SPIROCHETES

BACTERIA
 The genus Treponema belongs to the
family of Spirochaetaceae and includes
several significant human pathogen species
and subspecies. T. pallidum, subsp. pallidum
is the syphilis pathogen. T. pallidum, subsp.
endemicum is the pathogen that causes a
syphilis like disease that is transmitted by
direct, but not sexual contact.T. pallidum,
subsp. pertenue is the pathogen that causes
yaws, and T. carateum causes pinta, two non
venereal infections that occur in the tropics
and subtropics.
 Treponema pallidum, subsp. pallidum
(Syphilis)
Morphology and culture.
These organisms are slender
bacteria, 0.2 µm wide and 5–15 µm long;
they feature 10–20 primary windings and
move by rotating around their
lengthwise axis. Their small width makes
it difficult to render them visible by
staining. They can be observed in vivo
using dark field microscopy. In-vitro
culturing has not yet been achieved.
 Pathogenesis and clinical picture.
Syphilis affects only humans. The disease
is normally transmitted by sexual intercourse.
Infection comes about because of direct contact
with lesions containing the pathogens, which then
invade the host through micro traumata in the
skin or mucosa. The incubation period is two to
four weeks. Left untreated, the disease manifests
in several stages:
 Stage I (primary syphilis). Hard, indolent
(painless) lesion, later infiltration and ulcerous
disintegration, called hard chancre. Accompanied
by regional lymphadenitis, also painless.
Treponemes can be detected in the ulcer.
 Stage II (secondary syphilis). Generalization of the disease
occurs four to eight weeks after primary syphilis. Frequent
clinical symptoms include micropolylymphadenopathy and
macular or papulosquamous exanthem, broad
condylomas, and enanthem. Numerous organisms can be
detected in seeping surface efflorescences.
 Latent syphilis. Stage of the disease in which no
clinical symptoms are manifested, but the
pathogens are present in the body and serum
antibody tests are positive. Divided into early
latency (less than four years) and late latency
(more than four years).
Stage III (tertiary or late syphilis). Late
syphilis: manifestations in skin, mucosa,
and various organs. Tissue disintegration is
frequent. Lesions are hardly infectious or
not at all. Cardiovascular syphilis:
endarteritis obliterans, syphilitic aortitis.
Neurosyphilis: two major clinical categories
are observed: meningovascular syphilis,
i.e., endarteritis obliterans of small blood
vessels of the meninges, brain, and spinal
cord; parenchymatous syphilis, i.e.,
destruction of nerve cells in the cerebral
cortex (paresis) and spinal cord (tabes
dorsalis). A great deal of overlap occurs.
 Diagnosis.
Laboratory diagnosis includes
both isolation and identification of
the pathogen and antibody assays.
Pathogen identification. Only
detectable in fluid pressed out of
primary chancre, in the secretions of
seeping stage II efflorescence's or in
lymph node biopsies. Methods: dark
field microscopy, direct
immunofluorescence .
Antibody assays. Two antibody groups can be
identified:
 Antilipoidal antibodies (reaginic antibodies).
Probably produced in response to the
phospholipids from the mitochondria of
disintegrating somatic cells. The antigen used
is cardiolipin, a lipid extract from the heart
muscle of cattle. This serological test is
performed according to the standards .
Fig.1:Serous transudate from moist mucocutaneous primary
chancre. Direct immunofluorescence.
Fig.:2
 Antitreponema antibodies. Probably directed at T.
pallidum. — Treponema pallidum particle
agglutination (TP-PA). This test format has widely
replaced the Treponema pallidum
hemagglutination assay (TPHA). The antigens
(ultrasonically-treated suspension of Treponema
pallidum, Nichols strain, cultured in rabbit
testicles) are coupled to particles or erythrocytes.
— Immunofluorescence test (FTA-ABS).
 Therapy.
Penicillin G is the antibiotic agent of choice. Dosage and duration
of therapy depend on the stage of the disease and the galenic formulation
of the penicillin used.

Epidemiology and prevention.

Syphilis is known all over the world. Annual prevalence levels in
Europe and the US are 10–30 cases per 100 000 inhabitants. The primary
preventive measure is to avoid any contact with syphilitic efflorescences.
When diagnosing a case, the physician must try to determine the first-
degree contact person, who must then be examined immediately and
provided with penicillin therapy as required. National laws governing
venereal disease management in individual countries regulate the
measures taken to diagnose, prevent, and heal this disease. There is no
vaccine.
 BORRELIA(‫)لالطالع‬
RELAPSING FEVERS
 Taxonomy and significance.
The genus Borrelia belongs to the family
Spirochaetaceae. The body louse borne
epidemic form of relapsing fever is caused by
the species B. recurrentis. The endemic form,
transmitted by various tick species, can be
caused by any of a number of species
(at least 15), the most important being
B. duttonii and B. hermsii.
 Morphology and culture.
Borreliae are highly motile spirochetes with
three to eight windings, 0.3–0.6 µm wide, and 8–18
µm in length. They propel themselves forward by
rotating about their lengthwise axis. They can be
rendered visible with Giemsa stain . It is possible to
observe live borreliae using dark field or phase
contrast microscopy. Borreliae can be cultured
using special nutrient mediums, although it must be
added that negative results are not reliable .
Fig.3 :Preparation from the blood of an experimentally infected
mouse. Giemsa staining.
 Pathogenesis and clinical picture
B. recurrentis is pathogenic only in humans. The pathogens are
transmitted by body lice. B. duttonii, B. hermsii, and other species are
transmitted by ticks. Following an incubation period of five to eight days,
the disease manifests with fever that lasts three to seven days, then
suddenly falls. A number of fever free intervals, each longer than the last,
are interrupted by relapses that are less and less severe. The borreliae
can be detected in the patient’s blood during the febrile episodes. The
disease got its name from these recurring febrile attacks. The relapses
are caused by borreliae that have changed their antigen structure in such
a way that the antibodies produced in response to the last proliferative
episode cannot attack them effectively. Borreliae possess a highly
variable gene coding for the adhesion protein VMP (variable major
protein) in the outer membrane of the cell wall.
 Diagnosis.
Borreliae can be detected in patients’ blood when
the fever rises. They cannot be reliably cultured. One
method is to inject patient blood i.p. into mice. After two
to three days, the mouse develops a bacteremia that
can be verified by finding the pathogens in its blood
under a microscope.

Therapy.
The antibiotic of choice is penicillin G. Alternatives
include other betalactam antibiotics and doxycycline.
 Epidemiology and prevention.
B. recurrentis causes the epidemic form of relapsing
fever, which still occurred worldwide at the beginning of the
20th century but has disappeared for the most part today. The
pathogensare transmitted by the body louse. Prevention
involves eradication of the lice with insecticides. B. duttonii,
B. hermsii, and other borreliae cause endemic relapsing
fever, which is still observed today in Africa, the Near and
Middle East, and Central America. This is a tickborne disease.
Here again, the main preventive measure is elimination of the
insect vectors (ticks) with insecticides, especially in
residential areas.
Fig. 4 :Erythema chronicum migrans.
Table:1 : Clinical Manifestations of Lyme Disease
 LEPTOSPIRA
(LEPTOSPIROSIS, WEIL
DISEASE)
 Classification.
Leptospirae belong to the family
Leptospiraceae. The genus Leptospira comprises
two species. L. biflexa includes all apathogenic
leptospirae and L. interrogans represents the
pathogenic species. Based on its specific surface
antigen variety, L. interrogans is subclassified in
over 100 serovars in 19 serogroups. Some of the
most important serogroups are: icterohemorrhagiae,
canicola, pomona, australis, grippotyphosa, hyos,
and sejroe.
 Morphology and culture.
Leptospirae are fine spirochetes, 10–20
µm long, and 0.1–0.2 µm thick . no flagella, but
rather derive their motility from rotating
motions of the cell corpus. Visualization of
leptospirae is best done using dark field or
phase contrast microscopy. Can be grown in
special culture mediums under aerobic
conditions at temperatures between 27–30.8C̊
 Pathogenesis and clinical picture
Leptospirae invade the human organism
through microinjuries in the skin or the intact
conjunctival mucosa. There are no signs of
inflammation in evidence at the portal of
entry. The organisms spread to all parts of the
body, including the central nervous system,
hematogenously Leptospirosis is actually a
generalized vasculitis. The pathogens
 damage mainly the endothelial cells of the capillaries,
leading to greater permeability and hemorrhage and
interrupting the O2 supply to the tissues. Jaundice is caused
by a nonnecrotic hepatocellular dysfunction. Disturbances of
renal function result from hypoxic tubular damage. A clinical
distinction is drawn between anicteric leptospirosis, which
has a milder course, and the severe clinical picture of icteric
leptospirosis (Weil disease). In principle, any of the serovars
could potentially cause either of these two clinical courses. In
practice, however, the serogroup icterohemorrhagiae is
isolated more frequently in Weil disease.
Figure:5 : Serogroup icterohemorrhagiae. Culture
preparation. Dark field microscopy
 Both types of leptospirosis are characterized by fever
with chills, headache, and myalgias that set in after an
incubation period of seven to 12 days. This initial septic
stage of the disease lasts three to seven days and is then
followed by the second, so-called immune stage, which lasts
from four to 30 days. The most important clinical
manifestation of stage two anicteric leptospirosis is a mild,
aseptic meningitis. The second stage of Weil disease is
characterized by hepatic and renal dysfunctions, extensive
hemorrhaging , cardiovascular symptoms, and clouding of
the state of consciousness.
Diagnosis.
Detection and identification of leptospirae are
accomplished by growing the organisms in cultures. Blood,
cerebrospinal fluid, urine, or organ biopsies, which must not
be contaminated with other bacteria, are incubated in special
mediums at 27–30C̊ for three to four weeks. A microscope
check (dark field) is carried out every week to see if any
leptospirae are proliferating . The Leptospirae are typed
serologically in a lysis-agglutination reaction with specific
test sera. The method of choice for a laboratory diagnosis is
an antibody assay.
endemic serovars provide the test antigens. The reaction is read off under the
microscope.

Therapy.
The agent of choice is penicillin G.

Epidemiology and prevention.

Leptospiroses are typical zoonotic infections. They are reported from
every continent in both humans and animals. The most important sources of
infection are rodents and domestic animals, mainly pigs. The animals excrete
the pathogen with urine. Leptospirae show little resistance to drying out so that
infections only occur because of contact with a moist milieu contaminated with
urine. The persons most at risk are farmers, butchers, sewage treatment
workers, and zoo staff. Prevention of these infections involves mainly avoiding
contact with material containing the pathogens, control of Muridae rodents and
 successful treatment of domestic livestock. It is not
necessary to isolate infected persons or their contacts. There is no
commercially available vaccine.