Isolation of Novel Mycobacterium Species from Skin Infection in an Immunocompromised Person

An association between using coastal waters for recreation and staphylococcal skin infections has been reported by canoe paddlers and several physicians in Hawaii. A retrospective epidemiological/microbiological monitoring study was undertaken to determine the association between S aureus skin infections in youngsters (4 months to 16 years of age) and their exposure to recreational use of coastal waters. Telephone interviews were conducted of 53 patients with such skin infections and 53 similar (controlled for age and sex) patients with no infection. A significant association between skin infection and water exposure was found, the odds showing that those developing skin infection caused by S aureus were 4 times more likely to have had a history of seawater contact than the control group. Moreover, the antibiotic sensitivity patterns and phage types of S aureus isolated from patients were similar to those isolated from seawater at bathing beaches.

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Leukocytoclastic Vasculitis Associated with HHV6-A/ciHHV6-A and HHV6-B Coinfection in an Immunocompetent Woman

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530318666181106153758 ◽

2019 ◽

Vol 19 (2) ◽

pp. 221-225 ◽

Cited By ~ 1

Author(s):

Agata Calvario ◽

Caterina Foti ◽

Maria Scarasciulli ◽

Paolo Romita ◽

Eva Eliassen ◽

...

Keyword(s):

Transcriptional Activity ◽

Skin Infection ◽

Leukocytoclastic Vasculitis ◽

Human Herpesvirus ◽

Small Vessel Vasculitis ◽

Case Description ◽

Human Herpesvirus 6 ◽

Late Antigen ◽

Herpesvirus 6 ◽

Systemic Symptoms

Background and Objective: Leukocytoclastic vasculitis (LCV) is a small vessel vasculitis that can be limited to the skin but may also affect other organs. Often, its cause is unknown. LCV has previously been reported to occur with the reactivation of human herpesvirus 6 (HHV-6). Here, we report a second instance of HHV-6 reactivation in a 43-year-old woman with idiopathic cutaneous LCV. </P><P> Case Description: In this case, the patient was immunocompetent, and testing revealed that she had inherited chromosomally integrated human herpesvirus 6 variant A (iciHHV6-A) with a parallel skin infection of HHV-6B. The integrated ciHHV-6A strain was found to be transcriptionally active in the blood, while HHV-6B late antigen was detected in a skin biopsy. The patient’s rash was not accompanied by fever nor systemic symptoms and resolved over four weeks without any therapeutic intervention.Conclusion:In light of the transcriptional activity documented in our case, further examination of a possible role for HHV-6 in the etiology of LCV is warranted.

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GSDMD contributes to host defence against Staphylococcus aureus skin infection by suppressing the Cxcl1–Cxcr2 axis

Veterinary Research ◽

10.1186/s13567-021-00937-7 ◽

2021 ◽

Vol 52 (1) ◽

Author(s):

Zhen-Zhen Liu ◽

Yong-Jun Yang ◽

Feng-Hua Zhou ◽

Ke Ma ◽

Xiao-Qi Lin ◽

...

Keyword(s):

Staphylococcus Aureus ◽

Skin Infection ◽

Bacterial Colonization ◽

Critical Role ◽

Host Defence ◽

Skin Damage ◽

Microbial Infection ◽

Caspase 1 ◽

Deficient Mice

AbstractGasdermin D (GSDMD), a member of the gasdermin protein family, is a caspase substrate, and its cleavage is required for pyroptosis and IL-1β secretion. To date, the role and regulatory mechanism of GSDMD during cutaneous microbial infection remain unclear. Here, we showed that GSDMD protected against Staphylococcus aureus skin infection by suppressing Cxcl1–Cxcr2 signalling. GSDMD deficiency resulted in larger abscesses, more bacterial colonization, exacerbated skin damage, and increased inflammatory cell infiltration. Although GSDMD deficiency resulted in defective IL-1β production, the critical role of IL-1β was counteracted by the fact that Caspase-1/11 deficiency also resulted in less IL-1β production but did not aggravate disease severity during S. aureus skin infection. Interestingly, GSDMD-deficient mice had increased Cxcl1 secretion accompanied by increased recruitment of neutrophils, whereas Caspase-1/11-deficient mice presented similar levels of Cxcl1 and neutrophils as wild-type mice. Moreover, the absence of GSDMD promoted Cxcl1 secretion in bone marrow-derived macrophages induced by live, dead, or different strains of S. aureus. Corresponding to higher transcription and secretion of Cxcl1, enhanced NF-κB activation was shown in vitro and in vivo in the absence of GSDMD. Importantly, inhibiting the Cxcl1–Cxcr2 axis with a Cxcr2 inhibitor or anti-Cxcl1 blocking antibody rescued host defence defects in the GSDMD-deficient mice. Hence, these results revealed an important role of GSDMD in suppressing the Cxcl1–Cxcr2 axis to facilitate pathogen control and prevent tissue damage during cutaneous S. aureus infection.

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