Mycobacterioses can produce nonspecific clinical signs in dogs and cats that make diagnosis difficult. Furthermore, the full characterization of mycobacterial agents is not always possible or practical. We characterized mycobacteria detected through cytology in 12 dogs and 7 cats with generalized clinical signs from the province of Buenos Aires in Argentina. In dogs, molecular testing confirmed the presence of Mycobacterium avium subsp. hominissuis (MAH) in 8 cases and M. fortuitum in 1 case. All dogs were Miniature Schnauzers, suggesting that this breed may be more susceptible to M. avium than other dog breeds. The cat isolates were 2 M. bovis, 1 M. fortuitum, and 1 MAH. Mycobacterial interspersed repetitive unit-variable-number tandem repeat patterns suggested possible links with cattle, swine, and humans studied previously in Argentina. The results show that pets may act as susceptible hosts with the potential risk of transmitting the infection to humans and other animals.
Platelets and their interaction with cells of the immune system contribute through a variety of molecular mechanisms to support hemostasis and inflammation. These simple yet essential cells exert their effects in lymphocytes, monocytes, and neutrophils, both recruiting and modulating their function after activation. Emerging evidence is starting to define the mechanisms that allow platelets to also play pivotal roles in host defense. For example, platelet cell-surface expression of toll-like receptors allows platelets to direct neutrophil activation toward extracellular trap formation and facilitate the elimination of blood pathogens. In addition to these well-known receptors, two of the most recently discovered platelet receptors, C-type lectin receptor 2 (CLEC-2), and TREM-like transcript-1 (TLT-1), have been shown to modulate hemostatic and inflammation-related roles in platelets. This review will discuss the evolution of our understanding of platelet functions from hemostasis to inflammation, and highlight novel mechanisms that platelets use to mediate hemostasis under inflammatory pressure.
Objective:
Older age and cardiovascular comorbidities are well-known risk factors for all-cause mortality in COVID-19 patients. Hypertension (HT) and age are the two principal determinants of arterial stiffness (AS). The objective of this study is to estimate AS in COVID-19 patients requiring hospital admission and analyze its association with all-cause mortality.
Design and method:
This cross-sectional, observational, retrospective multicenter study includes 122170 patients who required hospital admission in 150 Spanish centers, included in the nationwide SEMI-COVID-19 Network. We compared estimated AS as pulse pressure > 60 mmHg and compared clinical characteristics between survivors and nonsurvivors.
Results:
Mean age was 67.5 ± 16.1 years, 42.5% were women. Most patients were white (90.0%). Globally, 2606 (21.4%) subjects died. Blood pressure (BP) < 120 mmHg and BP > 140 at admission predicted higher all-cause mortality (23.5% and 22.8%, respectively, p < 0.001), compared to BP between 120–140 mmHg (18.6%). 4379 patients with AS (36.0%) were older and had higher systolic and lower diastolic BP. Multivariate analysis showed that even adjusting for gender (males, OR: 1.6, p = 0.0001), age tertiles (second and third tertiles, OR: 2.0 and 4.7, p = 0.0001), Charlson-Index (second and third tertiles, OR: 4.8 and 8.6, p = 0.0001), heart failure, previous and in-hospital antihypertensive treatment, AS and BP < 120 mmHg significantly and independently predicted all-cause mortality (OR: 1.27, p = 0.0001 and OR: 1.48, p = 0.0001, respectively).
Conclusions:
Our data show that arterial stiffness, defined as pulse pressure above 60 mmHg at hospital admission, and BP at admission < 120 mmHg were important determinants with independent prognostic value for all-cause mortality in COVID-19 patients requiring hospitalization.
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