Background The cytopathic effects of cytomegalovirus (CMV) infection have been well described since the virus was first reported; however, the morphology of CMV infection has not been clearly studied. We examined the difference in detailed cytologic findings in bronchial washing cytology between liquid-based and conventionally prepared smears. Methods: Bronchial washing cytology was processed using either the conventional preparation (CP) or liquid-based preparation (LBP). Sixty-nine cells with typical cytopathic effects of CMV infection were detected on CP slides and 18 cells on LBP slides. Using the image analyzer, area, circumference, major axis, and minor axis of the cytoplasm, nucleus, and intranuclear inclusion were measured in singly scattered CMV-infected cells, and histiocytes were used as a control. Results: The mean cytoplasmic area of CMV-infected cells was 1.47 times larger than that of histiocytes in CP and 2.92 times larger in LBP (p<.05). The mean nuclear area of CMV-infected cells was 2.61 times larger than that of histiocytes in CP and 4.25 times larger in LBP (p<.05). The nucleus to cytoplasm ratio and intranuclear inclusion to cytoplasm ratio of the mean area, circumference, major axis, and minor axis in CP were larger than those in LBP (p<.05). Conclusions: The sizes of cytoplasm, nucleus, and intranuclear inclusion were larger in LBP than in CP, indicating that CMV-infected cells are easily detectable in LBP. However, the nucleus-to-cytoplasm ratio was larger in CP, suggesting that differentiation from malignancy or regenerative atypia requires caution in CP.
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Cytomegalovirus (CMV) infection is an uncommon association with idiopathic inflammatory bowel disease (IBD) often leading to a variety of serious complications. A total of 41 resected cases of IBD were examined to elucidate the pathologic features of intestinal CMV infection which was assessed by histologic examination and confirmed by immunohistochemistry with CMV antibody. Six cases were positve for CMV antibody; five cases in 19 ulcerative colitis (UC, 26.3%) and one case in 22 Crohn's disease (CD, 4.5%). Of 7 cases of the steroid-treated UC group, five cases were superinfected with CMV (71.4%) but none in 12 cases of the steroid-untreated UC group. All of the five CMV-positive cases in UC showed deep ulceration and transmural inflammation, while none of 10 UC cases without above features were CMV positive. Fibrinoid necrosis and thrombi were found in 83.3% of the CMV infected group, while none in the CMV-negative group of UC cases (p=0.01). We conclude that IBD, particularly UC, is susceptible to the CMV infection when steroid hormone is administered, and that deep colonic ulceration, transmural inflammation and fibrinoid necrosis of vasculature may suggest superinfection of CMV in UC patients. It seems that deep colonic ulceration may be the consequence of an ischemic change following vascular luminal occlusion or vasculitis by CMV infection.
Gastrointestinal cytomegalovirus(CMV) infection in adults is observed as a part of a generalized or localized infection in patients who are immunocompromized. We report a case of CMV infection of the small intestine. The patient is a 34 year-old woman who has complained of palpable purpura in the lower extremities and buttocks, and arthralgia of large joints. The skin biopsy showed fibrinoid necrosis and neutrophils with leukocytoclasis, which findings are compatible with hypersensitivity angiitis. The patient received steroid and cyclophosphamide. During the follow-up period, generalized edema and bloody stool were detected.
Resected specimen of small bowel has multiple aphthous ulcer. Microscopically, cytomegalic cells are observed along the endothelial cells and mesenchymal cells. In situ hybridization using DNA probes against CMV revealed positive staining in the cytomegalic inclusions in vascular endothelial and mesenchymal cells.
Cytomegalovirus(CMV) infection can be diagnosed by finding characteristic intranuclear inclusion body and enlargement of the cell size congenital CMV infection can be associated with various types of anomalies seen in different gestational age. These anomalies are probable due to direct virus infection of the parenchymal cell m early gestation.
Based on four autopsy cases of congenital CMV infection we have studied maturation process of virus particles in parenchymal cells, with special reference to me mode of replication and transmission. Virus particles in CMV-infected cells in brain and kidney showed nucleocapsids with characteristic concentric core, that were enclosed around fibrillar network in nucleus. During replication process virions showed various morphogenic mutation that was rather consistent in different tissues and individuals.
There were virions without core or with eccentric core.
Occasional cores were divided into 2~5 fragments. The virus particles reached the cytoplasm through the nuclear membrane, and here the virions increased twice in size.
After virions were fully matured in the cytop1asm. they showed exocytosis phenomenon through the cellular membrane to reach extracellular portion.
This is an autopsy-verifed case of the generalized cytomegalic inclusion disease occuring in a male fetus of a weeks gestation. The fetus revealed hydrocephalus and focal necrosis of brain, focal subcapsular necrosis of liver, and the typical cytomegalic inclusion cells having large acidophilic intranuclear inclusions in the liver, brain, kidney, lung, adrenal gland, pancreas and chorionic villi.
Prominent extramedullary hematopoiesis was noted in the liver and kidney. Immuohistochemical staining using anti-cytomegalovirus antibody revealed intranuclear or occasionally intracytoplasmic immunoreactivity in brain, liver, pancreas, lung, kidney, and intestine.
We analysed 8 cases of gastrointestinal cytomegalovirus(CMV) infection including one autopsy, three surgically resected and four endoscopic biopsy cases. Involved sites were colon in four,stomach in three and small intestine in one. Three of them were associated with immu-nosuppressed condition but others had no clinical evidence of immune deficiency.
Multiple aphthous mucosal ulceration was a common presentation, but one revealed a mucosal ulcer with segmental narrowing and thickening of wall. Microscopically, six showed cytomegalic inclusions in endothelial cells and fibroblasts, one in mucosal epithelial cells and the remaining one in both endothelial cells and mucosal epithelial cells. Immunohistochemical staining using monoclonal antibody against CMV confirmed postive result in seven cases. Serum IgM anti-CMV antibody was elevated in one case. We conclude that gastrointestinal CMV infection is currently not a rare condition and frequently associated with non-immunosuppressed condition, and thus a thorough histologic examination is required especially in the gastrointestinal ulcerative lesion. Once cytomegalic inclusion is suspected, immunohistochemical identification of CMV seems essential for specific diagnosis.
To provide ideas for the recognition of neonatal and infantile liver diseases caused by cytomegalovirus(CMV) infection, histopathological examinations were made on hepatic tissues obtained by biopsy or autopsy from 23 patients. All patients were sero-positive for IgM anti CMV and had no other known or suggested etiologic factors for their liver disease. There were five different types of liver diseases: 8 cases of giant cell hepatitis(34.8%), 4 cases of biliary atresia(17.4%), 5 cases of biliary atresia with changes of neonatal hepatitis(21.7%), 4 cases of diffuse hepatic fibrosis(17.4%) and 2 cases of hepatic necrosis with CMV inclusion(8.7%). The diffuse hepatic fibrosis involved both the hepatic lobules and portal areas without evidences of regeneration. This type of liver disease appeared to be a chronic progressive illness that began during the first week of life, and in 3 of 4 cases, the liver biopsy was dong at 5 to 9 months after birth. The two patients showing CMV inclusion in their liver were premature of debilitated, and died within I month after birth. Diffuse hepatic necrosis as well as the cytomegalic change of bile duct epithelium was characteristic. The findings suggest that the pattern of CMV liver disease depends on the major site of hepatic injury, the status of status of patient's defense mechanism and the chronicity of illness.
This is to describe a neonatal hepatitis with pericellular hepatic fibrosis and Mallory bodies in a sero-positive infant for IgM anti-CMV. A necropsy of the liver revealed severe heaptocellular swelling with many intracytoplasmic hyaline bodies, pronounced fibrosis of a creeping type, bile stasis with ductular proliferation, and the lack of parenchymal regeneration. These microscopical changes of the liver resembled those of Indian Childhood Cirrhosis (ICC).
In the present case the patient's serum IgM anti-CMV is the only clue for the etiological diagnosis.