scholarly journals American canine hepatozoonosis

2003 ◽  
Vol 4 (1) ◽  
pp. 27-34 ◽  
Author(s):  
R. J. Panciera ◽  
S. A. Ewing

AbstractAmerican canine hepatozoonosis is an emerging, tick-transmitted infection of domestic dogs caused by a recently recognized species of apicomplexan parasite,Hepatozoon americanum. The known definitive host of the protozoan is the Gulf Coast tick,Amblyomma maculatum. Presently recognized intermediate hosts include the domestic dog and the coyote,Canis latrans. Laboratory-reared larval or nymphalA. maculatumcan be infected readily by feeding to repletion on a parasitemic intermediate host; sporogony requires 35–40 days. Transmission of infection to the dog has been produced experimentally by oral administration of mature oocysts or oocyst-containing ticks. Canine disease follows experimental exposure in 4–6 weeks and is characterized by systemic illness, extreme neutrophilic leukocytosis, muscle and bone pain, and proliferation of periosteal bone. Histopathological findings include multifocal skeletal and cardiac myositis associated with escape of mature merozoites from within the host-cell environment. There is also rapid onset of periosteal activation and osteogenesis and, less frequently, glomerulopathy and amyloidosis. Sequential stages of development ofH. americanumin both the dog and the tick have been elucidated. Gamonts potentially infectious to ticks have been observed in peripheral blood leukocytes of the dog in as few as 28 days after exposure to oocysts. Young coyotes experimentally exposed to a canine strain ofH. americanumacquired disease indistinguishable from that of similarly exposed young dogs.

2020 ◽  
Vol 21 ◽  
pp. 100421
Author(s):  
Natalie D. Parkins ◽  
John V. Stokes ◽  
Nancy A. Gavron ◽  
Alexandra N. Frankovich ◽  
Andrea S. Varela-Stokes

2018 ◽  
Vol 14 (66) ◽  
pp. 075
Author(s):  
H. S. Lavryk ◽  
O. P. Korniychuk ◽  
Z. Ya. Fedorovych ◽  
Z. D. Vorobets

2020 ◽  
Vol 86 (5) ◽  
pp. 480-485
Author(s):  
Lior Segev ◽  
Ilana Naboishchikov ◽  
Diana Kazanov ◽  
Ezra Bernstein ◽  
Meital Shaked ◽  
...  

Background CD24 is a sialoglycoprotein anchored to the cell surface via glycosylphosphatidylinositol and is involved in intracellular signaling processes. It plays an important role in the early stages of the multistep process of colorectal carcinogenesis. Several single nucleotide polymorphisms in the CD24 gene are reported to exert a diverse effect on cancer risk. We aimed to elucidate whether CD24 TG/del genetic variants are associated with susceptibility to colorectal cancer (CRC). Methods The study included 179 subjects, 36 with CRC (prior to surgery) and 143 healthy control subjects. Deoxyribonucleic acid was purified from peripheral blood leukocytes, and by using restriction fragment length polymorphism analysis, the CD24 gene was genotyped for the specific genetic variant, TG deletion. Additionally, CD24 protein expression levels were determined by Western blotting analysis. Results The incidence of the TG/del was higher among the CRC patients compared with healthy controls, 14% and 10%, respectively ( P = .54). CD24 protein levels were significantly higher among CRC patients. There were no significant differences in CD24 expression between CRC patients at different stages of the disease or between patients who carry the mutation and those who did not. Conclusions CD24 genetic variant might be of clinical value for risk assessment as part of cancer prevention programs. Further study on larger populations is needed to validate the importance of this dinucleotide deletion in CRC development. Overexpression of CD24 protein occurs early along the multistep process of CRC carcinogenesis, and a simple blood sample based on CD24 expression on peripheral blood leukocytes can contribute to early diagnosis.


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