Systemic Pasteurella Haemolytica Infection as a Rare Sequel to Avirulent Live Pasteurella Haemolytica Vaccination in Cattle

Eleven cases of systemic Pasteurella haemolytica infection in cattle were identified from routine diagnostic laboratory submissions during the falls of 1988, 1989, and 1991. All cases came with a history of recent vaccination with an avirulent live culture P. haemolytica product. Nine of 11 cases involved cattle vaccinated between 2 and 18 days previously with this product. Ten of 11 cases involved 182-227-kg beef calves that were vaccinated between September and November during routine processing for entry into feedlots. The morbidity and mortality was generally low. The major pathologic findings included meningitis, injection site abscessation and/or cellulitis, and polyarthritis. Systemic infection was indicated in all cases by the isolation of P. haemolytica from 2 or more organs or distinct anatomical sites. In 6 cases, the vaccine injection site was cultured, and in all 6 cases, P. haemolytica was isolated. Three separate P. haemolytica isolates from 2 cases were further studied by restriction enzyme analysis (REA). These isolates were from tissues with suppurative inflammation, including the brain, joint, and injection site. The REA patterns of each of these 3 isolates were identical to the REA pattern of the vaccine masterseed, which strongly suggested that the organisms causing systemic infection were the same as the organism used to produce the vaccine. Because the overall incidence was quite low, other factors, such as stress, probably played a major role in the expression of this syndrome.

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Detection of Bovine Herpesvirus 4 (BoHV-4) DNA in the Cell Fraction of Milk of Dairy Cattle with History of BoHV-4 Infection

Journal of Clinical Microbiology ◽

10.1128/jcm.38.12.4668-4671.2000 ◽

2000 ◽

Vol 38 (12) ◽

pp. 4668-4671 ◽

Cited By ~ 22

Author(s):

Gaetano Donofrio ◽

Cesidio Filippo Flammini ◽

Franco Scatozza ◽

Sandro Cavirani

Keyword(s):

Dairy Cattle ◽

Bovine Herpesvirus ◽

Cell Fraction ◽

Enzyme Analysis ◽

Restriction Enzyme Analysis ◽

Cytopathic Effects ◽

Bovine Herpesvirus 4 ◽

Pcr Product ◽

History Of ◽

Herpesvirus 4

We have demonstrated, by PCR and restriction enzyme analysis of the PCR product, the presence of bovine herpesvirus 4 (BoHV-4) DNA in the cell fraction of milk from dairy cattle with a history of BoHV-4 infection. We next evaluated the infectious nature of BoHV-4 DNA in those cells. Cocultivation of a BoHV-4-sensitive cell line with BoHV-4 DNA-positive milk cell samples produced cytopathic effects. The same result was obtained from frozen and thawed milk cell fraction coming from the cell milk fraction PCR-positive cows, ensuring that cells were killed and only infectious virus could be recovered after cocultivation with sensitive cells. This report shows that infectious BoHV-4 can be present in milk cells and that therefore nursing may be one of the transmission routes of BoHV-4.

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Novel mutations of the thyroid peroxidase gene in patients with permanent congenital hypothyroidism

Acta Endocrinologica ◽

10.1530/eje.0.1450019 ◽

2001 ◽

pp. 19-24 ◽

Cited By ~ 29

Author(s):

P Ambrugger ◽

I Stoeva ◽

H Biebermann ◽

T Torresani ◽

C Leitner ◽

...

Keyword(s):

Congenital Hypothyroidism ◽

Enzyme Analysis ◽

Restriction Enzyme Analysis ◽

Thyroid Peroxidase ◽

Compound Heterozygous ◽

Single Strand Conformational Polymorphism ◽

Migration Patterns ◽

Exon 2 ◽

History Of ◽

Exon 9

OBJECTIVE: It is suggested that iodide organification defects account for 10% of all cases with congenital hypothyroidism (CH). One candidate gene for these defects is the thyroid peroxidase (TPO) gene. DESIGN: Exons 2, 8-10 and 14 of the TPO gene were examined in 30 patients with permanent CH without a family history of CH. This group was characterized by the presence of an orthotopic thyroid gland and elevated TSH levels. METHODS: The mutational screening was performed by single-strand conformational polymorphism followed by sequence analysis of fragments with abnormal migration patterns and by restriction enzyme analysis. RESULTS: In four patients we were able to identify mutations on both alleles which have not been described so far. One patient was a carrier of a new homozygous point mutation in exon 9 resulting in an exchange from Leu to Pro at codon 458. Another patient was found to be compound heterozygous for two mutations, a 20 bp duplication in exon 2 and a new mutation in exon 9 (Arg491His). Two brothers of consanguineous parents showed a homozygous T deletion in exon 14 at position 2512. CONCLUSIONS: Our findings confirm the genetic heterogeneity of TPO defects and support the suggested prevalence of organification defects.

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COMPLICATED MIGRAINE

JPHV (Journal of Pain, Vertigo and Headache) ◽

10.21776/ub.jphv.2021.002.02.2 ◽

2021 ◽

Vol 2 (2) ◽

pp. 28-33

Author(s):

Kadek Putri Paramita Abyuda ◽

Shahdevi Nandar Kurniawan

Keyword(s):

Genetic Disease ◽

Severe Headache ◽

Life Threatening ◽

History Of ◽

Complicated Migraine ◽

Abortive Treatment ◽

Migraine Pathophysiology ◽

Systemic Symptoms ◽

As Stress ◽

The Brain

Migraine is a chronic paroxysmal neurological disease characterized by attacks of moderate or severe headache accompanied by reversible neurologic and systemic symptoms. Although not life threatening, migraine can cause disability in the productive population. Migraine sufferers generally have a family history of migraine so that migraine is considered a genetic disease. Endogenous psychological factors such as stress or fatigue are the main triggers for migraine. Migraine pathophysiology involves various parts of the brain so that migraine symptoms are complex. Management of acute migraine can be done pharmacologically and non-pharmacologically. Migraine preventive management is needed if the patient has a chronic migraine or does not respond to abortive treatment.

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L2HGDH Missense Variant in a Cat with L-2-Hydroxyglutaric Aciduria

Genes ◽

10.3390/genes12050682 ◽

2021 ◽

Vol 12 (5) ◽

pp. 682

Author(s):

Matthias Christen ◽

Nils Janzen ◽

Anne Fraser ◽

Adrian C. Sewell ◽

Vidhya Jagannathan ◽

...

Keyword(s):

Current Knowledge ◽

Genetic Defect ◽

Clinical Signs ◽

Missense Variant ◽

Microcytic Anemia ◽

Abnormal Behavior ◽

Functional Candidate Gene ◽

History Of ◽

The Brain ◽

Hydroxyglutaric Acid

A 7-month-old, spayed female, domestic longhair cat with L-2-hydroxyglutaric aciduria (L-2-HGA) was investigated. The aim of this study was to investigate the clinical signs, metabolic changes and underlying genetic defect. The owner of the cat reported a 4-month history of multiple paroxysmal seizure-like episodes, characterized by running around the house, often in circles, with abnormal behavior, bumping into obstacles, salivating and often urinating. The episodes were followed by a period of disorientation and inappetence. Neurological examination revealed an absent bilateral menace response. Routine blood work revealed mild microcytic anemia but biochemistry, ammonia, lactate and pre- and post-prandial bile acids were unremarkable. MRI of the brain identified multifocal, bilaterally symmetrical and T2-weighted hyperintensities within the prosencephalon, mesencephalon and metencephalon, primarily affecting the grey matter. Urinary organic acids identified highly increased levels of L-2-hydroxyglutaric acid. The cat was treated with the anticonvulsants levetiracetam and phenobarbitone and has been seizure-free for 16 months. We sequenced the genome of the affected cat and compared the data to 48 control genomes. L2HGDH, coding for L-2-hydroxyglutarate dehydrogenase, was investigated as the top functional candidate gene. This search revealed a single private protein-changing variant in the affected cat. The identified homozygous variant, XM_023255678.1:c.1301A>G, is predicted to result in an amino acid change in the L2HGDH protein, XP_023111446.1:p.His434Arg. The available clinical and biochemical data together with current knowledge about L2HGDH variants and their functional impact in humans and dogs allow us to classify the p.His434Arg variant as a causative variant for the observed neurological signs in this cat.

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Molecular evolutionary analysis of human primary microcephaly genes

BMC Ecology and Evolution ◽

10.1186/s12862-021-01801-0 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Nashaiman Pervaiz ◽

Hongen Kang ◽

Yiming Bao ◽

Amir Ali Abbasi

Keyword(s):

Evolutionary History ◽

Genetic Basis ◽

Brain Size ◽

Primate Species ◽

Evolutionary Analysis ◽

Australopithecus Afarensis ◽

Primary Microcephaly ◽

Modern Humans ◽

History Of ◽

The Brain

Abstract Background There has been a rapid increase in the brain size relative to body size during mammalian evolutionary history. In particular, the enlarged and globular brain is the most distinctive anatomical feature of modern humans that set us apart from other extinct and extant primate species. Genetic basis of large brain size in modern humans has largely remained enigmatic. Genes associated with the pathological reduction of brain size (primary microcephaly-MCPH) have the characteristics and functions to be considered ideal candidates to unravel the genetic basis of evolutionary enlargement of human brain size. For instance, the brain size of microcephaly patients is similar to the brain size of Pan troglodyte and the very early hominids like the Sahelanthropus tchadensis and Australopithecus afarensis. Results The present study investigates the molecular evolutionary history of subset of autosomal recessive primary microcephaly (MCPH) genes; CEP135, ZNF335, PHC1, SASS6, CDK6, MFSD2A, CIT, and KIF14 across 48 mammalian species. Codon based substitutions site analysis indicated that ZNF335, SASS6, CIT, and KIF14 have experienced positive selection in eutherian evolutionary history. Estimation of divergent selection pressure revealed that almost all of the MCPH genes analyzed in the present study have maintained their functions throughout the history of placental mammals. Contrary to our expectations, human-specific adoptive evolution was not detected for any of the MCPH genes analyzed in the present study. Conclusion Based on these data it can be inferred that protein-coding sequence of MCPH genes might not be the sole determinant of increase in relative brain size during primate evolutionary history.

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Streptococcus pluranimalium meningoencephalitis in a horse

Journal of Veterinary Diagnostic Investigation ◽

10.1177/10406387211023465 ◽

2021 ◽

pp. 104063872110234

Author(s):

Dah-Jiun Fu ◽

Akhilesh Ramachandran ◽

Craig Miller

Keyword(s):

Ribosomal Rna ◽

Cross Sections ◽

Nucleotide Sequencing ◽

Formalin Fixed Paraffin ◽

Quarter Horse ◽

Formalin Fixed Paraffin Embedded ◽

History Of ◽

The Brain ◽

Gram Positive Cocci ◽

Formalin Fixed

A 3-y-old, female Quarter Horse with a history of acute neurologic signs was found dead and was submitted for postmortem examination. Areas of petechial and ecchymotic hemorrhage were present on cross-sections of the cerebrum, cerebellum, and brainstem. Histologic examination of the brain revealed severe, purulent meningoencephalitis and vasculitis with a myriad of intralesional gram-positive cocci. Streptococcus pluranimalium was identified from formalin-fixed, paraffin-embedded tissue obtained from sites with active lesions by PCR and nucleotide sequencing of bacterial 16S ribosomal RNA. S. pluranimalium should be considered as a cause of meningoencephalitis in a horse.

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A Rare Case of Spontaneous Arachnoid Cyst Rupture Presenting as Right Hemiplegia and Expressive Aphasia in a Pediatric Patient

Children ◽

10.3390/children8020078 ◽

2021 ◽

Vol 8 (2) ◽

pp. 78

Author(s):

Anne Bryden ◽

Natalie Majors ◽

Vinay Puri ◽

Thomas Moriarty

Keyword(s):

Cognitive Processing ◽

Arachnoid Cyst ◽

Memory Loss ◽

Acute Onset ◽

Word Finding ◽

Outpatient Visits ◽

The Family ◽

History Of ◽

Cyst Rupture ◽

The Brain

This study examines an 11-year-old boy with a known history of a large previously asymptomatic arachnoid cyst (AC) presenting with acute onset of right facial droop, hemiplegia, and expressive aphasia. Shortly after arrival to the emergency department, the patient exhibited complete resolution of right-sided hemiplegia but developed headache and had persistent word-finding difficulties. Prior to symptom onset while in class at school, there was an absence of reported jerking movements, headache, photophobia, fever, or trauma. At the time of neurology consultation, the physical exam showed mildly delayed cognitive processing but was otherwise unremarkable. The patient underwent MRI scanning of the brain, which revealed left convexity subdural hematohygroma and perirolandic cortex edema resulting from ruptured left frontoparietal AC. He was evaluated by neurosurgery and managed expectantly. He recovered uneventfully and was discharged two days after presentation remaining asymptomatic on subsequent outpatient visits. The family express concerns regarding increased anxiety and mild memory loss since hospitalization.

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