Relation of Pyrogenic and Emetic Properties of Enterobacteriaceal Endotoxin and of Staphylococcal Enterotoxin

Martin, W. J.; Marcus, Stanley

doi:10.1128/jb.87.5.1019-1026.1964

Cited by 15 publications

(3 citation statements)

References 10 publications

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“…Enterotoxin B was the first type obtained in a highly purified form (2) and has been the most studied. In view of the pyrogenic activity of purified enterotoxin B, which has been demonstrated after intravenous or intracerebroventricular administration to cats (7) and after intravenous injection into rabbits (12,16,20) and monkeys (8), it is likely that enterotoxin absorption is at least partially responsible for the sudden fevers that herald the development of Staphylococcus-induced enterocolitis (19). On the other hand, it is, perhaps, surprising that fever is not a commonly reported symptom of Staphylococcus-induced food poisoning.…”

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confidence: 99%

Pyrogenic Responses to Staphylococcal Enterotoxins A and B in Cats

Clark

Page

1968

J Bacteriol

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Pyrogenic responses, ranging up to 4.8 F, were induced in cats by oral administration of highly purified staphylococcal enterotoxin B in doses from 10 to 100 jig/kg. Fever was a more sensitive indicator of intoxication than was emesis. Highly purified preparations of enterotoxin A, whether administered intravenously (0.01 to 1.0 jAg/kg), orally (10 to 25 jig/kg), or into the cerebral ventricles (0.005 to 0.020 ,g in 0.20 ml), were also pyrogenic in cats. Tolerance to the pyrogenic activity was produced by repeated intravenous injection of a given dose of enterotoxin A but not by repeated intracerebroventricular injection. Enterotoxin A was more potent than enterotoxin B after intravenous injection in causing both fever and emesis. Crosstolerance could not be demonstrated between enterotoxin A and enterotoxin B or Salmonella typhosa endotoxin. This lack of cross-tolerance plus the inability of large oral doses (100 to 4,700 pg/kg) of endotoxin to cause fever or emesis indicate that the reported responses were attributable to the specific toxins administered and not to contamination by other pyrogens.

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confidence: 99%

Pyrogenic Responses to Staphylococcal Enterotoxins A and B in Cats

Clark

Page

1968

J Bacteriol

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“…This causes widespread T cell proliferation, cytokine production, and apoptosis (338). Several additional superantigens have been well characterized such as SEA and SEB (16,107,130,257,291) and have been associated with pathological inflammatory responses in the lung. The USA300 strain of S. aureus encodes three characterized superantigens: SelX, SEK, and SEQ (104,465).…”

Section: F T Cell Activation By S Aureusmentioning

confidence: 99%

Innate Immune Signaling Activated by MDR Bacteria in the Airway

Parker

Ahn

Cohen

et al. 2016

Physiological Reviews

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Health care-associated bacterial pneumonias due to multiple-drug resistant (MDR) pathogens are an important public health problem and are major causes of morbidity and mortality worldwide. In addition to antimicrobial resistance, these organisms have adapted to the milieu of the human airway and have acquired resistance to the innate immune clearance mechanisms that normally prevent pneumonia. Given the limited efficacy of antibiotics, bacterial clearance from the airway requires an effective immune response. Understanding how specific airway pathogens initiate and regulate innate immune signaling, and whether this response is excessive, leading to host-induced pathology may guide future immunomodulatory therapy. We will focus on three of the most important causes of health care-associated pneumonia, Staphylococcus aureus, Pseudomonas aeruginosa, and Klebsiella pneumoniae, and review the mechanisms through which an inappropriate or damaging innate immune response is stimulated, as well as describe how airway pathogens cause persistent infection by evading immune activation.

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“…Bacterial exotoxins such as staphylococcal enterotoxins (SEs) are known to stimulate emesis via gut chemoreceptors [ 116 , 117 , 124 ]. Worthy of note is that experimental induction of LPS-related emesis is achieved by intravenous or intraperitoneal routes [ 122 - 127 ], whereas SEs readily elicit vomiting when administered intragastrically [ 124 , 128 ]. Also of interest with respect to cyanobacteria-related G-I illness are some similarities of clinical symptoms in the case of staphylococcal food poisoning: enteritis due to ingestion of SEs is characterised by rapid onset (1–4 hours) of vomiting ± nausea and diarrhoea, abdominal cramping and dizziness [ 124 , 129 ].…”

Section: Introductionmentioning

confidence: 99%

Cyanobacterial lipopolysaccharides and human health – a review

2006

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Cyanobacterial lipopolysaccharide/s (LPS) are frequently cited in the cyanobacteria literature as toxins responsible for a variety of heath effects in humans, from skin rashes to gastrointestinal, respiratory and allergic reactions. The attribution of toxic properties to cyanobacterial LPS dates from the 1970s, when it was thought that lipid A, the toxic moiety of LPS, was structurally and functionally conserved across all Gram-negative bacteria. However, more recent research has shown that this is not the case, and lipid A structures are now known to be very different, expressing properties ranging from LPS agonists, through weak endotoxicity to LPS antagonists. Although cyanobacterial LPS is widely cited as a putative toxin, most of the small number of formal research reports describe cyanobacterial LPS as weakly toxic compared to LPS from the Enterobacteriaceae.We systematically reviewed the literature on cyanobacterial LPS, and also examined the much lager body of literature relating to heterotrophic bacterial LPS and the atypical lipid A structures of some photosynthetic bacteria. While the literature on the biological activity of heterotrophic bacterial LPS is overwhelmingly large and therefore difficult to review for the purposes of exclusion, we were unable to find a convincing body of evidence to suggest that heterotrophic bacterial LPS, in the absence of other virulence factors, is responsible for acute gastrointestinal, dermatological or allergic reactions via natural exposure routes in humans.There is a danger that initial speculation about cyanobacterial LPS may evolve into orthodoxy without basis in research findings. No cyanobacterial lipid A structures have been described and published to date, so a recommendation is made that cyanobacteriologists should not continue to attribute such a diverse range of clinical symptoms to cyanobacterial LPS without research confirmation.

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Relation of Pyrogenic and Emetic Properties of Enterobacteriaceal Endotoxin and of Staphylococcal Enterotoxin

Cited by 15 publications

References 10 publications

Pyrogenic Responses to Staphylococcal Enterotoxins A and B in Cats

Pyrogenic Responses to Staphylococcal Enterotoxins A and B in Cats

Innate Immune Signaling Activated by MDR Bacteria in the Airway

Cyanobacterial lipopolysaccharides and human health – a review

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