http://www.cdc.gov/std/treatment/2010/genital-ulcers.htm http://www.bcdecker.com/SampleOfChapter/1-55009-186-7.

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Case 8: A Problem at College Sarah, a sophomore college student, had moved into her apartment in September. It was a big change from last year s life in the dormitory and would have been a little lonely if it hadn t been for Steve. She had met Steve in the organic chemistry class, where she had drawn him as a partner in laboratory. Steve was a sharp, handsome chemical engineering major. Within a month they were in love, and on the final weekend in October after the homecoming celebration. Steve stayed at Sara s apartment. On Friday of the next week, Sara was at the student health clinic. She had an extreme amount of vaginal itching, dysuria and a mild headache and felt a little feverish. The physician obseved a mixture of vesicular pusular lesions and shallow coalesced ulcers bilaterally present on the labia. Local edema was extensive. An internal gynecologist examination could not be made because of extreme discomfort as the spectulum was inserted. One of the outer lesions was scraped as gently as possible and a microscopic smear was prepared. Acyclovir ointment was applied. Sara was told she would probably have recurrences of this condition and that she should avoid all sexual contact during the active stage of her disease and for 1 week thereafter. Questions: 1. How could Steve, in the absence of any obvious illness, transmit an STD to Sara? - Asymptomatic viral shedding is the presence of virus in the absence of clinical signs or symptoms. Up to 70% of new infections can be attributed to asymptomatic shedding.[8-10] Asymptomatic shedding occurs in virtually all HSV-2 infected patients, and shedding rates cannot be predicted on the basis of age, sex, or reported history of outbreaks.[7,11] Shedding of virus can occur from multiple genital sites, and 50% of asymptomatic shedding events occur more than 7 days before or after a clinical outbreak.[7] And although viral shedding tends to diminish over the course of infection, the rate of decay is measured in years and the potential of transmission persists. The presence of HSV-2 on the genital mucosal surface, whether associated with clinically recognized outbreaks, subclinical outbreaks, or asymptomatic shedding, can and does lead to the transmission of HSV-2.

Conclusion: Persons with asymptomatic HSV-2 infection shed virus in the genital tract less frequently than persons with symptomatic infection, but much of the difference is attributable to less frequent genital lesions because lesions are accompanied by frequent viral shedding.

2. Which STDs present as vesicular lesions? - Herpes Simplex Virus Type 2 Differential Diagnosis: Chancroid/ Syphilis - T. pallidum infection by darkfield examination of ulcer exudate or by a serologic test for syphilis performed at least 7 days after onset of ulcers.

3. Approximately how long will Sara have these lesions? - Pain lasts for 4 days and lesion usually heals within 10 days.

Recurrences of genital herpetic infections are common and tend to be mild. A limited number of vesicles appear and heal in about 10 days. Virus is shed for only a few days. Some recurrences are asymptomatic with anogenital shedding lasting less than 24 hours. Whether a recurrence is symptomatic or asymptomatic, a person shedding virus can transmit the infection to sexual partners.

4. What is the mode of action of Acyclovir? - Acyclovir, a nucleoside analog, is monophosphorylated by the HSV thymidine kinase and is then converted to the triphosphate form by cellular kinases. The acyclovir triphosphate is efficiently incorporated into viral DNA by the HSV polymerase, where it then prevents chain elongation. The drugs may suppress clinical manifestations, shorten time to healing, and reduce recurrences of genital herpes. However, HSV remains latent in sensory ganglia. Drugresistant virus strains may emerge. Acyclovir is phosphorylated by HSV- encoded thymidine kinase to the monophosphate. Acyclovir monophosphate is further converted to the triphosphate by cellular enzymes. Acyclovir triphosphate is incorporated into growing chain of viral DNA by viral DNA polymerase and acts as a chain terminator, preventing further virus complication. The triphosphate also inhibit HSV DNA polymerase to a much greater extent than cellular DNA polymerase.

5. What would be seen in the microscopic smear of the lesions? - The tzanck preparation of papanicolau stain shows cytoloic change in scraping from the base of the vesicle or the mucous membrane. The stain can t be differentiated between herpex simples and varicella zoster

In this process, scraping from lesions are stained and then examined under a microscope. This test is less accurate than viral cultures, as it is difficult to ascertain which type of HSV infection is present.

One common test is called a Tzanck smear.

Results of the tests take up to 2 weeks.

6. Does this disease pass from person to person only by sexual contact? - No. The virus is spread by direct contact with infected secretion. Lesion are highly infectious to susceptible individual. 7. Describe the basis of latency and recurrences of this disease - After initial replication of the virus on the skin, the virus migrate to dorsal route ganglion and establish lifelong latency. If stimulated, HSV return to the skin along sensory nerve and causes recurrent infection. 8. How can the etiologic agent be isolated between episodes? - Virus isolation is the reliable method in confirmation of the clinical diagnosis. HSV grows rapidly, so characteristic cytopathic effect are observed in 24 - 48 hours if adequate specimen is obtained. Vesicular fluid contains higher titer of virus. Virus is rarely obtained from crusted lesion. Specimens should be placed in viral transport media and inoculated into tissue culture as soon as possible. Specimens should be refrigerated after 24 hours after they are inoculated. If there is longer delay, then specimens and transport media should be frozen at -70 C. Storage at -20 C in standard freezer compartments results in significant loss of virus. - Virus isolation remains the definitive diagnostic approach. Virus may be isolated from herpetic lesions and may also be found in throat washings, cerebrospinal fluid, and stool, both during primary infection and during asymptomatic periods. Therefore, the isolation of HSV is not in itself sufficient evidence to indicate that the virus is the causative agent of a disease under investigation. - Inoculation of tissue cultures is used for viral isolation. HSV is easy to cultivate, and cytopathic effects usually occur in only 2 3 days. The agent is then identified by Nt test or immunofluorescence staining with specific antiserum. Typing of HSV isolates may be done using monoclonal antibody or by restriction endonuclease analysis of viral DNA but is only useful for epidemiologic studies. 9. Many patients with this disease have high specific antibody titers. Explain this in relationship to protective immunity 10. Compare this disease as it present in males and females. -