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Paramyxoviruses ( mumps , measles , rubella) Flashcards

(39 cards)

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1
Q

What familiy & genus is mumps in

A

genus: orthorubulavirus
Family: paramyxovirinae

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2
Q

what is the portal of entry for mumps

A

nasal & upper respiratory tract epithelial cells

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3
Q

whats the inucbattion period for mumps

A

2-4 weeks

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4
Q

What is the pathogenesis for mumps

A

• primary infections occurs in(portal of entry) nasal & upper respiratory tract epithelial cells
• Viremia disseminates virus to salivary glands + major systems epithelial cells ( i.e kidneys - can be detected in urine)
• Virus is shed in saliva from 3 days before & 9 days after onset of salivary gland swelling
• virsus may persist for 12 days after onset of symptoms

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5
Q

which salivary gland does mumps commonly infect

A

parotid gland

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6
Q

give some distinguishable characteristics of mumps

A
  • has hemagluttinin glycoprotien & fusion protein & neuroaminidase
  • single serotype
  • acute self limited viral infection
  • humans are only host
  • no cross immunity w other paramyxoviruses
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7
Q

epidemiology of mumps ? - how is mumps transmitted

A
  • airborne droplets /direct contact (very close )
  • fomites(e.gclothing,utensil) contamited w saliva / urine
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8
Q

epidemiology of mumps? - who are likely to be infected with mumps

A
  • children 5-9 years
  • can also occur in adolescents & adults
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9
Q

why is it difficult to control transmission of mumps

A
  • variable incubation periods
  • large number of asymptomatic cases
  • presence of virus in saliva before clinical symptoms develop
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10
Q

which organ does mumps frequently infect & how can it be detected

A
  • kidney
  • virus is present in urine
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11
Q

What are the clinical presentations of mumps

A

1.Parotitis(unilateral/bilateral) - swelling of parotid gland + pain

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12
Q

what are complications of mumps

A
  1. aseptic meningitis- MC in male than female
  2. Meningoencephalitis = occurs 5-7days after inflammation of salivary gland - most dont present w parotitis
    *these 2 usually resolve w/o sequelae**
    3.Orchitis(unilateral) - in 20-50% of youngmales who develop mumps
    4.oophoritis
    5.Pancreatitis
    6.myocarditis
    7.arthritis
    8.uveitis
    9.deafness
  3. guillain-barre syndrome
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13
Q

Immunity to mumps

A
  • one attack (clinical/subclinical) induces life long immunity
  • one antigenic type ( one serotype) w no variation
  • antibodies to NP (nucleocapsid) protein appear earliest(3-7daysafter onset of clinical symptoms) - usually gone within 6months
  • antibodies to HN develop more slowly (4wks after onset) - persist for years
  • cell mediated immune response
  • interferon induced early on in infection
  • IgA antibodies secreted in nasopharynx exhibit neutralizing activity
  • passive immunity from mother to offspring (rare to see mumps in children younger than 6months)
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14
Q

How mumps be diagnosed in lab ?

A

1.PCR - sensitive
2Culture : .saliva , CSF , urine (virus can be recovered for up to 2 wks) collected within few days after onset
nB : after collection inoculation done immediate since mump virus is thermoliable
- cytopathic effect: cell rounding & giant cell formation*
- hemadsoprtion test used to show presence of hemadsorbing agent 1 & 2 , weks after incoulation
-monkey kidney cells are preferred for viral isolation
- immunofluorescence via specific serum used for rapid diagnosis - as early as 2-3days after inoculation
3. serology
- fourfold or greater rise in antibody titer is evidence of mumps infection
- ELISA - detect IgM antibodies or IgG antibodies / HI test MC used
(IgM indicates recent infection - persist not longer than 60days)

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15
Q

Epidemiology of mumps

A
  • children 5-9years
  • outbreaks can occur = especially during crowding
  • Children younger than 5 = Respitatory tract infection w/o parotitis
  • highly contagious
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16
Q

which gene of mumps of variable

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A

SH gene : allowing for classification of known virus strains into 12 genotypes

17
Q

Treatment

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A

live attenuated virus mumps vaccine

18
Q

Control of mumps virus

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A

difficult due to high incidence of asymptomatic cases
children acquire mumps in school & work - should not go in until 5days after onset of parotitis

19
Q

MMR vaccine

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A
  • mumps , measles , rubella vaccine -
    2 doses are recommended for school entry
    2 doses of vaccine given to health care worker born before 1957 w/o evidence of mumps immuntiy
20
Q

What causes rubella (disease)

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A

Rubivirus rubellae

21
Q

Which virus (genus) is rubella (disease ) caused by ? and which familiy is it in

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A

family: matonaviridae (was previously in togaviridae family )
genus: rubivirus

22
Q

structure of rubivirus

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A
  • spherical 940-80nm)
  • (+)ssRNA
  • enveloped
  • has glycoproteins spikes E1 &E2
23
Q

what are the two types of rubella

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A
  1. Postnatal rubells - causes mild disease
  2. Congenital rubella syndrome - quite severe
24
Q

Pathogenesis of postnatal rubells

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A

Entry : respiratory epithelium
- invades the respiratory mucosa
- initial replication in RT
- then multiplication in cervical lymph nodes
- Viremia develops after 7-9 days - last till antibody appearance on day 13-15
(antibody appearance = coincides w rash appearance)
- secondary viremia (occurs 1-3wks after infection )
- dissemination to other organs (liver/spleen) , skin & mucosa

25
Epidemiology
- transmitted by respiratory route - not a contagious - occurs in neonates , childhood , adult
26
what is the incubation period of postnatal rubella
12-21 days
27
how is it spread
airdroplets /direct contact
28
clinical findings postnatal rubella
1. Non-specific signs : malaise & lowgrade fever 2. Morbilliform rash - starts on face, then trunk , extremeties (lasts not more than 3 days) - maculopapular rash - centrifugal - disappears affter 3-5 days 3. Forchheimer sign (20% of patients) - pinpoint lesions/petechiae in soft palate 4.suboccipital lymphadenopahty
29
complications of postnatal rubella
- arthralgia(joint pain) - arthritis (fingers, wrist /knees) - common in women - thrombocytopenic purpura - encephalitis
30
Immunity of postnatal rubella
- **antibodies appear in serum as rash fades - & rises rapidly over next 1-2 wks** - intitial antibody = IgM - not beyond 6wks after illness - indicate recent rubella infection - IgG antibodies persist for life - **one attack incurs life long immuniy** - only one antigenic type of virus exists - immune mothers transfer antibodies to their offsrping who are then protected for 4-6months
31
Lab Diagnosis of rubella
1. PCR /culture - by acquring nasopharyngeal/ throat swabs taken 6 days before & after onset of rash other sources of sample virus : urine , CSF , blood , cord blood for culture = cell lines of monkeys & rabbits can be used 2.Serology - HI test - requires pretreament for emoval of nonspecific inhibitors - ELISA test - no pretreatment & can detect IgM **NB detection of IgG is evidence of immunity cos there is only one serotype of rubivirus**
32
How to accurately confirm recent rubella infection esp in pregnant women ?
- rise in antibody titer(HI antibody) must be seen btwn 2 serum samples taken 10 days apart - rubella specific IgM detected in single specimen
33
Treatment of rubivirus + control
- no speciific treatment - since its mild & self limited - live attenuated rubella vaccine (single antigen / combine w measles & mumps vaccine) (induces lifelong immunity for at least 95% of ppl) role of vaccine : prevent congenital rubella infections
34
Pathogenesis of congenital rubella
- maternal viremia associated w rubella in pregnancy can cause infection of placents & fetus - Destroys fetal cells & inhibits mitosis(growth rate reduced) lead to hypoplastic organ devt = structural anomalies in newborn - time of infection determines teratogenic effect ( early in pregnancy = greater damage to fetus - **esp 1st trimester** = 85%cases of abnormalities) (birth defect uncommon if maternal infection occurs after 20th wk of gestation)
35
what are the 3 categories used to group congenital rubella ?
1. transient effects in infants 2. permanent manifestations that may be apparent at birth / are recognised during the 1st year 3. developmental abnormalities that appear & progress during childhood & adolescence
36
what is the classic triad of congenital rubella
cataract cardiac abnormalities(patent ductus arteriosus) deafness
37
other clinical findinds in congenital rubella
1. transient symptoms of ; - growth retardation - rash - hepatosplenomegaly - jaundice - meniningoencephalitis 2. progressive rubella panencephalitis - develops in second decade of life in child w congenital rubella
38
diagnosis of congenital rubella
- isolation of virus in cell culture of throat sample , urine & other secretions - detection of IgM in single serum sample shortly after birth(IgM des not cross placenta ,theri presence indicates that they must be synthesized by the infant in utero) - persistance of rubella IgG antibodies in serum beyond 1 year or rising anitbody titre anytime during infancy in an unvaccinated child -biopsy of tirrue/blood /CSF for viral antigen by monoclonal antibodies - detection of rubella RNA by insitu hybridization & PCR
39
Treatment & prevention of congenital rubella
no specific treatment prevention: childhood immunization w rubella vaccine to ensure that women of childbearing age are immune

Microbiology (3 decks)

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