SEXUALLY TRANSMITTED

DISEASES (STDs)
Microbiology review article

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QASIM HUSSAIN AL-HALEIMI

Names:

1- Qasim Hussain Mohsen AL-Haleimi AC : 207002113

2-Haider Hafez AL-Hashem AC:207001665

3-Yousef AL-Khars AC:207001631

4-Abdulaziz AL-Ateek AC:207001401

COLLEGE OF MEDICINE

KING FAISAL UNIVERSITY

2008-2009
 CONTENTS:

1-Introduction

2-Classification

3-Sexually transmitted bacterial infections

Chlamydial Infections.

Neisserial Infections.

Spirochetes Infections.

Ureaplasma urealyticum infections.

Haemophillus ducreyi.

4-Sexually transmitted Viral infections

Herpes simplex virus type 2

Human papilloma virus

Human cytomegalovirus infection

Human Immunodeficiency Virus

Hepatitis Virus B & C

5-Sexually transmitted fungal infections

Genital Candidiasis

6-Sexually transmitted parasitic infections

Trichomonas vaginalis infection

7-Resources & References

SEXUALLY TRANSMITTED INFECTIONS (STIs)

Introduction:

Sexually transmitted infections(STIs) are a group of contagious conditions whose principle mode of
transmission is by intimate sexual activity involving the moist mucous membranes of the penis, vulva,
vagina, cervix, anus, rectum, mouth, pharynx, & their adjacent skin surfaces. A wide range of infections
may be sexually transmitted , including syphilis, gonorrhea, HIV infection, genital herpes, genital warts,
chlamydial infection, trichomoniasis caused by trichomonas vaginalis, & genital candidiasis. Bacterial
vaginosis is not regarded as an STIs, because it can be transmitted by other modes, commonly causing
vaginal discharge.Hepatitis viruses specially B,C can be classified as an STI infection. Chancroid,
lymphogranuloma venerum, and granuloma inguinale are rare incidence is high in tropical regions.

Spread & control:

Spread:

The rate of spread of infection depends on the infectivity of the STIs (Virolence),the rate of partner
change of infected individuals, & the suseptability of the partners to transmit it.

This means that people with many sexual partners are the group which are at high risk.

In the other hand social, educational, & religious factors influence the patterns of sexual activity.

Control

Control of STIs depends on:

-Accurate diagnosis.

-Effective treatment.

-Condom use (Mechanical barrier).

-Partner notification about the problem.

-Immunoserology of most of the fluids to detect the early signs of the disease specially for donors e.g :
Detection of Hepatitis B,C, HIV infection in blood in blood donors.

-Serology of disease that are transmitted by vertical transmission from mother to fetus through
transplacental ,or through breast milk.

Terminology:

Sexualy transmited infection(STIs): simply means that a germ — virus, bacteria, or parasite — that can
cause disease or sickness is present inside a person’s body. An infected person does not necessarily have
any symptoms or signs that the virus or bacteria is actually hurting his or her body; they do not
necessarily feel sick.

Sexualy transmited disease (STDs): means that the infection is actually causing the infected person to
feel sick, or to notice something is wrong. This difference between STDs & STIs is like difference between
Microbial colonization & infection.

Classification:
1-Sexually transmitted bacterial infections.

2-Sexually transmitted viral infections.

3-Sexually transmitted fungal infections.

4-Sexually transmitted parasitic infections.

Some resources classify 3,4 in to Other genital condi9ons (Others).

Note: In our view we will study the diseases by the organism that it cause it.

1-SEXUALLY TRANSMITTED BACTERIAL INFECTIONS

Summery

Major cause of bacterial STIs

Organism Diseases Classification of IR
Urethritis
Chlamydial cervicitis
Chlamydia trichomatis 1
Chlamydial conjunctivitis
Trachoma
Gonococcal urethritis
Neisseria gonorrhoeae 2
Gonococcal ophthalmia neonatorum
Primary syphilis chancres of penis
Treponema pallidum Secondary syphilis on sole of feet 3
A gumma of tertiary syphilis
Ureaplasma urealyticum Non-gonococcal urethritis 4
Haemophilus ducreyi Chancroid 5

Abbreviations:
IR: Incidence Rate
(1)-Chlamydia trichomatis: It is an obligate intracellular parasite bacteria it depends on the
host for the formation of energy & NAD+. Chlamydiae are small ovoid to round organisms it is
one of the smallest prokaryotic cells.

Laboratory Investigations:

-Stainning: by direct immunoflourescence technique, more common is staining using Iodine.

-Chlamydial antigens.

-There are 11th serotypes every serotype is causing a specific disease(A-K):

 Serotypes Diseases
A,B,C Trachoma
Cervicitis
Endometritis
Epididymitis
Inclusion conjuctivitis
D-K
Infant pneumonia syndrome
Nongonococcal urethritis
Proctitis
Salpingitis

Clinical diseases:

1-Urethritis(NGU):

It is the most common cause in USA.In female it is usually associated with cervicitis. Also, it
may complicate to involve the epididmis in men & the fallopian tubes in female causing what
is called (Pelvic inflammatory disease). Also it is associated with recurrence rate of the
symptoms leading to sterility in both sexes or ectopic pregnancy in females. This disease is
associated with discharge of mucoid pus cells. Chlamydial urethritis is usually associated with
gonococcal infection so treatment includes both diseases. It is caused by D-K serotype.Also
these serotypes cause eye infections.

2-Lymphogranuloma venereum(LGV): It is caused by L1-L3 serotypes more common in Asia,

Africa, & South amarica. It is characterized by transient papules on external genitalia
followed by swelling in the inguinal & perirectal lymph nodes.

3-Trachoma:Caused by serotypes A,B,C CAUSING CHRONIC KERATOCONJUNCTIVITIS, that may

progress to blindness.

4-Neonatal conjunctivitis: It occurs through the passage of birth canal inclusions in the
conjuncFva is the characters. In 10% of the childrens the disease will progress to intersFFal
pneumonitis.

Treatments:

-Chlamydiae are sensitive to Azithromycin & Tetracyclines.

-Erythromycin can be used for pregnant & neonates.

(2)-Neisseria gonorrhoeae: It is a G-ve diplococci aerobic.Frequently associated with

polymorphoneuclear leukocytes.

Clinical diseases:

1-Genitourinary tract infections: easly diagnosed in males because the symptoms are
characteristics, yellow purulent exudates & painful urination. In females a greenish-yellow
discharge is most common it may progress in to the uterus causing salpigitis(PIDs)& fibrosis,
leading to infertility.

2-Rectal infections: prevalent in male homosexuals, characterized by painful defecation,

discharge , & conistipation.

3-Pharyngitis: is contracted by oral sex .Patient may show purulent exudates that mimic mild
viral infection or streptococcal sore throat.

4-Ophthalmia neonatorum: Infection of the conjunctival sac of a newborn aquaired through

the birth canal of an infected mother. If untreated it may leads to blindness.

5-Disseminated infection: disseminated infections caused by gonococci are rare.

Laboratory tools:

-Neutrophils containing G-ve diplococci in smear of urethral exudates.

-Thayer –Martin medium.

-Oxidase positive.

Treatments:

-Third generation cephlosporins.

-Streptomycin in allergic patient to cephalosporins.

(3)-Treponema pallidum: Anaerobic G-ve spiral shaped coiled motile thin from the genus of
spirochetes(Corkscrew or helical).It is characterized by a sheath composed of
GAGs(glycosaminoglycans).It is responsible for both syphilis, as well as chancre.

Transmission: It is transmitted by two ways by sexual contact, & by vertical transmission to

the fetus through transplacental transport or directly through breaks & abrasions.

Clinical diseases:

1-Syphilis:three stages are there:

-Primary stage: hard genital or oral ulcers(Chancre) it develops aIer 3 weeks of the
inoculation. It heals but the organism spread.

-Secondary stage: a symptomaFc stage 24 weeks aIer first characterized by red

maculopapular rash on almost all the body.It may be accompanied by systemic disease.After
this stage the disease goes to latancey period.

-Tertiary stage: characterized by degeneration of the nervous system, cardiovascular

problems may develops as anureysms & granulomatous lesions (Gummas) in the liver, skin,
and bones.

Note, that immunity to the disease is established in the primary stage but lost in the tertiary
stage.

2-Congenital syphilis: this occurs through transplacental transport aIer the first 10th to 15th
weeks of pregnancy. This may leads to spontaneous death of the fetus or abortion if the fetus
live the disease will be presented as secondary syphilis.

3-Other Treponemal infections: this includes three diseases(bejel associated with hot areas,
yaws found in humid, tropical countries, & pinta found in Mexico, Phillipines).

Laboratory investigations:

-Immunoflourescent stain, or dark-field illumination.

-Detection of antibodies:

1-Anti-treponemal antibodies that are specific to surface proteins.

2-Non-treponemal antibodies like reagain (RBR) produced aginst cardiolipins.

Treatments:

-Penicillin G is the drug of a choice.

-Erythromycin is used in allergic patients.

-Also Tetracycline can be used in allergic patients.

4-Ureaplasma urealyticum: It causes Urethritis in males with highly colonization rate.It causes
postpartum fever & chorioamnionitis in womens. It is associated in cases of endometritis, and
vaginal secretions of women with premature labor. In infected infant it is isolated from lower
respiratory tract.

5-Haemophilus ducreyi: It is a G-ve pleomorphic bacteria that needs an enrichment media to

grow. Containing one or both of :
-Factor X.

-Factor V. is not needed in the bacteria species but is required for other types.

It is the causative agent of soft chancre (Chancroid) characterized by swollen tender ulcer on
the genitalia which is accompanied by enlargement of the regional lymph nodes.

-Open genital sore facilitate the transmission of HIV, & Haemophilus ducreyi.

Laboratory investigation:

-Gram stain.

-Cultivation on chocolate agar containing isovitalex & vancomycin .

Treatment:

-Co-trimoxazole.

-Erythromycin, or 3rd generation cephalosporins.

2-Sexually transmitted viral infections:

Summery:

Causative agent Diseases Prevelence ratio n

Genital herpes
HSV-2 2
Neonatal herpes
Condyloma acuminatum
HPV Periungual verruca vulgaris 1
(on a finger)
HCMV CID 3
HIV AIDS 4

Abbreviations:
HSV-2: Herpes simplex type-2
HPV: Human papilloma virus
HCMV: Human cytomegalovirus
CID: Cytomegalic inclusion disease
HIV: Human immnodeficency virus
AIDS: Aquired immuno deficency syndrome
1-Human Papillomavirus: Double-stranded non-enveloped DNA virus from the family of
Papillomavirinae & subfamily of papovaviridae. HPVs exhibit there tissue & cell specificity by
infecting only the surface epithelia. HPV is associated with high malignant cervical carcinoma.
Other HPVs are associated with anogenital warts (Condyloma acuminate) & laryngeal
papillomas(Benign epithelial tumor of the larynx) while also others are associated with
benign lesions e.g: planter warts.

Notethat: all papillomaviruses induce hyperplastic epithelial lesions in their hosts.

Modes of transmission:

-Direct contact (Sexual contact).

-Through the birth canal from the mother to infant.

-Through abrasion in the skin in contaminated areas.

Pathology:

1-Wart formation:

-Each step in the replication of HPV is associated with induction of growth of certain skin
layer.

2-Development of malignancies:

Progression to malignancy occurs due to the affinity of binding between the HPV surface
proteins & the cellular anti-oncoproteins like P53,PRb by which inacFvate cellular regulatory
proteins.

Clinical diseases:

1-Cutaneous warts: classified as common, planter, or flat (disappear without treatment).

-Epidermodysplasia verruciformis warts (stay for several years) that spread to many sites of
the body. This type of wart may induce squamous cell carcinomas.

2-Mucosal infections: Genital infection by HPV is of a greatest clinical importance. Several

types of HPV produce anogenital warts (condyloma acuminate). HPV have been established
to be the primary cause of cervical carcinoma. Other infection include respiratory tract, oral
cavity, & conjunctiva.

Laboratory investigations:

-Biopsy or cervical swab.

-Genital area examination.

-PCR for HPV DNA detection.

-DNA hybridization.

Treatment:

-Surgical removal of the warts.

-Cidofovir an inhibitor of DNA synthesis but with adverse effect.

-Oral interferon is given.

2-Herpes simplex virus-2(HSV-2): It is classified in to the family of Herpes viruses DNA double
stranded. It establish recurrent infection despite to the immunity .

Mode of transmission:

-Sexual contact.

-Through the birth canal from the infected mother to her baby.

Clinical diseases:

1- Genital herpes:

- It is characterized by painful vesicular lesions of the male and female genital and anal area.

- Asymptomatic infections may occur which can be a source of infection to other individual.

2- Neonatal herpes:

- The newborn may acquire the infection in utero, during birth (most common) or after birth.

- The infection may be asymptomatic, mild local lesion, severe generalized disease or
encephalitis.

- 25% of cases may be caused by HSV-1.

- Babies with neonatal herpes may exhibit localized lesions (skin, eye or mouth), encephalitis
or disseminated disease (multiple organs involvement).

3- Skin infection:

- It may be caused by both HSV-1 and HSV-2.

Laboratory diagnosis:
1- Cytopathology:

- Detection of the multinucleated giant cells in the herpetic lesions after staining with
Giemsa’s stain.

2- Isolation of the virus in cell culture and detection of the virus is identified by specific fluorescent
antibody.

3- PCR which is sensitive and specific.

4- Serological determination of the antibody titer.

Treatments:

- Acyclovir is the drug of choice.

3-Human cytomegalovirus: Double stranded DNA virus from the family of Herpes viruses. It is
one of the most common intrauterine viral infection & also of neonates. It is associated with
teratogenic effect if transmiNed in the 1st trimester of pregnancy to the fetus.

Mode of transmission:

-Infected tears, urine, saliva, semen, blood, or vaginal secretions & breast milk.

Clinical diseases:

1-Cytomegalic inclusion disease In infants : it is a very severe condition in which damage is

usually associated at least to a milder degree to the liver, spleen, bone marrow, CNS.

2-Mental retardation: This may occur due to involvement of the CNS.

3- Infections of adults are usually asymptomatic.

A- Heterophile negative mononucleosis:

- It is characterized by fever, lethargy and the presence of abnormal lymphocytes in the blood.
B- Systemic CMV infections:

e.g. Pneumonitis, CMV retinitis

- More common in immunocompromised patients e.g. Patients with renal and bone marrow
transplants and AIDS patients.

Laboratory tools:

A) Detection of the inclusion bodies in the tissue.

B) Detection of the viral antigens.

C) Detection of the viral nucleic acid by PCR.

D) Detection of the antibodies serologically.

Treatments:

- Ganciclovir is effective in the treatment of CMV retinitis and pneumonia.

- No vaccine is available.

- Isolation of the infants who excrete the virus in the urine.

- Blood transfused to newborns should be CMV negative.

- Only organs from CMV antibody negative donors should be transplanted to antibody
negative recipients.

4-Human Immunodeficiency virus: HIV is an RNA single stranded enveloped virus classified in
to the family of Retroviruses. It causes AIDS The first case to be diagnosed was in Los Angeles
in 1981.

Modes of transmission:

-From all the body secretions (Semenal, vaginal, blood, and salivary seceretions ) through:

1-Sexual contact: Those of Syphilis & chancroid may facilitate the transmission of HIV-1.

2-Transfusions: through blood, plasma, clotting factors.

3-Contaminated needles: in sharing needles.

4-Perinatal transmission: this occur either transplacental or during birth from the birth canal,
or from the milk through breast feeding.

Pathology:
-The HIV disease resuls from either tissue distruction by the virus or the host immune response
to the infected cells. Also, HIV infection leads to increased incidence of opportunistic diseases
this may leads to progression to AIDS. High drop of the blood CD4+ cells is there.

Clinical disease significance:

1-Initial infection:

Initially HIV infect macrophages within the genital organs, after that it disseminate to the
blood & may localize in dendritic cells throughout the lymphoid tissue then HIV can infect
CD4+ lymphocytes.

2-Acute phase viremia(Primary infection):During this phase there is a high levels of the virus
replicaFon inside CD4+ leading to high levels of viral capsid anFgen to be in blood
(Seroconversion).

3-Latent period: the acute phase viremia is reduced with appearance of HIV-specific cytotoxic
T cell response followed by antibodies response.

4-Clinical complications of HIV infection during latent period: in this period there is:

-Generalized lymphadenopathy, Diarrhea, chronic fevers, night sweats, weight loss, more
opportunistic infections such as herpes zoster, & candidiasis.

5-Progression to AIDS: In this period there is high incidence to be infected by more than one
organism, that inhances the replication of HIV and escape from the immune response this
leads to exshustion of the immune system & the bone marrow. So the capacity to produce the
immunocells is lost.CD4+ levels in blood is less than 200/µl. The paFent is said to be AIDS +.
Laboratory Identifications:

-Demonistration of the virus or the virus components.

-Demonistration of the immune response.

Treatments:

-Nucleoside reverse transcriptase inhibitors: like Abcavir sulfate, Didanosine, Zidovudine,

Zalcitabine, Stavudine, & Lamivudine.

-Nonnucleoside reverse transcriptase: Delavirdine, Efavirenz, & Nevirapine.

-Protease inhibitors: Amprenavir, Indinavir sulfate, Lopinavir, Nelfinavir mesylate, Ritonavir,

& Saquinavir.

Multidrug regimens are recommended:

1-Two nucleoside + protease inhibitor.

2-Two nucleoside+ nonnucleoside.

3-Two nucleoside +two protease inhibitor.

5-Hepatitis Viruses: (Hepatitis B, & C): Hepatitis viruses are named because they involve the
distruction of hepatocytes.

- Viral hepatitis is a systemic disease primarily involving the liver.

- Hepatitis B virus → Serum hepatitis.

- Hepatitis C virus → Post-transfusion hepatitis.

1-Hepatitis B: Double stranded DNA virus classified in to the genus of Hepadenaviruses.It is

important to mention that Hepatitis viruses are all belonging to different Families of RNAs,
except HBV, but the acute stage of all are manifested as the same. StaFsFcs shows about 300
million peoples are infected by HBVs in Asia. Chronic hepatitis leads to liver cirrhosis, &
hepatocellular carcinoma.

Important Properties of Hepadnaviruses.1

Virion: About 42 nm in diameter overall (nucleocapsids, 18 nm)
Genome: One molecule of double-stranded DNA, circular, 3.2 kbp. In virion, negative DNA
strand is full length and positive DNA strand is partially complete. The gap must be completed
at beginning of replication cycle.
Proteins: Two major polypeptides (one glycosylated) are present in HBsAg; one polypeptide is
present in HBcAg.
Envelope: Contains HBsAg and lipid.
Replication: By means of an intermediate RNA copy of the DNA genome (HBcAg in nucleus;
HBsAg in cytoplasm). Both mature virus and 22-nm spherical particles consist of HBsAg
secreted from the cell surface.
Outstanding characteristics:
Family is made up of many types that infect humans and lower animals (eg, woodchucks,
squirrels, ducks).
Cause acute and chronic hepatitis, often progressing to permanent carrier states and
hepatocellular carcinoma.
Structure of HBV:

-Electron microscopy of HBsAg-positive serum reveals three morphologic forms. The most numerous
are spherical parFcles measuring 22 nm in diameter.

-The virion of HBVs are named as Dane particle, consists of of an icosahedral neucleocapsid
enclosed in an envelope.

-Viral proteins:

1-Viral capsid (containing capsid antigens[HBcAg]).

2-Viral Envelope(containing surface antigen[HBsAg]).

3-The multifunctional reverse transcriptase/DNA polymerase.

4-Regulatory proteins containing antigens.

Transmission modes:

Replication of Hepatitis B Virus:

The infectious virion attaches to cells and becomes uncoated . In the nucleus, the
partially double-stranded viral genome is converted to covalently closed circular double-
stranded DNA (cccDNA). The cccDNA serves as template for all viral transcripts, including
a 3.5-kb pregenome RNA. The pregenome RNA becomes encapsidated with newly
synthesized HBcAg. Within the cores, the viral polymerase synthesizes by reverse
transcription a negative-strand DNA copy. The polymerase starts to synthesize the positive
DNA strand, but the process is not completed. Cores bud from the pre-Golgi membranes,
acquiring HBsAg-containing envelopes, and may exit the cell. Alternatively, cores may be
reimported into the nucleus and initiate another round of replication in the same cell.

-Hepatitis D virus infection:

-It is usually present in those infected with HBV infected persons.

- Delta-Ag and anti-delta antibody are detected in some HBV infections.

- The antigen is found within certain HBsAg particles.

- In blood, HDV (delta agent) contains delta-Ag (HDAg) surrounded by HBsAg envelope.
- HDV is a defective virus that acquires an HBsAg coat for transmission.

- The genome of HDV consists of ssRNA, 1.7 kb in size (smallest human pathogen).

- HDAg is distinct from the antigenic determinants of HBV.

- Routes of transmission are similar to HBV (e.g. blood transfusion, IV drug abusers) but it
does not appear to be sexually transmitted disease.

- Incubation period is 2-12 weeks.

- HDV may cause to types of infection:

A- HDV Co-infection:

- Infection with both HDV and HBV for the first time simultaneously.

- Co-infections of HDV and HBV are usually acute and self-limiting infections.

- After resolution, no antibodies could be detected in the serum.

B- HDV Super-infection:

- It occurs in persons with an existing chronic hepatitis B infection.

- HDV Super-infection may be associated with fulminant hepatitis.

Laboratory diagnosis For HDVs:

1- Detection of HDV RNA in the serum by PCR.

2- Detection of HDV Ag by ELISA.

3- Serologic pattern:

- Presence of both Anti-HDV and Anti-HBc IgM → Co-infection with HDV and HBV.

- Presence of Anti-HDV and absence of Anti-HBc IgM → Super-infection of chronic HBV

infection with HDV.

- Hepatitis D could be prevented by vaccinating susceptible person with hepatitis B vaccine.

- Vaccination does not protect hepatitis B carriers from super-infection by HDV.

Laboratory Diagnosis For HBVs depends on the stage of the disease:

-Measuring antibody level (Wither IgG , or IgM).

- PCR for detection of the viral DNA.

-Detection of viral antigens.

Serum marker Resolved Chronic Vaccinated

HBeAg - + -
HBsAg - + -
Anti HBc + + -
Anti HBs + - +

Abbreviations:
HBeAg: Hepatitis B envelope Antigens
 HBsAg: Hepatitis B Surface Antigens
Anti HBc: Anti hepatitis B core antibodies
Anti HBs: Anti hepatitis B surface antibodies

Treatments:

-Interferon –α.

-Lamivudine : an oral nucleoside analog has significantly reduce the levels of HBV DNA.

Prevention:

-Vaccination. (Active & passive).

People at risk:

-People with multiple sexual partners.

-Sexual partners with HBsAg positive people.

-Homosexual activity.

-Travellers to regions of endemic disease.

-Patients receiving clotting-factor conc.

2-Hepatitis C HCV:

- It is an enveloped ssRNA virus classified as flavivirus.

- It causes Post-transfusion hepatitis.

- There are 6 serotypes (in addition to different mutants or subtypes).

- The response to antiviral therapy will differ according to the viral genotype.

Modes of transmission:
Clinical Disease:

- The incubation period is 15 – 160 days.

- Most primary infections are asymptomatic.

- The symptoms is usually mild with moderate elevation of liver enzymes and jaundice (10-
20%).

- 70 – 90 % of cases progress to chronic hepatitis.

- 20 – 50 % develop cirrhosis and ate at high risk for hepatocellualr carcinoma (5 – 25 %).

Laboratory diagnosis:

1- Detection of anti-HCV by ELISA.

- Detection of Anti-HCV does not distinguish between acute, chronic and resolved infection.

- Detection of Anti-HCV in previously negative patients (seroconversion) can indicate recent

infection.

- In some patients, false negative result may occur because anti-HVC may take few months to
develop detectable antibodies (seronegative phase).

2- Detection of HCV-RNA by PCR:

- PCR can detect viral RNA within 1-2 weeks of infection (specially important in seronegative
patients).

- HCV-RNA has first to be reverse transcribed (RT) into a copy of complimentary DNA
(cDNA) and then amplified by PCR (RT-PCR).

Positive PCR helps in:

1-Conformation of active viral replication.

2- Diagnosis of acute HCV infection in the early seronegative phase.

3- Determination of the viral load which is very important for monitoring of antiviral therapy
in chronic HCV infections.

4- Loss of HCV-RNA correlates with resolution of the infection.

5- Determination of the serotype of HCV.

Treatment:

- Combination of Ribavirin and Peginterferon (Pegylated alpha interferon) is recommended.

- Peginterferon consists of recombinant human interferon attached to polyethylene glycol

(PEG).

- PEG increases the half life of the drug in the bloodstream allowing weekly injection.

- It maintains a relatively constant level of the drug.

3-Other sexually transmitted infections other than viral or bacterial:

1-Sexually transmitted Fungal Infections:

-Genital Candidiasis (Candida albicans): Candida albicans is a dimorphic fungi and represents
the most common species of candida that causes candidiasis.

Pathology:

- Damage skin or epithelium permits local invasion of candida causing cutaneous or mucosal
candidiasis (superficial candidiasis).

- Systemic candidiasis occurs when candida enters the bloodstream specially if the host
defenses are inadequate.

- From the circulation, candida can infect any organ (e.g. kidney, heart valves) and cause
candidal infections (e.g. arthritis, meningitis, endophthalmitis).

- The risk factors associated with candidiasis include:

A- Physiological factors:

e.g. Pregnancy, young or old age, obesity.

B- Pathological factors:

e.g. Leukemia, lymphoma, aplastic anemia, immunodeficiency, diabetes, Most of AIDS patient
die due to fungal infections.

C- Drug administration:

e.g. Antibiotics, corticosteroids, chemotherapy, oral contraceptives.

D- Indwelling catheters and surgery.

E- Intravenous drug abuse.

F- Trauma, burns and damage of the skin or GIT.

Clinical Disease:

Vulvovaginal candidiasis: This leads to itching, borning pain of the vulva & vagina,
accompanied by white discharge.

Laboratory diagnosis:

1- Microscopic examination:

- Smears are examined by Gram stain for budding cells and pseudohyphae.

2- Cultivation on Sabouraud’s dextrose agar containing antibiotics.

- The pure colonies are identified by:

a- Germ tube formation:

- Germ tube (tube-like appendage) is a young immature hypha growing out of a yeast cell or
spore.

- This test is used for differentiating C. albicans from other candida species.

- A pure colony of C. albicans was inoculated in 0.5 ml of human serum.

- AIer 2 h incubaFon, the culture was examined microscopically.

b- Chlamydospore formation on corn meal agar.

- Chlamydospore is a thick-walled, large fungal spore that is derived from a hyphal cell.

c- Biochemical reacFons using API 20C kit.

Treatments:

- ketoconazole or fluconazole.

-amphotericin B in combination with fluconazole and flucytosine.

2-Sexually transmitted parasitic infections:

-Trichomonas Vaginalis: It causes trichomoniasis, the most common protozoal urogenital

tract infection of humans, It is largly transmitted through sexual contact. In females it causes
inflammation of the vagina(vaginitis),cervix(cervicitis),accompanied by yellowish
discharge.Less commonly it infect males causing urethritis, prostatitis, producing white
discharge.OpFmum growth is at Ph of 6.0. so the organism does not grow in the acidic Ph of
the vagina unless it become alkalinized.

Morphology:

-The parasite has no cystic stage.

-The trophozoite of T. vaginalis, measuring 14-17 mm x 5-15mm, has a single nucleus, four
free anterior flagella and one flagellum turns back and is attached to the body by an
undulating membrane. There is also axostyle or a central skeletal rod.
Diagnosis:

In female: by examination of vaginal secretion.

In males: by examination of prostatic secretion or in the semen.

Treatments:

* Treatment should cover both the infected female and her husband.

The drug of choice is the metronidazole.

-Scabies : It is caused by Sarcoptes scabiei but uncommon.

-Infestation By arthropods like:

Pediculosis pubis.

References & Resources:

Resources

(1)Kumar & Clark Clinical medicine 6th ed by Elsever Saunders CH:2 Infec4ous diseases,Tropical
medicine, and sexually transmitted diseases.

(2)R.Harvey, and P.Champe, Microbiology Lippinco6’s Illustrated Reviews.CH:14, 18, 20, 23, 24,
28, 29, and 31. Also summery of STDs page 238 in CH:20.

(3)C.Hasle6, E.Chilvers, N.Boon, N.Colladge, J.Hunter Davidson’s Principle & prac4ce of medicine
19th ED CH:1 Infec4on and immune failure. Pages 95-the end.

(4) http://en.wikipedia.org/wiki/STDs.

(5)Our course Lectures notes on microbiology.

References:

(6)Hrrison’s Principles and prac4ce of Internal medicine 17th ED Part: 7 Infec4ous diseases
(7)ABC series: Sexually transmi6ed infec4ons.

THE END