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Genital Herpes Case Study Analysis

Jill, a 29-year-old female patient went to her doctor complaining of painful blisters on her labia. Jill was in a monogamous relationship of 8 years with her husband. However, she admitted that they had recently been separated for a few months, but they were currently back together. Jill was unsure of her husband’s sexual practices during their separation. Additionally, her husband did not have any indications of illnesses. Laboratory tests of fluids from the blisters indicated the absence of gram-positive or gram-negative bacteria. This paper discusses the findings of the case study by describing the possible infection, causative organism, epidemiology, and treatment.

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Diagnosis and Justification

The correct diagnosis of the disease is genital herpes, which is a sexually transmitted infection (STI). The patient presents with painful blisters on her labia, indicating that she could be having an STI. Genital herpes is a viral contagion that causes eruptions of blisters on the genitals (World Health Organization, 2020). This diagnosis was selected because the patient’s history indicated that she was unsure of her husband’s sexual habits during their separation. Furthermore, the laboratory findings confirmed that Jill did not have a bacterial infection due to the absence of gram-positive and gram-negative bacteria, thereby ruling out the possibility of other bacterial STIs such as syphilis, chlamydia, or gonorrhea.

Background Information

Genital herpes is a viral infection caused by Herpes Simplex Virus type 2 (HSV-2), which is a subtype of the herpes simplex virus. HSV-2 is spread from one person to another exclusively through sexual contact (Gnann & Whitley, 2016). The other subtype (HSV-1) is transmitted through oral contact and is responsible for cold sores, which are also referred to as oral herpes. However, HSV-1 can also cause genital herpes. Most people with genital herpes do not display any symptoms. However, other people may show signs such as painful blisters or sores at the location of the infection, which may be the genitals or the anal area in genital herpes.

The microorganism that is to blame for this illness is herpes simplex virus type 2, which belongs to a family of viruses known as Herpesviridae. Herpes viruses originated from chimpanzees more than 6 million years ago and started infecting humans about 1.6 million years ago (Studahl et al., 2017). It has a distinct structure with four layers, which are a core, capsid, tegument, and envelope. The core holds the viral genome, which is a large fragment of double-stranded DNA. The genome is surrounded by an icosapentahedral capsid that is made up of capsomers (Ongrádi, 2016). A shapeless protein coat, the tegument, encloses the capsid. The final outer layer is a bilipid coating that also contains a glycoprotein. The key virulence factor of HSV is the evasion of the host immune responses, particularly through the production of a protein known as γ134.5 (Studahl et al., 2017). This protein works by inhibiting the major histocompatibility complex (MHC) classes I and II and the maturation of dendritic cells that mediate immune responses.

Information from the patient’s symptoms that contributed to the decision is painful blisters on the labia. The classic symptom of genital herpes is the appearance of painful labial lacerations in women (Gnann & Whitley, 2016). This information enabled the elimination of other possible culprits. However, syphilis is a bacterial STI that also causes ulcers in the genital areas. Additional information from the patient’s lab samples that contributed to the decision was the absence of gram-negative or gram-positive bacteria in the fluid samples from the blisters, which ruled out the possibility of syphilis.

The World Health Organization (2020) reports that approximately 491 million people between the ages of 15 and 49 years all over the world (this number translates into 13% of the world population in this age group) have HSV-2 infections. In the US, the incidence of genital herpes is estimated at 1 out of 6 people aged between 14 and 49 years (Bibbins-Domingo et al., 2016). Genital herpes is prevalent among women, men who have sex with other men, non-Hispanic blacks, and immunocompromised individuals. Neonatal herpes can occur when a pregnant mother transmits the infection vertically to their babies during childbirth.

The risk factors of genital herpes include having multiple sexual partners, being female, or having sexual encounters at an early age. Additional risk factors include having a weakened immune system and having another STI. During the symptomatic phase, active lesions contain a high viral load that causes viral shedding and increases the risk of infection (Ongrádi, 2016). Being infected in the late stages of gestation increase the risk of neonatal herpes. Having genital herpes may cause outcomes such as an elevated risk of getting other STIs such as Human Immunodeficiency Virus (HIV). Death may occur in infants who contract the disease from their mothers during childbirth. A mortality rate of 30% is associated with neonatal herpes (Ongrádi, 2016). Such infants can also develop encephalitis, which is the swelling of the brain.

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Genital herpes, like most viral infections, cannot be cured. However, several antiviral drugs can be used to suppress the incidence of outbreaks and reduce the frequency of recurrent outbreaks and minimize the probability of transmitting the virus from one person to another (Bibbins-Domingo et al., 2016). Antiviral therapy hastens the alleviation of symptoms and healing of lesions, in addition to reducing the shedding of the virus (Gnann & Whitley, 2016). Optimal outcomes are attained if therapy is initiated within 72 hours of manifestation of symptoms. The initial therapy for the disorder entails the administration of Acyclovir 400 mg thrice a day for 7 to 10 days or 200 mg of Acyclovir five times a day for the same duration. Valacyclovir may also be given at a dosage of 1 g twice a day or 250 mg of Famciclovir three times a day for 7 to 10 days.

Episodic treatment for recurrent herpes follows a different course. Acyclovir 400 mg may be administered thrice a day for 5 days, at a dose of 800 mg twice a day for 5 days, or 800 mg three times a day for 2 days. Valacyclovir and Famciclovir may also be given at doses of 1 g once a day for 5 days or 125 mg two times a day for 5 days, respectively. During pregnancy, Acyclovir and Valacyclovir should be initiated at 36 weeks of gestation at dosages of 400 mg thrice a day or 500 mg twice a day, respectively (Gnann & Whitley, 2016). The three drugs have similar efficacy and safety rates. The precise choice is determined by costs and patient preferences regarding the convenience of administration.

The treatments are effective at reducing the rate of infection because they have satisfactory safety profiles, minimal interaction with other drugs, and rare cases of allergic reactions. Complications of genital herpes include severe infections in immunocompromised people, which may present as recurrent outbreaks. In rare instances, genital herpes may cause eye and brain infections. Neonatal herpes may cause permanent neurologic debility or death. The symptoms associated with recurrent disease cause discomfort and a negative effect on sexual life and general quality of life. These symptoms can also cause psychological distress and social stigma.

References

Bibbins-Domingo, K., Grossman, D. C., Curry, S. J., Davidson, K. W., Epling, J. W., García, F. A., García, F. A., Kemper, A. R., Krist, A. H., Kurth, A. E., Landefeld, C. S., & Mangione, C. M. (2016). Serologic screening for genital herpes infection: US Preventive Services Task Force recommendation statement. JAMA, 316(23), 2525-2530. Web. 

This article contains a summary of recommendations proposed by the US Preventive Services Task Force (USPSTF) concerning the diagnosis and treatment of genital herpes. This source was chosen because it provides information about the benefits of prompt diagnosis and treatment. It also contains data on the prevalence of genital herpes in the US.

Gnann, J. W. & Whitley, R. J. (2016). Genital herpes. New England Journal of Medicine, 375, 666-674. Web. 

This article contains information about the incidence of genital herpes, course of infection, clinical presentation, and pharmacological interventions. This article was chosen because it describes the treatment of the disease during different phases of infection such as initial therapy, recurrent treatment, and suppressive therapy. The paper also describes the prevention of neonatal herpes through the management of the disease during pregnancy.

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Ongrádi, J. (Ed.). (2016). Herpesviridae. Books on Demand.

This book provides a detailed account of the family Herpesviridae. It also discusses the virulence of HSV and how it evades the immune response. This book was selected because of its in-depth elucidation of various aspects of the herpes virus.

Studahl, M., Cinque, P., Bergstrom, T. (2017). Herpes simplex virus. CRC Press.

This book describes the origin of the herpes simplex virus, the different classes of the microorganism as well as specific diseases that they cause. It also evaluates current treatment regimens and explains how the virus elicits and evades the immune response. Additional information such as the epidemiology, diagnosis, pathogenesis, and prevention of HSV infections is also elucidated in the book.

World Health Organization. (2020). Herpes simplex virus. Web. 

This website is a reputable source that distinguishes between the different types of herpes simplex virus. The article presents global statistics of genital herpes, the scope of the problem, symptoms as well as modes of transmission. This article was chosen because it also discusses the possible complications of genital herpes.

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