Lyme Disease Models of Tick-Mouse Dynamics with Seasonal Variation in Births, Deaths, and Tick Feeding.

Lyme disease is the most common vector-borne disease in the United States impacting the Northeast and Midwest at the highest rates. Recently, it has become established in southeastern and south-central regions of Canada. In these regions, Lyme disease is caused by Borrelia burgdorferi, which is transmitted to humans by an infected Ixodes scapularis tick. Understanding the parasite-host interaction is critical as the white-footed mouse is one of the most competent reservoir for B. burgdorferi. The cycle of infection is driven by tick larvae feeding on infected mice that molt into infected nymphs and then transmit the disease to another susceptible host such as mice or humans. Lyme disease in humans is generally caused by the bite of an infected nymph. The main aim of this investigation is to study how diapause delays and demographic and seasonal variability in tick births, deaths, and feedings impact the infection dynamics of the tick-mouse cycle. We model tick-mouse dynamics with fixed diapause delays and more realistic Erlang distributed delays through delay and ordinary differential equations (ODEs). To account for demographic and seasonal variability, the ODEs are generalized to a continuous-time Markov chain (CTMC). The basic reproduction number and parameter sensitivity analysis are computed for the ODEs. The CTMC is used to investigate the probability of Lyme disease emergence when ticks and mice are introduced, a few of which are infected. The probability of disease emergence is highly dependent on the time and the infected species introduced. Infected mice introduced during the summer season result in the highest probability of disease emergence.

The type of anticoagulant used for plasma collection affects in vitro Rhodococcus equi assays.

OBJECTIVE: The efficacy of Rhodococcus equi-specific hyperimmune plasma (HIP) is usually evaluated in vitro. Anticoagulants (AC) used for plasma collection can negatively impact bacterial replication but their effect on R. equi growth has not been evaluated. The aim of this study was to establish the effect that AC routinely used in veterinary medicine (ACD, K2EDTA, Li Heparin, and Na Citrate) have on in vitro R. equi growth. To assess this, in vitro assays commonly used to test HIP efficacy (direct effect on microorganism and macrophage infection), were performed using each AC and non-treated bacteria. RESULTS: There was no direct effect of ACD, Li Heparin or Na Citrate on R. equi growth. These AC significantly (p < 0.05) delayed growth for 12 h following opsonization. The number of R. equi colonies after macrophage infection was significantly (p < 0.05) lower 72 h post-opsonization with Na Citrate. K2EDTA inhibited the formation of R. equi colonies by 12 h in all the assays. In conclusion, AC should be taken into consideration when interpreting in vitro results as their negative effect on bacterial growth may be mistakenly interpreted as HIP efficacy. ACD and Li Heparin appear more appropriate for the selected assays.