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Virology Quiz 4 > Arbovirus, Rubella and Parvovirus B19 > Flashcards

Arbovirus, Rubella and Parvovirus B19 Flashcards

1
Q

Phenotypic Mixing

A

When two different viruses infect the same cell some of the progeny may exhibit phenotypic mixing: that is, the genome of one parent may be enclosed in a coat determined, at least in part, by the genome of the other parent.
Thus the phenotype may not correspond to the
genotype. This anomaly disappears after one cycle of growth if further mixed infections are avoided.”

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2
Q

Arbovirus Characteristics

A

Arbovirus is short for ARthropod-BOrne virus. This is not a formal classification term but an epidemiological subset of viruses.
Most togaviruses and flaviviruses are arboviruses (transmitted by an infected blood-sucking arthropod vector), (but this is NOT true of rubella virus, a togavirus, or hepatitis C virus, a flavivirus).
Togaviruses and flaviviruses share these
characteristics:
a. Small, enveloped.
b. Icosahedral nucleocapsid with a single molecule
of plus-stranded RNA that serves first as mRNA
upon entry into the cell.

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3
Q

Transmission of Arboviruses

A

Transmission of arboviruses requires multiplication in the arthropod host. Thus there are two incubation periods:
• INTRINSIC INCUBATION PERIOD in humans: about a week, occasionally longer.
• EXTRINSIC INCUBATION PERIOD in mosquito (or
other arthropod): about 14 days. After biting a viremic animal, a mosquito cannot transmit the
virus for 14 days. The mosquito is then infectious for life and is not harmed by the virus. During the extrinsic incubation period the arbovirus is multiplying in the arthropod.

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4
Q

Pattern of Transmission of Arboviruses

A

The pattern of natural transmission between arthropod (mosquitoes or ticks) and vertebrate hosts (omitting accidental hosts) is shown below: Transovarian transmission does not occur with all arboviruses.
• vertebrate -> arthropod -> vertebrate -> arthropod
• arthropod - transovarian ->arthropod progeny ->
vertebrate -> arthropod

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5
Q

Arbovirus disease in USA

A

In the USA the only serious arbovirus disease is encephalitis, caused by:
• Eastern equine encephalitis virus
• Western equine encephalitis virus
• St. Louis encephalitis virus
• West Nile virus
• the California group of encephalitis viruses, [and
Venezuelan encephalitis virus (occasionally seen in Texas).

For all arboviral diseases there is no direct human-to human transmission, with the rare exception of blood transfusions.

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6
Q

Aboviral Encephalitis

A

In arboviral encephalitis the incubation period in humans is short, about one week. Recognize the arthropod vector directly introduces the virus into blood so viremia occurs relatively quickly. Multiplication of the virus in vascular endothelium
rapidly increase viremia. A brief febrile malaise is followed by encephalitis with paralysis, coma, and death. No specific treatment is available.

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7
Q

Eastern Equine Encephalitis and Western Equine Encephalitis

A

Eastern equine encephalitis virus causes the most deadly arboviral encephalitis in the USA. [It was first identified as a cause of as human disease in Massachusetts in 1938: heavy rainfall in the preceding fall and then in the spring produced a
great mosquito excess.] This virus infects mostly children but also adults living in swampy and wetland areas with high fatality.
At the same time horses die of the same disease (hence the name).

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8
Q

Eastern Equine Encephalitis and Western Equine Encephalitis

Transmission

A

Humans and horses are DEAD-END HOSTS for Eastern and Western equine encephalitis. !Human (and horse) viremia rarely reaches the level required to infect mosquitoes. The virus is maintained in nature by birds and mosquitoes (both largely unaffected by the infection although ! some birds do
die):

  • Wild Bird -> Mosquito -> Wild Bird
  • Wild Bird -> Mosquito -> Humans
  • Wild Bird -> Mosquito -> Horse
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9
Q

Eastern Equine Encephalitis and Western Equine Encephalitis

Epidemic

A

Some hints of an impending epidemic are excessive rainfall and abnormally high mosquito populations. The best warning comes from finding a high prevalence of virus in mosquitoes (PCR).

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10
Q

Eastern Equine Encephalitis and Western Equine Encephalitis

Control Measures

A

The standard control measures are:
• reduction of mosquito population
• avoidance of mosquitoes during epidemic.

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11
Q

St. Louis Encephalitis Virus and West Nile Virus

A
  • Both are flaviviruses and are antigenically related to each other.
  • Both cause encephalitis. Fatal cases are mostly in the elderly.
  • Both are maintained by bird mosquitobird cycles. Humans are dead-end hosts, because they rarely have viremia high enough to infect mosquitos.
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12
Q

St. Louis Encephalitis Virus and West Nile Virus

Geographical Location

A

• St. Louis encephalitis virus is an indigenous North American virus. West Nile virus is native to North Africa and the Middle East. It was recently imported into the northeastern USA and rapidly spread across the USA. It seems likely to become permanently established. West Nile is now the most common arbovirus infection in the USA.
• On a world-wide basis, Japanese encephalitis virus (Japan and SE Asia ) causes the most common arboviral encephalitis.
A vaccine is recommended for travelers.

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13
Q

Arboviruses in General

A

• Other important arboviruses in USA are LaCrosse
encephalitis virus, a member of the California encephalitis virus group (rural forests). The names of arboviruses give no clue as to specific location
• In the temperate zones, arbovirus disease is seen as focal epidemics of short duration. The conditions have to be just right to allow transmission.
• Outside the USA, arboviruses show other patterns of disease, in addition to encephalitis:
a) Severe systemic disease with degeneration of liver, etc. (yellow fever)
b) Non-fatal systemic disease with muscle pain and rash (classical form of dengue fever)

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14
Q

Features of Arboviruses

St. Louis Encephalitis Virus

A
  • Virus Group: Flavivirus
  • Major Host: Wild and domestic birds
  • Age Incidence: Adults over 50
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15
Q

Features of Arboviruses

West Nile Virus

A
  • Virus Group: Flavivirus
  • Major Host: Wild and domestic birds
  • Age Incidence: Adults over 50
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16
Q

Features of Arboviruses

Western Equine Encephalitis Virus

A
  • Virus Group: Togavirus
  • Major Host: Wild birds
  • Age Incidence: Infants and adults over 50
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17
Q

Features of Arboviruses

Eastern Equine Encephalitis Virus

A
  • Virus Group: Togavirus
  • Major Host: Wild birds
  • Age Incidence: Mostly children under 10
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18
Q

Features of Arboviruses

LaCrosse

A
  • Virus Group: Bnow eunvavirus
  • Major Host: hares and rodents
  • Age Incidence: Children
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19
Q

Dengue

A

Classical DENGUE is (sometimes called “bone-break fever”) a severe but usually not life-threatening disease of the tropics and subtropics, especially S.E. Asia and the Caribbean islands. The incubation period of one week is followed by fever, severe headache (retro orbital), muscle and joint
pains, and a rash.

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20
Q

Dengue

Antigenic Types

A

There are four major cross-reacting antigenic types of dengue virus (types 1, 2, 3, 4). The pattern of transmission is exactly like that of yellow fever (see below). Note that humans are not dead-end hosts for dengue (or for yellow fever) and sufficient viremia occurs in humans to infect mosquitoes.

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21
Q

DENGUE HEMORRHAGIC FEVER

A

In S.E. Asia since about 1950 and more recently in the Caribbean there has emerged a much more severe, fatal form (DENGUE HEMORRHAGIC FEVER), characterized by hemorrhage, vomiting blood, and shock. Hemorrhagic dengue fever is seen primarily in the native population; most visitors
get the classical mild disease.

22
Q

Dengue

Reason fro Deadliness

A

The most likely theory to explain this lethal disease is that it is seen only in persons who have sequential infections with two different antigenically crossreacting dengue viruses (e.g., dengue-1 and
dengue-2). In the second infection, the nonneutralizing but cross-reacting antibodies from the first infection bind the virions to macrophages
through the Fc receptor and promote macrophage infection. The massive macrophage infection results in overproduction of lymphokines and cytokines resulting in increased vascular permeability and hemorrhage.

23
Q

Yellow Fever

A
  • The incubation period of YELLOW FEVER is about 7 days. The virus multiplies first in vascular endothelial cells and the resultant viremia serves to infect the liver and other organs
  • The disease is characterized by fever, nausea, jaundice (from viral damage to liver cells), hemorrhage (black vomit).
  • In addition to the liver, viral multiplication is extensive in spleen, liver, and kidney.
  • The mortality is high but there are occasional subclinical infections.
24
Q

Yellow Fever

Transmission Pattern

A

Pattern of transmission for Dengue and Yellow fever: humans are not dead end hosts for yellow fever or dengue. (Note that Aedes aegypti is also the arthropod host for dengue virus.)
• Mosquito (Aedes aegypti) -> Human -> Mosquito

25
Q

Jungle Yellow Fever

Transmission Pattern

A

Monkey -> Tree Mosquito -> Monkey -> Tree Mosquito -> Humans -> Mosquito -> Humans

26
Q

Yellow Fever

Vaccination

A

An excellent live-attenuated vaccine (17-D VACCINE) gives long-term protection.

27
Q

Yellow Fever

Epidemics

A

There is danger of epidemics wherever Aedes aegypti is present. If an unvaccinated person enters during the incubation period the yellow fever virus make may spread to the mosquitoes and then to the susceptible population.
This is the situation in the southeastern USA today.

28
Q

Types of Infectious Diseases

A

In the jargon of infectious disease
• neonatal infections acquired from the mother are called VERTICAL INFECTIONS.
• All other infections are termed HORIZONTAL.
Two pathways lead to vertical infection.

29
Q

Vertical Infections

Pathways

A

Two pathways lead to vertical infection:
• Perinatal
• Transplacental

30
Q

Perinatal Pathway

A

In the PERINATAL pathway, the neonate is infected
during birth by contact with maternal blood or other
fluids. Perinatal infections generally somewhat resemble horizontal pediatric infections with the same virus. Among the perinatally acquired viruses are HBV, HIV, and herpes simplex type 2.

31
Q

Transplacental Pathway

A

In the TRANSPLACENTAL pathway, the virus
crosses the placenta to invade the developing fetus.
Here the resulting disease is often different from horizontally acquired pediatric disease. Fetal infection distorts normal development resulting in congenital anomalies. Among the transplacentally acquired viruses are parvovirus B-19, rubella virus, cytomegalovirus, and lymphocytic choriomeningitis virus.

32
Q

Vertical Infections

Placental Defense

A

Embryonic cells and embryos are excellent hosts for growth of all types of virus. Fetal infections are uncommon because the placenta is a barrier to most viruses.
The placental barrier is impermeable to particles the
size of the smallest viruses. But some viruses can penetrate this barrier by replicating in placental tissue.

33
Q

Vertical Infections

Fetal Defense

A

The fetus has substantial defense mechanisms:
• Maternal IgG
• Fetal antibody after fourth month (mostly IgM).
• Interferon (probably adequate after fourth month)
• Cell-mediated immunity?

34
Q

Parvovirus B-19

A
  • Parvoviruses have small (smallest human virus), unenveloped, icosahedral virions that contain linear single-stranded DNA.
  • The route of infection is inhalation of a respiratory aersol from respiratory tract of an infected person.
35
Q

Parvovirus B-19

ERYTHEMA INFECTIOSUM

A

The infection is very common (~ 50% of adults are seropositive).
In normal individuals the infection is asymptomatic
or causes fever, malaise, and after a 14-day incubation period a rash known as ERYTHEMA INFECTIOSUM.
The rash is also called the fifth disease or the
“slapped cheek disease”, and is probably caused by immune complexes (virions plus antivirion antibody) deposited in capillaries.

36
Q

Parvovirus B-19

ERYTHEMA INFECTIOSUM

A

Parvovirus B-19 has a tropism for erythroid precursors (RBC precursors). Thus infection inhibits red cell production for about a week, by viral growth in these precursors.
Normal individuals tolerate a week without red
cell production without any symptoms. However, patients with a pre-existing deficit in red cell production or a pre-existing abnormally high rate of red cell destruction (example: sickle cell anemia) will have a TRANSIENT APLASIC CRISIS during infection with B-19 virus. This crisis can be fatal without transfusions.
Persons with immunological defects can suffer prolonged anemia from a parvovirus B-19 infection that they cannot eradicate.
Passive immunization with pooled human gamma globulin can cure these patients.

37
Q

Parvovirus B-19

Primary Infection

A

Primary infection with parvovirus B-19 in adults is often asymptomatic. The “slapped-cheek” rash is rarely seen or so transient it escapes notice. The most common symptom of infection is an acute and transient arthritis (sometimes can last a few weeks or months).

38
Q

Parvovirus B-19

Transplacental route

A

There is a transplacental route of infection. Primary B- 19 virus infection during pregnancy can lead to fetal death no matter when in gestation the infection takes place. When infection is in the first or second trimester, some fetal deaths are associated with severe edema (HYDROPS FETALIS). Hydrops fetalis is a relatively rare event of pregnancy and parvovirus B-19 is only an uncommon cause of hydrops fetalis. Infection in the third trimester can result in intra-uterine fetal death but hydrops is not seen.

39
Q

Rubella

Virus

A

!Rubella virus is a togavirus but it is NOT an arbovirus (no arthropod transmission). It has the same structure and pattern of multiplication as other togaviruses but there is no arthropod transmission.

40
Q

Rubella

Transmission

A

Rubella is transmitted by respiratory aerosols from the respiratory tract of an infected person. Local multiplication in the respiratory epithelium is followed by viremia.
Rubella is less contagious than measles allowing the persistence of seronegative adults.
The incubation period is 18 days.

41
Q

Rubella

Symptoms

A 
The rash (exanthem) lasts about 3 days with a fever and lymphadenopathy. Virus is excreted from the respiratory tract one week before and after the rash. Rubella is sometimes subclinical and even with a rash the clinical diagnosis can be difficult.
Rubella is sometimes more severe in adults, with transient arthritis.
42
Q

Rubella

Immunity

A

Even subclinical infections produce lifelong immunity.

Rubella is now very rare because of wide spread use of a live-attenuated vaccine (Part of MMR formulation)

43
Q

Congenital Rubella Syndrome

A

Virus from the viremia of primary infection during pregnancy (first trimester) crosses the placenta.
History: Gregg (1941) traced congenital cataracts to maternal rubella.

44
Q

Congenital Rubella Syndrome

Spectrum

A

Spectrum of possible congenital anomalies (in addition to spontaneous abortion):
• cataracts
• heart defects, especially patent ductus arteriosus
• deafness
• retardation

Some of these effects, particularly deafness, may not be obvious at birth but

45
Q

Congenital Rubella Syndrome

Mechanism

A

Mechanism of virus action on the fetus:
• When rubella virus is used to infect tissue culture
cells, many infected cells just grow more slowly and show no other cytopathic effect.
• In aborted infected fetuses only a small portion of fetal cells are infected (distributed in clones).

Infected cells are concentrated at site of malformation.

46
Q

Congenital Rubella Syndrome

Time for Fetal Infection

A

The time of fetal infection is critical: First month of gestation, 50% malformation; second month, 25%; third month, 9%; fourth month, 4%.

47
Q

Congenital Rubella Syndrome

Response to Infection

A

Response of fetus to infection:
• Virus production throughout gestation and gradually decreasing through first two years of life (mostly in the urine).
• This prolonged virus production does not represent
tolerance. Fetal IgM rubella antibody is made. After
birth IgG antibody to rubella is also made.

48
Q

Rubella Vaccine

A

The major purpose of the live vaccine is to prevent
congenital rubella. In the USA, the tactical plan is to interrupt the natural pattern of rubella epidemics by immunizing school children to provide herd immunity for non-immune pregnant women.
• Nearly all children must be immunized.
• Individual immunity must be maintained through
the child-bearing years to reduce the number of
susceptible pregnant women.

49
Q

Rubella Vaccine

Pregnant Women

A

The live-attenuated vaccine is also used for seronegative women of child-bearing age but they
should avoid pregnancy for two months. No transplacental infection or congenital anomalies have been seen in about 100 accidentally vaccinated pregnant women but there is a theoretical risk. The live rubella vaccine is a component of the MMR (mumps-measles-rubella) pediatric vaccine.

50
Q

Rubella Vaccine

Eradication and Concerns

A

Currently near-universal use of the rubella vaccine
has blocked all childhood disease acquired in the
USA and the congenital rubella syndrome has not
been reported in 2005. Major concerns are:
• children whose parents do not allow immunization,
• rubella cases in immigrant children, and
• seronegative immigrant women of child-bearing age.

Rubella remains a major public health problem in
many developing countries.

Virology Quiz 4 (6 decks)

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