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ID COPY Flashcards

1
Q

What is the ID suggestions for congenital infections acronym?

A

CHEAP TORCHES C: Chicken pox Hepatitis B, C,E Enterovirus AIDS Parvovirus B19 Toxoplasmosis Other (TB, WMV) Rubella CMV HSV Every other STD Syphilis

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2
Q

What are the clinical features of a CMV infection?

A

17-20% will have permanent sequelae Thromobocytopenia, petechiae Microcephaly, PV calcifictions Chorioretinitis SN HL

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3
Q

What is the one screening test you MUST consider in CMV?

A

HEARING

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4
Q

In whom should you consider PO valganciclovir for symptomatic congential CMV?

A

32 wk, wt>1.8, Sx: plts, petechiae, HM, SM, IUGR, hepatitis or CNS involvement End points: Best earing test at 6 months

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5
Q

What is the treatment approach for CMV?

A

All SX neonates with CNS, SNHL, chorioretinitis Valganciclovir x 6 months MONITOR CBC (neutrophils) and creatinine

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6
Q

What are the classic findings in syphilis?

A

SNUFFLES, maculopapular rash, microcephaly, HSM

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7
Q

When should you evaluate an infant for congenital syphilis?

A

Sx of congenital syphilis Mother not treated or treatment not adequately documented Mother treated with non-penicillin regime Mother treated within 30 days of the childs birth Less than 4-fold drop in mothers titer Mother had relapse or re-infection

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8
Q

What is the classic triad of congenital toxoplasmosis?

A
  1. Hydrocephalus 2. Cerebral calcifications 3. Chorioretinitis
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9
Q

How do you confirm toxo?

A

PCR on CSF blood urine

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10
Q

What is the treatment of confirmed toxo?

A

Triple therapy for 12 months Steroids for eye disease VP shunt

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11
Q

What are the characteristics of early GBS?

A

Generalized

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12
Q

What are the characteristics of late GBS?

A

Focal >7 days Vertical or horizontal transmission Meningitis, osteomyelitis, soft tissue infections sepsis

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13
Q

What are the indications for intrapartum antibiotic prophylaxis?

A

Positive GBS screening cx (35-37 weeks) Previous infant with GBS d/o GBS bacteriuria during current pregnancy Delivery at 18 hours Intrapartum fever >38

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14
Q

What is the antibiotic selection for GBS PPX?

A

No allergy= penicillin or ampicillin Mild pencillin allergy= cefazolin Severe pencillin allergy= clindamycin

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15
Q

What is the suggested approach to fever without a source?

A

Toxic infants= FSWU, admit, empiric ABx 0-28 days: FSWU, admit, ABx 29-90 days: clinical and lab screening and assess risk 3-36 months: Viral, clinical FU

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16
Q

What are the low risk criteria for febrile infants?

A

29-90 days: Previously healthy Non-toxic clinical appearance No focal infection Peripheral WBC count 5-15 Absolute band count

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17
Q

Most common bacterial pathogens in fever without a source

A

0-28 day: GBS, E, coli (Listeria, S. aureus, GAS, kleb) 29-90 day: GBS, E coli (Strep pneumonia, Neiseria) 3-36 months: Strep pneumonia

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18
Q

What % of women who delivery an HSV infected child have no history of genital herpes?

A

60-80%

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19
Q

Empiric pneumonia-stable

A

Ampicilin

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20
Q

Empiric pneumonia- shock

A

ceftriaxone/vanco

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21
Q

Meningitis bugs neonate?

A

GBS, E coli, Listeria Amp + Cefotaxime

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22
Q

Meningitis bugs >3 months?

A

Strep pneumo Neiseeria H. influenzae B Ceftriaxone + Vanco

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23
Q

What is the evidence behind dexamethasone in meningitis?

A

Reduces mortality and hearing loss in H flu and possiblity S pneumo meningitis

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24
Q

What are the etiologies of toxic shock syndrome?

A

S pyogenes S aureus Empiric cloxa plus clinda GAS: pencillin and clinda + IVIG for TSS

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25
Q

Impetigo bugs and rx

A

S aureus GAS Cloxacillin, cephalexin, topical mupircoin

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26
Q

Cellulitis

A

S. aureus GAS IV: Cloxa and ancef PO: cloa and keflex

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27
Q

Nec fas

A

GAS, S aureus Cloxa or ancef plus clinda think post varicella

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28
Q

What are the main bugs in asplenic children?

A

50-90% Strep pneumoniae HIB Neiseeria Salmonella

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29
Q

Approach to prevention in asplenic kids?

A

Prevnar 13 and 23-v polysacchirde vaccine 4CMenB Influenza annual S. typhi vaccine pre travel

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30
Q

Presentation of cat scratch?

A

Unilateral swollen Cx nodes and ipsilateral conjuctivitis NO FEVER

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31
Q

Chronically draining Cx LN

A

Atypical mycobacterium

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32
Q

Cat scratch RX?

A

Bartonella henselae Azithromycin for nodes Doxcycline + rifampin for neuroretinitis

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33
Q

How does early localized lyme present?

A

Ertherma migrains Systemic sx: fever, myalgia, neck stiffness

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34
Q

How does early disseminated lyme present?

A

Multiple EM Meninigitis FACIAL NERVE PALSY

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35
Q

How does late disease lyme present?

A

Pauciarticular arthritis, peripheral neuropathy, CNS manifestations

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36
Q

Treatment options for lyme disease?

A

PO: Doxycycline, amoxicillin, cefuroxime IV: ceftriaxone, pencillin G

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37
Q

Prevention of mosquito and tick bites?

A

Physical: screens on windows and doors, fine mesh netting for cribs, long loose clothing, hat, closed shoes Repellents: DEET 12 years 30%, Icaridin for children 6M-12Y Insepct skin daily for ticks Shower within 2 hours of removal

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38
Q

When do you consider ABx PPx for lyme?

A

Single dose doxy for children > 8 years of age in exposed endemic regions

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39
Q

How does west nile virus present?

A

Peak: late summer and fall Asymptomatic 80%, fever 20%, CNS

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40
Q

What are the CNS syndromes associated with WNV?

A

Aseptic meningitis, encephalitis, acute flaccid paralysis

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41
Q

What are the possible complications of chicken pox?

A

Cerebellar ataxia, encephalitis, reye syndrome, stroke, Zoster

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42
Q

What are the possibly causes of facial nerve palsy in children?

A

HSV Otitis media Lyme disease Varicella zoster virus Cholesteatoma Facial nerve schwannoma Vestibular schwannoma

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43
Q

What is Ramsey Hunt syndrome?

A

Facial nerve palsy Varicella zoster Worse prognosis Antivirals and corticosteriods

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44
Q

What are the acute medical emergenies in fever in the returned traveller?

A
  1. Malaria 2. Typhoid fever 3. Meinigococcemia 4. Viral hemorrhagic fever
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45
Q

Delayed onset prolonged fever in a traveller?

A

TB Brucellosis Leishmaniasis Typhoid fever

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46
Q

How do you distinguish between latent and active TB?

A

Chest Xray

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47
Q

What are the reasons for a positive TST?

A

Mycobacterium tuberculosis infection Non-tuberculosis mycobacteria BCG Incorrect technique

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48
Q

What are the reasons for a false negative TST?

A

Incorrect technique Active TB disease Immunodeficiency states Corticosteriods Young age Malnutrition Viral infections (measles, varicella, influenza) Live attenuated vaccines (measles)

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49
Q

Who is at increased risk of TB?

A

Infants and post-pubertal adolescents Recently infected (past 2 years) Immunodeficiency states (Primary ID, HIV, Malignancy, organ transplant, immunosuppressive medications, malnutrition)

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50
Q

How can you diagnose pulmonary TB?

A

TST INterferon gamma release assays Chest Xray Gastric aspirates (three consecutive AM aspirates) Bronchoalveolar lavage Microbiology (acid fast staining, DNA, PCR)

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51
Q

What is the treatment for latent TB infection?

A

Isoniazid for 9 months

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52
Q

What is the treatment for TB disease?

A

4 drugs (INH, RIF, PYR, ETH)

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53
Q

What are the adverse effects of isoniazid?

A

Hepatotoxicty, peripheral neuropathy,

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54
Q

What are the adverse effects of rifampin?

A

Hepatotoxicity, hypersensitivity reactions, memory impairment, drug interaction, body fluids turn orange

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55
Q

Pyrazinamide SE

A

Hepatotoxicity, increased uric acid levels

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56
Q

Ethambutol SE

A

Optic neuropathy

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57
Q

How can you prevent vertical HIV transmission?

A

Antiretroviral therapy: Triple ART starting in 2nd tri IV ziovudine during labor and to newborn for 6 weeks BF is contraindicated C/s if VL >1000

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58
Q

How do you exclude an HIV infection?

A

2 separate negative PCR tests at >1 and >2 months of age

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59
Q

How do you confirm HIV infection?

A

Positive PCR x 2 to 18 months Reactive serology >18 months

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60
Q

How to well controlled children with HIV compare to normal children?

A

Increased risk of pneumococcal disease Vaccine responses not as good as healthy children Management of acute illness same

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61
Q

How do you approach an HIV infected child in the ER?

A

Clinical status Immunologic status Virologic status Antiretroviral therapy and adherence

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62
Q

How do you approach vaccines in HIV infected children?

A

Live virus: MMR in absence of severe immune compromise VZV conisder in asymptomatic cihldren BCG and oral polio CI

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63
Q

How do you approach Hepatitis A PEP?

A

Vaccine within 2 weeks of exposure in those > 12 months

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64
Q

How do you manage bites in daycare?

A

Local wound care: allow bleeding, clean with soap and water Prevention: 1. Tetanus 2. Prophylactic ABx only for moder or severe, deep puncture, face/hand/gentalia/ foot 3. HIV PEP only if HIV infected PLUS exchange of blood

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65
Q

How do you manage a baby born to a known HBsAG positive mom?

A

HBIG and HB vaccine within 12 hours of birth HB vaccine at 1 and 6 months

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66
Q

How do you manage a baby born to a unknown Hep B positive mom?

A

Stat HBsAG on Mom If results are available within 12 hours, if positive, give HBIG and HB vaccine, if not, nothing If not available, seriously consider both

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67
Q

What is the transmission risk of Hep C?

A

5% Risk factors: HIV co-infection, higher HCV viral load, elevated ALT, cirrhosis

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68
Q

Approach to delivery with a Hep C + mom

A

No evidence to support C/s Avoid invasive procedures

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69
Q

Approach to breastfeeding with a Hep C + mom

A

No evidence of transmission in breast milk

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70
Q

Approach to testing baby with a Hep C + mom

A

HCV serology at 12-18 months

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71
Q

What are the infectious contraindications to breastfeeding?

A

HIV, HTLV, Variable: TB, HSV with lesions on breast

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72
Q

What are the 4 moments for hand hygiene?

A
  1. Prior to the patient or patient environment contact 2. Before aseptic procedure 3. After body fluid exposure 4. After patient/pateint environment contact
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73
Q

What are the antibiotic stewardship principles?

A
  1. Use clinical judgement 2. Treat infection, not contamination 3. Assessment of antibiotic allergies 4. Know your local antibiogram 5. Selecting an antibiotic (narrow, optimize dosing and duration) 6. Promote vaccinations to reduce likelihood for disease
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74
Q

Daycare exclusion: impetigo

A

24 hours after treatment start

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75
Q

Daycare exclusion: GAS pharyngitis

A

24 hours after treatment start

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76
Q

Daycare exclusion: Pertussis

A

5 full days after treatment start

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77
Q

Daycare exclusion: E coli 0157:H7

A

Resolution of diarrhea and stool negative x 2

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78
Q

Daycare exclusion: Shigellosis

A

Resolution of diarrhea and stool negative x 2

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79
Q

Daycare exclusion: tyhoid fever

A

resoltuion of Sx and stool negative x 3

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80
Q

Daycare exclusion: hepatitis A

A

until 1 week after onset of illness or jaundice

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81
Q

Daycare exclusion: scabies

A

after treatment given

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82
Q

Treatment of mild 1st episode c diff

A

PO flagy

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83
Q

Treatment of severe 1st episode c diff

A

PO vanco

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84
Q

Treatment of severe 1st episode c diff, complicated

A

PO vanco + IV flagyl

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85
Q

What is different about hand washing in C diff?

A

Alcohol doesn’t kill spores Must wash with soap and water

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86
Q

What are the risk factors for severe influenza?

A

6-59 months Chronic health conditions (NM, Cardiac or pulmonary, malignancy, IC

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87
Q

What are the options for PO antibiotics for febrile UTIS?

A

Cephalosporins, clavulin, septra

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88
Q

What are the indications for IV ABX in UTIs?

A

Toxic, unable to take PO, immunocompromised host Amp/Gent

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89
Q

When do you do an RBUS in febrile UTI?

A

First febrile UTI

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90
Q

What are the indications for a VCUG in febrile UTI?

A

US evidence of hydronephrosis, renal scarring or other findings suggestive of a high grade VUR Recurrence of febrile UTI

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91
Q

Who should NOT receive the LIVE ATTENUATED influenza vaccine?

A

infants

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92
Q

Contraindications to LAIV?

A

1.

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93
Q

How do you vaccine for influenza in children 6-23 months?

A

Quadrivalent inactiated vaccine (QIV)

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94
Q

What are general contraindications to vaccination?

A
  1. Anaphylaxis 2. Immunodeficiency (certain vaccines) 3. Pregnancy (live) 4. GBS
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95
Q

How do you approach vaccination in asplenic patients?

A

PCV13 (Prevnar) PPSV23 (Pneumovax) >8 weeks post prevnar, 2+ MCV4 4CMenB

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96
Q

What is the most common cause of medically attended gastro?

A

Norovirus

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97
Q

What are the age recommendations for rotavirus vaccines?

A

Universally given starting at 6 weeks no later than 15 weeks (Older kids get inssussception)

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98
Q

When should you not give rotavirus vaccine?

A

Immunocompromised History of intussussception

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99
Q

What are the high risk conditions for pneumococcal infections?

A

-Chronic pulmonary and cardiac disease -SNHL requiring cochlear implants -Chronic kidney, liver, metabolic -Immunosuppresion -neurologic swallowing disorders -Hgbopathies -Chronic CSF leak -Malignancy, past HSCT

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100
Q

What serogroup currently causes the most meningococcal disease?

A

B

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101
Q

What is the activity of pencillins?

A

Non-pencillinase producing gram + cocci and gram + anaerobic DOC: Syphilis, GBS, GAS pharyngitis

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102
Q

What is the mechanism of pencillins?

A

Beta lactam ring Interefere with peptidoglycan cross-linking that is required to produce stable bacterial cell walls DO NOT cross the blood brain barrier

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103
Q

What is the activity of anti-staph pencillins?

A

Eg: methicillin, oxacillin, dicloxacillin Side chains attached to pencillin lactam ring inhibit staph Excellent activity against Staph aureus

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104
Q

What is the activity of aminopencillins?

A

Similar to pencillin Additional activity against aerobic gram negative E. Coli, Listeria, Salmonella

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105
Q

Extended spectrum pencillins?

A

Anti-pseudo pencillins Expanded gram negative spectrum Pseudo aeruginosa and proteus

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106
Q

% of true pencillin allergy in those who report?

A
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107
Q

Teenage patient develops pruritic maculopapular rash 1 week after starting treatment with amoxicillin for pharyngitis, allergic?

A

No! Classic example of EBV + amoxicillin

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108
Q

Activity of first generation of cephalosporins?

A

Gram + organisms Some activity of E coli and klebsiella species

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109
Q

Activity of second generation of cephalosporins?

A

Increased spectrum of activity of gram negative organisms Treatment of nosocoimal pneumonia No antipseudonomal activity

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110
Q

Activity of third generation of cephalosporins?

A

Broad spectrum, excellent activity against gram negative bacteria General less activity gram positive organisms

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111
Q

What are the two primary mechanisms of resistance of beta lactam antibiotics?

A
  1. Penicillin binding proteins: crossing linking between glycan chains (target for beta lactam antibiotics) 2. Beta lactamase: enzymes that hydrolyze the beta lactam ring of the antibiotic. SPACE: Serratia, Pseudonomas, Actineobactera, Caitrobacter, and Enterobacter
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112
Q

What is redman syndrome?

A

-Rapid infusion of vancomycin -Complain of diffuse burning, itching, dizzines -Caused by histamine release from degradulaiton of mast cells underlies reaction -Reaction

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113
Q

What are the three stages of pertussis infection?

A

Catarrheal (1-2 weeks): low grade fever, URI Sx, mild cough, apnea in infants Paroxysmal (1-6 weeks): severe cough in paroxysms and inspiratory whoop Convalescent (2-3 weeks): resolution of sympoms, cough fits may persist

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114
Q

What is the classic triad of malaria?

A
  1. Spiking fevers 2. Anemia 3. Splenomegaly
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115
Q

How is malaria diagnosed?

A

thick and thin smears

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116
Q

Which illness if referred to as the breakbone fever?

A

Dengue fever -Fever, severe headache, retro-orbital pain, fatigue, severemyalgias Abrovirus, transmitted by mosquitos May develop dengue hemorrhagic dever

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117
Q

What are the characteristics of PFAPA?

A

Period fever, aphthous stomatitis, pharyngitis and cervical adenitits Childhood 4 day fevers 2-8 weeks in between

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118
Q

What are the characteristics of familial Mediterranean fever?

A
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119
Q

What are the three Cs of measles?

A

Cough, coryza and conjunctivitis

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120
Q

Risk factors for AOM?

A

Mid face hypoplasia

Dayare attendance

Aboriginal

Low SES

Second hand smoke

No BF

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121
Q

First choice for bite antibiotics?

A

Amox clav

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122
Q

What are the three phases of pertussis?

A

Catarrhal: 1 week (incubation 3-21 days) coryza, conjunctiviotis, mild cough Only phase that can be treated

Paroxysmal: 2-6 weeks: severe paroxxysms of coughing with inspiratory whoop. Apnea in small infants

Convalescent: up to 1 year, gradual decrease in cough

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123
Q

Organism and treatment of pertussis?

A

Bordetella

Azithromucin, clarithromycin, erthyromycin

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124
Q

When do you think of a brucella infection?

A

Food borne unpasteruized milk

Adults working with livestock

Triad: Fever, arthralgia, HSM

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125
Q

how do you tell the difference between periorbital and orbital cellulitis?

A

Orbital: proptosis, impairment of eye movement, pain, visual acuity decreased, SICK

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126
Q

Salmonella incubation

A

6-72 hours

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127
Q

Campylobactera incubation

A

Days with abdo pain

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128
Q

What are the two clinical syndromes caused by Salmonella?

A

Gastroenteritis

Typhoid fever

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129
Q

Which bug has the shortest incubation period for gastro?

A

Staph aureus

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130
Q
A
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131
Q

What causes eosinophilia?

A

CHINA

C: Connectiv tissue diseases

H: Helminithic infections

I: Idiopathic HES

N: Neoplasia

A: Allergies

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132
Q

What are the most common agents in infective endocarditis?

A

Viridans type strp

Staph aureus

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133
Q

Which is tender osler nodes or Janeway lesions?

A

Osler nodes

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134
Q

What are the Duke Critiera for IE?

A

Major:

  1. Positive blood cultures
  2. Evidence of endocarditits on echo

Minor:

1 Predisposing conditions

  1. Fever
  2. Embolic vascular signs
  3. Immune complex phenomena
  4. Single blood culture

Diagnosis: 2 major, 1 major and 3 minor, 5 minor

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135
Q

When can kids with diarrhea go back to daycare?

A

Salmonella-diarrhea resolves, 3 negative cultures

Shigella and e coli- diahrrhea reolves and 2 negative cultures

Campylobactera- diarrhea resolves

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136
Q

Vomiting daycare exclusion?

A

>2 in 24 hours until resolves

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137
Q

Scabies daycare exclusion?

A

Until completed treatment

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138
Q

VARICELLA daycare exclusion?

A

Well enough to go

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139
Q

Pertussis daycare exclusion?

A

5 days of antibiotics

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140
Q

Hep A virus daycare exclusion

A

1 week after onset of illness or jaundice

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141
Q

Things that do not require daycare exclusion

A

Nonpurulent conjuctivitis

Rash without fver

Parvo B19

CMV

HBV

HIV

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142
Q

Hep A characteristics

A

Acute, self-limited fever, jaundice, malaise

Highly contagious, fecal-oral

Exclude x 1 week

PEP: HepA IG within 2 weeks and Hep A vaccine if>12 M

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143
Q

Prevention of HIV transmission

A

Screening in pregnancy

Antiretrovirals for Mom in pregnancy

C section pre ROM
AZT for baby x 6 weeks

NO breastfeeding

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144
Q

Rheumatic fever diagnostic criteria

A

Major:

  1. Migratory polyarthritis
  2. Carditis
  3. Chorea
  4. Subcutaneous nodules
  5. Erthyema marginatum

Minor: Fever, AV block, Inflam markers, Arthralgia

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145
Q

Rheumatic fever treatment

A

Anti-inflammatory meds for the joints x2 months

Pen V 10 day course

PPx: minimum 5-10 years or until age 21 (longest)

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146
Q

What is the progression of sinus development?

A

Ethmoidal-Birth

maxillary- 4

Sphenoid 5

Frontal 7-8

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147
Q

What is the PEP for varicella?

A

Vaccine for susceptibles < 72 hours

VZIG within 96 hours if: IC, pregnant, newborn of mom’s with varicella 5 before, 2 after delivery, Prem <28 or <1000g

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148
Q

Hep A PEP?

A

PPX within 2 weeks

Vaccine

IG for IC, Infants, Liver Dz

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149
Q

PEP for Hep B

A

Neonate/Unvaccination: HBIg and Vaccine

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150
Q

What are the virulence factors of Staph aureus?

A

Polysaccharide capsule

Protein A (binds IG)

Catalase inactivated hydrogen perioxide

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151
Q

What is the most common cause of pyogenic infection of the skin?

A

Staph aureus

152
Q

What is the most common cause of nosocomial bactereima?

153
Q

What is the most common cause of bacteremia, pneumonia, AOM?

A

Strep pneumo

154
Q

Hordeolum

Stye

Chalazion?

A

Hordeolum-purulent infection of the sweat gland of the eye lid, red, tender swelling. S aureus

Stye-External hordeolum, skin side of the eyelid

Chalazion-internatl hordeolu, conjunctival side of the eyelid

155
Q

Top AOM bugs?

A
  1. Strep pneumonia
  2. Nontype H influenzae
  3. M. CATARRHALIS
156
Q

For whom is a TST positive for > 5mm?

A
  1. CLose contact with confirmed or suspected cases of TB
  2. Radiographic or clinical evidence of tubercular disease
  3. Immunosuppressive therapy
  4. CHldren with ID including HIV
157
Q

For whom is a TST of >10 mm positive?

A

CHildren < 4 years

Children with Hodgkin, lymphoma, DM, chorinc renal failure, malnutrition

Children born in high prevalence regions of the world

Children exposed to adulted HIV homeless, incarcerated, illict durg user

158
Q

In whom is TST positive if >15 mm?

A

>4 without risk factors

159
Q

What are clinical features of congenital CMV infection?

A

Cataracts
Purpuric rash (“blueberry muffin”)
Seizures from CMV CNS lesions
Hepatosplenomegaly
IUGR
Microcephaly
Prolonged neonatal jaundice

160
Q

What is the difference in location between congenital CMV and Toxoplasmosis CNS lesions?

A

CMV: periventricular calcifications
Toxoplasmosis: calcifications scattered throughout cortex

161
Q

What cells are involved in humoral immunity? What cells are involved in cellular immunity?

A

Humoral: B-cell
Cellular: T-cell

162
Q

Testing for HIV in child 18 months?

A

Child 18 months: HIV ELISA (enzyme linked immunosorbent assay to look for HIV IgG: 99% specificity and sensitivity); if positive, confirm diagnosis with Western Blot (direct visualization of antibodies against the virus)

163
Q

What is a soft tissue complication of varicella infection?

A

GAS invasive soft-tissue infection: necrotizing fasciitis, myositis, cellulitis, toxic shock syndrome

Treatment: Penicillin and clindamycin

164
Q

What is the classical triad of Wiskott-Aldrich syndrome?

  • Complications (2)
  • mode of inheritance
A

Classic triad (in 1/3 of patients):

  1. Eczema
  2. Thrombocytopenia
  3. Immunodeficiency

Complications:

  1. Immunodeficiency:
    - T and B cell function is reduced
    - recurrent pneumonia/otitis media/sepsis/meningitis/sinusitis
    - progressive
    - can have hepatomegaly
  2. Risk of malignancy (10-20%)
    - leukemia/lymphoma

Mode of inheritance:
-X-linked

165
Q

How do neonates with Wiskott-Aldrich usually first present?

A

Present at birth with thrombocytopenia features: bruising, petechiae, bloody diarrhea

Eczema by 1st month of life, recurrent infections by 3 months of life

166
Q

In Wiskott-Aldrich, describe the levels of immunoglobulins seen.

A

IgA & IgE: elevated
IgM: reduced
IgG: normal, reduced or elevated

167
Q

What investigations should be ordered for 1-3 mo febrile infants meeting clinical criteria for low risk SBI?

A
  1. CBC + diff
  2. Blood culture
  3. Bag for urine –> cath if positive
168
Q

What is the definition of a UTI?

A
  1. Urine with > 10 wbc/hpf
  2. Colony count of single organism > 50,000/ml

***Remember that if child has been symptomatic

169
Q

In children 3-36 months, what percentage of fevers are viral in origin?

170
Q

Clinical presentation of lyme disease (6)?

A
  1. Arthritis
  2. Erythema migrans: painless, annular, central clearing, minimum size 5 cm
  3. Aseptic meningitis
  4. Cranial nerve palsies
  5. Heart block
  6. Ocular involvement
171
Q

What are the most common clinical presentations of urethritis (2)?
-What is the most common etiology of urethritis?

A
  1. Dysuria
  2. Penile discharge

Most common etiology: Chlamydia trachomatis (3x more common than Neisseria gonorrhoeae)

172
Q

What is the best test for chlamydia and gonorrhea?

173
Q

What is the management of a patient diagnosed with urethritis?

  • medical therapy
  • advice to give patients (ie. how long to abstain from sex)
A
  1. Empiric treatment for chlamydia and gonorrhea
    - Azithromycin 1 g PO x 1 for chlamydia
    - Ceftriaxone 250 mg IM x 1 for gonorrhea
  2. Instruct patients to abstain from sexual intercourse x 1 wk after single-dose therapy and until all partners are treated to prevent reinfection
  3. Test for other possible STIs (syphillis, HIV, hepatitis, etc.)
174
Q

What is a possible GI side effect of ceftriaxone?

A

Increased gallbladder sludge and subsequent cholelithiasis

175
Q

What is the pathophysiology of retropharyngeal cellulitis/abscess?

A

The retropharyngeal nodes that drain the mucosal surfaces of the upper airway and digestive tracts (between the pharynx and the cervical vertebrae, extending down into the mediastinum) become infected

  • once infected, the nodes progress through 3 stages: cellulitis, phlegmon, abscess
  • most patients have history of recent ear/throat/nose infection
176
Q

What are the possible causes of retropharyngeal abscess?

A
  1. Localized infection of oropharynx extending to the retropharyngeal lymph nodes
  2. Penetrating trauma
  3. Vertebral osteomyelitis
  4. Dental infection
177
Q

Retropharyngeal abscess are most common in what age group and why?

A

This disease is most common in children between the ages of 1 and 6 years. There are several small lymph nodes in the retropharynx that usually disappear by the age of 4 or 5.

178
Q

What are clinical manifestations of retropharyngeal abscess? (7)`

A

Think upper airway obstruction!

  1. Respiratory distress
  2. Stridor
  3. Drooling
  4. Fever
  5. Refusal to eat
  6. Obstructive sleep apnea
  7. Neck stiffness/torticollis
179
Q

What is the differential diagnosis of retropharyngeal abscess? (5)

A
  1. Acute epiglottis
  2. Lymphoma
  3. Meningitis (if neck stiffness present)
  4. Foreign body aspiration
  5. Vertebral osteomyelitis
180
Q

What is the underlying bacterial etiology of retropharyngeal abscess?

A

Polymicrobial! Most commonly:

  1. GAS
  2. Staph aureus
  3. Oral anaerobes
181
Q

What is the treatment for retropharyngeal abscess?

  • abx choice
  • indications for surgical drainage (2)
A

Intravenous antibiotics until clinical improvement, then switch to PO abx (ideal duration of treatment unknown)

  • 3rd generation cephalosporin + clindamycin
  • studies have shown that > 50% of children can be successfully treated without surgical drainage

Indications for surgical drainage:

  1. Respiratory distress
  2. Failure to improve with IV abx
182
Q

What are 4 complications of retropharyngeal abscess?

A
  1. Significant upper airway obstruction
  2. Rupture leading to aspiration pneumonia
  3. Extension into mediastinum
  4. Thrombophlebitis of internal jugular vein
183
Q

What is Lemierre disease?
-causative organism

A

Infection from the oropharynx extending to cause septic thrombophlebitis of the internal jugular vein and embolic abscesses in the lungs

  • causative organism: fusobacterium necrophorum (oral anaerobe)
  • most commonly seen in pharyngitis where peritonsillar abscess forms (ie. with GAS) and this allows the oral anaerobes to flourish within the abscess and then spread to the IJV
  • infected clot forms within the IJV and can throw off emboli
184
Q

What is the Rochester Criteria?

  • 4 clinical criteria
  • 4 laboratory criteria
A

Used for management of febrile infants 1-3 months of age: if ALL criteria are present, then the risk of having occult bacteremia is less likely.

Well appearing infant

No skeletal, soft tissue, skin or ear infections

Full term birth

No prior illness

No prior hospitalizations

Not hospitalized longer than mother after delivery

No prior antibiotics

No Hyperbilirubinemia

No chronic or underlying illness

Complete Blood Count normal

White Blood Cell Count normal (5000 to 15,000/mm3)

Band Neutrophils < 1,500/mm3

Other Lab Findings

If Diarrhea is present, Fecal Leukocytes <5 WBC/hpf

Urine White Blood Cells <10 WBC/hpf

185
Q

What are the live vaccines?

A

BOY LoVe The crIME

  • BCG
  • OPV
  • Yellow fever
  • Live vaccines
  • Varicella
  • Typhoid
  • Influenza (intranasal)
  • Measles/mumps
  • Epidemic typhus
186
Q

A septic baby is born preterm to a mother with a febrile, flu-like illness. The placenta was noted to have white nodules. On later imaging, the infant’s organs was noted to have microabscesses. What infectious organism is the most likely culprit?

A

Listeria monocytogenes

187
Q

What is the chance of acquisition of neonatal HSV infection for:

  • an infant born via SVD to a mother with primary HSV genital infection?
  • an infant born via SVD to a mother with recurrent HSV genital infection?
A

Infant born to mom with primary HSV infection: 50%
Infant born to mom with recurrent HSV infection:1-3% (due to less viral shedding and presence of maternal neutralizing antibody)

188
Q

You scrape the base of a vesicle found on an infant and send it for the Tzanck test. You see multinucleated giant cells. What is the differential diagnosis? (3)

A
  1. HSV
  2. Varicella
  3. CMV
189
Q

What are the clinical features of infantile botulism?

  • which organism and found from which sources (3)?
  • why are infants affected but not older children?
  • diagnosis?
  • treatment?
A

Clostridium botulinum: intestinal colonization occurs from ingestion of spores from honey, dust, soil

  • spores secrete neurotoxin that irreversibly prevents acetylcholine, thus see anticholinergic effects
  • clinical features: constipation, urinary retention, symmetric progressive weakness (paralysis), ptosis, diplopia, respiratory failure, poor feeding
  • in older children, they have to ingest the actual neurotoxin itself (may be present in foods) to cause disease; eating spores alone does not result in disease since the spores cannot germinate and produce neurotoxin in the gut of a child > 1 yo
  • in infants
190
Q

Which medications are contraindicated in infantile botulism?

A

Aminoglycosides! Worsen neuromuscular blockade

191
Q

What are the clinical features of infectious mononucleosis?

  • infectious etiology?
  • complications (4)
A

EBV infection = infectious mononucleosis

  • clinical features: fever, exudative pharyngitis, fatigue, lymphadenopathy, hepatosplenomegaly, tonsillar hypertrophy
  • complications:
    1. Splenic rupture
    2. Encephalitis
    3. Hemolytic anemia/thrombocytopenia
    4. Airway obstruction
    5. Malignant association: Burkitt lymphoma, Hodgkin disease, etc.
192
Q

What is the utility of a Monospot to diagnose infectious mononucleosis?

A

Monospot = looks for heterophile antibodies produced by the immune system to EBV
-sensitive test in children > 4 yo (present in >90% if has infection)

193
Q

What is the organism causing cat-scratch disease?
-what are the clinical features? (1 predominant, 3 less common, 1 particularly in immunocompromised patients)

A

Bartonella Henselae (gram negative bacillus)

  • clinical features:
    1. Regional lymphadenopathy (predominant)

Less common:

  1. Parinaud oculoglandular syndrome: inoculation of eyelid conjunctiva –> conjunctivitis and ipsilateral preauricular lymphadenopathy
  2. Liver and spleen granulomas
  3. Encephalitis

Immunocompromised:
5. Bacillus angiomatosis: proliferation of blood vessels –> tumor like masses in skin and organs

194
Q

How do you diagnose cat-scratch disease?
-treatment for: mild disease? Severe disease?

A

Serology

  • mild disease: supportive care; self-limited with resolution in 2-4 mo, no need for abx
  • severe or systemic disease: 5 d course of azithromycin to treat severe, painful lymphadenopathy but does not shorten duration of symptoms
195
Q

What are the classic clinical features of roseola?

  • infectious etiology?
  • treatment?
A

3-5 d of high fever followed by macular papular rash which appears on TRUNK first, then spreads to extremities/neck/face as the fever resolves.

  • associated with febrile seizures
  • infectious etiology: Human herpes virus 6
  • treatment: supportive care
196
Q

What is the definition of AIDS?

A
  1. CD4 count 200 or less in a patient with HIV
    OR
  2. The presence of an opportunistic infection in a patient with HIV
197
Q

For a newborn born to HIV positive mom, what testing do you perform and when do you perform it?
-treatment until results are back?

A
  1. HIV PCR at 14-21 d; if negative, repeat at 2 and 6 mo.
  2. If still negative, HIV antibodies assay (ELISA) at 18 mo.
    - treatment: zidovudine is given to mother prenatally, during L&D. Then start zidovudine for infant x 6 wks or until HIV PCR is back.
198
Q

In general terms, what are the different classes of antiretroviral agents? (4)
-when initiating therapy, what is the principle?

A
  1. Nucleoside reverse transcriptase inhibitors (NRTI)
  2. Non-nucleoside reverse transcriptase inhibitors (NNRTI)
  3. Protease inhibitors
  4. Fusion inhibitors
    - use combination of 3 or 4 agents from at least 2 classes
199
Q

What are the complications of influenza infection? (5)

A
  1. Pneumonia with staph aureus, strep pneumo, GAS
  2. Otitis media
  3. Myocarditis
  4. Encephalitis
  5. Guillain Barre syndrome
200
Q

How is malaria transmitted?

  • which species of parasite causes the most severe disease?
  • clinical features?
  • diagnosis?
A

By the saliva of a female Anopheles mosquito - carries plasmodium protozoa (intracellular)

  • most severe disease is seen with plasmodium falciparum
  • clinical features:
    1. High fever
    2. Chills
    3. Hemolysis (anemia, jaundice, splenomegaly)
    4. Cerebral malaria: increased ICP, seizures, coma, death
  • diagnosis: thick and thin blood smears several samples per day x 3 days to identify parasite (thick is better to identify that parasite is there, thin is to identify species)
201
Q

The treatment of malaria is guided by which 3 main factors?

A
  1. Clinical status of patient: non-severe vs. severe
  2. Plasmodium species
  3. Drug susceptibility of the infecting parasite
202
Q

What is the treatment for malaria?

  • ie. which patients should receive oral vs. IV antimalarials?
  • how long to continue treatment?
A

For patients with non-severe, uncomplicated malaria, can treat with PO antimalarial (chloroquine = main one, other choices include primiquine, atovaquone proguanil or quinine sulfate plus doxycycline/tetracycline/clindamycin or mefloquine)

Patients with the following factors should receive IV antimalarials (IV quinidine plus doxycycline/tetracycline/clindamycin):

  1. Severe hemolysis: severe anemia, bleeding, jaundice, hemoglobinuria
  2. ARDS
  3. DIC
  4. Renal failure
  5. Impaired consciousness
  6. Parasitemia > 6%

-continue therapy until parasite level

203
Q

Which malaria species can result in relapse due to their latent hepatic stages?
-which malaria species can cause chronic asymptomatic parasitemia that can persist for several years?

A
  • Latent hepatic stages: Plasmodium vivax and ovale
  • chronic asymptomatic parasitemia: Plasmodium malariae
204
Q

When is a person with measles contagious?

A

5 days prior to onset of rash to 4 days after

205
Q

What are the clinical features of measles? (3 Cs)

  • what is the characteristic rash seen with measles?
  • how do you diagnose measles?
A

Measles (paramyxovirus):

  1. Cough
  2. Conjunctivitis
  3. Coryza
    - also see fever and Koplik spots
    - Morbilliform rash starting from head and spreading downwards (happens on day 5 of illness)
    - diagnose measles with IgG and IgM serology
206
Q

What are the complications of measles? (4)
-which is the most scary?

A
  1. Pneumonia
  2. Croup
  3. Otitis media
  4. Subacute sclerosing panencephalitis
    - rare degenerative encephalitis characterized by dementia and intellectual deterioration with seizures occurring many years after initial infection (11 yr on average)
207
Q

What is the treatment for measles?
-who should receive prophylactic treatment after exposure to measles? (3)

A

Supportive treatment

  • prophylactic treatment with IVIG within 6 days of exposure REGARDLESS of immunization status should occur for:
    1. Pregnant women
    2. Immunocompromised
    3. Infants
208
Q

What are the 3 main areas of the world where malaria is found?

A
  1. Africa
  2. Asia
  3. South America
209
Q

Which population of people resist are immune to malaria?

A

Hemoglobin S - sickle cell anemia patients

210
Q

What is the life cycle of a plasmodium parasite?

A
  1. Exoerythrocytic phase:
    - inoculation of parasite into bloodstream by female Anopheles mosquito
    - enters hepatocytes and multiplies asexually
    - hepatocytes burst releasing thousands of parasites into blood stream
  2. Erythrocytic phase:
    - parasites then enter the erythrocyte and multiplies asexually
    - erythrocyte bursts releasing parasites (this is what causes the high fevers) that then develop into male and female and then are sucked up by mosquito during a blood meal to be transmitted to the next victim.

GROSS.

211
Q

What is chemoprophylaxis recommended for travellers going to areas with malaria?

A

In Chloroquine sensitive areas: give chloroquine
-in chloroquine-resistant areas, use atovaquone, mefloquine

212
Q

What do you see on gram stain for Neisseria meningitidis?

A

Gram negative diplococci

213
Q

What is the treatment for meningococcemia?

  • mortality rate of meningococcemia?
  • postexposure chemoprophylaxis?
A

Pen G x 5-7 d
(remember that meningitis with N meningitidis is also treated with IV abx x 5-7 d only)
-mortality rate: 10%, most within 1st 48 hrs due to fulminant septic shock/DIC secondary to endotoxins
-postexposure chemoprophylaxis should occur for anyone who came into contact with oral secretions of an infected patient = use rifampin

214
Q

What is Waterhouse Friederischsen syndrome?

A

Diffuse adrenal hemorrhage secondary to meningococcemia infection

215
Q

What 6 groups are at increased risk of invasive meningococcal disease?

A
  1. Anatomical or functional asplenia
  2. Children with primary antibody deficiency disorders
  3. Children with complement, properdin or factor D deficiency
  4. Travellers to areas endemic for meningococcus
  5. Lab personnel with exposure to meningococcus
  6. Military
216
Q

What are complications of mumps? (5)

A

Mumps = paramyxovirus, mainly causing parotitis (inflammation of salivary glands)

  1. Meningoencephalitis
  2. Orchitis
  3. Arthritis
  4. Myocarditis
  5. Pancreatitis
217
Q

What are the clinical features of Parvovirus B19 infection? (ie. two types)

  • period of infectivity for parvovirus B19?
  • other clinical features
  • treatment
A

Two types of infection:

  1. Erythema infectiosum: -fever, headaches, myalgias, polyarticular arthritis followed by slapped check facial rash followed by lacy, reticular rash on trunk and extremities
    - period of infectivity occurs BEFORE the onset of rash (ie. once rash has developed, the child is no longer contagious).
  2. Aplastic anemia:
    - those with RBC aplasia ARE infectious at presentation and should be isolated for at least 1 wk or until resolution of fever
    - seen especially in children with hemoglobinopathies
    - treatment: supportive care, possible RBC transfusion
218
Q

What are the 4 stages of pertussis?
-do you see this in infants?

A

ICPC: “I caught pertussis coughing”

  1. Incubation stage x 7-10 d
  2. Catarrhal stage: most infectious stage, mild upper resp prodrome x 1 wk (catarrhal means INFLAMMATION OF MUCOUS MEMBRANES)
  3. Paroxysmal stage: severe cough with inspiratory whoop x 1-3 mo, post-tussive vomiting
  4. Convalescent stage: gradual resolution of symptoms
    - infants
219
Q

How do you make the diagnosis of pertussis?

  • what is the treatment of pertussis?
  • does treatment change severity or duration of disease?
A

Pertussis PCR or culture

  • may see leukocytosis with lymphocytosis
  • treatment: azithromycin x 5 d
  • treatment after paroxysmal stage begins does NOT change severity or duration of disease but does decrease infectivity
220
Q

What is the chemoprophylaxis for contacts of pertussis positive individuals?

A

Azithromycin x 5 d regardless of immunization status in order to prevent spread

221
Q

In a patient previously infected with pertussis OR previously immunized for pertussis, how long do their protective antibodies last?

A

Usually last 3-5 yrs only - this is why booster is needed in adolescence/adults

222
Q

What are the complications of pertussis? (5)

A
  1. Secondary pneumonia
  2. Apneas
  3. Pulmonary hypertension
  4. Acute otitis media
  5. Physical sequelae from forceful coughing: scleral hemorrhage, petechiae, laceration to frenulum
223
Q

What animal bites may transmit rabies?

A

Dogs, cats, skunks, raccoons, foxes, coyotes, bats (any exposure to bats, even being asleep in the same room since bites/scratches can be tiny and not noticed!)
-first the single stranded RNA virus replicates in the tissue at the site of the bite/scratch and over weeks-months, moves along peripheral nerves until it reaches the spinal cord (concentrated in brain stem) and spreads rapidly to the brain

224
Q

What are the clinical features of rabies?

A

Weeks-months after bite: rapidly progressive encephalopathy with seizures, delirium, dysphagia, hydrophobia

225
Q

What seen on histology is the hallmark of rabies?

A

Negri body (clump of viral nucleocapsides that create cytoplasmic inclusions)

226
Q

What are investigations that can be done to confirm diagnosis of rabies?

A
  1. Animal with unknown vaccination status that bit the patient should be quarantined and observed for signs of rabies - may need to be euthanized with brain intact in order to see virus-specific antigens on brain tissue
  2. Can take skin biopsy specimens of the patient or isolate the virus from saliva
227
Q

What is the treatment for rabies?

  • what do you use for postexposure prophylaxis?
  • when would you give postexposure prophylaxis?
228
Q

What is the timing of the rabies vaccine?

A

Day 0, 3, 7, 14, 28 (total of 5 doses)

229
Q

How is rabies immunoglobulin adminsitered?

A

Should be administered immediately after the animal bite and infiltrated directly into the wound if present. The remainder should be given IM.

230
Q

How is HPV transmitted?
-clinical manifestations?

A
  1. Direct contact
  2. Autoinoculation
  3. Fomites
    - clinical manifestations: common warts (verruca vulgaris), periungual warts, plantar warts, anogenital warts (condylomata acuminata), squamous cell carcinoma
    - all caused by different subtypes of HPV
231
Q

Which HPV subtypes cause cervical cancer?

232
Q

What is the differential diagnosis of genital warts in children?

A
  1. Inoculation during birth through infected birth canal
  2. Sexual abuse
  3. Incidental spread from cutaneous warts

***significant proportion of genital warts in children contain HPV types that are usually isolated from cutaneous warts

233
Q

What is the treatment for warts?

  • common warts
  • plantar/palmar warts
  • condylomata acuminata
A

More than 65% disappear spontaneously within 2 years

  • treatment is most successful when performed regular q2-4 wks
  • Common warts: liquid nitrogen or daily application of salicylic acid
  • plantar/palmar warts: salicylic acid
  • condylomata acuminata (anogenital warts): podophyllin application x 4-6 hr on weekly basis OR imiquimod cream 3 times weekly
234
Q

What are the 3 most common causes of eosinophilia in children?

A
  1. Atopic dermatitis
  2. Allergic rhinitis
  3. Asthma

*NOT parasites :)

235
Q

Which infections are associated with severe eosinophilia? (5)
-which one is the most common cause of severe eosinophilia in children?

A

***Remember that eosinophilia requires tissue-invasive/blood invasive parasites so you will NOT see eosinophilia with parasitic infections that are well contained within tissues or are solely intraluminal in the GI tract (ie. with giardia or enterobius vermicularis aka pinworms)

  1. Toxocariasis: visceral larval migrans = most common cause of severe eosinophlia in children
    - toxocara species (roundworms from dogs/cats/foxes) larvae migrating from blood into liver, heart, CNS, eyes
  2. Trichinosis: trichinella spiralis (roundworm) transmitted through raw or undercooked pork or bear meat
    - start off in the GI tract, then invade muscles causing edema of eyelids, myalgia, fever, eosinophilia, can become encysted in the muscle
  3. Hookworm
  4. Ascariasis: Ascaris lumbricoides from eating food/drink contaminated with feces
    - eggs hatch in intestines, burrow through the gut and migrate to lungs. Then break into the alveoli, pass up the trachea where they are coughed up and swallowed to continue the life cycle of being pooped out and passed onto the next victim
  5. Strongyloidiasis: roundworm infection
236
Q

Worldwide, what is the most common cause of GI blood loss in children?

A

Hookworm infection - causes microscopic blood loss

237
Q

What 2 fungal diseases can cause eosinophilia?

A
  1. Aspergillosis in the form of ABPA
  2. Coccidiodomycosis
238
Q

What 3 drugs can be used for chemoprophylaxis for contacts of N. meningitidis?
-pregnant women?

A
  1. Rifampin PO BID x 2 d (preferred in children)
  2. Ceftriaxone IM x 1
  3. Ciprofloxacin (for > 18 yo)
    - pregnant women: rifampin and cipro is contraindicated - use ceftriaxone
239
Q

Mom brings her baby to you with painful lesions on finger x 10 d. She frequently sucks on her fingers prior to the development of the lesions. There is diffuse erythema and vesicles on the finger.

  • diagnosis?
  • treatment?
A

Herpes whitlow = HSV infection of fingers or toes

  • most commonly seen in infants/toddlers who suck the thumb and who are experiencing symptomatic or subclinical oral HSV-1 infection
  • HSV-2 herpes whitlow develops in teenagers due to exposure to infectious genital secretions (ie. fingering)
  • have itching, pain, erythema
  • do NOT incise the lesion (even if it looks like it might contain pus) since this may prolong recovery and increases risk of secondary bacterial infection
  • rapid improvement/recovery within 18-20 d
  • no clinical trials assessing benefit of antiviral treatment for this
  • BUT can start high dose oral acyclovir (2 g/d div BID PO x 10 d)
240
Q

What is the likelihood of chronic hepatitis with the following:

  • Hep A
  • Hep B
  • Hep C
  • Hep D
  • Hep E
A
  • Hep A: 5% progress to chronic hepatitis (95% recover within 1-2 wks of illness, chronic disease is unusual)
  • Hep B: >90% of perinatally infected infants, 25-50% of young children who acquire Hep B during 1-5 yo, 10% of older children and adults
  • Hep C: 75% of children
  • Hep D: only if there is concurrent Hep B infection
  • Hep E: does not cause chronic hepatitis
241
Q

What are the clinical features of Hep A infection?

A

Acute febrile illness with abrupt onset of anorexia, nausea, malaise, vomiting and jaundice
-typical duration is 7-14 d

242
Q

What is the treatment for Hep A?

A

Supportive care and monitoring of liver enzymes and liver function tests for acute liver failure

243
Q

When are patients with Hep A contagious and be excluded from school/daycare?

A

ontagious 2 wks before and 7 days after onset of jaundice/symptoms

244
Q

What are the pre-exposure and post-exposure prophylaxis for Hepatitis A infection?

A

***Overall: infants 1 yo and healthy: Hep A vaccine
-> 1 yo and immunocompromised/chronic liver disease/chronic health problems: both Hep A vaccine and Hep A immunoglobulin

***Give post-exposure prophylaxis if

245
Q

What diagnostic testing do you order for Hep B?

A

Order: HBsAg, HBsAb, HBcAg, HBcAb, HBeAg, HBeAb, HBV DNA, liver function tests, liver enzymes

  • after exposure to HBV, the following occurs:
    1. HBsAg (hep B surface antigen) rises first and is the first detectable antigen to appear during infection
  • also gets cleared later on
  • this is what is inside the Hep A vaccine that then stimulates production of HBsAb
  • if your HBsAb AND HBcAb is positive, this means prior infection
  • if your HBsAb is positive but HBcAb is negative, this means prior immunization
    2. HBV DNA PCR will then become positive
    3. HBcAg (Hep B core antigen): found inside the virus, rises next. This is what stimulates formation of HBcAb
  • if your HBcAb is positive, this means that you have been previously infected with Hep B (this is how you distinguish between prior infection vs. immunization)
    4. HBeAg (Hep B e antigen): sometimes signals high levels of viral replication; induces HBeAb; not all Hep B strains have HBeAg

***If the host had Hep B and cleared the infection: see both HBsAb and HBcAb and possibly HBeAb

246
Q

What is the treatment of acute Hepatitis B?
-chronic?

A
  • Acute hep B: supportive care
  • Chronic hep B: interferon alpha or lamivudine
247
Q

What are the cilnical features of familial mediterranean fever?

  • diagnosis?
  • main complication?
  • treatment?
A

Acute recurrent episodes of fever + 1 or more of the following lasting 1-4 d:

  1. Sterile peritonitis
  2. Arthritis/arthralgia
  3. Pleuritis
    - can also have erysipelas-like rash, splenomegaly but less common
    - complication: may progress to development of renal amyloidosis
    - diagnosis: genetic testing for FMF gene to confirm
    - treatment: prevent attacks with prophylactic colchicine, also decreases progression to amyloidosis
248
Q

What are the clinical features of PFAPA (aka marshall syndrome)?

  • what differentiates PFAPA from other periodic fever syndromes?
  • treatment?
A

Periodic Fever lasting 4 d and recurs every 2-8 wks LIKE CLOCKWORK!
APHTHOUS STOMATITIS
Pharyngitis
Adenitis (cervical)
-most common cause of recurrent fevers in children
-other periodic fever syndromes have IRREGULAR intervals in between fevers whereas PFAPA has VERY regular intervals between fevers
-treatment: steroids, cimetidine

249
Q

What are clinical features of TRAPS?

  • mode of inheritance?
  • complication?
  • treatment?
250
Q

What are clinical features of Hyper-IgD syndrome? (HIDS)
-treatment?

A

Periodic fever syndrome with abdominal pain, cervical adenopathy, splenomegaly

  • fevers occur at irregular intervals
  • seen in Dutch families usually
  • see elevated IgD levels but is not diagnostic since other autoinflammatory disorders can cause this
  • treatment: steroids
251
Q

What are the 4 common periodic fever syndromes?

A
  1. PFAPA: most common
  2. TRAPS (TNF-receptor associated periodic syndrome)
  3. Hyper-IgD syndrome
  4. Familial mediterranean fever syndrome
252
Q

Name a distinguishing feature for each of the following:

  • PFAPA
  • Familial mediterranean fever
  • TRAPS
  • hyper IgD syndrome
A

PFAPA: fever occurs at REGULAR intervals like clockwork

Familial mediterranean fever: fevers are usually shorter in duration than in other periodic fever syndromes, only one treated with COLCHICINE (not steroids)

TRAPS: autosomal dominant, EYE involvement (periorbital edema, conjunctivitis)

Hyper IgD syndrome: elevated IgD levels, does NOT progress to amyloidosis

253
Q

Which infections have been found to cause guillain barre syndrome? (2)
-what about vaccines? (4)

A

Infections:

  1. Campylobacter
  2. Mycoplasma pneumoniae

Vaccines:

  1. Rabies
  2. Influenza
  3. Oral polio
  4. Conjugated meninococcal vaccine (serogroup C)
254
Q

Which children should receive the Pneumovax (PPV23) vaccine? (6)

A

High risk children > 2 yo:

  1. Asplenia
  2. Sickle cell disease
  3. Antibody deficiencies
  4. HIV infection
  5. Chronic lung, heart, kidney disease
  6. Diabetes mellitus
255
Q

What is the most common congenital infection?

256
Q

What is the most common outcome of congenital CMV infection?

A

Sensorineural hearing loss (58%)

257
Q

What are the clinical features of Q fever?

  • how is it acquired?
  • treatment?
A

Coxiella burnetii:

  • airborne, from FARM ANIMALS, EXTREMELY infectious and resistant to chemical and physical treatments
  • associated with farm visits, lamb birthing season
  • causes fever, mild interstitial lymphocytic pneumonitis (lives in the lungs) & hepatomegaly due to lymphocytic lobular hepatitis
  • only 40-50% of people infected with C. burnetii develop symptoms
  • can see leukocytosis, thrombocytopenia, elevated liver enzymes
  • diagnose by serology (abs to C. burnetii antigens)
  • self-limited illness
  • treat with doxycycline in any age (benefits >> tooth discoloration in children
258
Q

What is the main difference between neonatal chlamydial conjunctivitis and gonorrheal conjuncitivitis in terms of prognosis?
-what is the treatment for each?

A

Gonorrheal conjunctivitis: leads to corneal perforation and blindness if left untreated
-treatment: Ceftriaxone IM or IV x 1 dose, saline eye irrigation q10-30 minutes, until purulent discharge has cleared, must r/o sepsis

Chlamydial conjunctivitis rarely involves the cornea; usually isolated to conjunctiva and is self-limited (BUT can progress to chlamydial pneumonia which is bad)
-treatment: erythromycin PO x 2 wks (may prevent subsequent chlamydial pneumonia). CANNOT treat with topical therapy alone since this will NOT clear the chlamydia from their resp tract and thus not prevent pneumonia

259
Q

Among neonates with conjunctivitis: what is the timing for the various etiologies?

  • chemical
  • Neisseria gonorrhoeae
  • Chlamydia trachomatis
A

Chemical: onset less than 2 days
N. gonorrhea: onset 2-7 days
C. trachomatis: onset 5-14 days

260
Q

What is ophthalmia neonatorum?
-prophylaxis?

A

Conjunctivitis in the 1st month of life with concerns re: C. trachomatis and N gonorrhea perinatal acquisition
-prophylaxis: erythromycin 0.5% ophthalmic ointment

261
Q

What are the clinical stages of syphilis?

A
  1. Primary: painless, single genital ulcer (chancre) appearing 3-6 wks after inoculation
  2. Secondary: follows 6-8 wks later with fever, generalized lymphadenopathy (especially inguinal), disseminated maculopapular rash on body/palms/soles, condylomata lata, mucous membrane lesions
  3. Tertiary syphilis: does not happen in children; involves cardiovascular, neurologic and msk systems
  4. Latent syphilis = asymptomatic infection
    a. Early latent: acquisition within the preceding year
    b. late latent: acquisition within unknown duration
262
Q

What is the treatment of early syphilis (primary, secondary, early latent) vs. late syphilis (tertiary, late latent) vs neurosyphilis?

A

Early syphilis: single IM dose of benzathine pen G

Late syphilis: IM doses of benzathine pen G x 3 at weekly intervals

Neurosyphilis: IV aqueous crystalline pen G x 10-14 d

263
Q

What are clinical findings of congenital syphilis that are usually present within few days of birth?

A
  1. HSM
  2. Snuffles (rhinitis)
  3. Lymphadenopathy
  4. Copper rash on palms/soles/perioral/perianal
  5. Pneumonia
  6. Osteochondritis
264
Q

What are late clinical findings of untreated congenital syphilis? (7)

A

Usually appear after 2 years of age:

  1. interstitial keratitis (corneal scarring)
  2. 8th CN palsy (deafness)
  3. Hutchinson teeth (bifid teeth)
  4. Mulberry molars (multiple enamel spots on molars)
  5. Saddle nose deformity
  6. Frontal bossing
  7. Clutton joints (symmetrical joint swelling, usually in knees)
265
Q

What is Hutchinson’s triad?

A
  1. Interstial keratitis
  2. 8th cranial nerve palsy
  3. Hutchinson teeth

Indicative of congenital syphilis

266
Q

What testing should be completed for an infant if congenital syphilis is suspected?

A
  1. Quantitative treponemal syphilis test (TP-PA)
  2. Direct fluorescent antibody staining by scraping skin or mucous membrane (FTA-ABS)
  3. Nontreponemal reaginic antibody assays: VDRL (venereal disease research lab) & RPR (rapid plasma reagin)
267
Q

What is the treatment and f/u of congenital syphilis?
-neurosyphilis: treatment and f/u?

A

Pen G x 10-14 d with repeat of nontreponemal antibody titres at 3, 6, 12 months to document falling titres
-neurosyphilis: serologic testing + CSF q6months x at least 3 years or until CSF findings are normal

268
Q

What are the 2 most common causes of acute unilateral lymphadenitis in normal healthy children?

A
  1. S. aureus
  2. GAS
269
Q

What are the 2 most common causes of chronic infectious lymphadenitis in children?

A
  1. non-TB mycobacteria
  2. Bartonella henselae
270
Q

What is the most common organism causing meningitis in children with VP shunts?

A
  1. Staph aureus
  2. Coag neg staph
271
Q

When do you treat campylobacter with antibiotics? (4)

  • choice of abx?
  • resistent to which drugs/
A
  1. High fever
  2. Severe diarrhea
  3. Immunocompromised
  4. Toxic
  • treatment: Azithro or erythro PO, IV gent, tobra or meropenem
  • resistant to penicillins, cephalosporins, vanco
272
Q

Child is on prednisone for nephrotic syndrome. When would you give vaccines?

A

if on steroids for > 14 d, considered immunosuppressed and do NOT get live vaccines until off-steroids x 1 month

273
Q

What are clinical features of rubella?

  • period of infectivity?
  • most severe neuro complication?
A

Clinical features:

  1. Macular, coalescing rash on FACE, then moves downwards
  2. Fever
  3. Pharyngitis
  4. Conjunctivitis
  5. Lymphadenopathy
  6. Transient arthropathy
  7. Forckheiner spots: rose-colored spots on oropharynx

-period of infectivity 6 days pre rash up to 6 days
post rash
-CNS complication: rubella panencephalitis

274
Q

You have a 3 mo child with tender swelling over the mandible bilaterally with fever and irritability. Hyperostosis on xray. Diagnosis?
-differential diagnosis for hyperostosis on xray?

A

Caffey’s

  • usually related to mandible
  • differential diagnosis: hypervitaminosis A (but no fever/irritiability, subacute onset)
275
Q

What is the triple therapy for H. Pylori?

A
  1. Clarithro + amoxil OR flagyl + PPI
276
Q

What are 2 organisms that are transmitted via cat bites?

A
  1. Pasteurella
  2. Eichenella
277
Q

What is the most common congenital cardiac defect seen with congenital rubella syndrome?

278
Q

How long do children with congenital rubella syndrome stay infectious?

A

Shed virus in urine/stools x 1 year

279
Q

When do you treat salmonella infections?

A
  1. Infants meningitis
280
Q

What are clinical features of neonatal chlamydial pneumonia?
-treatment?

A
  1. Absence of fever
  2. Eosinophilia
  3. Cough
  4. Bilateral interstitial markings
    - treatment: erythromycin
281
Q

What are 3 viral causes of erythema nodosum?

  • common bacterial causes? (5)
  • common fungal causes? (3)
  • other causes?
A

Viral:

  1. Hep B
  2. EBV
  3. Mumps

Bacterial:

  1. Mycoplasma
  2. Bartonella henselae
  3. GAS
  4. Yersinia
  5. TB

Fungal:

  1. Histoplasmosis
  2. Blastomycosis
  3. Coccidiocomycoses

Other causes:

  1. OCP
  2. Sulfa drugs
  3. SLE
  4. IBD
282
Q

What are the types of meningococcus vaccines?

  • schedule for each?
  • what populations are at increased risk of meningococcal disease (6)?
A
  1. MCV-C: conjugate vaccine serogroup C (most common in adolescents)
    - brand names: mejugate, meningitec, neissvac-C
  2. MCV-4: conjugate quadrivalent serogroup: A/C/Y/W135
    - brand names: menactra, menveo
  3. 4CMenB: conjugate vaccine serogroup B (most common in preschool kids)

All children:

  • MCV-C @ 12 mo
  • MCV-4 @ 12 yo (grade 7)

Children at increased risk of meningococcal disease: (asplenia, immunocompromised = primary antibody disorder, complement deficiency, perperdin deficiency, factor D deficiency, travellers to high meningococcus areas, military, lab workers, cochlear implants )

  • MCV-C @ 2, 4, 6, 12 mo
  • MCV-4 @ 2 yo and q5yr
  • 4CMenB starting at @ 2 mo (also for outbreaks, close contacts of person with serogroup B)

Remember that conjugate >>> polysaccharide vaccines in inducing an immune response

283
Q

Worst prognosis of HIV occurs with which complication?

284
Q

What are the 2 side effects of isoniazid?
-prevention?

A
  1. Peripheral neuropathy: prevent by giving pyridoxine (vit B6)
  2. Elevated liver enzymes
285
Q

What TB medication causes retrobulbar neuritis?

A

Ethambutol

286
Q

When does a positive TST no longer be attributable to a BCG vaccine?

A

If the child received BCG vaccine more than 10 years ago, will not affect TST result

287
Q

In a child who requires immunosuppression and thus TST and MMR vaccine, what is the optimal timing for each test in order to avoid false negative TST caused by MMR vaccine?

A

Either give both the same day OR do TST 4 wks after MMR

288
Q

What 2 antibiotics can be used to treat chlamydia trachomatis?

A
  1. Azithromycin
  2. Doxycycline
289
Q

When do the sinuses develop during childhod? (ie. pneumatization)

A
  1. Ethmoid present by birth, pneumatises first!
  2. Maxillary present at birth but pneumatises 2nd at 4 yo
  3. Sphenoid: complete by 5 yo
  4. Frontal: begins at 3-7 years of age, complete by age 12 years
290
Q

Which injuries warrant inquiry into tetanus status? (3)
-pathogenesis of tetanus infection?

A
  1. Penetrating wounds from dirty object (nail, splinter, glass, etc.)
  2. Animal bites
  3. Burns/frostbite
    - clostridium tetani = produces tetanus toxin that blocks normal inhibition of antagonistic muscles on which voluntary coordinated movement depends = affected muscles sutain maximal contraction and cannot relax
    - does not affect sensory nerves so patients remain conscious and in severe pain

**Basically anything except a clean, minor wound

291
Q

What are common clinical features of tetanus infection?

A
  1. Most common presenting symptom: trismus (masseter muscle spasm or lockjaw)
  2. Risus sardonicus: abnormal spasm of the facial muscles that looks like a creepy smile
  3. Opisthotonos when abdo/lumbar/hip/thigh muscles are involved
  4. Laryngeal and resp muscle spasm = airway obstruction/asphyxiation
  5. Fever due to sustained muscle contraction (increased metabolic rate)
  6. Autonomic effects: tachycardia, dysrhythmias
    - lasts up to 4 wks
  7. Generalized tetanic spasms (seizures) leading to rhabdomyolysis and renal failure, intramuscular hematomas, spinal fractures
    - can be triggered by any sights/sounds/touch

**overall: see LOCKJAW, think tetanus!

292
Q

How do you make the diagnosis of tetanus?
-what is the single most common risk factor for neonatal tetanus?

A

Clinical findings - routine lab results are usually normal, neither EEG or EMG show characteristic pattern
-neonatal tetanus: lack of maternal immunization

293
Q

What is the management of tetanus infection?

A
  1. Tetanus immunoglobulin 500 U IM ASAP: if the tetanus toxin is already bound at the NMJ then there is nothing you can do about this but TIG neutralizes toxin that hasn’t bound yet
  2. Surgical wound debridement
  3. Antibiotics: Pen G x 10-14 d
  4. Muscle relaxants: diazepam or rocuronium (flaccid paralysis, requires I&V but at least gives muscles a break)
  5. Supportive care
294
Q

What is the immunization schedule for tetatnus prevention?

A

DTaP at 2, 4, 6, 18 months with booster at 4-6 yo and q10y after

295
Q

When would you consider giving tetanus prophylaxis with tetanus vaccine, tetanus immunoglobulin or both in a patient with a wound?

  • clean minor wounds vs. all other wounds
  • immunization status
  • dose of tetanus immunoglobulin
A

A) If the patient has received LESS than 3 tetanus toxoid vaccines or imm status unknown:

  • always give tetanus vaccine (Td or TdaP)
  • if wound is clean/minor: no TIG
  • if wound is contaminated: YES TIG

B) If the patient has received 3 or more tetanus toxoid vaccines:

  • don’t have to give tetanus vaccine UNLESS > 10 yrs since last dose for clean/minor wounds or > 5 yr for contaminated wounds
  • don’t have to give TIG ever

****So overall, clean/minor wounds NEVER need TIG; contaminated wounds only need TIG if patient has received 24 hrs since injury, unable to be debrided)

296
Q

What is the treatment of latent TB?

  • treatment of pulmonary TB?
  • treatment of TB with HIV coinfection?
  • treatment of TB meningitis?
A

A) Latent TB = positive TST in context of known exposure to TB positive close contact but normal CXR and asymptomatic
-treatment: isoniazid x 9 months to prevent reactivation

B) Treatment of pulmonary TB (fully drug susceptible): 6 months total isoniazid (+/- pyradoxine) + rifampin with pyrazinamide in first 2 months
-drug resistant or unknown susceptibility: add ethambutol to first 2 mo regimen

C) TB with HIV coinfection
-extend isoniazid + rifampin to 9 mo total

D) TB meningitis -extend isoniazid +rifampin to 12 mo total
-add corticosteroids (decrease mortality rates, decreases neurologic sequelae = prednisone 2 mg/kg/day x 4-6 wks, then taper

297
Q

What is the Ghon complex?

  • where is the most common site of TB infection?
  • Extrapulmonary sites?
A

initial focus of TB infection in the lung with enlarged regional lymph nodes

  • most common site of TB infection: lungs (80%)
  • extrapulmonary sites: lymph node (67%), meninges, pleura, miliary (disseminated), skeletal (13%)
298
Q

What are the 2 categories of TB infection?

A
  1. Latent: positive TST but asymptomatic and normal CXR
  2. Active TB: TB infection with symptoms and radiologic findings
299
Q

What is the most common form of extrapulmonary TB?

A

TB lymphadenopathy

300
Q

In TB CNS disease, where are the 2 sites of greatest involvement?

A

Brainstem and meninges

  • more common in children 6 mo-4 yo
  • get CN palsies (3, 6, 7 since they’re on brainstem)
301
Q

What is the immunization strategy to prevent pertussis?

A
  1. Immunize infants with DTaP vaccine at 2, 4, 6, 15 mo with booster at 4 yo
  2. Immunize adolescents with booster with single dose of Tdap
302
Q

What is Pott disease?

A

TB in the spinal vertebrae

303
Q

What test is the most specific way to confirm pulmonary TB?

A

Sputum culture
-can do induced sputum with jet nebulizer and chest percussion followed by NP suctioning

304
Q

What is the utility of gastric aspirate vs. bronchoscopy for diagnosing TB?

A

Gastric aspirates for culture may be the only option for young children BUT it only yields organism in AM

305
Q

If a patient has been infected with TB, when will the TST become positive?

A

Tuberculin sensitivity develops 3 wks-3 mo after infection

306
Q

When is a TST considered positive?

  • 0-4 mm (1)
  • 5-9 mm (6)
  • >10 mm (1)
A

-0-4 mm: HIV infection with immune suppression AND high likelihood of having TB (ie. close contact of active case, abnormal xray or from population with high prevalence)

  • 5-9 mm:
    1. HIV
    2. Immunosuppressed (chemotherapy)
    3. Children suspected of having TB
    4. Close contact of active contagious case within 2 years
    5. Abnormal CXR with fibronodular disease
    6. End stage renal disease

->10 mm: all other cases

307
Q

A child who you suspected may have TB ends up having a negative TST and IGRA. What is your diagnosis?

A

Could still have TB! Negative TST or IGRA does NOT exclude active TB!
-in all cases of suspected TB, you should do everything you can to get a culture diagnosis always always always

308
Q

Before starting therapy for TB disease, what baseline testing should be completed? (4)

A
  1. Liver enzymes (AST, ALT)
  2. Bilirubin
  3. HIV serology
  4. Baseline ophtho assessment in younger children (due to risk of retrobulbar neuritis due to ethambutol)
309
Q

What are the indications for use of pyridoxine in conjunction with isoniazid in treatment of TB? (5)

A
  1. Children who have milk/meat deficient diets
  2. Adolescents who are breastfeeding or pregnant
  3. Children with nutritional deficiencies
  4. Symptomatic HIV infection
  5. Breastfed infants
310
Q

A child with latent TB who you’ve been treating with Isoniazid for the last 3/9 months comes to you with anorexia, n/v, abdo pain, dark colored urine, jaundice and pale colored stools. What is your management?

A

Isoniazid can cause hepatotoxicity and lead to death or need for transplant!
-tell them to stop taking isoniazid ASAP and do liver work up

311
Q

What are 2 findings on lateral neck xray with retropharyngeal abscess?

A
  1. Air fluid level in retropharyngeal space
  2. Increased width of retropharyngeal space
312
Q

What are complications of otitis media? (6)
-what is the definition of chronic suppurative otitis media?

A
  1. Meningitis
  2. Lateral sinus thrombosis
  3. TM perf
  4. Intracranial abscess
  5. Hearing loss
  6. Cholesteatoma

***Chronic suppurative otitis media: purulent drainage from perforated tympanic membrane > 6 wks

313
Q

What are the indications for tympanostomy tubes?

A
  1. Failed antibiotics for recurrent AOM
  2. Chronic otitis media
  3. Tympanic membrane retraction with ossicular erosion or cholesteatoma formation
314
Q

What is the age range of children who typically get bacterial tracheitis?

  • what is the age range of peritonsillar abscess?
  • what is the age range of retropharyngeal abscess?
A

Between 3 mo - 3 yrs
-peritonsillar abscess: adolescents most common

315
Q

How do you diagnose mastoiditis?
-What is the treatment of mastoiditis?

A
  • Diagnosis: physical exam shows mastoid swelling and redness with protrusion of the ear forward
  • treatment: IV antibiotics (3rd generation cephalosporin ie. ceftriaxone) = if no improvement or if still febrile in 48 hrs, may need mastoidectomy
316
Q

A patient presents with trismus, drooling and a hot potato voice. What is the most likely diagnosis?

  • treatment?
  • most severe complication?
A

Peritonsillar abscess

  • will see unilateral tonsillar swelling with a deviated uvula
  • treatment: surgical drainage and antibiotic therapy x 10-14 days (usually IV penicillin or something with GAS coverage)
  • most severe complication: rupture of the abscess with resultant aspiration pneumonitis
317
Q

What is the treatment for PCP pneumonia?

A

TMP-SMX IV with or without steroids (for severe hypoxemia)

318
Q

What is the most common causative organism in endocarditis?

A

Strep viridans most common
-can also see S. epidermidis, S. auresua, HACEK organisms (hemophilus, actinobacter, cardiobacterium, Eikenella, Kingella)

319
Q

What are the clinical manifestations of cryptosporidium infection?
-treatment?

A

GI stuff! Crampy abdominal pain, vomiting, watery diarrhea

  • can cause bad disease in immunocompromised patients
  • treatment: supportive therapy for immunocompetent children, nitazoxanide for immunosuppressed with severe disease
320
Q

What is the underlying organism causing traveler’s diarrhea?

A

Enterotoxigenic E coli

321
Q

What is the principle reservoir of Yersinia?

322
Q

What is the most common cause of spontaneous bacterial peritonitis in a previously healthy child?

  • nephrotic syndrome?
  • children with dialysis catheters and VP shunts?
  • children with cirrhosis?

Treatment?

A

Previously healthy child, nephrotic syndrome = both strep pneumo

  • catheters/VP shunts: S. epidermidis, S. aureus
  • cirrhosis: E coli

***Treat with 3rd generation cephalosporin, add vanco if catheter related infection

323
Q

What is the management of necrotizing fasciitis?

A

Emergent surgical debridement with antibiotic therapy

324
Q

What is the msot common organism causing VP shunt infections?

A

Coag-negative staph

325
Q

What is the treatment for chlamydia trachomatis neonatal conjunctivitis?
-Neisseria gonorrhea neonatal conjunctivitis?

A

Chlamydia: Erythromycin PO x 14 d
Gonorrhea: Ceftriaxone x 1 dose

326
Q

A child has been bitten by a dog. What clinical feature can help differentiate other organisms from a pasteurella infection?

A

Pasteurella infections cause pain and swelling within the FIRST DAY of the bite whereas other bacteria cause pain and swelling AFTER the 1st day (take more time to develop)

327
Q

What is the diagnostic criteria for toxic shock syndrome?

A

Need all 3 major criteria:

  1. Acute fever
  2. Hypotension
  3. Erythroderma with convalescent desquamation rash

-AND-

3/7 minor criteria

  1. Mucous membrane inflammation (vaginal, oropharyngeal, strawberry tongue)
  2. GI: Vomiting or diarrhea
  3. Renal abnormalities (urea or cr > 2x normal)
  4. Liver abnormalities (bilirubin or liver enzymes > 2x normal)
  5. Muscle abnormalities (myalgia or CK > 2x normal)
  6. CNS abnormalities (altered LOC)
  7. Thrombocytopenia

-AND-

Absence of another explanation and negative blood cultures (except occasionally for Staph aureus)

328
Q

How can you differentiate between mumps and other viral infections?

A

Mumps = do NOT see rash
-usually have bilateral parotitis (2nd side can appear a day after the first side), can have displacement of the uvula, fever, orchitis

329
Q

What infectious disease has a rash that is described as “dewdrop on a rose petal”?

330
Q

What is the most common cause of death in Reye syndrome?

  • pattern of liver dysfunction? (ie. what do you see on liver enzymes and liver function tests?)
  • mortality risk?
  • two viruses involved in pathogenesis of Reye syndrome?
A

Increased ICP (from cerebral edema) and subsequent herniation

  • up to 40% mortality
  • see elevated liver enzymes and ammonia but NORMAL total bilirubin
  • two viruses involved: influenza and varicella in a patient on ASA therapy
331
Q

A patient presents to the ED with a GTC seizure and fever. During the lumbar puncture which turns out to be normal, he has a large watery stool with blood and mucus. What is the most likely diagnosis?

A

Shigella infection!
-in Shigella infection, increased risk of seizure and the seizure PRECEDES diarrhea which distinguishes shigella from other GI infections (like campylobacter)

332
Q

What type of organism causes leptospirosis?

  • where do cases typically occur?
  • which animals spread leptospirosis?
A

Spirochete = spiral bacteria

  • typically occur in tropical countries
  • found in livestock, birds, dogs (major reservoir in USA), cats, rats: usually people get exposed via contaminated water or soil or contact with animals
333
Q

What are the clinical manifestations of leptospirosis?

  • key distinguishing feature?
  • Weil syndrome?
  • how is the diagnosis made?
A

***Most infections are mild or subclinical!!!! Most patients clear the infection without any symptoms

KEY: illness follows biphasic course = initial (septicemic = see leptospires in blood, CSF, other tissues) phase lasting 2-7 days, followed by brief period of well-being before onset of a second symptomatic leptospiric phase (this is where leptospires move into the tissues and you can’t find them anymore in blood and csf)

  1. Septicemic stage: flu like symptoms with myalgia, headache, abdo pain, vomiting, fever, conjunctival injection, photophobia
    - —-asymptomatic phase—
  2. Second stage: aseptic meningitis (pleiocytosis aka elevated WBC and elevated proteins, normal glucose), uveitis, rash, fever

**Can also get icteric leptospirosis (Weil Syndrome) where immune phase is characterized by jaundice, renal failure, thrombocytopenia, cardiovascular collapse = this is very rare!

Diagnosis: serologies, microscopis agglutination test (serogroup specific assay), ELISA

334
Q

What is the treatment for leptospirosis?

A

Penicillin in children 9 yo x 7 days
-early treatment may shorten duration/severity of infectio

335
Q

How long can it take for osteomyelitis changes to show up on a plain radiograph?

A

Early soft tissue changes take 3 days to develop and bone changes take up to 12 days after onset of osteomyelitis

336
Q

What are the clinical features of Rocky Mountain Spotted Fever?

  • how is this infection transmitted?
  • treatment?
A

Classic triad: fever, headache, rash

  1. Prodromal period with headache, malaise, pain and tenderness of calf muscles in children is very common
  2. Abrupt onset of fever and chills
  3. Maculopapular rash on the flexor surfaces of the wrists and ankles, then moves in a central direction, typically involves palms and soles
    - rash can then become hemorrhagic within 1-2 days
    - can cause CNS depression, seizures, etc.
    - transmitted by ticks from Dermacentor family (rickettsia rickettsii is the organism carried by the tick)
    - treatment: Doxycycline regardless of the child’s age!
337
Q

A patient gets a puncture wound through a tennis shoe. What is the most likely organism to cause an infection?
-what about a patient who gets a puncture wound through her bare foot?

A

Tennis shoe = pseudmonas since shoe is warm and moist

Bare foot = staph aureus since it is bare skin

338
Q

What are 3 common complications of staphylococcal pneumonia?

A
  1. . Pleural effusion
  2. Empyema
  3. Pyopneumothorax
339
Q

What is the management of a perianal abscess?

A

Usually I&D only is adequate but depending on age/clinical status, may need antibiotics

340
Q

After what age should a genital wart in a child alert you towards the possibility of child abuse?

A

3-4 yo
-before then, perinatal or diaper changed by someone with a finger wart is more likely

341
Q

What is the risk of acute –> chronic Hep B infection based on mode of transmission?

A

****Likelihood of going onto chronic infection is inversely related to age

  • Perinatal infection is MOST likely to go on to chronic Hep B
  • horizontal transmission in childhood is in the middle
  • Adult infection is LEAST likely to go on to chronic Hep B infection
342
Q

What is the management of a patient who has been exposed to varicella?

  • healthy person
  • pregnant woman
  • immunocompromised
A

Healthy person: vaccinate with varicella vaccine

Pregnant women and immunocompromised:

  • check VZV IgG serologies,
  • If negative, give VZV IgG since they cannot receive the vaccine
343
Q

What is considered a positive TST?

A

> 5 mm IF:

  1. exposed to a close contact with known or suspected TB
  2. clinical symptoms of TB
  3. immunocompromized (HIV) or on immunosuppressants

> 10 mm IF:

  1. 15 mm IF:
    - any child > 4 yo without any other RFs
344
Q

First-generation cephalosporins

A

(e.g., cefazolin, cephalexin, cefadroxil)

•

Good activity against gram-positive organisms (especially Methicillin-susceptible S. aureus and streptococci spp.)

•

Frequently used as prophylaxis for orthopedic, cardiovascular, head and neck, and many types of neurosurgical or general surgical procedures (i.e., herniorrhaphy)

•

May have activity against some E. coli and Klebsiella species, but lack efficacy against Haemophilus influenza

•

May be considered as alternatives to penicillins for the treatment of group A streptococcal pharyngitis and group B streptococcal prophylaxis during labor.

345
Q

Second-generation cephalosporins

A

(e.g., cefuroxime, cefotetan, cefoxitin)

•

Increased spectrum of activity, including many gram-negative organisms

•

Increased activity against B. fragilis

•

Prophylaxis for intra-abdominal (e.g., cefotetan, cefoxitin)

•

Treatment for nosocomial pneumonia

•

No antipseudomonal activity

346
Q

Third-generation cephalosporins

A

(e.g., ceftriaxone, cefotaxime, cefixime, cefdinir, ceftazidime)

•

Broad spectrum, excellent activity against gram-negative bacteria

•

Generally less activity against gram-positive organisms than earlier generations, such as methicillin-susceptible S. aureus.

•

Very high blood and CSF levels achievable in relation to minimal inhibitory concentration for bacterial strains

•

Wide therapeutic index with generally minimal toxicity (similar to previous generations)

•

Some offer single-daily dosing

•

Ceftazidime: the first cephalosporin with antipseudomonal coverage

•

More expensive

347
Q

What are the two primary mechanisms of resistance to β-lactam antibiotics?

A

Penicillin-binding proteins (PBPs)

β-Lactamase

348
Q

What is the most common cause of death in children with whooping cough?

A

Ninety percent of deaths are attributable to pneumonia, which most often develops as a secondary bacterial infection

349
Q

What is the classic triad of malaria?

A

Spiking fevers, anemia, and splenomegaly.

Malaria is caused by species of Plasmodium (transmitted by the Anopheles mosquito), which infect red blood cells (RBCs); certain species (particularly P. vivax and P. ovale) can have a dormant liver stage. The classic malarial fever involves a periodicity (typically 48 to 72 hours) associated with the rupture of RBCs. Chills, headache, abdominal pain, and myalgias are also common symptoms.

350
Q

How is malaria diagnosed?

A

Thick and thin blood smears.

351
Q

How is the diagnosis of congenital syphilis made?

A

All pregnant women and infants should be screened for possible infection with a nontreponemal test for Treponema pallidum. Such tests include the rapid plasma reagin card test (RPR) and the Venereal Disease Research Laboratory (VDRL) slide test.

If blood from the mother or infant yields a positive nontreponemal serologic test, a specific treponemal test should be performed on the infant’s blood. Examples include the fluorescent treponemal antibody (FTA) absorption test and the microhemagglutination test for T. pallidum.

352
Q

Periodic fever syndromes

353
Q

What drugs are recommended for reducing the maternal-to-infant transmission of HIV?

A

All HIV-exposed newborn infants should receive zidovudine (AZT) at a dose of 4 mg/kg orally every 12 hours for the first 6 weeks of life.

Elective cesarean delivery is also recommended for women with high HIV loads.

354
Q

What are the risk factors for perinatal transmission of HIV?

A

AZT monotherapy during pregnancy (compared with combination antiretroviral therapy)

High maternal viral load at or near delivery

Rupture of membranes > 4 hours before delivery

Fetal instrumentation with scalp electrodes and forceps

Vaginal delivery (especially with high maternal viral loads)

Episiotomies and vaginal tears

Prematurity and low birth weight (possible impaired fetal or placental membranes)

Concurrent maternal HSV-2 infection (increased shedding of HIV in genital secretions)

Breastfeeding

Incidence of HIV during pregnancy and postpartum

355
Q

What is the natural course of serologic responses to EBV infection?

A

Acute infection is best characterized by the presence of high titers of VCA IgM or IgG with or without high titers of EA and with no or low titers of EBNA

356
Q

Valganciclovir monitoring?

A

CBC and Creatinine

ANC<0.5:STOP

LT Hearing and neurocognitive

357
Q

Toxoplasmosis treatment

A

Treat with pyrimethamine in combination with sulfadiazine (supplemented with leucovorin) for 1 yr.

358
Q

Diarrhea incubation periods?

A

Salmonella: 6-72 hrs

Campylobacter: days with abd pain that mimics appendicitis or intussusception

Ecoli is 2-3 days

Yersinia enterolitica: 4-6 days

Shigella: 2-4 days (spread person-person)

359
Q

HIV prevention of transmission?

A
  1. Screening in rpegnancy
  2. ARV in MOm
  3. Ziovudine intrapartum
  4. C/s
  5. Baby ziodovudine x 6 eeks
  6. No BF
360
Q

Canada notifiable diseases

A

Acute flaccid paralysis, AIDS, Anthrax, botulism, brucella, campylobacter, genital chlamydia, cholera, CJD, cryptosporidiosis, cyclospora, diphtheria, giardia, GBS disases of the newborn, hantavirus pulmonary syndrome, Hepatitis A,B,C, HIV, Influenza, Invasive HIb, Invasive GAS, Invasive pneumococcal or meningococcal disease, Legionella, leprosy, malaria, measles, mumps, pertussis, polio, rabies, rubella, salmonella, Shigella, smallpox, syphilis, tetanus, TB, tularaemia, typhoid, E.coli 0157:H7, west nile infections

361
Q

Lateral Xray measurements

A
  • Swelling of prevertebral tissue < 7mm at C2
    < 5 mm at C3-4
    < 40% AP diam of vert body
    < 14 mm at C6

Loss of cervical lordosis

362
Q

PEDIACEL®

A

DTaP
-IPV
Hib

363
Q

PNEUMOVAX® 23

364
Q

Prevnar® 13

365
Q

Menveo

A

Men-C-ACYW-CRM

366
Q

Menjugate®

A

Men-P-ACYW-135

367
Q

Menactra®

A

Men-C-C-CRM

368
Q

DtaP-IPV-HIB

A

2,4,6, 12/18

369
Q

DtaP-IPV

370
Q

Tdap

A

10 year post last dose

Approx 14-16

371
Q

Rota

A

2 or 3 doses

Complete before 8 months

372
Q

Men C-C

373
Q

pneuC-13

A

2/4/12 for 3 dose

2/4/8/12-15M for 4 dose

374
Q

Men C ACYW

A

12 years (Either mono or quad)

375
Q

MMR and V

A

12-15

18M or no later than school entry

376
Q

HepB

A

Either 0/1/6 OR

three doses at 12

377
Q

HPV

A

Girls 9-14

0/1/6

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