Summary Twelve adult ponies and 2 conventional foals were exposed intranasal to EHV‐1, strain Ab4 (TCID50 10−6.6) and samples of respiratory tract associated lymphoid tissues were recovered between 12 h and 13 days after infection. Infectious virus was detected in tissue homogenates using susceptible cell monolayers and expression of viral antigens was monitored using indirect immunoperoxidase histochemistry on paraffin sections. The results showed both infectious EHV‐1 and viral antigens in respiratory tract associated lymph nodes 12 h after exposure. Infected leucocytes were identified morphologically as lymphocytes, monocytes, macrophages and plasma cells. The rapid intracellular localisation of EHV‐1 in lymph nodes implies that cell mediated immunity is an important aspect of the equine response to this virus.

In July 1989 influenza A/equine-2 (H3N8) was isolated from a nasopharyngeal swab taken from a non-thoroughbred horse exhibiting acute clinical respiratory disease. This was the first isolation of equine influenza virus in the United Kingdom since 1981. Subsequent investigations of acute respiratory disease in horses indicated that the infection was dispersed throughout the UK. However, unlike the previous epidemic of 1979, the first horses from which the virus was isolated had been vaccinated. This outbreak of influenza provided an opportunity to evaluate an antigen capture ELISA, directed against the influenza virus nucleoprotein, as a rapid method for detecting virus in the nasopharyngeal secretions of naturally infected horses.

Summary Twelve adult ponies and 2 conventional foals were exposed to 106.6 TCID50 of Equid herpesvirus‐1 (EHV‐1), strain Ab4 and samples of respiratory tract tissues were recovered. Infectious virus in tissue homogenates was detected using susceptible cell monolayers and expression of viral antigens was monitored using indirect immunoperoxidase histochemistry of paraffin sections. The results illustrated the rapid dissemination of EHV‐1 throughout the respiratory tract, with early replication in the lungs one day after exposure. Endothelial cell infection was prominent in all areas of the nasopharynx by Day 4 emphasising the role of endotheliotropism and viraemia in dissemination of this virus to sites of secondary replication. Clinical disease in the adult ponies was mild.

IntroductionOveruse of CT Pulmonary Angiograms (CTPA) for diagnosing pulmonary embolism (PE), particularly in Emergency Departments (ED), is considered problematic. Marked variations in positive CTPA rates are reported, with American 4–10% yields driving most concerns. Higher resolution CTPA may increase sub-segmental PE (SSPE) diagnoses, which may be up to 40% false positive. Excessive use and false positives could increase harm vs. benefit. These issues have not been systematically examined outside America.AimsTo describe current yield variation and CTPA utilisation in Australasian ED, exploring potential factors correlated with variation.MethodsA retrospective multi-centre review of consecutive ED-ordered CTPA using standard radiology reports. ED CTPA report data were inputted onto preformatted data-sheets. The primary outcome was site level yield, analysed both intra-site and against a nominated 15.3% yield. Factors potentially associated with yield were assessed for correlation.ResultsFourteen radiology departments (15 ED) provided 7077 CTPA data (94% ≥64-slice CT); PE were reported in 1028 (yield 14.6% (95%CI 13.8–15.4%; range 9.3–25.3%; site variation p <0.0001) with four sites significantly below and one above the 15.3% target. Admissions, CTPA usage, PE diagnosis rates and size of PE were uncorrelated with yield. Large PE (≥lobar) were 55% (CI: 52.1–58.2%) and SSPE 8.8% (CI: 7.1–10.5%) of positive scans. CTPA usage (0.2–1.5% adult attendances) was correlated (p<0.006) with PE diagnosis but not SSPE: large PE proportions.Discussion/ ConclusionsWe found significant intra-site CTPA yield variation within Australasia. Yield was not clearly correlated with CTPA usage or increased small PE rates. Both SSPE and large PE rates were similar to higher yield historical cohorts. CTPA use was considerably below USA 2.5–3% rates. Higher CTPA utilisation was positively correlated with PE diagnoses, but without evidence of increased proportions of small PE. This suggests that increased diagnoses seem to be of clinically relevant sized PE.

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