Molecular mechanisms underlying group A streptococcal pathogenesis

Olsen, Randall J.; Shelburne, Samuel A.; Musser, James M.

doi:10.1111/j.1462-5822.2008.01225.x

Cited by 103 publications

(100 citation statements)

References 84 publications

(105 reference statements)

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“…Key to the ability of GAS to cause such disease diversity is the production of numerous freely secreted or cell-surface-associated virulence factors that modulate the host immune response and enhance bacterial survival (Olsen et al, 2009). Recently, progress has been made in the study of the molecular mechanisms governing GAS protein secretion, with several proteins shown to be targeted to a single distinct membrane microdomain termed the ExPortal for secretion (Rosch & Caparon, 2005;Rosch et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

2010

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The signal recognition particle (SRP) is a ribonucleoprotein complex that targets proteins for secretion in a co-translational manner. While originally thought to be essential in all bacteria, recent data show that the SRP is dispensable in at least some streptococcal species. The SRP from the human pathogen group A Streptococcus (GAS, Streptococcus pyogenes) is predicted to be composed of protein Ffh and 4.5S RNA. Deletion of ffh alters the secretion of several GAS proteins, and leads to a severe reduction in virulence. Here, we report that mutation of the gene encoding 4.5S RNA results in phenotypes both similar to and distinct from that observed following ffh mutation. Similarities include a reduction in secretion of the haemolysin streptolysin O, and attenuation of virulence as assessed by a murine soft tissue infection model. Differences include a reduction in transcript levels for the genes encoding streptolysin O and NADglycohydrolase, and the reduced secretion of the SpeB protease. Several differences in transcript abundance between the parental and mutant strain were shown to be dependent on the sensorkinase-encoding gene covS. Using growth in human saliva as an ex vivo model of upper respiratory tract infection we identified that 4.5S RNA mutation leads to a 10-fold reduction in colony-forming units over time, consistent with the 4.5S RNA contributing to GAS growth and persistence during upper respiratory tract infections. Finally, we determined that the 4.5S RNA was essential for GAS to cause lethal infections in a murine bacteraemia model of infection. The data presented extend our knowledge of the contribution of the SRP to the virulence of an important Gram-positive pathogen.

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Section: Introductionmentioning

confidence: 99%

The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

2010

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“…Spread of the infection from the subcutaneous tissue to the deep fascial planes is facilitated by bacterial enzymes and toxins. This causes vascular occlusion, ischemia, and tissue necrosis [4,6]. Superfi cial nerves are damaged, producing the characteristic localized anesthesia.…”

Section: Introductionmentioning

confidence: 99%

“…Facultative aerobic organisms grow because polymorphonuclear neutrophils (PMNs) exhibit decreased function under hypoxic wound conditions, thus, lowering the oxidation/reduction potential and enabling more anaerobic proliferation resulting in acceleration of the disease process [6]. Spread of the infection from the subcutaneous tissue to the deep fascial planes is facilitated by bacterial enzymes and toxins.…”

Section: Introductionmentioning

confidence: 99%

“…Third, these organisms produce proteins designed to subvert the body's immune system [6,9]. For instance, the protein Mac1 accomplishes this by both mimicking a host cell receptor and cleaving IgG, ultimately enhancing survival [6,9].…”

Section: Introductionmentioning

confidence: 99%

“…NF soft-tissue infections involve rapid and extensive necrosis of the superfi cial fascia that results in high morbidity and mortality despite prompt treatment [3]. cleaving immune molecules [6,9]. Third, these organisms produce proteins designed to subvert the body's immune system [6,9].…”

Section: Introductionmentioning

confidence: 99%

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Necrotizing Fasciitis caused by Streptococcus pyogenes: A case report and literature review of disease diagnosis and management

Aziz¹

2017

Arch Community Med Public Health

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Background: A 55-year-old male presented to the emergency room at a local hospital complaining of chest discomfort and severe left elbow pain.Case Presentation: Erythema and symptoms of peripheral neuropathy were evident in the left hand. The patient reported recent trauma to his left elbow; however a radiograph of the left arm was unremarkable for fracture. After being admitted to the intensive care unit for observation, he developed worsening pain out of proportion and progressive decreased sensation in his left hand. Diagnosis:Initially, left arm compartment syndrome was suspected and treated accordingly. After surgical intervention, the patient's subsequent symptoms and preliminary blood culture results revealed Gram positive cocci in chains, indicating necrotizing fasciitis. The isolate was identifi ed as group A betahemolytic Streptococcus (GABS). Treatment and Follow-up:Broad-spectrum antibiotics given at outset were extended with additional antibiotics. Treatment consisted of fi ve separate surgeries involving extensive debridement of necrotic tissue amounting to approximately 55 to 65 percent of the patient's body surface area. The patient was eventually released to a burn center for skin grafting and wound closure and in less than three months, he expired.

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Streptococcus pyogenes adhesion and colonization

et al. 2016

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Edited by Wilhelm JustStreptococcus pyogenes (group A Streptococcus, GAS) is a human-adapted pathogen responsible for a wide spectrum of disease. GAS can cause relatively mild illnesses, such as strep throat or impetigo, and less frequent but severe life-threatening diseases such as necrotizing fasciitis and streptococcal toxic shock syndrome. GAS is an important public health problem causing significant morbidity and mortality worldwide. The main route of GAS transmission between humans is through close or direct physical contact, and particularly via respiratory droplets. The upper respiratory tract and skin are major reservoirs for GAS infections. The ability of GAS to establish an infection in the new host at these anatomical sites primarily results from two distinct physiological processes, namely bacterial adhesion and colonization. These fundamental aspects of pathogenesis rely upon a variety of GAS virulence factors, which are usually under strict transcriptional regulation. Considerable progress has been made in better understanding these initial infection steps. This review summarizes our current knowledge of the molecular mechanisms of GAS adhesion and colonization.

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Molecular mechanisms underlying group A streptococcal pathogenesis

Cited by 103 publications

References 84 publications

The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

Necrotizing Fasciitis caused by Streptococcus pyogenes: A case report and literature review of disease diagnosis and management

Streptococcus pyogenes adhesion and colonization

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