Davao Doctors College, Inc.

Medical Laboratory Science Department

CASE STUDY 1 Trichomoniasis

CASE STUDY:

An 18 year old girl presents to her pediatrician with her mother for her pre-college check-up. She has no past medical history.
After her mother leaves the room for the social history component, the girl admits to having sex with her boyfriend for the
first time two weeks ago and complains of a yellow green malodorous vaginal discharge that started a week ago. She endorses
mild pelvic pain. A pelvic exam is performed and mild cervical tenderness is noted. The cervix is pink, nulliparous, inflamed
and is covered by small red punctate spots. A thin yellow green frothy discharge of fishy odor is also detected. A wet prep is
made and reveals squamous cells and numerous motile organisms.

Our patient was diagnosed with Trichomonas vaginalis (TV). TV is a flagellated parasitic protozoan for which humans are the
only known host. It is 10-20 um long and 2-14 um wide with multiple flagella projecting from the anterior and posterior sides.
It has a single trophozoite stage and does not survive well outside of its host. TV is a predatory obligate parasite that eats
bacteria, vaginal epithelial cells, and red blood cells. It uses fermentative metabolism to produce the carbohydrates needed
for fuel. TV is a sexually transmitted disease; however, because it is not reportable to local health departments, the true
epidemiologic incidence rate is unknown. Its prevalence is highly variable by population and location. For example, some
studies cite a prevalence of 3.1% of American pre-menopausal women (2.3% of adolescents) [1], while in certain high-risk
populations the rate might be as high as 47% [2]. Most affected patients are asymptomatic; about a third of females become
symptomatic within six months of infection. Symptoms for females include vulvar and vaginal irritation and itching, pain with
urination and a diffuse, malodorous, yellow-green vaginal discharge. The cervix becomes reddened in a punctuated fashion
causing the well-known strawberry cervix seen on colposcopy. In males, urethritis can develop. TV is often diagnosed via wet
mount microscopy, where the protozoa can be seen moving around (Video 1). However, the sensitivity is relatively low,
especially among males. Detection by nucleic acid probe from urine, endocervical, and vaginal swabs are considered more
sensitive. TV can also be incidentally discovered on Pap tests (Figures 1 and 2). Treatment typically consists of a single dose
of metronidazole [1,2]. It is critical that partners be treated as well, because otherwise reinfection may occur.

Table/ Result:

1. Physiology of Organs affected: X

The vulva is highly specialized tissue with regional distinctions in embryologic derivation and tissue structure. It is composed
of specialized tissue with regional differences in embryonic derivation, structure, and morphology. The vulva comprises the
mons, pubis, labia majora and minora, clitoris, vulvar vestibule and the vagina. Under the category of Protozoa, in its subgroup
Flagellate, Trichomoniasis is caused by Trichomonas Vaginalis. It is an inflammation of reproductive organs mostly in females.
In women, the organism causes an infection in the vagina, urethra, or both. Some women with the infection experience a
frothy, yellow-green vaginal discharge with a strong odor, discomfort during intercourse, pain during urination, itching in the
genital area or spotting between periods. In rare cases, pain in the lower abdomen can occur. Women infected with
Trichomonas are more at risk of acquiring human immunodeficiency virus (HIV) and other STDs.

Humans are the only host for T. vaginalis and direct transmission occurs from person to person during sexual intercourse. The
parasite reproduces by binary fission and there is no evidence of cyst formation. It is anaerobic, lacking a mitochondrion, and
is an obligate parasite inhabiting the urogenital tracts of males and females where it moves around using four thread-like
filaments called flagella. T.vaginalis attaches to several types of host cells, such as those lining the vagina and prostrate
(epithelial cells).
2. Pathophysiology of the Illness:

T vaginalis is approximately the size of a white blood cell (WBC)—about 10-20 μm long and 2-14 μm wide—though its size
may vary with physical conditions It has 4 flagella projecting from the anterior portion of the cell and 1 flagellum extending
backward to the middle of the organism, forming an undulating membrane. An axostyle, a rigid structure, extends from the
posterior aspect of the organism. In women, T vaginalis is isolated from the vagina, cervix, urethra, and bladder. In men, the
organism is found in the anterior urethra, external genitalia, prostate, epididymis, and semen. It resides both in the lumen
and on the mucosal surfaces of the urogenital tract. The flagella allow the trophozoite to move around vaginal and urethral
tissues.

During infection with T vaginalis, jerky motile trichomonads may be observed on wet mount microscopy. T vaginalis destroys
epithelial cells by direct cell contact and by release of cytotoxic substances. It also binds to host plasma proteins, thereby
preventing recognition by the alternative complement pathway and by host proteinases.

During infection, the vaginal pH increases, as does the number of polymorphonuclear leukocytes (PMNs). PMNs, a type of
white blood cell, are the predominant host defense mechanism. These cells respond to chemotactic substances released by
trichomonads. There is also evidence that lymphocyte priming occurs, as shown by the presence of antigen-specific peripheral
blood mononuclear cells.

An antibody response has been detected both locally and in serum. However, infection produces an immunity that is only
partially protective, at best. Despite the interaction the human immune system has with T vaginalis, there is little evidence
that a healthy immune system prevents infection. One study showed no association between trichomoniasis and the use of
protease inhibitors or immune status in HIV-infected women. Another study showed that HIV seropositivity did not alter the
rate of infection in males. Symptoms of trichomoniasis typically occur after an incubation period of 4-28 days. Infection may
persist for long periods in women but generally persists for fewer than 10 days in males. Anecdotal evidence suggests that
asymptomatic infection may persist for months or even years in women.
 Davao Doctors College, Inc.

Medical Laboratory Science Department

CASE STUDY 2 Genital Herpes ( Integumentary System)

CASE STUDY:

GENITAL HERPES

Roberta Patterson is a 26-year-old woman who presents for her first prenatal visit. She is concerned for her baby because of
her husband Franklin’s history of genital herpes. She states that she is six weeks pregnant.

 Roberta has never had symptoms of vaginal or oral herpes.

 She was diagnosed and treated for chlamydia seven years ago (age 19); no other STD diagnoses reported.

 Her 26-year-old husband had his first episode of genital herpes during his last year of high school; no other STD diagnoses
reported.

 Her husband (and sex partner for the last 16 months) has not had visible HSV lesions since she’s been sexually active
with him, and reports having had no prodromal symptoms or symptoms of active disease.

 She has had no sex partners other than her husband for the last 16 months.

Physical Exam

 Vital signs: blood pressure 112/68, pulse 58, respiration 13, temperature 38.5° C

 Cooperative, good historian

 Chest, heart, musculoskeletal, and abdominal exams within normal limits

 Uterus consistent with a six-week pregnancy

 Normal vaginal exam without signs of lesions or discharge

 No lymphadenopathy

Table/ Result:

1. Physiology of Organs affected: X

Herpes viruses cause cytolytic infections; therefore, pathologic changes are due to cell necrosis as well as inflammatory
changes. Fluid accumulates between the dermis and the epidermal skin layers, causing vesicle formation.
The fluid then is absorbed, scabs are formed, and healing is completed without evidence of scarring. Shallow ulcers form
after the vesicles rupture on mucous membranes.

The virus travels from the site of infection in the skin or mucosal surfaces (eg, oropharynx, cervix, conjunctiva) or through
small cracks in the skin to the sensory dorsal root and remains latent until a recurrent outbreak. Outbreaks are usually
due to some type of stress including ultraviolet radiation, trauma, emotional or psychological stress, or
immunosuppression. Two types exist: Both are closely related but differ in epidemiology.

° herpes simplex virus type 1 (HSV-1)

° type 2 (HSV-2)
HSV-2 is traditionally associated with genital disease. Usually transmitted via genital contact.
On the other hand, HSV-2 reactivates 8-10 times more commonly in the genital region than in the orolabial regions.
Reactivation is more common and severe in immunocompromised individuals.

Example: Genital herpes

Genital herpes virus or (STD) sexually transmitted disease can pass through a break in your skin during vaginal, oral,
or anal sex. It can enter the moist membranes of the penis, vagina, urinary opening, cervix, or anus. This causes sores,
blisters, and swelling. Besides the sex organs, genital herpes can affect the tongue, mouth, eyes, gums, lips, ngers, and
other parts of the body. Both viruses have the capacity to invade and replicate in the CNS and the capacity to establish
a latent infection in dorsal root ganglia (Roizman and Pellett, 2001).

The term, neurovirulence, encompasses both neuroinvasiveness from peripheral sites and replication in neuronal cells.
When paired isolates (brain and lip) from patients with HSV encephalitis are evaluated by PFU/LD50 ratios following
direct intracerebral inoculation in mice, the encephalitis isolates have lower PFU/LD50 ratios than isolates from lip
lesions. Latency (the establishment and maintenance of latent infection in nerve cell ganglia proximal to the site of
infection): In orofacial HSV infections, the trigeminal ganglia are most commonly involved, while, in genital HSV infection,
the sacral nerve root ganglia (S2-S5) are involved.

2. Pathophysiology of the Illness:

HSV-1 and HSV-2 exhibit two unique biologic properties that influence pathogenesis and subsequent human disease.

Example: Genital Simplex Herpes

According to the (American College of Obstetrician and Gynecologist). Once the virus gets into your body, it infects
healthy cells. Your body’s natural defense system then begins to get the virus. the virus gets into your body, it infects
healthy cells. Your body’s natural defense system then begins to get the virus.

Usually obtain during oral sex, herpes can be passed from a cold sore around the mouth to a partner’s genitals or vice
versa. You even can reinfect yourself if you touch a sore and then rub or scratch another part of your body, especially
your eyes.

Most people either have no or mild symptoms and thus do not know they are infected. When symptoms do occur, they
typically include small blisters that break open to form painful ulcers.

Flu-like symptoms, such as fever, aching, or swollen lymph nodes, may also occur. Onset is typically around 4 days after
exposure with symptoms lasting up to 4 weeks. Once infected further outbreaks may occur but are generally milder.

According to Folusakin O Ayoade, MD Clinical Fellow, Division of Infectious Diseases, LSU Health Science Center. Herpes
simplex viruses are ubiquitous, host-adapted pathogens that cause a wide variety of disease states.

With viral replication at the site of primary infection, either an intact virion or, more simply, the capsid is transported
retrograde by neurons to the dorsal root ganglia where, after another round of viral replication, latency is established.
The more severe the primary infection, as reflected by the size, number, and extent of lesions, the more likely it is that
recurrences will ensue. Although replication sometimes leads to disease and, infrequently, results in life.

The Neurovirulence appears to be the function of numerous genes (Roizman and Knipe, 2001). In fact, deletion of
virtually any of the genes dispensable for viral replication in cell culture reduces the capacity of the virus to invade and
replicate in CNS. Mutations affecting neuroinvasiveness have also been mapped in genes encoding glycoproteins. Access
to neuronal cells from usual portals of entry into the body requires postsynaptic transmission of virus and, therefore, a
particularly vigorous capacity to multiply and to direct the virions to appropriate membranes. In addition, since neuronal
cells are terminally differentiated and do not make cellular DNA, they lack the precursors for viral DNA synthesis that are
also encoded by the viral genes dispensable for growth in cell culture. Of particular interest, however, is the role of
γ134.5 gene in neurovirulence (Chou et al., 1990; Chou and Roizman, 1986; Hesselgesser and Horuk, 1999; Whitley et
al., 1993). Although γ134.5 deletion mutants multiply well in a variety of cells in culture, they are among the most
avirulent mutants identified to date in vivo.
Latency has been recognized biologically since the beginning of the century (Baringer and Swoveland, 1973; Bastian et
al., 1972; Stevens and Cook, 1971) and has been extensively reviewed (Roizman and Knipe, 2001; Nahmias and Roizman,
1973; Roizman and Sears, 1987). The molecular basis for latency is addressed in Chapter 33. Following entry, both HSV-
1 and HSV-2 infect nerve endings and translocate by retrograde transport to the nuclei of sensory ganglia. The virus
multiplies in a small number of sensory neurons, which are ultimately destroyed. In the vast majority of the infected
neurons, the viral genome remains for the entire life of the individual in an episomal state. In a fraction of individuals,
the virus reactivates and is moved by anterograde transport to a site at or near the portal of entry. Reactivations occur
following a variety of local or systemic stimuli.

The reactivation and replication of latent HSV, always in the area supplied by the ganglia in which latency was
established, can be induced by various stimuli (eg, fever, trauma, emotional stress, sunlight, menstruation), resulting in
overt or covert recurrent infection and shedding of HSV.

In immunocompetent persons who are at an equal risk of acquiring HSV-1 and HSV-2 both orally and genitally, HSV-1
reactivates more frequently in the oral rather than the genital region.

Cellular immunity is an important defense against herpes simplex. Dissemination of herpes simplex infection can occur
in people with impaired T-cell immunity, such as in organ transplant recipients and in individuals with AIDS. Herpes
simplex infection can also complicate burn wounds or damaged skin such as in atopic dermatitis or other allergic
dermatoses.
HSV is distributed worldwide. Humans are the only natural reservoirs, and no vectors are involved in transmission.
Endemicity is easily maintained in most human communities owing to latent infection, periodic reactivation, and
asymptomatic virus shedding.