Michaelis-Gutmann Research Articles

What is your diagnosis? Urine from a dog.

What is your diagnosis? Urine from a dog.

Malakoplakia in sclera of the left eye- A rare case report

“Malakoplakia” comes from Greek words malakos (soft) and plakos (plaque). It is a rare histiocytic disease that may occur in all organs, most frequently involving GU tract, particularly bladder. Other organs involved are gastrointestinal tract (most commonly colon, followed by stomach and duodenum), central nervous system and female genital tract. Malignancy and other forms of immunosuppression are predisposing factors. Malakoplakia in eye and orbit region are extremely rare and are usually appraised by the pathologist on histopathology sections with a few mimickers as differential diagnosis. Histopathological features showed. Collections of histiocytes with granular eosinophilic cytoplasm accumulated beneath the surface epithelium. Few cells showed round, concentrically layered intracytoplasmic inclusions known as Michaelis–Gutmann (MG) bodies which are characteristic of malakoplakia. The MG bodies are basophilic and are demonstrated by Periodic Acid–Schiff (PAS) stain and stains for iron and calcium. Rare histiocytic disease that can simulate a neoplasm. Gross appearance: Single or multiple white-yellow soft raised plaques on the mucosal surface. Pathological diagnosis/entity rather than a clinical impression and warrants special stains to arrive at the histological conclusion.More common in immunocompromised (HIV, renal transplant recipients) and women Noted in > 50 years of age Malakoplakia is presently regarded as a defect in the host macrophage (phagolysosomal) response to a bacterial infection, usually from gram-negative coliformbacilli. Malakoplakia should be kept as one of the differential diagnosis by the pathologist when dealing with ophthalmic specimen.

Ultrastructural evidence of the evolutional process in malakoplakia.

Malakoplakia can be caused by incomplete digestion of Escherichia coli by lysosomes, leading to recurrent urinary tract infections and consequential mass-forming events that mimic tumors. By using ultrastructural findings, we aimed to specify the process of phagolysosome to evoke malakoplakia. We observed a series of processes to form a peculiar Michaelis-Gutmann (MG) body in three patients with malakoplakia and compared with xanthogranulomatous pyelonephritis. The ultrastructural findings were realigned according to the sequence of events as pre-phagosomal, phagosomal, and post-phagosomal stages. For the mature MG body, numerous lysosomal aggregates targeting pathogens and subsequent incomplete digestion are prerequisite factors for the pre-phagosomal stage. Scattered lamellated residue is late evidence of the pre-phagosomal stage. Phagosomes can be formed by the fusion of multiple pathogens and multiple lysosomes. We utilized transmission and scanning electron microscopy to speculate on the process of phagolysosomal formation. The recognition of E. coli captured by phagosomes or partially damaged by lysosomal attack within the cell was recorded for the first time. Furthermore, SEM observation was performed on human tissue.

Malakoplakia of the colon following renal transplantation in a 73\u2009year old woman: report of a case presenting as intestinal perforation

BackgroundMalakoplakia is a chronic inflammatory disease characterized by tissue infiltrates of large granular macrophages containing distinctive intracytoplasmic inclusions termed Michaelis-Gutmann (MG) bodies. The genitourinary system is the most commonly involved site, followed by the gastrointestinal tract. Malakoplakia may occur as a complication of primary or secondary immunosuppression and, therefore, renal transplant recipients are at risk. The graft itself or extra-renal sites may be involved. Regarding the latter, six cases of colorectal malakoplakia have been reported following renal transplantation, with all but one patient experiencing significant morbidity. We describe a further example of colorectal malakoplakia following renal transplantation. The other previously reported cases are reviewed.Case presentationA 72 year old female presented with left lower quadrant abdominal pain and vaginal bleeding. She had received a cadaveric renal transplant for chronic renal failure ten months previously. Abdomino-pelvic computerized tomography (CT) scanning demonstrated two lesions in the mesocolon: the first adjacent to the descending colon and the second involving the sigmoid colon. A diagnosis of sub-acute perforated diverticulitis with two phlegmons was proposed. The sigmoid lesion was resected. The descending colon lesion was treated by creation of a cutaneous fistula. Microscopy of the sigmoid lesion showed the typical features of malakoplakia. She was discharged on sulfamethoxazole-trimethoprim. Nine months later, no longer receiving antibiotic therapy, the patient reported lower left quadrant discomfort. CT scanning showed para-rectal and pelvic abdominal masses with cutaneous and intestinal fistulas. Treatment with tazobactam-piperacillin was begun and sulfamethoxazole-trimethoprim was reinstated, with subsequent slow clinical improvement. Subsequent abdominal CT scans have shown persistence of the lesions.ConclusionsPhysicians caring for renal transplant recipients should be aware of colorectal malakoplakia as a rare but serious complication. The onset may be within months or as long as a decade or more following transplantation. The clinical presentation is varied, nonspecific, and will likely suggest more common diseases. Although radiologic imaging is also nonspecific, awareness of malakoplakia is of importance to radiologists when formulating the differential diagnosis of mass lesions of the colorectum in this clinical setting. Definitive diagnosis remains dependent on pathologic examination of a biopsy or surgical resection specimen.

Malakoplakia of the Kidney

Malakoplakia is a rare inflammatory disease associated with Escherichia coli infection. 1 von Hansemann D. Uber malakoplakia der harnblase. Virchows Arch A Pathol Anat Histopathol. 1903; 173: 302-308 Crossref Scopus (174) Google Scholar Despite some characteristic histological features, including the presence of large histiocytes with clusters of Michaelis-Gutmann (MG) bodies, malakoplakia of the kidney is difficult to diagnose because of its rarity and varying histological picture. We report the case of a 57-year-old man who had granulomatous interstitial nephritis caused by kidney parenchymal malakoplakia. Of note, using polymerase chain reaction (PCR), we were able to site-specifically amplify E coli DNA from his kidney biopsy specimens. Malakoplakia of the kidney should be considered in the differential diagnosis of granulomatous interstitial nephritis, and application of molecular biological approaches to the analysis of kidney tissues may be useful in the diagnosis of this disease.

こう丸マラコプラキアの二手術例の免疫組織化学的および電顕的検索 肉芽腫性こう丸炎との関連について

We report histochemical and immunohistochemical studies of two cases of testicular malacoplakia from 54-year-old (case 1) and 45-year-old (case 2) men and an ultrastructural study of case 1 with review of the literature. The testes were enlarged and the cut surface showed a neoplasma-like appearance. The testicular architecture was destroyed due to replacing by granulomatous lesion consisting predominantly of macrophages with abundant eosinophilic granular cytoplasm (so-called von Hansemann cell) in both cases. In the cytoplasm of von Hansemann cells, PAS-positive inclusion bodies were frequently observed. There was no histochemical evidence of iron or calcium deposition in the inclusion bodies. Immunohistochemically, positive materials for anti-α1-antitrypsin, anti-α1-antichymotrypsin and anti-Escherichia coli (E. coli) antibodies were seen in the cytoplasm of von Hansemann cells in granulomatous lesion. Thus, we considered the inclusion body as Michaelis-Gutmann (M-G) body. Electron microscopically, various kinds of phagosomes, including M-G structures which do not seem to contain calcium, were observed in the cytoplasm of von Hansemann cells in case 1. Although, the pathogenesis of testicular malacoplakia is still unclear, bacterial infection, especially E. coli infection, may be play an important role for the pathogenesis of testicular malacoplakia.

Lymphadenopathy due to fatal histiocytic proliferative disorder containing michaelis-gutmann bodies

A 59-year-old white man had generalized lymphadenopathy, fever, weight loss, and hypercalcemia. Histologic examination of seven lymph nodes from three different anatomic sites revealed a diffuse histiocytic infiltrate containing numerous typical Michaelis-Gutmann (MG) bodies. Histochemical and immunohistochemical results confirmed the histiocytic nature of the predominant cell within the infiltrate. Approximately equal numbers of residual normal B-cells, T-helper, and T-suppressor cells were present. Electron microscopy revealed extracellular and intracellular MG bodies, many of which were membrane-bound. Special stains, electron microscopy, and lymph node culture did not demonstrate microorganisms. The histologic features of the infiltrate were those of malacoplakia. However, the disease behaved like a lymphoma, with the occurrence of lymphadenopathy and a fatal outcome.

The histochemical features of the Michaelis-Gutmann body and a consideration of the pathophysiological mechanisms of its formation.

The reactions to a number of histochemical stains by Michaelis-Gutmann (MG) bodies in 13 cases of malakoplakia are described. All MG bodies contained calcium and phosphate. Iron was present in six cases. Special stains failed to reveal the presence of micro-organisms. In six cases the MG bodies contained either lecithin or sphingomyelin and in three both phospholipids were present. There was no evidence of phospholipid of bacterial cell membrane derivation. Carbohydrate staining reactions suggested the presence of a neutral polysaccharide and an acidic non-sulphated polysaccharide (such as a sialoglycan). No histochemical evidence could be adduced to implicate bacterial cell membranes in the structure of the organic matrix of the MG body. The implications of these findings in the light of the association between clinical bacterial infection and malakoplakia are discussed.

Alpha-1-antitrypsin in malakoplakia

Macrophages in malakoplakia contain large amounts of immunoreactive alpha-1-antitrypsin (AAT). The amount of AAT remains unchanged during the morphogenetic stages of the pathological process (early, granulomatous, fibrosing phases), and does not correlate with the number or the presence of Michaelis-Gutmann (M.G.) bodies. Macrophages from other pathological processes, closely resembling malakoplakia cells but without M.G. bodies, did not contain AAT, except for a few macrophages in tuberculosis and xanthogranulomatous pyelonephritis. Whatever the source and the pathogenic role of AAT in malakoplakia, its presence in all macrophages seems to be specific for this disease. Immunohistochemical staining for AAT is therefore proposed as a useful test for an early and accurate differential diagnosis of malakoplakia.

The ultrastructural features of malakoplakia.

The ultrastructural features of a case of disseminated malakoplakia are described and compared with available published cases. Generally macrophages were involved (although characteristic inclusions were seen in association with some plasma cells) and contained three types of cellular inclusions. These were (1) the phagolysosomes (2) and intermediate structure sharing features of the phagolysosome and the Michaelis-Gutmann (MG) body and (3) the MG body. All inclusions were delineated by unit membranes and their matrices (except those of large MG bodies) composed of membranous whorls and loops. It is suggested that these inclusions represent stages in the development of the MG body. Septate junctional complexes were observed between phagolysosomes and small MG bodies. These complexes may represent either a mechanism of organelle fusion or an abnormality of molecular organisation of the limiting unit membrane.