Strongyloides papillosus causes sudden death in weaned calves on New York dairies

Author(s):  
Toby L. Pinn ◽  
Amber M. Forrestal ◽  
Gerald E. Duhamel ◽  
Esther E. Crouch ◽  
Belinda S. Thompson ◽  
...  

Abstract CASE DESCRIPTION Outbreaks of sudden death in apparently healthy weaned dairy calves due to Strongyloides papillosus parasitism were diagnosed on 2 separate and independent New York (NY) dairies. CLINICAL FINDINGS Most calves were found dead; however, 1 calf observed while dying showed signs of tachycardia, tachypnea, vocalization, and convulsions shortly before death. In 6 affected heifers that underwent post-mortem examination, precocious bilaterally symmetric mammary gland enlargement was seen. A portion of their parasitized living cohorts also demonstrated similar mammary gland enlargement. A diagnosis of S papillosus hyperinfection was made based upon the presence of high numbers of S papillosus ova in feces, and confirmation by S papillosus–specific PCR assays. Consistent histopathological findings in affected calves included generalized mammary gland vascular congestion, interstitial edema and hemorrhage with ductal hyperplasia. Mild multifocal cardiomyocyte degeneration was found in 5 of 14 calves examined. Factors believed to contribute to the parasite’s environmental amplification and host hyperinfection included group housing on wood shavings and high environmental temperatures and humidity. TREATMENT AND OUTCOME Treatment of calves with doramectin pour-on stopped mortality and resolved the udder enlargement. CLINICAL RELEVANCE Similar outbreaks have previously been described in Japan and South Bohemia (Czech Republic), where researchers hypothesized that sudden death may be due to fatal arrhythmia caused by a parasite-associated cardiotoxin. This report highlights the importance of including S papillosus among the differential diagnoses for sudden death alone or together with precocious udder enlargement in calves kept in confinement housing.

2018 ◽  
Vol 5 (2) ◽  
pp. 74-78
Author(s):  
Danilo Silva Sousa ◽  
Eduardo Akio Pereira I ◽  
Carlos Roberto de Oliveira Júnior ◽  
Ricardo Mendonça de Paula ◽  
Genildo Ferreira Nunes

RESUMO Introdução - A miocardiopatia não compactada (MNC) é uma patologia de ocorrência familiar com histórico relevante de morte súbita e insuficiência cardíaca; é considerada como uma miocardiopatia não classificada pela Organização Mundial da Saúde (OMS). Segundo a Associação Americana de Cardiologia, é uma cardiomiopatia primária. Desenvolvimento - A MNC resulta de uma alteração genética que leva a uma parada do processo de compactação miocárdica, caracterizada pela persistência de trabeculações e recessos profundos que se comunicam com a cavidade ventricular. A apresentação clínica inicial varia de assintomático a apresentação de sintomas relacionados à dor torácica, insuficiência cardíaca e arritmias. Os principais métodos de diagnóstico para MNC são estudos ecocardiográficos e ressonância magnética cardíaca, tendo como principais diagnósticos diferenciais a forma apical de cardiomiopatia hipertrófica, a combinação de cardiomiopatia hipertrófica apical e MNC, cardiomiopatia hipertensiva, fibroelastose endocárdica, trombo apical ou tumores entre outros. Considerações finais - A terapêutica disponível inclui tratamento para insuficiência cardíaca, arritmias e eventos tromboembólicos, mas é necessário particularizar a terapêutica relacionada à anticoagulação e prevenção primária de morte súbita cardíaca.   Palavras-chave: Cardiomiopatias; insuficiência cardíaca; arritmias cardíacas. ABSTRACT The left ventricular noncompaction (LVNC) is a patology with a familiar occurrence and relevant historic of sudden death and heart failure; it's considered an unclassified cardiomyopathy by World Health Organization (WHO). According to American Heart Association (AHA), it's a primary cardiomyopathy. Development - The LVNC results in a genetic alteration which leads to stop miocardial compaction process, characterized by persistence of trabeculation and deep intertrabecular recesses communicating with the ventricular cavity. The initial clinical findings may vary from asymptomatic to chest pain, heart failure and arrhythmias. The main diagnosis methods for LVNC are echocardiography and cardiac magnetic resonance imaging, having as main differential diagnosis the apical form of hypertrophic cardiomyopathy, a combination of both apical hypertrophic cardiomyopathy and LVNC, hypertensive cardiomyopathy, endocardial fibroelastosis, apical thrombus, or tumours among others. Final considerations - The menagement available includes the treatment for heart failure, arrhythmias and thromboembolic events, but it's neceassary particularize the therapeutics related to anticoagulation and primary prevention of sudden death. Keywords: Cardiomyopathies; heart failure; cardiac arrhythmias.


1996 ◽  
Vol 105 (4) ◽  
pp. 312-316 ◽  
Author(s):  
James D. Williams ◽  
Oleh Slupchinskij ◽  
Anthony P. Sclafani ◽  
Claude Douge

Lingual thyroid gland is a rare clinical entity that is due to failure of descent of the gland anlage early in the course of embryogenesis. It may present with symptoms of dysphagia, upper airway obstruction, or even hemorrhage at any time from infancy through adulthood. We present two illustrative cases of lingual thyroid gland along with a protocol for diagnosis and management of the condition. Elements in the diagnostic and therapeutic evaluation are described with attention to the clinical findings, laboratory tests, and radiographic imaging studies employed in confirming the diagnosis and planning appropriate treatment The natural history of the condition is reviewed and a treatment strategy is outlined that focuses on the use of suppressive doses of thyroid hormone as the initial therapy. Surgical excision of the gland is reserved for more advanced cases of gland enlargement resulting in airway compromise, severe dysphagia that limits oral intake, or ongoing hemorrhage.


Lab Animal ◽  
2009 ◽  
Vol 38 (8) ◽  
pp. 258-259 ◽  
Author(s):  
Stephanie Blevins ◽  
Kelsie Gardner ◽  
Audra Wagner ◽  
Shay Elias ◽  
Susan Ball-Kell ◽  
...  

2008 ◽  
Vol 20 (1) ◽  
pp. 8-9 ◽  
Author(s):  
J. P. Brendemuehl

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Gregory Webster ◽  
Megan Puckelwartz ◽  
Lorenzo Pesce ◽  
Dellefave-Castillo Lisa ◽  
Carlos Vanoye ◽  
...  

Introduction: Genetic testing after sudden death in the young can identify pathogenic cardiac gene variants. Hypothesis: Genomic methods, coupled with phenotype evaluation, reveal non-Mendalian risks. Methods: We conducted clinical analysis and whole genome sequencing on 103 decedents aged 1-40 (mean age at death 23.7 years) accrued prospectively from 2015 to 2019 across 22 states. Postmortem pathological findings were classified as: known cardiac disorders, findings of uncertain significance (FUS), or sudden unexplained death (SUD, indicating no postmortem pathological diagnosis). Parental DNA and clinical data were obtained where possible. Variants were classified by an independent clinical genetic laboratory. Results: Among the 103 decedents, 34 had a postmortem clinical diagnosis, 23 had FUS, and 46 were classified as SUD. Pathogenic/likely pathogenic (P/LP) variants in arrhythmia or cardiomyopathy genes were identified in 17 (16.5%) decedents. The distribution of P/LP variants was not associated with age at death (OR 1.01 [0.97, 1.05], p=0.54); however, a multivariable analysis including decedent phenotype, ancestry and sex demonstrated that younger decedents had a higher burden of curated P/LP/VUS variants (effect size -1.5, p=0.0019). DNA from 31 parent-decedent trios and 14 parent-decedent dyads revealed 9 transmitted P/LP variants and 1 de novo P/LP variant. More than half of parents transmitting a P/LP variant (5/9) did not have clinical findings associated with the genotype. Conclusions: Whole genome sequencing effectively revealed P/LP variants in cases of sudden death in the young, implicating both arrhythmia and cardiomyopathy genes. In addition, both genotype and phenotype analyses suggest additional non-Mendelian risk mechanisms.


2001 ◽  
Vol 7 (4) ◽  
pp. 654-658 ◽  
Author(s):  
Don Weiss ◽  
Darcy Carr ◽  
Jacqueline Kellachan ◽  
Christina Tan ◽  
Michael Phillips ◽  
...  

2004 ◽  
Vol 72 (10) ◽  
pp. 5574-5581 ◽  
Author(s):  
Quan Lin ◽  
Yasuko Rikihisa ◽  
Robert F. Massung ◽  
Zerai Woldehiwet ◽  
Richard C. Falco

ABSTRACT A polymorphic multigene family (p44) of Anaplasma phagocytophilum encodes the immunodominant 44-kDa major outer membrane proteins. With p44-specific PCR and gene-specific probes, p44-1 was found in all human isolates from New York State but not in isolates from Minnesota, whereas p44-18 and two other p44 species were found in isolates from both regions. We therefore sequenced the genomic locus corresponding to the p44-1/p44-18 tandem locus of A. phagocytophilum HZ in 14 other geographically divergent strains from various hosts. The locus was found in all 14 strains, and p44-18 was conserved among all 13 United States isolates studied. In all nine northeastern strains, p44-1 was conserved. However, in three of the Minnesota strains and in one California strain, p44-1 was replaced at this genomic locus by the novel gene p44-61 (p44-61/18), whose hypervariable region (hv) was a chimera of p44-20hv and p44-23hv. The conserved base sequence within the hv region linked the two segments. In contrast, in the Old Sourhope strain isolated from sheep in the United Kingdom, only a single and distinct p44, p44-OS, was found in this locus. This suggests different rates of evolution of p44-1 and p44-18 at this locus and conservation of the locus within strains isolated from the same geographic region. Locus-specific reverse transcription-PCR revealed expression of p44-1 by New York and p44-61 by Minnesota strains at this locus. These p44 loci provide insight into the molecular evolution and functional divergence of p44 paralogs and may serve as markers for typing strains from different geographic regions.


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