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Toxic shock syndrome in a horse with Staphylococcus aureus pneumonia.

Abstract: A 3-year-old Thoroughbred gelding was examined because of clinical signs of pneumonia and shock. Mucous membrane petechiation and ventral edema were observed and considered to be a result of vasculitis. Epidermal necrosis developed on the distal portions of the limbs. The horse had a persistent high fever that was unresponsive to nonsteroidal anti-inflammatory treatment, and Staphylococcus aureus was isolated from a nasal swab specimen and 2 transtracheal wash fluid samples. Antimicrobial, anti-inflammatory, and supportive treatment resulted in clinical improvement. However, resolution of the pulmonary infection required long-term (42 days) antimicrobial administration. Staphylococcus aureus strains isolated from this horse were positive for the toxic shock syndrome toxin-1 gene and were shown to produce toxic shock syndrome toxin-1, the causative factor in toxic shock syndrome in humans. The horse's clinical signs were attributed to toxic shock syndrome secondary to pulmonary S. aureus infection.
Publication Date: PubMed ID: 12619842
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Summary

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The research article discusses a case where a horse developed toxic shock syndrome, a potentially fatal condition, due to a pneumonia infection caused by the Staphylococcus aureus bacteria. The horse showed improvement after antimicrobial therapy, however, complete recovery took a longer time.

Case Introduction

  • The study investigates a particular case of a 3-year-old Thoroughbred gelding horse that showed symptoms of pneumonia and shock. The horse also developed mucous membrane petechiation (small red or purple spots on the skin) and ventral edema (abnormal accumulation of fluid in the lower part of the body), which the veterinarians hypothesized to be due to vasculitis (inflammation of blood vessels).

Symptoms and Initial Treatment

  • Along with the aforementioned indications, the horse also developed epidermal necrosis (tissue death) on its limbs and did not respond to nonsteroidal anti-inflammatory treatment, characterized by a persistent high fever.
  • The Staphylococcus aureus bacterium was identified from nasal swab and fluid samples from the horse’s windpipe. The horse was thereafter administered with antimicrobial treatment, supportive care, and medicines to reduce inflammation. These measures resulted in the horse showing signs of clinical improvement.

Long-Term Treatment and Diagnosis

  • Despite the initial improvement, fully healing the lung infection required a long-term antimicrobial treatment that lasted for 42 days.
  • Further studies on the Staphylococcus aureus strains isolated from the horse revealed the presence of toxic shock syndrome toxin-1 gene, confirming the ability of these strains to produce the toxin that leads to toxic shock syndrome in humans.
  • This finding led the researchers to the conclusion that the clinical symptoms shown by the horse were indeed due to toxic shock syndrome, resulting from the pulmonary infection caused by the Staphylococcus aureus bacterium.

Cite This Article

APA
(). Toxic shock syndrome in a horse with Staphylococcus aureus pneumonia. .

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Citations

This article has been cited 3 times.
  1. Fungwithaya P, Boonchuay K, Narinthorn R, Sontigun N, Sansamur C, Petcharat Y, Thomrongsuwannakij T, Wongtawan T. First study on diversity and antimicrobial-resistant profile of staphylococci in sports animals of Southern Thailand. Vet World 2022 Mar;15(3):765-774.
  2. Little SV, Hillhouse AE, Lawhon SD, Bryan LK. Analysis of Virulence and Antimicrobial Resistance Gene Carriage in Staphylococcus aureus Infections in Equids Using Whole-Genome Sequencing. mSphere 2021 Aug 25;6(4):e0019620.
    doi: 10.1128/mSphere.00196-20pubmed: 34346711google scholar: lookup
  3. van Leeuwen WB, Melles DC, Alaidan A, Al-Ahdal M, Boelens HA, Snijders SV, Wertheim H, van Duijkeren E, Peeters JK, van der Spek PJ, Gorkink R, Simons G, Verbrugh HA, van Belkum A. Host- and tissue-specific pathogenic traits of Staphylococcus aureus. J Bacteriol 2005 Jul;187(13):4584-91.