENTIAL DIAGNOSIS
Cat scratch disease must
be differentiated from infectious mononucleosis, brucellosis, tularemia,
histoplasmosis and sporotrichosis.
TREATMENT
Usually the condition
heals spontaneously.
Antibiotics such as
Cephalosporin, Erythrocin may give good results.
Treatment of suppurating
lymph nodes is by aspiration with a needle and syringe and not by
incision.
DOG BITES
Dogs are perhaps the
most common assailants. They are capable of infecting soft tissue with a
number of organisms that are part of normal oral flora of healthy dogs
,cats and a number of other animals.
The injury varies from
local wound infection to fulminate septicemia.
Clinical Manifestations
Skin lesions include a
localized eschar at the site of the bite and cellulitis.
Non-specific macular or
maculopapular lesions, petechiae, purpura fulminans and symmetrical
peripheral gangrene are the mainfestations.
Septicemia and
disseminated intravascular coagulation may occur in severe cases.
Treatment
Treatment of the
lacerated wound.
Antibiotics: Penicillin,
Cephalosporin, Erythromycin, Tetracycline and Clindamycin are effective
medications .
Examination of the dog
for the possibility of infection with rabies where that needs thorough and
special treatment .
CHANCRIFORM PYODERMA
This is uncommon
infection that affects mainly children.
The etiology is uncertain
but a necrotizing reaction due to a strain of Staph. Aureus, inoculated by
minor trauma, has been suspected.
The lesion is usually
solitary and is often situated around the eyelids, near the mouth, or
occasionally on the genitalia.
CLINICAL FEATURES
Skin lesion presents with
a sharply marginated ulcer, sometimes exceeding 1 cm in diameter, with an
indurated base and a bright red areola that enlarges slowly after a few
days.
The regional lymph nodes are enlarged and
tender.
The ulcer may persist for
several weeks before healing. It leaves a superficial scar.
DIFFERENTIAL DIAGNOSIS
The disease has to be
differentiated from:
Epithelioma, syphilis,
primary tuberculosis, accidental vaccination, swimming-pool granuloma,
leishmaniasis and drug reaction. These are common dermatoses that may
cause confusion in the diagnosis of chancroid pyoderma.
TREATMENT
Antibiotics may improve
the condition.
PYODERMA VEGETANS
Pyoderma vegetans is
characterized by the development of epithelial hyperplasia and chronic
granulomatous changes accompanied by crusting, sinus tract formation and
ulceration.
Etiology
Dermatitis vegetans may
develop in any site but the flexures are often involved. Commonly, either
Staph. Aureus or Group A streptococci are isolated from lesions but as the
rash does not usually respond to antibiotics alone the role of these
bacteria in the pathogenesis of the condition is unclear. Pyoderma
vegetans may accompany ulcerative colitis and lymphomas.
Fig. 48. Pyoderma vegetans |
Fig. 49. Pyoderma
vegetans |
CLINICAL FEATURES
Hyperplastic and crusted
plaques appear on the skin surface. These may break down and weep and
there is often central clearing. When there is a prominent edge with crust
formation, the lesions may mimic blastomycosis. Alternatively, there may
be ulceration; the condition in this case simulates pyoderma gangrenosum.
In pyodermite vegetante,
crusted red plaques containing pustules have been described in multiple
sites of the oral cavity, the flexures and the scalp.
DIAGNOSIS
This is difficult and
largely depends on the exclusion of other conditions such as specific
infections, iododerma, pyoderma gangrenosum and pemphigus vegetans.
It is important to
exclude the underlying diseases such as ulcerative colitis, lymphoma or
leukemia. In doubt, repeated biopsies from the skin lesion may be
necessary.
TREATMENT
Antibiotics may be of no
value in controlling the condition.
Application of
antiseptics.
Topical corticosteroids
appear to produce some response.
Co2 laser skin
resurfacing of the lesion may be considered as one of the new methods of
treatment.
MASTITIS AND BREAST
ABSCESSES
Infection of the breast
is common in the second or third week of life, more often in girls than
boys. It is almost always unilateral.
CLINICAL FEATURES
The affected breast is swollen, red, hot
and tender. Systemic toxicity is usually absent. Fluctuation denotes
abscess formation, which will require surgical drainage.
The development of
long-term breast abscess may be associated with loss of some breast
tissues.
TREATMENT
Hot compresses on the
affected breasts
Proper antibiotics
Incision and drainage
REIER‘S SYNDROME
Reiter‘s disease is a
rare disease of unknown exact cause. Chlamydia and Mycoplasma were
suspected as causative organisms. It affects mainly adult males, although
it may sometimes occur in young children. The disease is characterized by
triad manifestations: Non-gonococcal urethritis, Conjunctivitis and
Arthritis.
CLINICAL FEATURES
The disease is usually
accompanied by skin and systemic manifestations.
Skin manifestations
Skin lesions appear as
small, yellowish vesicles and ulcers. Thick, dry, horny crust may develop
especially on the toes. Detachment of the crust and horny masses leaves a
residual pigmentation. The sites involved are mainly, the hands, feet,
genitalia, and the mucous membranes of the mouth, palate, pharynx, urethra
and conjunctiva. The soles characteristically show heavy crustations and
hyperkeratosis known as keratoderma blenorrhagica.
Systemic manifestations
Urethritis - is
non-bacterial, which manifests with pyuria, and bloody discharge. Symptoms
may be dysuria, stranguary, precipitancy and lower abdominal pain.
Complications such as cystitis , urethral stricture , seminal vesiculitis
and prostatitis may manifest with different signs and symptoms accordingly
.
Conjunctivitis, corneal
ulcer and iritis are other manifestations.
Arthritis - the onset is
a sudden with pain in the heels. It may involve any joint but the knee
joints are the ones commonly involved . The affected joint is swollen,
tender and hot.
Cardiac manifestations:
Endocarditis, myocarditis, pericarditis and aortic insufficiency are rare
manifestations of the syndrome.
Leucocytosis and raised
erythrocytic sedimentation rate are common findings.
DIFFERENTIAL DIAGNOSIS
Histopathology
Epidermis - there is
spongiform vesicopustules, acanthosis, parakeratosis, hyperkeratosis and
elongated intrapapillary processes.
Dermis - shows dilated
vessels and perivascular infiltrate.
TREATMENT
Rest
Special care to the eye.
Corticosteroids -
systemic steroids and topical eye drops.
Antibiotics in the form
of tetracycline may have good effect.
Antirheumatics and care
to the affected joints.
LEPTOSPIROSIS
(Weil‘s disease)
Leptospirosis is a
systemic disease that is caused by the strains of the genus Leptospira.
Modes of Infection
- Infected animals such as cats, dogs
and rodents.
-
Drinking or swimming
on infected water.
-
Direct infection from
humans that may have acquired the disease, accidentally from the urine or
tissues of infected animals.
-
Indirect infection
from contaminated soil with the organism.
CLINICAL MANIFESTATIONS
Systemic manifestations:
Sudden chills and high
fever.
Severe jaundice.
Hemorrhagic tendency,
hematuria and proteinuria.
Skin manifestations
Petechiae and purpura
appear on the skin and mucous membranes.
Severe conjunctivitis.
DIAGNOSIS
Blood picture
Severe leucopenia
Azotaemia
Blood culture: Detection
of the organism.
Rising of the antibodies
begin in the second week.
Urinalysis shows
hematuria and proteinuria.
TREATMENT
Symptomatic
Antibiotics such as
Tetracycline and Chloramphenicol may be of value in the adult age.
Children may be given
erythromycin or zithromax
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