As no alternative explanation exists for the neurological symptoms, this case supports that LCMV infection by percutaneous injection can cause neurological symptoms in people with untreated LCMV. It also shows that seroconversion can take more than a month and can occur even after all symptoms have disappeared. Seroconversion testing is recommended 30 and 60 days after exposure to confirm an individual’s infection status.
Interestingly, the Armstrong strain and the clone 13 variant of LCMV are considered risk group 2 pathogens by the Public Health Agency of Canada (https://health.canada.ca/en/epathogen). In this particular case, the infection occurred in a containment level 2 animal facility. Standard operating procedures include the use of a second pair of gloves and protective sleeves, as well as clear written instructions for handling mice in the biosafety cabinet. Symptoms associated with LCMV infection in humans are relatively mild in immunocompetent individuals (Figure 1). [2, 14, 15], we argue that containment level 2 is appropriate for conducting experiments with the Armstrong strain of LCMV. Additionally, the risk of self-injection still exists in containment level 3 facilities, so classifying LCMV Armstrong as a level 3 pathogen does not significantly reduce the risk of infection for laboratory workers.
Of note, this case differs from natural infection with LCMV both in terms of dose and route of administration. The solution prepared for injection into mice contained 2 × 10 .Five LCMV Armstrong plaque-forming units (PFU) per milliliter, and exposure was via percutaneous wounding. Although difficult to determine with precision, a typical needlestick injury may result in a volume injected between 0.3 µL and 6 µL, depending on the gauge and depth of needle exposure. [16]. Extrapolating this information to this case gives an infectious dose of LCMV of 60 to 1200 PFU. The higher virus titer in the inoculum and the transdermal route of exposure may explain the severity of symptoms. Interestingly, in contrast to natural exposure via the respiratory tract, the acute reaction was not followed by a second wave of worsening in this patient.
LCMV is an endemic virus spanning all temperate regions of the world. It is estimated that approximately 10% of wild mice are infected with her LCMV, but this number could be even higher in some circumstances. [17, 18]. One study reported that approximately 5% of humans have antibodies against LCMV. [2], but the number of people exposed is probably much higher. Studies in the 1960s showed that LCMV was one of the most common causes of aseptic meningitis. [19], however, the rate of LCMV meningitis reports has decreased recently. This latter point is compounded by the fact that the NML responsible for all his LCMV diagnoses in Canada only performs 50-60 LCMV tests a year, and in the past 16 years he has only found 5 positive cases. This is emphasized by the fact that there are only cases.
Previous case reports and epidemiological studies of laboratory personnel have associated LCMV infections with clone-13 variants or unknown strains. [14, 15, 20,21,22,23]. Common symptoms included fever, severe headache, flu-like symptoms, vomiting, and in some cases meningitis. [14, 15, 20, 21]. Recently, two cases of his LCMV clone-13 infection via the percutaneous route were reported. [7, 8]. Two patients developed neck pain, photophobia, nausea, vomiting, flu-like symptoms, pain in the limbs, and fever. [7, 8]. This highlights the clear clinical similarities between transdermal infections of LCMV Armstrong and LCMV clone-13, with the exception of symptoms that may be due to differences in the amount of virus administered or the type of strain. with differences in strength.
The case presented here is unique given the percutaneous route of exposure and serologic evidence of primary infection. Although a past history of cerebral venous sinus thrombosis makes the differential diagnosis a little broader for the patient’s initial symptoms, the absence of neurological symptoms in the years prior to LCMV exposure suggests that previous brain lesions may contribute. suggests that it is unlikely. Symptoms in seroconverted individuals may differ from those reported here, both in severity and duration. This hypothesis should be confirmed in future reports. This case report provides a framework for investigating and tracking patients exposed to LCMV Armstrong and fills a gap in our understanding of LCMV as an endemic pathogen and laboratory hazard.
