JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
DISCUSSION
further taxonomic classification was performed to subspeciate the isolate in our lab and is not usually performed in standard clinical laboratories. 19
Introduction
Each year in the United States, an estimated 486,000 people sustain burns which require medical attention. 1 With the loss of a natural barrier to the environment the underlying dermis and soft tissues are exposed to microbial colonization. The most common organisms associated with noscomial burn wound infections are Gram-positive organisms including Staphylococcus aureus (23%), Enterococcus species (11%), and coagulase-negative staphylococci (4.3%). Potential Gram- negative pathogens include Pseudomonas aeruginosa (19.3%), Escherichia coli (7.2%), Serratia marcescens (3.5%), and Klebsiella pneumonia (2.6%). 2 Isolation of fungal pathogens, most often Candida albicans (3.5%), is less common. Streptococcal species-associated sepsis in burn patients have been reported in the literature, but are usually due to Group A β-hemolytic Streptococcus . 3 Group G streptococcus is part of normal human commensal flora of the skin, upper airway, gastrointestinal tract, and genitourinary system. It most closely resembles Group A streptococcus in genetic sequencing and also shares many of the same virulence factors resulting in similar clinical manifestations. 4
Virulence Factors and Pathogenic Mechanisms
The majority of virulence factors found in Group G streptococci are also found in Group A streptococci (i.e., S treptococci pyogenes ), including adhesions, the M protein, Streptolysin O and Streptolysin S, C5a peptidase, streptokinase, and various superantigens.10, These factors are shared via horizontal gene transfer from S. pyogenes to SDSE via streptococcal phages. 4,18 Accordingly, these genetic similarities result in Group A streptococcus and Group G streptococcus sharing similar clinical manifestations, including skin and soft tissue infections, pharyngitis, bacteremia, and toxic shock-like syndrome. 16,18,22,23 The clinical features of Group G streptococcal infections can be attributed to its virulence factors which include adhesins, toxins, and proteases. Adhesions facilitate invasion of bacteria through damaged epithelial and mucosal surfaces. 12 The M protein virulence factor encoded by the emm gene facilitates the characteristic spreading of SDSE infections by resisting phagocytosis, inhibitingthecomplement cascadeanddisrupting the coagulation system. 10,12,16,24 This is further exacerbated by streptokinase, which converts plasminogen to plasmin and thereby prevents clot formation and facilitating spread of the organism. 10,12 Toxins of note in SDSE include Streptolysin O and Streptolysin S. These toxins are involved in necrotizing soft tissue infection and also are responsible for the phenotypic β-hemolysis seen on blood agar plates. 10,12 Superantigens also play a significant role in more severe streptococcal infections such as streptococcal toxic shock-like syndrome.
MICROBIOLOGY
Taxonomy
Group G β-hemolytic streptococci were first identified by Lancefield and Hare in 1935 and were not considered to be pathogenic organisms. 5,6 Today several species of streptococci carry the Lancefield G carbohydrate antigen on their cell wall, and are categorized as a Group G Streptococcus. These species include Streptococcus dysgalactiae, Streptococcus canis, and the Streptococcus anginosus group which includes S . anginosus, S. constellatus , and S. intestinalis . 4,7,8,9,10,11 Isolates found in humans were initially categorized as Streptococcus dysgalactiae subspecies which expressed either C or G antigens. Sixty years later, Vandamme et al. further divided Streptococcus dysgalactiae into two separate subspecies based on chemical properties and appearance. Group G streptococcus generally form large (>0.5mm) pearl gray colonies on sheep blood agar. 12,13 In 1999, Vieira et al classified all β-hemolytic, large-colony forming Group G streptococci found in human infections as Streptococcus dysgalactiae subspecies equisimilis (SDSE) 9,12,14,15,16 and Streptococcus dysgalactiae subspecies dysgalactiae (SDSD) for animal isolates of Group C. 17,18,19 The two subspecies are clustered together on phylogenetic trees because they share some genes but they do not have any identical alleles. 18 Zoonotic infections with SDSD infection have been reported as case reports in the the literature but are uncommon. 20 In our patient’s case, the streptococcal isolate was identified as beta-hemolytic based on the clear zones of total hemolysis and demonstration of large colony types greater than 0.5 mm with no odor. The isolate then underwent latex agglutination testing which determined the Lancefield group as G. No
EPIDEMIOLOGY
Group G streptococci inhabit human epithelial and mucosal surfaces. From these sites, the organism can invade into deeper structures or into normally sterile sites, such as the blood stream, to produce disease. 25 Group G streptococcal infections are more common in men than women 16,19 and increase in incidence with age. The organism can be transmitted from person to person. The median reported age at presentation of patients with GGS bacteremia varies in the literature, but generally falls between ages 55-67. 5,16,19,26,27 Adistinctive feature of GroupG streptococcal infection is its association with underlying chronic illness. Of patients with SDSE infection, some of the common coexisting comorbidities include cardiovascular disease, diabetes mellitus, malignancy, and alcohol abuse. 5,16,19,28 Multiple sources have reported an increase in the frequency of reports of Group G streptococcal infections. 21 The explanation for this increase remains unclear; Rantala et al. hypothesized that the aging population and increased survival of adults with chronic disease could be a factor. Watsky et al suggests that although virulence factors contribute to an organism’s pathogenicity it is disruption of mucosal barriers which plays the major role in overcoming host defense. 29
J La State Med Soc VOL 168 JULY/AUGUST 2016 21
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