MMR and Other Childhood Exanthems Flashcards
1
Q
Mumps
A
- Paramyxovirus genus of the Paramixoviridae family
- ( - ) ss RNA virus
- pleomorphic
2
Q
Mumps Structure
A
- (–) Single stranded RNA virus | Nucleoprotein complex
- Matrix protein surrounds nucleocapsid complex
- Envelope contains 2 spikes. One has both H and N activity. The other is called F (fusion) protein.
3
Q
Mumps Replication
A
- Replicates in the cytoplasm like (-) RNA viruses by using virion associated RNA dependent RNA polymerase
- Assembles in the cytoplasm
- Buds through cytoplasmic membranes
4
Q
Mumps Clinical Disease
A
- Enters respiratory tract
- Replicates in respiratory tract epithelium and local lymph nodes
- Viremia: spreads virus throughout body
- Fever followed by painful swelling of one or both parotid glands (parotitis) usually 12 to 29 days (16–18 days average) after exposure
- Symptoms last 7–10 days
- Immunity is life long
5
Q
Mumps Incubation Period
A
- usually 12 to 29 days (16–18 days average) after exposure
- symptoms last 7–10 days
6
Q
Mumps Common Complications
A
- Meningitis |Encephalitis (hearing loss)
- Pancreatitis
- Orchitis (10–20% of infected men)
- Oophoritis (inflammation of ovaries)
- Myocarditis (less common)
- 500 cases every year
7
Q
Mumps Diagnosis
A
- Clinical picture (most common)
- Isolate virus (saliva, urine)
- Serology
8
Q
Mumps Treatment
A
•supportive
9
Q
Mumps Prevention
A
•Live attenuated vaccine after 1st year of life or adults (particularly men)
10
Q
Measles
A
- Morbillivirus genus of the Paramyxoviridae family
- ( - ) ss RNA
- one antigenic strain
- causes rubeola (5 day measles) and hard measles
11
Q
Measles Structure
A
•same as mumps virus but the envelope protein of the measles virus lacks neuraminidase (N) activity
12
Q
Measles Replication
A
- same as mumps virus but the envelope protein of the measles virus lacks neuraminidase (N) activity
- Replicates like (-) RNA virus
- Assembles in the cytoplasm
- Buds out from the plasma membrane
13
Q
Measles Pathogenesis
A
- Enters respiratory tract and replicates in and destroys mucosal epithelium, necrosis and inflammation
- Spreads to local lymph nodes followed by viremia
- Virus transported to all body organs, conjunctiva, urinary tract, small blood vessels, CNS
- T and B lymphocytes, monocytes, polymorphonuclear leukocytes are infected
- Cell-mediated immunity is depressed by IL-12 downregulation, Natural killer cells impaired
- Enhanced susceptibility to bacterial superinfection
- Skin lesions show vasculitis; vascular dilation, edema and perivascular mononuclear cell infiltrates
- Viral components can be seen in the rash
- In some patients, an immune mediated post infectious encephalitis through CD8 T-cells infiltration in the CNS
14
Q
Measles Clinical Disease
A
- Spreads to local lymph nodes
- Viremia: transported to all body organs, symptoms occur 7-18 days (9–11 days average) post exposure
- Koplik spots first appear in mouth (buccal mucosa) as small bluish– yellow spots 1–2 days before rash.
- Rash first appears on head, then trunk and extremities.
15
Q
Measles Incubation
A
•symptoms occur 7-18 days (9–11 days average) post exposure
16
Q
Measles Koplik Spots
A
•Koplik spots first appear in mouth (buccal mucosa) as small bluish– yellow spots 1–2 days before rash.
17
Q
Measles Severity
A
•High fever, delirium, cough, photophobia (light–induced eye pain), conjunctivitis.
18
Q
Measles Complications
A
- Encephalitis: death or permanent impairments.
- Bacterial superinfection: otitis media, mastoiditis, pneumonia, sinusitis.
- Death: extensive progressive viral infection.
19
Q
Measles Epidemiology
A
- childhood disease; 6 mo. and older. Currently many infections found in teenagers, winter and spring.
- Measles cases have been on rise in US reaching 1250 in 2019
20
Q
Measles Diagnosis
A
- Clinical picture (most common)
- Virus isolation (throat, urine), Serology
21
Q
Measles Prevention
A
•live, attenuated vaccine after 1st year of life
22
Q
Measles Treatment
A
•supportive
23
Q
Measles - Subacute Sclerosing Pancencephalitis (SSPE)
A
- Rare, progressive neurologic disease of children, 2 to 10 years after a measles infection
- Insidious onset of personality change, poor school performance, progressive intellectual deterioration, development of myoclonic jerks (periodic muscle spasms), and motor dysfunctions (spasticity, tremors, loss of coordination, ocular abnormalities, blindness)
- Most of the pathologic features of the disease are localized to the CNS and retina
24
Q
Rubella
A
- Rubivirus genus of the Togaviridae family
- German or 3 day measles
- ( + ) ss RNA
- one antigenic strain
25
Rubella Structure
* Simple, icosahedral, enveloped virus
* The genome is (+) single stranded RNA
* Single species of capsid protein
26
Rubella Replication
* Entry by receptor mediated endocytosis
* (+) RNA is translated to produce viral proteins including RNA dependent RNA polymerase
* These proteins are required for the synthesis of replicative intermediates, the genomic RNA, and the subgenomic RNA
* The subgenomic RNA is the mRNA for viral structural proteins
* Virus assembly may take place at Golgi complex or plasma membranes
27
Rubella Clinical Disease
* Virus enters through inhalation
* Multiplies in upper respiratory tract
* Spreads, regional lymph nodes
* Viremia develops
* Symptoms appear 14–21 (average 16 days) days post infection
28
Rubella Incubation
•Symptoms appear 14–21 (average 16 days) days post infection
29
Rubella Rash
* Mild fever with rash
* Rash first appears on head, neck and trunk
* Rash may be mild or even inapparent
* Symptoms persist 1– 3 days
* Contagious from 7 days before to 7 days after the onset of rash
30
Rubella Clinical Disease
* Immunity (generally) life–long
* Mainly seen in the winter-spring season
* Maternal infection
* Placental infection
* Invasion of fetus
* Chronic fetal infection
* All organs are (may be) infected
31
Clinical Manifestations of Congenital Rubella
* Cardiac defects
* Ocular defects (cataracts)
* Hearing loss
* Liver and/or spleen enlargement
* Thrombocytopenia
* Failure to thrive (after birth)
* Low birth weight
* Mental retardation
* Mortality during first year of life
* Defects vary from very subtle to very severe
32
Rubella Diagnosis
•isolate virus, hemagglutination inhibition (most common)
33
Rubella Prevention
•live attenuated vaccine after 1st year of life, vaccine not given to pregnant females or immuno-compromised patients
34
Rubella Treatment
•supportive
35
Erythema infectiosum
* B19 of the Parvovirus genus of the Parvoviridae family
* A moderately benign contagious epidemic disease in children
* icosohedral ss DNA
36
Erythema infectiosum Structure and Replication
* Small (18–26 nm), icosahedral single– stranded DNA virus
* Replicates in the nucleus of dividing cells
* Virus assembly takes place in the nucleus
* Virus released by cell disruption
37
Erythema infectiosum Clinical Diseases
* Fifth disease
* Mild fever, headache, rash
* Rash first appears on face (slapped face) (lace–like) rash may persist 1– 2 weeks, may recur, children and young adults
38
Erythema infectiosum Diagnosis
•Clinical picture
39
Erythema infectiosum Treatment
•supportive
40
Roseola Infantum
* Rose colored rash
* Agent (?) human herpes virus type 6, adenovirus, coxsackieviruses, echoviruses
* Common disease in infants and children ages 6 months to 4 years
* Clinical diseases
- Abrupt onset of fever
- Brief convulsions
- After 3–5 days fever goes down followed in few hours by faint, transient rash
- Roset on face and body (Echo 19), Finger (Hand and Mouth-Coxsackie virus A)
41
Other Causes of Rubella like Rash
* Disease caused by numerous other agents can mimic rubella clinically.
* These agents are:
- 17 Echoviruses
- 9 Coxsackieviruses
- Several adenoviral serotypes
- Arboviruses
- Epstein-Barr virus (EBV)
