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Provoking factors:
1. Disturbances of integrity of integument as fracture, lesion, change T’ ,sharp trauma etc
2. Emotional stress & insolation & ↓ T’
3. Trauma of field / bruises with erysipelas ( Intercurrent dis angina, bronchitis etc.)
Contribution factors:
1. Concommitant diseases:
- DM, obesity, chronic venous failure (varicose dis of veins), chronic failure of absorbent vessels
(lymphostasis), eczema, psoriasis & other skin diseases (mycosis of the auto- podium)
2. Presence of the locuses of chronic streptococci inf contamination (tonsillitis, otitis, sinusitis,
karies, paradontitis) -> lead to oftenly to erysipelas of the foot, osteomyelitis, trophic ulcer etc.
3. Profesion trauma (bone trauma) with increasing of contamination of integument with________
(sportsman,drivers etc)
4. Chronic somatopathy with immunodeficiency (in advance ages)
5. End stage of pathogeny of erysipelas
- Erythematic
- Erythematic – bullous
- Erythematic – hemorrhagic
- Bullous – hemorrhagic
- Primary
- Repeated (arising in 2 years, other localization of process)
- Relapsing (at presence not less than 3 relapses of an erysipelas for a year expediently
determining “often relasing erysipelas” )
- Localized erysipelas
- Abundance erysipelas
- Metastatic erysipelas with the advent of remote from each other the locuses of an inflammation
5. Complications of an erysipelas:
6. Consequences erysipelas:
Pathogenesis of Erysipelas:
- Introduction of a streptococcus in a skin as a result of its damage (at a primary erysipelas) or by
a becoming infected from the locus of a dosing infection contamination can descend & is
immediate from the locus of independent disease of a streptococcal etiology (a pharyngitis,
sinusitis, otitis etc.)
- Breeding of streptococcus in lymphatic capillary vessel dermas
- Development bacteriemia, toxemias, that leads to originating symptoms to an intoxication (the
acute beginning of disease from rise in temperature, a cold fit,delicacy etc)
- Development of the aboriginal locus of an infectious – allergic inflammation of a skin with
participation of immune- complex process (are formed perivascular) the located cell – bound
immune complexes containing C-3 fraction of a complement).
- Disturbance capillary flows of lymph in a skin & microcirculation with formation of a
lymphostasis, possible formation of hemorrhages & bladders with serous & hemorrhagic
contents.
- Formation of the locuses of a chronic streptococcal infection contamination in a skin & partial
lymphonduses with presence of bacterial & L –forms of a streptococcu that leads at a part of
patients in development of relapse of disease (chronic course of erysipelas)
- Elimination of bacterial forms of a streptococcus by means of an engulment & formation of cell-
bound immune complexes both other immune mechanism & convalescence of the patient.
Indications for obligatory hospitalization in infectious diseases hospitals
(abjointings) are:
- Serious current of an erysipelas with sharply expressed intoxication or the widespread lesion of
a skin (especially at bullous – hemorrhagic to the form of an erysipelas)
- Frequent relapses of an erysipelas, irrespective of a degree of an intoxication, character of
aboriginal process
- Presence of serious general concomitant diseases
- Senile children’s age of patients
Incubation period:-
- From several hour till 3 – 5 days. At patients with relapsing course of the erysipelas,
development of the next attack of disease is preceded often with a frigorism, stress. At the
depressing majority o patients disease begins was acutely.
- Comes in terms from several hours till 1- 2 days after the first exhibiting disease. Reach the
maximum general – toxic exhibiting & a fever. There are characteristic aboriginal exhibiting an
erysipelas.
- More often inflammatory process is localized on the lower extremities (60 -70%), less often on
the face (20 -30%) and the top extremities ( 4 -7%), is rare only on a trunk, in the field of
mammary gland, perineum, outside of reproductive organs.
- From the beginning of the treatment and uncomplicated character of an erysipelas the fever
usually does not exceed 5 day. At 10 -15% of patients the fever is keptover 7days that is
observed usually at the widespread process & not enough a high grade causal treatment.
- The longest feverish period at bullous – hemorrhagic to the erysipelas. From above, 70% that
sizk of erysipelas, it is marked a lymphadenitis educing at all forms of disease.
The period of reconvalescence:-
*Infectious – allergic and immunocomplex mechanisms of the inflammation at the erysipelas cause its
serous- hemorrhagic character. Apposition of a purulent inflame testifies to the complicated disease.
Differential diagnosis:
- erysipelas should be compared with more than with 5 -10 diseases, concerning clinical features
of surgical, dermal and contagious and intrinsic diseases.
- First of all,we need t exclude abscess, phlegmon, supurative hematom, thrombophlebitis
(phlebitis), dermatitis,eczema, surrounding erysipeloid, a nodulose erythema.
Treatment of an erysipelas:
Treatment in hospital ;
- a preparation of choice – is Benzylpenicilin daily dose 6 -12 million U, IM for 10 days
- reserve preparation is cephalosporin I generation (Cefazolinum etc.) – in a daily dose 1,2 – 2,4 g
and more,IM) are appointed at the serious omplicated course of erysipelas
- In the serious course of disease, development of complications (an abscess, phlegmon etc) the
combination Benzylpenicillin (in the specified dosage) & gentamycin (240 mg – once daily,IM).
- Penicillin (in the specified dosage) & ciprofloxacin (400 – 800 mg IV drip)
- Penicillin & clindamycin (in specified dosages)
- Purpose of the combined antibacterial therapy is justified & at bullous hemorrhage of erysipelas
with an abundant exudates of fibrin.
- Disintoxication therapy (if necessary IV) , with use of diuretic & cardiovascular preparations
- Anti inflammatory therapy (Indomethacin, Butadionum, Aspirinum etc) – precaution to DM pt
- Desensitization therapy (under indication) – anti allergic (Suprastin etc)
- Apply bandages with 0,02% furosilinum / 0,1% solution of Rivanolum, shanging them sometimes
within day (erythematic erysipelas carrying out of aboriginal therapy is not required)
(IV) Physiotherapy:
- Use ultraviolet radiation on range of the locus of an inflammation & an electric current of
ultrahigh frequency on range regional lymph nodes
- Conservation in the period of a reconvalescence of an infiltration of a skin, hydropic syndrome,
regional a lymphadenitis are appointed an ozocerite or a bandage with warm taftaleneum
ointment (to the lower extremities), paraffin (on the face), electrophoresis of lydasum
(especially in initial stages of formation of an elephantitis), sodium chloridum of calcium, radon
baths, a magneto therapy
- Last year high efficacy low-energy laserotherapy in treatment of an thermal inflammatory
syndrome is established at varius clinical forms of an erysipelas.
- Laser radiance,as in red, and in infra-red range is used.
1st course:
2nd course:
- Lincomycin (30% a solution -2,0 ml – 3x /day, IM) or 0,5g 3x/day perorally for 7 – 10 days
Sequela M-Types
Acute rheumatic fever 1, 3, 5,6, 18
Glomerulonephritis
Postpharyngeal 1-4, 12, 15
Postpyoderma 49, 52, 55, 59, 60, 61
Streptococcal toxic shock syndrome 1, 3 predominantly; severa others
2. Systemic
Scarlet fever Is caused by production of erythrogenic toxin by a few strains of the organism.
2 of the most severe, but least common, forms of invasive GAS disease are called
“necrotizing fasciitis” and “streptococcal toxic shock syndrome” (STSS)
- Some of the antibodies produced during the above infections cross-react with certain host
tissues. These can indirectly damage host tissues even after the organisms have been cleared
and cause non-supurative complications
Rheumatic fever M protein cross reacts with sarcolemma Antibodies cross reacts with heart
tiua, fix complement and cause damage
Glomerulonephritis Antigen-Antibody complexes may be deposited in kidney, fix complement,
and damage glomeruli. Only a few M-types are nephritogenic.
Impetigo:
- Is an initially vesicular, later crusted, superficial inf of the skin.. Most cases occur in children.
Histopathologically, impetigo consists of a superficial intra epidermal, unilocular vesicopustule.
- In epidemiological studies, group A streptococcal acquisition on normal skin antedates the
appearances of impetigo by about 10 days.
- During that time,minor trauma (eg:insect bite,abrasion) predisposes to the development of
infected lesions.
- Impetigo is most common during hot, humid summer weather. 2 -3 weeks after skin acquisition
of streptococci, pharyngeal colonization by the same organism occurs in about 30% of children
with skin lesions.
- The sporadic cases of the facial impetigo occur in colder climates probably result from
contagious spread from an initial nasopharyngeal infection, and the serotypes involved are
those commonly causing pharyngeal disease.
- In contrast, in the case of staphylococcal impetigo,(in case of only S. aureus is the pathogen),
nasal colonization precedes that of the normal skin; skin lesions then occur after such
colonization.
Classification of Bacterial superficial infections of the skin
- Erysipelas involves the more superficial layers of the skin & cutaneous lymphatic, whereas
cellulitis extens more deeply into the subcutaneous tissues.
- This anatomical distinction is the basis for the clinical differentiation of the 2 entities.
- In typical erysipelas, the area of inflammation is raised above the surrounding skin, and there is
a distinct demarcation between involved & normal skin. In cellulitis, neither of these clear
distinction between infected nor not infected one is present.
A) a normally sterile site (eg: blood,CSF, pleural fluid or peritoneal fluid, tissue biopsy, surgical
wound etc.)
B) a non sterile site (eg: throat, sputum, vagina, superficial skin lesion etc)
i) Renal impairment: creatinine ≥ 177 µM for adults or ≥ 2 of the upper limit of normal age. N
patients with pre-existing renal disease, in ≥ 2-fold elevation over the baseline level.
ii) Coagulopathy: platelets ≤ 100 x 109 /L or disseminated intravascular coagulation defined by
prolonged clotting times, low fibrinogen level and the presence of fibrin degradation
products
iii) Liver involvement: alanine aminotransferase, aspartate aminotransferase or total bilirubin
levels ≥2 x the upper limit of normal age. In patients with preexisting liver disease, a ≥ 2-fold
elevation over the baseline level
iv) Adult resp distress syndrome defined by acue onset of diffuse pulmonary infiltrates &
hypoxemia in the absence of cardiac failure or evidence of diffuse capillary leak manifested
by acute onset of generalized edema or pleural or peritoneal effusions with
hypoalbuminemia
v) A generalized erytematous macular rash that may desquamate
vi) Soft tissue necrosis, including necrotizing fasciitis or myositis or gangrene
An illness fulfilling criteria IA and II (A and B) is defined as definitive case. An illness fulfilling criteria IB
and II (A and B) is defined as a probable case if no other etiology for the disease is identified.