IMPETIGO AMPOLLOSO EN NIOS PDF

El impétigo, una de las afecciones de la piel más comunes entre los niños. El impétigo no ampolloso comienza como pequeñas ampollas que se revientan y. Impétigo ampolloso Niños pequeños Siempre causado por S. aureus Por acción de una toxina epidermolítica Ampollas superficiales de. ABSTRACT. Impetigo is a common cutaneous infection that is especially prevalent in children. Historically, impetigo is caused by either group A β- hemolytic.

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Impetigo is a common cutaneous infection that is especially prevalent in children. Currently, the most frequently isolated pathogen is S. Topical agents for impetigo therapy are reviewed. Anti-Bacterial agents; Impetigo; Staphylococcus aureus ; Streptococcus pyogenes.

Normal skin is colonized by large numbers of bacteria that live as commensals in its surface or in hair follicles. Sometimes, the overgrowth of these bacteria causes skin diseases, and in other occasions, bacteria that are normally found on the skin can colonize it and cause diseases. Recent genetic studies have shown a large quantity of Pseudomonas spp. Biofilms are complex and sessile aggregates comprising one or more bacterial species associated with an extracellular polymeric substance.

Bacteria in biofilms are 50 to times more resistant to antibiotics than bacteria in plankton organisms that have little or no ability to move. Besides inducing antibiotic tolerance, biofilms can increase bacterial virulence. Host factors, such as integrity of the skin barrier with its acidic pH, presence of sebaceous secretion fatty acids, particularly oleic acidlysozyme and production of defensins and adequate nutritional status, play an important role in resistance to infection.

The act of handwashing, with antiseptic soap or even regular soap, especially amongst children caretakers, severely decreased their chance of acquiring infections such as pneumonia, diarrhea and impetigo. Lancefield classification of streptococci is based on the cell wall’s C carbohydrate antigens, going from A to T.

Various streptococci may be commensals on the skin, mucous membranes, and gastrointestinal tract. The isolation of streptococci of groups other than A can mean a secondary infection of preexisting lesions or colonization on cutaneous surface. Group A streptococci can be subdivided into several serotypes, according to their M protein antigenicity.

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Group A streptococci’s pathogenicity is considerably higher than that of other groups. These are germs with invasive potential, which can reach several tissular planes, such as the epidermis impetigodermis ecthyma or deeper subcutaneous tissue cellulite. The discovery of these agents in the skin of healthy children precedes the appearance of lesions in about 10 days and they can be isolated from the oropharynx between 14 and 20 days after appearing on the skin.

Thus, their path goes from normal skin to injured skin and may subsequently reach the oropharynx. Several decades of epidemiological studies indicate that there are some strains of group A streptococci that elicit oropharyngeal infections, but rarely cause impetigo. On the other hand, there is a distinct group of strains that cause cutaneous infection but that do not affect the throat. Rheumatic fever can be a complication of streptococcal pharyngitis or tonsillitis, but it does not occur after skin infections.

El impétigo

Rather, glomerulonephritis may result from streptococcal cutaneous or upper respiratory tract infections, but the skin is the main previous site. Treatment of impetigo does not reduce the risk of glomerulonephritis, but it reduces the dissemination of nephritogenic strains in the population. Beta-hemolytic streptococcus group A is not commonly observed before two years of age, but there is a progressive increase in older children.

Streptococci can be retrieved by culture of oropharynx or skin lesion materials. Dosage of antistreptolysin O may not be useful for cutaneous infections since its titles do not increase satisfactorily. For skin diseases, serological im;etigo B test, useful to demonstrate a previous streptococcal infection group A streptococcuscan be performed. A crucial factor to niios infection virulence is the ability of these bacteria to produce circulating toxins that act as superantigens.

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This response may lead to the formation of exfoliative cutaneous eruption, vomiting, hypotension and shock.

Bullous impetigo and scalded skin syndrome, caused by staphylococcal toxins and toxic shock syndrome, caused by staphylococcal or streptococcal toxins are examples of toxin-mediated diseases. Coagulase negative staphylococci are the most common organisms on the impftigo skin flora, with about 18 different species, and Staphylococcus epidermidis being the most common of the resident staphylococci.

The path would be from the nares or perineum to normal skin, and later to injured skin. Host factors seem to determine the onset of disease. Immunosuppression and amolloso damage are considered important in the pathological process genesis, since the ability to produce coagulase, leukocidin and toxin appears to be the same in the carrier’s normal flora and in imperigo isolated from cutaneous lesions.

Staphylococci are transmitted primarily by hand, particularly in hospital settings. Staphylococcal infections are present in all age groups. Bullous impetigo is almost universally caused by a single organism, S. Other phage types involved are 3A, 3C and Toxins are een greatest virulence factor of S.

Blisters are localized in bullous impetigo and disseminated in scalded skin syndrome. There are at least two different types of exfoliative toxins, so that exfoliative toxin A relates to bullous impetigo and toxin B with scalded skin syndrome. Scalded skin syndrome usually begins after a localized infection on the conjunctiva, ej, navel or perioral region and more rarely after pneumonia, endocarditis and arthritis. Bullous impetigo starts with smaller vesicles, which become flaccid blisters, measuring up to 2 cm in diameter, initially with clear content that later becomes purulent Figure 1.

The roof of the blister ruptures easily, revealing an erythematous, shiny and wet basis. The remainder of the roof can be seen as a collarette at the periphery and the confluence of lesions promotes the appearance of polycyclic figures Figures 2 and 3. Bullous impetjgo occurs most commonly in intertriginous regions such as the diaper area, axillae and neck, although any cutaneous area can be affected, including palms and soles Figures 1 and 2.

It is particularly important in the neonatal period, starting usually after the second week of life, although it can be present at birth in case of premature membranes rupture. Bullous impetigo is most common among children aged two to five years. Bullous impetigo in the genital area – intact and flaccid pustules, exulcerations and scaling in collarette. Bullous impetigo —desquamation collarette and flaccid blisters. Bullous impetigo in diaper area.

It occurs in adults and children but rarely in those under two years of age. The main etiological agent has varied over time. In studies conducted over the past three decades, there has been a resurgence of S.

Although we have not found any Brazilian studies conducted in recent decades regarding the epidemiology of impetigo, these data are corroborated in studies conducted in different countries, such as United States, Israel, Thailand, Guyana, India, Chile, and Japan. Crusted impetigo can occur in normal skin or impetiginisation may appear over a nips dermatosis such as atopic dermatitis, contact dermatitis, insect bites, pediculosis and scabies.

Malnutrition and poor hygiene are predisposing factors. The initial lesion is a vesicle, located on an erythematous base, which iseasily ruptured. The resulting superficial ulceration is covered with purulent discharge that dries as an adhering and yellowish honey-colored crust.

Each lesion measures 1 to 2 cm in diameter and grows centrifugally Figure 4. The discovery of satellite lesions, caused by self-inoculation, is frequent. There is a predominance of lesions in exposed areas, especially in the limbs and face Figures 5 and 6. Regional lymphadenopathy is common and fever can occur in severe cases.

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Crusted impetigo—vesicles, honey-colored and hematic crusts. Crusted impetigo located on the arm. Crusted impetigo non-bullous on the face.

These enzymes hydrolyze the beta lactam ring, and they are, so far, the main mechanism of resistance to betalactam antibiotics. Cases of infections caused by MRSA in the community were reported in the 80’s, but the importance of this group has increased significantly in recent years.

The presence of MRSA as impetigo’s causative agent in non-hospitalized patients is considered unusual and with heterogeneous distribution. Staphylococcal impetigo is usually caused by S.

Staphylococci that possess PVL gene cause suppurative cutaneous infections such as abscesses and furuncles. Therefore, concern about MRSA in community-acquired infections, should be greater in the presence of furuncles and abscesses and smaller in impetigo.

In patients with impetigo, lesions should be kept clean, washed with soap and warm water and secretions and crusts should be removed. Common soaps or those containing antiseptic substances such as triclosan, chlorhexidine and povidone iodine, may be used.

In the impetigo treatment review performed by the Cochrane Database of Systematic Reviews, the authors report a relative lack of data on the efficacy of topical antiseptics. On the other hand their use is not discouraged, because they do not seem to increase bacterial resistance. Topical antibiotics are the treatment of choice for most cases of impetigo. The spectrum of the selected antibiotic must cover staphylococci and streptococci, both for bullous impetigo as well as for crusted impetigo.

Thus, benzathine penicillin or those sensitive to penicillinases are not indicated in the treatment of impetigo. The first-generation cephalosporins, such as cephalexin and cefadroxil, may be used, since no differences between them was found in a metaanalysis.

Impetjgo, being less expensive, can become the antibiotic of choice for the most impoverished populations. One should take into account the possibility of resistance to S. Other macrolides such as clarithromycin, roxithromycin and azithromycin have the advantage of presenting fewer side effects in the gastrointestinal tract, as well as a more comfortable posology, although with a higher cost. Staphylococcal strains that are resistant to erythromycin will also be resistant to clarithromycin, roxithromycin and azithromycin.

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The amoxicillin associated with clavulanic acid is the combination of one penicillin with a beta-lactamase inhibiting agent clavulanic acidthus enabling adequate coverage for streptococci and staphylococci. There is strong evidence on the superiority, or at least the equivalence, of topical antibiotics compared to oral antibiotics in the treatment of localized impetigo.

In addition, oral antibiotics have more side effects than topical antibiotics. Mupirocin and fusidic acid are the first choice options. In meta-analyses publications, no difference between these two agents was demonstrated. Fusidic acid ampplloso highly effective against S.

It is also effective, to a lesser extent, against Streptococcus and Propionibacterium acnes.

Gram-negative bacilli are resistant to fusidic acid. Resistance, in vitro and in vivo, to fusidic acid has been verified but at low levels. The incidence of allergic reactions is low and cross-allergy has not been seen. This antibiotic is not marketed in the United States. Mupirocin pseudomonic acid A is the major metabolite of Pseudomonas fluorescens fermentation. Mupirocin acts by inhibiting bacterial protein synthesis, by binding with isoleucyl-tRNA synthetase enzyme, thus preventing the incorporation of isoleucine into protein chains.