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Micro Exam 2 > Freji: Perinatal and Pediatric Infections > Flashcards

Freji: Perinatal and Pediatric Infections Flashcards

1
Q

Cytomegalovirus (CMV)

Structure:
Genome:

A

Structure: enveloped, dsDNA virus

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2
Q

Cytomegalovirus (CMV)

What happens after primary infection?
How is it spread?

A

Persists after primary infection: in low-grade chronic or latent states with periodic reactivation

Transmission: spread of infected oropharyngeal secretions, sexual intercourse, blood transfusions or mother to fetus spread (transplacental)

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3
Q

Maternal CMV Infection

What can happen to pregnant women?
Where can they shed CMV from?

A

Many adults in the population have Abs to CMV, however, pregnant women can have a primary infection

Pregnant women can shed CMV from cervix, urinary tract, throat, and in breast milk post-partum

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4
Q

Primary CMV Infection in Pregnancy

How many are symptomatic?

What symptoms? (4)

A

Most are asymptomatic (~90%)

Symptomatic cases present with many symptoms, including:
o	Infectious mononucleosis
o	Hepatitis
o	Thrombocytopenia
o	Myocarditis
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5
Q

Primary CMV Infection in Pregnancy

How often does transmission of CMV to fetus occur in mothers infected for the first time?

A

Transmission of CMV to fetus occurs ~50% of the time in mothers infected for the first time during pregnancy

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6
Q

Primary CMV Infection in Pregnancy
Diagnosis

Isolate virus from what?
Measure what type of abs?
Rapid diagnosis via what?

A

Isolate virus from urine, buffy coat or cervical secretions

Measure anti-CMV IgM antibodies (indicates primary infection)

Rapid diagnosis using PCR (can perform on any tissue- urine, blood, CSF etc.)

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7
Q

What percentage of live births have congenital CMV?

A

~1% of live births: however, only a small amount of these are symptomatic at birth

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8
Q

Congenital CMV

Diagnosis:

A

Isolation of CMV from urine or saliva within the first 2 weeks of life

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9
Q

Symptomatic Congenital CMV

Mortality Rate:

Common Findings:

Neurological abnormalities:

***Sensorineuronal hearing loss:

A

Mortality Rate: 15-30%; most survivors have long-term sequelae

Common Findings: petechiae, jaundice, hepato- and splenomegaly, thrombocytopenia, conjugated hyperbilirubinemia

Neurologic abnormalities: microcephaly, seizures, hypotonia, intracranial calcifications

Sensorineuronal hearing loss: most common cause of non-genetic congenital hearing loss

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10
Q

Symptomatic Congenital CMV

Eye abnormalities:
- Most frequent

Dental Defects

Urinary CMV shedding:

Treatment:

A

Eye abnormalities: chororetinitis most frequently; also optic atrophy, micopthalmia and cloudy cornea

Dental defects

Urinary CMV shedding: continues for months or years

Treatment: Ganciclovir in symptomatic CMV infection

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11
Q

Asymptomatic Congenital CMV

What percent?
Can follow what?
What continues for months or years?

A

90%

Can follow primary or reactivate CMV infection in the mother

Urinary CMV shedding: continues for months or years

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12
Q

Asymptomatic Congenital CMV

Is there hearing loss?
Mental/behavioral problems?
Antiviral therapy:

A

Sensorineural hearing loss: found less often than in symptomatic CMV

Mental or behavioral problems: seen in some cases

Antiviral therapy NOT recommended

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13
Q

Perinatal CMV

How is it acquired?
Are most cases symptomatic or asymptomatic?

A

CMV is acquired during passage through infected birth canal or by ingestions of CMV-positive breast milk

Most cases are asymptomatic

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14
Q

Perinatal CMV

What is the most common clinical illness?
Long term hearing loss?

A

Most common clinical illness: self-limited infantile pneumonitis (can be severe in premature infants)

No long-term hearing or neurologic deficits

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15
Q

Maternal HSV Infection During Pregnancy

What percentage of infected women will have symptoms?

What happens if infection occurs shortly before delivery?

When can asymptomatic shedding occur?

A

Only 1/3 of women infected with HSV during pregnancy will have symptoms

If infection occurs shortly before delivery, ~50% of newborns will get infected (not enough Ab to pass on yet)

Asymptomatic shedding: can occur in pregnant women at or near term (most common type of shedding)

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16
Q

Neonatal HSV

What is the usual route of infection?
Risk of vertical Transmission:

A

Transmission: intrapartum is usual route; can also occur via transplacental spread as well

Risk of Transmission: much higher for mothers with primary HSV infection than those with recurrent infection

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17
Q

Neonatal HSV

Risk Factors: (6)

A

o Cervical HSV infection
o Multiple genital lesions
o Prematurity
o Prolonged rupture of maternal membranes
o Intrauterine instrumentation
o Low/absent titers of maternal neutralizing Ab (which normally blocks virus action)

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18
Q

Intrauterine HSV

What happens in intrauterine HSV infections?
Hallmarks:
Associated abnormalities:
Mortality rate:

A

Intrauterine HSV Infections: baby born already sick; only small percentage of neonatal cases

Hallmarks: vesicular rash present at birth/appears shortly after

Associated Abnormalities: microcephly, chorioretinitis, microphthalmia, intracranial calcifications, seizures

High Mortality Rate: ~50%; survivors have long-term complications

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19
Q

Clinical Manifestations of Neonatal HSV

How common is asymptomatic infection?
Three Presentations:

A

Asymptomatic Infection: very rare

  1. Skin/Eyes/Mucous Membranes (SEM)
  2. Localized CNS Involvement (Encephalitis)
  3. Disseminated Disease
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20
Q

Neonatal HSV
Skin/Eyes/Mucous Membranes (SEM)

Cutanteous lesions:
Eye disease:
Mouth:
Neurological abnormalities:

A

Cutaneous Lesions: discrete vesicles, large bullae, or denuded skin (10-11 days old)

Eye Disease: keratoconjunctivitis and chorioretinitis

Mouth: ulcerative lesions

Neurological Abnormalities: can develop in some, although CNS involvement was not evident during acute illness

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21
Q

Neonatal HSV
Localized CNS Involvement (Encephalitis)

Symptoms: 
What makes it difficult to diagnose?
CSF:
Mortality:
- What do survivors have?
A

Symptoms: focal or generalized seizures, lethargy, or apnea

Skin lesions often absent: makes it hard to diagnose

CSF: mononuclear pleocystosis and elevated protein

Mortality Rate: fairly high; survivors have long-term sequelae (a small number have a CNS relapse within one month of completing therapy)

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22
Q

Neonatal HSV
Disseminated Disease

Presents similar to:
Usual age at presentation:
How often is the CNS involved?

A

Presentation: similar to sepsis patient (around age 9-11 days)

CNS involvement: only in about 2/3 of cases

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23
Q

Neonatal HSV
Disseminated Disease

Other infected organs:
Mortality:

A

Other severely infected organs: adrenal glands, GI tract, liver, pancreas, heart, and kidneys

High mortality rate: over 50% even with therapy; majority of survivors have severe neurologic impairment

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24
Q

HSV

Treatment:

A

Treatment: acyclovir (almost always) or vidarabine

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25
HSV Prevention If there are signs at the onset of labor: Late in pregnancy for women with frequent genital recurrences:
C-section for women with signs and symptoms suggestive of genital HSV at onset of labor (as long as membrane rupture is not greater than 4-6 hours) Oral acyclovir or valcyclovir given late in pregnancy for women with frequent genital recurrences (in practice, many more than just this receive this therapy)
26
HSV Diagnosis What does PCR detect?
Isolate virus from vesicular lesions or CSF PCR: detects HSV DNA in CSF, blood and skin lesions (very sensitive and test of choice)
27
Varicella | General:
Highly communicable and usually benign disease of childhood 95% of women have Abs to VZV
28
Varicella Typical Illness: (3) Rash:
Typical Illness: fever, malaise, pruritic rash Truncal rash characterized by crops of maculopapules that evolve in to vesicles, which eventually crust over (presence of lesion in various stages of evolution)
29
Varicella Complications: What population is more likely to have complications?
Complications: bacterial superinfection (most common), pneumonia, arthritis, encephalitis, bleeding diathesis Adults are more likely to have complications
30
*Zoster (General)* Rash: Pain in adults vs children
Rash: unilateral, usually follows distribution of one or more sensory nerve roots (shingles) - Follows same evolutionary pattern as varicella Painful in adults; not so much in kids
31
Varicella Zoster Diagnosis: How is the laboratory confirmation possible?
Diagnosis: usually done clinically with laboratory confirmation rarely being needed Laboratory confirmation possible via: o Recovery of virus from vesicle fluid or detection of VZV Ags from base of fresh vesicles o PCR detecting VZV DNA (most common now)
32
Fetal Varicella Syndrome Cause: When does it occur?
Cause: occurs after maternal chicken pox during the first 20 weeks of pregnancy (although risk of transmission is small)
33
Fetal Varicella Syndrome Clinical Findings: (6)
o Cutaneous scars, denuded skin o **Limb hypoplasia: usually unilateral; most commonly leg** o Shingles during infancy o CNS abnormalities: microcephaly, seizures, focal brain calcifications o Ocular abnormalities o Autonomic dysfunction: dysphagia, loss of urinary or bowel sphincter control
34
Neonatal Varicella Syndrome | Cause:
Most often due to maternal chickenpox during the last 3 weeks of pregnancy (no Abs transferred to help)
35
Neonatal Varicella Syndrome How many days of maternal varicella before delivery for severe infection? Mortality: How many days of maternal varicella before delivery for mild infection?
Maternal infection within 5 days of delivery and 2 days after delivery: may be mild but can become severe (fever, hemorrhagic rash, generalized visceral involvement) - Mortality high for severe infection: ~30%; usually due to pneumonia Infection 5-21 days before delivery: illness usually mild
36
Neonatal Varicella Syndrome Treatment: Prevention:
Treatment: acyclovir Prevention: infants born to mothers who develop varicella 5 days before or 2 days after delivery should receive 125 units of varicella zoster immune globulin ASAP
37
Maternal B19 Infection Source: In what instances are there higher rates of infection?
Source: infected respiratory secretions or blood transfusions (uncommon) Higher rates of infections in some women: school teachers, healthcare workers, homemakers
38
Maternal B19 Infection What % are asymptomatic? What symptoms are seen in kids? Adults?
Asymptomatic: ~20% Erythema infectiosum (slapped cheek appearance; most common, usually seen in kids) Influenza-like illness and symmetric polyarthropathy (in adults)
39
Maternal B19 Infection | Chronic Condition: (3)
Anemia Transient aplastic crisis Hemophagocytic syndrome
40
What can serious fetal B19 infection lead to?
Serious infection that can result in death: | - Hydrops fetalis, spontaneous abortion, or stillbirth possible after maternal infection during pregnancy
41
How does fetal B19 infection lead to chronic anemia? How does fetal B19 infection affect the heart?
Chronic anemia (B19 suppresses fetal bone marrow RBC production) Cardiac dysfunction (direct infection of fetal heart muscles possible)
42
Parvovirus B19 Infection Diagnosis What is seen by day 3? What is seen by the end of the first week? What does PCR detect?
B19 specific IgM (seen by day 3; can persist for up to 4 months) B19 specific IgG (by the end of the first week; persists for life) B19 DNA detected in serum/tissues using PCR
43
Toxoplasmosis What type of protozoan? What are the 3 forms? Hosts: Infects:
Obligate intracellular protozoan 3 forms: tachyzoite, tissue cyst or oocyst Hosts: cats and other felines Infect: humans and other warm blood animals
44
Toxoplasmosis Transmission Ingestion of what? Consumption of: Oocysts from:
Ingestion of oocyst contaminated food or water Consumption of cyst-containing raw/undercooked meat Oocysts from cat litter box material, dust or soil
45
Toxoplasmosis Transmission Other Methods: Intrauterine Transmission:
Other Methods: eating raw infected eggs, blood transfusion, organ transplants from positive donors Intrauterine Transmission: from mother to fetus
46
Maternal Toxoplasmosis Acute infection is most often: Symptoms: Possible complications:
Acute Infection: most often asymptomatic If Symptomatic: lymphadenopathy (head and neck region) is the most common illness; causes a small number of infectious mononucleosis cases Possible Complications: hepatitis, pneumonia, myocarditis, encephalitis, deafness
47
Maternal Toxoplasmosis When is risk of transmission lowest? How severe is the disease in early infection? Risk and severity in Infection Late in Pregnancy:
Infection Early in Pregnancy: risk of transmission is the lowest, but transmission during this time causes the most severe disease Infection Late in Pregnancy: risk of transmission is highest, but disease not as severe
48
Maternal Toxoplasmosis Treatment What is given to reduce risk of infection? If fetal infection occurs, the mother is treated with:
Spiramycin sometimes give to reduce risk of fetal infection If fetal infection occurs, mother treated with pyrimethamine and sulfadiazine (folic acid antagonists)
49
Congenital Toxoplasmosis How many are asymptomatic at birth? Symptomatic disease at birth: How many are born premature? How many are born with severe disease?
At least 2/3 are asymptomatic at birth: but still affected by disease. Symptomatic disease at birth: can be mild, moderate or severe o ~ 50% born premature o Only a small number (10%) are born with severe disease (survivors have major neurologic sequelae)
50
Congenital Toxoplasmosis CNS Symptoms: Eye Symptoms:
CNS Symptoms: vasculitis, thrombosis, infarction of brain tissue, hydrocephalus, intracranial calcifications, hypotonia, microcephaly, seizures Eye Symptoms: chorioretinitis, chorioretinal scars (important), iritis, optic atrophy, cataracts
51
Congenital Toxoplasmosis Sensorineural hearing loss: Other Symptoms:
Sensorineural hearing loss: not as common as in congenital CMV Other Symptoms: hepatosplenomegaly, jaundice, petechiae, purpura, anemia, thrombocytopenia
52
Congenital Toxoplasmosis Diagnosis When should you suspect congenital infe
o Isolation of parasite from placenta or blood o PCR to detect DNA in urine, CSF or serum o Specific IgM Abs o Specific IgG Abs (transferred from mother to fetus; typically drop by ~50% per month- if levels do not fall, suspect congenital infection)
53
Congenital Toxoplasmosis Treatment (3) for 1 year: Who are steroids given to? What is monitored?
Pyrimethamine, sulfadiazine and leucovorin for one year Steroids to treat chorioretinitis or high CSF protein levels Need a lot of monitoring during therapy (platelet count, neutrophil count etc.)
54
Congenital Toxoplasmosis Prognosis What will develop by age 10-20? Recurrence of: What can occur even with treatment?
Regardless of treatment, most will develop chorioretinitis or chorioretinal scars by age 10-20; treatment reduces the severity and frequency of these adverse sequelae Recurrences of ocular toxoplasmosis occur even if treated infants (although less often than untreated) Neurologic problems (hydrocephalus, seizures) can occur even with treatment
55
Sepsis Neonatorum Disease of what population? Early vs Late onset:
General: disease of infants who are less than 1 month of age, are clinically ill, and have positive blood cultures Early Onset: first week of life (often caused by Group B Streptococci and E.coli) Late Onset: after first week of life (often caused by Coagulase-negative Staph picked up in the NICU)
56
Sepsis Neonatorum Early Onset is often caused by:
Often caused by Group B Streptococci and E.coli
57
Sepsis Neonatorum Late Onset is often caused by:
Often caused by Coagulase-negative Staph picked up in the NICU
58
Sepsis Neonatorum Risk Factors: (5)
- Premature labor - Prolonged rupture of fetal membranes - Chorioamnionitis - Maternal fever - Use of arterial and venous umbilical catheters, central venous catheters, or endotracheal tubes
59
Sepsis Neonatorum Symptoms: Lab abnormalities: (3)
Symptoms (Non-Specific): temperature instability (hyper- or hypothermia), lethargy, apnea, poor feeding,tachypnea, vomiting, diarrhea, abdominal distention Lab Abnormalities: abnormal WBC count, unexplained metabolic acidosis, hyperglycemia
60
Sepsis Neonatorum Group B Streptococcal Sepsis Vertical Transmission of GBS Occurance: Result: Prevention of Transmission Prophylaxis:
Vertical Transmission of GBS: occurs often, but does not always result in infant colonization Prevention of Transmission: intrapartum antibiotic (usually penicillin) as prophylaxis in women who are carriers of GBS
61
Early Onset GBS Sepsis How old? Most often in what population? Other risk factors (a lot, just get the gist):
~around 20 hours old Most often in premature infants Other risk factors: low birth weight, early membrane rupture, intrapartum fever, maternal GBS rectovaginal colonization, race (African American), young maternal age (<20) , GBS bacteriuria during pregnancy, previous stillbirth/abortion, previous child with GBS infection
62
Early Onset GBS Sepsis Sudden onset and can be: Where is the primary focus of inflammation? What can also occur? Mortality rate
Sudden onset and can be fulminant (life-threatening) Primary focus of inflammation occurs in the lung (meningitis can also occur) - Respiratory distress, apnea, hypotension, DIC Can be treated so mortality rate not very high (but is inversely related to birth weight)
63
Late Onset GBS Sepsis Age: Symptoms: - What are the most common signs? Presentation:
~2-4 weeks of age Symptoms: insidious onset (poor feeding and fever most common signs) Presentation: bacteremia without specific focus, follow by meningitis
64
Late Onset GBS Sepsis Neurologic deficits: Relapse/Reinfections:
Neurologic deficits: may occur ~1/2 the time after GBS meningitis Relapse/Reinfection: possible but uncommon
65
Epstein-Barr Virus What animals is it found in? How is it spread?
Transmission: only found in humans and spread by intimate contact
66
Epstein-Barr Virus Most common clinical outcome: Other clinical manifestations: - What is the most common if symptomatic?
Most common clinical outcome: NOTHING (most often asymptomatic) Other clinical manifestations: infectious mononucleosis (most common if symptomatic), Burkitt’s lymphoma, nasopharyngeal lymphoma, B-cell lymphoma in immunodeficient children
67
What is infectious mononucleosis caused by?
Epstein-Barr Virus
68
Infectious Mononucleosis | Classic Disease: (5)
Classic Disease: fever, exudative pharyngitis, lymphadenopathy, hepatosplenomegaly, atypical lymphocytes
69
Infectious Mononucleosis | Complications: (6)
Aseptic meningitis, encephalitis, *rupture of spleen (avoid sports)*, hemolytic anemia, myocarditis, thrombocytopenia
70
Infectious Mononucleosis Diagnosis: What can be done quickly? What is reserved for more severe cases?
Diagnosis: o Heterophile Abs (non-specific; can be done quickly) o EBV specific Abs (ie. to viral capsid Ag, early Ag, nuclear Ag; reserved for more severe cases due to increased accuracy)
71
Infectious Mononucleosis Treatment: What are steroids used for?
Treatment: bed rest in acute phase and avoid sports until spleen not palpable Steroids are used for specific problems: to control tonsilar swelling, splenomegaly, hemolytic anemia and hemophagocytic syndrome
72
Human Herpesvirus-6 (HHV-6) What is the symptom in most cases? Transmission:
Most cases are asymptomatic Transmission: infected respiratory secretions
73
Human Herpesvirus-6 (HHV-6) What is the most common symptom in symptomatic cases? When can reactivation occur?
Symptomatic cases: most commonly show up as roseola infantum (exanthema subitum) Reactivation of virus infection can also occur in immunosuppressed patients (BM suppression, hepatitis, pneumonia)
74
Human Herpesvirus-6 (HHV-6) Roseola (Exanthem Subitum) Basics: Type of fever:
Basics: acute febrile illness of infants and young children (6 months-3 years) Fever: abrupt and high spiking, lasts 3-7 days
75
Human Herpesvirus-6 (HHV-6) Roseola (Exanthem Subitum) When does the rash occur? How long does it last? Where does it start? What complication is the most common? Others?
Rash: follows fever; erythematous macular/popular rash that lasts for 2 days, beginning on trunk and spreading outward Complications: febrile seizures most common; others include hemiplegia, encephalopathy, thrombocytopenia purpura
76
Staphylococcal Scalded Skin Syndrome Caused by: Diagnosis: Therapy:
Cause: exotoxin of S.aureus Diagnosis: clinical grounds alone (organism can be isolated from skin or nose but often not needed) Therapy: oral or parenteral Abx; no topical Abx or steroids
77
Staphylococcal Scalded Skin Syndrome Symptoms What often happens to children? Severe Form
Children often febrile and uncomfortable Severe Form: o Bullous desquamation of large areas of the skin o Tender erythroderma (baby will cry if you hold them in attempt to soothe) o Positive Nikolsky sign (separate epidermis from dermis when you drag your finger over the skin)
78
Staphylococcal Scalded Skin Syndrome Symptoms Mild Form:
Mild Form: o Diffuse scarlantiform erythroderma with sandpaper texture (skin is also tender, but not as extreme) o Cracks appear around the eyes and mouth
79
Kawasaki Disease Results from: What is most severely affected?
Disease resulting from blood vessel inflammation (medium size arteries most severely affected- coronary and renal arteries are examples)
80
Kawasaki Disease Classic diagnostic criteria
``` Fever for at least 5 days, AND Four of the following five signs: -Bilateral conjunctival injection without exudate (limbic sparing) -Changes of the oral mucosa -Changes of the hands and feet -Rash -Cervical lymphadenopathy (>1.5 cm), AND Disease not explained by another disease process ```
81
Kawasaki Disease | Treatment for the fever:
Treatment: immunoglobulin IV + high dose aspirin
82
Kawasaki Disease Changes of the oral mucosa Lips: Oral/Pharyngeal mucosa: Tongue: Note: What signs, if present, indicate that it is not Kawasaki?
Lips: erythema, dryness, fissuring, peeling, bleeding Oral/Pharyngeal mucosa: erythema Strawberry tongue Note: if oral ulcers, Koplik spots or exudates present it is NOT Kawasaki
83
Kawasaki Disease Changes of the hands and feet ``` Palms/Soles: Swelling of: Periungual desquamation of: Beau’s Lines: - When? ```
Palms/Soles: erythema Swelling: of hands and feet Periungual desquamation: of fingers and toes Beau’s Lines: transverse grooves across nails (1-2 months after onset of disease)
84
Kawasaki Disease Which of the signs is most likely to be missing?
Cervical lymphadenopathy
85
Kawasaki Disease Clinical Phases Why is it not seen anymore? How long is the acute febrile phase?
Clinical Phases: without treatment (therefore, not seen anymore because usually treated) Acute Febrile Phase: 1-2 weeks
86
Kawasaki Disease | Rash
Rash (often a diffuse maculopapular erythematous rash; vesicles and bullae not seen)
87
Kawasaki Disease Clinical Phases When does subacute phase begin? What usually develop in this phase? How long is the convalescent phase?
Subacute Phase: begins when fever, rash and lymphadenopathy resolve (risk of sudden death the highest) - Aneurysms: usually develop at this stage Convalescent Phase: usually 6-8 weeks after onset of fever
88
Kawasaki Disease Laboratory Features WBC count: ESR and other acute phase reactants: What type of anemia?
- Can have normal or elevated WBC counts - Elevation of ESR and other acute phase reactants - Normocytic anemia
89
Kawasaki Disease Laboratory Features What is uncommon and associated with severe coronary disease and MI? Thrombocytosis seen when? What is urine containing pus?
- Thrombocytopenia (uncommon; associated with severe coronary disease and MI) - Thrombocytosis seen during 2nd and 3rd week - Sterile pyruia (urine containing pus)
90
Kawasaki Disease What age in most cases? Who are at the highest risk?
Most cases in children under 4 years of age (rare <3 months), but can occur in older children and adults Occurs around the world but Asians are at highest risk
91
Kawasaki Disease Cardivascular Manifestations What do many untreated patients develop? What happens to 1/2 of the aneurysms? Other abnormalities:
15-25% of untreated patients develop coronary abnormalities (ie. diffuse dilation or aneursyms) Aneurysms: ~50% resolve, but the rest have persistent aneurysm (can lead to increased risk of MI and stenosis) Other Abnormalities: myocarditis, vavulitis, pericardial effusion, MI
92
Kawasaki Disease Therapy in Acute Phase: When should it be started? Management:
Therapy in Acute Phase: should be started in first 10 days of illness to reduce risk of coronary artery disease o IGIV high dose (often 2 doses needed) + high dose aspirin for the fever Management: follow up echocardiograms, aspirin for life with those with aneurysms

Micro Exam 2 (18 decks)

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