ABSTRACT
BACKGROUND: Contact dermatitis (CD) is very common but can be mimicked by numerous dermatologic conditions. Thus, a wide differential must be considered before a definitive diagnosis of CD is made to ensure the patient receives appropriate treatment and follow-up. OBJECTIVE: To describe conditions that can present similarly to contact dermatitis. METHODS: We retrospectively analyzed patients referred to the Occupational Disease Specialized Program at St. Michael's Hospital in Toronto between 2009 and 2011 for CD investigations but with a final diagnosis other than CD. RESULTS: We report cases of 2 feet-1 hand syndrome, Dermatitis Herpetiformis, Sézary syndrome and two cases of Pityriasis Rubra Pilaris misdiagnosed as CD and referred for patch testing at our busy tertiary care centre. Failing to recognize these mimickers of CD resulted in a significant delay in diagnosis for the patients and resulting initiation of necessary intervention. CONCLUSIONS: It is important to consider numerous mimickers before making a diagnosis of CD to ensure optimal outcome for patients.
Subject(s)
Dermatitis, Allergic Contact/diagnosis , Dermatitis, Occupational/diagnosis , Occupational Exposure/adverse effects , Skin/pathology , Tertiary Care Centers , Adult , Humans , Male , Middle Aged , Ontario , Patch Tests/methodsSubject(s)
Acute Pain/diagnosis , Blister/pathology , Fingers/pathology , Hand Dermatoses/pathology , Skin Diseases, Bacterial/pathology , Aged , Anti-Bacterial Agents/therapeutic use , Blister/drug therapy , Blister/surgery , Cephalexin/therapeutic use , Debridement , Diagnosis, Differential , Fingers/surgery , Hand Dermatoses/drug therapy , Hand Dermatoses/surgery , Humans , Male , Skin Diseases, Bacterial/drug therapy , Skin Diseases, Bacterial/surgery , Treatment OutcomeABSTRACT
The lower intestine of adult mammals is densely colonized with nonpathogenic (commensal) microbes. Gut bacteria induce protective immune responses, which ensure host-microbial mutualism. The continuous presence of commensal intestinal bacteria has made it difficult to study mucosal immune dynamics. Here, we report a reversible germ-free colonization system in mice that is independent of diet or antibiotic manipulation. A slow (more than 14 days) onset of a long-lived (half-life over 16 weeks), highly specific anticommensal immunoglobulin A (IgA) response in germ-free mice was observed. Ongoing commensal exposure in colonized mice rapidly abrogated this response. Sequential doses lacked a classical prime-boost effect seen in systemic vaccination, but specific IgA induction occurred as a stepwise response to current bacterial exposure, such that the antibody repertoire matched the existing commensal content.
Subject(s)
Antibodies, Bacterial/immunology , Escherichia coli/growth & development , Escherichia coli/immunology , Immunoglobulin A/immunology , Intestinal Mucosa/immunology , Intestinal Mucosa/microbiology , Animals , Antibodies, Bacterial/biosynthesis , Antibody Specificity , Colony Count, Microbial , Dose-Response Relationship, Immunologic , Germ-Free Life , Half-Life , Immunoglobulin A/biosynthesis , Immunologic Memory , Intestines/immunology , Intestines/microbiology , Mice , Mice, Inbred C57BL , Mucous Membrane/immunology , Plasma Cells/immunology , Time FactorsABSTRACT
Commensal bacteria in the lower intestine of mammals are 10 times as numerous as the body's cells. We investigated the relative importance of different immune mechanisms in limiting the spread of the intestinal microbiota. Here, we reveal a flexible continuum between innate and adaptive immune function in containing commensal microbes. Mice deficient in critical innate immune functions such as Toll-like receptor signaling or oxidative burst production spontaneously produce high-titer serum antibodies against their commensal microbiota. These antibody responses are functionally essential to maintain host-commensal mutualism in vivo in the face of innate immune deficiency. Spontaneous hyper-activation of adaptive immunity against the intestinal microbiota, secondary to innate immune deficiency, may clarify the underlying mechanisms of inflammatory diseases where immune dysfunction is implicated.
