The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario

1976 ◽  
Vol 54 (5) ◽  
pp. 634-643 ◽  
Author(s):  
Sherwin S. Desser ◽  
Andrée K. Ryckman
Keyword(s):  
Red Blood Cells ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Primary Infection ◽  
Clinical Signs ◽  
Peripheral Circulation ◽  
Branta Canadensis ◽  
Canada Geese ◽  
Severe Anemia ◽  
Branta Canadensis Interior

The development of Leucocytozoon simondi was studied in naturally and experimentally infected Branta canadensis maxima, Branta canadensis interior, and Anser domesticus. The number of mature round gametocytes in the peripheral blood of the Canada geese increased between days 9 and 15 post exposure (PE) and decreased rapidly thereafter. Mean peak parasitemias recorded on day 13 PE were (per 1000 red blood cells (RBC)): 8 gametocytes in B.c. maxima, 16 gametocytes in B.c. interior, and 17 gametocytes in A. domesticus. About 3 weeks PE, gametocytes disappeared from the peripheral circulation and were not observed again during the autumn, winter, and spring in birds kept in the laboratory.Haematocrit determinations in the Canada geese revealed a low fluctuating anemia during the primary infection which subsided by day 21 PE. A more severe anemia was recorded in A. domesticus with a mean low packed RBC value of about 18% on day 11 PE. Immature and mature hepatic schizonts were observed in the Canada and domestic geese between days 3 and 8 PE. Neither megaloschizonts nor elongate gametocytes were seen. Clinical signs, pathology, and mortality commonly associated with L. simondi infection in ducks were not observed. Hypotheses are advanced to explain reports of severe pathogenesis associated with L. simondi infections in Canada geese in other localities.

scholarly journals EXPERIMENTAL BONE MARROW REACTIONS

1926 ◽  
Vol 43 (4) ◽  
pp. 533-553 ◽  
Author(s):  
Gulli Lindh Muller
Keyword(s):  
Bone Marrow ◽  
Red Blood Cells ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Circulation ◽  
Similar Type ◽  
Bone Marrow Aplasia ◽  
Clear Cut ◽  
Initial Stage ◽  
Small Doses

1. The effect produced by the intravenous administration of collargol on the bone marrow of rabbits varies directly with the amount of collargol injected, and three fairly well defined stages could be recognized. (a) An initial stage after comparatively few and small doses, with erythrocytic and endothelial hyperplasia in the bone marrow and with evidences of this stimulation in the peripheral blood in the form of young erythrocytes and normoblasts. (b) An intermediary stage which followed the injection of larger amounts of collargol, and which was characterized by a predominant myeloid hyperplasia. (c) A final stage with marked bone marrow aplasia and with colloidal silver deposited in endothelial cells, as well as in clasmatocytes. This was associated with a high grade anemia with low color index, resembling aplastic anemia in its main features. This stage terminated fatally. 2. There was no evidence of injury to blood cells in the peripheral circulation. The erythrocytic bone marrow aplasia was present before any appreciable decrease of red blood cells was found in the peripheral blood. 3. The results were less clear-cut in a series of rats, but anemia of a similar type was produced in all animals when sufficiently large doses were injected. 4. Splenectomy did not alter the course in rats materially. 5. It is fair to conclude that the cause of the anemia produced may be sought in the deviation of the parental endothelial cell toward clasmatocyte formation at the expense of the development of erythrocytes. 6. It is suggested that the results may be offered in support of the theory of the endothelial origin of both clasmatocytes and red blood cells.

scholarly journals The mechanism of adaptation of the organism of patients with chronic heart failure combined with vitamin D deficiency and the morphofunctional state of peripheral blood erythrocytes

2019 ◽  
Vol 10 (3) ◽  
pp. 352-357
Author(s):  
N. I. Baryla ◽  
I. P. Vakaliuk ◽  
S. L. Pоpеl’
Keyword(s):  
Heart Failure ◽  
Vitamin D ◽  
Chronic Heart Failure ◽  
Red Blood Cells ◽  
Vitamin D Deficiency ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Functional Class ◽  
Exercise Stress ◽  
Control Group

The problem of structural changes in peripheral blood erythrocytes in patients with chronic heart failure in combination with vitamin D deficiency during exercise stress remains insufficiently studied. Vitamin receptors are located on smooth myocytes, endothelial cells, cardiomyocytes and blood cells. It affects the state of the cell membrane, the contractile function of the myocardium, the regulation of blood pressure, cardiac remodeling and reduction of left ventricular hypertrophy. Therefore, it is important to assess the level of vitamin D in blood plasma in individuals with chronic heart failure and to identify the effect of its deficiency on the state of peripheral red blood cells when performing a 6-minute walk test. A total of 75 patients of the main group with chronic heart failure stage II A, I–II functional class with different levels of vitamin D deficiency were examined. The control group included 25 patients with chronic heart failure stage II A, functional class I–II without signs of vitamin D deficiency. The average age of patients was 57.5 ± 7.5 years. All patients were asked to undergo the 6 minutes walking test. The level of total vitamin D in plasma was determined by enzyme immunoassay. Morphological studies of erythrocytes were performed on the light-optical and electron-microscopic level. The obtained results showed that patients of the main group with chronic heart failure had a decrease in vitamin D by 2.2 times compared with the control group. Correlation analysis showed a directly proportional relationship between vitamin D deficiency and the number of red blood cells of a modified form and red blood cells with low osmotic resistance. Dosed exercise stress in patients with chronic heart failure against a background of vitamin D deficiency leads to an increase in the number of reversibly and irreversibly deformed erythrocytes and a decrease in their osmotic stability. This indicates a disorder in the structural integrity of their membrane and can have negative consequences for the somatic health of such patients.

scholarly journals OVERVIEW OF MALARIA PARASITE AND ITS PREVENTION IN INDIA

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Adil Raza ◽  
Megha Chaudhary ◽  
Sonika Devi
Keyword(s):  
Red Blood Cells ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Malaria Parasite ◽  
Plasmodium Species ◽  
Peripheral Blood Smear ◽  
Infected Mosquito ◽  
Protozoan Parasites ◽  
Malaria Parasites ◽  
Genus Plasmodium

Background: Malaria is a systematic disease caused by a parasite called Plasmodium which is transmitted into the human blood via female Anopheles mosquito. Malaria in humans is caused by four species of protozoan parasites of the genus Plasmodium: P. falciparum, P. vivax, P. ovale, and P. malariae. The parasite enters the human body through a mosquito bite and travel to the very crucial organ, the liver, where they multiply and come back to the bloodstream and destroy red blood cells. Malaria causes symptoms that typically include fever, tiredness, vomiting, and headaches. In severe cases it can cause yellow skin, seizures, coma, or death. Symptoms usually begin ten to fifteen days after being bitten by an infected mosquito. In those who have recently survived an infection, reinfection usually causes milder symptoms. Objectives: Isolation of different species of malaria parasites. The prevalence of malaria parasite in India. Methods: The procedure follows these steps: collection of peripheral blood, staining of smear with Leishman’s stain and examination of red blood cells for malaria parasites under the microscope. Results: We observed the plasmodium species in peripheral blood smear. Conclusion: Worldwide, the number of cases of malaria caused by Plasmodium falciparum, the most dangerous species of the parasite, is on the rise.

Establishment of a murine model of cerebral malaria in KunMing mice infected with Plasmodium berghei ANKA

Parasitology ◽  
2016 ◽  
Vol 143 (12) ◽  
pp. 1672-1680 ◽  
Author(s):  
YAN DING ◽  
WENYUE XU ◽  
TAOLI ZHOU ◽  
TAIPING LIU ◽  
HONG ZHENG ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Cerebral Malaria ◽  
Plasmodium Berghei ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
Clinical Signs ◽  
Necrosis Factor Alpha ◽  
Experimental Cerebral Malaria ◽  
Km Mice

SUMMARYMalaria remains one of the most devastating diseases. Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection resulting in high mortality and morbidity worldwide. Analysis of precise mechanisms of CM in humans is difficult for ethical reasons and animal models of CM have been employed to study malaria pathogenesis. Here, we describe a new experimental cerebral malaria (ECM) model with Plasmodium berghei ANKA infection in KunMing (KM) mice. KM mice developed ECM after blood-stage or sporozoites infection, and the development of ECM in KM mice has a dose-dependent relationship with sporozoites inoculums. Histopathological findings revealed important features associated with ECM, including accumulation of mononuclear cells and red blood cells in brain microvascular, and brain parenchymal haemorrhages. Blood–brain barrier (BBB) examination showed that BBB disruption was present in infected KM mice when displaying clinical signs of CM. In vivo bioluminescent imaging experiment indicated that parasitized red blood cells accumulated in most vital organs including heart, lung, spleen, kidney, liver and brain. The levels of inflammatory cytokines interferon-gamma, tumour necrosis factor-alpha, interleukin (IL)-17, IL-12, IL-6 and IL-10 were all remarkably increased in KM mice infected with P. berghei ANKA. This study indicates that P. berghei ANKA infection in KM mice can be used as ECM model to extend further research on genetic, pharmacological and vaccine studies of CM.

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