Sexually Transmitted
Diseases Of Bacterial Origin
Gonorrhea is
the most frequently reported communicable disease in many of the more developed
countries. Rates are 5–50 times higher than in the less developed world. The
Gram-negative coccus that causes the disease is called Neisseria
gonorrhoeae. It is a highly specialized organism that requires a mucosal
surface to gain access to the body. The most important health consequence of
gonorrheal infections is fallopian tube damage and the associated predisposi-
tion to ectopic (tubal) pregnancies and infertility.
In men,
urethritis is the most common clinical manifestation of gonorrhea. Symptoms
include dysuria and/or a purulent urethral discharge. Complications of
gonorrhea are uncommon in men, but ure- thral stricture, epididymitis and
prostatitis can occur. Between 20 and 30% of heterosexual men with symptomatic
gonococcal urethritis are simultaneously infected with Chlamydia trachomatis.
Gonococcal
infection in women is often asymptomatic. Morbidity associated with the
infection, however, is far greater than that seen among infected men. A
significant number of women diagnosed with gonorrhea are identified in sexually
transmitted disease (STD) clinics as the asymptomatic consort of an infected
partner. Uncomplicated urogenital gonococcal infection in women may present as
dysuria from urethritis, vaginal discharge from cervicitis, or purulent
drainage from the Skene or Bartholin glands at the vaginal introitus. Pelvic
inflammatory disease (PID) is a term used to describe infection of the
upper genital tract, including endometritis, salpingitis and peritonitis. Neisseria
gonorrhoeae and C. trachomatis are the two pathogens most commonly
isolated from women with positive cultures for PID. Women with gonococcal
PID present with lower abdominal pain, abnormal uterine bleeding,
dyspareunia (pain with intercourse) and fever. Although mortality from PID is
low, morbidity is extremely high. PID is an important risk factor for chronic
pelvic pain, infertility and tubal pregnancies. In some areas of Africa, up to
50% of women are infertile as a result of tubal occlusion from gonococcal PID.
Other
serious clinical manifestations include disseminated gonococcal infection (DGI)
and gonococcal ophthalmia neonatorum, a severe form of conjunctivitis affecting
newborn infants who acquire the infection in the birth canal. Neonatal
gonococcal ophthalmia can result in blindness if left untreated. It is a rarity
in developed countries because neonatal ocular prophylaxis is mandated at
birth, but remains a significant problem in many resource-poor parts of the
world.
Gonorrhea is
treated with antibiotics. Due to antibiotic resistence profiles, a parenteral
cephalosporin plus doxycycline or azithromycin is currently first-line therapy
for uncomplicated infections, but the choice of antibiotic evolves with
resistence profiles and the propensity for the organism to be associated with
other STDs.
Epidemiology of gonorrhea
Gonorrhea is
largely a disease of youth. Incidence peaks in men and women at ages 18–24
years. In addition to age, the risk factors include low socioeconomic status,
urban residence, unmarried status, non- white race, male homosexuality and
prostitution.
Biology of N. gonorrhoeae
Gonococci
enter the body by attaching to nonciliated columnar mucosal epithelial cells
using specialized surface structures on the bacteria known as pili (Fig.
46.1). Following attachment by the pili, the gono- cocci are endocytosed by the
cell. At this stage, a lipopolysaccharide (LPS; endotoxin)-mediated event is
activated and nearby cells are killed. Following endocytosis of the bacteria,
vacuoles containing viable and replicating gonococci pass through the cell from
the mucosal surface to the subepithelial membrane. They are then released into
the underlying tissues. The surface damage caused by the gonococcus allows
other pathogens, such as chlamydia, to gain access to the upper reproductive
tract and cause multiorganism PID. Movement of the gonococci to subepithelial
sites also explains frequent failure to document its presence in the fallopian
tube despite cervical culture-positive PID.
Gonococci
develop their antibiotic resistance through plasmidmediated and chromosomal
mechanisms. Most plasmid-mediated resistance is to penicillin and tetracycline.
Chromosomally mediated resistance is more general and involves mutations that
alter cell wall permeability or the affinity of binding proteins to
antibiotics.
Chlamydia
There are
many similarities between the infections caused by N. gonorrhoeae and Chlamydia
trachomatis (CT). Chlamydiae access the body by invading the same
epithelial cells of the endocervix, urethra, endometrium, fallopian tubes,
rectum and conjunctivae that are host to the gonococcus. Infections in men are
relatively asymptomatic and of low morbidity; the major consequence of
infection in the male is the risk of transmission to a female partner. In
women, gonococcal and chlamydial infections can result in PID, chronic
abdominal and pelvic pain, infertility and ectopic
pregnancy. There is risk to the newborn infant from a birth canal infected with
gonococci or chlamydiae. The greatest clinical difference between female
infection with gonococci and CT is that chlamydial PID is often
asymptomatic. Hence, chlamydial infection is a major public health hazard
because of the potential for undetected serious damage to the upper
reproductive tracts of women.
Chlamydia
trachomatis is the most common STD in the USA and Europe. Chlamydiae are
unique bacteria. Like viruses, they are obligate intracellular parasites and
can only be propagated in cell culture. Chlamydia causes about 50% of the cases
of nongonococcal urethritis in men. In women, chlamydia can cause mucopurulent
cervicitis and the “urethral syndrome.” In the latter, pain on urination is
associated with the presence of white blood cells, but no bacteria, in the
urine. Unlike gonorrhea, chlamydial infection of the upper genital tract often
invades the endometrium and even the fallopian tubes without causing overt
signs of PID. Such subclinical infection may first be recognized with diagnosis
of the consequent infertility or ectopic pregnancy.
Several
strains of chlamydia cause a unique disorder known as lymphogranuloma
venereum (LGV), a chronic disease that, like syphilis, has three clinical
stages. The primary lesion of LGV is a small, inconspicuous papule of the
genitalia that quickly and quietly disappears. The secondary stage of LGV is
characterized by fever, malaise and either acute lymphadenitis of the inguinal
region (bubo formation = inguinal syndrome) and/or acute hemorrhagic proctitis
(anogenitorectal syndrome). Most people recover uneventfully from the second
stage. In an unfortunate few, the chlamydiae persist in the anogenital tissues
and incite a chronic inflammatory response that can cause genital tract ulcers,
fistulae and strictures. LGV is endemic in much of the less developed world but
sporadic in the USA and Europe. Neonates exposed to chlamydia in the birth
canal may develop afebrile pneumonia or conjunctivitis that can progress to
blindness.
Unlike gonococci,
chlamydiae require prolonged treatment to eradi- cate the intracellular
reservoir of the bacteria. First-line therapy is presently azithromycin or
doxycycline. In vitro data and clinical experience indicate that CT may
persist within certain infected cells for many years. Because of frequent
coexistence of gonorrhea and chlamydial infection, most treatment regimens
include antibiotics active against gonococci and chlamydia. True antibiotic
resistance is rare in chlamydial infections.
Epidemiology of chlamydial
infection
Chlamydia
infection is a disease of the young. Additional risk factors include low
socioeconomic status, a high number of sexual partners and oral contraceptive
use. Barrier methods of contraception (condom, diaphragm, diaphragm plus
spermicide) reduce risk.
Biology of chlamydia
The
chlamydiae are structurally complex microorganisms. Like viruses, chlamydiae
are obligate intracellular parasites. They are classified as bacteria because
they contain both DNA and RNA. Like Gram-negative bacteria, they possess outer
membrane proteins and an LPS. Chlamydiae differ from all other bacteria in that
their growth cycle is characterized by transformation between two distinct
forms: the elementary body and the reticulate body (Fig. 46.2).
The elementary body is a highly infectious, rigid extracellular growth form
that is metabolically inactive. The elementary body attaches to nonciliated
columnar or cuboidal epithelial cells and induces ingestion by the host cell.
The elementary body-containing phagosome does not fuse with host cell
lysosomes, a characteristic crucial to CT survival and unique to only a few
organisms (Mycobacterium tuberculosis is another). Within the phagosome,
the elementary body reorganizes into a larger, metabolically active, fragile
and noninfectious reticulate body. The reticulate bodies divide repeatedly by
binary fission within the phagosome of the host cell. They will ultimately
reorganize back into infectious elementary bodies that are released when the
host cell dies.
There are 15
different serotypes or serovars of chlamydiae. These serovars are identified as
A–K, Ba, and L1, L2 and L3. Strains D–K are associated
with chlamydial STDs. L1, L2 and L3 cause LGV.
