RHEUMATIC FEVER

Bold/ underline = IMPORTANT; gray = extra explanation

Definition & Etiology:

 A systemic immune process complicating group A beta-hemolytic

streptococcal pharyngitis resulting in diffuse inflammation involves
mainly heart, joints, skin, CNS and blood vessels
– Autoantibodies is formed against autoantigen of the connective tissue
– Antibodies produced against streptococci can react with heart tissue
Antigens
Clinical picture and Diagnosis:
 Usually affects children between the ages of 5 and 15; rare after 25.
 Incubation period: occurs 1–5 weeks after throat infection
Tonsillitis
Chorea
Subcutaneous nodules
Erythema marginatum
Diagnosis based on Jones criteria (two major OR
one major and two minor)

Jones criteria for the diagnosis of rheumatic fever

Major manifestations
• Carditis • Polyarthritis
• Chorea • Erythema marginatum
• Subcutaneous nodules
Minor manifestations
•Fever • Arthralgia
• Previous rheumatic fever • Raised ESR or CRP
• Leucocytosis • First-degree AV block (ECG)
 Plus supporting evidence of preceding streptococcal infection:
 recent scarlet fever ‫رمزية‬4‫لق‬44‫ىا‬4‫لحم‬44‫ ا‬, raised antistreptolysin O (ASOT)

‫لسبحي‬44‫لميكروبا‬44‫ا‬or other streptococcal antibody titre, positive throat

culture
Major criteria
• Carditis:
 Pericarditis ( dry with retrosternal pain increase with respiration or effusion),

 Myocarditis (tachycardia, systolic murmur, diastolic gallop)

 Endocarditis: valvatitis (carey comb murmur then value stenosis or incompetence)

• Erythema marginatum: skin rash with red raised edges and clear center, mainly on
trunk, thighs and arms
• Migratory polyarthritis: affects the large joints
•Subcutaneous nodules: small, mobile and painless nodules on the extensor surface of
joints
• Sydenham’s chorea: common in female. It is unilateral involuntary semi purposeful
movements with hypotonia and emotional lability
Minor criteria
 fever, arthralgias, elevated erythrocyte sedimentation rate, elevated C-
reactive protein, PR prolongation on ECG, and history of rheumatic
fever
Treatment:
Bed rest until vital signs and ECG become normal
*Salicylates and nonsteroidal anti-inflammatory drugs reduce fever
and joint complaints but do not affect the natural course of the disease
*If streptococcal infection is still present, penicillin is indicated
*In penicillin allergy, cephalosporin and erythromycin
*Prevention of recurrent streptococcal pharyngitis in patients less than
25 years old (a monthly injection of benzathine penicillin is most
commonly used)
Infective endocarditis
Definition:
Infective endocarditis, an infection of the endocardial surface
of the heart which may include:
-heart valves ,
-mural endocardium
-septal defects ‫لقلبمثال‬44‫يا‬444‫قبف‬444‫ث‬
and is caused by :a wide variety of bacteria and fungi.
The pathogens entry are facilitated by underlying heart disease
Incidence of infective endocarditis :
 Higher in patients with underlying valvular heart disease: native or
prosthetic, congenital or rheumatic, and those with intravenous drug abuse.
- Mitral valve prolapse, mitral regurge and aortic valve disease are the most
frequent.
- Prosthetic valvular heart disease about %20 of all cases of endocarditis.
- Pacemaker-endocarditis
- Intravenous drug abuse and catheterrelated infection .
- Rare in: Congenital cyanotic heart disease
- Uncommon in: Isolated mitral stenosis
 The commonest organisms causing infective endocarditis and their
possible route of entry

Possible source Organism

Periodontal infection Streptococcus viridans

Bowel or urinarv tract Other streotococci

Skin infections: Abcesses Staphylococcus aureus

Vascular access sites (intravenous and central
lines) IVDA

Surgical wound infection Coagulase negative staphylococcus

Albus

Periodontal region Gram negative bacteria of HACEK group

Venous access Fungi ( candida. Aspergillus)

Pathophysiology
l. Endothelial damage occurs
 On top of damaged valves.

 Due to high pressure jet of blood (VSD , PDA , regurgitant mitral or aortic lesion)

2. Adherence of micro-organisms to endovascular surfaces

3. Deposition of fibrin and platelets which are colonized by blood born organisms
creating vegetations.
 
Sequalae:
 Vegetations may become large enough to cause obstruction.

 Break away as emboli.

 Perforation of a cusp or disruption of chordae that may because of increased regurge

Classification of infective endocarditis:
Acute, subacute, chronic
 Acute : Fulminating form associated with high fevers and systemic

toxicity. Virulent bacteria, such as Staphylococcus aureus, frequently

cause this syndrome, if untreated, death may occur within days to
weeks
 Subacute: more indolent and caused by less-invasive organisms,

such as streptococci viridans, usually occurring in preexisting

valvular heart disease.
MANIFESTATION
S

OF
INFECTIVE
ENDOCARDITIS
Extracardiac manifestations
due to emboli or immune complex causing:
 * Vasculitis and skin lesions.

 * Mycotic aneurysms at the sites of infected emboli may develop in the arteries.

 * Focal glomerulonephritis.

-Fever and Weight loss

 *The illness often begins as a "flu-like" illness with a dry cough, body aches and

fatigue, which follows a subacute or chronic course.

 * Low grade fevers, night sweats and weight loss are cardinal manifestations.

- Myalgia and joint pain.

 * May present as fever of unknown origin , so high index of suspicion is needed.
Skin lesions
 Skin or mucosal lesions are seen in about 50% of cases. These include:

 * Purpuric or petechial rash.

 * Subconjunctival and soft palate petechiae, hemorrhages within the nail

beds ("splinter hemorrhages")

 * Painful subcutaneous nodules on the palms or soles ("Osler's nodes") at the

finger tips, and generalized rash.

 * Janeway lesions are macular (round), nonblanching (pale on pressure), nonpainful,

erythematous lesions on the palms and soles.

Fundus
 *Roth spots
Cardiac manifestations
 * New murrnur: Almost always, usually in the mitral or aortic valve position.
 * In patients with pre-existing murrnurs, a new or changing murmur is noted in about 30%

of cases. This may be a sign of valve dehiscence and require urgent surgical intervention.
 A widening pulse pressure due to a significant regurgitant lesion.

 Bradycardia due to possible conduction defect and require immediate attention.

 Heart failure due to valve affection or myocarditis in (40-50 %) of cases.

 Splenomegaly: Splenomegaly is reported in about 20% of cases, more likely in patients

who have been ill for months rather than days or weeks.
 Systemic embolization : causing peripheral arterial embolism , cerebral emboli

causing stroke , renal emboli causing hematuria .

 A systemic immune reaction (eg, glomerulonephritis' arthritis).
Diagnosis:
 careful history and physical examination,
 blood culture

 echocardiogram.

- A minimum of three blood cultures should be obtained over a time

period based upon the severity of the illness.
Diagnosis of infective endocarditis (modified Duke
criteria)
Major criteria

• Positive blood culture

Typical organism (eg. Strept. Viridans) from two cultures
1. Persistent positive blood cultures taken > 12 hrs apart
2. Three or more positive cultures taken over > 1 hr
• Endocardial involvement
3. Positive echocardiographic findings of vegetations
4. New valvular regurgitation
• Minor criteria
Predisposing valvular or cardiac abnormality
• Intravenous drug misuse
• Pyrexia ≥ 38 °C
• Embolic phenomenon
• Vasculitic phenomenon
• Blood cultures suggestive: organism grown but not achieving major criteria
Suggestive echocardiographic findings •
Definite endocarditis = two major,
or one major and three minor,
or five minor
Possible endocarditis = one major and one minor, or three minor

Other laboratory tests: are relatively nonspecific:

- An elevated erythrocyte sedimentation rate (ESR) and/or an elevated level of C-reactive protein (CRP).
- A normochromic normocytic anemia.
- The white blood cell count may be normal or elevated in patients with subacute presentations of
endocarditis.
Complications:
1.Heart failure.
2. Neurological complications: stroke, encephalopathy, and retinal
emboli.
 Brain abcess and mycotic aneurysms are relatively infrequent.

3. Annular or ring abcesses in different organs.

4. Metastatic infection (eg, vertebral osteomyelitis), septic arthritis
5. Immune-mediated damage (eg, glomerulonephritis)
6. Complications associated with prolonged parenteral antimicrobial
therapy or surgery.
Treatment:
 It is difficult because organisms reside within a protected site within the vegetation.
 High concentration of intravenous antibiotics for prolonged periods are required.

 Synergistic combinations of antibiotics are used to maximize the microbicidal effect.

Principles of drug therapy:

 - Empiric antibiotics are started only after cultures are taken.

 - The treatment should continue for 4-6 weeks

 - Serum levels of Gentamicin and Vancomycin need to be monitored.

 - In patients with penicillin allergy, one of the glycopeptides antibiotics, vancomycin,

can be used.
Prevention
Any source of infection ( e.g. dental abscess ) should be removed as soon as possible
Chemoprophylaxis before the following procedure:
 • Dental procedures known to produce bleeding

 • Tonsillectomy

 • Surgery involving GI, respiratory mucosa

 • Esophageal dilation

 • ERCP for obstruction

 • Gallbladder surgery

 • Cystoscopy, urethral dilation

 • Urethral catheter if infection present

 • Urinary tract surgery, including prostate

IMPORTANT!
Chemoprophylaxis:
 Amoxicillin 2g PerOral 1h before procedure or Ampicillin 2g IM/IV

30m before procedure

 Penicillin Allergic: Clindamycin 600 mg PO 1h before procedure or

600 mg IV 30m before, Cephalexin OR Cefadroxil 2g PO 1 hour

before , Cefazolin 1.0g IM/IV 30 min before procedure,
Azithromycin or Clarithromycin 500mg PO 1h before
Treatment (skipped!)
 – Antimicrobial therapy
 – Empirical therapy once infective endocarditis is suspected:
 • Benzyl penicillin + vancomycin if onset is acute
 • Benzyl penicillin + gentamycin if onset is subacute
 – According to the results of the culture
 – Surgery: Indications:
 • Congestive cardiac failure
 • Uncontrolled infection despite maximal antimicrobial therapy
 • Pseudomonas aeruginosa, Brucella species, Coxiella burnetti, Candida and fungi
 • Presence of prosthetic valve endocarditis unless late infection
 • Large vegetation
 • Major embolus
 • Heart block
 Dental management of infective endocarditis patient

Dental treatment is important routes for entry of the organism into the blood
stream
– Streptococcus viridans: Is the usual etiologic agent
– Usually is subacute
– Incubation period approximately two week
 Oral hygiene should be practiced with methods that improve gingival health yet

minimize bacteremia. In patients with significant gingival inflammation, oral

hygiene is initially limited to gentle procedures.
 Oral irrigators
are generally not recommended
because their use may induce
bacteremia.

 Susceptible patients should be encouraged to maintain the highest level of oral hygiene
once soft tissue inflammation is controlled.
 Severe periodontal disease and areas of periodontal suppuration or dental focus of
infection require elimination.
 Pretreatment chlorhexidine mouth rinses are recommended before all procedures,
including periodontal probing,
because they significantly reduce the presence
of bacteria on mucosal surfaces.

-Dental extraction should be avoided in healthy mouths whenever possible.

-Endodontic therapy is the treatment of choice.
Also, single extractions are preferable to
multiple extractions.
All dental treatment procedures require antibiotic prophylaxis.
 When possible, at least 7 days are kept between appointments

(preferably 10–14 days).

 If this is not possible, an alternative antibiotic regimen is selected

for appointments within a 7-day time period.

 Regular recall appointments, with an emphasis on oral hygiene

reinforcement and maintenance of oral health, are extremely

important for patients with infective endocarditis.