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STREPTOCOCCAL AND ENTEROCOCCAL INFECTIONS

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mariam kavtaria

on 30 September 2018

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Transcript of STREPTOCOCCAL AND ENTEROCOCCAL INFECTIONS

Spread of infection from pharyngeal mucosa to deeper tissues:
cervical lymphadenitis, peritonsillar or retropharyngeal abscess, sinusitis, otitis media, meningitis, bacteremia, endocarditis, and pneumonia
.
should be considered in a patient with
unusually severe or prolonged symptoms
or
localized pain associated with high fever and a toxic appearance.

Spares the palms and soles
characteristic “sandpaper rash”
Circumoral pallor
“Strawberry tongue”
Accentuation of the rash in skin folds
- Pastia’s lines
Subsidence of the rash in 6–9 days

Desquamation
of the palms and soles.
Is seen most often in
young children
, living in
poor hygiene
conditions
Minor trauma inoculates organisms into the skin.
Impetigo is best prevented by adequate hygiene.
The usual sites of involvement are the
face
- around the nose and mouth and the legs
Lesions begin as:
Red papules vesicular pustular lesions break down and coalesce to form characteristic
honeycomb-like crusts

STREPTOCOCCAL AND ENTEROCOCCAL INFECTIONS
Mariam Kavtaria
Gram Positive Cocci
Catalase
catalase
Staphylococcus
STREPTOCOCCUS
Alfa (Partial)
hemolysis
Beta (Complete hemolysis)
Gamma
(NO Hemolsis)
Bacitracin sensitive
Bacitracin resistant
Group A
S. Pyogenes
Group B
S. Agalactiae
optochin sensitive
capsulated
Bile soluble
optochin resistant
No capsule
bile insoluble
S. Pneumoniae
Viridans Streptococci
group D
grows in bile
grows in 6.5% NaCl
Non - enterococcus
Grows in bile
No growth in 6.5 %NaCl
Enterococcus Faecalis
Streptococcus Bovis
Cause of suppurative infections
Triggers the postinfectious syndromes:
1. Acute Rheumatic Fever
2. Post-Streptococcal GlomeruloNephritis (PSGN)
M protein
on the surface inhibits phagocytosis - interferes with complement activation and opsonisation

Antibodies to a given M type are protective
against the same M type, but not against different M types
Has toxins -
Streptolysins S and O -
damage cell membranes and cause hemolysis
Has Streptokinase; DNAses; protease; and pyrogenic exotoxins A, B, and C.
The pyrogenic exotoxins, previously known as erythrogenic toxins, cause the rash of scarlet fever.

The onset of symptoms is acute:
Severe pain at the site
Malaise, fever, chills and a toxic appearance
MANAGEMENT
Early surgical exploration
Drainage and debridement
Antibiotic treatment
Screening
for anogenital colonization
at 35–37 weeks of pregnancy
- Identifies carrier mothers
Administration of
ampicillin/penicillin
during delivery reduces the risk of infection in the newborn
Women who develop
premature labor (<37 weeks)
should also receive intrapartum chemoprophylaxis
1)

Urinary tract infections

- patients who received antibiotics or undergone urinary tract Catheterisation.
2)
Nosocomial bacteremia
in patients with
intravascular catheters
10–20% of cases of
bacterial endocarditis
on both native and prosthetic valves
Treatment:
penicillin or ampicillin
plus
gentamicin
for at least 4 weeks
Infectious complications of
biliary surgery
and in liver abscesses
.
Polymicrobial infections arising from the bowel flora (intraabdominal abscesses),
Abdominal surgical wounds,
Diabetic foot ulcers



diagnosis on clinical grounds alone is
not reliable

The

throat culture
- diagnostic gold standard.
Latex agglutination or enzyme immunoassay of swab
- A rapid diagnostic test
A positive result is reliable and eliminates the need for throat culture
Rapid diagnostic tests are
less sensitive than throat culture
- a negative result should be confirmed by throat culture
In uncomplicated streptococcal pharyngitis, symptoms resolve after 3–5 days.
Prevention of Acute Rheumatic Fever
= eradication of the organism from the pharynx
Erythromycin
may be substituted for
penicillin
in cases of penicillin allergy.
Treatment :
Streptococcus Pyogens
(Group A Streptococci)
One of the most common bacterial infections of childhood
20–40% of all cases of
Exudative pharyngitis
in children
Spread by respiratory droplets
The incubation period is 1–4 days
Intense
erythema and swelling
of the pharyngeal mucosa
presence of
purulent exudates
on the posterior pharyngeal wall and tonsillar pillars.
Enlarged, tender cervical
lymph nodes

GAS pharyngitis
sore throat,
fever and chills,
malaise
NO COUGH
Symptoms :
Diagnosis of GAS Pharyngitis:
Suppurative complications:
both results from
immune responses
to streptococcal infection
Antibodies produced against the organism attack host tissues
Penicillin treatment of streptococcal pharyngitis reduces the risk of ARF, but
not of PSGN
.
ARF - caused
only
by streptococcal throat infections
PSGN may follow either skin infection or pharyngitis
Nonsuppurative complications
1. Acute Rheumatic Fever (ARF)
2. Post-Streptoccocal GlomeruloNephritis (PSGN)
Pathogenesis of Acute Rheumatic Fever
Pathogenesis of PSGN
Scarlet fever
Impetigo
Superficial skin infection - Caused by GAS
occasionally by other streptococci or
Staphylococcus Aureus
.
Necrotizing fasciitis (hemolytic streptococcal gangrene)
Organisms are introduced into the tissue:
a) through the skin trauma
b) the bowel flora - released during abdominal surgery
c) from an occult source - diverticular or appendiceal abscess.
Infection of superficial or deep muscle fascias caused by:
Group A Streptococci alone
Or Combination with other organisms (S. aureus).
GAS is implicated in ∼60% of cases of necrotizing fasciitis.
The general features of the illness:
Fever
Hypotension
Renal impairment
Respiratory distress syndrome.
Rash usually does not develop.

Management:
Supportive + antibiotics
clindamycin is effective - rapidly
terminates toxin production
Streptoccocal Toxic Shock Syndrome
Erysipelas
The lesion is
Tender and warm
to the touch
Appears
shiny and swollen
.
The skin has a
peau d’orange texture
- involvement of superficial lymphatics;
Develops over a few hours
Is associated with
fever and chills
.
Tends to occur on the
face and lower extremities.
After one episode,
recurrence at the same site
is common
Streptococcal Cellulitis
- infection involving the skin and subcutaneous tissues.
The portal of entry -
a trauma, surgical wound, previous fungal skin infection
- bright red appearance of the involved skin
- sharply demarcated
GAS infections associated with shock and multisystem organ failure
It shares certain features with staphylococcal TSS
Laboratory abnormalities:
Marked shift to the left in the WBCs, with many immature granulocytes;
Hypocalcemia
Hypoalbuminemia
Thrombocytopenia,
Treatment of GAS Infections
1. Pharyngitis -
Benzathine penicillin G, or penicillin V, - 10 days
2. Impetigo-
Same as pharyngitis
3.
Erysipelas/cellulitis
Severe: Penicillin G,
Mild to moderate: Procaine penicillin
4. Necrotizing fasciitis
: - Surgical debridement; plus penicillin G, ; plus clindamycin,
5. Pneumonia/empyema
- Penicillin G IV, plus drainage of empyema
6. Streptococcal toxic shock syndrome: -
Penicillin G, IV plus clindamycin, plus IV immunoglobulin - a single dose
Group B Streptococci (s. Agalactiae)
5–40% of women are
vaginal or rectal carriers

of GBS.
50% of infants delivered vaginally by carrier mothers become colonized
The infection is

acquired during birth
from the colonized maternal genital tract

The incidence is high among infants of women with:
Early rupture of membranes
(>24 h interval before delivery)
,
Prolonged labor
Fever
Chorioamnionitis.
Early onset infection
- Sepsis and Bacteremia
First week of life - 20 h at onset.
Symptoms:
respiratory distress, lethargy, and hypotension

Late-onset infections
- in infants 1 week - 3 months old.
Acquired during delivery, or
later contact with a colonized mother, nursery personnel
Meningitis
is the most common manifestation
Fever, lethargy or irritability
,
poor feeding
Seizures
Penicillin -
agent of choice for all GBS infections.
Enterococci
Have the ability to grow in the presence of 6.5% sodium chloride


Vancomycin plus gentamicin
for Penicillin allergic patients.
Enterococci are resistant to all cephalosporins
High - Risk Patents:
Elderly
Disrupted Mucosal or epithelial barriers
Altered normal flora by antibiotic treatment.
E. faecalis
E. faecium
Streptococcus gallolyticus

formerly
S. Bovis

(Group D streptococci)
Endocarditis
- associated with
neoplasms of the GI tract
— colon carcinoma, polyps
When GI lesions are carefully searched, abnormalities are found in ≥60% of patients with S. gallolyticus endocarditis
Treatment:
penicillin
as a single agent
VIRIDANS STREPTOCOCCI
Treatment:
1. neutropenic patients with bacteremia -
resistant to penicillin
these patients should be treated with
vancomycin.

2. Viridans streptococci isolated in other clinical settings usually are sensitive to penicillin.
S. Mutans
-
dental caries
metabolizes
sucrose to lactic acid
-
The acid makes tooth enamel vulnerable to decay.
Bacteremia
- induced by eating, tooth-brushing, flossing
Adherence to biologic surfaces
- ability of these organisms to cause
endocarditis.
Risk factors for bacteremia
:
High-dose cytarabine
Treatment with
trimethoprim- sulfamethoxazole
or a
fluoroquinolone
,
Treatment with
antacids or antihistamines
,
Mucositis
Profound
neutropenia
S. salivarius, S. mitis, S. sanguis, and S. mutans
- part of the normal flora of the mouth
Alfa-hemolytic
References:

1. Harrison's Infectious Diseases- 17th Edition

2. Harrison'sPrinciples of Internal Medicine - 19th Edition
Streptococcal infection -
pharyngitis plus characteristic rash

The rash due to one of 3 toxins - streptococcal pyrogenic exotoxins A, B, and C
Lesions are generally
not painful
Patients do not appear ill
Presence of Fever -
suggests either infection extending to deeper tissues or another diagnosis.
Cultures of lesions often yield S. aureus as well as GAS.
streptococci are isolated initially and staphylococci appear later
S. aureus may have become more prominent cause of impetigo, thus
Medications should cover both
streptococci and S. aureus:
For example, either
dicloxacillin or cephalexin
Antibodies
against the
GAS
M protein
may cross-react with host's connective tissues:
Heart
Joints
Skin
Brain


Migratory Polyarthritis
- large joints
Carditis - may lead
to Mitral stenosis
Subcutaneous nodules
: Painless, firm collections of collagen fibers over bones or tendons.
Erythema marginatum:
This rash typically spares the face
Sydenham's chorea
- involuntary movements of the face and arms - late presentation
Minor Jones criteria

Fever
of 38.2–38.9 °C (100.8–102.0 °F)
Arthralgia
Raised
erythrocyte sedimentation rate
(ESR)
Reised
C reactive protein
(CRP)
Leukocytosis
ECG changes:
prolonged PR
interval
Previous episode
of rheumatic fever
Diagnosis of Rheumatic fever:
2 Major
1Major + 2 minor
plus evidence of streptococcal infection
Hematuria
Oliguria
Edema
Hypertension
Fever (headache, malaise, anorexia, nausea
immune-complex-mediated disease
a type III hypersensitivity reaction
Antigen-antibody complexes
"get stuck" into glomerular capillaries and
activate complement
- inflammation ensues
The rash begins over the
upper trunk,
spreads to extremities
Major Jones criteria
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