Diagnosing leg swelling. S. pyogenes are a catalase-negative, coagulase-negative

Diagnosing a superficial skin infection
must be approached in a systemic manner. The first branch point is to determine
the extent of penetration of the infection – is it localized to the dermal
layer or does the infection extend into the subcutaneous tissue? The former
leads one to an erysipelas diagnosis while the latter is indicative of a
cellulitis infection.i On
inspection, it is difficult to assess the depth of infection so classic signs
are looked for. Erysipelas is indicated as a well-demarcated, erythematous,
painful lesion, with high fevers and chills commonly present.ii Usually,
erysipelas results as a consequence of lymphatic obstruction, local trauma or
abscess, or fungal infections. Ms. V had signs that were dissimilar to this
presentation and as such, an alternate to erysipelas was considered.

Cellulitis is an acute inflammatory
skin condition characterized by localized pain, erythema, swelling, and heat
with or without signs of fever.iii It is important to distinguish a
purulent infection from a non-purulent one as that is key to identifying the
most common pathogens – Staphylococcus
aureus purulent and Streptococcus
pyogenes non-purulent. Ms. V’s
presentation was non-purulent and the blood cultures came back positive for S. pyogenes. Cellulitis usually presents
unilaterally, so a bilateral involvement should raise flags for other possible
etiologies, namely, necrotizing fasciitis, toxic shock syndrome, and gas
gangrene.3 The absence of any major
systemic symptoms along with the clinical presentation of a subacute
progression led to a low clinical suspicion of these alternate diagnoses, despite
Ms. V having bilateral leg swelling.

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S. pyogenes are a catalase-negative,
coagulase-negative Lancefield Group A bacteria that are non-spore-forming
cocci. Histology frequently shows them in pairs or chains. S. pyogenes has a variety of virulence factors that makes it
pathogenesis so widespread.iv The outermost
capsule is made of hyaluronic acid, which has a chemical structure similar to
human connective tissue. This enables the bacteria to escape host recognition
and allows for evasion by macrophages and neutrophils.  The major virulence factor is the M protein,
which has been largely associated with community-based streptococcus
infections. The M protein binds to the host fibrinogen and blocks complement
binding to the peptidoglycan layer of the bacterium.v Although
antibodies may develop to a specific M protein, there are more than 80
serotypes of the protein, making it difficult to establish immunity to S. pyogenes infection. Increasing the
invasive capacity of S. pyogenes is
mediated largely by its capsular polysaccharide (C-substance), which is
composed of a branched polymer of L-rhamnose and N-acetyl-D-glucosamine.vi

The pathophysiology of host cell damage
and inflammatory response is similarly exhaustive in nature. 2 hemolysins –
Streptolysin O and Streptolysin S – are implicated in tissue damage.
Streptolysin O is highly immunogenic, and is more helpful in assessing other S. pyogenes infections apart from
cellulitis. Streptolysin S damages neutrophils and mediates organelle damage,
which is the relevant pathogenesis for cellulitis and systemic inflammatory
responses.vii Ms. V’s
subacute presentation plus marked widespread edema can raise a concern for
toxic shock syndrome (TSS) if improvement does not occur within one week.viii Streptococcal
TSS encodes certain factors that function as superantigens; they induce a
rapidly elevated febrile response, proliferation of T cells, and promote the
release of cytokines such as TNF, IL-1B, and IL-6. This widespread, nonspecific
T cell proliferation is a cause of serious concern, as patients who develop TSS
must be treated aggressively. Death is a likely complication, as mortality
rates can vary from 30% – 70%.ix

Monitoring Ms. V’s clinical
improvements is essential to her diagnosis. As per the guidelines for skin and
soft tissue infection by the Infectious Diseases Society of America, Ms’ V’s infection
is on the severe scale as evidenced by the progression of edema and extent to
which the edema presents. Additionally, her hospitalization makes her
susceptible to MRSA infection and a MRSA-specific antibiotic regimen must be
included in her treatment plan. Vancomycin plus either piperacillin- tazobactam or imipenem/meropenem has a
strong/moderated recommendation for an empiric regimen of severe infections. A
strong/high recommendation is for treatment duration of 5 days but treatment
should continue past this if the infection has not improved. Furthermore,
elevation of the affected area and treatment of other factors such as edema is
recommended. Because Ms. V’s edema is widespread, a diuretic should be included
in the regimen, taking care to note her renal impairment and adjusting the drug
and dose accordingly.x

Ms.
V’s presentation is not classic for a cellulitis infection; however, the
proposed pathogenesis is most likely when considering all the possible risk
factors along with the patient’s recollection. Ms. V states she was near her
grandchildren while on vacation and was aware of the “flu” going around the
area and attributes her cause of infection to those factors. She also had a solitary
case of diarrhea, vomiting, and nausea. It is hard to assess the cause of these
findings, especially because they were standalone factors. But, Ms. V’s likely
etiology of an infectious cause where she does not remember a bruise or injury
at the site can be likely as that is the most likely proposed mechanism for S. pyogenes infections that cause
cellulitis. Additionally, the positive blood cultures for S. pyogenes indicates an infectious process, although repeat
cultures should be attained for establishing strength of association. This
likelihood of an infectious cause coupled with negative tests for other severe,
but likely etiologies such as DVT or emboli from endocarditis makes this
treatment plan highly tailored for Ms. V’s presentation a favorable prognosis.

x

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