Viral Skin Infections (Virus) Flashcards Preview

Skin MS: Week 4 > Viral Skin Infections (Virus) > Flashcards

Flashcards in Viral Skin Infections (Virus) Deck (168):
1

Vesicular or Pustural Rash Diseases - major viral causes

HHV-1* (Neuro, HRM)
HHV-2* (Neuro, HRM)
HHV-3
Coxsackieviruses A and B
Smallpox
Orf virus* (in handout)

2

Maculopapular Rash Diseases - major viral causes

Measles* (Neuro, IHO)
Rubella
Parvovirus B19
Roseoloviruses (HHV-6 and HHV-7)
HHV-4* (in IHO)
ECHO virus* (in handout)
West Nile Virus* (in handout)

3

Wartlike eruptions - major viral causes

HPV
Molluscum contagiosum

4

Steps of Viral Infection inside organism

Replication at site of entry
Primary viremia
Replication
Secondary viremia
Replication
Transmission to other hosts
*See picture*

5

Herpesvirus infections last a life time in a state called ____

latency

6

Herpesvirus do/do no integrate into host genome

Do not
They make proteins that mediate genome persistence in host cells by binding to the viral genome and ensuring that as the host cell divides that the viral genome is copied.

7

Herpesvirus can/cannot reactivate

Can - more infectious

8

virus - dsDNA (group I) - linear genome - icosahedral nucleocapsid - enveloped

herpesvirus family

9

herpesvirus subfamilies

alpha:
simplexvirus (1 and 2)
Varicellovirus (VZV)
beta:
cytomegalovirus (HCMV, HHV-6/7)
gamma:
Lymphocryptovirus (EBV)
Kaposisarcoma-associated herpesvirus

10

herpesvirus tree

virus - dsDNA (group I) - linear genome - icosahedral nucleocapsid - enveloped

11

Herpes simplex 1

alpha - Human herpesvirus 1 (HHV-1)
Above waist - gingivostomatitis, herpes labialis, etc.

12

Herpes simplex 2

alpha - Human herpesvirus 2 (HHV2)
Below wait - genital herpes or neonatal herpes

13

Varicella-Zoster virus

alpha - HHV-3
Chickenpox or shingles

14

Human cytomegalovirus

beta - HHV 5
Congenital CMV infection, systemic, mono-like

15

Roseoloviruses

beta - HHV 6(a,b)/7 - exanthem subitum (6th disease), encephalitis in IC

16

Epstein-Barr Virus

gamma- HHV-4 - mononucleosis, lymphoid-organ related cancers

17

Kaposi Sarcoma-Associated Herpesvirus

gamma - HHV8 - Kaposi sarcoma

18

first disease

measles

19

second disease

strep pyogenes (scarlet fever)

20

third disease

rubella

21

fourth disease

staph aureus (SSSS)

22

fifth disease

parvovirus B19 (slapped cheek)

23

sixth disease

HH6/7 - roseola

24

Virus lifecycle

attachment - penetration/adsorption - synthesis - assembly - release

25

HHV1 and HHV2 cause

mucosal lesions, encephalitis

26

HHV1 and HHV2 transmission

saliva, vaginal secretions, lesion fluid
1 - mainly oral
2 - mainly sexual

27

HHV1 and HHV2 vaccines

no vaccine

28

HHV1 and HHV2 drugs

acyclovir etc.

29

HHV1 and HHV2 disease mechanism

virus spreads cell to cell, not neutralized by antibody
cell-mediated immunopathology --> damage and sxs
cell mediated immunity required for resolution of infection
virus establishes latency in neurons
reactivated by stress or immune suppression

30

VZV diseases

chickenpox, shingles

31

VZV transmission

respiratory droplets or contact

32

VZV risk factors

contact, IC
disease severity worsens as get older

33

VZV vaccines

Live vaccine for both (separate)

34

VZV drugs

antiviral drugs - acyclovir, foscarnet

35

VZV disease mechanisms

infects epithelial cells and fibroblasts, spread by viremia to skin, causes lesions (CP)
CM-immunopathology contributes to sxs
CM-immunity required for resolution of infection
Latent infection in neurons
Reactivation by immune suppression (from DRG) Reactivation leads to zoster or shingles, formation of lesions over entire dermatome

36

VZV incubation period

15 days, contagious period for 10, then latency in DRG

37

Poxvirus

virus - dsDNA (group 1) - linear genome - complex nucleocapsid - enveloped - poxviridae

38

Poxvirus subfamilies

Molluscipoxvirus (Molluscum contagiosum)
Orthpoxvirus (smallpox)
Parapoxvirus (Orf virus)

39

Poxvirus disease mechanisms

infects respiratory tract, spreads through lymphatics and blood
MC and zoonoses transmitted by contact
Sequential infection of multiple organs
cell-mediated and humoral immunity important to resolve

40

Picornavirus (enterovirus) disease mechanism

Enter oropharyngeal or intestinal mucosa
secretory IgA can prevent infections
spread by viremia to target tissues
serum Ab blocks spread
virus shed in feces
high asymptomatic infection rate

41

virus - dsDNA (group 1) - linear genome - complex nucleocapsid - enveloped -

poxvirus

42

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucleocapsid - picornavirdidae

enterovirus

43

enterovirus

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucelocapsid - picornaviridae

44

enterovirus subfamilies

poliovirus
coxsackievirus A & B --> HFM
Echovirus --> various rashes
Rhinovirus
Enterovirus

45

Hand Foot Mouth caused by

Coxsackie A virus predominantly

46

Measles virus aka

Rubeola

47

virus - ssRNA (-) Group V - nonsegmented - helical nucleocapsid - enveloped - paramyxoviridae - morbillivirus

measles virus (rubeola)

48

Rubeola tree

virus - ssRNA (-) Group V - nonsegmented - helical nucleocapsid - enveloped - paramyxoviridae - morbillivirus - measles virus

49

measles disease mechanism

infects epithelial cells of respiratory tract, spreads to lymphocytes and by viremia
replicated in conjunctivae, respiratory tract, urinary tract, lymphatic system, blood vessels and CNS
T-cell response to virus-infected capillary endothelial cell --> rash
cell mediated immunity required to control infection
complications d/t immunopathogenesis or viral mutants

50

infects epithelial cells of respiratory tract, spreads to lymphocytes and by viremia
replicated in conjunctivae, respiratory tract, urinary tract, lymphatic system, blood vessels and CNS
T-cell response to virus-infected capillary endothelial cell --> rash
cell mediated immunity required to control infection
complications d/t immunopathogenesis or viral mutants

measles disease mechanisms

51

infects respiratory tract, spreads through lymphatics and blood
MC and zoonoses transmitted by contact
Sequential infection of multiple organs
cell-mediated and humoral immunity important to resolve

poxvirus disease mechanisms

52

Enter oropharyngeal or intestinal mucosa
secretory IgA can prevent infections
spread by viremia to target tissues
serum Ab blocks spread
virus shed in feces
high asymptomatic infection rate

picornavirus disease mechanisms

53

virus spreads cell to cell, not neutralized by antibody
cell-mediated immunopathology --> damage and sxs
cell mediated immunity required for resolution of infection
virus establishes latency in neurons
reactivated by stress or immune suppression

HHV 1 and 2 disease mechanisms

54

infects epithelial cells and fibroblasts, spread by viremia to skin, causes lesions
CM-immunopathology contributes to sxs
CM-immunity required for resolution of infection
Latent infection in neurons
Reactivation by immune suppression (from DRG) Reactivation leads to zoster or shingles, formation of lesions over entire dermatome

VZV disease mechanisms

55

rubella virus aka

German measles

56

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucleocapsid - enveloped - togaviridae - rubivirus -

Rubella virus

57

rubella virus tree

virus - ssRNA (+) Group IV - nonsegmented - icosahedral nucleocapsid - enveloped - togaviridae - rubivirus -

58

erythema infectiosum

fifth disease
mild by highly contagious disease - slapped-cheek appearance

59

fifth disease causative agent

parvovirus B19

60

Parvovirus B19

Virus - ssDNA group II - linear genome - icosahedral nucleocapsid - nonenveloped - parvoviridae - erythrovirus (parvovirus B19)

61

Virus - ssDNA group II - linear genome - icosahedral nucleocapsid - nonenveloped -

parvoviridae - erythrovirus (parvovirus B19)

62

Parvovirus complications

aplastic crisis, acute polyarthritis, abortion

63

Sixth disease "Roseola"

young children, babies
high fever up to 105 then maculopapular rash (or not)
First on chest and trunk
by time rash, disease almost over

64

Roseola causative agent

HHV6/7 - can remain latent

65

IF HHV6/7 reactivate from latency in adulthood

mono-like, hepatitis-like

66

vaccine or drugs for roseola?

None

67

Virus - dsDNA group 1 - circular genome - icosahedral nucleocapsid - nonenveloped - papoviridae

papillomavirus

68

infects epithelial cells of skin, mucous membranes
replication depends on stage of epithelial cell differentiation
cause benign outgrowth of cells into warts
some types are associated with dysplasia --> cancerous

HPV disease mechanisms

69

HPV disease mechanisms

infects epithelial cells of skin, mucous membranes
replication depends on stage of epithelial cell differentiation
cause benign outgrowth of cells into warts
some types are associated with dysplasia --> cancerous

70

HPV tree

Virus - dsDNA group 1 - circular genome - icosahedral nucleocapsid - nonenveloped - papoviridae

71

Molluscum contagiosum type of virus and spread

poxvirus
direct contact (STD) or indirect

72

viral mechanisms of disease

1. tumorigenesis
2. host cell destruction (lysis, autophagy, apoptosis)
3. host immune response leading to tissue damage

73

Koplik spots

measles
lesions on buccal mucosa that precede the rash and are considered pathognomonic

74

chickenpox vs. smallpos

vesicles --> pustules (often displayed at same time in chickenpox) whereas in smallpox are generally all at same stage

75

Which strains of HPV --> cervical cancer?

16, 18 - cause genital warts --> cervical cancer

76

HPV: : transmitted by _______, virus infects ________.

transmitted by close contact, virus infects squamous cells in the epidermis or mucous membranes.

77

HPV: Lysogenic vs lytic

Lysogenic - basal cells, cannot replicate by transform using E6 and E7 - benign cell growth and vacuolization
Lytic - upper keratinized epithelium or basal cell and it rises and differentiates. Replication --> lysis --> further infection.

78

HPV: Infection controlled through

cell mediated immunity

79

dx of hpv

1% acetic acid turns lesions white
colposcopy + biopsy of white lesions
PCR

80

Tx and vaccines for HPV

spontaneously regress in 1 to 2 years
Ablation
HPV vaccines - gardasis cervarix

81

Molluscum Contagiosum (MCV): spread

autoinoculation, in which virus from one lesion spreads to other parts of the body via scratching, is common in children

82

MCV: location

Unlike varicella or HSV infections, MCV infection is limited to the epidermis and does not establish a dormant state. The rash associated with this virus is most often seen on the trunk and anogenital regions.

83

MCV in immunocompromised people

Immunosuppressed individuals may have multiple, large lesions that do not resolve spontaneously. MCV is most often seen in AIDS patients.

84

MCV clinical presentation

pearly skin papules and nodules.

85

HPV clinical presentation

Acute – warts (on penis, vulva, cervix, fingers, hands, soles, knees, elbows, oropharynx, larynx). Chronic – asymptomatic or carcinomas (cervical carcinoma, squamous cell carcinoma, laryngeal carcinoma).

86

MCV pathology (spread, cause of nodules)

Virus transmitted by casual contact and infects epidermal cells creating large eosinophilic inclusion bodies that contain virus particles (molluscum bodies) within them. The molluscum bodies enlarge the infected cells to form dome-like structures that leads to the eventual rupture of the infected cells forming a central crater.

87

MCV dx

clinical presentation (non-painful domes with dimpled center). Skin biopsy (molluscum bodies and in epidermal layer, limited inflammation)

88

MCV tx

self resolves in 6 to 12 months or surgically remove lesions (cryotherapy, laser treatment)

89

Smallpox eradication

The last case of smallpox was reported in Somalia in 1977. Now only a few vials of the virus exist including a couple here in the United States. The eradication effort against smallpox worked because only one smallpox stereotype existed, there is no smallpox carrier state, and there are no animal reservoirs of the virus.

90

Smallpox causative agent

Variola virus

91

Smallpox clinical presentation

rash (macules --> vesicles)

92

Smallpox: pathology when inhaled in aerosols

virus infects upper respiratory epithelium and from here it penetrates the mucosa and enters the bloodstream establishing primary viremia. At this point the virus infects and multiplies within the internal organs and a large number of virions are released into the bloodstream establishing secondary viremia. From here the virus spreads throughout the body, giving focal infections in the skin, lungs, intestines, kidneys, and brain.

93

Smallpox: pathology when skin is infected

virus particles collect and replicate in the epidermis. These collections form macules first in the head and then later in the extremities. The virus replicates and generates a host immune response and the macules become puss-filled vesicles. Crusts form in 2 to 3 weeks and infectious particles are released.

94

Smallpox dx

detection in vesicular fluid, serology

95

Smallpox tx

vaccination (now only to those in military)

96

Orf virus clinical presentation

Exanthemous disease causing denuded lesions.
Ecthyma contagiosum

97

Orf virus pathology

Zoonotic disease where humans contract infections by coming in direct contact with infected sheep and goats or fomites carrying the virus. This virus causes a local, purulent-appearing papule. Generally there are no systemic infections with an immunocompetent host. Serious damage may be inflicted on the eye if the eye becomes infected by this virus, even with healthy individuals.

98

Orf virus dx

case hx and clinical presentation

99

orf virus tx

1% topical cidofovir

100

Varicella-Zoster Virus (HHV-3) clinical presentation

Varicella (chickenpox) or zoster (shingles)

101

VZV spread

high contagious
respiratory secretions or contact w/ ruptured vesicles

102

VZV pathology

The virus infects the respiratory tract and following a two-week incubation period the virus establishes viremia in the host. This is accompanied by flulike symptoms and widespread vesicles with a red base appearing as “dew on a rose petal” (varicella). The rash continues to spread centrifugally and is typically mild in children but may be severe in adults where it can progress to pneumonia or encephalitis. The varicella resolves within two weeks and the virus enters local sensory nerve endings where it is axonally transported proximally to sensory ganglion cell bodies establishing latent infection of the dorsal root ganglion.

103

VZV reactivation

Stress or some other form of immunocompromise can lead to viral reactivation. This results in axonal transport of virus from the ganglia to the nerve endings where a recurrent painful vesicular rash appears over the sensory dermatome (zoster).

104

VZV dx

detection of virus. Clinical inspection of the rash. Multinucleate giant cells on Tzanck smear of skin lesions. Eosinophilic Cowdry intranuclear inclusion bodies on skin biopsy.

105

VZV tx

Supportive. For severe infections acyclovir or famciclovir can be used. Anti-VZV immunoglobulin can be effective in immunocompromized individuals. There is a vaccine available (live-attenuated VZV).

106

_______ can be associated with aspirin treatment for chickenpox in children.

Reye’s syndrome (liver damage and encephalomyelitis)

107

HSV-1 epidemiology

most common cause of sporadic encephalitis in the United States (HSV-1 in adults and HSV-2 in neonates). Most adults have been infected by HSV-1 or -2, but very few infections are symptomatic and only 25% of latent infections exhibit recurrent infections.

108

HSV-1 clinical presentation

Gingivostomatitis, keratoconjunctivitis, herpes labialis (cold sores), temporal lobe encephalitis

109

HSV-1 pathology: (reservoir, transmission, infection)

humans are only reservoir
transmitted by saliva
invades mucous membranes --> primary local infection-typically asymptomatic but can cause vesicular lesions that ulcerate in the mouth (gingivostomatis) and eye keratoconjuctivitis (on cornea, typically presents as branching “dencritic ulcer”). The primary infection resolves after 2 to 3 weeks.
virus enters local sensory nerve endings and is transported along the axon proximally to the sensory ganglion cell bodies to establish latent infection in the trigeminal ganglion or other sensory ganglia.

110

HSV-1 reactivation

Stress (fever, menstruation, sunlight) can lead to virus reactivation.
axonal transport of the virus from the ganglia to the nerve endings where it establishes a local recurrent infection which may result in herpetic labialis (cold sores around the mouth), gingvostomatitis or keratoconjunctivitis.
Rarely - via cranial nerves to brain --> focal necrotic lesions in the temporal lobe leading to inflammation, encephalitis and permanent neurological abnormalities or death.

111

HSV-1 dx

detection of virus (PCR, good for early detection in encephalitis), multinucleate giant cells on Tzanck smear of skin lesions, eosinophilic Cowdry intranuclear inclusion bodies on skin biopsy. Fluorescent antibody test available.

112

HSV-1 tx

acyclovir, trifluridine (topical, for eye infections)

113

HSV-2 clinical presentation

genital herpes or neonatal herpes

114

HSV-2 reservoir and spread

humans are the only reservoir for this virus and infection transmission is by sexual contact.

115

HSV-2 infection

virus invades mucous membranes and sets up a local primary infection that is typically asymptomatic but can cause vesicular lesions in the genital and perianal area.
The primary infection resolves after 2 to 3 weeks when the virus enters the local sensory nerve endings and is transported via the axon proximally to sensory ganglion cell bodies and establishes latent infection of the lumbosacral ganglia.

116

HSV-2 reactivation

Stress (fever, menstruation, sunlight) can initiate viral reactivation leading to axonal transport of the virus from the ganglia to the nerve endings resulting in a milder, recurrent vesicular infection at the primary site.

117

HSV-2 to fetus

If a pregnant mother is infected the virus may transfer to the fetus through the placenta or during delivery. The infected child typically will have congenital defects or the infection may result in abortion or neonatal encephalitis.

118

HSV-2 dx

detection of virus (PCR, good for early detection in encephalitis), multinucleate giant cells on Tzanck smear of skin lesions, eosinophilic Cowdry intranuclear inclusion bodies on skin biopsy.

119

HSV-2 tx

Prevention – cesarean section in infected mothers.

120

Roseoloviruses HHV6/7 Clinical presentation

Exanthem subitum (sixth disease)
Reactivation can occur in organ transplant patients leading to enchepalitis, bone marrow suppression and pneumonitis.

121

HHV6/7 spread

Virus is transmitted through aerosols.

122

HHV6/7 epidemiology

Infection is typically seen in children ages 3 months to 3 years. This infection can occur year-round but has a higher incidence in the spring.

123

HHV6/7 pathology

Primarily an infection in children that typically results in either a subclinical infection or an acute febrile illness. A fine maculopapular rash on the neck and trunk can be seen in some cases.

124

HHV6/7 dx

clinical presentation. In severe cases definitive diagnosis by ELISA or indirect immunofluorescence is possible.

125

HHV6/7 tx

Ganciclovir, supportive

126

EBV (HHV-4) risks

patients with infectious mononucleosis are at risk for splenic rupture due to splenomegaly and should avoid contact sports.
A rash occurs in a few cases of mononucleosis however if ampicillin is given to treat tonsillitis (before EBV is diagnosed) then a rash occurs in most cases.

127

EBV clinical presentation

infectious mononucleosis (“kissing disease”), lymphoid organ-related cancers: Burkitt’s lymphoma, nasopharyngeal cancer (East Asia).

128

EBV spread

transmitted by saliva and respiratory secretions.

129

EBV infection

Infects the oropharynx epithelium, which leads to viremia. Here the virus binds to and infects B cells. The virus remains latent in B cells as episomal DNA. The infected and B cells are transformed and multiply. This creates an immune response to the infected B cells and the lymph nodes and spleen both enlarge and the host experiences flulike symptoms and a painful, red sore throat (mononucleosis). The immune response eventually controls the B cell expansion and the infection resolves.

130

EBV in immunocompromised people

If the immune system is compromised you get uncontrolled B-cell proliferation and unrepaired mutations accumulate which may increase chances for neoplasms like Burkitt’s lymphoma.

131

EBV dx

monospot test – detects heterophil antibody (nonspecific antibody that agglutinates sheep RBCs.)
Blood smear – atypical lymphocytes (cytotoxic T lymphocytes that react against infected B cells)
Serology – anti-EBV IgM (acute infection), IgG (past infection).

132

EBV tx

acyclovir in severe cases

133

Parvovirus B19 in IC, fetuses

in immunodeficiency patients parvovirus infection can lead to chronic severe anemia. Fetuses who require higher red blood cell production and are immunodeficient are especially vulnerable to parvovirus infections. Infected fetuses may develop severe anemia and hydrops fetalis.

134

Parvovirus B19 clinical presentation

erythema infectiosum (“fifth disease” - slapped cheeks), transient aplastic anemia crisis

135

Parvovirus B19 pathology

virus establishes infection in nasal cavity followed by a six day incubation which leads to viremia and fever.
virus infects and lyses erythoid precursor cells in the bone marrow. This leads to mildly reduced reticulocytes, lymphocytes, neutrophils, and platelets. Normal hosts can tolerate a lack of erythropoiesis for 1 week.
Immune complexes form which leads to erythema infectiosum which is a rash with a “slapped cheek” appearance. This is accompanied by muscle aches for several days.

In patients requiring increased erythropoiesis (sickle cell anemia, thalassemias) there is a transient aplastic crisis and severe reticulocytopenia with normal myeloid lineage.

136

Parvovirus B19 dx

detect viral DNA, serology

137

Parvovirus B19 tx

Supportive. RBC transfusion. In immunocompromised individuals – Ig transfer.

138

Coxsackievirus A & B clinical presentation

Coxsackie A – herpangia, hand-foot-and-mouth disease.
Coxsackie B – pleurodynia, myocarditis, pericarditis.
A and B – aseptic meningitis, paralysis, upper respiratory tract infection.

139

Coxsackievirus epidemiology

infections are typical in summer and fall and the virus is transmitted via aerosols or fecal to oral route.

140

Coxsackievirus pathology

The virus travels in the G.I. tract and infects mucosal epithelial cells. Local replication ensues and virus spreads in the bloodstream. From here the virus infects and can lyse skin and mucosal epithelium (Group A) to form vesicles leading to herpangina (red oropharynx vesicles, fever, sore throat), hand-foot-and-mouth disease.

141

Coxsackievirus complications

In Group B infections the virus travels to the heart and pleural surfaces to cause pleurodynia, myocarditis, and pericarditis.

In Group A and B infections the virus can travel to the meninges and anterior horn motor neurons to cause meningitis and paralysis.

142

Coxsackievirus dx

isolate virus, serology

143

Coxsackievirus tx

Symptomatic infections – anti-inflammatory agents. No antivirals or vaccines available.

144

ECHO virus clinical presentation

Acute febrile illness often in male children. Non-specific exanthem.

145

ECHO virus spread

Fecal to oral route of transmission, sometimes salivary aerosols.

146

ECHO virus pathology

Infection in neonates can be fatal. Myocarditis is a frequent complication in adult infections. Infection typically causes a non-specific illness with fever. Sometimes a rash can be produced that spreads from the face down to the neck and upper extremities and chest.

147

ECHO virus dx

serology

148

ECHO virus tx

Supportive. New antiviral called pleconaril interferes with viral attachment and penetration.

149

Measles virus clinical presentation

Rubeola. Flu-like symptoms, Koplik’s spots followed by rash, and sometimes encephalitis. Subacute sclerosing panaencephalitis (SSPE) can occur in infections with complications.

150

Measles virus epidemiology

this virus spreads human to human by respiratory aerosol droplets.

151

Measles virus spread throughout body

The virus infects, replicates within, and eventually destroys epithelial cells. This leads to the first (primary) viremia. From here the virus infects and replicates in reticuloendothelial cells leading to secondary viremia which allows the virus to spread to several other areas in the body.

152

Measles virus pathogenesis: mucosa, koplik's, rash

At the mucosa, infection promotes inflammation around capillaries.
In the mouth you see Koplik’s spots (red lesions with a blue-white center).
At the dermis, infection also promotes inflammation around capillaries that forms a rash starting at the head and progressing to the feet, disappearing in the order that it appears.

153

Measles virus in the CNS

In the brain, infection can lead to meningitis and encephalitis.
Infections with measles virus variants can lead to a chronic low-level infection of the central nervous system. This creates inflammatory lesions in the brain that gradually present as personality and cognitive changes (subacute sclerosing panenchalitis or SSPE) this eventually leads to death.

154

Measles virus pathogenesis in GI and lungs

In the respiratory tract and lung, giant cells form with inclusion bodies (Warthin-Finkeldey cells) this cell damage leads to a cough.

155

Measles dx

isolate the virus from nasopharyngeal secretions, blood, and urine. Warthin-Finkeldey cells (multinucleated giant cells with inclusion bodies in the nucleus and cytoplasm) in respiratory secretions. Serology.

156

Measles tx

Vaccine of a live-attenuated virus in the MMR vaccine. In severe cases in infants administer high doses of vitamin A.

157

Rubella Virus clinical presenation

German measles
rubella – fever followed by descending rash.
Congenital rubella – congenital malformations (deafness, patent ductus arteriosus, pulmonary artery stenosis, cataracts, microcephaly)

158

Rubella virus spread

this virus is transmitted by aerosol and infects nasopharynx

159

Rubella virus pathology

replicates in the local lymph node. Systemic spread is through the bloodstream. An antibody mediated reaction leads to maculopapular rash beginning in the face and spreading to the extremities. Antibody complexes many result in arthritis in women.

160

Rubella in a pregnant woman

If the virus infects pregnant women in their first trimester then the virus may cross the placenta and reach the fetus. Here the virus infects fetal cells and promotes mitotic arrest, necrosis, or chromosomal damage. This leads to congenital defects in the brain, heart, and eyes.

161

Rubella dx

Detection of anti-rubella antibodies. IgM if recent infection – IgG if immune. Virus in aminocentesis indicates congenital rubella.

162

Rubella tx

self-limiting – no antiviral. Vaccine – live-attenuated rubella virus in MMR vaccine.

163

clusters of dead crows usually herald human cases of ______

West Nile Virus

164

West Nile Virus clinical presentation

most infections are asymptomatic. West Nile Fever – fever, fatigue, headache, myalgia, anorexia, eye pain, nausea, vomiting, diarrhea, rash. West Nile encephalitis – neuroinvasive disease causing encephalitis (more typical in the elderly) or meningitis (more typical in children). Symptoms range from mild confusion to tremor, extrapyramidal symptoms, flaccid paralysis, or severe encephalopathy that may progress to coma or death, particularly in the elderly or immunocompromised.

165

West Nile virus epidemiology

Virus is maintained in a cycle of infection that includes mosquitos, birds and humans. Spreads to incidental human host by a mosquito bite

166

West Nile Virus pathology

replicates in the skin Langerhans cells which migrate into the regional lymph nodes followed by viremia and infection of multiple organs including the CNS.

167

West Nile Virus dx

IgM Ab in serum or CSF. PCR of the CSF.

168

West Nile Virus tx

Supportive. Prevention against mosquito bites.