ERYSIPELAS. ERYSIPELOID

ERYSIPELAS

Erysipelas is an acute inflamation of the skin,with marked involvement of cutaneus lymphatic vessels.

Etiology

Erysipelas is almost always caused by group A streptococci (sometimes by group C or G). Group  streptococci cause erysipelas of newborn children.

Epidemiology

Erysipelas is common disease of infants, children of early age, and old people. Formerly, the face was often involved, and antecedent streptococcal respiratory tract infection preceded cutaneous involvement in about one-third of patients, even though streptococci might not be found on culture when skin lesions became evident.

Pathogenesis

Most interest is focused on streptococcal pyrogenic exotoxins (SPEs). In edition to mediating the scarlatinal rush, SPE exibit a variety of adverse biologic effects, including the multiorgan damage and lethal shock. There is an amino acid homology of 50 % and immunologic reactivity between SPE A and staphylococcal enterotoxins  and C. SPE of group A streptococcus is a superantigen and it is a potent inducer of tumor necrosis factor.

The antistreptolysin Πresponse after cutaneous streptococcal infection is weak. There is experimental evidence to suggest that this may be due to local inactivation of streptolysin Πby skin lipids. The immune response to antiDNase  is brisk, and antihyaluronidase reactivity is also a useful test in the serodiagnosis of erysipelas.

Clinical manifestations

Now the localization of erysipelas has changed: 70-80 % of the lesions are on the lower extremities and 5-20 % are on the face. Entry gates are commonly skin ulcers, local trauma or abrasions, psoriatic or eczematous lesions, fungal infections; in the neonate,erysipelas may develop from infection of the umbilical stump. Predisposing factors include venous stasis, paraparesis, diabetes mellitus, and alcohol addiction. Patients with the nephrotic syndrome are particularly susceptible. Erysipelas tends to occur in areas of preexisting lymphatic obstruction or edema (e.g. after radical mastectomy). Also, because erysipelas itself produces

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lymphatic obstruction, it tends to recur in an area of earlier infection. Over a 3-year period, the recurrence rate is about 30 %, predominantly in individuals with venous insufficiency or lymphedema.

Streptococcal bacteremia occurs in about 5 % of patients with erysipelas; group A, C, or G streptococci can be isolated on throat culture from about 20 % of cases.

Erysipelas is a painful lesion with a bright red,edematous,indurated ("peau d'orange") appearance and an advancing, raised border that is sharply demarcated from the adjacent normal skin. Fever is a feature. A common form of erysipelas involves the bridge of the nose and the cheeks (Fig. 10). Uncomplicated erysipelas remains confined primarily to the lymphatics and the dermis. Occasionally, the infection extends more deeply, producing cellulitis, subcutaneous abscess, and necrotizing fasciitis.

Leukocytosis is common sign of erysipelas. Group A streptococci usually cannot be cultured from the surface of the skin lesion, and only rarely they can be isolated from tissue fluid aspirated from the advancing edge of the lesion. In cases of erysipelas complicating infected ulcers,group A streptococci have been isolated from the ulcerated area in 30 % of patients.

Complications

Bacteremic spread of the streptococci may result in a variety of metastatic

foci of infection, for example, suppurative arthritis, endocarditis, meningitis or

brain abscess, osteomyelitis, liver abscess, and so forth. The local complications

are abscess and streptococcal cellulitis, skin necrosis and ulcers, thrombophlebitis,

otitis and others. Suppurative lymphadenitis may also occur.

.. . Diagnosis

Diagnosis is usually easy due to characteristic manifestatioms of erysipelas. It is difficult to isolate culture of erysipelas infectious agent from the lesion,but it may occasionally be cultured from the blood.

Differential diagnosis

The diagnosis is made on the basis of characteristic manifestatioms of the lesion and the clinical setting. Early herpes zoster involving the second division of the fifth cranial nerve may resemble unilateral facial erysipelas but can be distinguished by the pain and hyperesthesia preceding the skin lesions. Occasionally contact dermatitis or giant urticaria may look like erysipelas but can be distinguished by the absence of fever and the presence of pruritus. Lesions closely resembling erysipelas, but apparently not due to streptococcal infection, may occur recurrently in patients with familial Mediterranean fever. Diffuse inflammatory carcinoma of the breast may mimic a low-grade erysipelas. Erythema chronicum migrans, the cutaneous lesion of Lyme disease, resembles

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erysipelas but is not painful and progresses much more slowly,and the associated fever is less marked. An erysipelas-like skin lesion has occurred in several patients with hypogammaglobulinemia and Campylobacter jejuni bacteremia.

Treatment

Treatment is carried out according to the clinical form and gravity of disease. Antibiotics of penicillinic lines are effective. In case of initial and repeated erysipelas benzylpenicillin has to be given during 7-10 days. At serious course, complications, rapid local inflammatory changes, enlarge daily dose of preparation up to 8 - 12 million units. Among semisynthetic penicillines, ampicillin, oxacillin, amoxacillin (bactox, ospamox) are considered effective. At serious course of disease, development of a sepsis one have to use a combination of two antibiotics, for example ampicillin and gentamicin. For treatment of frequently relapsing erysipelas one should apply ampicillin, ampiox, amoxyclav, oletetrin, lincomicin, cefaloridin, cefazolin (kefzol), cefotaxim (claforan), at intolerance of antibiotics -furazolidon, bactrim. Course of treatment is 8 -10 days. If the residual phenomena of disease are keeping, after 7-10 days one should indicate repeated course of treatment by other antibiotic. Indicate fluoroquinolones - ofloxacin, ciprofloxacin (ciprobai, ciprobid) etc.

Patients with the mild form of erysipelas can be treated ambulatory,using bactrim, furazolidon, furagin, chingamin (delagil) in average therapeutic doses during 10 days.

At presence of expressed infiltration and pain syndrome indicate non steroid anti-inflammatory preparations - indomethacin, mefanamic acid, paracetamol. Indication of immunostimulators is proved - prodigiosan, sodii nucleinat, splenin, methyluracil. The best results is reached in case of the combination of 2 - 3 imunostimulatores. Course of treatment is 10 days.

The patients with frequently relapsing erysipelas and the phenomena of lymphostasis should administer, besides antibiotic therapy, prednisolon in tablets 0.005 gm - 20-30 mg per day with a gradual dose decline or its analogue.

It is expedient to apply preparations which reduce a permeability of capillaries - rutin in tablets 0.02 gm, ascorutin in tablets, an ascorbic acid in tablets 0.05 gm, calcii gluconat in tablets 0.5 gm, vitamin preparations of  group, retinoli acetat and also desensitizing agents - dimedrol in tablets 0.05 gm, suprastin in tablets 0.025 gm, tavegil in tablets 0.001 gm, diazolin in tablets 0.05 gm.

The patients with serious form of erysipelas and expressed intoxication are given reopoliglycin, 5 % solution of glucose with addition of corglykon, cocarboxylase, ascorbic acid, diuretic preparations - furosemid, etacrin acid, spironolacton (veroshpiron) are also indicated.

At bullous form large bubbles should be cut off and use bandage with solution of aethacridin, 0.02 % solution of furacilin or ectericid with chlorophylypt, juice of calanhoe - fifty-fifty with 0.5 % solution of novocain.

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If purulent-septic process appeares, phlegmon is formed, applications with 30 % a solution of dimexidum with the dissolved antibiotic in a single dose 5000 units of heparinum in every 12 hours during 4-5 days are locally applied. The same antibiotics are infused parenterally. Unguentai bandages at local purulent processes are contrindicated.

Local treatment is combined with indication of physiotherapeutic procedures: in acute period ultra violet radiation and photoradiotherapy, during reconvalescence period - inductothermy, electroforesis of potassii iodidi, calcii chloridi, lydasi; ozocerit or parafin, radon baths.

After transferred initial, repeated and seldom relapsing erysipelas at presence of the residual phenomena give bicillin-5 (in bottles 1,500,000 units): in muscle in every 4 weeks during 3-4 months. The patients with often and repeated relapses are treated. Bicillin-5 is infused monthly during 2-3 years. Necessity of repeated injections with bicillin-5, it is expedient for checking with the help of thermal imager researches. Paralelly with bicilinoprofilaxis stimulators of immune system - methyluracil, prodigiosan, natrii nucleinici, fortifying treatment -polyvitamines, eleuterococ extract, tinctura araliae, pantocrin etc are indicated. The sanitation of chronic streptococcal infection, mycosis is indicated.

Prophylaxis

Adherense to good regimens of personal hygiene, with special attention to frequent scrubbing with soap and water, is the most effective preventive measure currently available. The in time treatment of streptococcal pharyngitis is of much importance.

ERYSIPELOID

Erysipeloid is an acute, but slowly ewolwing, skin infection.

Historic reference

First isolated from mice by Robert Koch in 1878 and from swine by Louis Pasteur in 1882,it was established as the etiologic agent of swine erysipelas in 1886 by Loeffler and as a human pathogen in 1909 when Rosenbach isolated it from a patient with localized cutaneous lesions. Rosenbach coined the term "erysipeloid" to avoid confusion with "erysipelas", a superficial cellulitis with prominent lymphatic involvement that is almost always caused by group A streptococci.

Etiology

Erysipelothrix rhusiopathiae is a straight or slightly curved aerobic or facultatively anaerobic bacillary organism; it is 0.2-0.4 mm diameter and 0.8-2.5 mm in length. It is gram-positive but may appear gram-negative because it "decolorize" readily. Organisms may be arranged singly, in short chains, in pairs in a "V" configuration or grouped randomly. Nonbranching filaments that can

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be greater than 60 mm in length are sometimes seen. There is a dual colonial and microscopic appearance that varies with the medium, pH and temperature of incubation. After growing for 24 hours at 37 °Ñ, colonies are small and transparent with a smooth glistening surface.

Erysipelothrix rhusiopathiae is sometimes confused with other gram-positive bacilli, in particular with Listeria monocytogenes, Actinomyces (Corynebacterium) pyogenes, and Arcanobacterium (Corynebacterium) haemolyticum, but these three species are p-hemolytic on blood agar and do not produce hydrogen sulfide in the butt on TSI agar slants. Furthermore, L. monocytogenes is catalase-positive and motile.

Epidemiology

Erysipelothrix rhusiopathiae is found worldwide. It has been reported as a commensal or a pathogen in a wide variety vertebrate and invertebrate species, but the major reservoir believed to be domestic swine. It doe» not appear to cause disease in fish but can persist for long periods of time in the mucoid • exterior slime of these animals. It may live long enough in soil to cause infection weeks or months after initial contamination. The greatest commercial impact of E. rhusiopathiae infection is due to disease in swine, but infection of turkeys, ducks, and sheep is also important. The organism is communicable from animals to human by direct cutaneous contact. The risk of human infection with Erysipelothrix is related to the opportunity for exposure to the organism, and hence, most human cases are related to occupational exposure. Although infection with Erysipelothrix has been associated with a wide variety of occupations, those at greatest risk include, fisherman, fish handlers, butchers, slaughterhouse workers, veterinarians, and housewives. Infection is especially common among individuals who handle fish. "Whale finger" is erysipeloid seen in those who sustain cuts to their fingers and hands while engaged in whaling. Human-to-human transmission of infection has not been mentioned.

Pathogenesis

Abrasions or puncture wounds of the skin probably serve as the portal of entry of E. rhusiopathiae in most cases of infection in humans and in other animals. Erysipelothrix rhusiopathiae produces a neuraminidase and a hyaluronidase. The activity of these enzymes may correlate with virulence. The neuraminidase may have a role in the pathogenesis of arteritis and thrombocytopenia in an experimental rat model of Erysipelothrix infection. The rhomboidal skin lesions seen in swine are the result of thrombotic vasculitis of end arterioles.

Clinical manifestations

Three clinical categories of human disease have described: (1) erysipeloid, a localized skin lesion, (2) a diffuse cutaneous eruption with systemic symptoms, and (3) bacteremia, which is often associated with endocarditis.

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The localized'cutaneous form or "erysipeloid of Rosenbach", a subacute cellulitis, is the most common type of infection seen in humans. It is a cellulitis. Because the organism is acquired through contact with infected animals,fish,or their products, with organisms gaining entrance via cuts or abrasions on the skin, most lesions are on the fingers. Following an incubation period of 2-7 days, pain (which is often severe and described as burning, itching or throbbing) and swelling of the involved digit or part of the hand develop. The lesion is well-defined, slightly raised, and violaceous in color. As it spreads peripherally, the central area fades. Vesiculation may occur. Regional lymphadenopathy and lymphangitis occur in approximately one-third of cases. There may be arthritis of an adjacent joint. Systemic symptoms are uncommon. Part of patients have low-grade fever and arthralgias. Erysipeloid can be distinguished clinically from staphylococcal or streptococcal cellulitis by the absence of suppuration, the lack of pitting edema, the violaceous color, and the disproportionate pain. Because pathogens are located only in deeper layers of the skin in cases of erysipeloid, aspirates or biopsy specimens should be of the entire thickness of the dermis and from the periphery of the lesion to maximize the chance of recovery of the organism. Erysipeloid usually resolves without treatment within 3 or 4 weeks.

The diffuse cutaneous form, which is rare, occurs when the violaceous cutaneous lesion progresses proximally from the site of inoculation or appears at remote areas. Lesions may appear urticarial with the rhomboid pattern characteristic of swine erysipelas. Fever and arthralgias are common. Blood cultures are negative. The course is more protracted than in the localized form and recurrence is common.

Systemic infection with E. rhusiopathiae is unusual. In approximately 60 % of patients, E. rhusiopathiae endocarditis developed on previously normal heart valves. In patients with bacteremia and/ or endocarditis, routine blood culture techniques are adequate for recovery of the organism.

Complications

Complications of Erysipelothrix endocarditis include congestive heart failure, myocardial abscess, aortic valve perforation, meningitis, and glomerulonephritis.

Bacteremia without endocarditis has been reported with increasing frequency. It has occurred primarily in immunocompromised hosts. Brain abscess, osteomyelitis, and chronic arthritis have also been reported.

Diagnosis

Definitive diagnosis of infection with Erysipelothrix requires isolation of the organism from a biopsy specimen or blood. There are no reliable serologic tests for the diagnosis of infection in humans.

Differential diagnosis

Erysipeloid must be differentiated from erysipelas, arm of hand herpes zoster, contact dermatitis and angioneurotic edema.

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Treatment

Susceptibility data for E. rhusiopathiae are limited. Most strains are highly susceptible to penicillins, cephalosporins, clindamycin, imipenem,and ciprofloxacin. Penicillin and imipenem are the most active agents in vitro. Susceptibility to chloramphenicol, erythromycin, and tetracycline is variable. Most strains are resistant to vancomycin, sulfonamides, trimethoprim-sulfamethoxazole, novobiocin, teicoplanin, and aminoglycosides. Resistance to vancomycin is important because this agent is often used empirically to treat bacteremia due to gram-positive organisms. Use of fluoroquinolones maybe considered inErysipelothrix infections when b-lactams are contraindicated. In cases of endocarditis, the duration of intravenous antibiotic therapy should be 4-6 weeks, although shorter courses (2 weeks of intravenous therapy followed by 2-4 weeks of oral therapy) have been successful. Although erysipeloid usually resolves spontaneously, healing is hastened by antibiotic therapy.

Prophylaxis

Prevention of infection for those in high-risk occupations depends on the use of protective attire such as gloves. Unprotected direct contact with animal body tissues and secretions should be avoided. There are live attenuated vaccines available for veterinary use. Use of vaccination along with other measures such as improved waste disposal has helped to control swine erysipelas.

Control questions:

1. Etiology, epidemiology and incidence of erysipelas and erysipelotrix.

2. Pathogenesis of erysipelas and erysipelotrix.

3. Clinical manifestations of erysipelas and erysipelotrix.

4. Laboratory methods of diagnosis.

5. Criteria of diagnosis.

6. Differential diagnosis of erysipelas and erysipelotrix.

7. Treatment of erysipelas and erysipelotrix.

8. Prophylaxis of erysipelas and erysipelotrix.

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Date: 2014-12-21; view: 1500