Professional Documents
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Task 1: Diagnosis
The 2014 Guidelines for Rheumatic Fever will help you.
1) Find out what the "Jones Criteria" are. Make notes about these criteria.
Major manifestations (least likely to lead to an incorrect diagnosis) at that time included carditis, joint symptoms,
subcutaneous nodules and chorea
Minor manifestations (suggestive, but not su cient for the diagnosis) included clinical signs such as fever, erythema
marginatum, and abdominal pain and laboratory markers of in ammation such as ESR and leukocytosis.
These de nitions are now incorporated into the New Zealand RF Criteria. De nitions of raised temperature, ESR and
CRP were used. However the criteria need not be rigidly adhered to when ARF is the most likely diagnosis i.e. a
possible case of ARF.
2) Why is it now recommended that the Jones Criteria be replaced by the New Zealand guidelines for the diagnosis of
ARF?
The history and evolution of the Jones criteria for the diagnosis of ARF is detailed in Appendix B. For the 1st edition of
the New Zealand Rheumatic Fever guideline (2006) the main modi cation made to the Jones 19924 criteria was the
acceptance of echocardiographic evidence of carditis as a major manifestation.2,3
3) What are the generic diagnostic criteria that are given that would lead the doctor to make a de nitive (initial) diagnosis
of ARF?
2 major or 1 major and 2 minor manifestations plus evidence of a preceding GAS infection*
4) What common manifestation included in the generic criteria that would lead the doctor to have a very high suspicion
of ARF?
guidlines are important as they keep care and treatment consisstent and to an agreed upon standard
Disadvantages of guidlines is they might not be correct and may lead to miss diagnoses.
The 2014 Guidelines for Rheumatic Fever (section A and pages 5, 24-26) will help you.
C-reactive protein
Throat swab (preferably before giving antibiotics) - culture for group A streptococcus Anti-streptococcal serology:
both anti-streptolysin O and anti-DNase B titres, if available (repeat 10-14 days later if 1st test not con rmatory)
TREATMENT
Observation prior to anti-in ammatory treatment (use paracetamol [1st line] for fever or joint pain)
Once diagnosis of ARF or recurrence is made, refer to rheumatic fever register for prophylaxis programme and
public health for contact tracing.
ARF is a noti able disease in New Zealand. All patients should be noti ed to the regional Public Health service. The
Public Health service will refer to Episurv, the national noti able disease data base at ESR.
Antibiotics
naproxen (NSAID) but also works like aspririn and is considered safer alternative
Task 2: Strategies to detect GAS and curb rates of ARF in NZ children
1) Outline strategies implemented by government for the detection of GAS infections to try and curb rates of rheumatic
fever in children in the most a ected areas of New Zealand.
Radio New Zealand's Morning Report feature and the Ministry of Health's Rheumatic Fever updates will help you.
1) In the International Collaboration on Endocarditis Prospective Cohort Study (ICE-PCS), what was the primary causative
organism found to be for infective endocarditis (IE) in New Zealand?
How did this compare internationally?
S. aureus Worldwide
2) Based on the ICE-PCS study, if you were asked what demographic and clinical features might be seen in the patient
who presents with IE in New Zealand in the 21st century, what would you include?
most New Zealand patients with IE were men (68%) with a median age of 60 years
prosthetic valves or degenerative heart disease rather than underlying rheumatic heart disease; common
3) For those patients who had a coagulase-negative staphylococcus infections as the bacteria responsible for their IE,
what did this put them at higher risk for developing and why?
Those with IE caused by coagulase-negative staphylococci had an increased risk of death compared with those with IE
caused by viridans streptococci (RR 4.7, 95% CI 1.2, 17).
intracardiac abscess
4) Where some of the IE cases caused by less common bacteria caused blood cultures to be negative, how was the
organism able to be identi ed?
PCR
5) Why do you think that for many of the patients recruited in to the study, the time of onset of the IE was unknown?
Might not have known it was IE at rst because patients report after the onset of symptoms
Growths of bacteria.
endocardium is damaged then platelets and brin form clot providing surface for bacterial colonisation
Clinical signs of IE were less frequent in this cohort than traditional descriptions of the disease, with very few exhibiting
the classical Roth spots, Osler's nodes or Janeway lesions.
The inclusion of 'probable' endocarditis in this analysis may have also contributed to an apparently lower mortality.
8) Supposing a causal link did exist for the patient having developed IE as a result of repeated episodes of acute
rheumatic fever, you should know how this came about.
Draw a ow diagram to show the relationship between Streptococcus pyogenes (Group A Streptococcus or GAS) and
Viridans Streptococci group bacteria in a patient who:
You can use real paper (remember to bring it with you to tutorial two! ),
OR
Click annotate to open and use the virtual paper (and bring your device to tutorial two!).