STUDENT PROJECT

HERPES SIMPLEX TYPE 2 INFECTION

Arranged by:
SGD B2

Albertus Imanuel Krisna Sandyawan (1702511093)

Cindy Liora Driansha (1702511207)
Gustinara Bakti Pangala (1702511040)
Johanes Prasetyo Harjanto (1702511096)
Louisa Gisela Maura Gutama (1702511167)
Made Ratna Sandra Dewi (1702511011)
Ni Komang Pasek Nurhyang Jumantini (1702511064)
Ni Luh Putu Mulia Laksmi Dewi (1702511068)
Putu Dewinadya Saraswati (1702511139)
Renaldy Frederich Nathanael Magat (1702511081)
Dharsnee Perimaisivam (1702511227)
Elianora Viliana Hi Freitas (1702511219)

UDAYANA UNIVERSITY
FACULTY OF MEDICINE
2020
 PREFACE

Om Swastyastu,
First of all the writer praises God before the Almighty God, because
thanks to His mercy, this Student Project Task can be completed in time.
On this occasion, allow the author to express deepest gratitude to our
facilitator in the Reproductive System and Disorders block, dr. I Kadek Swastika,
M.Kes, who have provided input, suggestions, objections, and corrections so that
the Student Project's assignments can be realized. The writer also delivered
gratitude to our evaluator. The contents of this Student Project are about Herpes
Simplex type 2 Infection.
We realize that this student project is far from perfect and has a number
of errors. We apologize for errors that have occurred in terms of format, topic
suitability, and so on. The constructive criticism and advice from the readers is
very much needed to improve writing in the future.
Finally, we say Parama Santih. Om Santih Santih Santih Om.

Denpasar, Mei 16th 2020

Writers

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 TABLE OF CONTENT
Page

PREFACE ................................................................................................................i

TABLE OF CONTENT ..........................................................................................ii

TABLE OF FIGURES...........................................................................................iii

CHAPTER I THEORY ...........................................................................................1

1.1 Etiology .................................................................................................1

1.2 Risk Factor ............................................................................................1

1.3 Process...................................................................................................1

1.4 Pathophysiology.....................................................................................2

CHAPTER II DIAGNOSIS ....................................................................................3

2.1 Anamnesis..............................................................................................3

2.2 Physical Examination.............................................................................3

2.3 Supporting Examination........................................................................4

2.4 ICD X.....................................................................................................5

2.5 Differential Diagnosis............................................................................5

CHAPTER III MANAGEMENT............................................................................7

3.1 Treatment...............................................................................................7

3.2 Prognosis................................................................................................8

3.3 Prevention..............................................................................................9

REFFERENCES ...................................................................................................10

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 TABLE OF FIGURE

Figure 1....................................................................................................................4

Figure 2....................................................................................................................8

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 CHAPTER I
THEORY

1.1 Etiology
Herpes Simplex Virus Type-2 (HSV-2) dominantly contributes to
infections in genitalia called Herpes genitalis. The virus mainly causes genital
ulcer disease then the infection expands and causes complications in central
nervous system disease. Initial mode of HSV-2’s transmission is through direct
contact, specifically through sexual intercourse that most likely to escalate after
puberty (Balaeva et al., 2016; Matthew and Sapra, 2020). Not only through sexual
intercourse, HSV-2 can also be carried to neonates via intrauterine or by maternal
genital’s infection during delivery. In further, the mothers are generally
asymptomatic since there wasn’t any genital herpes’s history (Matthew and Sapra,
2020).

1.2 Risk Factor

Age groups that have active sexual intercourse is one of the risk factors of
HSV-2 infections. The age group ranging from 15-35 years old applies to Asia
and could be younger in Western countries due to geographic differences that
affect both sexual lifestyle and behavior (Bonita and Murtiastutik, 2017). In
addition, people who have history contact with numbers of sexual partners raise
the risk of HSV-2 infection and in details arising the risk of HIV infection. Direct
exposure like saliva (fluids) from a seropositive individual holds the amount of
viral most at the time of sexual intercourse also adding another risk factor that
brings in infection. Considering its low stability apart from the body, the virus can
only last infectious for days on a humid area or surface. Thus, other transmission
approaches are often found insignificant aside from sexual intercourse (Balaeva et
al., 2016; Matthew and Sapra, 2020). 

1.3 Process
Primary infection of HSV-2 commonly caused by close contact with
infected person on mucous membrane of genital organ or abrashed skin (Mustafa

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et al., 2016; Monroe-Wise, McClelland and Farquhar, 2017). HSV-2 transmission

through contact with contaminated objects is uncommon. HSV-2 is commonly
transmitted in population of men that are actively having sexual intercourse with
another men. The incubation period of this infection is relatively short, only about
5 days (Mustafa et al., 2016).

1.4 Pathophysiology
The virus can enter the skin and replicate themselves in epidermis and
dermis cells. Early infection of this virus is often asymptomatic; clinical
manifestation may appear after replication of the virus is sufficient to begin
infection in sensory and autonomic neurons. Virus that have entered the neuron
cell will be transported intra-axonal to the nerve cell body (Mustafa et al., 2016).
In HSV-2 that is located in genital area, the most common location they migrate
to is S2-S5 dorsal root ganglion (Mustafa et al., 2016; Monroe-Wise, McClelland
and Farquhar, 2017). After that, the virus will inoculate and replicate again in
neural ganglion. At this time, neuron tissue can be really contagious. And then,
the virus will spread centrifugally to other skin area via peripheral sensory nerves,
causing new lesions that may develop distant from the initial vesicle. Contagious
virus spread can also facilitate them to expand the spread of infection to another
parts of the body. In primary HSV-2 infection, viremia is reported for about 25%
of the cases and can affect the severity and reactivation frequency (Mustafa et al.,
2016). Host factor like immunocompromised people can also aggravate this
condition, because immune responses such as cytotoxic T lymphocyte have role to
control the activities of the virus (Mustafa et al., 2016; Monroe-Wise, McClelland
and Farquhar, 2017).  

After the primary infection, HSV-2 will enter the area of infection, and
then go to the neuron cells body, and become dormant or latent in neural ganglion
(Mustafa et al., 2016). If there are factors that triggering the reactivation such as
immunosuppression, UV light, trauma, and fever, the virus will go to epithelial
cells via axons and replicate themselves, causing the production of lesion that less
severe than primary infection (Monroe-Wise, McClelland and Farquhar, 2017).
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 CHAPTER II
DIAGNOSIS

2.1 Anamnesis
Herpes can be diagnosed through anamnesis, physical examination and
test for herpes. For the anamnesis symptoms will appear between three days to
one week after exposure to HSV-2. Patients will generally experience typical viral
prodromal symptoms, such as malaise, anorexia, fever, lymphadenopathy,
localized pain, burning, or throbbing before the appearance of the lesion. The
patient will then complain of the emergence of group vesicles at the base of the
erythema. The vesicles will then become pustules, erosions, and ulcerations in the
part of the broken vesicle. Within 2 to 6 weeks, the lesion will be covered by
crusting and the symptoms will disappear. In genital herpes clinical
manifestations that can be extracted from the history include a classic syndrome in
the form of a group of bilateral erythema papules, vesicles or ulcers in external
genitalia, perianal, or buttocks of patients that appear within 4-7 days after sexual
exposure. This classic syndrome only appears in 10-25% of cases of primary
infection. Patients generally complain of genital pain and itching. 80% of cases in
women report dysuria. The symptoms, such as headache, fever, headache,
malaise, myalgia (World Health Organization, 2016). After 2-3 weeks, new
lesions will appear and old lesions will turn into pustules which then merge into
ulcers, scab, then heal. Lesions on the genital mucosa may form ulcers without
previous vesicle formation. Atypical presentations of HSV-2 can be in the form of
small erosions and fissures, as well as dysuria or urethritis, without the appearance
of skin lesions (World Health Organization, 2016).

2.2 Physical Examination

Physical examination of genital herpes, from the inspection we can get the
appearance of painful vesicles or lesions in the form of ulcers may look similar to
chancroid or syphilis. In addition, inguinal lymphadenopathy can also be found.
Lesions in the urethra can provide complaints in the form of transient urine
retention in women (Sauerbrei, 2016).

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Figure 1. Herpes simplex type 2 infection (Sauerbrei, 2016).

2.3 Supporting Examination

1. Herpes simplex virus culture

Herpes virus culture aims to diagnose the presence of herpes virus.
Herpes virus culture is done by wiping the infected skin or genital area,
taking genital fluid or other bodily fluids that are suspected of having
herpes to then be examined in the laboratory using a microscope
(Sauerbrei, 2016).
2. Blood Test (Antibody test)
HSV 2 virus specific antibody tests can be performed to detect the
presence of primary herpes infections, but cannot detect recurrent herpes
infections. Antibody tests are carried out by taking blood samples from the
body, then analysed in the lab to check for the presence of HSV-2 specific
antibodies. The body takes about 12-16 weeks to form anti HSV-2
antibodies, after the HSV virus has entered into the body first. The HSV-2
antibody tests are very helpful in diagnosis, especially if the patient has no
sores or blisters on the skin (Sauerbrei, 2016).
3. PCR Test
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The PCR test aims to find out whether a person has genital herpes
even if he has no symptoms. PCR testing is done by looking for pieces of
viral DNA in samples taken from fluids or cells or in the urinary tract or
genital injuries. This test is very accurate and it’s commonly used to
diagnose HSV-2 (Sauerbrei, 2016).
Cell culture, antibody tests or PCR tests can give false negative results if
the wound begins to heal or if you have just been infected. False negative tests
show you don’t have a HSV 2 condition although in fact you have it. False
positive test results are also possible. If your test results are positive, but you have
a low risk of contracting the virus. It’s mean you have to do further testing
(Sauerbrei, 2016).

2.4 ICD X
A60.00: Herpesviral Infection of Urogenital System, Unspecified

2.5 Differential Diagnosis

Differential Diagnosis of HSV-2 Infection such as :

1. Syphilis ( ICD X: A51.0 Primary genital syphilis)

Treponema pallidum infection is mostly can caused Syphilis. This
bacterium is spiral-shaped which is can infected one person from sexual
contact infected partner and also can infected fetus from infected mother
(Lola V. Stamm, 2016). There are 4 stages that infected person through if
the infection is untreated:
- primary (regional lymphadenopathy)
- secondary (generalized lymphadenopathy, skin eruptions)
- latent (no symptoms)
- tertiary (cardiovascular syphilis and late neurological symptoms).
(Lola V. Stamm, 2016).
2. Chancroid (ICD X: A57)
Haemophilus ducreyi infection is the cause of chancroid through a
sexual activity. Symptoms of this infection is genital ulcers that soft and
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pain, regional lymphadenitis can also appear in this condition, that can
develop to buboes. This organism is fastidious that  hard to culture from
material of the genital ulcer. The genital ulceration as symptoms of
chancroid can associated with transmission of human immunodeficiency
virus (HIV) infection. (Stephan Lautenschlager, 2017)
3. Psoriasis (ICD X: L40.9)
Psoriasis is a systemic inflammation disease that can associated
with many comorbidities include malignancy and cardiovascular disease.
This disease is a chronic and effect multisystem in the body that can
caused inflammatory disease with mostly involve the skin and joint. (Kim
W.B, et al, 2017)
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CHAPTER III
MANAGEMENT

3.1 Treatment
The management of HSV-2 infection consists of antiviral medications.
Dosage & duration depends on whether it is a first-time clinical episode or a
recurrent episode, but in general all cases are treated when a clinical episode is
confirmed. The treatment for adults and adolescents with a first-time clinical
episode, the usage of Aciclovir is preferred over famciclovir or valaciclovir, with
the duration of the drug regimen being 10 days. The preference of Aciclovir over
famciclovir & valaciclovir is based on the lower cost of Aciclovir, not efficacy. 
On patients with recurrent clinical episodes, the same type of drugs are
recommended, Aciclovir being preferred. The duration and dosage of the drugs
are adjusted on whether the patient is immunocompromised or not. The
medications should be taken during the prodromal phase. In patients with frequent
recurrent clinical episodes with cause extreme distress (generally considered to be
around 4-6 times a year), suppressive therapy is recommended over episodic
therapy. Suppressive therapy means that the medications are taken year-round.
(World Health Organization, 2016)

Recommendations Treatment

Adults and adolescents with a first-  Aciclovir 400 mg 3dd tab 1 for 10
time clinical episode days 
 Aciclovir 200 mg 5dd tab 1 for 10
days
 Valaciclovir 500 mg 2dd tab 1 for
10 days
 Famciclovir 250 mg 3dd tab 1 for
10 days

Patients with recurrent clinical For adults, adolescents and pregnant

episodes women: 
 Aciclovir 400 mg 3dd tab 1 for 5
days/ 800 mg 2dd tab 1 for 5 days/
800 mg 3dd tab 1 for 2 days 
 Valaciclovir 500 mg 2dd tab 1 for
3 days
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 Amciclovir 250 mg 2dd tab 1 for 5

days 
For people living with HIV and people
who are immunocompromised:
 Aciclovir 400 mg 3dd tab 1 for 5
days
 valaciclovir 500 mg 2dd tab 1 for
5 days
 famciclovir 500 mg 2dd tab 1 for 5
days

Patients with frequent recurrent Dosages for adults, adolescents and

clinical episodes with cause extreme pregnant women:
distress (around 4-6 times a year)  Aciclovir 400 mg 2dd tab 1 
 valaciclovir 500 mg 1dd  tab 1
 famciclovir 250 mg 2dd tab 1
Dosages for people living with HIV and
people who are immunocompromised: 
 Aciclovir 400 mg 2dd tab 1  
 valaciclovir 500 mg 2dd tab 1 
 famciclovir 500 mg 2dd tab 1

Figure 2. Dosage recommendations for the treatment of HSV type 2 infections

(World Health Organization, 2016).

3.2 Prognosis
For a person who already infected by the HSV-2 cannot cure the virus, so
the virus is persists for a lifetime with that person, but the viral replication can be
suppression by the early identification of sign and symptoms and early
pharmacotherapy treatment can provide a good prognosis. To decrease the risk of
transmission to other person have to abstinence during known the viral shadding
(Sauerbrei, 2016). Generally, the prognosis of genital herpes will be good if the
patient’s immune system is maintained because the herpes simplex virus will be
dormant in the body of an infected person throughout their life.

HSV-2 infection can lead to others complication such as:

1. Sexually transmitted disease

People that already infected by HSV-2 have a high risk for other
complication of sexually transmitted disease such as HIV (Human
immunocompromised Virus). Increased risk acquiring of HIV infection is
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associated with HSV-2 infection, which is 60%-90% patient HIV is also

infected by HSV-2. For the patient who infected by both HIV and herpes
virus type 2 is more likely to transmitted HIV to other people (Sauerbrei,
2016).
2. Meningitis
Meningitis is one of the complication that can cause by HSV-2
infection and this virus can affected in any part of the nervous system.
Meningitis is occur when infection of HSV-2 is untreated. Meningitis is a
rare but a serious complication in HSV-2 infection (Sauerbrei, 2016).
3. Herpes virus type-2 infection in Neonatal
In pregnant woman that infected by HSV-2 can transmit the virus
to the baby. Transmission of the HSV-2 from mother to the infant is
occurs during vaginal delivery, where that time the baby will be in direct
contact with the virus that is in the genital area of the mother. HSV-2
infection in neonatal is rare but it can lead to a serious condition such as
permanent neurologic disability or can cause death. The risk of
transmission will high when the mother is infected by HSV-2 for the first
time in third trimester of pregnancy because in early infection the level of
the virus is highest in genital tract (Sauerbrei, 2016).

3.3 Prevention
As HSV- 2 infections are classified as an STI, practicing safe sex is a tool
in prevention. Safe sex can be applied by using condoms during sex. Practicing
abstinence will also prevent HSV infections. Counselling may be beneficial in
preventing future infections as well as overcoming current difficulties if done on a
confirmed patient. Knowledge of both partners’ serostatus’ is important as
patients may be symptomatic or asymptomatic. To date, there are no effective
prophylactic vaccines against HSV (Sauerbrei, 2016).
 REFFERENCE

Balaeva, T., Grjibovski, A.M., Sidorenkov, O., et al. (2016). Seroprevalence and
correlates of herpes simplex virus type 2 infection among young adults in
Arkhangelsk, Northwest Rusia: a population-based cross-sectional study.
BMC Infectious Disease, 16(616).
Bonita, L., Murtiastutik, D.A. (2017). Retrospective Study: Clinical Manifestation
of Genital Herpes Infection. Periodical of Dermatology and Venereology,
29(1): 33.
Kim WB, Jerome D, Yeung J. (2017). Diagnosis and management of psoriasis.
Can Fam Physician. 63(4):278‐285.
Lautenschlager, Stephan, et.al. (2017). European guideline for the management of
chancroid. International Journal of STD&AIDS. Vol. 28:4
Matthew, Jr.J., Sapra, A. (2020). Herpes Simplex Type 2 [Internet]. In: StatPearls.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK554427/ [accessed
9 May 2020]
Monroe-Wise, A., McClelland, R. and Farquhar, C., (2017). Chapter 44 - Genital
Ulcer Disease. In: C. Sanford, P. Pottinger and E. Jong, ed., The Travel and
Tropical Medicine Manual, 5th ed. Philadelphia: Elsevier, pp.545-553.
Mustafa, M., Illzam, E., Muniandy, R., Sharifah, A., Nang, M. and Ramesh, B.,
(2016). Herpes simplex virus infections, Pathophysiology and Management.
IOSR Journal of Dental and Medical Sciences, 15(07), pp.85-91.
Sauerbrei, A., (2016). Herpes Genitalis: Diagnosis, Treatment and Prevention.
Geburtshilfe und Frauenheilkunde, 76(12), pp.1310-1317.
Stamm L. V. (2016). Syphilis: Re-emergence of an old foe. Microbial cell (Graz,
Austria), 3(9), pp. 363–370.
World Health Organization. WHO Guideline For The Treatment of Genital
Herpes Simplex Virus. (2016). Available from :
https://www.who.int/reproductivehealth/publications/rtis/genital-HSV-
treatment-guidelines/en/. [accessed on 11 May 2020]

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