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SB_Infectious Disease (Pediatrics Royal College 2018) > ID (To be sorted) > Flashcards

ID (To be sorted) Flashcards

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1
Q

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

A

CMV: periventricular calcificationsToxoplasmosis: calcifications scattered throughout cortex

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2
Q

What are clinical features of congenital CMV infection?

A

Cataracts Purpuric rash (“blueberry muffin”)Seizures from CMV CNS lesionsHepatosplenomegalyIUGRMicrocephalyProlonged neonatal jaundice

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3
Q

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

A

Humoral: B-cellCellular: T-cell

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4
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)

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5
Q

What is a soft tissue complication of varicella infection?

A

GAS invasive soft-tissue infection: necrotizing fasciitis, myositis, cellulitis, toxic shock syndromeTreatment: Penicillin and clindamycin

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6
Q

What is the classical triad of Wiskott-Aldrich syndrome?-Complications (2)-mode of inheritance

A

Classic triad (in 1/3 of patients):1. Eczema2. Thrombocytopenia3. ImmunodeficiencyComplications:1. Immunodeficiency: -T and B cell function is reduced-recurrent pneumonia/otitis media/sepsis/meningitis/sinusitis-progressive-can have hepatomegaly2. Risk of malignancy (10-20%)-leukemia/lymphomaMode of inheritance: -X-linked

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7
Q

How do neonates with Wiskott-Aldrich usually first present?

A

Present at birth with thrombocytopenia features: bruising, petechiae, bloody diarrheaEczema by 1st month of life, recurrent infections by 3 months of life

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8
Q

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

A

IgA & IgE: elevatedIgM: reducedIgG: normal, reduced or elevated

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9
Q

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

A
  1. CBC + diff2. Blood culture3. Bag for urine –> cath if positive
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10
Q

In febrile patients, when should a UA always be ordered? (5)

A
  1. All boys age
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11
Q

What is the definition of a UTI?

A
  1. Urine with > 10 wbc/hpf2. Colony count of single organism > 50,000/ml***Remember that if child has been symptomatic
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12
Q

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

A

> 95%

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13
Q

Clinical presentation of lyme disease (6)?

A
  1. Arthritis2. Erythema migrans: painless, annular, central clearing, minimum size 5 cm3. Aseptic meningitis4. Cranial nerve palsies5. Heart block6. Ocular involvement
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14
Q

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

A
  1. Dysuria2. Penile dischargeMost common etiology: Chlamydia trachomatis (3x more common than Neisseria gonorrhoeae)
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15
Q

What is the best test for chlamydia and gonorrhea?

A

Urine PCR

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16
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 gonorrhea2. Instruct patients to abstain from sexual intercourse x 1 wk after single-dose therapy and until all partners are treated to prevent reinfection3. Test for other possible STIs (syphillis, HIV, hepatitis, etc.)
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17
Q

What is a possible GI side effect of ceftriaxone?

A

Increased gallbladder sludge and subsequent cholelithiasis

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18
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

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19
Q

What are the possible causes of retropharyngeal abscess?

A
  1. Localized infection of oropharynx extending to the retropharyngeal lymph nodes2. Penetrating trauma3. Vertebral osteomyelitis4. Dental infection
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20
Q

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

A

Most common in children

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21
Q

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

A

Think upper airway obstruction!1. Respiratory distress2. Stridor3. Drooling4. Fever5. Refusal to eat6. Obstructive sleep apnea7. Neck stiffness/torticollis

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22
Q

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

A
  1. Acute epiglottis2. Lymphoma3. Meningitis (if neck stiffness present)4. Foreign body aspiration5. Vertebral osteomyelitis
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23
Q

What is the underlying bacterial etiology of retropharyngeal abscess?

A

Polymicrobial! Most commonly:1. GAS2. Staph aureus3. Oral anaerobes

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24
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 drainageIndications for surgical drainage:1. Respiratory distress2. Failure to improve with IV abx

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25
Q

What are 4 complications of retropharyngeal abscess?

A
  1. Significant upper airway obstruction2. Rupture leading to aspiration pneumonia3. Extension into mediastinum4. Thrombophlebitis of internal jugular vein
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26
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

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27
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

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28
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

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29
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

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30
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)

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31
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. HSV2. Varicella3. CMV
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32
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

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33
Q

Which medications are contraindicated in infantile botulism?

A

Aminoglycosides! Worsen neuromuscular blockade

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34
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 rupture2. Encephalitis3. Hemolytic anemia/thrombocytopenia4. Airway obstruction5. Malignant association: Burkitt lymphoma, Hodgkin disease, etc.

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35
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)-in children

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36
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:2. Parinaud oculoglandular syndrome: inoculation of eyelid conjunctiva –> conjunctivitis and ipsilateral preauricular lymphadenopathy3. Liver and spleen granulomas4. EncephalitisImmunocompromised:5. Bacillus angiomatosis: proliferation of blood vessels –> tumor like masses in skin and organs

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37
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

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38
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

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39
Q

What is the definition of AIDS?

A
  1. CD4 count 200 or less in a patient with HIVOR2. The presence of an opportunistic infection in a patient with HIV
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40
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.
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41
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 inhibitors4. Fusion inhibitors-use combination of 3 or 4 agents from at least 2 classes
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42
Q

What are the complications of influenza infection? (5)

A
  1. Pneumonia with staph aureus, strep pneumo, GAS2. Otitis media3. Myocarditis4. Encephalitis5. Guillain Barre syndrome
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43
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 fever2. Chills3. 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)

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44
Q

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

A
  1. Clinical status of patient: non-severe vs. severe2. Plasmodium species 3. Drug susceptibility of the infecting parasite
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45
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, hemoglobinuria2. ARDS3. DIC4. Renal failure5. Impaired consciousness6. Parasitemia > 6%-continue therapy until parasite level

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46
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

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47
Q

When is a person with measles contagious?

A

5 days prior to onset of rash to 4 days after

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48
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. Cough2. Conjunctivitis3. 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

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49
Q

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

A
  1. Pneumonia2. Croup3. Otitis media4. Subacute sclerosing panencephalitis-rare degenerative encephalitis characterized by dementia and intellectual deterioration with seizures occurring many years after initial infection (11 yr on average)
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50
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 women2. Immunocompromised3. Infants

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51
Q

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

A
  1. Africa2. Asia3. South America
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52
Q

Which population of people resist are immune to malaria?

A

Hemoglobin S - sickle cell anemia patients

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53
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 stream2. 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.
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54
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

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55
Q

What do you see on gram stain for Neisseria meningitidis?

A

Gram negative diplococci

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56
Q

What 2 age groups are most commonly affectd by Neisseria meningitidis?-which are the common serotypes causing disease?

A

Children

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57
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

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58
Q

What is Waterhouse Friederischsen syndrome?

A

Diffuse adrenal hemorrhage secondary to meningococcemia infection

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59
Q

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

A
  1. Anatomical or functional asplenia2. Children with primary antibody deficiency disorders3. Children with complement, properdin or factor D deficiency4. Travellers to areas endemic for meningococcus5. Lab personnel with exposure to meningococcus6. Military
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60
Q

What are complications of mumps? (5)

A

Mumps = paramyxovirus, mainly causing parotitis (inflammation of salivary glands)1. Meningoencephalitis2. Orchitis3. Arthritis4. Myocarditis5. Pancreatitis

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61
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 transfusions

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62
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 d2. 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 vomiting4. Convalescent stage: gradual resolution of symptoms-infants

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63
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

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64
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 yo2. Immunize adolescents with booster with single dose of Tdap
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65
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

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66
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

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67
Q

What are the complications of pertussis? (5)

A
  1. Secondary pneumonia2. Apneas3. Pulmonary hypertension4. Acute otitis media5. Physical sequelae from forceful coughing: scleral hemorrhage, petechiae, laceration to frenulum
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68
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

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69
Q

What are the clinical features of rabies?

A

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

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70
Q

What seen on histology is the hallmark of rabies?

A

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

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71
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 tissue2. Can take skin biopsy specimens of the patient or isolate the virus from saliva
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72
Q

What is the treatment for rabies?-what do you use for postexposure prophylaxis?-when would you give postexposure prophylaxis?

A

In people who are bitten, should give postexposure prophylaxis with RIG and administer rabies vaccine immediately to decrease chance of developing rabies UNLESS the animal was a dog, cat or ferret who was healthy and can be observed for 10 days, then prophylaxis can wait-once rabies symptoms have developed, unfortunately no specific treatment available-all animals other than the healthy dog/cat/ferret who can be observed should be caught and euthanized and have its brain tested for rabies

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73
Q

What is the timing of the rabies vaccine?

A

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

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74
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.

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75
Q

How is HPV transmitted?-clinical manifestations?

A
  1. Direct contact2. Autoinoculation3. 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
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76
Q

Which HPV subtypes cause cervical cancer?

A

16, 18

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77
Q

What is the differential diagnosis of genital warts in children?

A
  1. Inoculation during birth through infected birth canal2. Sexual abuse3. Incidental spread from cutaneous warts***significant proportion of genital warts in children contain HPV types that are usually isolated from cutaneous warts
78
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

79
Q

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

A
  1. Atopic dermatitis2. Allergic rhinitis3. Asthma*NOT parasites :)
80
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, eyes2. 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 muscle3. Hookworm4. 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 victim5. Strongyloidiasis: roundworm infection

81
Q

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

A

Hookworm infection - causes microscopic blood loss

82
Q

What 2 fungal diseases can cause eosinophilia?

A
  1. Aspergillosis in the form of ABPA2. Coccidiodomycosis
83
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 13. Ciprofloxacin (for > 18 yo)-pregnant women: rifampin and cipro is contraindicated - use ceftriaxone
84
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)

85
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

86
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

87
Q

What is the treatment for Hep A?

A

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

88
Q

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

A

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

89
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 immunoglobulinGive post-exposure prophylaxis if

90
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 immunization2. HBV DNA PCR will then become positive3. 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

91
Q

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

A

-Acute hep B: supportive care-Chronic hep B: interferon alpha or lamivudine

92
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/arthralgia3. 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

93
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 STOMATITISPharyngitisAdenitis (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

94
Q

What are clinical features of TRAPS?-mode of inheritance?-complication?-treatment?

A

TNF-receptor-associated periodic syndrome-periodic fever lasting 1-3 weeks, with abdominal pain, pleuritis, rash, myalgias, EYE involvement (periorbital edema, conjunctivitis)-mode of inheritance: AD-complication: amyloidosis-treatment: steroids

95
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

96
Q

What are the 4 common periodic fever syndromes?

A
  1. PFAPA: most common2. TRAPS (TNF-receptor associated periodic syndrome)3. Hyper-IgD syndrome4. Familial mediterranean fever syndrome
97
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 clockworkFamilial 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

98
Q

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

A

Infections:1. Campylobacter2. Mycoplasma pneumoniaeVaccines:1. Rabies2. Influenza3. Oral polio4. Conjugated meninococcal vaccine (serogroup C)

99
Q

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

A

High risk children > 2 yo:1. Asplenia2. Sickle cell disease3. Antibody deficiencies4. HIV infection5. Chronic lung, heart, kidney disease6. Diabetes mellitus

100
Q

What is the most common congenital infection?

A

CMV

101
Q

What is the most common outcome of congenital CMV infection?

A

Sensorineural hearing loss (58%)

102
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&raquo_space; tooth discoloration in children

103
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 sepsisChlamydial 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

104
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 daysC. trachomatis: onset 5-14 days

105
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

106
Q

What are the clinical stages of syphilis?

A
  1. Primary: painless, single genital ulcer (chancre) appearing 3-6 wks after inoculation2. Secondary: follows 6-8 wks later with fever, generalized lymphadenopathy (especially inguinal), disseminated maculopapular rash on body/palms/soles, condylomata lata, mucous membrane lesions3. Tertiary syphilis: does not happen in children; involves cardiovascular, neurologic and msk systems4. Latent syphilis = asymptomatic infection a. Early latent: acquisition within the preceding yearb. late latent: acquisition within unknown duration
107
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 GLate syphilis: IM doses of benzathine pen G x 3 at weekly intervalsNeurosyphilis: IV aqueous crystalline pen G x 10-14 d

108
Q

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

A
  1. HSM2. Snuffles (rhinitis)3. Lymphadenopathy4. Copper rash on palms/soles/perioral/perianal5. Pneumonia6. Osteochondritis
109
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 deformity6. Frontal bossing7. Clutton joints (symmetrical joint swelling, usually in knees)

110
Q

What is Hutchinson’s triad?

A
  1. Interstial keratitis2. 8th cranial nerve palsy3. Hutchinson teethIndicative of congenital syphilis
111
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)
112
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

113
Q

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

A
  1. S. aureus2. GAS
114
Q

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

A
  1. non-TB mycobacteria2. Bartonella henselae
115
Q

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

A
  1. Staph aureus2. Coag neg staph
116
Q

When do you treat campylobacter with antibiotics? (4)-choice of abx?-resistent to which drugs/

A
  1. High fever2. Severe diarrhea3. Immunocompromised4. Toxic-treatment: Azithro or erythro PO, IV gent, tobra or meropenem-resistant to penicillins, cephalosporins, vanco
117
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

118
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 downwards2. Fever3. Pharyngitis4. Conjunctivitis5. Lymphadenopathy6. Transient arthropathy7. Forckheiner spots: rose-colored spots on oropharynx -period of infectivity 6 days pre rash up to 6 days post rash-CNS complication: rubella panencephalitis

119
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)

120
Q

What is the triple therapy for H. Pylori?

A
  1. Clarithro + amoxil OR flagyl + PPI
121
Q

What are 2 organisms that are transmitted via cat bites?

A
  1. Pasteurella2. Eichenella
122
Q

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

A

PDA

123
Q

How long do children with congenital rubella syndrome stay infectious?

A

Shed virus in urine/stools x 1 year

124
Q

When do you treat salmonella infections?

A
  1. Infants meningitis
125
Q

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

A
  1. Absence of fever2. Eosinophilia3. Cough4. Bilateral interstitial markings-treatment: erythromycin
126
Q

What are 3 viral causes of erythema nodosum?-common bacterial causes? (5)-common fungal causes? (3)-other causes?

A

Viral:1. Hep B2. EBV3. MumpsBacterial:1. Mycoplasma2. Bartonella henselae3. GAS4. Yersinia5. TBFungal:1. Histoplasmosis2. Blastomycosis3. CoccidiocomycosesOther causes:1. OCP2. Sulfa drugs3. SLE4. IBD

127
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-C2. MCV-4: conjugate quadrivalent serogroup: A/C/Y/W135-brand names: menactra, menveo3. 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&raquo_space;> polysaccharide vaccines in inducing an immune response
128
Q

Worst prognosis of HIV occurs with which complication?

A

PCP infection

129
Q

For a child

A

5 mm is positive

130
Q

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

A
  1. Peripheral neuropathy: prevent by giving pyridoxine (vit B6)2. Elevated liver enzymes
131
Q

What TB medication causes retrobulbar neuritis?

A

Ethambutol

132
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

133
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

134
Q

What 2 antibiotics can be used to treat chlamydia trachomatis?

A
  1. Azithromycin2. Doxycycline
135
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 yo2. Sphenoid: complete by 5 yo3. Frontal: begins at 3-7 years of age, complete by age 12 years
136
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 bites3. 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
137
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 smile3. Opisthotonos when abdo/lumbar/hip/thigh muscles are involved4. Laryngeal and resp muscle spasm = airway obstruction/asphyxiation5. Fever due to sustained muscle contraction (increased metabolic rate)6. Autonomic effects: tachycardia, dysrhythmias-lasts up to 4 wks7. 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!
138
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

139
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 yet2. Surgical wound debridement3. Antibiotics: Pen G x 10-14 d4. Muscle relaxants: diazepam or rocuronium (flaccid paralysis, requires I&V but at least gives muscles a break)5. Supportive care
140
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

141
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 TIGB) 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)

142
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 reactivationB) 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 regimenC) TB with HIV coinfection-extend isoniazid + rifampin to 9 mo totalD) 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

143
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%)

144
Q

What are the 2 categories of TB infection?

A
  1. Latent: positive TST but asymptomatic and normal CXR2. Active TB: TB infection with symptoms and radiologic findings
145
Q

What is the most common form of extrapulmonary TB?

A

TB lymphadenopathy

146
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)

147
Q

What is Pott disease?

A

TB in the spinal vertebrae

148
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

149
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

150
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

151
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 TB4. Close contact of active contagious case within 2 years5. Abnormal CXR with fibronodular disease6. End stage renal disease->10 mm: all other cases

152
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

153
Q

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

A
  1. Liver enzymes (AST, ALT)2. Bilirubin3. HIV serology4. Baseline ophtho assessment in younger children (due to risk of retrobulbar neuritis due to ethambutol)
154
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 diets2. Adolescents who are breastfeeding or pregnant3. Children with nutritional deficiencies4. Symptomatic HIV infection5. Breastfed infants
155
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

156
Q

In infants and children

A

40%

157
Q

How would you treat the following:1. TB exposure, > 4 years old and immunocompetent2. TB exposure

A
  1. TB exposure in > 4 yo and immunocompetent:-no treatment-TST now and repeat 2-3 mo after contact with source case is broken (since incubation period before TST will become positive is 3 wks - 3 mo)-further treatment will be based on TST results +/- symptoms +/- CXR findings2. TB exposure in
158
Q

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

A
  1. Air fluid level in retropharyngeal space2. Increased width of retropharyngeal space
159
Q

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

A
  1. Meningitis2. Lateral sinus thrombosis3. TM perf4. Intracranial abscess5. Hearing loss6. Cholesteatoma***Chronic suppurative otitis media: purulent drainage from perforated tympanic membrane > 6 wks
160
Q

What are the indications for tympanostomy tubes?

A
  1. Failed antibiotics for recurrent AOM2. Chronic otitis media3. Tympanic membrane retraction with ossicular erosion or cholesteatoma formation
161
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-retropharyngeal abscess:

162
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

163
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

164
Q

What is the treatment for PCP pneumonia?

A

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

165
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)

166
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

167
Q

What is the underlying organism causing traveler’s diarrhea?

A

Enterotoxigenic E coli

168
Q

What is the principle reservoir of Yersinia?

A

Pigs!

169
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

170
Q

What is the management of necrotizing fasciitis?

A

Emergent surgical debridement with antibiotic therapy

171
Q

What is the msot common organism causing VP shunt infections?

A

Coag-negative staph

172
Q

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

A

Chlamydia: Erythromycin PO x 14 dGonorrhea: Ceftriaxone x 1 dose

173
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)

174
Q

What is the diagnostic criteria for toxic shock syndrome?

A

Need all 3 major criteria:1. Acute fever2. Hypotension3. Erythroderma with convalescent desquamation rash-AND-3/7 minor criteria1. 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)

175
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

176
Q

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

A

Varicella

177
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

178
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)

179
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

180
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 symptomsKEY: 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, feverCan 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

181
Q

What is the treatment for leptospirosis?

A

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

182
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

183
Q

What are the clinical features of Rocky Mountain Spotted Fever?-how is this infection transmitted?-treatment?

A

Classic triad: fever, headache, rash1. Prodromal period with headache, malaise, pain and tenderness of calf muscles in children is very common2. Abrupt onset of fever and chills3. 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!

184
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 moistBare foot = staph aureus since it is bare skin

185
Q

What are 3 common complications of staphylococcal pneumonia?

A
  1. Pleural effusion2. Empyema3. Pyopneumothorax
186
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

187
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

188
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

189
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 vaccinePregnant women and immunocompromised:-check VZV IgG serologies, -If negative, give VZV IgG since they cannot receive the vaccine

190
Q

What is considered a positive TST?

A

> 5 mm IF:1. exposed to a close contact with known or suspected TB2. clinical symptoms of TB3. immunocompromized (HIV) or on immunosuppressants> 10 mm IF:1. 15 mm IF:-any child > 4 yo without any other RFs

SB_Infectious Disease (Pediatrics Royal College 2018) (10 decks)

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