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. 2022 Sep;46(3):837-852.
doi: 10.1007/s11259-022-09908-5. Epub 2022 Mar 3.

Evaluation of the clinical evolution and transmission of SARS-CoV-2 infection in cats by simulating natural routes of infection

Sandra Barroso-Arévalo  1   2 , Lidia Sánchez-Morales  3   4 , Jose A Barasona  3   4 , Belén Rivera  3   4 , Rocío Sánchez  3   4 , María A Risalde  5   6 , Irene Agulló-Ros  5 , José M Sánchez-Vizcaíno  3   4
Affiliations

Evaluation of the clinical evolution and transmission of SARS-CoV-2 infection in cats by simulating natural routes of infection

Sandra Barroso-Arévalo et al. Vet Res Commun. 2022 Sep.

Erratum in

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the current pandemic disease denominated as Coronavirus Disease 2019 (COVID-19). Several studies suggest that the original source of this virus was a spillover from an animal reservoir and its subsequent adaptation to humans. Of all the different animals affected, cats are one of the most susceptible species. Moreover, several cases of natural infection in domestic and stray cats have been reported in the last few months. Although experimental infection assays have demonstrated that cats are successfully infected and can transmit the virus to other cats by aerosol, the conditions used for these experiments have not been specified in terms of ventilation. We have, therefore, evaluated the susceptibility of cats using routes of infection similar to those expected under natural conditions (exposure to a sneeze, cough, or contaminated environment) by aerosol and oral infection. We have also evaluated the transmission capacity among infected and naïve cats using different air exchange levels. Despite being infected using natural routes and shed virus for a long period, the cats did not transmit the virus to contact cats when air renovation features were employed. The infected animals also developed gross and histological lesions in several organs. These outcomes confirm that cats are at risk of infection when exposed to infected people, but do not transmit the virus to other cats with high rates of air renovation.

Keywords: Air renovation; Cats; Routes of infection; SARS-CoV-2; Transmission.

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Conflict of interest statement

The authors have no relevant financial or non-financial interests to disclose.

Figures

Fig. 1
Fig. 1
BioFlex® B90 Flexible Film Trolley Isolator with HEPA filters containing pairs inside cages measuring 124.8 × 51.6 × 60 cm used in this experiment
Fig. 2
Fig. 2
Diagram of inoculation of infected animal 1 (INF1) and sentinel contact control (contact animal 1, CNT1); inoculation of infected animal 2 (INF2) and sentinel contact control (contact animal 2, CNT2); and inoculation of contact animal 1 (CNT1) cohoused with a sentinel contact control (CNT2). DPI: day post-infection. DPC: day post-contact. *The asterisk indicates the period after which CNT1 became infected
Fig. 3
Fig. 3
Viral loads based on Ct value measured by employing RT-qPCR on both oropharyngeal and rectal swabs as well as blood (left axis; continuous lines), and neutralizing antibody production based on the percentage of inhibition measured by employing SARS-CoV-2 surrogate virus neutralization test (right axis; bars) with infected animal 1 (IFN1)
Fig. 4
Fig. 4
Viral loads based on Ct value measured by employing RT-qPCR on both oropharyngeal and rectal swabs as well as blood (left axis; continuous lines), and neutralizing antibody production based on percentage of inhibition measured by employing SARS-CoV-2 surrogate virus neutralization test (right axis; bars) with infected animal 2 (IFN2)
Fig. 5
Fig. 5
Viral loads based on Ct value measured by employing RT-qPCR on both oropharyngeal and rectal swabs as well as blood during contact and infection period in CNT1. Neutralizing antibodies were not produced before euthanasia (6 days post-inoculation)
Fig. 6
Fig. 6
Average viral loads based on Ct values on sponges taken from INF 1 (A), INF2 (B), CNT1 (C), and CNT2 (D) during the experiment
Fig. 7
Fig. 7
Gross lesions were found in tissues of the inoculated animals (INF1, INF2, and CNT1). Congestion and interstitial pneumonia were found in the three animals (INF1 = A; INF2 = B; CNT1 = C), and animal INF1 (A) had alveolar edema and seromucosal tracheitis, while animal CNT2 lungs were perfectly normal (CNT2 = D). The spleens of all three animals were enlarged and congested (INF1 = E; INF2 = F; CNT1 = G), while animal CNT2 had no gross lesions (CNT2 = H)
Fig. 8
Fig. 8
SARS-CoV-2 infection caused several respiratory lesions in the cats. INF1 (A) and INF2 (B), both euthanized at 11 DPI, had an intense congestion, alveolar (black asterisk), and perivascular edema (arrows), along with bronchial glandular and epithelial hyperplasia (arrowheads). Hyperplasia of type II pneumocytes (A, inset) and alveolar macrophages (B, inset) was also observed in these animals. These lesions were slighter in CNT1 (C), but there was a greater alveolar septal thickening as a result of light-to-severe interstitial aggregations (green asterisk) composed mainly of lymphocytes and macrophages (C, inset). Epithelial hyperplasia (grey arrowheads) and mononuclear infiltrates were observed in the lamina propria (grey asterisks) of the nasal turbinates of INF1 (E), INF2 (F), and CNT1 (G). No histological lesions were observed in tissues from CNT2 (D, H)
Fig. 9
Fig. 9
Pathological findings found in lymphoid tissues after SARS-CoV-2 infection in cats. Hyperemic splenomegaly was observed in INF1 (A), INF2 (B), and CNT1 (C), also accompanied by moderate lymphoid depletion in this last animal (C and C inset). A decrease in lymphocytes and images of apoptosis within germinal centers with evidence of pyknosis, cellular fragmentation, and macrophages with engulfed cell debris (tingible body macrophages) (E, inset) were also evident in several of the lymph nodes of INF1 (E), INF2 (F) and CNT1 (G). No histological lesions were observed in tissues from CNT2 (D, H)
Fig. 10
Fig. 10
Viral loads based on average Ct values in tissues obtained from INF1 and INF2 on 11 DPI and CNT1 on 6 DPI*
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