Hélène Amory

European outbreaks of atypical myopathy in grazing equids (2006-2009). Spatiotemporal distribution, history and clinical features

REASONS FOR PERFORMING STUDYnImproved understanding of the epidemiology of atypical myopathy (AM) will help to define the environmental factors that permit or support the causal agent(s) to exert toxicity.nnnOBJECTIVESnThis European survey of AM aimed to describe spatiotemporal distribution, survival, clinical signs, circumstances in which AM develops and its different expressions between countries and over time.nnnMETHODSnThe spatiotemporal distribution, history and clinical features of AM cases reported to the Atypical Myopathy Alert Group from 2006 to 2009 were described. Comparisons of data from the most severely affected countries and from the large outbreaks were made with Fishers exact and Welchs tests with Bonferroni correction.nnnRESULTSnOf 600 suspected cases, 354 met the diagnostic criteria for confirmed or highly probable AM. The largest outbreaks occurred during the autumns of 2006 and 2009 in Belgium, France and Germany. For the first time, donkeys, zebras and old horses were affected, and clinical signs such as gastrointestinal impaction, diarrhoea, penile prolapse, buccal ulceration and renal dysfunction were observed. Affected horses spent >6u2003h/day on pastures that almost always contained or were surrounded by trees. The latency period was estimated at up to 4 days. Overall survival rate was 26%. Although differences between countries in affected breeds, body condition, horse management and pasture characteristics were recognised, the common presenting clinical signs and mortality were similar between countries.nnnCONCLUSIONS AND POTENTIAL RELEVANCEnThis study describes new data on case details, history and clinical course of AM that is of preventive, diagnostic and therapeutic value. However, the true impact of the findings of this study on the development of or severity of AM should be tested with case-control studies.

European outbreaks of atypical myopathy in grazing horses (2006–2009): determination of indicators for risk and prognostic factors

REASONS FOR PERFORMING STUDYnAppropriate management of atypical myopathy (AM) requires the establishment of an accurate diagnosis and prognosis. Furthermore, preventive measures to avoid AM need to be refined.nnnOBJECTIVESnThe aims of the study were as follows: 1)u2003to improve the diagnosis of AM; 2)u2003to identify prognostic predictors; and 3)u2003to refine recommended preventive measures based on indicators of risk factors.nnnMETHODSnAn exploratory analysis of cases in Europe between 2006 and 2009 reported to the Atypical Myopathy Alert Group was conducted. Based on clinical data, reported cases were allocated into 2 groups: confirmed or highly probable AM (AM group; further divided into survivors and nonsurvivors); and cases with a low probability of having AM or with another final diagnosis (non-AM group). Using Welchs test and odds ratios corrected for multiple comparisons, the AM vs. non-AM groups were compared to identify indicators for diagnosis and risk factors, and survivors vs. nonsurvivors in the AM group were compared to identify prognostic factors. Sensitivity, specificity and positive and negative predictive values were calculated for specific clinical signs related to final diagnosis and outcome.nnnRESULTSnFrom 600 reported cases, 354 AM cases (survival rate of 26%) and 69 non-AM cases were identified, while there were insufficient data to categorise the remainder. Variables valuable for diagnosing AM compared with similar diseases were as follows: presence of dead leaves and wood and/or trees on pastures; sloping pastures; full-time pasture access; no food supplementation; normal body condition; pigmenturia; normothermia; and congested mucous membranes. Nonsurvival was associated with recumbency, sweating, anorexia, dyspnoea, tachypnoea and/or tachycardia. Survival was associated with remaining standing most of the time, normothermia, normal mucous membranes, defaecation and vitamin and antioxidant therapy.nnnCONCLUSIONS AND POTENTIAL RELEVANCEnThis study refines the list of risk factors for AM. Clinical signs valuable for diagnosis and prognosis have been identified, enabling clinicians to improve management of AM cases.

Faecal microbiota characterisation of horses using 16 rdna barcoded pyrosequencing, and carriage rate of clostridium difficile at hospital admission.

BackgroundThe equine faecal microbiota is very complex and remains largely unknown, while interspecies interactions have an important contribution to animal health. Clostridium difficile has been identified as an important cause of diarrhoea in horses. This study provides further information on the nature of the bacterial communities present in horses developing an episode of diarrhoea. The prevalence of C. difficile in hospitalised horses at the time of admission is also reported.ResultsBacterial diversity of the gut microbiota in diarrhoea is lower than that in non-diarrhoeic horses in terms of species richness (p-value <0.002) and in population evenness (p-value: 0.02). Statistical differences for Actinobacillus, Porphyromonas, RC9 group, Roseburia and Ruminococcaceae were revealed. Fusobacteria was found in horses with diarrhoea but not in any of the horses with non-diarrheic faeces. In contrast, Akkermansia was among the three predominant taxa in all of the horses studied. The overall prevalence of C. difficile in the total samples of hospitalised horses at admission was 3.7xa0% (5/134), with five different PCR-ribotypes identified, including PCR-ribotype 014. Two colonised horses displayed a decreased bacterial species richness compared to the remaining subjects studied, which shared the same Bacteroides genus. However, none of the positive animals had diarrhoea at the moment of sampling.ConclusionsThe abundance of some taxa in the faecal microbiota of diarrhoeic horses can be a result of microbiome dysbiosis, and therefore a cause of intestinal disease, or some of these taxa may act as equine enteric pathogens. Clostridium difficile colonisation seems to be transient in all of the horses studied, without overgrowth to trigger infection. A large proportion of the sequences were unclassified, showing the complexity of horses’ faecal microbiota.

Samaras and seedlings of Acer pseudoplatanus are potential sources of hypoglycin A intoxication in atypical myopathy without necessarily inducing clinical signs

REASONS FOR PERFORMING STUDYnIngestion of sycamore seeds (Acer pseudoplatanus) is the likely source of hypoglycin A in atypical myopathy (AM) but ingestion of seedlings in spring might also contribute to intoxication.nnnOBJECTIVESnTo test for hypoglycin A in seeds and seedlings collected on pastures where AM cases were reported and compare its concentration in serum of affected and healthy horses.nnnSTUDY DESIGNnField investigation of clinical cases.nnnMETHODSnWhenever present, samaras (the winged nuts that each contain one seed) and/or seedlings were collected from pastures of 8 AM cases and 5 unaffected horses from different premises. Two AM cases were each co-grazing with an apparently healthy horse. Acylcarnitines and hypoglycin A were quantified in blood samples of all horses involved in the study.nnnRESULTSnHypoglycin A was detected in serum of AM (5.47 ± 1.60 μmol/l) but not in healthy controls pasturing where A. pseudoplatanus trees were not present. However, hypoglycin A was detected at high concentrations (7.98 μmol/l) in serum of a clinically healthy horse grazing a pasture with seedlings and samaras and also in the 2 healthy horses co-grazing with AM cases (0.43 ± 0.59 μmol/l). Hypoglycin A was detected in all samples of seeds and spring seedlings of A. pseudoplatanus.nnnCONCLUSIONSnAtypical myopathy can be associated with the ingestion of sycamore samaras and also ingestion of seedlings. Hypoglycin A can be detected in the blood of horses with no detectable clinical signs at pasture in which there is A. pseudoplatanus. Determination of hypoglycin A concentration in blood is useful for screening for exposure in suspected cases of AM.

European outbreak of atypical myopathy in the autumn 2009.

BACKGROUNDnAtypical myopathy is an acute, severe rhabdomyolysis occurring in grazing horses. In the beginning of October 2009, a new outbreak occurred in several European countries. Geographic, demographic and clinical data of the reported cases in the month October 2009 are described.nnnKEY FINDINGSnThe survival rate in this outbreak was 25%. The most frequently observed clinical signs were congested mucous membranes, dyspnea, tachycardia, depression, weakness, stiffness, recumbency, trembling, sweating, and myoglobinuria. Nonsurvivors were significantly more likely to be recumbent than survivors. Prognostic factors, symptomatic treatment, and preventive measures are discussed.nnnSIGNIFICANCEnDifferences were encountered during the described outbreak of atypical myopathy in October 2009 compared with previous outbreaks reported. Equine practitioners should be aware that previous epidemiological studies have shown that after a high prevalence in the autumn, new cases are likely to occur in the following spring.

The composition of the inflammatory infiltrate in three cases of polyneuritis equi

Polyneuritis equi (PNE) is a rare neurological disease in the horse. Because of the suspicion in PNE of a T-lymphocyte mediated immune response against the myelin, the objective of this study was to determine the composition of the inflammatory infiltrate in the involved nerves of 3 horses with PNE, studied retrospectively. T-lymphocytes were demonstrated in the lesions, which suggests a T-lymphocyte mediated immune response against myelin. In addition, the presence of B-lymphocytes indicated a local production of antibodies. More research, involving a prospective study, is needed to determine whether the T-lymphocytes are cytotoxic or T-helper lymphocytes.

Carriage and acquisition rates of Clostridium difficile in hospitalized horses, including molecular characterization, multilocus sequence typing and antimicrobial susceptibility of bacterial isolates

Clostridium difficile has been identified as a significant agent of diarrhoea and enterocolitis in both foals and adult horses. Hospitalization, antibiotic therapy or changes in diet may contribute to the development of C. difficile infection. Horses admitted to a care unit are therefore at greater risk of being colonized. The aim of this study was to investigate the carriage of C. difficile in hospitalized horses and the possible influence of some risk factors in colonization. During a seven-month period, faecal samples and data relating the clinical history of horses admitted to a veterinary teaching hospital were collected. C. difficile isolates were characterized through toxin profiles, cytotoxicity activity, PCR-ribotyping, antimicrobial resistance and multilocus sequence typing (MLST). Ten isolates were obtained with a total of seven different PCR-ribotypes, including PCR-ribotype 014. Five of them were identified as toxinogenic. A high resistance to gentamicin, clindamycin and ceftiofur was found. MLST revealed four different sequencing types (ST), which included ST11, ST26, ST2 and ST15, and phylogenetic analysis showed that most of the isolates clustered in the same lineage. Clinical history suggests that horses frequently harbour toxigenic and non-toxigenic C. difficile and that in most cases they are colonized regardless of the reason for hospitalization; the development of diarrhoea is more unusual.

Traditional and Quantitative Assessment of Acid-Base and Shock Variables in Horses with Atypical Myopathy

BACKGROUNDnDescriptions of acid-base disturbances in atypical myopathy (AM) are limited.nnnOBJECTIVESnDescribe and compare traditional and quantitative acid-base abnormalities and cardiovascular shock status in horses with AM at admission.nnnANIMALSn34 horses with AM, 15 healthy controls.nnnMETHODSnRetrospective case-control study. Records were searched for shock variables (packed cell volume [PCV], blood urea nitrogen [BUN], heart and respiratory rate) and acid-base variables (venous blood gas analysis, electrolytes, total protein, lactate) on admission. Base excess (BE) of free water (BEfw), chloride (BEcl), total protein (BEtp), and unidentified anions (BEua), anion gap (AG), measured strong ion difference (SIDm), and concentration of total nonvolatile weak acids ([Atot]) were calculated. Acid-base classifications, using simplified strong ion model and traditional approach, and shock grades were assigned. A 2-sample Wilcoxon rank-sum test and Bonferroni correction compared variables in AM cases versus control horses. Significance was P < .05/16 for acid-base and P < .05/5 for shock variables.nnnRESULTSnTachycardia, tachypnea, and normal to increased PCV and BUN were common in AM cases. Respiratory, metabolic acid-base alterations, or both were mainly caused by respiratory alkalosis, lactic acidosis, and SIDm alkalosis, alone or in combination. Evaluated variables (except pH, potassium concentration, total protein, and related calculations) were significantly different (P < .001) between AM cases and control horses. The strong ion model provided a more accurate assessment than the traditional approach and identified mixed derangements.nnnCONCLUSIONS AND CLINICAL IMPORTANCEnAcid-base derangements should be evaluated in horses with AM and this preferably with the strong ion model.

Mitochondrial function is altered in horse atypical myopathy.

Equine atypical myopathy in Europe is a fatal rhabdomyolysis syndrome that results from the ingestion of hypoglycin A contained in seeds and seedlings of Acer pseudoplatanus (sycamore maple). Acylcarnitine concentrations in serum and muscle OXPHOS capacity were determined in 15 atypical myopathy cases. All but one acylcarnitine were out of reference range and mitochondrial respiratory capacity was severely decreased up to 49% as compared to 10 healthy controls. The hallmark of atypical myopathy thus consists of a severe alteration in the energy metabolism including a severe impairment in muscle mitochondrial respiration that could contribute to its high death rate.

Can horses be clinically screened for West Nile Fever

In Europe, the frequency of West Nile Fever (WNF) outbreaks in horses and/or human beings is on the increase, especially in mid-eastern and southern Europe (Dauphin and others 2004, Rabel and others 2011). However, in several western European countries no activity of the virus has been detected so far, for example, in The Netherlands (Rockx and others 2006), Belgium and the UK (Morgan 2006)). However, considering the presence of migratory birds and suitable vectors in those countries, and the reports of changing epidemiology of the virus (Petersen and Marfin 2005, Blitvich 2008), the West Nile virus (WNV) is a genuine threat. Horses are considered good sentinels for WNV infection surveillance (Petersen and Marfin 2005) by the use of syndromic surveillance followed by laboratory confirmation. Syndromic surveillance aims at early identification of disease clusters before laboratory confirmation, thereby reducing morbidity and mortality (Leblond and others 2007). Clinical signs of WNF in horses are, however, difficult to distinguish from those of other neurological diseases (Leblond and others 2007, Porter and others 2011).nnThe aim of this study was to identify clinical variables that could be indicators for WNF in horses, which will be attempted …