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Biomedical subjects

Z Ali-Khan

Publications and source records attributed to Z Ali-Khan.

At least 55 records · Page 3Linked to original sources
PubMed1982

Amyloidosis in experimental murine alveolar hydatidosis.

Male mice (eight to ten weeks old, C57BL/6J, H-2b strain) were inoculated intraperitoneally with 50 Echinococcus multilocularis cysts each and killed 12 and 17 weeks later. The alveolar cyst masses were weighed and the spleens and kidneys fixed for light and electron microscopy of sections. Amorphous eosinophilic deposits in both were extensive and there were apple-green birefringent deposits visible under polarized light in all the glomeruli. The presence of amyloid was confirmed by electron microscopy.

Amyloid↗
PubMed1981

Cysticercus racemosus in an eosinophilic phlegmon in the brain.

Cysticercus racemosus in a tumour-like mass from the brain of a 30-year-old Canadian was identified by histological and specific immunofluorescent techniques. The patient possibly acquired the infection during her stay in India. She had a mild peripheral eosinophilia and complained of pounding headaches and convulsions. Examination of tissue sections revealed the larva enclosed in an eosinophilic phlegmon and the surrounding brain tissue infiltrated by histiocytes and eosinophils. Loss of microtriches and degenerative changes in the larva were apparent in areas with adherent eosinophils. With the appropriate reagents, both intracellular and interstitial specific immune complexes were detected in the biopsied tissue. The course of infection in the cystic and racemosus types of cysticercosis and the role of tissue eosinophilia in neurocysticercosis have been discussed.

Adult↗
PubMed1980

Pathogenesis and host response in subcutaneous alveolar hydatidosis. I. Histogenesis of alveolar cyst and a qualitative analysis of the inflammatory infiltrates.

C57L/J male mice were infected subcutaneously in their left flank with 10 cysts of Echinococcus multilocularis. The dimensions and histologic features of the larval cyst mass (LCM) were determined at three days, at weekly intervals for 12 weeks, and at 22 weeks postinfection. The LCM doubled its size between 3 and 12 weeks, and at 22 weeks it was five times larger than at three weeks. During the proliferative phase, the LCM was infiltrated massively by neutrophils, macrophages, and progenitors of the plasma cell series. The first two cell types were found firmly bound to the laminated layer of both intact and degenerating cysts, whereas plasma cells colonized the fibrohistocytic corona and the interlacunar stroma harboring individual cysts. By 22 weeks, the proliferation of the cysts had ceased and histologically the LCM consisted of fibrous and fibrohistiocytic stroma, thick-walled fertile and sterile brood capsules, and predominantly plasmacytic and histiocytic infiltrates. In addition to exogenous budding evidence has been presented also suggesting the role of free germinal cells in the histogenesis of LCM. Regulation of cyst proliferation in susceptible hosts is discussed with reference to antibody-dependent cell mediated cytotoxicity with nonlymphoid inflammatory cells.

Animals↗
PubMed1980

Pathogenesis and host response in subcutaneous alveolar hydatidosis. II. Intense plasmacellular infiltration in the paracortex of draining lymph nodes.

Male C57L/J mice were infected subcutaneously in the left flank with 10 cysts of Echinococcus multilocularis. The draining and contralateral nodes were excised at weekly intervals, weighed, and examined histologically. Lymphoproliferation occurred in both the follicles and the paracortex (PCA) of the draining lymph nodes at one week postinfection (p.i.). Disorganization in the PCA of the draining nodes, was characterized by replacement of lymphocytes by plasma cells and the flattening of the endothelial cells lining the postcapillary venules. This began at three weeks p.i. and was completed by 12 weeks p.i. No comparable alterations occurred in the contralateral nodes during this period, but at 22 weeks p.i. these nodes were disorganized and histologically identical to the draining nodes. The growth and histogenesis of the subcutaneous alveolar cysts correlated with the expansion and disorganization of the PCA. The regulation of subcutaneous murine alveolar hydatidosis is discussed with reference to immune-deviation which is brought about by the antigenic load and plasmacellular infiltration in the draining lymph nodes.

Animals↗
PubMed1979

Humoral response to sheep red blood cells in C57L/J mice during early and chronic stages of infection with Echinococcus multilocularis cysts.

C57L/J male mice infected with Echinococcus multilocularis cysts were challenged intraperitoneally at 4, 8, and 12 weeks postinfection (p.i.) with 3 x 10(9) sheep erythrocytes. The direct plaque forming cells, 2-mercaptoethanol (2-ME) sensitive (4-day sera) and 2-ME-resistant (8-day sera) haemagglutinin responses were significantly elevated at eight and 12 weeks p.i. as compared to controls or the fourweeks postinfected mice. Possible mechanisms of immunopotentiation in the chronically infected mice is discussed in relation to the larval cyst mass, splenomegaly, and B cell hyperplasia in the lymphoid tissues during the course of infection.

Animals↗
PubMed1979

Human cysticercosis: a probable case of cerebral cysticercosis with generalized subcutaneous nodular lesions.

A case is reported in Montreal of human cysticercosis in a 44-year-old man who emigrated from Italy in 1956. Numerous subcutaneous nodules were found throughout his body. X-ray of his thighs and chest showed oblong calcific densities measuring 1 x 0.5 cm in size. Examination of an excised nodule from the right biceps revealed a cysticercus larva morphologically similar to Cysticercus cellulosae although the scolex lacked hooks. On the basis of the intensity of infection, focal and generalized epileptic seizures, changes in the CSF, and well demarcated lucencies observed in brain scan, cerebral cysticercosis was considered the most likely diagnosis.

Adult↗
PubMed1978

Pathological changes in the lymphoreticular tissues of Swiss mice infected with Echinococcus granulosus cysts.

Swiss mice infected intraperitoneally with approximately 1,500 protoscolices of Echinococcus granulosus and sacrificed at three and 13 months post infection yielded both viable and degenerated hydatid cysts. The mean cyst weights in the three and 13 months post infected mice were 0.13 and 2.1 g, respectively. Sections of spleens and lymph nodes in the three months post infected mice showed hyperplastic follicles and blastoid cells in thymus dependent areas. At 13 months post infection T cells from paracortex and periarterial areas were replaced by plasma cells and confluent sheets of histiocytes; follicles had retained germinal centres and medullary areas showed intense plasmacytosis and sinus histiocytosis. Failure of mice to control the histogenesis of hydatid cyst with reference to numerical reduction in T cells is discussed.

Animals↗
PubMed1978

Cellular changes in the lymphoreticular tissues of C57L/J mice infected with Echinococcus multilocularis cysts.

The pathology of the spleen, lymph nodes and thymus of C57L/J mice, infected intraperitoneally with 20 and 100 cysts of Echinococcus multilocularis is described at 2, 4, 8 and 12 weeks postinfection (p.i.). For the first 8 weeks, growth of the larval cyst mass (LCM) was slow and blastogenesis in T-dependent areas of both spleen and lymph nodes was moderate whereas in B-cell compartments it was intense. A rapid growth of the LCM between 8 and 12 weeks p.i., 15-20 times greater than for the first 8 weeks, was associated with depletion of lymphocytes in thymus dependent area (TDA) of both spleen and lymph nodes, gross expansion of the red pulp with extramedullary haemopoiesis, partial atrophy of spleen follicles, but not those of the lymph node, and involution of the thymus. At 12 weeks p.i. the TDA had mainly plasma cells and histiocytes among occasional lymphocytes and blast cells; germinal centre activity and plasmacytosis persisted in B-cell areas. Morphological aspects of these changes are discussed in relation to the invasiveness and proliferation of the LCM during the course of infection.

Animals↗
PubMed1977

Tissue pathology and comparative microanatomy of Onchocerca from a resident of Ontario and other enzootic Onchocerca species from Canada and the U.S.A.

The microanatomy of one male and one female specimen of a zoonotic Onchocera sp in a fibrous nodule excised from the wrist of an Ontario resident, two bovine Onchocerca from Saskatchewan and Manitoba, Canada, and O. cervicalis from the ligamentum nuchae of a horse in Georgia, U.S.A., were compared. In dimensions and cuticular morphology, the three Canadian specimens of Onchocera shared certain features and closely resembled both O. cervicalis and O. gutturosa. The number of cuticular striae in some species of Onchocerca, particularly in male worms, is briefly discussed and its taxonomic value questioned. The Canadian patient visited Radlett, Hertfordshire, England, and then her summer cottage in the Muskoka region, Ontario, prior to the appearance of her symptoms, so that it is uncertain where she acquired the infection. Zoonotic onchocerciasis has yet to be described from Ontario. All nine cases of bovine onchocerciasis (the two described here and seven others) have occurred in Manitoba and Saskatchewan.

Adult↗
PubMed1975

Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis.

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.

Colon↗