R F Canalis1, L Zamboni. 1. Division of Head and Neck Surgery, Department of Surgery, Harbor-UCLA Medical Center and the UCLA School of Medicine, Los Angeles, California 90509, USA.
Abstract
OBJECTIVE: To identify the structural changes of the proliferative phase of rhinoscleroma which could be responsible for the chronicity of the disease. STUDY DESIGN: Observational research. METHODS: Samples of friable tissue taken from the nasal mucosa of nine untreated patients were processed for light and ultrastructural microscopy. RESULTS: The majority of changes contributing to the chronicity of the disease occurred in the subepithelium and followed three closely related but distinct events. In the first (infiltrative), subepithelial invasion by the Klebsiella was followed by its active multiplication and proliferation of capillaries. In the second (neutrophilic), large numbers of neutrophils were delivered into this space. Neutrophils actively phagocytized the Klebsiella but appeared to die at an accelerated rate without completing digestion of the microorganisms. In the third event (histiocytic), histiocytes entered the subepithelium and engaged in unrestrained phagocytosis of decaying neutrophils, Klebsiella, and debris. During this process, the histiocytes' phagosomes underwent massive dilation, thus becoming Mikulicz cells. Mikulicz cells were unable to consistently destroy the Klebsiella and eventually ruptured, releasing them into the interstitium. Evidence was found that an autophagic process might contribute to phagosome distention and to the rupture of the vacuolar membranes and cell wall. CONCLUSIONS: Several critical changes responsible for the chronicity of rhinoscleroma occur during the proliferative phase of the disease. The majority of these take place in the subepithelium and include: 1) factors leading to the transformation of histiocytes into Mikulicz cells, 2) the inability of these cells to consistently destroy the Klebsiella, 3) their rupture releasing viable Klebsiella, and 4) the intrinsic resistance of the pathogen.
OBJECTIVE: To identify the structural changes of the proliferative phase of rhinoscleroma which could be responsible for the chronicity of the disease. STUDY DESIGN: Observational research. METHODS: Samples of friable tissue taken from the nasal mucosa of nine untreated patients were processed for light and ultrastructural microscopy. RESULTS: The majority of changes contributing to the chronicity of the disease occurred in the subepithelium and followed three closely related but distinct events. In the first (infiltrative), subepithelial invasion by the Klebsiella was followed by its active multiplication and proliferation of capillaries. In the second (neutrophilic), large numbers of neutrophils were delivered into this space. Neutrophils actively phagocytized the Klebsiella but appeared to die at an accelerated rate without completing digestion of the microorganisms. In the third event (histiocytic), histiocytes entered the subepithelium and engaged in unrestrained phagocytosis of decaying neutrophils, Klebsiella, and debris. During this process, the histiocytes' phagosomes underwent massive dilation, thus becoming Mikulicz cells. Mikulicz cells were unable to consistently destroy the Klebsiella and eventually ruptured, releasing them into the interstitium. Evidence was found that an autophagic process might contribute to phagosome distention and to the rupture of the vacuolar membranes and cell wall. CONCLUSIONS: Several critical changes responsible for the chronicity of rhinoscleroma occur during the proliferative phase of the disease. The majority of these take place in the subepithelium and include: 1) factors leading to the transformation of histiocytes into Mikulicz cells, 2) the inability of these cells to consistently destroy the Klebsiella, 3) their rupture releasing viable Klebsiella, and 4) the intrinsic resistance of the pathogen.