Viral Skin Infections (Virus) Flashcards
(168 cards)
1
Q
Vesicular or Pustural Rash Diseases - major viral causes
A
HHV-1* (Neuro, HRM) HHV-2* (Neuro, HRM) HHV-3 Coxsackieviruses A and B Smallpox Orf virus* (in handout)
2
Q
Maculopapular Rash Diseases - major viral causes
A
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
Q
Wartlike eruptions - major viral causes
A
HPV
Molluscum contagiosum
4
Q
Steps of Viral Infection inside organism
A
Replication at site of entry Primary viremia Replication Secondary viremia Replication Transmission to other hosts *See picture*
5
Q
Herpesvirus infections last a life time in a state called ____
A
latency
6
Q
Herpesvirus do/do no integrate into host genome
A
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
Q
Herpesvirus can/cannot reactivate
A
Can - more infectious
8
Q
virus - dsDNA (group I) - linear genome - icosahedral nucleocapsid - enveloped
A
herpesvirus family
9
Q
herpesvirus subfamilies
A
alpha: simplexvirus (1 and 2) Varicellovirus (VZV) beta: cytomegalovirus (HCMV, HHV-6/7) gamma: Lymphocryptovirus (EBV) Kaposisarcoma-associated herpesvirus
10
Q
herpesvirus tree
A
virus - dsDNA (group I) - linear genome - icosahedral nucleocapsid - enveloped
11
Q
Herpes simplex 1
A
alpha - Human herpesvirus 1 (HHV-1)
Above waist - gingivostomatitis, herpes labialis, etc.
12
Q
Herpes simplex 2
A
alpha - Human herpesvirus 2 (HHV2)
Below wait - genital herpes or neonatal herpes
13
Q
Varicella-Zoster virus
A
alpha - HHV-3
Chickenpox or shingles
14
Q
Human cytomegalovirus
A
beta - HHV 5
Congenital CMV infection, systemic, mono-like
15
Q
Roseoloviruses
A
beta - HHV 6(a,b)/7 - exanthem subitum (6th disease), encephalitis in IC
16
Q
Epstein-Barr Virus
A
gamma- HHV-4 - mononucleosis, lymphoid-organ related cancers
17
Q
Kaposi Sarcoma-Associated Herpesvirus
A
gamma - HHV8 - Kaposi sarcoma
18
Q
first disease
A
measles
19
Q
second disease
A
strep pyogenes (scarlet fever)
20
Q
third disease
A
rubella
21
Q
fourth disease
A
staph aureus (SSSS)
22
Q
fifth disease
A
parvovirus B19 (slapped cheek)
23
Q
sixth disease
A
HH6/7 - roseola
24
Q
Virus lifecycle
A
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.
