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Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
The exfoliative toxins are also known as epidermolytic toxins, epidermolysins, and exfoliatins. Production of exfoliative toxin occurs in 5% of all S. aureus strains [160–162]. The two main exfoliative toxins are exfoliative toxin A (ETA) and exfoliative toxin B (ETB) [160,163,164]. Bullous impetigo (also known as bullous varicella or measles pemphigoid) presents with a few localized, fragile, superficial blisters that are filled with colorless, purulent fluid [165]. The lesions re-epithelialize in 5‒7 days. This form of SSSS is usually seen only in children. Typically, there are no associated systemic symptoms. The lesions are located in the area of the umbilicus and perineum in infants and over the extremities in older children [166].
A Case of Hospital-Acquired Mrsa
Published in Meera Chand, John Holton, Case Studies in Infection Control, 2018
TSST-1 is a superantigen that stimulates a broad range of T-cells to release TNF and IL-1, leading to a generalized acute inflammatory reaction and shock. This leads to the toxic shock syndrome. S. aureus enterotoxins (SEA-SE/U2) are superantigens and have a similar mechanistic effect to TSST-1, but induce food poisoning with rapid onset of nausea, vomiting, and sometimes diarrhoea. Alpha toxin is a pore-forming toxin, which induces cell necrosis by allowing intracellular contents to leak out of the affected cells, causing local host cell death. PVL is associated with necrotizing pneumonia and severe invasive skin or bone infections. It induces cytolysis of cells, particularly neutrophils, thus abrogating the host innate immune response. Exfoliatin A and B produced by S. aureus affects cadherin intercellular adhesion proteins and their loss leads to separation of the upper skin layers, with desquamation of the epidermal layer. This illness is called scalded skin syndrome.
Infections and infestations affecting the nail
Published in Eckart Haneke, Histopathology of the NailOnychopathology, 2017
Impetigo contagiosa is the most frequent superficial skin infection and mainly seen in children between 2 and 5 years although, in principle, any age may be affected. Heat and humidity favor its outbreak.62 Approximately 30% of impetigo cases are bullous, which is due to staphylococcal exfoliatin toxins. Staphylococcus aureus and, more rarely, β-hemolytic streptococci, are the most common causes of putrid infections of the nail. Around the nail, they give rise to bulla repens (bulla rodens), also called runaround. This starts as a clear blister of the proximal to lateral nail fold, which soon becomes cloudy and yellow. Removal of the blister roof and disinfective baths are usually sufficient for treatment; systemic antibiotics are rarely needed for this superficial infection. The clinical differential diagnoses are burns and congelations as well as other blistering dermatoses.
Echtyma gangrenosum caused by coinfection with group A Streptococcus and Staphylococcus aureus: an emerging etiology? Case reports and literature review
Published in Acta Clinica Belgica, 2021
Antonio Ulpiano Trillig, Véronique Y. Miendje Deyi, Pierre Youatou, Deborah Konopnicki
The Gram staining of several lesion swabs showed white blood cells and gram-positive cocci both in chains and in clusters; cultures grew both GAS (abundant or confluent) and SA (moderate quantity) later found to be sensitive, respectively, to methicillin and penicillin. Resistance to clindamycin was found in the SA but not in the GAS strain. Typing showed an emm81 Streptococcus and the absence of gene coding for toxin production by the SA (Panton-Valentin TSST-1, exfoliatin toxins a and b, spa type t359). Blood cultures were negatives as well as serology tests for HIV, Rickettsia, Syphilis, Hepatitis B and C and Bartonella.
Pediatric impetigo: an expert panel opinion about its main controversies
Published in Journal of Chemotherapy, 2022
Luisa Galli, Andrea Novelli, Giuseppe Ruggiero, Stefania Stefani, Anna Belloni Fortina
Worldwide bacterial impetigo is one of the most common pediatric skin infection, in particular among children aged 2–5 years [1], with a peak in tropical areas and low-income settings [2]. Poor hygiene, high humidity, maceration, skin lesions with disruption of the epidermis barrier (e.g., scabies, atopic dermatitis, insect bites), comorbidities and adverse reactions (rash, itch) associated with drugs administration are well-established risk factors for impetigo. Impetigo presents in bullous or non-bullous forms. Non-bullous impetigo accounts for 70% of cases and is caused by Staphylococcus aureus and Streptococcus pyogenes, which is still the dominant pathogen in tropical areas, while in temperate regions such as USA and Europe S. aureus has become the most prevalent aetiological pathogen, with a rising role of community acquired methicillin-resistant S. aureus (CA-MRSA) [3]. It is characterized by vesicles progressing to pustules and then to yellow crusts. Bullous impetigo is caused by S. aureus, even capable to produce the extracellular exfoliatins A and B [3], and presents with clear or purulent, fluid-filled blisters and shallow erosions. The diagnosis is mainly clinical. Prompt identification of its common or atypical presentations is necessary to differentiate impetigo from other skin conditions with similar presentation including herpes simplex, scabies, and eczema for non-bullous impetigo, or burns, Stevens-Johnson syndrome, and other bullous diseases (e.g., bullous pemphigoid) for the bullous form. Topical treatment (e.g., fusidic acid, mupirocin, ozenoxacin) is recommended in patients with limited extension (<2% of total body surface area) of the disease, while systemic antibiotics (e.g., first-line oral treatment with isoxazolyl penicillins such as flucloxacillin or a first-generation cephalosporin such as cephalexin or cefadroxil or amoxacillin/clavulanic acid) should be recommended in cases with extensive/multiple lesions, relapses and/or a systemic involvement, poor response to topical treatment as well as in children <1 year of age. An adequate coverage with clindamycin or trimethoprim-sulfamethoxazole should be considered when MRSA is confirmed or suspected [4]. In 13–52% of patients, impetigo spontaneously resolves within 7–10 days without scarring [5,6]. Occasionally, patients will present a systemic involvement with fever and lymphadenopathy; rare complications include cellulitis, osteomyelitis, septic arthritis, pneumonia, sepsis, and acute glomerulonephritis [1]. Complicated impetigo is increasing due to the emergence of MRSA colonization which varies between 0.5 and 15.1% of pediatric population according to the local area. Patients with impetigo often receive inappropriate management, due to misdiagnosis, under- or over-estimation of the disease severity, failure to recognize patient’s risk factors, and misuse of diagnostic tools. MRSA colonization and antimicrobial-resistant pathogens increase the challenge of treating pediatric impetigo. As a consequence, a better knowledge about its adequate management is desirable. The present paper aims at providing a practical guide on the best practice for appropriately managing pediatric impetigo, with particular emphasis on its main controversies.