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A Clear-cut Case of Acute Rheumatic Fever After Group G Streptococcal Pharyngitis in New Zealand

Lennon, Diana, MBChB

The Pediatric Infectious Disease Journal: April 2018 - Volume 37 - Issue 4 - p 376–377
doi: 10.1097/INF.0000000000001834
Letters to the Editor

Population Child and Youth Health, University of Auckland, Auckland, New Zealand, Starship Children’s Hospital, Auckland District Health Board, Auckland, New Zealand, Kids First Public Health Nursing, Kidz First Community, Auckland, New Zealand

Supported by a grant (13-969) from the Health Research Council of New Zealand in partnership with the New Zealand Ministry of Health and the Heart Foundation of NZ. The author has no other funding or conflicts of interest to disclose.

Address for correspondence: Diana Lennon, MBChB; E-mail:

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To the Editors:

We note with interest a recent report of a case of acute rheumatic fever (ARF) possibly associated with group G streptococcal pharyngitis and perhaps group A streptococcal pyoderma in the subtropics.1

We draw readers’ attention to a case of ARF with a much closer temporal association with pharyngeal group G streptococcus in our randomized trial published in your journal in 2009.2 It was isolated from a student with pharyngitis and cultured within the accepted latent period of 3 weeks before the onset of ARF. The most closely associated group A streptococcal pharyngitis in the same student was 4 months before the onset of ARF. In addition, this student had raised streptococcal antibody titers (aspartate aminotransferase and anti-DNase B) to support this as an active infection rather than carriage. Students in the intervention group in this trial presented with sore throats for management to school clinic, so, if consented and an active participant, we had access to their longitudinal throat swabbing history. Over the 4-year study, throat swab cultures for symptomatic 5–18 year olds consistently threw up group A (7%) (a higher percentage in younger children) as well as group C (1%), B (4.4%) and G (3.8%). The New Zealand (NZ) primary prevention program for ARF control is sore throat management with treatment of group A streptococcal pharyngitis (

There has been important success for indigenous Maaori in NZ with a significant reduction of first presentation ARF after the introduction of the primary prevention program. Maaori carry two-thirds of the NZ ARF disease burden (Fig. 1).



There are ongoing challenges to control ARF in the last third (the up-swinging graph above) who are predominantly Auckland-domiciled Pacific New Zealanders. Note the y axis for this graph is rates not number of cases. The formula for Ministry of Health funding underestimated the ARF burden for this urban area.

Published robust evidence from a circumscribed area of the NZ program with high density of ARF and more than 90% in a school with a clinic has demonstrated that school clinics for 5–13 year olds has been successful (2010–2016) (88/100,000 to 37/100,000, P = 0.008), a proof of principle for this approach (and a global first).3

Regarding the role of skin in the NZ environment, a 1-year antibiotic audit of the school clinics in the same evaluation area above and where skin infection treatment is part of a comprehensive school health approach found antibiotic treatment for skin infections was less than 10% of total antibiotics used in the program.4 This is in the face of seasonal epidemic post-streptococcal glomerulonephritis usually preceded by impetigo (which continues to this time).5

However, there is no doubt the emm types seen in our ARF endemic region are more typically those classed as skin-associated types or “generalists” (skin and/or throat infectors) though at least one outbreak with a “rheumatogenic” group A streptococci has been described.2 , 6–8 So-called rheumatogenic emm types are uncommon. A plausible hypothesis is the requirement for a skin-type isolate to induce pharyngitis for ARF to ensue.9 This scenario is not ruled out in the case presented. Very high streptococcal titers are seen in our ARF endemic population, which suggests repeated infection leading to priming, which is now supported by experiments using newer modalities.10 , 11 This may help unravel the pathogenesis of ARF. A potential flaw in the case of O’Sullivan et al is that a child self-presenting from a school classroom may not have declared a sore throat and therefore not presented for a swab within the latent period, that is, less than 3 weeks before the onset of ARF.

The pathogenesis of ARF indeed needs more elucidation with modern tools. The evidence presented by O’Sullivan et al (and our case) for alternative pathways for the triggering of ARF produce evidence for guilty only by possible association but not by causation. It is an insufficient evidence to support a change to a very extensive public health program, which appears successful to date.

Diana Lennon, MBChB

Population Child and Youth Health

University of Auckland

Auckland, New Zealand

Starship Children’s Hospital

Auckland District Health Board

Auckland, New Zealand

Kids First Public Health Nursing

Kidz First Community

Auckland, New Zealand

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1. O’Sullivan L, Moreland NJ, Webb RH, et alAcute rheumatic fever after group a Streptococcus pyoderma and group G streptococcus pharyngitis. Pediatr Infect Dis J. 2017;36:692–694.
2. Lennon D, Stewart J, Farrell E, et alSchool-based prevention of acute rheumatic fever: a group randomized trial in New Zealand. Pediatr Infect Dis J. 2009;28:787–794.
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11. Raynes JM, Frost HR, Williamson DA, et alSerological evidence of immune priming by group A streptococci in patients with acute rheumatic fever. Front Microbiol. 2016;7:1119.
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