Monitoring an epidemic of Theileria-associated bovine anaemia (Ikeda) in cattle herds in New Zealand.

Monitoring an epidemic of an emerging vector-borne disease can be problematic; particularly in a country where vector-borne disease has previously had minimal impact on livestock. This paper describes methods of past and current surveillance of the Theileria-associated bovine anaemia (Ikeda; TABA) epidemic in New Zealand, and the resulting inferences made. Over the three year period of the TABA epidemic a portfolio of surveillance methods has been used: case reporting (with subsidised PCR testing), syndromic surveillance, sentinel surveillance, testing convenience samples for herd infection, as well as specific active surveillance initiatives to understand the tick vector distribution. Surveillance data have shown that the number of affected cattle herds has continued to increase over time with seasonal peaks in spring and autumn coinciding with peak activity of nymph and adult ticks respectively. In spring 2014, the epidemic extended south into areas that were previously considered to be unsuitable for the tick vector. As a result a survey was initiated that showed that ticks were present in areas outside of the known distribution. Testing pooled blood samples from cattle herds across New Zealand showed there still remained a significant percentage of herds where only non-Ikeda type infections were present, indicating that these herds were at risk of future TABA (Ikeda) outbreaks. For some regions there had been a noticeable increase in the percentage of herds infected, yet with only a small increase in the number of outbreaks compared with the previous year. Thus, outbreaks had either gone unobserved or had not been confirmed by testing. In these regions extensive low-input beef farming could explain the non-detection observed. There was a close relationship between the number of syndromic reports of anaemia and the number of confirmed cases of TABA (Ikeda), (P<0.01, adjusted R-squared=0.74). Active monitoring of the epidemic for a three year period has provided valuable insight into seasonal nature of the disease and its continuing impact. Information from multiple surveillance sources can help build up an understanding of the epidemiology, even when data from each individual surveillance stream are limited. The TABA (Ikeda) epidemic in New Zealand represents a useful case study of long term monitoring where disease is caused by an emerging pathogen.

Moxonidine acting centrally inhibits airway reflex responses.

We examined the role of I1-imidazoline (I1-IR) receptors in control of airway function, by testing the effects of systemic administration of the I1-IR agonist moxonidine on reflex responses of tracheal smooth muscle (TSM) tone to either lung deflation or mechanical stimulation of intrapulmonary rapidly adapting receptors. Experiments were performed in either alpha-chloralose anesthetized or decorticate, paralyzed, and mechanically ventilated beagle dogs. Moxonidine (10-100 micrograms/kg) administered via three different routes (femoral vein, muscular branch of superior thyroid artery, and vertebral artery) attenuated TSM responses to stimulation of airway sensory nerve fibers by two different ways and caused a decrease in arterial pressure and heart rate. These effects were dose dependent and were significantly reversed by efaroxan (an I1-IR and alpha 2-adrenergic blocker) administered via the vertebral artery. Intravertebral efaroxan abolished the hemodynamic effects of moxonidine. Intravenous moxonidine (10-100 micrograms/kg) did not alter airway smooth muscle responses to electrical stimulation of the peripheral vagus nerve. In addition, in vitro moxonidine (1-100 micrograms/ml) had no effect on contractile responses to increasing doses of acetylcholine. These findings indicate that moxonidine may act at a central site to suppress reflex airway constriction, even when given into the systemic circulation. Given the presence of I1-IR sites and alpha 2-adrenergic receptors in brain regions participating in airway reflexes, these receptor classes may be involved in brainstem control of the cholinergic outflow to the airways.

I1-imidazoline receptors and cholinergic outflow to the airways.

We examined the role of I1-imidazoline receptors in the control of airway function, by testing the effects of systemic administration of the I1-imidazoline agonist moxonidine on reflex responses of tracheal smooth muscle (TSM) tone to either lung deflation or mechanical stimulation of intrapulmonary rapidly adapting receptors. Experiments were performed in either alpha-chloralose anaesthetized or decorticate, paralyzed and mechanically ventilated beagle dogs. Moxonidine (10-100 microg/kg) administered via three different routes (the femoral vein, muscular branch of superior thyroid artery, and vertebral artery) attenuated TSM responses to stimulation of airway sensory nerve fibers by two different ways, and caused a decrease in arterial pressure and heart rate. These effects were dose-dependent, and were significantly reversed by efaroxan (an I1-imidazoline and alpha2-adrenergic blocker) administered via the vertebral artery. Intravertebral efaroxan abolished the hemodynamic effects of moxonidine. Intravenous moxonidine (10-100 microg/kg) did not alter airway smooth muscle responses to electrical stimulation of the peripheral vagus nerve. In addition, in vitro moxonidine (1-100 microg/ml) had no effect on contractile responses to increasing doses of acetylcholine. These findings indicate that moxonidine may act at a central site to suppress reflex airway constriction, even when given into the systemic circulation. Given the presence of I1-imidazoline sites and alpha2-adrenergic receptors in brain regions participating in airway reflexes, these receptor classes may be involved in brainstem control of the cholinergic outflow to the airways.

The influence of parasympatholytics on the resolution of acute attacks of asthma.

PURPOSE: To evaluate the role of parasympatholytics in the resolution of acute attacks of asthma. METHODS: This study employed a prospective sequential design in which the influence of 0.5 and 1.0 mg of ipratropium bromide on peak expiratory flow rates (PEFR), hospital admissions, and length of stay (LOS) in the emergency department (ED) was evaluated. The parasympatholytic was added to a well-investigated standard therapeutic regimen that was anchored by the use of repetitive doses of albuterol, and employed pretested decision algorithms. RESULTS: One hundred and thirty-one patients received ipratropium (l) and 123 who did not (NI) served as controls. There were no significant pretreatment between group differences in gender, racial composition clinical signs and symptoms, or PEFR. The presence of ipratropium in the regimen did not influence discharge/admission patterns, LOS, the rate of improvement of the patients, or the level of PEFR achieved. CONCLUSION: Anticholinergic agents such as ipratropium are not first-line treatments for acute asthma. They do not add any therapeutic benefit to the effects of albuterol given in divided doses over 1 hour, nor do they facilitate recovery in patients whose immediate response to sympathomimetics is impaired.