1. What is your diagnosis?Bronchiolitis2. What is the causative agent?Respiratory Syncytial Virus (RSV)3. How does it enter the body?RSV enters through the mucous membranes of the nose or mouth.
The virus may also enter through the eyes and is carried in respiratory droplets in the air from an infected persons sneeze or cough, but also by contact with contaminated surfaces (American Lung Association). 4. How does it spread? a. Within the body Attachment and entry of RSV is dependent on the viral G protein.
After binding to its receptor on respiratory ciliated epithelial cells in the mucous membranes of the throat and mouth, the viral envelope and host cell membrane are positioned close together. The F protein facilitates fusion of the membranes. The RSV nucleocapsid is then released into the host cell (Harris et al., 2003). RSV spreads to neighboring cells and form syncentia through the binding of the F protein expressed on the host cell to surrounding uninfected cells. The virus may also be spread to more distant regions through the viral shedding at the apical surface of the respiratory epithelial cells (Tian, J. et al.
, 2013). b. From person to personRSV is spread through infected respiratory droplets that travel through the air. RSV can also be spread through contaminated surfaces. Often these droplets are passed via infected individual sneezing, coughing, and then touching surfaces (American Lung Association). 5. What is the host response to the infection and what is the disease pathogenesis? RSV infection induces an innate immune response that uses recognition receptors such as toll-like receptors (TLRs) and to recognize the RSV virion and express this recognition to other cells. Inflammatory cells are then able to be recruited and also begin adaptive immunity if the virus is not killed by macrophages.
Antibodies and t- cell immunity is established during the adaptive immunity; however, RSV does not usually produce neutralizing antibodies due to antigenic changes of the virion particle. This is why re-infections can be common in many people (Domachowske, J. 1999).
Pathogenesis of RSV involves the movement of the virus further down mucosal surfaces and the respiratory tract. As the virus proliferates, more immune cells and inflammatory cytokines are produced which is what causes the inflammation of the bronchioles. The virus can also cause edema which brings fluid to the alveoli and often interferes with airflow to the lungs (Domachowske, J. 1999).
6. What is the typical clinical presentation and what complications can occur?I’m almost done, will copy and paste into here soon! -B Betsy: he changed the due date to Thursday so you still have time. Go get some sleep and soup!7. How is this disease diagnosed and what is the differential diagnosis?Bronchiolitis can be diagnosed by the presence of two common clinical symptoms, hyperinflation of the lungs and wheezing. This can be detected by the use of a chest X-ray and chest auscultation. Another indication of bronchiolitis is hypoxemia which can be quantified through the use of a pulse oximeter which measures oxygen saturation in the blood. Normal oxygen saturation ranges from 95 to 100 mm Hg. The causative agent of bronchiolitis can be confirmed through the use of several laboratory tests including detection of viral antigens, detection of viral nucleic acid, enzyme immunoassay and polymerase chain reaction (PCR).
Most clinical laboratories use antigen tests to detect RSV. Samples from the upper respiratory tract are obtained with the use of nasopharyngeal washes or nose and throat swabs. An enzyme immunoassay test can be used to detect viral antigens and a polymerase chain reaction is often used to detect viral RNA. PCR tends to be the most reliable test and is beginning to be used more in hospitals. The differential diagnosis is asthma, whooping cough (pertussis), croup (laryngotracheitis), pneumonia, and epiglottitis. Bronchiolitis itself can also be caused by other viruses including, but not limited to, adenovirus, influenza, or corona viruses which all are capable of causing respiratory tract infections.
8. Explain the likely test depicted in Figure 2, and how that could give a definitive indication of the microorganisms? The test in Figure 2 is a photomicrograph of the epithelial cells taken from the respiratory tract of an infected 2-month old child using immunofluorescence techniques. Epithelial cells were treated with a fluorescently tagged antibody specific to RSV. Under ultraviolet light, the antibody bound to RSV fluorescences and confirms the presence of RSV. From the test, you can see the binucleated cells which is an indicator of RSV.
This image may also allow for the study of morphological changes in cells potentially caused by RSV. In this graph we see the membrane fusion between infected cells which is uncommon for uninfected cells, but often occurs in RSV infection. While that is not as definitive as a specific antibody target, it does reveal viral infection (TIWARI, P. M. et al., 2014). 9. How is the disease managed and prevented?Most cases of bronchiolitis can be managed at home.
Intake of fluids must be managed as dehydration of the patient can occur easily. Fever can be managed with over the counter drugs such as ibuprofen. In severe cases, the patient can be treated through oxygen or intubation (RSV: Symptoms and Care). In cases where RSV is the causative agent of bronchiolitis, the drug Ribavirin can be administered to immunocompromised patients. This antiviral drug is not typically used as it has a low rate of efficiency (Marcelin, J.R. et al.
, 2014). There is currently no vaccine for RSV. Therefore, prevention can include not contacting those experiences signs of infections, most importantly not making contact with an infected person’s mucosal surface (i.e. kissing, running nose). Also washing hands with soap and water, as well as disinfecting surfaces near infected people can also prevent spread (American Lung Association). An immunoprophylaxis drug, Palivizumab, can be used to target RSV’s F protein to prevent fusion of the viral envelope and the host cell membrane. By inhibiting fusion of the two membranes, entry of the virus into the host cell can be prevented.
This drug is typically used for young, high-risk patients (Mejias, 2008).