ABSTRACT
Bacteria, particularly Gram-negative bacilli, can develop abnormal morphology after the administration of subinhibitory concentrations of antibacterial agents. Filamentation is a common response in which bacteria replicate but incompletely divide, leading to long slender chains that resemble fungal hyphae. Pathologists are frequently consulted to examine direct smears of body fluids, which often contain microorganisms. Antibiotic-related filamentous morphology may resemble fungal hyphae and this potential misinterpretation can lead to inappropriate treatment for presumed fungal infections. Two cases are described in which direct smears of body fluids were examined by on-call pathology residents who misinterpreted filamentous bacteria as fungal organisms, with one case leading to the initiation of antifungal medication. Although well-established within the field of microbiology, many residents and practising pathologists are less familiar with antibiotic-related bacterial morphology, as it may not be routinely encountered. It is important for pathologists to be aware of this phenomenon in order to avoid misinterpretation.
Subject(s)
Bacteriological Techniques , Diagnostic Errors/prevention & control , Fungi/isolation & purification , Gram-Negative Bacteria/isolation & purification , Gram-Negative Bacterial Infections/diagnosis , Mycoses/diagnosis , Anti-Bacterial Agents/adverse effects , Antifungal Agents/therapeutic use , Cerebrospinal Fluid/microbiology , Female , Fungi/ultrastructure , Gram-Negative Bacteria/drug effects , Gram-Negative Bacteria/ultrastructure , Gram-Negative Bacterial Infections/drug therapy , Gram-Negative Bacterial Infections/microbiology , Humans , Hyphae/ultrastructure , Mycoses/drug therapy , Mycoses/microbiology , Predictive Value of Tests , Unnecessary Procedures , Urine/microbiologyABSTRACT
BACKGROUND: Grover disease is a clinicopathologic entity characterized by acantholysis. The histologic changes typically occupy circumscribed foci, therefore early stages could go unnoticed and be misdiagnosed. OBJECTIVE: To report on early histopathologic changes in Grover disease. MATERIAL AND METHODS: We analyzed 22 cases of Grover disease histologically diagnosed at Wake Forest University School of Medicine, NC, between 2000 and 2009. Early changes were defined as elongation of rete ridges and mild focal acantholysis. RESULTS: Six cases (27%) showed elongation of the rete ridges with focal acantholysis. Mild spongiosis was seen in 4 cases. Superficial perivascular inflammatory infiltrate was found in all cases, 5 of which showed eosinophils. CONCLUSIONS: These findings may represent a diagnostic clue in cases of early Grover disease, if clinical correlation is made.
Subject(s)
Acantholysis/pathology , Ichthyosis/pathology , Keratinocytes/pathology , Skin/pathology , Acantholysis/immunology , Aged , Biopsy , Eosinophils/immunology , Eosinophils/pathology , Female , Humans , Ichthyosis/immunology , Lymphocytes/immunology , Lymphocytes/pathology , Male , Middle Aged , Retrospective Studies , Skin/immunologySubject(s)
Carcinoma, Verrucous/pathology , Lymphoma, T-Cell, Cutaneous/pathology , Neoplasms, Second Primary/pathology , Skin Neoplasms/pathology , Adult , Carcinoma, Verrucous/drug therapy , Humans , Lymphoma, T-Cell, Cutaneous/drug therapy , Male , Neoplasms, Second Primary/drug therapy , Skin Neoplasms/drug therapyABSTRACT
Nephrogenic systemic fibrosis (NSF), also known as nephrogenic fibrosing dermopathy (NFD), occurs in renal failure patients after gadolinium contrast exposure. The fibrosis of the dermis and subcutaneous septae accompanies fibrosis of other organs, including the heart, liver, lungs, and muscle. The fibrotic skin demonstrates increased dermal collagen, fibroblasts, and mucin. The mechanism by which gadolinium is associated with fibrosis is not known. We tested the hypothesis that upregulation of transglutaminases contributes to the fibrosis seen in the organs, including skin, of renal failure patients exposed to gadolinium contrast. We performed immunohistochemical studies using antibodies to transglutaminase-2, factor XIIIa, transglutaminase isopeptide, and the histiocyte marker CD68 on five archived skin biopsies of NSF. The results indicate that the dermal fibroblasts and histiocytes of NSF express transglutaminase-2, CD68, factor XIIIa, and transglutaminase isopeptide, indicating increased expression and/or activation of transglutaminases in NSF. We recommend further research into the use of transglutaminase inhibitors in the treatment and prevention of NSF.
