LIVING THE LAB LIFE
A BLOG FOR ASCLS REGION V
Any who has been paying attention to the news recently knows that Hennepin County in Minnesota has been facing a public health crisis. There is an active outbreak of measles (rubeola) among young children, all who are unvaccinated. So far, no fatalities have been reported, but this event has highlighted the potential dangers associated with failing to vaccinate children as recommended by medical professionals. As laboratory professionals, we must be prepared to handle these outbreaks and appropriately consult other members of the healthcare team.
The measles virus is a member of the Paramyxovirus family, along with the mumps virus, respiratory syncytial virus, parainfluenza viruses, Nipah virus, and Hendra virus. They are single-stranded, enveloped RNA viruses. These viruses are transmitted via the respiratory route, which is what makes them so contagious.
The measles virus has a few tricks up its sleeve that aide in its ability to causes serious infection in hosts. Unlike most respiratory viruses, the measles virus readily disseminates throughout the body by binding to receptors on various somatic cells (a skill few viruses have). By latching on to dendritic cells in the respiratory mucosa, the measles virus scores a free ride the lymphatic system. From there, the virus can spread throughout the body and can cause mischief.
Children are most likely to be infected with measles, particularly under the age of five. The first symptoms to appear in a measles infection include cold-like symptoms (coryza), high fever, cough, sore throat, and conjunctivitis. While these symptoms are present, the patient is most contagious (which is a problem since these symptoms are so nondescript, those around the patient likely have no idea of how serious of an illness they are exposing themselves to).
Last month, the microbiology department at the lab that I work in got a unique request from one of our Infectious Disease attending physicians. The doctor informed us that she had a patient who she suspected had been infected with Leishmania. She had been in contact with experts at the Centers for Disease Control and Prevention about how to diagnose this patient, and therefore, we should expect to receive a special kit from them with materials to properly process a culture for Leishmania.
Since I live and work in Minnesota, a disease like Leishmaniasis is not routinely seen. But as we live in an increasingly diverse world where our hospitals may be treating patients from all over the world, we laboratorians need to be ready to handle the unexpected. Here, I will do a brief review of Leishmaniasis.
Leishmania is intracellular, flagellate parasite transmitted through the adult female sand fly. Over twenty species of Leishmania have been identified. It is endemic throughout the tropical and sub-tropical regions of the world. For this reason, most patients in the United States who present with the disease will either be immigrants or travelers. The disease manifests in three forms: cutaneous, muco-cutaneous, and visceral leishmaniasis.
In cutaneous leishmaniasis, a self-limiting, red, cutaneous papule appears at the site of the sand fly bite. It takes two to eight weeks for the lesion to form after the initial bite. With time, the lesion will pruritic, enlarged and eventually ulcerates. The ulcer will then crust over and exude a serous fluid. At this point, the lesion is prone to secondary infections. Best case scenario, the lesion will heal over but leave a pronounce scar. Depending on the species of Leishmania, the infection may spread to other cutaneous sites, causing more lesions. Another route for spread of Leishmania infection is through direct contact with skin lesions.
Human chorionic gonadotropin (hCG) is a peptide glycoprotein hormone composed an α- and β-chain subunits. The trophoblastic cells of the placenta are the primary producer of hCG. There is also evidence that a very small amount of hCG is produced by the pituitary gland in menopausal women. The α-chain component of hCG is identical to the α-chain in luteinizing hormone, thyroid stimulating hormone, and follicle stimulating hormone; the β-chain is unique. HCG is responsible for maintaining the corpus luteum and stimulating the synthesis of progesterone. It is also has proangiogenic functions critical for maintaining blood supply to the fetus.
By far, the most common test for hCG is the urine pregnancy test. Urine pregnancy tests are available over the counter for women to test for new pregnancy. Hospital also routinely use this point-of-care testing to screen non-sterile women of child-bearing age. Urine pregnancy tests are qualitative immunoassays that detect hCG by drawing the urine specimen through a porous membrane to an immobilized section imbedded with anti-hCG. Once an hCG-anti-hCG complex forms, its presence is visualized by a colorimetric detection reaction step (the exact methodology for detection varies depending on the manufacturer).
This week, NPR featured a news article about a young boy born with serious birth defects due to CMV infection. While Zika has been a hot topic in the news for the past couple of years due to the potential devastating birth defects associated with infection, CMV has a record of doing much more damage. While CMV has flown under the radar for most in the general population, as laboratorians, CMV is an ever-present part of our world. We may perform testing on obstetric patients, tittering out IgM and IgG antibodies to evaluate for current, recurrent, or past infection. We may see the cytopathic effects of CMV upon microscopic examination of tissue specimens. Or we transfuse CMV-negative blood products to vulnerable populations. Here I will discuss the virus further in depth.
Human cytomegalovirus, or CMV, is a member of the Herpesviruses family, along with other well-known viruses like herpes simplex virus types 1 and 2, Epstein-Barr, and varicella-zoster. The Herpesviridae are large, complex, double-stranded DNA viruses. The hallmark of this family of viruses is their ability to establish latent infections and re-emerge periodically throughout the life of their host. In the case of CMV, the virus establishes latency by residing in monocytes.
About half of all people in the human population developed nations are infected with CMV. At any given time, 10% of people are shedding the virus, either through tears, urine, saliva, stool, semen, cervical secretions, or breast milk. The virus is commonly transmitted via sexual and oral routes, but is also transmitted through blood transfusions, tissue transplants, in utero. In adults, CMV is often an asymptomatic, benign infection. Some cases present like the common cold, or a less severe mononucleosis-type disease (remember the causative agent of mononucleosis is another member of the Herpesviruses family, EBV).
Last month, many news outlets featured a very buzzy story about a potentially breakthrough treatment for severe sepsis patients. The lead physician involved in the study treated his patients with a cocktail drug combination of vitamins and corticosteroids, with the principle ingredient of vitamin C. Now, much more research will need to be done to determine whether this treatment is truly the next breakthrough in severe sepsis care or just another fluke study that does not work out in follow-up studies. But if this treatment were to become standard in hospitals across the country, where would that leave us in the laboratory?
Vitamin C (ascorbic acid) is a water-soluble vitamin, meaning the body absorbs whatever is can use and the excess is excreted in urine. It is a reducing agent (anti-oxidant), meaning it gives up electrons to other molecules, protecting them from damaging oxidation. In 1928, Albert Szent-Gyorgi first isolated Vitamin C. He would go on to win a Nobel Prize for his discovery.