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STREPTOCOCCAL AND ENTEROCOCCAL INFECTIONS

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mariam kavtaria

on 3 April 2017

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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.
Streptococcal infection, usually pharyngitis plus characteristic rash
The rash is the effect of one of 3 toxins - streptococcal pyrogenic exotoxins A, B, and C
The rash begins on the 1st or 2Nd day of illness over the upper trunk, spreads to extremities
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 - particularly 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
Lesions are generally not painful
Patients do not appear ill
Fever, if present, 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
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
M protein on surface inhibits phagocytosis - interferes with complement activation and opsonisation.
Antibodies to a given M type are protective against same M type, but not against that with different M types.
Has toxins - Streptolysins S and O that 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 of involvement
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
- among 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 (e.g., intraabdominal abscesses),
Abdominal surgical wounds,
Diabetic foot ulcers



diagnosis of streptococcal pharyngitis on clinical grounds alone is not reliable.
The throat culture remains the diagnostic gold standard.
.A rapid diagnostic kit for latex agglutination or enzyme immunoassay of swab is a useful adjunct to throat culture.
A positive result is reliable for definitive diagnosis and eliminates the need for throat culture.
Rapid diagnostic tests are less sensitive than throat culture thus a negative result should be confirmed by throat culture.
In the usual course of uncomplicated streptococcal pharyngitis, symptoms resolve after 3–5 days.
Prevention of Acute Rheumatic Fever depends on 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
Respiratory droplets are the usual mechanism of spread.
The incubation period is 1–4 days
intense erythema and swelling of the pharyngeal mucosa
presence of purulent exudate on the posterior pharyngeal wall and tonsillar pillars.
Enlarged, tender cervical lymph nodes
GAS pharyngitis
sore throat,
fever and chills,
malaise
Symptoms :
Diagnosis:
Suppurative complications:

both results from immune responses to streptococcal infection.
Penicillin treatment of streptococcal pharyngitis reduces the risk of ARF, but not of PSGN.
ARF is 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 infection of the skin Caused by GAS and 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, such as a diverticular or appendiceal abscess.
Infection of superficial and/or deep muscle fascias caused by:
Group A Streptococci alone or
Combination with other organisms (S. aureus).
Overall, 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
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
Erysipelas
Streptococcal Cellulitis
- infection involving the skin and subcutaneous tissues.
The portal of entry may be a trauma or surgical wound
- 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 intravenous immunoglobulin, a single dose
Group B Streptococci (s. Agalactiae)
5–40% of women are vaginal or rectal carriers of GBS.
Up to 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 before delivery),
Prolonged labor
Fever
Chorioamnionitis.
Early onset infection
- Sepsis and Bacteremia
Occur within the first week of life, 20 h at onset.
Symptoms: respiratory distress, lethargy, and hypotension.
Late-onset infections
- occur 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 is the agent of choice for all GBS infections.
Enterococci
Have the ability to grow in the presence of 6.5% sodium chloride


Vancomycin plus gentamicin may be used in 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
S. Bovis (Group D streptococci)
Endocarditis - often associated with neoplasms of the GI tract— colon carcinoma, polyps
When gastrointestinal lesions are carefully searched, abnormalities are found in ≥60% of patients with S. bovis endocarditis
Treatment:penicillin as a single agent
VIRIDANS STREPTOCOCCI
Treatment:
1. neutropenic patients with bacteremia are resistant to penicillin; thus these patients should be treated with
vancomycin
.
2. Viridans streptococci isolated in other clinical settings usually are sensitive to
penicillin
.
Development of
dental caries

Bacteremia
induced by eating, tooth-brushing, flossing
Adherence to biologic surfaces
accounts for the ability of these organisms to cause endocarditis.
Risk factors for bacteremia
:
High-dose cytarabine
Prior Treatment with trimethoprim- sulfamethoxazole or a fluoroquinolone,
Treatment with antacids or antihistamines,
Mucositis
Profound neutropenia.
S. salivarius, S. mitis, S. sanguis, and S. mutans, are part of the normal flora of the mouth
Alfa-hemolytic
References:

1. Harrison's Infectious Diseases- 17th Edition

2. Harrison'sPrinciples of Internal Medicine - 18th Edition
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