Detection of rat lungworm (Angiostrongylus cantonensis) infection by real-time PCR from the peripheral blood of animals: a preliminary study.

Rat lungworm disease or neuroangiostrongyliasis is a cerebral parasitic infection that affects humans and animals alike. Its clinical signs and symptoms can range from mild self-resolving to serious life-threatening conditions. Studies suggest therapeutic interventions during the early stages of infection to be more effective than in later stages. However, early diagnosis of infection is usually problematic without the knowledge of exposure and/or detection of the parasite's DNA or antibody against the parasite in the cerebrospinal fluid. This requires a lumbar puncture, which is an invasive procedure that generally requires hospitalization. This study evaluates an affordable and less invasive alternative to detect parasitic DNA by PCR from the peripheral blood of potentially infected animals. Blood samples from 58 animals (55 dogs and 3 cats) with clinical suspicion of infection were submitted to our lab between February 2019 and August 2022 by local, licensed veterinarians. DNA was extracted from whole blood, plasma, serum, and/or packed cells using the Qiagen DNeasy Blood & Tissue Kit as per the manufacturer's protocol. All 58 animals were tested by real-time PCR using the AcanITS1 assay and 32 of these animals (31dogs; 1 cat) were also tested using the AcanR3990 assay. The PCR results for both assays were classified into strongly positive > positive > weakly positive > negative, and equivocal for ambiguous results, based on the strength of the signal. The percent infection detected using the AcanITS1 and AcanR3990 assays was 12.72% (7/55) and 20.68% (6/29), respectively. The overall percent infection detected was 34.37% (11/32), with only two animals testing positive by both assays. The three cats involved in this study tested negative by both assays. These results are promising and warrant further investigations to increase sensitivity including variables that might affect detection in the blood, such as parasite load, and laboratory methodologies.

Effects of antiplatelet agents on outcomes for elderly patients with traumatic intracranial hemorrhage.

BACKGROUND: Recent literature on elderly patients with traumatic intracranial hemorrhage receiving preinjury antiplatelet agents shows a mortality rate of 47%. METHODS: In a retrospective analysis, patients older than 50 years presenting to the hospital over the past 4 years with traumatic intracranial hemorrhage and the use of aspirin, clopidogrel, or a combination were compared with a control group that had hemorrhage but no antiplatelet medications. Patient demographics, mechanism of injury, and injury scores were recorded. RESULTS: No significant differences were found between the 90 study patients and the 89 control subjects in terms of demographics, mechanism of injury, Injury Severity Score, Glasgow Coma Score, or hospital length of stay. Patients receiving antiplatelet therapy had significantly more comorbid conditions (71% vs. 35%; p < 0.001). In this series, 21 study patients and 8 control patients died (23% vs. 8.9%; p = 0.016). Age older than 76 years and a Glasgow Coma Score lower than 12 were correlated significantly with increased mortality. CONCLUSIONS: The use of antiplatelet agents with elderly trauma patients significantly increases the risk of mortality when head injury involves intracranial hemorrhage.

Complications of preinjury warfarin use in the trauma patient.

BACKGROUND: The frequency of use of warfarin anticoagulation increases significantly in the elderly population. It remains controversial whether this puts these patients at increased risk for hemorrhagic complications after trauma. METHODS: We prospectively evaluated consecutive trauma patients who were taking warfarin and compared their outcomes to a group of age-matched patients with head injuries but not taking warfarin. RESULTS: One hundred fifty-nine trauma patients on warfarin were evaluated, 94 (59%) with some type of head trauma; 25 of these 94 patients (27%) had documented intracranial trauma. Fifteen patients died (9.4%); they had an international normalized ratio of 3.3 +/- 1.6 versus 3.0 +/- 2.1 for survivors in the warfarin group (p = 0.585). Twelve deaths were in the group of 25 patients with intracranial injuries (48%). Three patients without head injury died (5%) of other causes not related to warfarin or hemorrhage at a mean of 13 days after admission. Ten of 12 patients on warfarin with intracranial injuries who died had documented loss of consciousness (LOC); two patients who died secondary to an isolated intracranial injury had no LOC. Of 70 age-matched patients with head trauma not taking warfarin, 47 (67%) had intracranial injury and 5 of these died (10%) (p < 0.001 for both values compared with study patients). There were no significant differences for patients with intracranial injury comparing those on warfarin and those who were not in terms of age, gender, mechanism of injury, Injury Severity Score, or Glasgow Come Scale score. CONCLUSION: We conclude that the preinjury use of warfarin does not place the trauma patient at increased risk for fatal hemorrhagic complications in the absence of head trauma. Furthermore, the presence of a head trauma alone is not predictive of mortality. However, the presence of intracranial injury is strongly associated with a mortality rate that is significantly higher than patients with head trauma who are not taking warfarin. LOC is also associated with mortality, but the absence of loss of consciousness does not reliably indicate the absence of intracranial injury or risk of death.

Intracranial complications of preinjury anticoagulation in trauma patients with head injury.

BACKGROUND: We have evaluated our recent experience as a Level I trauma center to test the hypothesis that preinjury anticoagulation adversely affects the morbidity and mortality of trauma patients with an intracranial injury. METHODS: Records of 380 patients admitted to the trauma service from January 1997 to December 1998 who at the time of admission were taking warfarin, low-molecular-weight heparin, aspirin, nonsteroidal anti-inflammatory drugs, clopidogrel, dipyridamole, pentoxifylline, or naproxen were reviewed. Thirty-seven patients with intracranial injuries were identified and compared with a matched (age, gender, mechanism, and severity of injury) control group of 37 patients with similar head injury but not taking any anticoagulant randomly selected from the trauma registry for that same time period. RESULTS: The control and anticoagulated groups were comparable in terms of age, 75 +/- 8 versus 74 +/- 11 years (p = 0.655); gender, 22 men/15 women versus 21 men/16 women; mechanism of injury, 30 falls/7 motor vehicle crashes versus 30 falls/7 motor vehicle crashes; and length of hospital stay, 11 +/- 14 versus 10 +/- 11 days (p = 0.853). In the anticoagulated group, the mean Injury Severity Score was 17.0 +/- 7.8 and the mean Glasgow Coma Scale score was 11.8 +/- 4.0; these were not significantly different from the control group, which had a mean Injury Severity Score of 19.8 +/- 8.1 (p = 0.143) and a Glasgow Coma Scale score of 12.5 +/- 2.6 (p = 0.378). There were 14 deaths (38%) in the anticoagulation group, versus 3 deaths in the control group (8%) (p = 0.006). In the anticoagulation group, 4 of 12 patients (33%) taking warfarin died, whereas 9 of 19 patients (47%) taking aspirin died (p = 0.285). All deaths were secondary to head injuries; all deaths in the control group and all but one in the anticoagulated group were the result of a fall; 6 of 10 anticoagulated patients who fell on stairs died, and 5 of these were taking aspirin only. CONCLUSION: These data indicate that the trauma patient with preinjury anticoagulation such as warfarin or even aspirin who has an intracranial injury has a four- to fivefold higher risk of death than the nonanticoagulated patient. The efficacy of reversing the anticoagulant effect at the time of hospital admission remains to be evaluated.