Scarlet fever and other Streptococcal diseases. Flashcards

1
Q

what is the EPIDEMIOLOGY OF SCARLET FEVER ?

A

Peak incidence: 5–15 years (although it may affect individuals of any age)

Generally occurs in association with streptococcal cases of tonsillopharyngitis

most commonly during the late fall to early spring in temperate
environments

highly contagious

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2
Q

what is the ETIOLOGY OF SCARLET FEVER ?

A

Group A β‑hemolytic streptococci (Streptococcus pyogenes) produce erythrogenic exotoxin A, B, or C

( These exotoxins cause the rash of scarlet fever via a delayed-type skin reaction.)

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3
Q

what is the ROUTE OF TRANSMISSION OF SCARLET FEVER ?

A

aerosol / via respiratory droplets

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4
Q

what is the INCUBATION PERIOD OF SCARLET FEVER ?

A

2–5 days

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5
Q

what’s the CLINICAL FEATURES OF SCARLET FEVER ?

A

Characteristic triad:

  1. Sore throat - flame colored,
  2. fever,
  3. vomiting

============

initial phase (acute tonsillitis)

Fever
chills,
myalgias
Tonsillopharyngitis - Sore throat and difficulty swallowing

sharp borderline of the hyperemia between
the hard and soft palate

enlarged tonsils

White coating on the tongue

Enlarged cervical lymph nodes

Gastrointestinal symptoms (possible in young children)
Abdominal pain
 vomiting

=========
Exanthem phase

Rash appears 12–48 hours after the onset of fever

Fine, erythematous, sandpaper‑like texture (occlusion of sweat glands imparts a sandpaper texture)
Blanches with pressure

PASTIA LINES
key sign of scarlet fever: linear, petechial
Most pronounced in the groin, underarm, and elbow creases (i.e., flexural areas)

all of this
Begins on the neck
Disseminates to the trunk and extremities

Duration: ∼ 7 days

========
Tonsillopharyngitis

Pharyngeal erythema, possibly with tonsillar exudates

Strawberry tongue: with papillary hyperplasia, which is revealed once the white coating has sloughed off

Scarlatinous face - Typical red, flushed appearance of the cheeks with perioral pallor

Zischinskis Symptom
: several pale yellow vesicles at the base
of the nails

Rosenbergs scarlatinous erythema
: on 10th day of disease,
erythema on gluteal parts appear -> important for putting
diagnosis

==========

Desquamation phase

Appears 7–10 days after resolution of rash

Skin desquamation: desquamation of the skin in flakes
Affects face, trunk, hands, fingers, and toes

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6
Q

what symptoms should not be mistaken with scarlet fever

A

CORYZA, RHINORRHEA, COUGH, HOARSENESS, ANTERIOR STOMATITIS, CONJUNCTIVITIS, and ulcerative lesions are atypical for scarlet fever and warrant further investigation.

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7
Q

DIAGNOSIS OF SCARLET FEVER ?

A

primarily a clinical diagnosis

========
Pathogen detection
Throat culture - golden standard - but is not always used because of the time it takes (∼ 24 hours)

rapid strep test

======
During the course of disease: elevated antistreptolysin O (ASO) and anti‑deoxyribonuclease B (ADB) titers
are a late finding. THEY ARE USUALLY NOT USED IN AN ACUTE setting but are helpful when investigating POTENTIAL COMPLICATIONS SUCH AS RHEUMATIC FEVER AND POST‑STREPTOCOCCAL GLOMERULONEPHRITIS.

///positive tourniquet test (Rumpel-Leede capillary‑fragility test)

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8
Q

TREATMENT OF SCARLET FEVER ?

A

Drug of choice: oral penicillin V

In patients allergic to penicillin: macrolides

In cases of recurrence due to antibiotic resistance: cephalosporins

After 24 hours of antibiotic treatment, the patient is no longer infectious and may return to daycare or school

aim of antibiotic treatment is to prevent complications and shorten the period of infectivity.

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9
Q

what are the COMPLICATIONS OF SCARLET FEVER ?

A

Scarlet fever is considered one of the nonsuppurative (i.e., non-pus forming) complications of streptococcal tonsillopharyngitis. /////

========
early: otitis,
mastoiditis,
Ludwig Angina

=======
late:

POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

ACUTE RHEUMATIC FEVER (RARE)

SYDENHAM CHOREA

RHEUMATOID ARTHRITS

Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
Definition: a rare disorder that is characterized by sudden onset or exacerbation of obsessive-compulsive disorder (OCD) and/or a tic disorder following infection with S. pyogenes

=========
SUPPURATIVE:
peritonsillar cellulitis, peritonsillar abscess,
retropharyngeal abscess, suppurative cervical lymphadenitis,
mastoiditis, acute sinusitis, and otitis media

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10
Q

to become infected with s progenies what are needed?

A
  1. ## Highly toxic strain
  2. Sensitization from previous infections with streptococci /e.g.
    tonsillitis, otitis
    -
  3. Lack of antibodies to the erythrogenic exotoxin
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11
Q

dd for rash?

A
allergic/contact dermatitis
-
viral exanthema
-
staphylococcal scalded skin syndrome
-
erythema toxic
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12
Q

dd for strawberry rash?

A

viral stomatitis with eruptive lingual papillitis
-
diphteria

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13
Q

what are the OTHER INFECTIONS CAUSED BY STREP?

A

Streptococcal Toxic Shock Syndrome

erysipelas

tonsilopharyngitis

impetigo

Necrotizing Fasciitis.
Cellulitis.

Rheumatic Fever.
Post-Streptococcal Glomerulonephritis.

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14
Q

pathogenesis of stss?

A

Streptococcus enters via vagina, pharynx, mucosa, and skin in 50%
of cases, otherwise during surgery, but rarely as a secondary
infection from streptococcal pharyngitis

======
athogen enters the organism and goes into the deeper tissues and bloodstream

group A streptococci avoid phagocytosis largely due to
their antiphagocytic properties

induction of cytokine synthesis
within the deeper tissues and
bloodstream due to super antigens such as :

Streptococcal pyrogenic exotoxins (SPE) serotypes: ∼
SPE-A
SPE-B

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15
Q

clinical manifestation of Streptococcal Toxic Shock Syndrome?

A

first signs: influenza-like prodrome phase characterized by fever - 38.9°C

chills, myalgias, nausea, vomiting, and diarrhea that precedes
hypotension by 24 to 48 hours

confusion

without portal entry in develop necrotizing fasciitis or frank
myonecrosis, postpartum infection, peritonitis, or joint space
infection, pain that progressively increases ( soft tissue pain out of proportion to physical findings in necrotizing fascitis )

in children and adults: soft tissues are the most common primary site
of infection

=========

Second phase: patients suffer from tachycardia,
tachypnea,
persistent fever,

in patients with necrotizing fasciitis or myonecrosis, have increased pain at site of infection

hypotension, renal impairment,
and respiratory distress syndrome

==========

Third phase: sudden onset of shock and organ failure -> rapid progression,
and many patients die within 24 to 48 hours of hospitalization
-
Early diagnosis is essential for survival

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16
Q

diagnosis of stss?

A

leukocytosis
enal creatine clearance
hypoalbuminemia
and thrombocytopenia (at later stages)
creatine phosphokinase levels in serum are markedly elevated in
those with necrotizing fasciitis and myonecrosis

serum bicarbonate, lactate, and blood gas pH determinations are
crucial tests to follow therapeutic progress

17
Q

management of stss?

A

prompt and aggressive surgical exploration and
débridement of suspected deep-seated streptococcal infection
-
must find the cause and the extent of necrosis
-
helpful are CT and MRI to locate the primary site of infection

=======

Fluid resuscitation : several liters of crystalloid intravenous fluid to
improve blood pressure; the goal is to maintain a pulmonary artery
occlusion pressure of 12 to 16 mm Hg

======

not cause improvement, transfusion with packed red
blood cells, with or without albumin

========

empirical broad-
spectrum coverage for septic shock should be instituted initially

=======

diagnosis is made: high-dose
penicillin and clindamycin
should be given

===========

Dialysis and hemoperfusion in patients that develop renal failure

==========

Intravenous Immune Globulin

18
Q

what is erysipelas?

A

superficial cutaneous process, usually restricted to the dermis but
with prominent lymphatic involvement

19
Q

what are the clinical features of erysipelas?

A

  1. ## lesions are raised above the level of the surrounding skin- edematous
  2. ## clear line of demarcation between involved and uninvolved tissu
  3. lesions are a salmon red

lower extremities are more frequently involved
than the face

lesions are accompanied by chills, fever, and toxicity

there can also be lymphadenetitis
and bullae

20
Q

epidemic of erysipelas?

A

more common in infants, young children and oder

adults

21
Q

pathogenesis of erysipelas?

A

portals of
entry: these include surgical incisions, trauma or
abrasions, dermatologic diseases such as psoriasis,
or local fungal infections
-
the cutaneous lesions begin as localized area of
erythema and swelling -> then spreads rapidly with the lymphatic system

22
Q

what is the diagnosis of erysipelas?

A

usually clinical

soft tissue ultrasound - for skin abcess
CT and MRI

culture and gram stain not routine
- consider skin biopsy

23
Q

what is the treatmnet for erysipelas ?

A

empiric antibiotic therapy for strep and staph - systemic therapy usually required

choice penicillin or cephalosporin