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Pediatric Primary Care Exam 4 > Infectious Diseases Part II > Flashcards

Infectious Diseases Part II Flashcards

1
Q

Varicella Primary Infection clinical Manifestations (7)

A
  1. Generalized pruritic vesicular rash in varying stages of healing
  2. Vesicles, papules, scales
  3. Usually between 250 to 500 lesions
  4. Establishes viral latency in the dorsal root ganglia
  5. Reactivation causes herpes zoster pain located to 1-3 sensory dermatomes)
    * Burning feelings on dermatome
    * Will not pass midline ***
    * Predominantly in the dermatome that its in
  6. Postherpetic neuralgia may last for week
  7. Starts as truncal rash then spreads (vesicles and papules)
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2
Q

Varicella Transmission and Incubation (8)

A
  1. Humans are only host
  2. Virus comes in contact with mucosa
  3. Person to person by direct contact or airborne spread from respiratory tract secretions or contact with zoster
  4. Household spread is common
  5. Peak incidence in late winter and early spring
    * February is chief season
  6. Incubation is 14 to 16 days with range from 10-21 days
  7. Subsequent household contacts get much worse cases
  8. If child gets it and gets vaccine it will be more mild
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3
Q

Varicella Diagnosis (3)

A
  1. Largely clinical
  2. VZV can be identified with PCR or direct fluorescent antibodies
  3. Serum varicella IgG antibody can be used to confirm infection
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4
Q

Varicella Treatment (3)

A
  1. Must be given with 72 hours of onset of the rash
  2. Oral acyclovir not recommended for routine use in otherwise healthy children
  3. When to use oral acyclovir:
    - Children older than 12 years
    - Child with chronic pulmonary or metabolic disease
    - Long term salicylate
    - Children on short or long term corticosteroids.
    - Not recommended in children less than 12
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5
Q

The Classic Exanthems of Childhood (12)

A
  1. First Disease: Measles
  2. Second disease: Scarlet fever
    * Toxin producing en-protein strain of strep
  3. Third disease: Rubella
  4. Fourth disease: Duke’s disease; variant of scarlet fever/a toxin producing staph
  5. Fifth Disease: Parvovirus B19
  6. Sixth disease: roseola
  7. Measles
  8. Scarlet fever (Strep)
  9. Rubella
  10. Filatov-Dukes disease (not a separate exanthem but a variant of scarlet fever or toxin-producing staphylococcus infection)
  11. Erythema infectiosum (Parvovirus B 19)
  12. Exanthem subitum (HHV-6/Roseola)
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6
Q

Measles Overview (5)

A
  1. Acute disease
  2. Fever, cough coryza, conjunctivitis an erythematous maculopapular rash, and koplick spots
  3. Incubation: 8-12 days before onset of rash
  4. Contagious for 3-5 days before rash to 4 days after the appearance of the rash goes away
  5. HIGHLY AIRBORNE CONTAGIOUS DISEASE
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7
Q

Measles 3 C’s

A
  1. Conjunctivitis
  2. Cough
  3. Clear nasal discharge (coryoza)
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8
Q

Measles Rash

A

Measles spreads opposite of varicella; goes from behind ears → face → down body

  • Rash starts behind ears!
  • More billiform; maculopapular confluent rash
  • Affects palms and soles
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9
Q

Rubella Overview (5)

A
  1. Mild: generalized erythematous maculopapular rash with generalized lymphadenopathy (usually posterior occipital, post-auricular, and cervical) with slight fever
  2. Transient polyarthralgia and polyarthritis rarely in children but more common in adolescent
  3. 25-50% infections are asymptomatic
  4. Infectious three days before to 5-7 days after the rash
  5. Incubation period is 14-23 days; long incubation period
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10
Q

Rubella Clinical Manifestations (3)

A
  1. Fine rash
  2. Enanthem
  3. Mild: generalized erythematous maculopapular rash with generalized lymphadenopathy (usually posterior occipital, post-auricular, and cervical) with slight fever
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11
Q

Parvovirus B19 Clinical Manifestations (3)

A

Three phases:

  1. Prodrome: malaise myalgias, headaches, low grade fever
  2. Slapped cheek appearance with arthritis/arthralgia in adolescent
  3. Lacy symmetric maculopapular rash which waxes and wanes for six weeks
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12
Q

Parvovirus B19 Incubation Period

A

4-14 days

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13
Q

Parvovirus B19 Overview (7)

A
  1. Infection in pregnancy: hydrops and fetal death
    * Baby can develop heart failure and die; doesn’t matter what trimester
  2. Need to know your parvovirus titers
  3. Very bad for children with hemolytic anemia and pregnant adolescents
  4. Causes 7-10 days of bone marrow aplasia
  5. Cannot produce reticolocytes
    * Very bad for SCD patient b/c lack of oxygen carrying capacity
    * Aplastic crisis in patient with SCD
  6. Prolonged course with HIV and bone-marrow transplant patients
  7. OCCURS IN SPRING
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14
Q

Clinical Associations with Parvovirus B19 (9)

A
  1. Asymptomatic disease
  2. Erythema infectiosum
  3. Arthropathy/arthritis
  4. Transient aplastic crisis
  5. Chronic anemia
  6. Hydrops fetalis
  7. Neurologic disease
  8. Rheumatologic disease
  9. Vasculitis
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15
Q

Roseola Clinical Presentation (5)

A

Sixth Disease

  1. Well appearing 6 months to 3 year old with a fever.
  2. Can have a little diarrhea and anorexia
  3. Fever breaks and the child breaks out in a rash.
    * Rash can last 3-4 days and requires no treatment
  4. Number 1 cause of febrile convulsions
  5. Fever can be as high as 104 but they don’t act sick!
    * When mother gives Tylenol they can be running around the house
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16
Q

Adenovirus transmission (2) and incubation

A

Transmission:

  1. Can maintain infectivity at room temperature for 2 weeks after freezing but is destroyed by heat of 129 for 30 minutes or by standard disinfectants
  2. Spread by direct contact, droplets from respiratory tract and eye as well as feces if it is enteric (not airborne)

Incubation: 5-10 days of incubation

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17
Q

Adenovirus general presentation (3)

A
  1. Illness lasts for 1 week but can be asymptomatically shed for years
    * Can present as a multisystem disease
  2. Cough, sore throat, runny noise, bronchitis, etc
  3. Croup may present but if there is croup it’s more likely to be parainfluenza
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18
Q

Adenovirus Upper Respiratory Symptoms (4)

A
  • 2% to 3% of all acute infectious respiratory
  • Up to 8% of acute respiratory illnesses in infants younger than 2 years of age.

An Upper respiratory tract infection

  1. Nonspecific nasal congestion
  2. Coryza
  3. Cough.
  4. Exudative pharyngitis (25%) with malaise fever, and chills
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19
Q

Adenovirus GI and Urinary Symptoms (3)

A
  1. Diarrhea
  2. Hepatitis in immunocompromised host

Urinary
3. Hemorrhagic cystitis (Dysuria, Polyuria with gross hematuria that lasts about 3 days, with microscopic hematuria persisting for a few more days before spontaneous resolution)

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20
Q

Adenovirus Nervous System, Cutaneous, Disseminated Infection Symptoms (6)

A
  1. Aseptic meningitis
  2. Encephalitis, meningoencephalitis
  3. Myelitis, acute flaccid paralysis
  4. Myositis

Cutaneous
5. Exanthemata

Disseminated infection (newborns, immunocompromised)
6. Multiorgan failure
21
Q

Pharyngoconjunctival Fever General Info (7)

A
  1. Extremely contagious
    * If the child gets it usually the both parents will get it and even the provider; WASH HANDS!
  2. Fever, sore throat, and conjunctivitis.
    * Pretty sick kid with high fever and sore throat
  3. Bloody conjunctivitis
  4. Hallmark: preauricular adenopathy
  5. Rhinitis and cervical adenitis may be present.
  6. Onset may be monocular, and a granular appearance may be seen on the palpebral conjunctivae.
  7. Think ADENOVIRUS
22
Q

Outbreak of pharyngoconjunctival fever (3)

A
  1. Exposure to contaminated ponds and inadequately chlorinated swimming pools
  2. Usually lasts from 7-10 day and up to 2 weeks
  3. Very severe papular rash that occurs on the conjunctiva of the eye
    * Could be limited on one eye but can be on both
    * If bloody conjuncitivits is very severe then refer to opthamology
23
Q

Eye and Adenovirus (4)

A

Adenovirus is the most common cause of acute conjunctival infection.

  1. Acute follicular conjunctivitis
  2. Epidemic keratoconjunctivitis
  3. Pharyngoconjunctival fever
  4. Conjunctivitis occurring in association with respiratory illness.
24
Q

Adenovirus as a Neurological Presentation (8)

A
  1. Occurs with or without concomitant respiratory infection.
  2. Encephalitis
  3. Aseptic meningitis
  4. Acute flaccid paralysis
  5. Meningoencephalitis
  6. Encephalomyelitis
  7. Reye-like syndrome have been described.
    *Can lead to respiratory failure
    Used to be a common cause of an encephalitis before it was realized that aspirin is causing it
  8. Illness is more severe in immunocompromised’ Disseminated disease with multiorgan failure
25
Q

Poliovirus (6)

A
  1. Generally spreads via the lymph nodes and in various internal organs
  2. Prefer the epithelial cells lining the alimentary tract and for cells of the central nervous system.
  3. Poliovirus infection is quite common in nonimmunized individuals, but only about 1 percent of these cases progress to the paralytic form of the disease.
  4. Primary replication of poliovirus takes place in the oropharyngeal and intestinal mucosa (the alimentary phase).
  5. Spreads to the tonsils and Peyer’s patches of the ileum and to deep cervical and mesenteric nodes, where it multiplies abundantly (the lymphatic phase).
  6. Carried by the bloodstream to various internal organs and regional lymph nodes (the viremic phase). In most cases, no further virus spread occurs,
26
Q

Poliovirus presentation

A

Asymptomatic or mild febrile undifferentiated illness, such as fever, malaise, headache, nausea, gastrointestinal disturbances, and sore throat, or combinations of these.

27
Q

Staph Aureus Problems (4)

A
  1. Resurgence of infection
  2. Resurgence of toxin-mediated disease/virulent disease
  3. Escalation of antibiotic resistance
  4. MRSA prevalence can be as high as 40%!
28
Q

Staph risk groups (5)

A
  1. Crowding and skin conditions with/without antibiotic exposure
  2. Lower socioeconomic groups
  3. Daycare
  4. Sports team
  5. Contact games
29
Q

Staph Common Clinical Syndromes (4)

A
  1. Impetigo
    * When it starts to go deeper into the soft tissue it becomes cellulitis
  2. Cellulitis
  3. Lymphadenitis
  4. Abscesses; puss formation beneath the skin
30
Q

Staph Serious Clinical Syndromes (7)

A
  1. Septicemia
  2. Shock
  3. Toxic shock (TSST-1)
  4. Scaled skin Syndrome
  5. Arthritis/osteomyelitis
  6. Endocarditis
  7. Disseminated abscesses
31
Q

Community Acquired MRSA (6)

A
  1. Started over 20 years ago
  2. Most robust strains are winning
  3. Changes in genetic structure of the bacteria.
  4. Presence of Panton-Valentine Leukocidin (PVL) which injures WBC that kill organism
    * If you have a leukocidin produced by the bacteria then there neutrophils can’t kill the bacteria and MRSA develops and takes over
  5. Causes outbreaks in closed populations
  6. Recurrent disease
32
Q

Risk Factors for Community Acquired MRSA (16)

A
  1. Exposure to another child
  2. Age < 2 years; especially neonates in NICU’s
  3. Skin conditions such as eczema
  4. Shaving (need to change razor often!)
  5. Abrasions
  6. Tattooing, drug use, other needle use
  7. Sports
  8. More in African Americans, Native Americans, Pacific Islanders, Alaskan
  9. Prison or day-care exposure
  10. Military service
  11. Sports activities
  12. Nasal carriage of CAMRSA
  13. Obesity and other comorbid conditions
  14. Prior antibiotic use
  15. Influenza
  16. Old age
33
Q

Antibiotic Sensitivity/Resistance to MRSA/Staph (6)

A
  1. Cephalexin (Keflex) and 1st generation cephalosporins work well
  2. 2nd generation don’t work very well
  3. 4th and 3rd generation cover staph aureus, but 3rd covers gram(-) slightly better and MRSA/staph are gram(+)
  4. BACTRIM DOES NOT COVER STREP or any gram(+) strep infection
  5. Bactrim is effective against MRSA which is gram(+)
  6. Clindamycin is very effective against strep and staph but not against clindamycin-resistant staph
34
Q

Kirby-Bauer Sensitivities

A

Zone of inhibition; larger area of inhibition around disc=more sensitive the organism is

35
Q

The D test for CA-MRSA (Clindamycin resistant) (2)

A
  • Worrisome because Clinda treats MRSA/Staph
    1. If D-Test positive—cannot use clindamycin
    2. If D-Test negative—may use clindamycin
36
Q

MRSA Problems of Resistance (3)

A
  1. Resistant organisms; affect patients with compromised host defenses (e.g. neutropenic patients)
  2. Can spread to affect patients with both intact and compromised host defenses; especially onc patients receiving chemo
  3. Spread from the healthcare system to the community
37
Q

MRSA Resistance Due to Selection Steps (5)

A

1st: Spontaneous mutation occurs in the absence of drug selection in a sensitive population
2nd: drug treatment is introduced
3rd: mutant is selected for by drug treatment as sensitive strain dies off
4th: resistant clone grows within what used to be a sensitive population
5th: resistance becomes clincally manifested during therapy

38
Q

Recent MRSA (2)

A
  1. In the past 5 years –> USA300 clone of SA has replaced others throughout the US (and world)
  2. Community-associated MRSA –> Replaced more than 50% of skin and soft tissue infections are MRSA positive
39
Q

Treatment of Impetigo (5)

A
  1. If localized, Bactroban (muprocin) or
  2. Altabax can be used.
  3. If extensive, Keflex is a nice first line if you do not suspect MRSA

For MRSA Impetigo:

  1. Clindamycin if you suspect that it is strep
  2. Bactrim
40
Q

Treatment of Paronchya (3)

A
  1. I and D (draining)
  2. Local therapy if not extensive
    * Usually this is all that is required
  3. Antibiotic for this is Clindamycin as first line
    * If it doesn’t get better then start Bactrim
41
Q

Treatment of MRSA (5)

A
  1. Alters transpeptidase
  2. Penicillin binding protein to which B-lactam attach
    * Binding site is different so antibiotic cannot attach
  3. First Line = Clindamycin/clinda with rifampin or TMP-SMX
  4. Second line = Linezolid ($$)
  5. Newest drug: Daptomycin (Fifth generation of cephalosporin)
42
Q

Serious Staph Infections (3)

A

Diffuse erythematous rash

  1. Tender to palpation
  2. Warm to palpation
  3. Sandpaper like
43
Q

Staphylococcal Scalded Skin Syndrome (SSSS) (6)

A
  1. Exotoxin produced by Staph aurues
  2. Infection occurs at a site (oral, nasal cavity, throat, skin) and exotoxin acts at remote sites
  3. 98% of cases are younger than 6y/o
  4. Presents with fever, malaise, irritability, and skin tenderness
  5. Bullae and Nikolsky’s sign
    * Nikolsky’s sign: Large portion of the epidermis separates in sheets after light friction
  6. Exfoliation
44
Q

SSSS Labs (3)

A
  1. Increased WBC, ESR
  2. Blood culture (usually negative)
  3. Gram stain and culture from remote infection site
45
Q

SSS Treatment (2)

A
  1. Burn care

2. IV Antibiotics- Clindamycin

46
Q

Toxic Shock Syndrome (4)

A
  1. Staphylococcal
  2. Strep Toxic Shock Syndrome (STSS)

Varicella and strep like each other

  1. Begins with localized infection by coagulase – positive staph
  2. Puncture wound
47
Q

Toxic Shock Sydrnome Presentation (5 in stages)

A
  1. Prodrome (how it starts): Fever, malaise, myalgias, vomiting
  2. Followed abruptly by worsening symptoms (developing shock) →Abdominal pain, dizziness, and weakness
  3. Diffuse erythroderma
  4. Erythroderma; Resembles sunburn
    * Ex: African American child will look very red
  5. Desquamation → skin is peeling
    * Begins 1 week after rash
    * Palms, soles
    * Thick sheets shed
48
Q

Staphylococcal TSS – Criteria (6)

A
  1. Fever
  2. Rash
  3. Desquamation
  4. Hypotension; <5%; orthostatic drop in DBP of > 15mmHg
  5. Multisystem involvement (includes >3)
    o GI- V/D
    o Muscular- myalgias
    o Renal-increased BUN, creatinine, U/A with >5 WBCs
    o Hepatic- increased bilirubin, AST, ALT
    o Hematologic- decreased platelets (<100,00)
    o CNS- alteration in consciousness, no focal signs
  6. Otherwise negative culture and studies
49
Q

TSS Treatment (5)

A
  1. Fluid management
  2. Anticipation of multi-system organ failure
  3. Parenteral Antibiotics; B-Lactamase resistant Penicillin and clindamycin
  4. Remove source of toxin production
  5. Consider IVIG if in bad shape

Pediatric Primary Care Exam 4 (8 decks)

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