Preparing for biological threats: Addressing the needs of pregnant women

Watson, Amelia K.; Ellington, Sascha; Nelson, Christina; Treadwell, Tracee A.; Jamieson, Denise J.; Meaney‐Delman, Dana

doi:10.1002/bdr2.1016

Cited by 18 publications

(10 citation statements)

References 51 publications

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“…This blockade of neurotransmitter release accounts for the flaccid paralysis and autonomic dysfunction that are characteristic of the disease botulism [ 5 ]. Botulinum neurotoxins (BoNTs) are considered some of the most potent toxins known to mankind and due to their extreme toxicity have become potential bio-warfare agents [ 6 , 7 , 8 , 1 ]. The two most likely forms of botulism that could arise from the deliberate release of BoNT are foodborne and inhalational botulism [ 1 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Therapeutic efficacy of equine botulism antitoxin in Rhesus macaques

et al. 2017

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BackgroundThere are currently no licensed vaccines available for prevention of botulism in humans. The vaccination is not desirable due to expanding therapeutic indications of botulinum toxins. The only available specific treatment for botulism is antitoxin to remove circulating toxin, thus, preventing further neuronal damage. BAT® (Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G)—(Equine)) has been developed and its therapeutic efficacy evaluated against botulinum neurotoxin serotype A (BoNT/A) in Rhesus macaques.Methods and findingsIn a post-exposure prophylaxis (PEP) study, animals were exposed to 4x LD50/kg of BoNT/A and administered intravenously with either BAT (1x or 0.1x scaled human dose), or placebo at 4 hours post-exposure. The animals were monitored for 14 days. For the therapeutic intervention studies, animals were exposed to a 1.7x LD50/kg of BoNT/A and treated intravenously with either placebo or BAT at a 1x scaled human dose at the onset of clinical signs. Animals were monitored on an hourly basis for 14 or 21 days. In the PEP study, all animals tolerated equine based antitoxin without any adverse clinical signs. A 100% survival was observed in groups treated with the BAT compared to 0% survival in those treated with the placebo (p<0.001, Fisher’s exact test). BAT antitoxin prevented the development of signs of neurotoxicity of botulinum toxin. In a therapeutic study, treatment with the BAT at scaled 1x human dose after the onset of clinical signs significantly enhanced survival compared to the placebo (46.6% vs. 0%, p<0.0001, Fisher’s exact test). Additionally, treatment with the BAT delayed the progression of signs (muscular weakness, respiratory distress, oral/nasal discharge) of toxin intoxication and reduced the severity of the disease.ConclusionsA single dose of BAT, when administered to symptomatic monkeys, resulted in a statistically significant survival benefit compared to the placebo. Additionally, BAT completely protected monkeys from the clinical signs of intoxication and subsequent death when administered as PEP treatment. These data in part supported the licensure of BAT under the Animal Rule in the United States by the Food and Drug Administration.

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Section: Introductionmentioning

confidence: 99%

Therapeutic efficacy of equine botulism antitoxin in Rhesus macaques

et al. 2017

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“…Moreover, alcohol consumption has only been identified in the literature as a cause of panhypopituitarism rather than IGHD ( 4 ). Suspicion of neurological damage secondary to maternal ingestion of other toxins was low as the patient demonstrated no other physical abnormalities or cognitive deficits on evaluation, both of which are typical sequaele ( 5 ). Nutritional deficit was not suspected given serum albumin and pre-albumin levels were within normal reference ranges and proportionate weight change prior to treatment.…”

Section: Discussionmentioning

confidence: 95%

A surprising treatment response in a patient with rare isolated growth hormone deficiency, type IB

Amar

Borden

Watson

et al. 2017

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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Isolated Growth Hormone Deficiency (IGHD) is a rare cause of short stature, treated with the standard regimen of subcutaneous synthetic growth hormone (GH). Patients typically achieve a maximum height velocity in the first year of treatment, which then tapers shortly after treatment is stopped. We report a case of a 9-year-old male who presented with short stature (<3rd percentile for age and race). Basal hormone levels showed undetectable serum IGF1. Skeletal wrist age was consistent with chronologic age. Cranial MRI revealed no masses or lesions. Provocative arginine-GH stimulation testing demonstrated a peak GH level of 1.4 ng/mL. Confirmatory genetic testing revealed a rare autosomal recessive single-nucleotide polymorphism (SNP) with mutational frequency of 2%. GH supplementation was started and pursued for 2 years, producing dramatically increased height velocity. This velocity persisted linearly through adolescence, several years after treatment had been discontinued. Final adult height was >95th percentile for age and race. In conclusion, this is a case of primary hypopituitarism with differential diagnosis of IGHD vs Idiopathic Short Stature vs Constitutional Growth Delay. This case supports two objectives: Firstly, it highlights the importance of confirmatory genetic testing in patients with suspected, though diagnostically uncertain, IGHD. Secondly, it demonstrates a novel secondary growth pattern with implications for better understanding the tremendous variability of GH treatment response.Learning points:GHD is a common cause of growth retardation, and IGHD is a specific subtype of GHD in which patients present solely with short stature.The standard treatment for IGHD is subcutaneous synthetic GH until mid-parental height is reached, with peak height velocity attained in the 1st year of treatment in the vast majority of patients.Genetic testing should be strongly considered in cases of diagnostic uncertainty prior to initiating treatment.Future investigations of GH treatment response that stratify by gene and specific mutation will help guide treatment decisions.Response to treatment in patients with IGHD is variable, with some patients demonstrating little to no response, while others are ‘super-responders.’

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“…The clinical presentation of gestational infection is not different from that in nonpregnant women. 5,6 Placental infection can occur through bacteremia or through the genitourinary tract. 7,8 In the literature, there are few neonatal melioidosis reports.…”

Section: Discussionmentioning

confidence: 99%

Case Report: Gestational Melioidosis through Perinatal Transmission

Rodríguez

Huertas

Rodríguez

et al. 2020

The American Journal of Tropical Medicine and Hygiene

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Burkholderia pseudomallei is an emerging pathogen in the Americas. Cases of mother-to-child transmission of B. pseudomallei are rare and probably occur by placental or perinatal infection. We report the first case of native gestational and neonatal melioidosis in the Western hemisphere. The isolated strains in the mother and newborn were confirmed by whole-genome sequencing and identified as a novel sequence type ST1748. The comparison of both genomes revealed a nucleotide similarity of 100%. Melioidosis should be considered within the differential diagnosis of febrile illness or pneumonia in pregnant women and newborns from endemic areas of the Americas.

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Preparing for biological threats: Addressing the needs of pregnant women

Cited by 18 publications

References 51 publications

Therapeutic efficacy of equine botulism antitoxin in Rhesus macaques

Therapeutic efficacy of equine botulism antitoxin in Rhesus macaques

A surprising treatment response in a patient with rare isolated growth hormone deficiency, type IB

Case Report: Gestational Melioidosis through Perinatal Transmission

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