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 Viral Disease Slackers Facts by Mike  Viral Disease Slackers Facts by Mike

Viral Disease Slackers Facts by Mike - PowerPoint Presentation

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Viral Disease Slackers Facts by Mike - PPT Presentation

Ori Disclaimer The information represents my understanding only so errors and omissions are probably rampant It has not been vetted or reviewed by faculty The source is our class notes The document can mostly be used forward and backward I tried to mark questionable stuff with ID: 775288

virus describe disease rubella virus describe disease rubella respiratory rabies rash vaccine fever occurs ssrna hpv day days small

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Slide1

Viral Disease

Slackers Facts by Mike

Ori

Slide2

Disclaimer

The information represents my understanding only so errors and omissions are probably rampant. It has not been vetted or reviewed by faculty. The source is our class notes.

The document can mostly be used forward and backward. I tried to mark questionable stuff with (?).

If you want it to look pretty, steal some crayons and go to town.

Finally…

If you’re a gunner, buck up and do your own work.

Slide3

What are the three types in

Orthomyxoviruses

Slide4

A, B, C

Slide5

Seasonal flu is what type?

Slide6

Type A

Slide7

Describe the genome of

orthomyxovirus

Slide8

Segmented ssRNA (-)

Slide9

To what do H and N refer to

Slide10

Hemagglutinin and neuraminidase spikes on the viral surface

Slide11

In which portion of the cell

orthomyxovirus

replicate and why?

Slide12

In the nucleus because they cannot prime their RNA strands

Slide13

Why is the seasonal flu shot seasonal?

Slide14

A new vaccine is required each year because of antigenic drift due to polymerase errors

Slide15

Why does bacterial pneumonia often follow influenza?

Slide16

The virus causes destruction of ciliated respiratory epithelium in the upper respiratory tract. This degrades the mucociliary elevator and prevents efficient clearance of bacteria.

General immune system down regulation occurs as the influenza infection is controlled.

Slide17

What is the basis for the increased virulence seen in H1N1 of swine origin

Slide18

Antigenic shift has substantially altered the virus to reduce its antigenic similarity to previous strains and to allow it to replicate in both the upper and lower respiratory tract.

Slide19

Why are people over 50 less likely to get sick from H1N1 swine origin.

Slide20

An similar pandemic occurred within their lifetime.

They do not have as robust an immune system and cannot generate as much of a cytokine storm

Slide21

Why is avian flu H5N1 difficult to get

Slide22

Currently the strain’s H antigen interact with

sialic

acid alpha 2,3 gal receptors which are situated in the lower respiratory tract. Thus it take larger exposures to transmit the disease.

Slide23

What would occur if H5N1

reassorts

in swine

Slide24

Why are swine important intermediates in the assortment of avian and human influenza?

Slide25

Swine upper respiratory epithelium contains

sialic

a2,3 gal and

sialic

a2,6 gal receptors thus they can be easily

coninfected

with both human and avian virus. This allows nature to tinker.

Idle goddesses are the devils workshop.

Slide26

What will happen if H5N1

reassorts

or mutates to efficiently infect both upper and lower respiratory epithelium.

Slide27

The potential for significant mortality

Slide28

What are the requirements of a pandemic influenza

Slide29

New human type A strain

Causing serious illness

Easily spreads person to person

Slide30

What diseases are caused by

paramyxovirus

Slide31

Mumps

Parainfluenza

and croup

Rubeola (5 day measles)

Respiratory syncitial virus

Slide32

Describe the

paramyxovirus

spikes

Slide33

Combined H and N on single spike (

para

=next to hence H is

para

to N)

Fusion (F) protein on second spike

Slide34

What is a

syncitia

and why do they form

Slide35

A

syncitia

is a giant cell that forms by fusion of multiple cells.

Paramyxovirus

tends to form

syncitia

through the action of F protein deposited on cell surfaces.

Slide36

Distinguish

parainfluenza

from Respiratory syncitial virus

Slide37

Parainfluenza

= bronchitis

RSV =

bronchiolitis

Slide38

Describe RSV epidemiology

Slide39

Occurs from the late fall to the spring. Predominantly affects small children < 1

yo

.

Slide40

Describe RSV immunity

Slide41

Immunity is incomplete. Repeated

infections occur with lessened

severity but its unclear if there is an immune basis.

Slide42

RSV diagnosis

Slide43

Immunofluorescence of nasal swabs

Slide44

RSV prophylaxis

Slide45

Injection of monoclonal antibody against factor F is indicated in high risk children

Slide46

Its flu if?

Slide47

It looks like a cold but also has

Myalgia

/

arthralgia

Fever

Slide48

Adenovirus structure

Slide49

Linear dsDNA

Slide50

Adenovirus disease

Slide51

URI particularly in children

Slide52

Adenovirus persistence

Slide53

DNA virus can establish latent/carrier state

Slide54

What viruses are responsible for the common cold?

Slide55

Rhinovirus

Coronavirus

Reovirus

Slide56

What is a exanthema?

Slide57

Circle the correct answer

Choose wisely grasshopper

A widespread rash

An out of date national anthem.

Last years skirt lengths

Slide58

List the common

exanthem

viruses and families

Slide59

Illness

Genus

family

Mumps

Paramyxovirus

paramyxoviridae

Measles

Morbillivirus

paramyxoviridae

Rubella

Rubivirus

togaviridae

Roseola

infantum

HHV6,

adenovirus,

coxackie

virus, echovirus

Erethema

Infectiosum

Parvovirus B19

Slide60

What is the basis of the vaccine for these diseases

Slide61

Combined attenuated vaccine for measles, mumps, and rubella. This avoids a rash of shots.

Slide62

Mumps time course

Slide63

16 day incubation

7 day clinical disease

Slide64

Mumps complications

Slide65

Orchitis

Meningitis

Encephalitis

Slide66

Rubeola (Measles) time course

Slide67

10 day incubation

5 days of rash

Koplik

spots 1-2 days prior to exanthema

Slide68

Rubeola epidemiology

Slide69

Occurs in unimmunized people typically in childhood or teens during the winter and spring.

Slide70

What is unique about

morbillivirus

spikes

Slide71

Even though they are

paramyxoviridae

they lack N activity. Thus they have H and F spikes as opposed to H/N and F typical of other

paramyxoviridae

.

Slide72

What are

koplik

spots

Slide73

Small bluish

y

ellow spots that appear on the oral mucosa in advance of the rubeola rash

Slide74

Rubeola complications

Slide75

Post infectious encephalitis in near term

SSPE (encephalitis) in 2-10 years

Slide76

Rubeola

sx

Slide77

Progressive rash extending from head to toe.

High fever

Delirium

Photophobia

Conjunctivitis

Slide78

Rubella time course

Slide79

Incubation period 16 days

Exanthema for 3 days

Contagious -7 to +7 from rash

Slide80

Rubella epidemiology

Slide81

Occurs in unimmunized people usually in the winter and spring

Slide82

Should pregnant women receive MMR vaccine?

Slide83

No, MMR is a live vaccine and rubella is a

transplacental

infective agent. Reversion of rubella to a virulent form could lead to congenital rubella in the child.

Slide84

Congenital rubella

sx

Slide85

Cataracts

Cardiac defects

Reticuloendothelial

defects (liver, spleen, thrombocytes)

Mental retardation

Slide86

What is the mechanism of spread for MMR?

Slide87

All enter the respiratory tract to cause

viremia

before moving to their tropic tissue

Slide88

What are the tropic tissues for MMR?

Slide89

Mumps – salivary glands, testes, ovary, CNS?

Measles – skin and Lymph nodes?

Rubella – skin and lymph nodes?

Slide90

What is agent for

Erythema

Infectiosum

?

Slide91

Parvovirus B19

Slide92

Where does the exanthema appear?

Slide93

On the face. It has a characteristic slapped face appearance.

Slide94

What is the alternative name for

Erythema

Infectiosum

?

Slide95

Fifth disease

Slide96

A child presents with a faint rash and convulsions. What is a likely diagnosis?

Slide97

Roseola

infantum

Slide98

Describe the structure of

Enteroviruses

Slide99

They are small naked icosahedral virus with ssRNA (+) in

picornaviridae

Pico = small

rna

= RNA

Slide100

What is the transmission path for

enterovirus

Slide101

Fecal-oral

Slide102

Describe the stability of

enterovirus

Slide103

They are very stable and are resistant to acidic pH, detergents, disinfectants, and alcohol

Slide104

Describe the epidemiology of

enterovirus

Slide105

Summer and fall in temperate climes. Year round in the tropics. Transmitted by direct or indirect fecal-oral contact. Vectors occasionally spread the virus.

Slide106

What are the

picornaviridae

genus?

Slide107

Polio

Echo

Rhino

Coxsackie

Hep

A

(PERCH)

Slide108

What are the three possible outcomes of polio infection

Slide109

Abortive poliomyelitis

Aseptic meningitis

Paralytic poliomyelitis

Slide110

What is the entry point tissue for polio

Slide111

Oropharynx

. Resulting viruses swallowed and infect intestines. Then infect CNS

Slide112

What vaccines are available for polio

Slide113

Salk = killed

Sabin = Attenuated

Slide114

Polio diagnostic

Slide115

Viral visualization

Ab

titer

Slide116

What is the potential contagious period for polio

Slide117

Intestinal shedding can occur for weeks

e

ven in the face of effective immune response

Slide118

What is the structure of

papillomavirus

Slide119

dsDNA circular. Naked icosahedral

Slide120

How many genotypes of HPV are known

Slide121

70+

Slide122

What is the transformation potential of HPV

Slide123

It’s a DNA virus and thus can be stabilized in the cell. Higher stain numbers are more oncogenic (?). Malignant strains seem to insert DNA into host genome.

Slide124

HPV Transmission Routes

Slide125

Occupational exposure (meat packers)

Sexual contact

Public showers/swimming pools (suspected)

Perinatally

Slide126

List the diseases associated with common HPV genotypes

Slide127

1,2 – common warts

7 – meat handler warts

6,11 – benign genital warts

16,18,31,45 – warty lesions with malignant potential in the

nethers

Slide128

What percent of females in US are HPV positive?

Slide129

20%-60%

Slide130

Where does HPV replicate?

Slide131

Nucleus – it’s a DNA virus

Slide132

How is HPV typically diagnosed in females

Slide133

Detected by cytoplasmic vacuolization and nuclear enlargement on routine pap smear

Slide134

What is

cryotherapy

Slide135

Removing HPV infected epithelium with extremely cold substances such are liquid nitrogen

Slide136

Describe PML

Slide137

Degenerative brain disease that causes focal areas of

demyelination

surrounded by bizarre

astrocytes

.

Slide138

What is the virus of PML?

Slide139

The JC

Polyomavirus

Slide140

What is a likely

comorbidity

in PML PT?

Slide141

HIV

Slide142

A bone marrow transplant patient presents a few weeks after discharge with hemorrhagic cystitis. What is the likely agent

Slide143

BK

polyomavirus

Slide144

What is the tropic tissue for BK virus?

Slide145

Kidney

Slide146

What are the general

sx

of

arbovirus

Slide147

Encephalitis

Hemorrhagic fever

Slide148

What is the characteristic of an

arbovirus

?

Slide149

They are all transmitted via insect vectors such as mosquitoes or ticks.

Slide150

What is the family for

arboviruses

involving horses?

Slide151

Togavirus

Slide152

What commonly

togavirus

is commonly vaccinated for?

Slide153

Rubella

Slide154

What is the distribution of western, eastern and St

Loius

encephalitis

Slide155

Western – western us

Eastern – Eastern US

St Louis – central US?

Slide156

Describe a typical WEE,EEE victim

Slide157

People in association with horses where mosquitoes are present

Slide158

What is the age range for St

Loius

and West Nile Virus

Slide159

St

Loius

> 40

West Nile > 50

Slide160

What is the classic distribution for yellow fever

Slide161

Caribbean and south and central

america

Slide162

What is the classic distribution of Dengue

Slide163

World wide.

Middle east, far east, Africa, Caribbean

Slide164

What is the vector for yellow fever and dengue

Slide165

Aedes

aegypti

Slide166

Describe Yellow Fever SX

Slide167

Fever, chills, headache, hemorrhage, jaundice, and shock

Slide168

Describe Dengue

sx

Slide169

Severe back and joint pain, fever, rash.

Slide170

What is the reservoir for west

nile

Slide171

Birds

Slide172

What is the vector for west

nile

?

Slide173

Mosquitoes

Slide174

West

nile

sx

Slide175

Flu-like, Rash on torso and upper extremities

Slide176

Describe the morphology of

bunyavirus

Slide177

ssRNA (-) , enveloped, spherical, segmented

Slide178

California virus family and

sx

Slide179

Bunyavirus

Encephalitis with seizures

In north central mid west states

Slide180

Hantavirus family

Slide181

Bunyavirus

Slide182

Hantavirus epidemiology

Slide183

Direct exposure to rodent feces. Occurs in the southwestern US

Slide184

Hantavirus

sx

and mortality

Slide185

Fulminant

respiratory disease with > 50% mortality.

Slide186

Reovirus

arbovirus

disease

Slide187

Colorado tick fever

Slide188

Arenavirus

morphology

Slide189

Spherical enveloped ssRNA (+/-) segmented

Slide190

Arenavirus

unique characteristics

Slide191

Ambisense

(+/-) RNA

Presence of host cell ribosomes within virus

Slide192

Filovirus

morphology

Slide193

Enveloped ssRNA (-)

Slide194

Filovirus

sx

Slide195

Hemorrhagic disease

Slide196

Famous

filovirus

diseases

Slide197

Marburg and

ebola

Slide198

What disease is cased by a

rhabdovirus

Slide199

Rabies

Slide200

Rabies virus morphology

Slide201

Bullet shaped enveloped helical ssRNA (-)

Slide202

What is the initial

tx

for rabies

Slide203

Injection of IgG near bite. Vaccination with killed attenuated virus.

Slide204

Describe the

timecourse

of rabies

Slide205

Occurs from 10 days to one year depending on inoculum size

Slide206

Classify the final stages of rabies infection

Slide207

Prodrom

Acute neurologic phase

Coma

Death

Slide208

What is the mortality of rabies

Slide209

100%

(only a few exceptions are known)

Slide210

What is the furious phase of rabies infection?

Slide211

Occurs during the acute neurologic phase. Patients are often aggressive and disoriented

Slide212

What is the

d

umb phase of rabies infection

Slide213

Occurs during the acute neurologic phase. Patients are lethargic and paralytic.

Slide214

Why isn’t everyone vaccinated against rabies

Slide215

The vaccine is a killed attenuated vaccine so people receiving it are double protected form conversion but the protection does not last long so repeated vaccine would be necessary. Rabies is uncommon with proper precautions

Slide216

Rotavirus family

Slide217

Reoviridae

Slide218

Rotavirus structure

Slide219

Small wheel shaped ssRNA (+). 1 segments

Slide220

What are the segmented virus

Slide221

Bunya

Orthomyxo

Arena

Reo

(BOAR)

Slide222

What is the epidemiology of rotavirus

Slide223

Infection during cooler months in children < 2 years old. Highly contagious and spreads rapidly in institutions and families

Slide224

Describe Rotavirus disease

Slide225

1-3 day incubation period followed by abrupt onset of vomiting. Subsequent diarrhea lasting 5-8 days. Virus shedding for 2-12 days

Slide226

Rotavirus prevention

Slide227

Hand washing. Vaccine in development.

Slide228

Rotavirus death factors and numbers

Slide229

Malnutrition and

immunodeficient

children

600K die worldwide

Slide230

Norwalkvirus

family

Slide231

Calcivirus

Slide232

Calcivirus

morphology

Slide233

Naked small round ssRNA (+)

Slide234

Norwalk disease

Slide235

1-2 day incubation

1-2 day vomiting and diarrhea

Slide236

Other diarrhea agents

Slide237

Astrovirus

(star shaped naked)

Adenovirus