- viral particles from cornified layer, the keratinized skin cells get sloughed off of

Different Types of Warts:

- Butcher wart: present in butchers, they auto-inoculate their hands

when they would Knick their fingers with a knife and not getting virus
from the animal (?)
- When kids gets older, they have bigger warts because their immune
system stimulates stronger response to Warts
epidermis
HPV 1- Diagnosis
 virus infx - clinical presentation
 Late genes : genes that virus expresses to make the virus particle - Histology
o L1- Major capsid protein Treatment
o L2- Minor capsid protein - Topical Application of caustic agent (compound W)
- Cryotherapy: warts frozen with liquid nitrogen but warts can’t be fully
Host cells and Papilloma virus eliminated bc

- for long periods

- common in infections in kids: kids going to school are covered
by loose fitting bandage

Clinical presentation:
o Self limiting disease: Cluster of lesions, Papular

o Smooth (warts are scaly and rough) and

umbilicated in the center
o Raised and shiny appearance
o Cluster lesions: 6-8 in Localized areas on pts bodies
o Self resolving disease, benign

Pathophysiology
- Target epidermal keratinocytes
- Typical inclusion bodies
- Hyperplastic (Similar to Papilloma virus)

Viral replication:
- basal layer cells replicating and as they differentiate thru the super-basal,
granular and cornified layer (inside to outside of epidermis)
- When infected with papilloma virus, the viral genome is present in the basal cells
- Red areas: infected with papilloma virus, the basal cells will replicate and the
virus genes are going to be expressed including E6 and E7 genes will be expressed
- First genes that are expressed E6 and E7 will cause the cells to replicate outside
the bounds of

Treatment:
- Curettage, cryosurgery
- Topical agents
- Self limiting disease (unsightly, covered in loose fitting
bandage)
 Individuals at high risk for severe illness and complications from
measles:
Measles Virus - Infants and children aged <5 years
- Adults aged >20 years
Transmission: most contagious of all infectious diseases (9/10)- high rate
- Pregnant women
of contagion
- People with compromised immune systems, such as from
- direct contact with infectious droplets
leukemia and HIV infection
- From airborne spread when an infected person breathes,
Diagnosis
coughs, sneezes
- Laboratory confirmation is essential
- Remains infection in air up to 2 hours
- Detection (measles virus is RNA virus)
Symptoms
o Measle-specific IgM antibody in serum
- Characterized by a prodrome: before rash appearance
o Measles- RNA- real time PCR (RT-PCR)
o Fever (as high as 105F)
- Urine samples
o Malaise
o May also contain the virus
o 3Cs: coryza, cough, and conjunctivitis (these
o Collecting both respiratory (nasal-pharyngo) and
symptoms are indicative that they have measles
urine samples can increase likelihood of detection
before the rash appears)
Treatment:
o Koplik spots- pathognomonic enanthema: whitish
- No specific antiviral therapy
lesions on soft palates, hard to see, not true
- Supportive care to help relieve symptoms and address
vesicles (think measles, even if the rash hasn’t
complications such as bacterial infections
developed and you see kolpik spots)
- Severe measles cases among children
o Treated with Vitamin A (dec severity of infx) 
administered immediately on diagnosis and
repeated the next day
Prevention: Vaccination
- combination measles-mumps-rubella (MMR) vaccine
Koplik spots - combination measles-mumps-rubella-varicella (MMRV)
- approximately 97% effective
- Followed by a maculopapular rash - For people w/o evidence of immunity  administer MMR
o Appears ~14 days after exposure within 72 hrs of initial measles exposure or give them IG
o Spreads from head  trunk  lower within 6 days of exposure
extremities

- : abrupt onset of fever 40C (104F)

- Last 3 days, development of rash: maculopapular exanthem
- Rash

Diagnosis:
- Based on clinical presentation
- Roselola infantum, 6th disease
Treatmtent:
- 1st day of rash kolpik spots on buccal mucosa and small and - Symptomatic
discrete appearance of rash rash keeps developing  3rd Complications:
day confluent and discrete macupapules - Immunologically suppressed patients
- Rash is related to vasculitis and antigen antibody complex
deposition, this is why it takes 14 days after primary infection
to develop full blown rash
Complications:
- otitis media, bronchopneumonia, laryngotracheobronchitis,
and diarrhea
- One out of every 1,000 - acute encephalitis, which often
results in permanent brain damage
- One to three out of every 1,000 children will die from
respiratory and neurologic complications
- Subacute sclerosing panencephalitis (SSPE) - rare, but fatal
degenerative disease of the central nervous system that
generally develops 7 to 10 years after measles infection