Molluscum Contagiosum, Rocky Mountain Spotted Fever, Erythema Migrans, Lyme Disease, ERYSIPELAS, Bollous Erysipelas, SCARLET FEVER, peritonsillar abscess, IMPETIGO, NECROTIZING FASCIITIS Flashcards | Quizlet
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Molluscum Contagiosum, Rocky Mountain Spotted Fever, Erythema Migrans, Lyme Disease, ERYSIPELAS, Bollous Erysipelas, SCARLET FEVER, peritonsillar abscess, IMPETIGO, NECROTIZING FASCIITIS

Terms in this set (31)

Molluscum Contagiosum
Intraepidemral tumors of the skin; More common in children
Mildly contagious by direct contact
Can self inoculate
POX DNA Virus
Etiology of Molluscum Contagiosum
Treatment of Molluscum Contagiosum
depends on the number, size, and age of the patient
No treatment
Tretinoin gel
Cantharone solutions
Manual curettage of big lesions
Cryotherapy w liquid nitrogen
Rocky Mountain Spotted Fever
Acute febrile illness with significant constitutional symptoms and a characteristic rash; Transmitted by dog, wood, or lone star tick; Rash begins on hands and feet and includes palms and soles, then spreads to the ankles, wrists, abdomen and trunk
Laboratory presentation in Rocky Mountain Spotted Fever
CBC normal to low
Thrombocytopenia, bandemia, anemia, hyponatremia, hypoalbuninemia, elevated CPK
Weil-Felix serologic test + 10-14 days after onset of illness
Rickettsia rickettsia
Etiology of Rocky Mountain Spotted Fever
Treatment of early Rocky Mountain Spotted Fever
Doxycycline: >8 years old: 2mg/kg PO BID (max 100 mg per dose x 10- 21 days
Amoxicillin 50mg/kg/day TID. Max 500mg per dose x 14 - 21 days
Cefuoxime 30 mg/kg/day divided BID PO. Max 500 mg per dose x 14-21 days
2 days to 2 weeks
Time from tick bite to symptoms of Rocky Mountain Spotted Fever
Symptoms of Rocky Mountain Spotted Fever
Fever
Headache
Muscle ache
N/V
Confusion
Coma
Erythema Migrans
The early cutaneous manifestation consisting of an expanding annular lesion around the original tick bite
Lyme Disease
Fever, facial paralysis, rash, arthritis
EM 70 - 80 % of people
Expands gradually over days up to 12 inches across
May feel warm but non tender
May appear on any area of body
May clear as it enlarges
Days to Months after Lyme Disease infection
Severe headaches and neck stiffness
Additional EM rashes on other areas of the body
Arthritis with severe joint pain and swelling, particularly the knees and other large joints.
Facial or Bell's palsy (loss of muscle tone or droop on one or both sides of the face)
Intermittent pain in tendons, muscles, joints, and bones
Heart palpitations or an irregular heart beat (Lyme carditis)
Episodes of dizziness or shortness of breath
Inflammation of the brain and spinal cord
Nerve pain
Shooting pains, numbness, or tingling in the hands or feet
Problems with short-term memory
ERYSIPELAS (St. Anthony's Fire)
A distinctive type of infection of the skin; spreads rapidly like a fire to involve very large areas of skin; Some times a chronic ulcer of the skin may be a predisposing factor; rapidly spreading, fiery red or crimson plaque with a sharp advancing border
group A beta-hemolytic streptococcus
Etiology of Erysipelas
Labortory findings in Erysipelas
High WBC with left shift
GABS may be cultured from Blood, oropharynx, or aspirate from the advancing margin of the lesion
Treatment for Erysipelas
IV antibiotics for 48 hours.
PCN, EES, Clindamycin, Cepahlxin
Cool wet dressings, and rest
Bollous Erysipelas
Well-circumscribed lesion
Fiery red plaque
Spreads peripherally 2 -10 cm/day
Lesion is hot and tender
Common sites: face and extremities
Fever, chills, malaise and headache
SCARLET FEVER
A specific toxic and erythematous exanthem and enanthem; Children 2 - 8years affected most often; Oropharynx is the portal of entry
The rash is produced by the erythrogenic toxin
Group A beta-hemolytic streptococcus strains that produce erythrogenic toxin
What etiology is responsible for Scarlet fever?
Winter and early spring
When is Scarlet fever most prominent?
2 to 4 days (range 1-7 days)
Incubation period for Scarlet fever
Clinical features of Scarlet Fever
Sore throat, HA, malaise, fever.
Rash
Punctiform, erythematous papular sandpaper texture.
Blanches with pressure
Intertriginous areas predominate.
Strawberry tongue
White strawberry tongue, edematous red apapillae project through the white -coated tongue in the first two days.
Red strawberry tongue occurs when the white coating disappears and the red lingual papillae stand out.
Petechiae on the palate.
Tonsils enlarged, erythematous, with patches of white exudate
Marked desquamation 7 - 10 days later
PCN LA injection, PCN orally, EES, or clindamycin
Treatment for Scarlet fever
desquamation
One of the most common symptoms of Scarlet fever
Extent and duration is directly related to intensity of the rash
Seen at end of the first week.
Appears as large areas of skin peeling off giving rist to a punch hole appearance
hands and feet may be a presenting sign if the initial acute phase was mild and overlooked:
This process is complete in most cases in 2 - 3 weeks
peritonsillar abscess
prolonged sore throat, fever, worsening symptoms, including trismus and visible swelling of the left tonsil with deviation of the uvula to the right. Trismus, by the way, comes from the Greek word trismos, which was used to describe the "lockjaw" appearance of tetanus. Now, anything that causes pain or limits the ability to open the mouth is referred to as trismus.etiology often includes Streptococcus pyogenes and/or Staphylococcus aureus.obvious abscess, as shown in this patient, the preferred treatment is surgical drainage and IV antibiotics
IMPETIGO
Affects all children except newborns
My be preceded by eczema, inset bite
Lesions are vesicopustuler with a "honey-colored crust surrounded by a ring of erythema"
Group A beta-hemolytic streptococcus
Etiology for impetigo
Treatment for impetigo
Beta - lactam antibiotic : Augmentin or Clindamycin if the patient is allergic to PCN
Topical mupirocin.
New drug just out in June 2007 is retapamulin ointment 1% (Altabax) over 9 mos of age
NECROTIZING FASCIITIS
a life-threatening infection of the fascia and adjoining tissues; bacterial infection can cause small blood vessels in the infected area to clot. This clotting causes the tissue fed by these vessels to die from lack of blood. Because the body's immune defenses that travel through the bloodstream (such as white blood cells and antibodies) can no longer reach this area, the infection spreads rapidly and may be difficult to control
Streptococcal toxin may be the direct cause of the necrosis
etiology of NECROTIZING FASCIITIS
CLINICAL FEATURES of NECROTIZING FASCIITIS
begins as an erythematous, painful, tender, ill defined plaque
May involve any area of the body.
Duskiness or vesiculation may appear in the center of the affected area
Crepitance may be present over affected area.
Toxic signs include: high fever, malaise, altered sensorium.
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