Intraocular metallic-appearing foreign bodies after phacoemulsification.

Intraocular metallic-appearing foreign bodies in the anterior segment were seen in six eyes after cataract extraction by two-handed phacoemulsification. These fragments produced no symptoms and had no clinically significant effect on visual function. Similar-appearing foreign bodies were experimentally produced by applying ultrasound power with a phacoemulsification handpiece to the surface of a cyclodialysis spatula in vitro. Microscopic examination of the phaco handpiece tip and cyclodialysis spatulas revealed numerous surface irregularities, suggesting a possible source of these fragments. These results suggest that instrument touch during phacoemulsification may be the cause of the fragments. Long-term follow-up of these patients is required to determine the overall effect of the fragments.

Murine chronic tubulointerstitial nephritis: induction by human uveitis mycoplasma-like organisms.

Mycoplasma-like organisms (MLO) are non-cultivated intracellular cell wall deficient pathogenic bacteria with a distinctive ultrastructural appearance. Diagnosis of MLO disease rests on finding the organisms in parasitized cells using a transmission electron microscope. MLO are a well studied cause of transmissible chronic plant vascular disease responsive to antibiotics. MLO have recently been found to cause human chronic progressive ophthalmic disease including uveitis. In human uveitis MLO are readily found within parasitized intraocular fluid leucocytes. Inoculation of human uveitis MLO into mouse eyelids produced a high incidence of chronic progressive ophthalmic disease including uveitis. MLO also disseminated to produce randomly distributed lethal systemic inflammatory disease. MLO parasitized leucocytes and microvascular alterations were found in the disease sites by electron microscopy. This report describes the chronic progressive tubulointerstitial nephritis in 12 of 100 human uveitis MLO eyelid inoculated mice versus 0 in 200 control mice (p < 0.0001). MLO parasitized leucocytes accompanied by tubular and microvascular alterations were found by electron microscopy in all 12 inflamed kidneys versus 0 of 4 control kidneys. Pathobiology of the MLO-induced murine nephritis, resemblance of this nephritis to human idiopathic chronic tubulointerstitial nephritis, bacterial molecular biology, and antibiotic therapy of MLO disease are discussed.

Experimental murine chronic hepatitis: results following intrahepatic inoculation of human uveitis mycoplasma-like organisms.

Mycoplasma-like organisms (MLO) are non-cultivated intracellular cell-wall deficient pathogenic bacteria with a distinctive ultrastructural appearance. Diagnosis of MLO disease depends on finding the organisms in parasitized cells using a transmission electron microscope. MLO are a well studied cause of transmissible chronic plant disease responsive to antibiotics. MLO have recently been found to cause human chronic uveitis, orbital, and retinal disease with autoimmune features. Ophthalmic leucocytes in these patients display MLO parasitization. Inoculation of human uveitis MLO into mouse eyelids produced chronic uveitis. MLO also disseminated to produce randomly distributed lethal systemic disease including chronic hepatitis. MLO parasitized leucocytes were present in all disease sites. Direct intrahepatic inoculation of human hepatic pathogens is a simple and efficient technique to produce murine hepatitis. This report describes the delayed onset widespread inflammatory liver disease produced by direct intrahepatic inoculation of human chronic uveitis MLO in 12 of 20 mice versus 0 in 40 controls (P < 0.05). The liver disease was accompanied by elevated serum SGOT levels, splenomegaly, and accelerated mortality. All 12 inflamed livers displayed MLO parasitized leucocytes versus 0 of 10 control livers. The resemblance of human chronic active hepatitis, massive hepatic necrosis, and post-necrotic cirrhosis to the MLO induced murine liver disease, the role of molecular biologic techniques in the detection and classification of those bacteria, and in therapy of MLO disease are discussed.

Postinflammatory cataracts in the mouse: induction by human mycoplasma-like organisms.

Cataracts often occur in humans secondary to uveitis. Uveitis may be caused by various infectious agents, but rarely is the agent detected in the cataract. Mycoplasma-like organisms (MLO) were recently reported to cause human uveitis and retinitis. Cataracts were often present in those inflamed eyes. MLO are intracellular cell wall deficient pathogenic bacteria. They are pleomorphic tubulospherical and filamentous organisms with a characteristic ultrastructural appearance. No MLO culture system has been found despite 20 years of effort. The diagnosis of MLO disease rests on detection of the organisms in parasitised cells by a transmission electron microscope and response to antibiotics. In human intraocular inflammatory disease MLO are detectable in parasitised leucocytes and retinal pigment epithelial cells at the disease sites. Inoculation of MLO from a human source into mouse eyelids produced intraocular, chronic, progressive, inflammatory disease, with intraocular leucocytes parasitised by MLO in 15 of 100 mice versus 0 in 200 controls (p less than 0.05). This report describes the cataracts with MLO-parasitised intralenticular leucocytes in the inflamed eyes of 14 of those 15 mice versus 0 in 200 control mice (p less than 0.05). The results indicate that MLO penetrated the lens capsules to produce the cataracts, and they suggest that MLO could cause human cataracts. Alternative methods for detection of MLO and rifampin treatment of MLO intraocular disease are discussed.

Ulcerative colitis associated chronic uveitis. Parasitization of intraocular leucocytes by mollicute-like organisms.

Uveitis is inflammation of the ocular vascular coats. Most uveitis is chronic, idiopathic, and considered to have an endogenous, possibly autoimmune pathogenesis. Chronic idiopathic uveitis occurs in isolation or with various systemic diseases including inflammatory bowel diseases. Using a transmission electron microscope vitreous leucocyte parasitizing and destroying mollicute-like organisms (MLO) are often found to cause chronic uveitis. Mollicutes are cell wall deficient bacteria. Mollicutes have a characteristic ultrastructural appearance. Extracellular mollicutes are fastidious, lipid-rich, and contain various potent cytotoxins. They cause human and animal diseases with autoimmune features. Morphologically similar organisms are intracellular non-cultivable pathogens that bear the eponym MLO. MLO are cytopathogenic, and cause host cell proliferation, destruction, and dysfunction. Uveitis producing MLO are detectable within parasitised vitreous lymphocytes, monocytes, and polymorphonuclear leucocytes. They appear as intracytoskeletal 0.005-0.01 micron diameter filaments and undulating pleomorphic trilaminar membrane bound 0.01-1.0 micron tubulo-spherical bodies. Cell wall deposition to form distinctive 'spore-like' cocci may also be seen. Inoculation of human uveitis MLO into mouse eyelids produces chronic uveitis. MLO also disseminate to produce chronic inflammatory disease in all organs including the gut. MLO are detectable in all the diseased organs. This report describes MLO parasitised vitreous and aqueous leucocytes in five ulcerative colitis patients with chronic uveitis. No microorganisms were cultivated using a wide variety of cultural techniques. The results indicate that MLO caused the uveitis of these patients. The possible role of this pathogen in human gut disease and Rifampin treatment of MLO disease are discussed.

Chronic orbital inflammatory disease: parasitisation of orbital leucocytes by mollicute-like organisms.

Chronic orbital inflammatory disease (COID) is usually considered non-infectious and idiopathic. Treatment is empirical, palliative, and may not prevent disease progression. COID occurs in isolation or in association with various systemic diseases. Exophthalmos may be an important presenting sign. Vasculitis, lymphoid infiltrates, and granulomas are common. Mollicute-like organisms (MLO) parasitising and destroying vitreous leucocytes are often found to cause human chronic uveitis when an appropriate search is made. Inoculation of these MLO into mouse eyelids produced chronic uveitis and exophthalmic orbital inflammatory disease. Mollicutes are cell wall deficient bacteria. Extracellular mollicutes cause human and animal diseases characterised by lymphoid infiltrates, immunosuppression, and autoantibody production. Intracellular morphologically similar bacteria are non-cultivable pathogens termed MLO. Identification is based on direct detection in diseased cells by transmission electron microscopy. MLO are cytopathogenic and detection is aided by the alterations they produce. MLO replace the cytoplasm, destroy the organelles, and alter the nucleus. This results in cell proliferation, destruction, and dysfunction. MLO parasitise lymphocytes, monocytes, and polymorphonuclear leucocytes. This report describes orbital leucocytes parasitised by MLO in three patients with isolated COID. Rifampicin treatment of MLO disease is discussed.

Sarcoidosis associated uveitis. Parasitization of vitreous leucocytes by mollicute-like organisms.

Mollicute-Like Organisms (MLO) have been reported to be a cause of uveal tract and orbital chronic inflammatory disease. MLO are intracellular cytopathogenic cell wall deficient bacteria. No culture system exists for MLO, MLO disease diagnosis is based chiefly on direct detection of the organisms within diseased cells using a transmission electron microscope. Uveitis producing MLO are detectable within vitreous leucocytes as 0.005-0.01 micron filaments and undulating pleomorphic 0.01-1.0 micron tubulo-spherical bodies. Human uveitis producing MLO can be passed to laboratory animals. Inoculation into mouse eyelids produced intraocular, orbital, and lethal systemic chronic progressive inflammatory disease. MLO parasitised lesional leucocytes were found in all the disease sites. The MLO induced mouse chronic interstitial pneumonitis displayed 'sarcoid-like' granulomas. This report describes MLO parasitised vitreous leucocytes in the chronic uveitis of four sarcoidosis patients. The results indicate that MLO caused the uveitis. The implications of the results and Rifampin treatment of MLO disease are discussed.

Crohn's disease. Rifampin treatment of the ocular and gut disease.

Idiopathic Uveitis (IU) may occur as either an isolated ocular disease or with other systemic diseases such as Crohn's Disease (CD). As many as 33% of CD patients demonstrate IU, and frequently their gut and IU course and severity are similar. Rifampin produces remissions of isolated IU, and Rifampin has been used to treat gut CD with varying success. In this investigation 4 CD patients, whose gut but not IU had partially responded to corticosteroids, the addition of Rifampin was associated with improvement in both their CD Activity Index and IU, allowing steroid discontinuation; Rifampin withdrawal was associated with exacerbations of both gut disease and IU; and re-institution of Rifampin was associated with another gut and IU disease remission. Since mouse ocular and systemic inflammatory disease producing non-cultivatable ultrastructurally unusual bacteria are commonly found within isolated chronic IU vitreous polymorphonuclear (PMN) leukocytes, a search for these bacteria in CD eye and gut disease seems justified, as the beneficial results of Rifampin in this study may have been an antimicrobial action on these bacteria.

Chronic idiopathic vitritis. Cytopathogenicity of unusual bacteria for vitreous polymorphonuclear leukocytes.

In acute exacerbations of chronic idiopathic vitritis (CIV) non-cultivatable ultrastructurally unusual 0.5-0.7 micron cell walled coccal bacteria (B) are commonly present within phagolysosomes of 3-5% of vitreous polymorphonuclear (PMN) leukocytes. Inoculation of that CIV vitreous into mouse eyelids produces chronic mouse vitritis (CMV) with identical B within CMV PMN leukocyte phagolysosomes. This transmission electron microscopic restudy of all PMN leukocytes in those 8 CIV and 3 CMV specimens demonstrated in all 11 severe cytoskeletal lytic damage associated with pleomorphic 0.1-1.4 micron cell wall deficient B in 1-2% of the cells; both those cell wall deficient and the unusual cell walled B within the same cell in 1-3 cells per specimens; and within the cell walled B complex internal structures resembling the cell wall deficient B. The study results suggest that the morphologically diverse B may be subportions of a single unusual pathogenic B, which parasitizes, undergoes complex morphologic differentiation within, and produces profound cytoskeletal damage to host PMN leukocytes.

Transmission of chronic idiopathic vitritis in mice by inoculation of human vitreous containing leucocyte phagolysosomal bacteria-like bodies.

Vitreous humour from chronic idiopathic vitritis (CIV) patients containing 0.5-0.7 micron diameter bacteria-like bodies (BLB) in polymorphonuclear leucocytes was inoculated into the eyelids of 100 mice. 200 control mice received either eye-bank vitreous or saline. After 12 months, 53 mice that received CIV vitreous, but none of the controls, had clinical signs of ocular inflammation (p less than 0.05); 15 of the mice that received CIV vitreous and none of the controls had histological evidence of chronic deep ocular inflammation, including vitritis (p less than 0.05); 95 CIV-vitreous-inoculated and 38 control mice were dead (p less than 0.05); and 3/3 of the CIV-vitreous group, compared with 0/3 controls, that were killed for histological assessment had phagolysosomal BLB identical to those in the CIV-vitreous inocula. The findings indicate that the BLB are pathogenic for mice.