Distribution Of Pathological Lesions Research Articles

Histopathological analysis of placental lesions caused by Chlamydia abortus 1B vaccine strain in vaccinated ewes

Background Chlamydia abortus is one of the most diagnosed causes of infectious abortion in small ruminants. Infections can be controlled using the live, attenuated C. abortus strain 1B vaccine, which has been associated with infection and abortion in animals. This study aimed to compare the severity and the distribution of lesions caused by this vaccine strain (vt) with those resulting from a wild-type (wt) infection. Methods Two grossly affected and 1B-positive (by qPCR and RFLP analysis) placentas from a vaccinated sheep flock were analysed. Histopathological lesions and immunohistochemical labelling (IHC) were graded (increasing score from 0 to 5) according to their severity and distribution. Pathology in the vt infected placentas was compared with that in two wt infected placentas. Datasets generated for observed histological and pathological features were analysed using principal component analysis (PCA). Results Histopathologically, the lesions in both vt and wt-placentas presented as typical multifocal necrosuppurative placentitis, associated with vasculitis, mural necrosis, and thrombosis. IHC for C. abortus revealed intense staining with a multifocal distribution in most cotyledons in both vt and wt placentas. Comparison of the pathological lesions between vt and wt by PCA revealed a similar distribution and severity, revealing a strong association with features such as necrosis and inflammatory infiltration between vt and wt placentas. A weaker association with IHC was observed. Conclusion This study shows that the C. abortus attenuated 1B vaccine strain presents no significant differences in severity and distribution of pathological lesions from those typically observed following a wt infection.

Retrospective Analysis of Oral and Maxillofacial Biopsies: An Institutional Study.

ABSTRACTAim:To determine the preponderance and the distribution of pathological lesions in oral and maxillofacial region reported in and around the Madurai city.Study Design:Retrospective study on the oral and maxillofacial biopsies taken during 11 years period from 2007 to 2018 in a CSI Dental College, Madurai, Tamilnadu. A total of 1000 cases were analyzed and 904 were selected. The parameters recorded were age, sex, area, and the histopathological report obtained. Descriptive statistics was used for analysis.Result:The most common soft tissue lesion was traumatic fibroma (16.1%) and the prevalent hard tissue lesion was periapical cyst (12.7%). The more common oral malignant tumour observed was squamous cell carcinoma (7.3%) and benign tumor was ameloblastoma (5.3%). The frequently affected sites were mandible (36.1%) and buccal mucosa (19.8%). There was more predilection among male than females. The frequency of lesion is common in age group of 31-60 years. A considerable similarity was observed between age, type of lesion and its location.Conclusions:This study evaluated chronic periapical lesions were the most common hard tissue lesions and fibromas in soft tissue category. The idea of this histopathological study concludes on the requirement for biopsy to rule out type of the lesion and its severity to start up the earlier management.

Pathomorphological changes of flunixin meglumine toxicity in layer chicks

The aim of the 21 day toxicity study was to evaluate the pathomorphological effect of flunixin meglumine in layer chicks. The chicks of Group I were kept as control while groups II, III and IV were fed with diet containing flunixin meglumine @ 10 ppm, 25 ppm and 50 ppm respectively for 21 days. Clinical signs viz. anorexia, dullness,lethargy, lameness and uneven growth were noticed in chicks of treatment groups III and IV only. Maximum mortality was observed in group IV (12%) followed by group III (4%). A dose dependant reduction in body weight was observed in all the treatment groups. The mean values of Kidney: Body weight ratio was significantly increased in group IV. The plasma uric acid, creatinine and BUN values were significantly increased in group III whereas increase in group IV was highly significant. Grossly, there was deposition of chalky white urates on serosal surface of kidney, heart and liver in chicks of group IV which died during experiment. Microscopically, lesions were characterized by varying degrees of congestion, haemorrhages, degeneration, necrosis and deposition of urate crystals in visceral organs of group III and group IV chicks. The intensity and distribution of pathological lesions were more severe in chicks of group IV, followed by chicks of group III. The overall lesions gave an impression that flunixin meglumine was nephrotoxic in nature.

Meeting an Early Medieval Community: A Preliminary Analysis of the Human Skeletal Remains from the Jucu Cemetery (Cluj-Napoca, Romania)

Necropola de la Jucu (jud. Cluj) – „ Tetarom III” – a fost cercetată în 2007 în urma săpăturilor arheologice de salvare determinate de necesitatea descărcării de sarcină arheologică a terenului pe care urma să fie amenajat parcul industrial Nokia. Zona este bogată în situri arheologice a căror datare merge din epoca neolitică până în secolul al XVIII-lea. Articolul de faţă prezintă rezultatele preliminare ale analizei antropologice efectuate pe 60 de schelete din această necropolă. S-a constatat astfel o rată ridicată a mortalităţii infantile, o slabă diferenţă între sexe în ceea ce priveşte patologia şi o talie medie apropiată de cea a altor populaţii europene din Evul Mediu timpuriu. Perioada în care necropola de la Jucu a fost folosită este caracterizată de intense migraţii. Numărul de surse scrise ce conţin informaţii referioare la această perioadă din istoria Transilvaniei fiind limitat, materialele arheologice şi osteologice reprezintă o sursă fundamentală în cunoaşterea istoriei acestei regiuni. Chiar şi într-o formă preliminară, studiul de faţă a permis obţinerea unor date preţioase asupra comunităţii de la Jucu.

Co-Infection with the Friend Retrovirus and Mouse Scrapie Does Not Alter Prion Disease Pathogenesis in Susceptible Mice

Prion diseases are fatal, transmissible neurodegenerative diseases of the central nervous system. An abnormally protease-resistant and insoluble form (PrPSc) of the normally soluble protease-sensitive host prion protein (PrPC) is the major component of the infectious prion. During the course of prion disease, PrPSc accumulates primarily in the lymphoreticular and central nervous systems. Recent studies have shown that co-infection of prion-infected fibroblast cells with the Moloney murine leukemia virus (Mo-MuLV) strongly enhanced the release and spread of scrapie infectivity in cell culture, suggesting that retroviral coinfection might significantly influence prion spread and disease incubation times in vivo. We now show that another retrovirus, the murine leukemia virus Friend (F-MuLV), also enhanced the release and spread of scrapie infectivity in cell culture. However, peripheral co-infection of mice with both Friend virus and the mouse scrapie strain 22L did not alter scrapie disease incubation times, the levels of PrPSc in the brain or spleen, or the distribution of pathological lesions in the brain. Thus, retroviral co-infection does not necessarily alter prion disease pathogenesis in vivo, most likely because of different cell-specific sites of replication for scrapie and F-MuLV.

Survival rate of airborne Mycobacterium bovis

Despite years of study the principle transmission route of bovine tuberculosis to cattle remains unresolved. The distribution of pathological lesions, which are concentrated in the respiratory system, and the very low dose of Mycobacterium bovis needed to initiate infection from a respiratory tract challenge suggest that the disease is spread by airborne transmission. Critical to the airborne transmission of a pathogenic microorganism is its ability to survive the stresses incurred whilst airborne. This study demonstrates that M. bovis is resistant to the stresses imposed immediately after becoming airborne, 94% surviving the first 10 min after aerosolisation. Once airborne the organism is robust, its viability decreasing with a half-life of approximately 1.5 hours. These findings support the hypothesis that airborne transmission is the principle route of infection for bovine tuberculosis.

Development and distribution of pathologic lesions are related to immune status and tissue deposition of human granulocytic ehrlichiosis agent-infected cells in a murine model system.

To evaluate pathology and the role of immune status in a murine model system of human granulocytic ehrlichiosis (HGE), C3H/HeJ, C3H-SCID, and Peromyscus leucopus mice were infected with an HGE agent. All mice remained healthy. Ehrlichemia was not detected after day 14 in P. leucopus and C3H/HeJ mice but increased between days 14 and 90 in C3H-SCID mice. In tissues examined at day 21 and later, infection was rarely detected in immunocompetent mice but was present in all C3H-SCID mice and included pulmonary endothelialitis and hepatic mononuclear cell aggregates with apoptoses. HGE agent was demonstrated in mature and immature myeloid cells in hematopoietic tissues and infrequently in lung and liver lesions with deposition of infected cells. HGE agent infection in immunocompromised mice progresses slowly, has a higher infectious burden and more tissue pathology and is persistent. A murine model for HGE may be useful to assess pathologic lesions, transmission, and persistence.

Atypical form of Alzheimer's disease with prominent posterior cortical atrophy: A review of lesion distribution and circuit disconnection in cortical visual pathways

In recent years, the existence of visual variants of Alzheimer's disease characterized by atypical clinical presentation at onset has been increasingly recognized. In many of these cases post-mortem neuropathological assessment revealed that correlations could be established between clinical symptoms and the distribution of neurodegenerative lesions. We have analyzed a series of Alzheimer's disease patients presenting with prominent visual symptomatology as a cardinal sign of the disease. In these cases, a shift in the distribution of pathological lesions was observed such that the primary visual areas and certain visual association areas within the occipito-parieto-temporal junction and posterior cingulate cortex had very high densities of lesions, whereas the prefrontal cortex had fewer lesions than usually observed in Alzheimer's disease. Previous quantitative analyses have demonstrated that in Alzheimer's disease, primary sensory and motor cortical areas are less damaged than the multimodal association areas of the frontal and temporal lobes, as indicated by the laminar and regional distribution patterns of neurofibrillary tangles and senile plaques. The distribution of pathological lesions in the cerebral cortex of Alzheimer's disease cases with visual symptomatology revealed that specific visual association pathways were disrupted, whereas these particular connections are likely to be affected to a less severe degree in the more common form of Alzheimer's disease. These data suggest that in some cases with visual variants of Alzheimer's disease, the neurological symptomatology may be related to the loss of certain components of the cortical visual pathways, as reflected by the particular distribution of the neuropathological markers of the disease.

Pathology of shigellosis and its complications.

One hundred and thirty-three colonic biopsies of proven cases of Shigella colitis were examined and post-mortem examinations were carried out on 29 fatal cases at the International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR, B) hospital between 1988 and 1992. The distribution of pathological lesions and the spectrum of histopathological changes in the intestinal tract of these patients, and the features of intestinal and extra-intestinal complications of shigellosis are presented. Septicaemia, hyponatraemia, hypokalaemia and hypoglycaemia were present in a high percentage of these cases. All but two patients were malnorished at the time of autopsy. Shigellosis patients rapidly became hypoproteinaemic and were susceptible to other infections including opportunistic infections. Mortality amongst shigellosis patients admitted to our hospital continues to be high in spite of adequate antibiotic and supportive therapy.

Neuropathology of Parkinson’s Disease and Related Syndromes

A progressive parkinsonian disorder predicts pathology in the substantia nigra and possibly elsewhere in the basal ganglia. Parkinson's disease is a manifestation of Lewy body disease, which is characterized by the association between Lewy bodies and cell degeneration in specific neuronal populations. Striatonigral degeneration is part of multiple system atrophy and is characterized by striatal and nigral degeneration without neuronal inclusion bodies, but glial inclusions have been described. Steele-Richardson-Olszewski disease is characterized by the globose neurofibrillary tangle and predominant brain stem pathology. Corticobasal degeneration shows similar midbrain pathology and a round, filamentous inclusion in the substantia nigra, not unlike the globose tangle, but there is also focal frontoparietal cortical atrophy. The combination of the distribution of degeneration and nerve cell morphology identify apparently distinct disorders, but most of the neuronal inclusions are not disease specific.

An Anatomic Substrate for Visual Disconnection in Alzheimer's Diseasea

During a recent clinical and neuropathologic evaluation of a large population of brains collected at autopsy, attention was drawn to a subset of Alzheimer's disease (AD) patients presenting with prominent visual symptomatology as the first sign of the disease. In this population, a shift in the distribution of pathologic profiles had occurred such that the primary visual areas and the visual association areas had an increased number of lesions, whereas the prefrontal cortex had fewer lesions than usually observed in AD. Previous quantitative analyses have shown that generally in AD, primary sensory cortical areas are less damaged than association areas of the frontal and temporal lobes, as demonstrated by the laminar and regional distribution of two neuropathologic hallmarks of the disease, neurofibrillary tangles and neuritic plaques. Furthermore, the distribution of pathologic lesions in the AD cases with visual symptomatology revealed the disruption of specific visual association pathways, which are normally affected to a lesser degree in AD. These data suggest that in some cases of AD, the particular psychologic and neurologic symptomatology may be caused by the selective loss of specific corticocortical systems, as reflected by a differential distribution of the neuropathologic markers of the disease.

Selective Disconnection of Specific Visual Association Pathways in Cases of Alzheimer's Disease Presenting with Balint's Syndrome

During a recent clinical and neuropathological evaluation of a large autopsy population of brains our attention was drawn to a subset of patients with Alzheimer's disease (AD) presenting with a major impairment of visuospatial skills referred to as Balint's syndrome. In this subset a shift in the distribution of certain pathological profiles had occurred in that the visual areas of the occipital and posterior parietal regions had an increased number of lesions, whereas the prefrontal cortex had fewer lesions than usually observed in AD. Previous quantitative analyses have shown that generally in AD, primary sensory cortical areas are less damaged than association areas of the frontal and temporal lobes, as demonstrated by the laminar and regional distribution of two neuropathological features of the disease, neurofibrillary tangles and neuritic (senile) plaques. The distribution of pathological lesions in the AD cases with Balint's syndrome revealed that specific visual association pathways were disrupted, which are normally spared in AD. These data suggest that in some cases of AD, the particular psychological and neurological symptomatology may be caused by the selective loss of specific corticocortical systems, as reflected in the differential distribution of the neuropathological markers of the disease.

Why do frontal lobe symptoms predominate in vascular dementia with lacunes?

We studied 30 necropsy cases of vascular dementia with a lacunar state. Manifestations included dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, urinary incontinence, grasp reflex, pyramidal signs, paraplegia in flexion, and akinetic mutism. Pathologically, there was diffuse incomplete softening of white matter in all cases. Both lacunes and diffuse softening were found predominantly in the frontal lobes. The prominent clinical features were therefore frontal lobe symptoms, with good correlation between the symptoms and the distribution of pathologic lesions.

Why do frontal lobe symptoms predominate in vascular dementia with lacunes?

We studied 30 necropsy cases of vascular dementia with a lacunar state. Manifestations included dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, urinary incontinence, grasp reflex, pyramidal signs, paraplegia in flexion, and akinetic mutism. Pathologically, there was diffuse incomplete softening of white matter in all cases. Both lacunes and diffuse softening were found predominantly in the frontal lobes. The prominent clinical features were therefore frontal lobe symptoms, with good correlation between the symptoms and the distribution of pathologic lesions.