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Infectious Disease > Viral Diseases > Flashcards

Viral Diseases Flashcards

1
Q

What is a virus?

A
  • submicroscopic, obligate intracellular parasite (Can’t survive outside of cell, use host machinery -> can’t replicate or express genes w/o help of living cell)
  • Formed within cells from the assembly of preformed components, whereas other agents reproduce
  • Virons are the complete infective particle and don’t grow. It lacks needed components that cells have to reproduce.
  • No viruses known to have the genetic info needed to produce metabolic energy for replication
  • When a virus infects a cell, it marshals the cell’s ribosomes, enzymes and much of cellular machinery to replicate
  • Viral replication produces many progeny, that when complete, leave the host cell to infect other cells in the organism
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2
Q

What kind of cells do viruses infect?

A
  • all types of living cells - animals, plants and bacteria

- viroids: small circular RNA molecules with a rod like secondary structure that possess no capsid or envelope

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3
Q

What is a virus made of?

A

A virus particle, also known as a vision is essentially a nucleic acid (DNA or RNA) enclosed in a protein shell or coat.
- Viruses are extremely small, approx: 15-25 nm in diameter

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4
Q

Variations in viruses?

A
  • may be dsDNA, dsRNA, ssDNA, or ssRNA
  • The type of genetic material found in a particular virus depends on the nature and function of the specific virus
  • so dsDNA viruses must enter the host cell’s nucleus before it can replicate
  • ssRNA viruses replicate in host cell’s cytoplasm.
  • the genetic material isn’t typically exposed but covered by a protein coat. The viral genome can consist of a very small number of genes or up to hundreds of genes depending on the type of virus
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5
Q

The viral capsid?

A
  • the protein coat that envelopes viral genetic material
  • composed of protein subunits called capsomeres
  • have several shapes: polyhedral, rod, or complex
  • fxn is to protect the viral genetic material from damage
  • in addition to protein coat: some viruses have specialized structures -> the flu virus has a membrane-like envelope around it’s capsid, and the envelope has both host cell and viral components and assists the virus in infecting its host
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6
Q

The process of the viral infection?

A
  • adsorption: virus binds to host cell
  • penetration: virus injects its genome into host cell
  • viral genome replication: viral genome replicates using host’s cellular machinery
  • assembly: viral components and enzymes are produced and begin to assemble
  • Maturation: viral components assemble and viruses fully develop
  • release: newly produced viruses are expelled from the host cell
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7
Q

Key components of current classification system?

A
  • type of symmetry of the virus capsid
  • presence or absence of a lipid envelope
  • type and structure of the viral nucleic acid and the strategy used in its replication
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8
Q

What does hemagglutinin allow viruses to do?

A
  • binds to host cells, this is how viruses can switch b/t strains so they can infect other species -> virulent, lethal to humans -> can become pandemics
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9
Q

What are the Class 1 viruses?

A

HAPP viruses: dsDNA

  • Herpesvirus (cold sores, genital herpes, chicken pox, mono)
  • Adenovirus (resp diseases)
  • Papovavirus (warts, cervical cancer)
  • Poxvirus (small pox, cowpox)
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10
Q

Class II viruses?

A

ssDNA

- parvovirus

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11
Q

Class III viruses?

A 
- dsRNA
coronavirus
picornavirus (polio, common cold)
Togavirus (rubella, yellow fever)
Hep C virus
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12
Q

Class IV viruses?

A

positive ssRNA itself acting as mRNA

  • Rhabdovirus (rabies)
  • Paramyxovirus (measles, mumps)
  • Orthomyxovirus (influenza viruses)
  • Bunyavirus (Korean hemorrhagic fever)
  • Arenaviruses
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13
Q

Class V viruses

A
  • negative ssRNA used as template for mRNA synthesis

Reovirus (diarrhea)

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14
Q

Class VI viruses

A

positive ssRNA with DNA intermediate in replication

- retrovirus (leukemia, AIDS)

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15
Q

Class VII viruses

A

dsDNA with an RNA intermediate in replication

- Hep B virus

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16
Q

Viral exanthematous diseases?

A
  • chickenpox/Herpes zoster
  • infectious mono
  • Roseola infantum (6th disease or Erythema subitum)
  • 5th disesae (Erythema infectiosum)
  • Measles
  • Rubella
  • Enteroviral exanthems: coxsackievirus, echovirus
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17
Q

What does exanthematous disease mean?

A
  • characterized by or of the nature of an eruption or rash
  • the most frequent cause of exanthematous diseases are viral infections, which provoke skin alterations either directly or via the reaction of the immune system
  • in many distinct parainfectious clinical pictures, several viruses from quite different groups are able to produce a specific exanthem
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18
Q

Ddx of exanthematous eruptions?

A
  • Rickettsial infections (tick borne illnesses)
  • Mycoplasma pneumoniae
  • syphilis (hands and soles)
  • typhoid fever
  • bacterial toxins (staph aureus: TSS -> pinpoint rash on abdomen
  • drug eruptions
  • live-virus vaccinations
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19
Q

All of the Human Herpes Viruses?

A 
HHV-1: Herpes Simplex Virus 1 (HSV1)
HHV-2: HSV2 
HHV-3: VZV
HHV-4: EBV (mono: elev lympho)
HHV-5: CMV 
HHV-6: exanthema or Roseola
HHV-7: T-lymphotropic virus
HHV-8: virus assoc with Kaposi's sarcoma (AIDS defining illness)
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20
Q

HSV 1 and 2 generally associated with what?

A

orolabial herpes: typically HSV-1
genital herpes: HSV-2
can affect almost all body tissue
- these are mutlinucleated giant cells, intranuclear inclusion bodies (where viral assembly is taking place)

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21
Q

Epidemiology of HSV

A

> 90% have abs to HSV-1 by age 30
- HSV 2 abs are rare b/f puberty
10-40% of general U.S. adult pop. have HSV-2 abs

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22
Q

Pathophysiology of HSV?

A

virus infects through mucosal membranes or abraded skin

- latent infections are harbored in neuronal cells: in trigeminal ganglia and in pre-sacral ganglia

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23
Q

Clinical presentation of HSV oral-facial lesions?

A
  • dew-drop on a rose petal
  • oral-facial lesions: primary infections: Gingivostomatitis (painful -> swollen lips) and pharyngitis most frequent, this is commonly seen in children and young adults
  • fever, malaise, myalgias, inability to eat, irritability and cervical adenopathy lasts 3-14 days
  • recurrence: Herpes labialis (cold sores)
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24
Q

Clinical presentaion of HSV urogenital lesions

A
  • dew drop on rose petal
  • caused by either HSV-1 or 2
  • systemic: HA, fever, malaise, and myalgia
    local: vesicular lesions of external genitalia with pain, itching, dysuria, vagina and urethral d/c, tender inguinal lymph adenopathy
  • usually present with early, tingly sensation and tenderness in affected area, with low grade fever
  • tx during this time= best results
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25
Q

What is often more severe primary infection or recurrent infections?

A
  • primary infection usually more severe than recurrences but may be asymptomatic
  • vesicles form moist ulcers after several days, and crust over in 1-2 weeks if left unaddressed

recurrences often: involve fewer lesions

  • tend to be labial
  • heal faster
  • are induced by stress, fever, infection, sunlight, chemo, pregnancy
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26
Q

What complications can HSV cause?

A
  • ocular disease (#1 cause of blindness (hepatic keratitis)
  • Neonatal and congenital infections
  • Bells palsy (facial droop)
  • Encephalitis and recurrent meningitis
  • Herpes is most common cause of viral encephalitis in US
  • will see disseminated herpes in immunocompromised (AIDS)
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27
Q

What should be tested during pregnancies?

A 
TORCHS:
To: toxoplasmosis
 R: rubella
 C: CMV
 H: herpes and HIV
 S: syphilis
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28
Q

Dx of HSV?

A
  • usually clinically made
  • clinical dx should be confirmed with lab testing, the dx can be made by viral culture( can’t be crusted over), PCR, Tzanck prep, direct fluorescence AB, and type-specific serologic tests. The choice of test varies with the clinical presentation
  • Viral culture - 50% sensitive
  • real-time HSV PCR: more sensitive to confirm HSV in clinical specimens obtained from genital ulcers, mucocutaneous sites, and CSF (amplifies the virus), its particularly useful for the detection of asymptomatic HSV shedding
  • **There is enhanced sensitivity of HSV PCR compared to viral culture
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29
Q

What is the preferred dx test of HSV?

A
  • PCR assay
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30
Q

Describe the HSV direct fluorescent ab test?

A
  • many dx labs provide a rapid type-specific direct fluorescent ab (DFA) test to detect HSV in clinical specimens. This test is specific and reproducible (have to have an immune response though)
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31
Q
  • What is the HSV serology test?
A
  • type specific abs to HSV develop during the first several weeks after infection and persist indefinitely. The availability of type-specific abs has also facilitated greater accuracy in epidemiological surveys
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32
Q

Tzanck smear for HSV?

A
  • Tzanck smear: may demonstrate the cytopathic effect of the virus (multinucleate giant cells), and can be performed on lesion scrapings from pts with active genital lesions. However it has limited utility since it has low sensitivity and specificity and is only helpful if +
  • furthermore, only a viral culture can determine whether the infection is due to HSV-1 or HSV-2
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33
Q

Management of HSV?

A
  • acute infections: antiviral agents only shorten duration of sxs by 1-2 days (acyclovir, famciclovir, valcyclovir)
  • suppressive therapy: taken daily to prevent reactivation (spendy)
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34
Q

Where will Herpes present?

A
  • can present on fingers (herpetic whitlow)
  • in the mouth -> primary: gingivostomatitis (sores all over mouth)
  • On the cornea (hepatic keratitis)
  • genitals (don’t miss the cervix)
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35
Q

What are the 2 clinical presentations of VZV?

A
  • primary infection: chicken pox

- recurrent infections: Herpes zoster

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36
Q

Epidemiology of VZV?

A
  • humans only known reservoir of VZV
  • primary infection: transmission likely by resp. route
  • recurrent infection: VZV probably infects dorsal root ganglia during primary infection. Mechanism or stimulus for reactivation of latent infection in unknown.
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37
Q

Pathophys of VZV?

A

incubation pain: 10-21 days (usually 14-17)
- infected persons are infectious 48 h before onset of vesicular rash, throughout vesicle formation (4-5 days), and until all vesicles are crusted.

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38
Q

Clinical presentation of primary infection: chickenpox

A
  • rash, fever (100-103F), lasting 3-5 days, malaise
  • skin lesions are hallmark of disease: maculopapules, vesicles, and scabs in varying stages of development (“crops” of lesions - compared to small pox which lesions occur at same time ) on an erythematous base of 5-10 mm
  • distribution is centripetal (see on trunk)
  • Not as umbilicated as smallpox
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39
Q

Clinical presentation of recurrent VZV recurrent infection: Herpes zoster or “shingles”

A
  • unilateral vesicular eruptions which develop within a single dermatome (T3 to L3 most common). Often assoc. with severe pain
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40
Q

Dxs in VZV?

A
  • usually clinically made
  • tests can include:
    specialized complement fixation and virus neutralization in cell culture
    Fluorescent ab test of smear of lesions
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41
Q

progress of VZV infection?

A
  1. thin walled vesicle with clear fluid forms on a red base
  2. The vesicle becomes cloudy and depressed in center (umbiliicated) with and irregular (scalloped) border
  3. A crust forms in the center and eventually replaces the remaining portion of the vesicle at the periphery
42
Q

When would you tx Herpes Zoster with IV acyclovir?

A
  • when it is on the face and the eye is involved (can lead to blindness)
43
Q

Management of VZV infections?

A
  • primary infection prevention: vaccination (reduce outbreak by 50%)
  • primary disease: prevent secondary infections
  • Recurrent infection: zoster
    take antivirals (high dose): - acyclovir, famciclovir
    and analgesics
  • can give immunoglobulin w/in days of outbreak will decrease severity of outbreak
44
Q 
Infectious mononucleosis (EBV)
epidemiology
A
  • EBV (HHV-4) -> 2 variants: EBV-1, EBV-2
  • B-cell lymphotropic virus primarily transmitted in saliva
    (4-8 wk incubation period)
  • 50% have had primary infection before adolescence (80% of daycare kids exposed to mono -> get over it easily)
    -Peak incidence occurrence: (big problem in adolescents and adults)
    ages 14-16 for girls
    ages 16-18 for boys
  • EBV shed from oropharynx for up to 18 months post-infection
45
Q

Clinical presentation of mono (EBV)

- clinical triad?

A
  • subclinical or mild when infected during childhood
  • infectious mono defined by transient appearance of heterophil Ab and clinical triad:
  • fever/chills: 7-14 days duration (may be prodromal)
  • lymphadenopathy: rarely exceed 3 weeks duration (posterior chain -B cells multiplying)
  • Severe pharyngitis with exudates: maximal for 5-7 days and resolved over following 7-10 days (only exception when virus causes exudates)
46
Q

Other common signs/sxs of primary infection of mono?

A
  • HA, malaise, anorexia
  • soft palatal petechiae
  • maculopapular rash (especially with admin. of amoxicillin/PCN)
  • splenomegaly and mild hepatic tenderness in up to 50%
47
Q

What neoplasms is EBV associated with?

A
  • nasopharyngeal carcinoma

- B-cell lymphomas (Burkitt’s lymphoma)

48
Q

Lab findings in infectious mono (EBV)

A
  • throat culture to check for B-hemolytic strep
  • monospot
  • Heterophil abs (90-95% of adolescents will be Ab +)
    become positive w/in 4 weeks after onset of sxs, are specific but not sensitive in early illness
  • atypical lymphocytosis in about 75%
  • EBV-specific immune response: EBV ab titers directed at several Ags -> EB virus capsid antigen (VCA), ABs to EBV nuclear antigen - EBNA
49
Q

Complications of infectious mono?

A
  • bacterial strep pharyngitis (develop a rash)
  • hematologic: thrombocytopenia, neutropenia
  • splenic rupture
  • neurologic: CN palsies (Bell’s palsy); Guillain-Barre syndrome; encephalitis
50
Q

Management of infectious mono? (EBV)

A
  • 95% of pts have self-limited disease in most cases requiring only supportive therapy
  • Acetaminophen or NSAIDS
  • warm salt water gargles
  • adequate rest (return to work/school based upon sx)
  • avoid contact sports for 6-8 weeks from onset
  • fever disappears in 10 days
  • lymphadenopathy and splenomegaly in 4 weeks
51
Q

Epidemiology of CMV

A
  • approx 1% of newborns infected
  • virus spread by: prolonged close contacts, blood/body fluids: transfusion (containing viable leukocytes), maternal-fetal transmission, STD
  • lifelong “infection” once infected
  • Congenital CMV occurs almost exclusively when preg. woman acquires primary infection (vs. reactivation)
  • perinatal CMV occurs when infant is infected at time of delivery through an infected birth canal or postnatal contact with maternal milk or or other secretions (40-60% transmission rate through nursing if mother infected)
52
Q

When are the three times that you are most likely going to see CMV (worry about infection)?

A
  • in pregnancy (babies)
  • transplant patients
  • in HIV (AIDS defining illness, shows up when CD4
53
Q

Clinical presentation of congenital CMV?

A
  • cytomegalic inclusion disease
  • ranges from inapparent infection (most) to severe/disseminated (-5%)
  • Petechiae, hepatosplenomegaly, jaundice common (60-80%)
  • microcephaly, growth retardation, prematurity (30-50%)
54
Q

Clinical presentation of perinatal CMV?

A
  • poor wt gain, adenopathy, rash, hepatitis, anemia, and atypical lymphocytosis
55
Q

Clinical presentation of CMV mono?

A
  • heterophil Ab negative mono syndrome (looks like mono but negative for mono spot, usually don’t have strep throat)
  • prolonged high fevers, profound fatigue and malaise
  • myalgias, HA, and splenomegaly are frequent
  • exudative pharyngitis and cervical adenopathy are rare
  • occasional rubelliform rash
56
Q

Dx of CMV mono

A
  • viral culture: MOST impt dx study in the eval of suspected CMV disease is the viral culture
  • CMV may be cultured from virtually any body fluid or organ system. Blood, urine, saliva, cervicovaginal secretions, CSF, bronchoalveolar lavage fluid, and tissues from bx specimens are all approp. specimens for culture
  • PCR
  • Ag assays
  • Tissue confirmation w/ AIDS related CMV : CMV GI or neuron disease, CMV pneumonitis = death
57
Q

What is characteristic to CMV congenital infection in babies?

A

blueberry muffin lesions

58
Q

Tx of CMV

A

Ganciclovir

59
Q

What is fifth disease (Erythema infectiosum)?

A

caused by Human parvovirus B19

- respiratory tract is probably route of transmission

60
Q

Clinical presentation of fifth disease?

A
  • mild febrile exanthematous disease with little or no prodrome
  • low-grade fever, varying degrees of conjunctivitis, upper respiratory complaints, cough, myalgia, itching, nausea, and diarrhea are initial signs and sxs
  • Classic “slapped face” lesion: indurated, confluent erythema of the cheeks, fiery red
  • circumoral pallor
  • bilateral symmetric eruptions (maculopapular slightly raised blotchy areas with reticular or lacy pattern) appear on the arms, legs and trunk about one day later
  • Rash (when it occurs) usually lasts 1 week and may disappear then reappear in the same area a few hours later
61
Q

Dx of Fifth disease?

A
  • usually made clinically in kids
  • labs: elevated titer of IgM anti-parvovirus abs
  • PCR in serum
62
Q

Tx of Fifth disease?

A
  • symptomatic tx: NSAIDS
63
Q

Roseola (infantum) epidemiology and pathophysiology?

A
  • epidemiology: benign disease of infants 6 m to 4 yo (most commonly seen in children
64
Q

Clinical presentation of Roseola (infantum)?

A
  • first manifestations occur after 5-15 days incubation period with abrupt onset irritability and fever (up to 105 F) lasting 3-5 days
  • rash appears several hours after sudden drop in temp: faint small (2-3 mm) macules or maculopapules over neck and trunk extending to thighs and buttocks
    will last a few hours or up to 1-2 days
    management: symptomatic only
65
Q

If child has seizure what test should be done?

A
  • Lumbar puncture because you are worried about meningitis and encephalitis
66
Q

Measles (Rubeola) epidemiology

A
  • occurs only in human and remains worldwide health problem despite a vaccine
  • transmitted through nasopharyngeal secretions (directly or airborne droplets) to respiratory mucous membranes or conjunctivae of susceptible persons
  • Highly contagious: infectious from 5 days after exposure to 5 days after skin lesions appear
67
Q

Clinical presentation of measles (rubeola)

A
  • Koplik’s spots (small, red, irregular lesions with blue white centers) appear on oral mucosa 1-2 days before rash (look like salt on mucosa)
  • Brick red, irregular maculopapular rash: first appears on forehead, spreads downward over face, neck, and trunk and appears on feet by 3rd day “outward and downward”
  • can affect palms and soles last
  • lesions usually coalescence and disappear in same order as appearance after about 3 days
  • prodromal sxs subside 1-2 days after rash appears
68
Q

Dx Measles (rubeola)

A
  • usually clinical

- labs: neutropenia, detection for IgM abs with ELIZA

69
Q

Tx of measles (rubeola)

A
  • isolation of pt
  • bedrest
  • antpyuretics
  • fluids
  • can have some bacterial disease complications, if so, tx with approp. abxs.
  • This is a vaccine preventable disease!!!
    complications: heart, and encephalitis
70
Q

Rubella (german measles, 3-day measles) epidemiology

A
  • nasopharyngeal secretions transmit virus
  • caused by Togavirus
  • transplacental transmission results in congenital rubella syndrome
  • age is an important determinant of the severity of Rubella (milder than measles)
71
Q

Clinical presentation of Rubella?

A
  • viral exanthemous primary disease is generally milder than rubeola
  • no prodromal in children
  • adults: prodromal illness precedes rash by 1-8 days and consists of malaise, HA, and fever (devastating in pregnancy: congenital rubella syndrome)
  • lymphadenopathy: large, tender, post-auricular and sub occipital nodes are most often involved, splenomegaly or generalized lymphadenopathy may be present
  • Rash appears 14-21 days after exposure and follows same pattern as rubeola (starts cephalically)
    lesions have lighter hue than measles, lesions usually remain discrete versus coalescent form and last 1-5 days (most commonly 3 days). Small red lesions (Forchheimer’s spots) may appear on soft palate (not pathognomonic)
72
Q

Clinical presentation of congenital rubella syndrome?

A
  • heart malformations (patent ductus arteriosus, interventricular septal defect, pulmonic stenosis)
  • eye lesions (corneal clouding, cataracts, chorioretinitis, microphthalmia)
  • microcephaly
  • mental retardation
  • deafness
  • thrombocytopenic purpura
  • hepatosplenomegaly
  • intrauterine growth retardation
73
Q

Management of congenital rubella syndrome?

A
  • Prevention
  • vaccinate all women of childbearing age (if already pregnant, wait until 2nd trimester when not as immunocompromised because it is a live virus
74
Q

Dx and Tx of rubella

A
  • leukonpenia
  • virus isolation and serologic tests of immunity: fluorescent ab tests, IgM abs to Togavirus

Tx: acetaminophen provides symptomatic relief

75
Q

Complications of Rubella

A
  • exposure during pregnancy: congenital rubella: heart defects, cataracts, glaucoma, psychomotor retardation
  • post infectious encephalopathy
  • This is vaccine preventable disease!!!!
76
Q

Epidemiology of mumps?

A
  • etiologic agent: paramyxovirus
  • disease occurs most frequently in the spring
  • spread by respiratory route but less contagious than measles or chickenpox
77
Q

Clinical presentation of the mumps

A

12-25 days incubation period

  • at least 25% of infections are subclinical
  • parotitis: parotid swelling (salivary adenitis) is first indication of illness and usually occurs suddenly: may be preceded by prodrome of malaise, anorexia, fever (up to 103F) and pharyngitis
  • glandular enlargement progresses over 1-3 days and subsides about a week after max enlargement
  • pain and tenderness may be marked or absent
  • epididymoorchitis: complicates 20-35% of post pubertal males, testicular involvement usually appears 7-10 days after onset of parotitis but may precede it or be simultaneous:
  • usually unilateral
  • acutely tender painful swollen testicle persist 3-7 days and subsides gradually
  • epididymis often palpable as swollen tender cord
  • heralded by recurrence of malaise, fever (103-106F), chills, HA, N/V
  • tx: no specific tx
78
Q

Worst possible complication of mumps:

A

meningitis

79
Q

What are the common cold viruses?

A

rhinovirus
coronavirus
adenovirus

80
Q

influenza like illnesses?

A

influenza A virus

influenza B virus

81
Q

Influenza etiology?

A
  • caused by members of Orthomyxoviridae family of viruses
  • Types A, B, and C are based on antigenic characteristics of the nucleoprotein (NP) and matrix (M) protein Ags.
  • Type A viruses undergo further surface antigenic classification:
    Hemagglutinin (H) ags (H1-3)
    Neuraminidase (N) ags (N1-2)
  • major antigenic shifts occur regularly:
    type A viruses about every 3 years (changes frequently, can swap with swine or avian, makes it very deadly)
    type B viruses about every 5 years
  • influenza outbreaks occur every year
82
Q

Clinical presentation of influenza?

A
  • abrupt onset of systemic sxs: HA, fever (38-41C), chills, myalgia, malaise:
  • accompanied by respiratory signs/sxs: cough, pharyngitis
  • dyspnea, hyperpnea, cyanosis, diffuse rales or signs of consolidation are evidence of pulmonary complications
  • acute illness generally resolves within a week
83
Q

Complications of influenza?

A
  • pneumonia (staph aureus)
  • Reye’s syndrome (especially children 2-16 yo)
  • Myositis, rhabdomyolysis, myoglobinuria (elderly: dehydrated and confused)
  • myocarditis and pericarditis
84
Q

Dx influenza?

A
  • rapid flu swab (Nasal, throat)

- Leukopenia

85
Q

Symptomatic tx for influenza?

A
  • acetaminophen
  • rest
  • fluids
  • abx if pneumonia suspected
86
Q

Anti-influenza virus drugs

A
  • Neuraminidase inhibitors (used the most)
    Oseltamivir (Tamiflu)
    Zanamivir (Relenza)
  • Adamantane derivatives/M2 inhibitors (proton channel through viral envelope -> blocks acidification):
    amantadine
    rimantadine
87
Q

Management and prevention of influenza?

A
  • vaccination: trivalent inactivated influenza virus vaccine provides partial immunity for few months to 1 year
  • given in Oct or Nov of each year
  • CI when allergic eggs
  • Vaccination of high risk groups:
  • chronic cardiac or pulmonary disease (including asthma)
  • pregnant women
  • residents of chronic care/nursing facilities
  • over age 65
  • chronic medical disorders: DM, renal disease, hemoglobinopathies, immunosuppressed
  • individuals who care for high risk populations
88
Q

Epidemiology of Bronchiolitis?

A

RSV (member of paramyxovirus genus) major respiratory pathogen of young children

  • transmitted primarily by close contact with contaminated fingers or fomites
  • annual epidemics occur in late fall, winter or spring
  • incidence rates are highest in infants 1-6 months of age and accounts for 20-25% of hospitalizations in infants/young children (babies can’t cough up the thick bronchial secretions)
  • disease is milder in older children/adults
89
Q

Clinical presentation of Bronchiolitis (RSV)?

A

infants: commonly presents as rhinorrhea, low-grade fever, cough, wheezing, mild systemic sxs
severe illness: tachypnea, dyspnea, hypoxia, cyanosis even apnea may ensue
- diffuse wheezing, rhonchi and rales (may not see wheezing)
- clinical presentation of adults/older children: common cold presentation
- younger children/infants: bronchiolitis, tracheobronchitis and pneumonia

90
Q

Dx of bronchiolitis?

A

Get O2 sats!!!

  • rapid RSV with nasal washings using viral Ag ID using ELIZA or immunofluorescent assay
  • culture of nasopharyngeal secretions
91
Q

Tx of bronchiolitis?

A
  • antiviral therapy: ribavirin

- sx relief: contact isolation, respiratory therapy, oxygen, secretion removal, hydration, antibronchospastic agents

92
Q

Epidemiology of Croup

A
  • caused by parainfluenza viruses: 4 major serotypes
    type 1: most frequent cause of croup (laryngotracheobronchitis) in children
    type 2: similar but less severe
    type 3: causes bronchiolitis and pneumonia in infants
  • account for up to 22% of respiratory illness in children, very mild disease in adults
93
Q

Clinical presentation of Croup?

A
  • acute febrile illness in children (50-80%)
  • coryza, sore throat, hoarseness, and variably croupy cough
  • breathing difficulty accompanied by a barking cough
  • much worse at night (day 3 the worst!)
94
Q

Management of croup

A

sx relief:
cool or moist air can bring relief
- try bringing child into steamy bathroom or outside into the cool night air
- a cool air vaporizer, set it up in the child’s bedroom and use it for the next few nights
- Acetaminophen
- ER tx: aerosolized racemic epinephrene
predisone in ER and to go (oral)
- after 3 hours of good presentation -> send them home
- avoid cough medicines because they suppress coughs and you want to get rid of inflammation, but don’t want to suppress cough and make child lethargic and sleepy

95
Q

Rabies epidemiology

A
  • caused by rhabdovirus
  • 2 epidemiologic forms:
    urban: unimmunized domestic cats/dogs
    sylvatic: skunks, foxes, raccoons, wolves and bats
96
Q

Clinical presentation of rabies (4 stages)

A

1) Prodrome: usually persists 1-4 days. Fever, HA, malaise, myalgias, increased fatigability, anorexia, N/V, pharyngitis, nonproductive cough
-paresthesias and/or fascicultations around site of inoculation suggestive of rabies
2) Acute encephalitis: development of excessive motor activity, excitation, and agitation
- confusion, hallucinations, combativeness, muscle spasms, meningismus, seizures and focal paralysis quickly follows
- hyperesthesia with excessive sensitivity to bright light, noise or touch is common
- Fever (up to 105F), dilated irregular pupils, increased lacrimation, salivation, perspiration, and postural hypotension occur
-3) Profound brainstem dysfunction:
occur shortly after onset of encephalitic phase, difficulty swallowing (with increased salivation) produces characteristic foaming at the mouth.
Violent involuntary contractions of diaphragm and accessory, respiratory, pharyngeal and laryngeal muscles
- coma and respiratory failure follow
- recovery (rarely)

97
Q

lab findings of Rabies

A
  • isolation of virus (saliva, CSF or brain tissue)
  • indirect serologic evidence of immune response
  • direct antigent detection (skin or brain bxs)
98
Q

Management of rabies?

A
  • prevention: pre-exposure vaccinations:
    domestic animals, high risk individuals: animal handlers, veterinarians, cave explorers, lab workers
  • post-exposure prophylaxis: immunoglobulin
99
Q

Ddx Variola versus varicella?

A

Variola (smallpox): rash starts on the face, lesions same stage, deep lesions, often palms, soles, centrifugal rash, Back>abdomen, multiloculated vesicles

Varicella: rash starts trunk, lesions in crops, superficial lesions, never palms/soles, centripedal rash, back=abdomen, uniloculated vesicles

100
Q

disease course of smallpox?

A
  • Day 0 -> exposure
  • Day 12-14 -> fever, malaise, non-productive cough, HA, backache, joint pain
    -Day 14-16 -> papular rash on face -> extremities
  • Day 16-18 -> papular -> vesicular -> pustular
  • Day 22-26 -> crusted lesions
  • Day 28-30 -> resolving
    10% will develop malignant disease and die 5-7 days after incubation
101
Q

Vaccine for small pox?

A
  • d/c’d in early 1970’s, but has been reinstituted b/c of concerns about bioterrorism,
  • routine vaccine, in the absence of a case of small pox is not recommended for those under 18

live vaccine:
site becomes red, itchy in 3-4 days
vesicle umbilicates and evolved into well formed pustule by day 6-11
- pustule scabs over b/t week 2 and 3
- scab falls off by end of 3rd week, leaving a scar

Infectious Disease (27 decks)

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