skin 7: karposi sarcoma, measles, rubella, NPEs Flashcards Preview

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Flashcards in skin 7: karposi sarcoma, measles, rubella, NPEs Deck (56):

Kaposi sarcoma caused by ??

Low endemicity in US, but high endemicity in underdeveloped countries.
Secreted in saliva; unknown if shed chronically or only during primary infection. B
cells are one site of latency
HHV-8 is associated with all forms Karposi sarcoma (KS)


Kaposi sarcoma risk factors:

older than 60yr males of Mediterranean and Middle Eastern
extraction; AIDS


kaposi sarcoma Clinical Manifestation

bluish-red or purple bumps (tumors) on the skin (rich in blood vessels)
lesions may first appear on the feet or ankles, thighs, arms, hands, face, or any other part of the body. They also can appear on sites inside the body.


kaposi sarcoma ddx

Bacillary angimatosis cause by Bartonella sp


karposi sarcoma tx

localized nodular disease may respond well to surgical excision, radiotherapy, and
intralesional and outpatient low-dose vinblastine chemotherapy



(Rubeola or “hard” measles or "1st disease")
acute highly contagious disease characterized by fever, a generalized maculopapular rash, and a high rate of complications and/or post-infection sequelae.
characterized by: *cough, coryza, conjunctivitis, Koplik spots*


measles is a ??

Paramyxovirus virus -
measles: an enveloped ssRNA virus with *one serotype* (genus: Mobillivirus)

also includes mumps, parainfluenza and respiratory syncytial viruses (RSV), human metapneumovirus (hMNV), which all cause *syncytia formation* (HSV, HIV)


measle: infectious?

*one of the most communicable diseases known* -aerosolized!!
-Humans and other primates are the only known hosts; there is no carrier state.
-1 in 8 children and adolescents are at risk for measles (entire pop vulnerable)
-2% further reduction in immunity will result in levels below need for herd immunity: 1/1000 will dev. acute encephalitis/BD
1/2000 will die


age ??
seasonality ??

-Major cause of death in *younger than 5 years old* (2-3 million primarily due to diarrhea and pneumonia) where there is malnutrition and poor medical care
-winter and spring peak incidence (crowding, like chickenpox, 5th disease, UNLIKE HHV6 (6th disease), which is yr round))


measles POE is ??
pass how??

infectious period begins when??

URT and perhaps conjunctivae (like VZV, 5th, 6th disease), passed by direct contact with respiratory secretions through *aerosols*,
direct contact, or less commonly by fomites freshly soiled with respiratory secretions.

Period of communicability begins with prodrome until about 4 or 5 days after onset of rash.


measles: high attack rate ??

what protects newborns??

Primary attack rate- 99%! (beats influenza virus, about 95%) and secondary attack rate is 90%. Herd immunity must be 90 to 95%. (need almost everyone vaccinated!)
can remain infectious in air up to 2 hrs
-Maternal antibodies prevent efficacious immunization until 12 months, vaccinate after 1 yr


is measles eliminated in the US?

not completely, Sporadic epidemics and microepidemics in the nonimmunized and immigrant populations have thus far prevented it elimination in the U.S. Most outbreaks have been urban areas (Houston, L.A., etc.)


measles incubation period
virus replicates ??

10-14 days
n the URT and draining lymph nodes


what happens 2 to 3 days post-exposure to measles ??

*primary viremia*
due to the virus spreading to lymphoid tissue throughout body within monocytes.


A ?? occurs from day 5 or 6 onward (post-measles exposure)- wide dissemination to ??.
Induces ??
The infection must be controlled by ??

secondary, prolonged viremia
wide dissemination to GI, RES, CNS, UT (virus can be detected in urine) – this viremia results in s/s
Induces multinucleated giant cell (syncytia) formation in all infected cells.
The infection must be controlled by *CMI*


measles immune (CMI) response results in ??

-Rash - measles virus-specific T cells target viral antigens processed with HLA class I and class II molecules in the surface of cells in the capillary endothelium and in small blood vessels.
*UNLIKE 5th, 6th diseases: due to Ab-Ag deposition
-Full-body desquamation of all epithelial surfaces (exfoliation of epithelial cells).
-Anergy lasting weeks to months following measles infection. Anergy may also
occur immediately following immunization with MMR vaccine. (may have secondary pneumonia)


measles clinical manifestations: prodromal phase

0-12 days post-infection and 3-4 days before the exanthem
roughly coincides with a persisting secondary viremia indicates onset of the adaptive immune response (note the 3 Cs below).
High fever, Fatigue/malaise
*Coryza*, Persistent, brassy, non-productive *Cough* (a measles bronchitis), *Conjunctivitis* with photophobia
Pharyngitis, Cervical lymphadenopathy
Koplik's spots


Koplik's spots

Fleeting (last only 1-2 days) lesions that appear on buccal mucosa and can also be present on the conjunctiva and vagina
Early lesions are mm sized bluish-gray enanthem; Late lesions are white “grains of salt” on a red base.
virtually *pathognomonic* for measles in a patient with other prodromal s/s


measles clinical manifestations: eruptive phase (rash)

appears at about 3 days following onset of prodromal stage
-A symmetrical, non-pruritic, bright (florid) red maculopapular rash (morbilliform) appears on the face (scalp line) and descends to lower extremities.
-Rash is confluent on the head and as the rash descends it thins and becomes discrete.
-Viral antigen can be demonstrated in lesions
(rash does not go away when fever defervesces)
*viral Ag and T cells in lesion, but lesions not infections*

*UNLIKE 5th, 6th diseases: due to Ab-Ag deposition


measles clinical manifestations: resolution phase

1-2 days later (post-eruption), as antibody titers rise, disseminated viremia halts and symptoms abate - there is rapid defervescence and the rash clears by a fine briny desquamation, first on the face and then descends (fading in the same order as it appears).


measles complications related to CMI suppression? Epithelial compromise? Both?

Not known.


measles complications

-OM: most common complication, due to 2o bacterial infection of inner ear (1/10 lose hearing)
-Pneumonia occurs in 2-3 % of all measles cases – primary viral Giant cell pneumonia or a secondary bacterial infection or a bacterial superinfection as a
result of desquamation of RT epithelial surfaces.
-Diarrhea (can be protracted) as a result of desquamation of GI tract epithelial surfaces (particularly if Vitamin A or protein malnourished)


measles CNS complications

Primary viral encephalitis and post-measles encephalomyelitis (immune- mediate) occurs in 1 in every 1,000 to 2,000 cases of measles. It is more likely to occur in children >10-y-o-age


measles CNS complications: SSPE

Subacute sclerosing panencephalitis (SSPE) occurs in 1 of every 500 cases of measles encephalitis.
It is a fatal, slowly progressive, inflammatory, demyelinating disease of the CNS which occurs primarily in children & young adults caused by defective measles virus infection in the CNS.
SSPE is very rare in US-born children, more common in developing countries


measles complications: congenital disease

Maternal primary infection during pregnancy may result in virus crossing placenta, infecting fetus, causing still birth, spontaneous abortion, fetal malformation.


measles immunity is ??

lifelong and both antibody and cellular immunity are important.


measles dx

Clinical appearance of rash 3-4 days after typical prodromal symptoms.
Laboratory diagnosis via serology or FAT and giant cell formation in affected tissues. (syncytial cell formation)
*reportable disease*
consider in pts with febrile rash illness esp. with recent exposure or travel hx


measles tx

-Supportive therapy is recommended. Vitamin A supplementation may speed recovery due to increased epithelial cell regeneration. (esp malnourished populations)
-IgG for immunocompromised or unvaccinated individuals w/in 6 days of exposure.
-Disease resolution confers life-long immunity?? up for debate, may need re-vaccination?


measles ppx

trivalent measles, mumps, rubella live attenuated vaccine (MMR). Attenuated vaccine. (2 doses better than 1)
-First dose is recommended at 15-18 months
-second dose at 4-6 years (school-entry age) or age 11-13 years but can be administered at any time after the first dose so long as at least 4 weeks have elapsed
(US currently at less than 85% herd immunity)


measles vaccine risks ??
given to adults??

Risk of vaccine-associated febrile seizures – are not associated with any long-term adverse outcomes (e.g. autism or rheumatic diseases).

In adults, one dose is recommended if not previously immunized. Two doses in the occupationally or geographically exposed.


contraindications for MMR vaccine

should not be administered to the immunocompromised, pregnant, or those who may wish to become pregnant within 3 months of administration.
(like other live attenuated vaccines)



(German measles, “soft” measles, 3 day measles)

mild benign exanthematous disease characterized by minimal or absent prodromal stage, a *3 day rash (mobilliform), generalized lymph node enlargement*
(Virus originally isolated by a German doc., hence name)


rubella etiology

Togavirus (an enveloped ssRNA) unlike other Togaviridae, is NOT arthropod-borne. There is only *one serotype*


rubella host

Humans are the sole hosts; there is no carrier state. (like measles)


rubella POE

is URT and perhaps
conjunctivae, passed by direct contact with respiratory secretions


rubella: age??

higher incidence in older children, adolescents and young adults.

peak incidence is in the winter and spring (like other viruses exp. HHV6)


rubella communicability

Patient is communicable from 5 days before to 5 days after appearance of rash.
Not as communicable as measles or chicken pox - about 20% of pre-vaccine era persons reached adulthood without exposure.


rubella in the US: common or rare??

Due to vaccination the incidence of rubella and congenital disease is now rare in US. (seropositivity due to vaccination)
Populations at risk include immigrants from developing countries and continental Europe.
on the rise due to anti-vaccine movement (MMR)


rubella incubation period is ??
prolonged viral replication in the ??

14-21 days
pharynx (for up to 2 weeks) Then a viremia occurs
which results in s/s


rubella clinical manifestations: prodrome??

Prodromal symptoms are minimal or absent (relatively asymptomatic) but virus replicates in the pharynx for up to 2 weeks


rubella clinical manifestations: symptoms (if present)

Low-grade fever, Fatigue/malaise
Conjunctivitis, Coryza, Pharyngitis
Pronounced lymph node enlargement/*lymphadenitis*(postauricular, suboccipital, cervical)
Discrete pink-red (not brick red like measles) maculopapular rash lasting 3-5 days. Appears initially on face then spreads downward to involve the trunk and extremities.
Arthralgia (like Parvovirus B19)
thrombocytopenia purpura and encephalitis (more common in adults)


rubella arthralgia

arthropathy, increasing incidence with age, more common in women – very similar to parvovirus B19 in this regard. Adults may manifest with only mild fever and joint involvement. Some think many “viral syndromes with fever and arthralgia” may be secondary rubella or breakthrough rubella in adults.


rubella complications: Congenital Rubella Syndrome (CRS):

No risk to mother.
-Maternal viremia may result in placental infection leading to fetal viremia. *first trimester* is the most critical time:
-Organogenesis is disrupted by viral infection of fetal cells (50-60% risk that maternal viremia will result in fetal infection and teratogenic effects).
-Chronic and persistent infection of the infant/child is likely.
-Isolation is required for infected neonate because of prolonged (months) shedding of virus in urine and respiratory secretions.


clinical manifestations associated with Congenital Rubella Syndrome (CRS)

Cardiac defects: *pulmonary artery stenosis, patent ductus arteriosis*
Eye defects: cataracts, glaucoma.
Hearing loss or deficit.
CNS involvement (learning and/or speech deficits).
-purpuric lesions: destruction of vasculature

15% mortality: The lower the birth weight, the greater likelihood of severe complications.


rubella dx

-lab dx for newborn: (Syphilis, Toxoplasmosis, Rubella, Cytomegalovirus, Herpes virus ([S]TORCH or TORCH[S]) by measuring agent-specific IgM Ab titers in cord blood.
-Tests for immune status via latex agglutination tests in prenatal exam, not TORCH.


clinical diagnosis of rubella is difficult because ??

many ECHO viruses and can mimic manifestations of rubella and are more common than rubella. (summer/fall)


rubella tx: IgG??

Treatment with immunoglobulin (IgG) is NOT recommended under most conditions
Most treatments are supportive
Based on risks above, some physicians provide counsel that includes therapeutic abortion if
CRS is likely.


rubella ppx

MMR vaccine (see above)
Immune globulin: Post-exposure prophylaxis does not prevent rubella infection or viremia.


If a susceptible pregnant woman is exposed to rubella and wishes not to consider termination of the pregnancy under any circumstance, then ?? within ?? might reduce (not eliminate) the risk of CRS.

20 ml IgG IM
72 hours (3 days) of exposure


Preventive measures for CRS: Vaccinate non-pregnant women; how to deal with preggos??

pregnant women should avoid exposure and immunization. Screen pregnant women and those who plan to become pregnant for rubella antibody. Non-pregnant women wishing to become pregnant and are seronegative or have no history of immunization should be immunized.


Since the advent of the MMR vaccine, ?? has become the leading cause of infection and morbidity in the neonate.


It is estimated that 40,000 CMV-infected neonates are born each year in the USA and 8,000 (20%) of these will have serious neurological sequelae due to congenital disease.


NPEs: importance?
causes ??
seasonality ??

ne of the most common and important viral pathogens in humans, causing 5 to 15 million cases of
nonspecific febrile illness with or without rash/year in the US
with peak incidence in summer and fall months.


NPEs are responsible for ??

more than 1⁄2 of all febrile illness in infants and young children during the summer and early fall months.
Major reason why blood culture and/or spinal taps are
done on infants and young children in the U.S


NPE etiologic agents

ECHOvirus (enteric cytopathic human orphan virus – many [31] serotypes)
Coxsackie viruses (A and B - many [30] serotypes).
Enteroviruses 68-71

(very little cross-protection between serogroups occurs and there are many (>70) serotypes)


NPE manifestations

(In children and adults)
Abrupt onset of undifferentiated febrile illness (nonspecific, constitutional s/s):
Sore throat, Vomiting and diarrhea, Malaise


sometimes NPE febrile illness develops into the ??

*classic common syndromes*:

Fever + rash (mostly maculopapular, can be petechial, vesicular)
Hand, foot and mouth disease (HFMD)
Epidemic pleurodynia.

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