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Michael J Fliotsos,1 Donovan Stephen Reed,2 Gregory Giles,3 Adam HH Altman,2 Joseph A Santamaria,2 Sidra Zafar,1 Darrel K Carlton,3 Anthony J Johnson,3 Brett W Davies,2 Gary L Legault,3,4 Fasika A Woreta,1 Grant A Justin3,4 1Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; 2Department of Ophthalmology, Wilford Hall Eye Center, San Antonio, TX, USA; 3Department of Ophthalmology, Brooke Army Medical Center, San Antonio, TX, USA; 4Department of Surgery, Uniformed Services University of the Health Sciences, Bethesda, MD, USACorrespondence: Michael J FliotsosWilmer Eye Institute, The Johns Hopkins University School of Medicine, 600 N Wolfe Street, Baltimore, MD, 21287, USATel +1-260-409-7314Email michael.fliotsos@yale.eduPurpose: To describe the frequency and type of eye injuries in fighters in mixed martial arts (MMA) competition.Methods: Fight result data were collected from the Nevada Athletic Commission database from 2001 to 2020. Any fighters in a professional mixed martial arts (MMA) contest with an eye injury were included. Main outcome measures included frequency and rate of eye injuries per fight and the types of eye injuries. Secondary outcome measures were gender, laterality, decision type, and length of no-contact recommended.Results: Of the 256 MMA events in the database, 187 events (73.3%) had at least one eye injury. Of a total 2208 fights at these events, there were 363 fighters who sustained 369 eye injuries, with the yearly rate of eye injuries per 100 fighters ranging from 2.56 to 12.22. The most common injuries were eyebrow and eyelid lacerations (n=160, 43%), lacerations around the eye (n=98, 27%), and orbital fractures (n=62, 17%). Most eye injuries were right sided (n=197, 53.3%) and the majority of fighters with eye injuries lost their match (n=228, 62.8%). Fifty-seven fighters were recommended for further ophthalmology clearance after the match. The most common reasons for recommended ophthalmology follow-up was orbital fracture (n=25, 44%) and retinal injury (n=7, 12%). Forty-three fighters received no-contact requirements relating to their injury for an average of 8.9 weeks (range 1– 24 weeks).Conclusion: Ophthalmic injuries in professional MMA were prevalent, were most often lacerations surrounding the eye, and often accompanied the fighter losing their match.Keywords: ophthalmic trauma, eye trauma, mixed martial arts, boxing, MMA, combat sports

Hemorrhagic smallpox was a rare but severe manifestation of variola virus infection that resulted in nearly 100% mortality. Here we describe intravenous (IV) inoculation of cowpox virus Brighton Red strain in cynomolgus macaques (Macaca fascicularis) which resulted in disease similar in presentation to hemorrhagic smallpox in humans. IV inoculation of macaques resulted in a uniformly lethal disease within 12days post-inoculation in two independent experiments. Clinical observations and hematological and histopathological findings support hemorrhagic disease. Cowpox virus replicated to high levels in blood (8.0–9.0 log10 gene copies/mL) and tissues including lymph nodes, thymus, spleen, bone marrow, and lungs. This unique model of hemorrhagic orthopoxvirus infection provides an accessible means to further study orthopoxvirus pathogenesis and to identify virus-specific and nonspecific therapies. Such studies will serve to complement the existing nonhuman primate models of more classical poxviral disease.

Smallpox, caused by variola virus (VARV), is a devastating human disease that affected millions worldwide until the virus was eradicated in the 1970 s. Subsequent cessation of vaccination has resulted in an immunologically naive human population that would be at risk should VARV be used as an agent of bioterrorism. The development of antivirals and improved vaccines to counter this threat would be facilitated by the development of animal models using authentic VARV. Towards this end, cynomolgus macaques were identified as adequate hosts for VARV, developing ordinary or hemorrhagic smallpox in a dose-dependent fashion. To further refine this model, we performed a serial sampling study on macaques exposed to doses of VARV strain Harper calibrated to induce ordinary or hemorrhagic disease. Several key differences were noted between these models. In the ordinary smallpox model, lymphoid and myeloid hyperplasias were consistently found whereas lymphocytolysis and hematopoietic necrosis developed in hemorrhagic smallpox. Viral antigen accumulation, as assessed immunohistochemically, was mild and transient in the ordinary smallpox model. In contrast, in the hemorrhagic model antigen distribution was widespread and included tissues and cells not involved in the ordinary model. Hemorrhagic smallpox developed only in the presence of secondary bacterial infections - an observation also commonly noted in historical reports of human smallpox. Together, our results support the macaque model as an excellent surrogate for human smallpox in terms of disease onset, acute disease course, and gross and histopathological lesions.

Mice with generalized influenza or tularemia of similar lethality were studied in an effort to compare biochemical responses of the myocardium during infections of viral and bacterial etiology. A progressive loss of body weight characterized the course of both infections. Accompanying this, the myocardial content of protein and the activities of lactate dehydrogenase, citrate synthase, and cytochrome c oxidase all decreased. However, myocardial protein degradation appeared earlier and was more pronounced in influenza, and the protein changes were accompanied by a rapid decline of myocardial RNA. Activation of acid hydrolases, such as cathepsin D and beta-glucuronidase, occurred in tularemia but not in influenza, whereas leakage of beta-glucuronidase into the plasma occurred in both infections. Conversely, there was a considerably greater activation of myocardial catalase in influenza. These findings suggested that different control mechanisms or metabolic pathways were operative in the degradation of myocardial constituents in influenza as compared with tularemia. The absence of histological signs of myocarditis in either infection appeared to exclude any direct local effects of an inflammatory process on myocardial cells. Since the infections were of comparable lethality (based upon the inoculated dose of organisms), the observed differences in pattern and extent of metabolic responses of the myocardium to these infections may be attributed to different pathophysiological mechanisms evoked by the different microorganisms.