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1
Q

Measles Virus

A

morbillivirus, Paramyxoviridae family, “new” human virus

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2
Q

How is the Measles Virus different that other paramyxoviruses?

A

1) Lacks neuraminidase activity (protein H, not HN)

2) Forms intracellular inclusion bodies

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3
Q

Measles Illness

A
  • Childhood infection spread by respiratory route.
  • Latent: 10-14 days
  • 2-3 day prodrome of fever, cough, conjunctivitis
  • maculopapular rash, T cell response, virus clearance
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4
Q

Measles Clinical Case Definition

A

1) Rash >3 days
2) Temp > 38.3/101
3) Cough, rhinorhea, conjunctivitis
* If more than 1 case, contact health department.

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5
Q

Measles: Early Infection Stage

A

1) First, virus replication restricted to tracheal and bronchial epithelium.
2) After 2-4 days, spreads to lymph nodes
( appearance of reticuloendothelial giant cells-warthin-Finkeldy cells)
3) Amplification of lymph nodes leads to viremia, causes infection of other tissues/organs

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6
Q

Measles Virus Viremia/Disease Progression

A

1) Symptoms soon after onset of viremia
2) Patient is infectious 1-2 days before symptoms
(10-20 days after exposure)
3) Symptoms:maculopapular (morbilliform) rash and Koplik spots

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7
Q

Measles Virus Complications

A

1) Immune suppression during infection
-suppression of delayed type hypersensitivity
skin test response
-Antibody/cellular immune responses to new antigens are impaired
2) Acute Disseminated Encephalomyelitis - Autoimmune demyelination disease
- immune response to myelin basic protein
- mechanism unknown/not restricted to measles
3) Measles Inclusion Body Encephalitis/Subacute Scleerosing Panencephalitis
-establishment of perisistent infections in the
brain
-mechanism of entry not understood

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8
Q

Measles Prevention/Control

A

1) Vaccine (MMR) at 12-15 months and 4-6 years
- live-attenuated provides “life-long” protection
2) Virus is antigenically stable monotypic
- once recovered, individual is immune for life
- different strains (AA different in H or HN) but
Ab to one protects from all

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9
Q

Why is measles ideal to eradicate through Immunization?

A

1) 1 serotype
2) Cases are clinically identifiable
3) No animal reservoir
4) Eradication requires herd immunity-98% population is immune

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10
Q

What limits measles vaccine?

A

1) Pregnancy statue

2) Immune status/illness

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11
Q

Mumps Virus

A

rubulavirus, Paramyxoviridae family

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12
Q

Mumps Illness

A

1) Initially Infects nasal mucosa/upper respiratory tract epithelium
- incubation is ~18 days
- spreads to draining lymph nodes
- sheds in saliva for ~6 days before clinical onset
2) 1st clinical sign: infection of parotid gland (95%)

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13
Q

Mumps Complications

A
  • CNS involvement: Aseptic meningitis, deafness
  • post-pubertal men: symptomatic gonadal issues
  • mumps with type 1 insulin-dep diabetes
  • MI occurs frequently
  • Fetal wastage leading to spontaneous abortion in first trimester of pregnancy.
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14
Q

Mumps Prevention/Control

A

Vaccine - Live-attenuated, safe, effective, few adverse effects

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15
Q

Rubella Virus

A

-small, enveloped, nonsegmented, + strand RNA
-Togaviridae family
- alpha virus: western equine encephalitis, EEE,
VEE, arthropod-borne
- rubiviruses: rubella, distinguished from alpha
by limited (human) host range

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16
Q

Rubella Virus Replication Cycle

A

1) Entry: receptor mediated endocytosis, viral envelope fuses with endosomal membrane in pH dependent manner
2) Genome serves as mRNA for translation of viral polymerase - polymerase makes 1 sense antigenome to make:
-subgenomic mRNA encoding viral capsid and
envelope proteins
-more full-length + strand genomic RNA

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17
Q

Rubella Virus Transmission

A

By aerosols: initial replication in mucosa of upper respiratory tract and nasopharyngeal lymph nodes

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18
Q

Rubella Illness

A 
mild disease
low-grade fever
occasional conjunctivitis
sore throat
lymphadenopathy
morbilliform rash- starts on face and spreads
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19
Q

Rubella Disease Progression

A

~7-9 incubation before virus in in serum, then it starts shedding, isolated from nasopharynx and stool

  • rash at 16-21 days after exposure
  • virus still shed after rash disappears (up to a month from exposure)
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20
Q

Rubella: worst effect

A

Congenital Birth Defects (congenital rebella syndrome)
-highest risk in 1st/2nd trimester
1st month-spontaneous abortion/mental retardation/motor disabilities/hearing loss/congenital heart disease/ cataracts

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21
Q

Rubella Prevention/Treatment

A
  • Vaccine in 1969 - before there were epidemics every 3-9 years
  • Developed to protect the fetus, not illness in kids/adults
  • No antiviral treatment needed b/c mild disease
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22
Q

Leprosy

A

Hansen’s Disease
Chronic Granulomatous - affecting peripheral nerves and superficial tissues (nasal mucosa)
Caused by Mycobacterium leprae (like MTB)
Can’t grow on agar media/cell culture
Humans and Armadillos
1) Tuberculoid
2) Lepromatous

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23
Q

Leprosy Transmission

A
  • via small droplets from nasal secretions of lepromatous leprosy patients
  • low infectivity, prolonged close contact with infected
  • 2-7 years incubation
  • most common in India and Braxil
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24
Q

About M. leprae

A
  • obligate intracellular parasite, primarily of macrophages and Schwann cells
  • also invade peripheral neurons
  • Lepromatous causes lack of TH1 mediators
  • disease extent determined by T cell-mediatated immunity
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25
Q

Leprosy Disease

A
  • single skin lesions on face, limbs, buttocks
  • peripheral nerve involvement can leave lesions anesthetic (not normally facial)
  • low # of organisms in lesions, not normally contagious
  • Tuberculoid heal and prognosis is good
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26
Q

Lepromatous Leprosy Progression

A

1st - edema and rhinitis
Lesions on face, buttocks, limbs
Infiltration notable on ear lobes (acid fast bacilli)
Severe Damage - perforation of nasal septum
- collapse of nose (cartilage loss)
- finger loss, neurotrophic atrophy
- atrophy of testicles
Spread to reticuloendothelial system

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27
Q

Leprosy Diagnosis/Treatment

A
  • skin biopsies, acid-fast bacilli
  • abx resistance is a problem, multiple drugs
  • sulfone (inhibits para-aminobenzoic acid metabolism) + rifampin (cure tuberculoid leprosy in 6 months)
  • with lepromatous form +clofazimine and 2 years
  • prophylaxis for kids: sulfones
  • early diagnosis/treatment is key
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28
Q

Herpesviruses

A

Linear, ds DNA genome of 150-250 kbp
Icosahedral capsid
enveloped
dozen glycoproteins
DNA replicated/virus assembled in nucleus
*normally self-limiting, but can be life-thretening in immunocompromised host

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29
Q

Herpesvirus Classifications

A 
-Alpha: herpes simplex virus type 1 (HSV-1)
           HSV-2
           Varcella-zoster virus (VZV)
-Beta: Cytomegalovirus (CMV)
          Human herpesvirus 6 (HHV-6)
          HHV-7
-Gamma: Epstein-Barr virus (EBV)
               HHV-8 (Kaposi's Sarcoma-asscoiated herpies)
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30
Q

Herpes Virus Latency

A

-occurs soon after initial infection
-no virus particles produced (entire genome is extrachromosomally maintained), few viral genes expressed
3 stages: establishment, maintenance, reactivation

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31
Q

Herpes Virus Neurotrophic Latency

A

HSV-1
HSV-2
VZV

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32
Q

Herpes Virus Lymphotrophic Latency

A 
CMV
EBV
HHV-6
HHV-7
KSHV
33
Q

Varicella-Zoster Virus

A

-Primary infection: Chicken pox
-Highly communicable, aerosol
-Late winter/early spring
-Fever, itchy rash starting on scalp/trunk
-Adult cases more sever-pneumonia
-Reactivation: shingles - sudden onset of pain, rash along thoracic dermatome or forehead
rash last 2-4 weeks, pain longer, postherpetic neuralgia

34
Q

Varicella-Zoster Virus - Diagnosis/Treatment

A

Diagnosis is clinical
FDA approved attenuated vaccine (MMR regimen)
Treat chickenpox itchiness and aches
Adult pneumonia require VSV Ig
Zoster treated with oral ACV and steroids
Vaccine designed to boost immunity to or lessen zoster

35
Q

HHV-6 and HHV-7

A

Cause roseola (exanthem subitum)

  • mild respiratory illness followed by high fever
  • after fever, 25% children will exhibit rash on face and body that lasts 2-3 days
  • affect 3months-6 years of age
  • > 90% US is seropositive
36
Q

Parvovirus B19

A

autonomous replication

Genus: Parvovirus

37
Q

Adeno-associated virus

A

Genus: Dependovirus

require helper virus

38
Q

Family Parvoviridae Structure

A
  • linear, ssDNA, 5.6kbp
  • icosahedral capsid, no envelop
    • or - strand
  • replication/assembly in nucleus
  • replicate in rapidly dividing cells-providing replication function
39
Q

Parvo B19: Epidemiology

A

Erythema infectiosum- “slapped cheek” rash
- “lacy red rash”
“fifth disease” - resolve in 7-10 days
mild, common childhood rash
-50% of population seropositive
1)conversion after school age
2)Ab offer protective immunity

40
Q

Parvo B19: Pathogenesis

A

Can spread before rash shows-respiratory secretions!
Biphasic- 4 of 5 will show symptoms
1) initial viremia - may have flu-like symptoms
2) second phase is rash
3) symptoms are immune mediated
-Adults have joint pain/swelling “polyarthritis”, flu-like symptoms

41
Q

Parvo B19 in certain populations?

A

Sickle Cell- transient aplastic crisis-B19 infects and lyses erythroid precursor cells
-results in loss of red blood cell production during infection (7-10 days)
-shortened life span of RBC in sickle cell patients, get anemia
Immune compromised: chronic anemia-hard to clear
Transplacentally Transmitted: normally not concerning, 5% fetal anemia, hydrops fetalis, miscarriage-most common in first 1/2 of pregnancy

42
Q

Parvo B19 Diagnosis

A

Rash, serological and viral DNA testing of blood

43
Q

Parvo B19 Treatment

A

treat flu-like symptoms and itchy rash

anemia patients may need blood transfusion

44
Q

Parvo B19 Prevention

A

hard-infectious period before rash

  • no vaccine
  • genreal hygiene may limit spread
45
Q

Family Poxviridae

A

1) Variola (small pox)
2) Vaccinia (small pox vaccine)
-molluscum contagiosum
Non-ocosahedral complex structure- virus can be seen in light microscope “brick-shaped”
-intracellular virus has core & lateral bodies surround by envelope, extracellular virus has additional envelope
-large, double-strand linear DNA genomes that are complexed with proteins

46
Q

Family Poxviridae Replication

A

Cytoplasmic replication

makes everything by ribosomes

47
Q

Variola

A

Small Pox
-Variola Major (25% fatality)
-Variola Minor (1% fatality)
Systemic disease with generalized rash

48
Q

Variola Spread

A

Inhalation from virus being released from ruptured mouth lesions

49
Q

Variola Virus

A

Small Pox (eradicated in 1977)

50
Q

Molluscum Contagiosum

A 
nodular skin lesions
Childhood: lesions-face,trunk, limbs
                 skin to skin spread
                 tropical
Young Adult: lower abdomen
                   sexual transmission
disappear spontaneous in 2 to 12 months
LARGE CYTOPLASMIC INCLUSIONS in eosinophils of affected area
51
Q

Variola Virus symptoms

A

prodrome of high fever, malaise, body aches, viremia
-red spots in mouth/tongue: contagious when rupture
Second viremia: infected macrophages go to epidermis-lesions (toxemic)

52
Q

Variola Virus second viremia

A

-skin lesion is raised bump with depression in middle
-become pustules (BB inside)
-pustules scab, pitted scar
-contagious until last scab is gone
ALL LESIONS IN SAME STAGE

53
Q

Variola Virus prognosis

A

Death or Recovery (complete clearance)

54
Q

Smallpox vaccine

A

disease know 2000, Jenner milkmaids (cowpox not bad, provide immunity to all)-1789

  • then in 1950s, use vaccinia -live, enoculate in epidermis (local lesion that heals in 2 weeks)
  • not effective after 20 years
55
Q

What key features let smallpox be eradicated?

A

1) Humans only reservoir
2) No healthy carriers
3) No sub-clinical infections
4) Effective vaccine

56
Q

Smallpox vaccine effects

A
  • not safe
  • NO: pregnant women, immune suppression, eczema, atopic dermatitis, acne, <18, heart disease patients

1 million: 50-1000 severe, 15 life-threatening,
1-3 die
can give VIG: Vaccine immune globlin
can give Cidofovir

57
Q

Vector-borne/Zoonotic

A 
rare
"flu-like" initially
rapid treatment critical
human to human is rare
-have animal/insect reservoir
58
Q

Vector Borne Transmission

A

tick, flea, louse

transmit during blood meal

59
Q

Zoonotic Transmission

A

aerosol, fluid, direct contact

60
Q

Rickettsia

A

gram - rods, obligate intracellular bacteria
Can’t culture on media
3 phyla: rickettsia (vector-borne), ehrlichia (vector)
coxiella (non-vector)
-diagnosis relies heavily on patient presentation & travel
-confirm by serology
all responsive to doxycycline

61
Q

Rickettsia Symptoms

A

Classic: fever-headache-rash (rash 3-5 days)

  • replicate in cytoplasm of endothelial & muscle cells of small blood vessels
  • Hemorrhage & edema
  • Vasculitis leading to rash & headache
62
Q

R. Rickettsia

A

“Rocky Mountain Spotted Fever”
-ticks
2000 cases a year, seasonal, in NC, SC, AR, MO, OK
endemic in TN

63
Q

R. Rickettsia symptoms

A

Initial: flu with severe headache, then rash

  • spreads from ankles & wrists to soles, palms, trunks
  • calf muscle tenderness
  • Septicemia, DIC
64
Q

R. Rickettsia Diagnosis

A

-presentation/history
-Weil-Felix serologic test (non-specific)
Indirect Fluorescent Antibody (need early blood draw, then one several weeks later) -need 4 fold increase in titers
-25% mortality if untreated

65
Q

R. prowazekii

A

Epidemic Typhus

  1. Human to human by body lice (flying squirrels?)
  2. Historical - poverty & wars
  3. Rash similar to Rocky, but spreads from trunk to extremities, not palms/soles
  4. Not in US
  5. 10-60% mortality rate- myocarditis, CNS
66
Q

R. typhi

A

Endemic (murine) typhus
-southern Texas, southern California, Hawaii
Rat flea to human
less severe than epidemic typhus, less mortality

67
Q

Ehrlichia

A

southern tick borne disease 1,400/year

68
Q

E. chaffeensis

A 
Human Monocytic ehrlichiosis
Transmitted by Lone Star deer tick
replicates in monocytes
***form inclusions called morulae*** (wright/Giemasa stain)
-treat with doxycycline
69
Q

A. phagocytophilia

A 
Human granulocytic anaplasmosis
"rocky moutain spotless fever"
Ixodes deer tick
-wright/giemsa stian - morulae in granulocytes
-serology
treat with doxycycline
70
Q

Borrelai

A

Spirochetes

  • most to thin for gram staining (use Wright/Giemsa)
  • antigenic variation (1 in 1000 change surface antigens)
71
Q

B. burgdorferi

A

Lyme Disease
Ixodes deer tick nymph to humans-prevented if removed in 24 hours
-most common tick disease (22,000)
-Endemic New England, Mid-Atlantic, Upper Midwest, TN

72
Q

B. burgdorferi Symptoms

A 
Early: flue-like
Classic Bull's Eye Rash at sight of tick
Secondary: disseminated
-weeks/months after initial infection
-arthritis, facial palsy, peripheral neuropathy
Tertiary: chronic
-months/years 
-erosive arthritis (knees)
-numbness, Bell palsy
73
Q

B. burgdorferi Diagnose/ Treatment

A

2 step seriological test: ELISA
Western Blot
-PCR-based NAATs

Treat: early (doxy or amoxicilllin)
chronic (IV cephalosporines extended)

74
Q

B. hermsii

B. recurrentis

A

“relapsing fever”
tick-hemsii, endemic in high, dry west US
louse-recurrentis
-3 day on, 1 week off,(antigenic variation) rash uncommon
microbes in wright/giemsa stain
serology needed to confirm
Treat: doxycycline

75
Q

Leptospira interrogans

A

Spirochetes-Leptospirosis

  • water with animal urine (break in skin)
  • NO skin lesions
  • flu-like, jaundice/renal (Weil’s disease), meningitis

DDX: serologic
Treat: Penicillin
-vaccine cattle & pets

76
Q

Bartonella henselae

A 
Cat Scratch
can reservoir (no symptoms)
-mostly kids (24,000)
swollen lymph glands near scratch
Adults: flu-like, 
Both: disseminated disease involving CNS in immune compromised
DDX: presentation, history (scratch)
most clear on own, immunocomprised
77
Q

Anthrax

A

eschar at site

78
Q

Plague

A

swollen gland (bubo) in groin/axilla

79
Q

Tularemia

A

ulcer at infection site

Dermatology (9 decks)

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