Can Streptococcal TSS follow pharyngitis?

[CBG23]

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So, I am reading conflicting things about the sequelae caused by S. pyogenes.

It seems like you can break it down S. pyogenes diseases into three categories:

1.) Pharyngitis

2.) Skin infections

3.) Necrotizing fasciitis

Now, AFTER infecting the oropharynx, scarlet fever is a possibility if the strain expresses the pyrogenic toxins needed.

Rheumatic fever is also a possibility following ONLY pharyngitis.

Post-streptococcal GN can follow BOTH pharyngitis and a skin infection.

So, basically, that leaves Streptococcal TSS; can it follow pharyngitis and/or a skin infection? Can it occur in isolation? The sources I've read aren't very clear on this...

 

[CBG23]

Also, on a related note; Goljan's RR3 says that Patients with post-streptococcal GN will not have a positive ASO titer:

"Increased anti-DNase B titers; ASO is degraded by oil in the skin and is not
increased; streptozyme test is positive (can detect anti-DNase B, ASO, anti-AH,
and anti-NAD antibodies)". - p. 402.

However, other sources like First Aid say the opposite? Is Goljan wrong here?

 

[ArcGurren]

So, I am reading conflicting things about the sequelae caused by S. pyogenes.

It seems like you can break it down S. pyogenes diseases into three categories:

1.) Pharyngitis

2.) Skin infections

3.) Necrotizing fasciitis

Now, AFTER infecting the oropharynx, scarlet fever is a possibility if the strain expresses the pyrogenic toxins needed.

Rheumatic fever is also a possibility following ONLY pharyngitis.

Post-streptococcal GN can follow BOTH pharyngitis and a skin infection.

So, basically, that leaves Streptococcal TSS; can it follow pharyngitis and/or a skin infection? Can it occur in isolation? The sources I've read aren't very clear on this...

Also, on a related note; Goljan's RR3 says that Patients with post-streptococcal GN will not have a positive ASO titer:

"Increased anti-DNase B titers; ASO is degraded by oil in the skin and is not
increased; streptozyme test is positive (can detect anti-DNase B, ASO, anti-AH,
and anti-NAD antibodies)". - p. 402.

However, other sources like First Aid say the opposite? Is Goljan wrong here?

1. I think TSS is more common in pharyngitis but it can probably occur with both. You have to suspect it with a patient who is hypotensive and has signs of shock (obviously) with a recent sore throat or skin infection, but with skin infection it'd prob be tough to differentiate that from S. aureus toxic shock. I suppose they could say something like "gold crusted rash" but I dunno.

2. Er to my knowledge PSGN almost always has an increased ASO; if it's inconclusive you the anti-DNase B usually helps to confirm. That's odd.

 

[Rollo]

Here's quick excerpts from medscape:

M protein is an important virulent determinant of GAS; strains lacking M protein are less virulent. M protein is a filamentous protein anchored to the cell membrane, which has antiphagocyte properties. M types 1, 3, 12, and 28 are the most common isolates found in patients with shock and multiorgan failure; furthermore, 3 distinct streptococcal pyrogenic exotoxins (ie, A, B, C) also have been identified. These toxins induce cytotoxicity and pyrogenicity and enhance the lethal effects of endotoxins. Recently, the streptococcal super antigen, a pyrogenic exotoxin, has been isolated from an M-3 strain. In some studies, strains producing exotoxins B and C have been implicated in this syndrome, to a lesser extent.

Colonization or infection with certain strains of S aureus and GAS is followed by the production of 1 or more toxins. These toxins are absorbed systemically and produce the systemic manifestations of TSS in people who lack a protective antitoxin antibody. Possible mediators of the effects of the toxins are cytokines, such as interleukin 1 (IL-1) and tumor necrosis factor (TNF). Pyrogenic exotoxins induce human mononuclear cells to synthesize TNF-alpha, IL-1-beta, and interleukin 6 (IL-6).

Estimates from population-based studies have documented an incidence of invasive GAS infection of 1.5-5.2 cases per 100,000 people annually.[8] Approximately 8-14% of these patients also will develop TSS.[9] A history of recent varicella infection markedly increases the risk of infection with GAS to 62.7 cases per 100,000 people per year. Severe soft tissue infections, including necrotizing fasciitis, myositis, or cellulitis, were present in approximately half of the patients.

And some information about ASO in AGN:

The streptozyme tests test includes many streptococcal antigens that are sensitive for screening but are not quantitative, such as DNase, streptokinase, streptolysin O, and hyaluronidase.

The antistreptolysin O (ASO) titer is increased in 60-80% of patients (in AGN). The increase begins in 1-3 weeks, peaks in 3-5 weeks, and returns to normal in 6 months. ASO titer is unrelated to severity, duration, or prognosis of renal disease.

With ASO titer or streptozyme titer, increasing titers confirm recent infection. In patients with skin infection, anti-DNase B (ADB) titers are more sensitive than ASO titers for infection with Streptococcus.

 

[turkeyjerky]

Yeah, I think ASO is only about 50% sensitive following skin infections.

 

[ArcGurren]

Yeah, I think ASO is only about 50% sensitive following skin infections.

Fair point. It would however be the first standard test to order if you have a pediatric patient with recent sore throat with 2+ hematuria, 2+ proteinuria on an exam question i think.

 

[werd]

so, i think of strep toxic shock syndrome as usually being associated with a bad skin infection, but i don't think you can box it in completely; it can be a/w any infection if it's the right type of GAS.

as a side note, s. pyogenes can (rarely) do a whole lot more than the list you have. i saw a patient die from a rapidly progressive strep pyogenes pneumonia when i was an intern. i've also seen GAS bacteremia and osteo. it's a much more sensitive bug than staph, but its infections can move much faster. any time you think an infection is moving way faster than normal, consider strep pyo.