Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats with tick paralysis caused by Ixodes holocyclus: a pilot survey

Objective To determine the incidence and nature of adverse reactions of dogs and cats to tick antitoxin serum and to re-evaluate the role of atropine in the treatment of tick paralysis. Design A retrospective questionnaire of veterinarians. Procedure Questionnaires were posted to 320 veterinarians in tick-endemic regions of Australia. Questions referred to dogs and cats treated for tick paralysis over a period of three years: the number treated, treatment protocols and adverse systemic reactions to tick antitoxin serum. Ninety completed questionnaires were returned and responses analysed. Results Veterinarians reported that approximately 3% of dogs exhibited adverse reactions immediately following treatment with tick antitoxin serum, Eighteen percent of these reactions were described as anaphylaxis, with the remaining 82% attributed to the Bezold-Jarisch reflex. Six percent of cats treated with tick antitoxin serum reacted adversely and the majority of reactions (63%) were ascribed to the Bezold-Jarisch reflex. Atropine was used routinely by 10% of responding veterinarians in the treatment of dogs and cats with tick paralysis. A similar number of veterinarians used atropine only in selected cases. Most veterinarians (76%) reported that they never used atropine in the treatment of tick paralysis in either dogs or cats. Within the survey population, premedication with atropine reduced the number of Bezold-Jarisch reactions following tick antitoxin administration approximately five-fold in dogs and four-fold in cats. Conclusions Data from this pilot survey indicate that more cats than dogs have adverse systemic reactions to tick antitoxin serum and that the majority of these reactions in both dogs and cats could be related to the Bezold-Jarisch reflex. The number of reactions to tick antitoxin serum in dogs and cats could be significantly reduced by the routine use of atropine prior to administration of tick antitoxin serum.

Prospective survey of tick paralysis in dogs

Objective To obtain information on tick paralysis in dogs, including the nature of disease, host signalment, tick-host relationship, treatment, disease progression and recovery, and preventive measures. Design A prospective survey of 577 dogs affected by tick paralysis was conducted during 1998. Forty-two veterinary clinics along the eastern coast of Australia were instructed to complete survey forms for the first 15 dogs that presented with tick paralysis during September to November. Results Five percent of dogs died from tick paralysis. Younger dogs were more likely to survive. Long coat length was associated with a greater tick burden but not greater tick size, whereas coat thickness had no bearing on either. Dogs with mild disease recovered more quickly from tick paralysis. Respiratory and gait scores reflected disease severity and were good prognostic indicators. The size of the tick did not reflect the severity of the clinical condition it induced in the host. No method of tick removal or in situ treatment improved recovery time or reduced mortality. However, the time spent in hospital was significantly less for dogs from which the live tick was manually removed. Inspiratory strider. evident in some dogs with tick paralysis, was not related to tick attachment on the neck. The use of acepromazine maleate or dexamethasone did not reduce recovery time or mortality. Increasing the dose of tick antitoxin serum (TAS) above 0.1 mL/kg had no effect on mortality or recovery time. Dogs with severe disease that received an additional dose of TAS were significantly less likely to survive. Subcutaneous use of TAS at the site of tick attachment was of no benefit in reducing mortality or time to initial clinical improvement. A registered preventative product had not been used on the majority of dogs. Clipping the coat to search for ticks did not reduce mortality. Conclusions Therapy needs to address cardiopulmonary dysfunction that may be due directly to the effect of tick toxin and not just respiratory compromise caused by progressive respiratory muscle failure.

Low intraspecific variation in the rRNA internal transcribed spacer 2 (ITS2) of the Australian paralysis tick, Ixodes holocyclus

Ixodes holocyclus has a narrow, discontinuous distribution along the east coast of Australia. We studied ticks from 17 localities throughout the geographic range of this tick. The ITS2 of I. holocyclus is 793 bp long. We found nucleotide variation at eight of the 588 nucleotide positions (1.4%) that were compared for all ticks. There were eight different nucleotide sequences. Most sequences were not restricted to a particular geographic region. However, sequences F, G and H, which had an adenine at position 197, were found only in the far north of Queensland - all other ticks had a guanine at this position. The low level of intraspecific variation in this tick (0.7%) contrasts with the sequence divergence between L holocyclus and its close relative, I. cornuatus (13.1 %). These data indicate that L holocyclus does not contain cryptic species despite possible geographic isolation of some populations. We conclude that variation in the ITS2 is likely to be informative about the phylogeny of the group.

The Australian paralysis may be the missing link tick in the transmission of Hendra virus from bats to horses to humans

Hendra virus is a new virus of the family Paramyxoviridae. This virus was first detected in Queensland, Australia, in 1994; although, it seems that the virus has infected fruit-eating bats (flying-foxes) for a very long time. At least 2 humans and 15 horses have been killed by this virus since it first emerged as a virus that may infect mammals other than flying-foxes. Hendra virus is thought to have moved from flying-foxes to horses, and then from horses to people. There is a reasonably strong hypothesis for horse-to-human transmission: transmission of virus via nasal discharge, saliva and/or urine. In contrast, there is no strong hypothesis for flying-fox-to-human transmission. I present evidence that the Australian paralysis tick, Ixodes holocyclus, which has apparently only recently become a parasite of flying-foxes, may transmit Hendra virus and perhaps related viruses from flying-foxes to horses and other mammals. (C) 2003 Elsevier Science Ltd. All rights reserved.

Effects of the paralysis tick, Ixodes holocyclus, on the electrocardiogram of the Spectacled Flying Fox, Pteropus conspicillatus

Objective To evaluate cardiac electrical function in the Spectacled Flying Fox (bat) infested with Ixodes holocyclus. Design Prospective clinical investigation of bats treated for naturally occurring tick toxicity. Procedure ECGs were performed on bats with tick toxicity (n = 33), bats that recovered slowly (n = 5) and normally (n = 5) following treatment for tick toxicity, and on normal bats with no history of tick toxicity (n = 9). Results Bats with tick toxicity had significantly prolonged corrected QT intervals, bradycardia and rhythm disturbances which included sinus bradydysrhythmia, atrial standstill, ventricular premature complexes, and idioventricular bradydysrhythmia. Conclusions The QT prolongation observed on ECG traces of bats with tick toxicity reflected delayed ventricular repolarisation and predisposed to polymorphic ventricular tachycardia and sudden cardiac death in response to sympathetic stimulation. The inability to document ventricular tachycardia in bats shortly before death from tick toxicity may be explained by a lack of sympathetic responsiveness attributable to the unique parasympathetic innervation of the bat heart, or hypothermiainduced catecholamine receptor down-regulation. Bradycardia and rhythm disturbances may be attributable to hypothermia.

Does diaphragmatic breathing technique really improve its range of motion? An objective assessment

Purpose - To verify the results of a diaphragmatic breathing technique (DBT) on diaphragmatic range of motion in healthy subjects. Methods - A total of 51 healthy subjects (10 male; 41 female), mean age 20 years old and a body mass index (BMI) ranging from 15.6 to 34.9 kg/m2, were enrolled in this study. Diaphragmatic range of motion was assessed by M-mode ultrasound imaging. Measurements were made before and after the DBT implementation in a standard protocol, based on 3 seconds of inspiration starting from a maximum expiration. Differences between assessments were analyzed by descriptive statistics and t-test (p < 0.05). Results - Mean value range of motion before DBT was 55.3 ± 13.4 mm and after DBT was 63.8 ± 13.2 mm showing a significant improvement of 8.5 ± 14.7 mm (p < 0.001). A strong correlation between the slope and the range of motion was found (r = 0.71, p < 0.001). Conclusions - Based on ultrasound measurements, it has been proved that DBT really contributes to a higher diaphragmatic range of motion. Future studies are needed in order to understand the influence of protocol parameters (e.g. inspiration time). Clinical implications - In the contest of evidence-based practice in physiotherapy, it has been showed by objective measurements that DBT improves the diaphragm range of motion, translating into a more efficient ventilatory function and thus can be used in clinical setting. To our knowledge this is the first study to assess the effects of DBT on range of motion of diaphragm muscle with ultrasound imaging.

Multiple Haemangiomas, Diaphragmatic Eventration and Beckwith-Wiedemann Syndrome: An Unusual Association

A 6-month-old girl with Beckwith-Wiedemann syndrome, multiple haemangiomas (axillary, laryngeal, pulmonary and hepatic) and diaphragmatic eventration was reported. All tumours responded to treatment with propranolol. The surgical correction of diaphragmatic eventration was crucial to a better outcome.

Tick paralysis cases in Argentina

Tick paralysis (TP) occurs worldwide and is caused by a neurotoxin secreted by engorged female ticks that affects the peripheral and central nervous system. The clinical manifestations range from mild or nonspecific symptoms to manifestations similar to Guillain-Barré syndrome, bulbar involvement, and death in 10% of the patients. The diagnosis of TP is clinical. To our knowledge, there are no formal reports of TP in humans in South America, although clusters of TP among hunting dogs in Argentina have been identified recently. In this paper, clinical features of two cases of TP occurring during 1994 in Jujuy Province, Argentina, are described.

Heart hypoplasia in an animal model of congenital diaphragmatic hernia

PURPOSE: In previous papers, we described a new experimental model of congenital diaphragmatic hernia in rabbits, and we also reported noninvasive therapeutic strategies for prevention of the functional and structural immaturity of the lungs associated with this defect. In addition to lung hypoplasia, pulmonary hypertension, biochemical, and structural immaturity of the lungs, the hemodynamics of infants and animals with congenital diaphragmatic hernia are markedly altered. Hence, cardiac hypoplasia has been implicated as a possible cause of death in patients with congenital diaphragmatic hernia, and it is hypothesized to be a probable consequence of fetal mediastinal compression by the herniated viscera. Cardiac hypoplasia has also been reported in lamb and rat models of congenital diaphragmatic hernia. The purpose of the present experiment was to verify the occurrence of heart hypoplasia in our new model of surgically produced congenital diaphragmatic hernia in fetal rabbits. METHODS: Twelve pregnant New Zealand rabbits underwent surgery on gestational day 24 or 25 (normal full gestational time - 31 to 32 days) to create left-sided diaphragmatic hernias in 1 or 2 fetuses per each doe. On gestational day 30, all does again underwent surgery, and the delivered fetuses were weighed and divided into 2 groups: control (non-surgically treated fetuses) (n = 12) and congenital diaphragmatic hernia (n = 9). The hearts were collected, weighed, and submitted for histologic and histomorphometric studies. RESULTS: During necropsy, it was noted that in all congenital diaphragmatic hernia fetuses, the left lobe of the liver herniated throughout the surgically created defect and occupied the left side of the thorax, with the deviation of the heart to the right side, compressing the left lung; consequently, this lung was smaller than the right one. The body weights of the animals were not altered by congenital diaphragmatic hernia, but heart weights were decreased in comparison to control fetuses. The histomorphometric analysis demonstrated that congenital diaphragmatic hernia promoted a significant decrease in the ventricular wall thickness and an increase in the interventricular septum thickness. CONCLUSION: Heart hypoplasia occurs in a rabbit experimental model of congenital diaphragmatic hernia. This model may be utilized for investigations in therapeutic strategies that aim towards the prevention or the treatment of heart hypoplasia caused by congenital diaphragmatic hernia.

Prenatal tracheal ligation or intra-amniotic administration of surfactant or dexamethasone prevents some structural changes in the pulmonary arteries of surgically created diaphragmatic hernia in rabbits

PURPOSE: Characterization of the structural changes occurring in the pulmonary arteries resulting from surgically produced congenital diaphragmatic hernia in rabbits, with particular emphasis on the preventive effects of prenatal tracheal ligation or administration of intra-amniotic dexamethasone or surfactant. METHODS: Twenty rabbit fetuses underwent surgical creation of a left-sided congenital diaphragmatic hernia on the 24th or 25th gestational day. They were divided according to the following procedures: congenital diaphragmatic hernia (n = 5), congenital diaphragmatic hernia plus tracheal ligation (n = 5), congenital diaphragmatic hernia plus intra-amniotic administration of dexamethasone 0.4 mg (n = 5) or surfactant (Curosurf 40 mg, n = 5). On gestational day 30, all the fetuses were delivered by caesarean section and killed. A control group consisted of five nonoperated fetuses. Histomorphometric analysis of medial thickness, cell nuclei density, and elastic fiber density of pulmonary arterial walls was performed. RESULTS: Arteries with an external diameter > 100 mum have a decreased medial thickness, lower cell nuclei density, and greater elastic fiber density when compared with arteries with external diameter <= 100 mum. Congenital diaphragmatic hernia promoted a significant decrease in medial thickness and an increase in cell nuclei density in artery walls with external diameter > 100 mum. Prenatal treatments with tracheal ligation or intra-amniotic administration of dexamethasone or surfactant prevented these changes. In arteries with external diameter <= 100 mum, congenital diaphragmatic hernia promoted a significant increase in medial thickness and in cell nuclei density and a decrease in elastic fiber density. The prenatal treatments with tracheal ligation or intra-amniotic administration of dexamethasone or surfactant prevented these changes, although no effect was observed in elastic fiber density in the congenital diaphragmatic hernia plus dexamethasone group. CONCLUSIONS: Congenital diaphragmatic hernia promoted different structural changes for large or small arteries. The prenatal intra-amniotic administration of dexamethasone or surfactant had positive effects on the lung structural changes promoted by congenital diaphragmatic hernia, and these effects were comparable to the changes induced by tracheal ligation.

When pneumonia becomes a double congenital diaphragmatic hernia

When pneumonia becomes a double congenital diaphragmatic hernia

Lower NPAS3 expression during the later stages of abnormal lung development in rat congenital diaphragmatic hernia

Purpose Congenital diaphragmatic hernia (CDH) is characterized by a developmental defect in the diaphragm, pulmonary hypoplasia and pulmonary hypertension. NPAS3 is a PAS domain transcription factor regulating Drosophila tracheogenesis. NPAS3 null mice develop pulmonary hypoplasia in utero and die after birth due to respiratory failure. We aimed to evaluate NPAS3 expres- sion during normal and abnormal lung development due to CDH. Methods CDH was induced by administering 100 mg/ml nitrofen to time-pregnant dams on embryonic day (E) 9 of gestation. Lungs were isolated on E15, E18 and E21 and NPAS3 localization was determined by immunohisto- chemistry and quantified using Western blotting. Results We found that only E21 hypoplastic CDH lungs have reduced expression of NPAS3 in the terminal sac- cules. Western blotting confirmed the down-regulation of NPAS3 protein in the nitrofen-induced hypoplastic lungs. Conclusions We demonstrate for the first time that ni- trofen-induced hypoplastic CDH lungs have reduced NPAS3 expression in the terminal saccules during the later stages of abnormal lung development. Our findings suggest that NPAS3 is associated with pulmonary hypoplasia in CDH.