Rubella virus

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Rubella virus

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Paeds

Newborn management: Clinical
Congenital TORCH infections: Pathology review
Perinatal infections: Clinical
Congenital heart defects: Clinical
Miscellaneous genetic disorders: Pathology review
Disorders of amino acid metabolism: Pathology review
Glycogen storage disorders: Pathology review
Lysosomal storage disorders: Pathology review
Disorders of fatty acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Autosomal trisomies: Pathology review
Congenital disorders: Clinical
Neonatal jaundice: Clinical
Neonatal ICU conditions: Clinical
Immunodeficiencies: Clinical
Pediatric allergies: Clinical
Kawasaki disease: Clinical
Pediatric ear, nose, and throat conditions: Clinical
Congenital adrenal hyperplasia: Clinical
Pediatric constipation: Clinical
Pediatric gastrointestinal bleeding: Clinical
Pediatric vomiting: Clinical
Developmental milestones: Clinical
Vaccinations: Clinical
Precocious and delayed puberty: Clinical
Disorders of sex chromosomes: Pathology review
Child abuse: Clinical
Disorders of sexual development and sex hormones: Pathology review
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Pediatric infectious rashes: Clinical
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Viral exanthems of childhood: Pathology review
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BRUE, ALTE, and SIDS: Clinical
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Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
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Rubella virus

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A 1 month-old girl is brought to the clinic for a routine evaluation. The patient was delivered via a cesarean at 38-weeks gestational age due to arrested labor. The mother immigrated from Zambia ten months ago and received minimal prenatal care. During the first trimester of pregnancy, she developed an upper respiratory infection and self-limited joint pain affecting the wrists, knees, and ankles. Family history is notable for retinitis pigmentosa. The patient’s weight is at the 20th percentile, and head circumference is at the 50th percentile. Vitals are within normal limits. She does not move her head in response to sounds. Facial features appear normal. Physical examination is notable for petechiae and purpura over the arms, trunk, and legs. A cardiac examination reveals a continuous murmur heard in the left infraclavicular area. Abdominal examination is notable for hepatosplenomegaly. Which of the following findings is most likely present on this patient’s ophthalmologic examination?  

External References

First Aid

2024

2023

2022

2021

Rubella p. 166

cardiac defect association p. 304

cataracts p. 550

heart murmur with p. 296

rash p. 178

ToRCHeS infection p. 181

unvaccinated children p. 183

Lymphadenopathy

rubella p. 166, 181, 178

Cataracts p. 550

rubella p. 181

Congenital heart disease p. 302-304

rubella p. 181

Deafness

rubella p. 181

Blueberry muffin rash

rubella p. 166, 181

Polyarthralgias

rubella p. 181

Polyarthritis

rubella p. 181

Rashes

rubella p. 166, 178

Arthralgias

rubella p. 166, 181

Togaviruses

rubella as p. 164

Transcript

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Rubella, the infection formerly known as “German Measles,'' is caused by the Rubella virus.

Thanks to vaccination, it’s a disease we see less and less, although because some groups are under-immunized, it’s still possible to see outbreaks.

The Rubella virus is part of the Togaviridae family.

Togaviruses are single-strand RNA viruses surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces, all within a spherical outer lipid envelope.

They’re also positive sense RNA viruses, which means that their genetic material is actually mRNA, so it can be used right away by the host cell to make viral proteins.

Now, the Rubella virus is transmitted through respiratory droplets, which are released into the environment when you sneeze or cough on another person.

Within the nasopharynx mucous membrane, the virus binds to a specific receptor on the membrane of epithelial cells.

It’s then surrounded by a little section of cell membrane that pinches off to form an endosome, that’s brought into the cell.

The low pH in the endosome uncoats the viral RNA and the virus causes changes to the endosome.

Now, when the Rubella virus enters the cell it also rearranges some of the organelles, gathering the endoplasmic reticulum, golgi apparatus, and mitochondria around the endosome.

The result is a membrane-bound Viral Replication Complex where - like the name says - the virus replicates.

So, after the virus replicates, its structural proteins are synthesized using the rough endoplasmic reticulum and these proteins are then transported to the golgi apparatus to be assembled and surrounded by membrane, a process called viral budding.

The new virus copy eventually exits the cell by exocytosis and enters nearby lymphatic and blood vessels, travelling to lymph nodes where it will replicate once again.

From the lymph nodes, it enters blood vessels again, and spreads to various parts of the body, making its way into various bodily fluids like urine, cerebrospinal fluid, and synovial fluid of joints.

Finally, the Rubella virus has a cytopathic, or cell-damaging, effect, that’s linked to viral replication.

This happens because the host body reacts to replication by causing apoptosis, or cell death, in infected cells, in an attempt to prevent the virus from spreading further.

Another way that Rubella can spread is from a pregnant female to her unborn child, through the placenta.

This causes Congenital Rubella Syndrome in the fetus. In fact, Rubella is among the most common infections that cause congenital defects in fetuses, which are grouped under the acronym TORCH. T stands for Toxoplasmosis, O for Other infections - like Syphilis, R for Rubella, C for Cytomegalovirus, and H for Herpes Simplex.

We’re not sure exactly how Rubella causes defects in the developing fetus but it’s possible that it causes vasculitis, or inflammation of blood vessels, which damages the vessels.

As a result, there’s not enough blood flow to developing organs which can result in tissue death.

It’s also possible that the Rubella virus slows down the process of mitosis, or cell division, in infected fetal cells.

Since mitosis helps drive the development of the fetus, infected tissues might not grow properly.

The timing of the infection in mom will determine the risk of the fetus also getting congenital Rubella.

Congenital defects are much more likely if the maternal infection happens between 4 weeks before and 20 weeks after conception.

After 20 weeks, there aren’t usually fetal defects, but there may be some intrauterine growth restriction, meaning the baby will be smaller than expected for their gestational age.

The biggest risk factor for Rubella is being unvaccinated—which is more common in countries with lower vaccination rates—and coming into contact with someone who is in the contagious period of their Rubella infection—which starts about 3 days after being exposed to the virus and lasts around 3 to 4 weeks.

Ok, now, many Rubella infections are asymptomatic, but when there are symptoms they typically show up after a 14 day incubation period.

Children tend to have fewer and milder symptoms which can last anywhere from 3 to 8 days on average.

Summary

Rubella virus is a single-strand, positive-sense RNA virus of the Togaviruses family, which is known to cause rubella, sometimes referred to as German measles. The virus is spread through respiratory droplets and infects and replicates in mucous membrane cells of the nasopharynx, then does the same in lymph nodes, triggering apoptosis in infected cells. Infected children are often asymptomatic or might have mild symptoms like fever, lymphadenopathy, and a rash, whereas adults tend to show more serious symptoms and get sick longer. Complications of rubella are rare but may include arthritis, encephalitis, and thrombocytopenia. Treatment for Rubella is supportive and prevention involves a live attenuated vaccine.