scholarly journals The Pathology of Natural Fasciola hepatica Infection in Cattle

1969 ◽  
Vol 6 (3) ◽  
pp. 244-256 ◽  
Author(s):  
Timo Rahko

The pathology of bovinc livers during the parenchymal and chronic phases of natural Fasciola hepatica infections is described. Immature infections occurred from September to the middle of January. Significant changes of the hepatic parenchyma caused by immature flukes occurred in association with large migrational tracks. The changes included frequent thrombosis and haemorrhages, extensive disintegration and coagulative necrosis of hepatic cells, and abundant infiltrates of inflammatory cells. In chronic infections the proliferation and destruction of the mucosa of main bile ducts were pronounced. Normal mast cells were lacking in the portal areas surrounding fresh migrational tracks. In chronically infected livers mast cells occurred in great numbers.

Parasitology ◽  
1963 ◽  
Vol 53 (1-2) ◽  
pp. 135-143 ◽  
Author(s):  
Ben Dawes

During the early stages of infections of mice with Fasciola hepatica (6–11 days) the young flukes feed almost exclusively on hepatic cells which the oral sucker and the pharynx have broken down into a kind of homogenate containing Kupffer cells, invading leucocytes and some erythrocytes. As the flukes increase in size liver damage also increases in amount because of the larger burrows which are made. In some instances this does not adversely affect the host but in many infections excessive liver damage produces critical conditions which threaten the life of the host and its parasites. A comparison of the lesions produced in infections lasting 17–25 days with lesions produced after only 6–7 days has shown that the former, unlike the latter, are not due entirely to the feeding activities of the fluke. In short-term infections the inflammatory reaction produces the characteristic effects which are concerned with the healing of fluke tracts, but in older infections this reaction appears to be much more violent and tremendous leucocytic infiltrations break down apparently normal hepatic parenchyma and convert the terminal part of the burrow into a pool containing enormous numbers of invading leucocytes, broken hepatic cells and blood. These are the conditions which prevail at the onset of the critical period, when flukes have their growth inhibited as if by nutritional deficiencies. Some hosts are able to survive the critical period and nurture well-grown flukes for long periods, and may be able to obviate the critical conditions. It is suggested that the excessive damage which occurs in many instances during the critical period is not due to the feeding activities of the larger flukes but is a consequence of less restrained or even unrestrained inflammatory reactions which may lead to more serious pathogenic effects bordering on malignancy. This may be related to differences in the time spent by flukes in the hepatic parenchyma, early entry into the biliary system obviating these effects, late entry facilitating them.


1978 ◽  
Vol 15 (6) ◽  
pp. 763-769 ◽  
Author(s):  
R. A. Masake ◽  
R. B. Wescott ◽  
G. R. Spencer ◽  
B. Z. Lang

Primary and secondary infections of F. hepatica in mice were compared to determine how prior exposure to the parasite affected host response. Mice with primary parenchymal Fasciola infections initially had hemorrhagic tunnels filled with inflammatory cells and connective tissue. These lesions were progressive and became most severe 30 days after exposure as the parasites entered the bile ducts. At this time there was much hyperplasia and thickening of all layers of the duct system near the parasites and occasionally severe periportal fibrosis. By 2 months after exposure regeneration of the damaged liver cells was complete although hyperplasia persisted in bile ducts containing flukes. In mice with secondary infections (mice exposed 40 to 50 days after first infection), the inflammatory response was faster and shorter. Most lesions were resolved by 30 days after the second exposure. There was little difference in histology of primary and secondary infections during the chronic phase of the disease.


2005 ◽  
Vol 57 (2) ◽  
pp. 181-185 ◽  
Author(s):  
F. Kleiman ◽  
S. Pietrokovsky ◽  
S. Gil ◽  
C. Wisnivesky-Colli

The sensitivity and utility of a standard faecal sedimentation method (FSM) and a modified stool sieving staining method (FSSM), both currently employed for the diagnosis of Fasciola hepatica infection were compared. Faecal samples were obtained from 51 bovines of an endemic area for fasciolosis in Southwestern Argentina. Each sample was placed in a recipient containing 5% formalin. Eight millilitres of the suspension, equivalent to 2g of faeces, were used for each of the two methods tested. The number of eggs found per sample was recorded. The proportion of positive samples obtained by the FSSM (27/51) was significantly higher than that by the FSM (11/51) (P<0.05). The percent of agreement between methods was 41%. Over a total of 27 positive samples detected by the FSSM, the FSM missed 16, yielding 60% false negative samples. The FSSM enhanced 2.5 times the sensitivity of diagnosis. The complexity of the FSM may decrease its sensitivity through missing and loss of eggs during sample processing. These results confirmed that the commonly used FSM underestimates the prevalence and the egg output in cattle and that the FSSM is a more reliable diagnostic method.


Nature ◽  
1963 ◽  
Vol 198 (4876) ◽  
pp. 204-204 ◽  
Author(s):  
D. TEODOROVIĆ ◽  
I. BERKEŠ ◽  
M. MILOVANAVIĆ

2016 ◽  
Vol 38 (7) ◽  
pp. 387-402 ◽  
Author(s):  
L. Garza‐Cuartero ◽  
J. O'Sullivan ◽  
A. Blanco ◽  
J. McNair ◽  
M. Welsh ◽  
...  

2018 ◽  
Vol 09 (01) ◽  
Author(s):  
Carrera de Medicina ◽  
Mabel G ◽  
Greta M ◽  
William C ◽  
Maritza C ◽  
...  

1995 ◽  
Vol 182 (5) ◽  
pp. 1181-1190 ◽  
Author(s):  
M Triggiani ◽  
A Oriente ◽  
M C Seeds ◽  
D A Bass ◽  
G Marone ◽  
...  

Increasing evidence suggests that the metabolism of arachidonic acid (AA) may be different in inflammatory cells isolated from blood or migrating into tissues. To explore the possibility that changes in AA metabolism between blood and tissue inflammatory cells could be due in part to a different content or distribution of AA in glycerolipid classes, we studied these parameters in six human inflammatory cells isolated from blood (eosinophils, monocytes, neutrophils, and platelets) or from the lung tissue (mast cells and macrophages). Lung cells generally had a higher total cellular content of AA than that found in the blood cells. In addition, both mast cells and macrophages had a large endogenous pool of AA associated with triglycerides (TG), containing 45 and 22% of their total cellular AA, respectively. To address the hypothesis that cells migrating into the lung had a higher cellular level of AA and a larger AA pool in TG, we studied neutrophils isolated from the bronchoalveolar lavage (BAL) of patients with adult respiratory distress syndrome. BAL neutrophils had a fourfold increase in cellular AA as compared with blood neutrophils and contained 25% of their AA in TG versus 3% in blood neutrophils. BAL neutrophils also had a higher number of cytoplasmic lipid bodies (8 +/- 3/cell) relative to blood neutrophils (2 +/- 1/cell). High concentrations of free AA were also found in the cell-free BAL fluid of adult respiratory distress syndrome patients. To explore whether changes in BAL neutrophils may be due to the exposure of the cells to high concentrations of exogenous AA found in BAL, we incubated blood neutrophils in culture with AA (10-100 microM) for 24 h. Neutrophils supplemented with AA had a 10-fold increase in the amount of AA associated with TG and a sixfold increase in the number of lipid bodies. In addition, supplementation with AA induced a dose-dependent formation of hypodense cells. Taken together, these data indicate that human inflammatory cells undergo a fundamental and consistent remodeling of AA pools as they mature or enter the lung from the blood. These biochemical and morphological changes can be mimicked in vitro by exposing the cells to high levels of AA. This mechanism may be responsible for the changes in AA mobilization and eicosanoid metabolism observed in tissue inflammatory cells.


2018 ◽  
Vol 11 (1) ◽  
Author(s):  
Caroll Stoore ◽  
Constanza Andrade ◽  
Christian Hidalgo ◽  
Felipe Corrêa ◽  
Mauricio Jiménez ◽  
...  

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