Cogley T P
Independent Laboratory of Veterinary Entomology, Clearwater, FL 34618-269.
Vet Parasitol. 1989 Jun;31(3-4):317-31. doi: 10.1016/0304-4017(89)90081-2.
Lesions were formed in the mouth of the horse by first- and second-stage Gasterophilus intestinalis larvae. The lesions resulted as larvae burrowed through the top millimeter of the tongue and then became embedded in the interdental gingiva. Appearance of the lesion was dependent on the degree of larval burrowing activity and healing that had taken place. Active tunneling production occurred at the posterior end of the lesion. Extensive change in configuration and color was apparent along the longer lesions with active larvae. Virtually all tissue in the path of the larvae was removed while forming a tunnel. Tissue destroyed included tops of the lamina propria mucosae evaginations and the deeper portions of the lamina epithelialis mucosae. Histopathologic findings showed that the tissue removed included the nerve and blood supply of the proprial evaginations. Hemorrhage and exocytosis into the tunnels included erythrocytes mixed with some macrophages, lymphocytes and scant numbers of eosinophils. Air shafts excavated in the tongue by larvae enabled bacteria to enter into the tunnels. Bacteria became adhered to larvae and initiated microabscesses. Microabscesses were composed of clotted erythrocytes, bacteria, disintegrating epithelial cells, and large numbers of neutrophils. Cells surrounding the tunnel exhibited pyknosis, epithelial hydropic degeneration and became separated from each other. Healing of tongue lesions occurred as epithelial cell growth below raised the tunnel upward and affected tissue desquamated. Interdental gingiva invaded by larvae were hyperemic and denuded of epithelia. Recession and ulceration of the gingiva produced periodontal pockets. Extensive invasion by larvae led to compound periodontal pockets. Larval mouth hooks were embedded in the submucosa of the pockets and tore at engorged capillaries. The cephalic portion of embedded larvae became surrounded by a cellular exudate containing erythrocytes and mononuclear cells. Attachment of second-stage larvae at the root of the tongue did not produce observable damage.
马胃蝇肠道一期和二期幼虫在马口腔中形成病变。这些病变是幼虫钻入舌面顶部一毫米后,嵌入齿间牙龈所致。病变的外观取决于幼虫挖掘活动的程度以及已经发生的愈合情况。病变后端出现活跃的隧道形成。活跃幼虫所在的较长病变处,形态和颜色有明显的广泛变化。幼虫在形成隧道的过程中几乎将其路径上的所有组织都移除了。被破坏的组织包括固有层黏膜突起的顶部和上皮层黏膜的较深部分。组织病理学检查结果显示,被移除的组织包括固有层突起的神经和血液供应。隧道内有出血和胞吐现象,包括红细胞与一些巨噬细胞、淋巴细胞和少量嗜酸性粒细胞混合。幼虫在舌部挖掘的气穴使细菌进入隧道。细菌附着在幼虫上并引发微脓肿。微脓肿由凝结的红细胞、细菌、解体的上皮细胞和大量中性粒细胞组成。隧道周围的细胞出现核固缩、上皮细胞水肿变性并彼此分离。舌部病变的愈合是由于下方上皮细胞生长使隧道向上抬起,受影响的组织脱落。幼虫侵入的齿间牙龈充血,上皮剥脱。牙龈退缩和溃疡形成牙周袋。幼虫广泛侵入导致复合性牙周袋。幼虫的口钩嵌入牙周袋的黏膜下层,撕裂充血的毛细血管。嵌入幼虫的头部被含有红细胞和单核细胞的细胞渗出物包围。二期幼虫附着在舌根处未产生可观察到的损伤。