Histopathological changes in skeletal muscle associated with chronic ischaemia

Muscle biopsy is an essential part in the diagnostic workup in patients with suspected neuromuscular disorders. It is therefore important to be aware of morphological alterations that can be caused by systemic factors or natural ageing. Chronic limb ischaemia is frequent in elderly individuals. This study was performed to examine histopathological and mitochondrial changes in muscle in patients with chronic critical limb ischaemia. Muscle biopsy of skeletal muscle of the lower limb of patients with chronic ischaemia leading to amputation was performed and compared with muscle biopsies of healthy, age‐matched controls. The histopathological abnormalities included fibrosis, necrosis, atrophy, glycogen depletion, internal nuclei, rimmed vacuoles, fibre type grouping, cytochrome c oxidase deficient fibres, MHC‐I upregulation, and signs of microangiopathy. The only alteration found in age‐matched controls was a few cytochrome c oxidase deficient fibres. There were also increased levels of multiple mitochondrial DNA deletions in ischaemic muscles compared with controls. Critical limb ischaemia is associated with significant histopathological changes in muscle tissue and also increased levels of mitochondrial DNA deletions. Since the alterations mimic different primary myopathic changes, chronic ischaemia is important to consider as a differential diagnosis in elderly individuals, investigated with muscle biopsy for muscle disease.     

Histopathological and ultrastructural alterations of induced Yersinia enterocolitica infection in mice

Yersinia enterocolitica is an enteric bacterium and infections by this organism are mostly foodborne. It has been implicated to cause enterocolitis, terminal ilitis. diarrhoea, mesenteric lymphadenitis and arthritis in man. Due to paucity of information regarding histopathological and specially ultrastructural alterations in tissues affected, this study was planned with mice as the experimental model. Nine pathogenic Y.enterocoliticaisolates were used to infect 80 albino mice by oral and intraperitoneal route. Pathological alterations were studied by light and electron microscopy. Histopathological examination of intestines showed severe edema, purulent enteritis, goblet cell hyperplasia infiltration of mononuclear cells, thickening of mucosa and necrosis of the tips of villi. Liver showed congestion, hepatocellular degeneration and necrosis, atrophy of hepatocytes and microabcesses. The lungs revealed congestion, edema, haemorrhage and purulent ronchopneumonia, while kidneys showed mild necrotic changes and bacterial emboli in glomeruli. Ultrastructural changes were indicative of mitochondrial degeneration and their loss in kidneys, membranous degeneration with formation of myelin figures in lungs and disorganization, disruption and bleb formation of microvilli in intestines. Y.enterocolitica caused significant histopathological and ultrastructural alterations in experimentally infected mice. Variation in pathogenicity of different strains of Y.enterocolitica was also observed.     

Histopathological changes in simian immunodeficiency virus infection

The histological lesions were studied in seven rhesus and three cynomolgus monkeys infected with simian immunodeficiency virus for periods ranging from nine weeks to 18 months. Lymphoreticular changes included hyperplasia, follicular involution and depletion, and one animal had amyloidosis of the spleen. Hyperplastic changes also took place in mucosa-associated lymphoid tissue and infiltrations occurred in the vaginal mucosa of one animal, which could be significant in sexual transmission of the infection. The range of opportunistic infections was small compared with that in human AIDS patients, although two monkeys had Pneumocystis carinii pneumonia. Enterocolitis was a common finding and brown adipose tissue was transformed into a large vacuolated type. Lesions of the central nervous system were found in five of nine monkeys, and consisted of foci of glial activity and perivascular and meningeal lymphocytic infiltration. A lymphoma involving the lumbar spinal cord developed in one animal.     

Histopathological and ultrastructural changes in 57 cases of high altitude heart disease]

This paper reports the histopathologic and ultrastructural changes in 37 children and 20 adults with high altitude heart disease. Its clinicopathologic features, diagnostic criteria and differential diagnosis from Ke-shan disease and other heart diseases are discussed. The right heart of 37 children showed hypertrophy and dilatation. Microscopically, necrosis and scarring were found mainly in the right ventricular wall (29/37) and the anterior papillary muscles (29/37) of the right ventricle. The hearts of 20 adults (19 Hans and 1 Tibetan) were enlarged and increased in weight. Heart weight increased to 400-500g in 15 cases, and hypertrophy of both ventricles was seen in 16 cases. Necrosis and scarring were found mainly in the papillary muscles (20:16) and the ventricular walls (11:19) of the left and right ventricles. Electronmicroscopy showed that myofibrils were dissolved or degenerated, mitochondria swelled, endoplasmic reticula dilated and glycogen granules decreased. As regards the pathogenesis, the authors stress the role of chronic hypoxia which causes myocardial damage, and advocate the importance of early diagnosis and treatment.     

Histopathological classification of lesions associated with natural paratuberculosis infection in cattle

Paratuberculosis-associated lesions in 116 naturally infected adult cows, with or without clinical signs, were classified histopathologically. Tissue samples obtained focused on gut-associated lymphoid tissue. Lesions were divided into five categories. Focal lesions (n=68 cases), consisted of small granulomas in the ileal and jejunal lymph nodes or the ileocaecal lymphoid tissue. In the multifocal type (n=13 cases), small granulomas or scattered giant cells appeared in some intestinal villi, as well as in the lymph nodes. Diffuse multibacillary lesions (n=15 cases), associated with severe granulomatous enteritis affecting different intestinal locations and lymph nodes, were formed by macrophages containing large numbers of acid-fast bacilli. In diffuse lymphocytic lesions (n=3 cases), lymphocytes were the main inflammatory cells, with some macrophages or giant cells containing few if any mycobacteria. In diffuse intermediate forms (n=17 cases), the infiltrate was formed by abundant lymphocytes and macrophages, and mycobacteria were present to varying degrees related to the number of macrophages. Clinical signs and gross lesions were mainly associated with diffuse forms. Thickening of the intestinal wall, which was the most common macroscopical finding, was related to the degree of submucosal change. Mycobacterium avium subsp. paratuberculosis was identified by culture or PCR in all cows with diffuse lesions, and in 55.5 and 37% of those with multifocal or focal forms, respectively. The importance of sampling the ileal and caudal jejunal lymph nodes to find histological lesions of paratuberculosis in cattle is emphasized.     

人巨细胞病毒感染胎鼠大脑皮质神经元显微和超微结构观察

目的：研究人巨细胞病毒（HCMV）经小鼠胎盘垂直传播致胎鼠大脑皮质神经元病理改变的显微和超微结构特征。方法：在8－12周龄Balb/c雌雄小鼠腹腔内接种HCMV后,交配,特孕鼠临产时剖腹取出10份胎鼠双侧大脑皮质,用光镜和透射电射观察了神经元的显微和超微结构,同时进行了病毒分离。结果：光镜下可见胎脑微血管扩张充血,神经元数目明显减少,残存的神经元缺血性改变,间质水肿;可见到软化灶及受染神经元核内及胞质内HCMV特征性哮碱性和哮酸性包涵体,电镜下可见受染神经元核仁消失,胞质内线粒体,内质网和高尔基复合体等重要细胞器结构严重破坏呈空泡状或溶解;并找到人类疱疹病毒样颗粒。病毒分离阳性,在同时设置的正常对照组则无上述阳性发现。结论：HCMV能通过小鼠胎盘感染子代胎鼠大脑皮质神经元,并导致神经元结构破坏死亡。     

Potassium accumulation in smooth muscle and associated ultrastructural changes

1. The water content, extracellular ((60)CoEDTA) space, ionic composition and ultrastructure of several mammalian smooth muscles were studied after incubation in solutions of varying ionic compositions and osmolarities.2. Substitution of KCl for NaCl resulted in an increase in cell water, K and Cl, accompanied by little change in total wet weight. This was due to a reduction in the extracellular space.3. Changes in extracellular osmolarity produced a wider range of cell volumes in high KCl solutions than in Krebs. The addition of 29-58 mM sucrose to high KCl prevented the swelling.4. Electron microscopy of smooth muscle swollen in high KCl solution revealed light (less electron opaque than normal) fibres of increased diameter, reduction in extracellular space, and nuclear swelling. The normal thick filament lattice was destroyed in swollen, osmium-fixed smooth muscles.5. The ultrastructural changes ascribed to swelling were absent in smooth muscles, (a) depolarized in high K(2)SO(4) solutions, (b) in high KCl solutions with 29-58 mM sucrose, and (c) returned to normal Krebs solution for recovery from swelling.6. Smooth muscles incubated in high KCl (swollen) and high K(2)SO(4) (unswollen) exhibited similar contractile responses, suggesting the filament lattice was intact until fixation, and that the contractile mechanism can operate over a relatively wide range of actin to myosin separations.7. Shrinkage of smooth muscles in high KCl solutions made hypertonic with the addition of 10% sucrose was accompanied by an aggregation of the thick filaments.8. The cell water of fixed taenia coli was reduced (a) by incubation in hypertonic solution followed by fixation in normal glutaraldehyde, or (b) by fixation of normal tissue in hypertonic glutaraldehyde. Osmotic responses during aldehyde fixation may be a source of artifact in the visualization of the normal filament lattice.     

Early ultrastructural changes in rat duodenal mucosa associated with cysteamine-induced ulcer

The early morphologic sequelae induced by the duodenal ulcerogen, cysteamine, have been studied in rats by transmission electron microscopy. Cysteamine was administered per os at 70 mg/100 g body wt to groups of female rats sacrificed at 30 min, 1, 2, 4, 8, 12, 20, and 24 hr after chemical treatment, and duodenal tissue sampled from the antimesenteric side of the proximal duodenum, where ulcers develop, was studied. Emphasis was placed on early times as our previous scanning electron microscopic data had demonstrated enhanced in situ cellular necrosis and surface cavitation at 2-4 hr after cysteamine treatment. Results indicated intracellular changes as early as 30 min after treatment and prior to damage of the columnar cell microvilli or epithelial tight junctions. A staging of observed cellular degenerative changes suggested early apical endoplasmic reticular swelling and loss of cytoplasmic ground substance, followed later by moderate internal disruption of mitochondria. Through these stages the cell surface microvilli remained morphologically normal. Subsequently, microvilli degenerated and mitochondrial fine structure became severely disrupted and cell contents were expelled. Deeper villous changes such as separation of columnar cells from the lamina propria and alterations of selected elements within the lamina propria were observed. These data suggest that intracellular cytotoxic reactions at the villous tips occur early and may precede the influence of intraluminal damaging factors induced by cysteamine.     

Histopathological and ultrastructural changes in the gills of Poecilia reticulatus induced by an organochlorine pesticide

After exposure to 1.2-3.0 ppb of DDT in an aquatic-terrestrial model ecosystem, the gills of guppies showed histopathological changes when examined by light and electron microscopy. The secondary lamellae of the gills were shortened and deformed and the epithelial cells were disoriented with regard to the pillar cell system. In many places erythrocytes were virtually absent from the blood laguna, which was filled with the flanges of pillar cells. The microfilament bundles in the pillar cell cytoplasm had disintegrated. The chloride cells were swollen and alterations had occurred in their mitochondria and nuclei. The changes did not resemble the typical non-specific pattern of pesticide poisoning, and were probably specific to DDT.     

Kaposi's sarcoma associated with previous human herpesvirus 8 infection in kidney transplant recipients

This study investigates the prevalence of human herpesvirus 8 (HHV-8) infection in kidney transplant patients, evaluating the risk of HHV-8 transmission via transplantation and the association between pre- and posttransplantation HHV-8 infection and the subsequent development of Kaposi's sarcoma (KS). Immunofluorescence and an enzyme immunoassay were used to determine HHV-8 seroprevalence in 175 patients awaiting kidney transplantation and 215 controls who were attending our clinic for other reasons. All patients in the study came from central or southern Italy. Seroprevalence was similar in both groups (14.8 versus 14.9%), with no significant difference between the rates for male and female patients. Of the 175 patients, 100 were tested for anti-HHV-8 antibodies at various times during follow-up. During follow-up, seroprevalence increased from 12% on the date of transplantation to 26%. This increase was paralleled by an age-related increase in seroprevalence in the control group. During follow-up from 3 months to 10 years after transplantation, KS was diagnosed in seven patients (4.0%). Six of these patients were positive for HHV-8 prior to transplantation. Overall, 23.0% of patients who were HHV-8 positive before transplantation developed KS, whereas only 0.7% of seronegative patients developed the disease (relative risk, 34.4; 95% confidence interval, 4.31 to 274.0). This finding suggests that the key risk factor for KS is infection prior to transplantation and that antibody detection in patients awaiting transplantation could be useful in identifying patients at high risk for KS. In patients from geographic areas with a high prevalence of HHV-8, serological tests on donors may be less important.     

Kaposi's sarcoma associated with previous human herpesvirus 8 infection in heart transplant recipients

The aim of this study was to evaluate the seroprevalence of human herpesvirus 8 (HHV-8) in a group of 150 patients awaiting heart transplants and to detect HHV-8 seroconversion after transplantation. Four patients were HHV-8 seropositive before transplantation, and one of them developed Kaposi's sarcoma. One patient converted to seropositive HHV-8 status after transplantation.     

Morphofunctional changes in guinea pig ovaries in experimental chronic herpesvirus infection

The ovaries of adult guinea pigs infected with herpesvirus-2 were examined by light microscopy under conditions of latent infection and relapse of infectious process. Morphofunctional changes in the ovarian follicles at all stages of folliculogenesis and in ovarian stroma were caused by the negative effects of type 2 herpes simplex virus. Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 146, No. 8, pp. 221–225, August, 2008     

Trichodinosis associated with pathology of the reproductive tract in waterfowl

Trichodinid ciliophorans are opportunistic parasites of many species of fish, amphibians, and molluscs, but yet never reported in association with lesions in birds. Postmortem and histopathological evaluation of a commercial adult Toulouse gander and female goose, and a wild Mallard drake revealed the presence of severe pathological parasitic colonization of their reproductive tracts. Histopathological findings included moderate to severe granulocytic inflammation, acanthosis, accentuation of the rete pegs, and proliferative hyperplastic squamous metaplasia of the mucosa of the ejaculatory ducts and groove, sulcus spermaticus, glandular part of the phallus (cavum penis), and oviduct in association with large numbers of ciliated protozoa anchored to the tissues or free in the lumen. These protozoa had characteristic morphological features analogous to the family of Trichodinidae. The source of this parasitism could not be determined. To our knowledge, this is the first report of trichodinosis associated with pathology in birds.     

Histopathological and ultrastructural studies on human cutaneous leishmaniasis

Leishmania, a genus of intracellular protozoan parasites of macrophages, is the etiologic agent of cutaneous and visceral disease in man. In our study, localized cutaneous infections with leishmania were studied by light and transmission electron microscopy in 16 patients at phases ranging from onset to a progressive disease. In early infections, epidermal changes could be detected as deep hemorrhagic ulcer characterized by focal massive necrosis of the epidermal layers. Spongiotic vesicles in the epidermis were prominent containing the amastigotes. The dermal changes appeared in the form of diffuse inflammatory infiltrate predominantly composed of macrophages, epithelioid cells, lymphocytes, mast cells, and few plasma cells and eosinophils. Macrophages laden with the parasites were seen dissociating the striated muscle and the collagen bundles which showed degenerative and necrotic changes. In late stages of the disease, multiple granulomas formed predominantly of macrophages containing promastigotes and amastigotes, giant cells, epithelioid cells, and some mast cells were seen in the dermis. Some macrophages appeared vacuolated and loaded with the parasite. The dermal vasculature showed congestion, swelling of the endothelial cells, and fibrinoid necrosis of the wall. Some congested blood vessels demonstrated margination and diapedesis of inflammatory cells. By transmission electron microscopy, intact and degenerated amastigotes were seen phagocytosed inside the macrophagal parasitophorus vacuoles. Erythrophagocytosis and the reaction of other inflammatory cellular components were also described. These results clarified the lesions of leishmania invasion into the skin of the affected patients and its defensive mechanism. Moreover, the host macrophagal–parasite relationship was shown on ultrastructural level.     

针刺损伤兔椎间盘退变模型组织病理变化及软骨样细胞的迁移规律**☆

背景：兔椎间盘退变模型间盘退变表现为随时间进展脊索细胞将被软骨样细胞逐渐替代,但兔针刺纤维环间盘退变模型中软骨样细胞的来源和移行规律尚不明确。 目的：观察针刺兔纤维环间盘退变模型椎间盘病理变化过程,并初步探讨软骨样细胞来源及移行规律。 方法：将24只新西兰大白兔随机分为手术组与假手术组。手术组使用16 G穿刺针针刺L2/L3、L3/L4、L4/L5及L5/L6椎间盘纤维环,假手术组暴露至相同椎间盘前方后冲洗闭合伤口。 结果与结论：针刺损伤椎间盘退变过程中的软骨样细胞来源于终板。在髓核与上下终板交界处,软骨细胞脱离终板成串向髓核中心迁移;在髓核与内层纤维环交界处,软骨细胞沿纤维走行迁移并随之向皱缩的髓核边缘迁移。椎间盘退变过程中非钙化层逐渐变薄,非钙化层/钙化层比值逐渐降低。 关键词：椎间盘退变;软骨细胞;软骨终板;纤维环穿刺;新西兰大白兔  doi:10.3969/j.issn.1673-8225.2012.09.018     

Histopathological changes in the oviduct of hens producing shell-less eggs associated with precipitins to adenovirus

Histopathological changes in oviducts of laying hens which produced shell-less eggs associated with the presence of precipitins to adenovirus appeared to be limited to the uterus (shell-gland). Changes could not be seen macroscopically. Microscopically extensive atrophy of the glandular tissue, oedema and infiltration by plasma cells and lymphocytes in the uterine villi were observed. The changes are compared with those described for infectious bronchitis virus infection.     

Congenital infection with human herpesvirus 6 variant B associated with neonatal seizures and poor neurological outcome

Human herpesvirus 6 (HHV 6) has neurotropic and neuroinvasive properties. The virus has been found in the cerebrospinal fluid of many children with aseptic meningoencephalitis. Intrauterine transmission has been documented by HHV 6 DNA detection in cord blood specimens of apparently healthy newborns and in fetuses following spontaneous abortions. A patient is described with early neonatal afebrile seizures resulting from a congenital HHV 6 variant B infection disclosed by repeated detection of viral genome by polymerase chain reaction (PCR) in cerebrospinal fluid in the first days of life. At follow-up, magnetic resonance imaging (MRI) studies disclosed hyperintensities in the periventricular white matter and basal ganglia, associated with cerebral atrophy. Further follow-up at 18 months revealed poor neurological outcome with mild neurodevelopmental retardation, strabismus and hypertonia of legs. This report provides evidence of neurological involvement after HHV 6 vertical transmission, and the association with neurological sequelae.     

Histopathological and ultrastructural features of dermal telangiectasias in systemic sclerosis

AIMS: To investigate the histological, ultrastructural and immunohistochemical features of the vascular lining of dermal telangiectasia, a characteristic clinical finding in scleroderma. METHODS: Standard histological, electron microscopic and immunohistological techniques were used to examine dermal telangiectasias in five patients with limited scleroderma, the most common scleroderma variant in Caucasian populations. RESULTS: The telangiectasias were dilated postcapillary venules located in the papillary and superficial reticular dermis. The vessel walls consisted of non-fenestrated endothelial cells surrounded by a variable number of pericytes and smooth muscle cells. There were no unique ultrastructural features. Thickened collagen fibres in the reticular or deep dermis were seen in all but one patient, although in variable and generally minimal quantities. Surrounding infiltrating inflammatory cells were scarce. No enhanced endothelial staining was obtained with antibodies directed against endoglin, endothelin, E-selectin and ICAM-1 suggesting a resting or inactivated state. CONCLUSION: The immunohistological and ultrastructural features of the lining endothelium of established telangiectasias in long-standing, limited scleroderma appear benign. It would be of interest to examine telangiectasias in the early phase of their formation. Alternatively, other explanations need to be explored in understanding the aetiopathogenesis of telangiectasia in scleroderma.     

Epididymal ultrastructural changes associated with chronic cholestasis after bile duct ligation in adult rats

Testicular atrophy and testesterone insufficiency have been commonly reported associated with chronic liver diseases. Though testosterone dependent, the epididymal changes induced by liver disease have never been studied before. Thus, this study aimed to assess the ultrastructural events in the epididymis of rats with chronic obstructive jaundice. Chronic cholestasis induced many epididymal structural alterations manifested by the reduced tubular diameters, thickening of the tubular basement membrane, and regression of the principal cells. This was accompanied with reduction of principal cell organelles, cytoplasmic vacuolations, nuclear alterations, and stereovilli loss. The results establish that chronic cholestasis causes epididymal structural changes due to androgen deficiency.