Download THE HISTORY OF MICROBIOLOGY. CLASSIFICATION OF

Chair of Medical Biology, Microbiology, Virology,
and Immunology
Pathogenic spirochetes.
Rickettsia. Mycoplasmas.
Clamidia.
Lecturer As. Prof. O.V. Pokryshko
Spirochetes
 Treponema
 Borrelia
 Leptospira
Main pathogenic bacteria of
Spirochetaceae
Genus
Species
Subspecies
Treponema
T.pallidum
T.pallidum
T. pallidum
T.сarateum
T.vincentii
Borellia
B.recurrentis
B.caucasica,
B.duttoni,
B.persica та ін
Epidemic relapcing fever
Endemic relapsing fever
B.burgdorferi
Lyme disease
Icterohaemorrhagiae
Leptospirosis
Leptospira
pallidum
endemicum
Pertenue
Disease
Syphilis
Bejel
Yaws
Pinta
Vincent’s angina
Spirochetes structure
Spirochetes morphology
Treponema
Leptospira
Borrelia
Spirochetes ultrastructure
Borrelia
Leptospira
Classification of Human Terponema
 Non-pathogenic



T.denticola
T.macrodenticum
T.orale
 Conditionally
pathogenic

T.vincentii
 Pathogenic




T.pallidum pallidum
(syphilis)
T.pallidum
endemicum (bejel)
T.pallidum pertenue
(yaws)
T.carateum (pinta)
Vincent’s angina
Noma (gangrenous stomatitis)
Treponema in tested material
Cell attacked by treponema
Hard chancre
Clinical findings of Syphilis
Secondary syphilis
Hetchinzone
teeth
Microbiologic diagnosis of Syphilis
 Microscopy (native an
 Serologic diagnosis
fixed material)



Romanovsky-Giemsa
stain
Phase contrast
Dark field




Chain polymerase
reaction
Wassermann’s test (CFT)
Sedimentation reartions
(Каhn’s and SachsWitebsky’s tests)
Microreaction of Treponema
pallidum immobilization
IFT, ELYSA, IHAT
Tropic trepanematoses:
pinta (T.carateum), bejel (T.endemicum), yaws
(T.pertenue)
Yaws (tropic granuloma)
Bejel (endemic syphilis)
Yaws
Pinta
Bejel
Borrelia morphology
Borrelia in blood smear
Lyme disease
Causative agents:
Borrelia burgdorferi
Borrelia garinii
Borrelia afzelii
B. burgdorferi
Leptospira morphology
Clinical findings of
leptospirosis
Rickettsia
General Features
The rickettsia are bacteria which are obligate
intracellular parasites. They are considered a separate
group of bacteria because they have the common feature
of being spread by arthropod vectors (lice, fleas, mites
and ticks). The cells are extremely small (0.25 u in
diameter) rod-shaped, coccoid and often pleomorphic
microorganisms which have typical bacterial cell walls, no
flagella, are gram-negative and multiply via binary fission
only inside host cells. They occur singly, in pairs, or in
strands.
General Features
They occur singly, in pairs, or in strands. Most species
are found only in the cytoplasm of host cells, but those
which cause spotted fevers multiply in nuclei as well as in
cytoplasm. In the laboratory, they may be cultivated in
living tissues such as embryonated chicken eggs or
vertebrate cell cultures.
The family Rickettsiaceae is
taxonomically divided into three genera:
 1. Rickettsia (11 species)--obligate intracellular
parasites which do not multiply within vacuoles and do
not parasitize white blood cells.
 2. Ehrlichia (2 species) – obligate intracellular
parasites which do not multiply within vacuoles but do
parasitize white blood cells.
 3. Coxiella (1 species) – obligate intracellular parasite
which grows preferentially in vacuoles of host cells.
 4. Bartonella (3 species) – intracellular parasite
which attacks the red blood cell.
Structure
The structure of the typical rickettsia is very similar to
that of Gram-negative bacteria. The typical envelope
consists of three major layers: an innermost cytoplasmic
membrane, a thin electron dense rigid cell wall and an
outer layer. The outer layer resembles typical
membranes in its chemical composition and its trilaminar
appearance. The cell wall is chemically similar to that of
Gram-negative bacteria in that it contains diaminopimelic
acid and lacks teichoic acid. Intracytoplasmic
invaginations of the plasma membrane (mesosomes)
and ribosomes are also seen. There are no discrete
nuclear structures
Pathogenicity
In their arthropod vectors, the rickettsia
multiply in the epithelium of the intestinal tract;
they are excreted in the feces, but occasionally
gain access to the arthropods salivary glands.
They are transmitted to man, via the arthropod
saliva, through a bite. In their mammalian host,
they are found principally in the endothelium of
the small blood vessels, particularly in those of
the brain, skin and heart.
Pathogenicity
Hyperplasia of endothelial cells and localized thrombus
formation lead to obstruction of blood flow, with escape of
RBC's into the surrounding tissue. Inflammatory cells also
accumulate about affected segments of blood vessels.
This angiitis appears to account for some of the more
prominent clinical manifestations, such as petechial rash,
stupor and terminal shock. Death is ascribed to damage
of endothelial cells, resulting in leakage of plasma,
decrease in blood volume, and shock.
Pathogenicity
It is assumed that the observed clinical
manifestations of a rickettsial infection are due to
production of an endotoxin, although this
endotoxin is quite different in physiological effects
from that produced by members of the
Enterobacteriaceae.
Laboratory Diagnosis
Presumptive laboratory diagnosis is based on the
finding of rickettsial-like organisms in tissue or blood.
Although the organisms are gram-negative, they only
weakly take the counter stain, safranin. Therefore, special
staining procedures are used. Infected tissue may be
stained with:
 1. Macchiavello stain--organisms are bright red against
the blue background of the tissue.
 2. Castaneda stain--blue organisms against a red
background.
 3. Giemsa stain--bluish purple organisms.
Laboratory Diagnosis
Confirmative diagnosis is based on a serological reaction (WeilFelix reaction) in which the titer of the agglutinins in the patient's serum
against the Proteus strains OX-19, OX-2 and OX-K are determined.
These Proteus strains have no etiological role in rickettsial infections,
but appear to share antigens in common with certain rickettsia. These
antigens are alkali stable polysaccharide haptens which are distinct
from the group-specific and type-specific antigens. In interpreting the
results, it must be kept in mind that Proteus infections are fairly
common (especially in the urinary tract) and that they, too, may evoke
antibodies to the Proteus-OX strains. This test is usually positive seven
days after the initial infection.
Laboratory Diagnosis
A more specific complement fixation test is available but
does not show positive results until 14 days into the
infection.
The indirectfluorescent antibody test is also useful for
the detection of IgM and IgG antibodies against rickettsia.
In fact, this is the diagnostic test of choice for ehrlichiosis.
Diseases
1. Louse-borne:
European epidemic typhus (Rickettsia prowazekii),
Brill's disease (Rickettsia prowazekii),
Trench fever (Bartonella quintana)
2. Flea-borne
Endemic murine typhus (Rickettsia typhi),
Cat scratch fever /Bacilliary angiomatosis/ (Bartonella
henselae)
3. Mite-borne
Scrub typhus (Orientia /Rickettsia tsutsugamushi),
Rickettsialpox (Rickettsia akari)
Diseases
4. Tick-borne
Rocky Mountain Spotted Fever (Rickettsia rickettsii),
North Asian tick typhus (Rickettsia siberica),
Fievre boutonneuse (Rickettsia conorii),
Queensland tick typhus (Rickettsia australis),
Q-fever (Coxiella burnetii),
Spotted fever (Rickettsia rhipicephali),
Ehrlichiosis (Ehrlichia canis, Ehrlichia chaffeensis)
5. Fly-borne
Oroyo fever / Verruga peruana (Bartonella bacilliformis)
Chemotherapy
The drugs of choice for the treatment of
rickettsial diseases are chloramphenicol and
tetracycline. Each of these is highly toxic,
especially in children, and must be used with care.
The sulfonamides stimulate rickettsial growth and
thus are contraindicated in the treatment of these
diseases.