rICKETTSIACEA, CHLAMYDIACEAE, AND MYCOPLASMATACEAE Flashcards
(159 cards)
1
Q
RICKETTSIACEAE us transmitted ia
A
arthropod vectors (lice, fleas, mites and
ticks)
2
Q
how does ricettsiae ultiply
A
Most multiply by transverse binary fission inside cytoplasm of host cells
except for the spotted fever group which multiply in nuclei
and in cytoplasm
3
Q
Grown in a yolk sac of embryonated eggs and several cell
line
A
rickettsiae
4
Q
3 groupd of rickettsiae
A
o Typhus group
o Spotted fever group
o Transitional group
5
Q
o Typhus group
A
contains only two species, R.
prowazekii and R. typhi.
6
Q
o Spotted fever group
A
includes a number of species
generally recognized as human pathogens, such
as R. rickettsii, R. conorii, and R. africae.
7
Q
o Transitional group
A
contains R. akari, R. australis,
and R. felis
8
Q
Rickettsials that are potential bioterror agents.
A
R. rickettsii, R. prowazekii, R. typhi, and R. conorii are
considered potential bioterror agents.
9
Q
Cell wall contains DAP (di-aminopimelic acid), no teichoic
acid
A
Ricketssiae
10
Q
Macchiavello stain
Castaneda stain
Giemsa stain
ricketssia rection to these tests
A
Macchiavello stain (organisms appear bright red against the
blue background of the tissue);
Castaneda stain (blue
organisms against a red background) or
Giemsa stain
(bluish purple organisms
11
Q
Confirmatory serological test for rickettsiae
A
Weil-Felix reaction
Complement-fixation
Indirect fluorescent antibody test
12
Q
diseases
Spotted fever group Rickettsioses
A
o Rocky Mountain spotted fever
o Rickettsial pox
13
Q
Typhus fever group Rickettsioses
A
o Flea-associated rickettsioses caused by R. typhi
and R. felis
o Murine typhus
o Epidemic typhus caused by R. prowazekii
o Scrub typhus
14
Q
- Other Rickettsioses
A
o Ehrlichiosis
o Anaplasmosis
o Q-fever
o Trench fever
15
Q
rocky mountain spotty fever is caused by
A
- Caused by R. rickettsia
16
Q
The nature of the agent was a mystery because no bacteria
were apparent on direct examination or on culture.
A
RMSF
17
Q
zoonosis, and humans typically acquire the
infection by tick bites. Ticks are the principal vectors and
reservoirs for R. rickettsii.
A
Rocky Mountain Spotted Fever
18
Q
The most common tick vectors are:
(iN RICKETTSIAE(
A
o Dermacentor variabilis- Southeastern United
States
o Dermacentor andersoni- Western
19
Q
nduce vasculitis in internal organs, including the brain,
heart, lungs, and kidney
Symptoms: fever, headache, myalgia, nausea, vomiting,
rash
o Rash begins as erythematous patches on ankle
and wrist during 1st week
o It extend to palms of hands and soles of feet
o Maculopapular patches eventually consolidate into
larger areas of ecchymoses
A
ROCKY MOUNTAIN SPOTTED FEVER
20
Q
Also known as Mediterranean spotted fever
A
Boutonneuse fever
21
Q
Boutonneuse fever IS CAUSED BY
A
r, is caused by R.
conorii and occurs in France, Spain, and Italy.
22
Q
The rash is similar to RMSF except that it also involves the
face
A
Boutonneuse fever
23
Q
Characterized by the presence of taches noires (black
spots) at the primary site of infection
A
Boutonneuse fever
Edema secondary to increased vascular permeability
reduces blood flow to the area and results in local necrosis
24
Q
Its reservoirs include ticks and dogs
A
Boutonneuse fever
25
are lesions caused by the introduction of R.
conorii into the skin of a nonimmune person
Taches noires
26
which causes endemic typhus, also referred to as
murine typhuS
R. typhi
27
MURINE TYPHS
Arthropod vector for R. typhi is the oriental rat flea
Xenopsylla cheopis, and the rat (Rattus exulans) is the
primary reservoir
28
Arthropod vector for R. typhi is the ????
Arthropod vector for R. typhi is the oriental rat flea
Xenopsylla cheopis,
29
is the
primary reservoir OF MURINE THYPUS
and the rat (Rattus exulans)
30
Cat flea
Ctenocephalides felis,
31
Survive in nature, to a lesser extent, by transovarial
transmission.
Murine Typhus
31
typhus can cause fever, headache, and rash
* Endemic typhus: fever, headache, and rash
32
epidemic typhus is caused by
R. prowazekii.
33
also called recrudescent typhus, is
seen in patients who previously had louseborne typhus.
Brill-Zinsser disease,
34
R.
prowazekii lies dormant in the
lymph tissue of the human
host until the infection is reactivated.
35
Rickettsial pox
cause, reservoir and vector
Caused by R. akari,
the reservoir is the common house
mouse,
and the vector is the mouse mite Liponyssoides
sanguineus
36
Papule progresses to a pustule and then to an
indurated eschar.
* Patient becomes febrile as the rickettsiae are disseminated
throughout the body via the bloodstream
experiences headache, nausea, and chills
Rash appears in face, trunk, and extremities.
self limitingg
rickettsial gropup
rickettsial pox
37
Causative agent is Orientia (formerly Rickettsia)
tsutsugamushi.
Orientia
38
vector and reservoirof oerentia
* Vector is the chigger, Leptotrombidium deliensis
reservoir rat
39
A tache noire (black spot), similar to that of boutonneuse
fever, forms at the site of inoculation.
Orientia
40
Rash starts on trunk and spread to extremities.
orienta rash starts with
41
Obligately intracellular, arthropod-borne coccobacilli. OF RICKETSIA
EHRLICHIA
42
multiply in the phagosomes of host leukocytes, and
other cells derived from the bone marrow, not in the
cytoplasm of endothelial cells.
Ehrlichia
43
2 FORM OF RICKETSIA
Two forms: Denser and infective EB, and the RB that
replicates in the phagosome and prevent phagolysosome
formation
44
morulae (mulberry-like bodies)
RICKETSSIACEAE
45
round to oval clusters of bacteria 1 to 3 μm in
diamete
MORULAE OF M. EHRLICHIA
46
causes human monocytic
ehrlichiosiS
Ehrlichia chaffeensis
47
produces a disease indistinguishable from
E. chaffeensis, and no currently available serologic test can
distinguish these agents
Ehrlichia ewingii
48
NATURAL HOST AND VECTOR OF ERLICHIA
Natural hosts of the organism include dogs and deer humans,
lone star ticK
(Amblyomma
americanum) being the primary vector
49
DYMPTOMS, COMPLICATIONS IN EHRLICHIA
- Symptoms: high temperature, headache, malaise, and myalgia
- severe complications, including
toxic shock–like syndrome, CNS involvement, and acute
respiratory distress syndrome`
50
diagnosing E. chaffeensis
- Pediatric patients infected with E. chaffeensis
- Patients may also have evidence of leukopenia
andneutropenia, thrombocytopenia, and elevated liver
enzyme levels
have a rash;
however, adults rarely experience a rash
Direct staining (Giemsa or Wright) of peripheral blood
smears or buffy coats for morulae
51
produces a disease indistinguishable from
E. chaffeensis, and no currently available serologic test can
distinguish these agents
Ehrlichia ewingii
52
HOW IS EHRLICHIA CHAFEENSIS DIAGNOSED
Most cases of HME are diagnosed retrospectively by
serologic testing; the IFA test is the most widely used
method
53
causes a disease referred to as human
granulocytic anaplasmosis (HGA).
Anaplasma phagocytophilum,
54
Anaplasma phagocytophilum, EAS FORMEYLY KNOWN AS
Ehrlichia
phagocytophilum
55
Ehrlichia chaffeensis causes
human monocytic
ehrlichiosis (hme)
56
* The symptoms closely resemble those of HME
anaplsma
57
tick vector of anaplsma
* Tick vectors include Ixodes scapularus and I. pacificus.
58
diagnosis of anaplasma what specimen
Stained smears of buffy coat preparations are preferred.
59
Diagnosis of anaplsma can also be made by using
smears, direct antigen
detection, NAATs, and isolation in cell culture
60
c burnetii characteristics
* Does not transport ATP across its plasma membrane
* Develops within the phagolysosomes of infected cells
* Acidic environment activates its metabolic enzymes. Spore
formation by C. burnetii allows it to survive harsh
environmental conditions.
* Not transmitted by arthropods, although it is known to infect
more than 12 genera of ticks and other arthropods
61
Can infect fishes, birds, rodents, livestock, and other
mammals
coxiella bunetii
62
coxiella burnetii causes
Causative agent of Q (query) fever, a disease found
worldwide.
highly contagious and, as such, is considered a
potential bioterrorism agent
63
coxiella burnetii is transmitted by
nfections are spread by the inhalation of dried birthing
fluids of several animals
64
enerally has an abrupt onset of an
undifferentiated febrile disease consisting of high
temperature that can be accompanied by headaches,
myalgia, arthralgia, cough, and rarely, a rash
acute q fever
65
May present with elevated liver enzyme levels, increased
erythrocytic sedimentation rate, and thrombocytopenia.
acute q fever
66
isolation of coxieklla burnetii should only be done in
Isolation in cell cultures should be attempted only in
biosafety level 3 facilities.
67
The drugs of choice are ___-_
for Rickettsial diseases
Chloramphenicol and Tetracycline
68
Within the genus Chlamydia, four species were previously
recognized
C. pecorum, C. pneumoniae, C. psittaci, and
C. trachomatis. All except C. pecorum have been
associated with human disease
69
The family Chlamydiaceae now consists of two genera
(1)
Chlamydia
- C. trachomatis
(2) Chlamydophila
- C. pneumoniae,
- C. psittaci, and
- C. pecorum
70
depends on the phosphorylated sugar, d-glucose 6-
phosphate, from the host cell
CHLAMYDIACEAE
71
unable to synthesize most
amino acids, cofactors, and purine and pyrimidine
nucleotides
chlamydiaaceae
72
Tricarboxcylic acid (Krebs) cycle is incomplete
Chlamydiaceae
73
Unique growth cycle involves two distinct forms,
an
elementary body (EB), which is infectious, and a reticulate
body (RB), which is noninfectious
74
has sporelike features in that they are resistant
to environmental physical stress
elementary body (EB) of chlamydiaceae
75
In vivo, host cells are primarily the nonciliated, columnar, or
transitional epithelial cells that line the conjunctiva,
respiratory tract, urogenital tract, and rectum.
chhlamydiaeceae
76
EM TO OF CHLAMYDIAECEAE
The most prominent component of
this membrane is the
major outer membrane protein
(MOMP)
77
is a transmembrane protein that contains
both species-specific and subspecies-specific
epitopes that can be defined by monoclonal
antibodies
MOMP
78
Chlamydial outer membrane also contains
lipopolysaccharide (LPS).
79
LPS is exractable with ________________. It is the primary
antigen detectable in genus-specific test and serologic
assays for chlamydiae
ketodeoxyoctonate
80
Resemble bacteria except that it cannot multiply
outside the cells
CHLAMYDIAE
81
" Energy Parasites" because they depend on host cell for
ATP generation and nutrient sources
CHLAMYDIACEAE
82
CHLAMYDIACEAE
IMPORTANT SPECIES AND DISEASE
* C. trachomatis - eye and genital infections, LGV
(Lymphogranulomavenereum)
* Chlamydophila pneumoniae - respiratory infections
* C. psittaci - psittacosis in man, ornithosis in birds
* C. pecorum
83
Elementary body -
extracellular, infective form; enters cell
via endocytosis
o Inert
o Growth cycle begins when the small EB infects
host cells by inducing energy-requiring active
phagocytosis when they remain within membrane bound phagosome
o Bacteria prevent interaction of the phagosome with
endosome
84
Reticulate body -
intracellular, growing and replicative form
o collections of reticulate bodies can be seen in the
cytoplasm called "inclusion bodies"
o mature inclusion body contains 100-500 elementary bodies
85
ANTIGENIC PROPERTIES
OF CHLAMYDIACEAE
* Genus specific antigens - heat stable, a LPS similar to gram negative bacilli present in all stages
* Species specific protein antigens - found at the surface
envelope which help in classifying them into species
* Intraspecies antigens - present in some species located
on major outer membrane proteins which classifies species
into serotypes
86
CHLAMYDIA TRACHOMITIS
Divided into two biovars- trachoma and lymphogranuloma
venereum
o TRIC- trachoma, inclusion conjunctivitis divided
into 12 serotypes
o LGV- lymphogranulomavenereum, 3 serovars
87
has separated C.
trachomatis into 20 serovariants or serovars
Characterization of the MOMP
88
Trachoma biovar includes
serovars A through K.
Serovars A, B, Ba, and C are associated with the severe eye infection trachoma,
serovars D through K, Da, Ia, and Ja are associated with
inclusion conjunctivitis, a milder eye infection, and urogenital infections
Serovars L1, L2, L2a, L2b, and L3 are associated
with lymphogranuloma venereum (LGV), an
invasive urogenital tract disease.
89
Its unique characteristic is it carries 10 stable plasmids
(unknown function
chlamydia trachomitis
90
It is the major reason for the applications of nucleic
acid amplification by PRC and identification by
nucleic acid hybridization
chlamydia trachomitis
91
trachoma is caused by
Caused by C. trachomatis types A, B & C
92
Chronic keratoconjunctivitis
trachoma
93
trachoma transmission
Transmitted by fingers, fomites, flies or dust
94
trachoma stages
Stages I-IV, infectivity is maximum in early cases, stage IV
is non-infectious
95
Number one cause of preventable blindness in the world
* Found near the equator and seen with high temperature an
C. trachomitis, trachoma
96
trachoma prevention and treatment
Prevention and treatment includes antimicrobial treatment,
facial cleanliness, environmental improvement, and a
simple surgical procedure on the eyelid
97
trachoma begins as
* It is a chronic disease that begins as follicular conjunctivitis.
* The chronic inflammation causes the eyelid to turn inward,
which results in continual abrasion to the cornea from the
eye lashes. The condition results in scarring and ulceration
of the cornea. This can result in secondary bacterial
infection and blindness
98
* Laboratory Diagnosis
of trachoma
o Demonstration of characteristic inclusion bodies
(Halberstaedter Prowazek or HP bodies) in
conjunctival scrapings by Giemsa
o Culture - yolk sac, cell lines
99
treatment and control of trachoma
Treatment and Control
o Local application of antibiotics
o Oral Administration of Tetracycline or Doxycycline
; single dose of Azithromycin
100
most common STD
Genital chlamydiasis: m
101
Genital chlamydiasis in men and women
o Men - non-gonococcal urethritis, epididymitis,
proctitis and Reiter's syndrome
o Women - acute urethral syndrome, mucopurulent
cervicitis, endometritis, salpingitis, PID, infertility,
ectopic pregnancy, premature delivery,
postpartum fever
102
most commonly caused by type L2 in the regional
lymph nodes; 3days - 5 weeks incubation period
LGV
103
o Presents with Inguinal and Anorectal symptoms
LGV
104
o Bacteria enter the lymph nodes and produce a strong inflammatory response that often results in bubo formation and subsequent rupture of the lymph node.
o Proctitis is common in women as a result of
lymphatic spread of bacteria from the vagina or
cervix.
o Men can develop proctitis as a result of analreceptive intercourse or lymphatic spread from the
urethra
LGV
105
common in women as a result of
lymphatic spread of bacteria from the vagina or
cervix
Proctitis
106
Men can develop proctitis as a result of
anal receptive intercourse or lymphatic spread from the urethra
107
The LGV serovars have also been linked to
Parinaud oculoglandular conjunctivitis
108
STAGE OF LGV
POTA ANG DAMI
109
Inclusion conjunctivitiS
* Caused by C. trachomatis types D to K
* Naturally present in the genital tract
* Neonatal form - "inclusion blenorrhoea" develops when the
infant is in birth canal, appears 5-12 days after birth;
prevented by local application of antibiotics
* Adult form - "swimming pool conjunctivitis" associated with
bathing in community swimming pools contaminated with
chlamydia from genital secretions
110
Serovars D through K IN C TRACHOMITIS
are associated with these clinical
infections, which can be persistent and subclinical as well
as acute
CONJUNCTIVITIS IN MEN AND WOMEN'
Typical clinical manifestation:
o cervicitis
o endometritis
o salpingitis
o proctitis
o nongonococcal urethritis (NGU)
o epididymitis
o prostatitis
o proctitis in men
111
can lead to scarring and dysfunction of the
oviductal transport system, resulting in infertility or ectopic
pregnancy.
Salpingitis
C TRACHOMITIS
112
also known as reactive
arthritis, is believed to be caused by C. trachomatis
Reiter syndrome (urethritis, conjunctivitis, polyarthritis,
and mucocutaneous lesions)
113
Microscopic demonstration of inclusion bodies or
elementary bodies
Microscopic demonstration of inclusion bodies or
elementary bodies
o Gram negative but stain better with Giemsa,
Castaneda or Machiavello stains
o With Giemsa stain, the elementary and the
reticulate body stains blue in cytoplasm
o With Lugol's Iodine, rapid and simple screening
method for ocular infections, stains glycogen
matrix of C. trachomatis
o With Immunofluorescent staining, it is more
sensitive and specific with the use of monoclonal
antibodies. It identifies inclusion and elementary
bodies. It is used for ocular, cervical or urethral
specimens
114
Culture of Chlamydia
o Yolk sac, 6-8 days old chick embryo
o Tissue culture, McCoy, Hela cell line
115
Demonstration of Chlamydial antigen
o Micro-immunofluorescent - infected ocular or
genital samples are stained with fluorescent
conjugated antibody
o ELISA - best for staining large number of
specimens, detects LPS antigen
o PCR method
o Demonstration of antibodies or hypersensitivity
116
READ PAGE 6 TO 7 SKNIP DITO
117
Formerly known as _______
was
originally identified in 1965 from a conjunctival culture of a
child (TW) enrolled in a Taiwan trachoma vaccine study
CHLAMYDPOPHILIA PNEUMONIAE
118
cause of sinusitis, pharyngitis, acute
respiratory disease, bronchitis, and pneumonia.
Isolated from patients with otitis media with effusion,
pneumonia with pleural effusion, and aseptic pharyngitis
Implicated as a possible factor in asthma and cardiovascular
disease.
Isolated from atherosclerotic tissue, but its possible
pathogenic role remains under investigation.
* Association of this organism with other vascular diseases,
such as abdominal aortic aneurysm, has also been
considered
CHLAMYDOPHILIA PNEUMONIAE
119
second phase of the biphasic illness often results in
pneumonia (approximately one in nine infections) and
bronchitis but is rarely accompanied by sinusitis
C PNEUMONIAE
120
* Third most common cause of infectious respiratory disease.
CHLAMYDOPHILA PNEUMONIAE
121
Present method of choice is the MIF assay, which is more
sensitive and specific than CF.
o It does not cross-react with C. trachomatis and C.
psittaci.
o Can distinguish an IgM from an immunoglobulin G
(IgG) response
122
PRIMARY INFECTION AND REINFECTION OF CHLAMYDOPHILIA PNEUMONIAE
* Primary infection:
o IgM does not appear until 3 weeks after onset of
symptoms
o IgG does not reach diagnostic levels for 6-8 weeks
o Traditional convalescent serum obtain is
approximately 14-21 days after onset does not
contain MIF-detectable antibody
* Reinfection:
o IgG titer of 1:512 or more appear within 2 weeks
o IgM are detectable but low
123
also known as
ornithosis or parrot fever
psittacosis
124
Cause of psittacosis
CHLAMYDOPHILA PSITTACI
125
If C. pneumoniae–specific and C. trachomatis–specific IgG
and IgM are not detected by MIF and a fourfold rise in the
levels of chlamydiae antibodies is detected by CF, then
C.
psittaci should be strongly suspected.
126
shed in the droppings or nasal discharges and aerosols are
liberated; infection by inhalation
* Mild influenza like syndrome to fatal pneumonia
Psittacosis
127
occupational disease in humans (poultry workers, pigeon
farmers, pet shop owners, veterinarians)
Psittacosis
128
SPECIMEN FOR PSITTACOSIS
* Blood in early stage, later on sputum
* Demonstration of LCL (Levinthal-Cole-Lillie Inclusion
bodies) in alveolar macrophages, mouse brain, yolk sac, cell
cultures
* LCL bodies are more diffuse and irregular, not stained by Iodine
* Serology: complement-fixation test, microIMMUNOFLOURESCEBT
129
MycoplasmaTACEAE
* Smallest replicating organisms in nature
* Lack cell wall
* Coccoid
* Tapered rods:
* Can pass through bacterial filters
130
MOST SIGNIFICANT PAHOTGENS IN MYCPLASM
Most significant pathogens
o Mycoplasma pneumoniae, causes respiratory
diseases
o Mycoplasma hominis, associated with urogenital
tract diseases
o Ureaplasma urealyticum, associated with
urogenital tract diseases
131
* Family Acholeplasmataceae contains the single genus
Acholeplasma
. The most significant human pathogen in this
genus is A. laidlawii
132
Pleiomorphic organisms that do not possess a cell wall but
have a triple-layered cell membrane
MYCOPLASM
133
CELL WALL OF MYCOPLASM
* Resistant to cell wall-active antibiotics (penicillin and
cephalosporins)
* Cell-wall-deficient bacteria different from the L-forms
o Not classified as L-forms which are bacteria that
have temporarily lost their cell wall as a result of
environmental conditions
* Outermost part of the organism is the plasma membrane
and unique because of high content of sterols that act to
prevent osmotic lysis
MAY HAVE CAPSULE
134
Requires cholesterol and fatty acids for growth
MYCOPLASM except aerobic M. pneumoniae and the more
rapidly growing M. hominis
135
GROWTH ON MEDIA
Mycoplasm
* Often grow embedded beneath the surface of solid media
o transferring colonies with a loop is ineffective
* On solid media, some species form "fried-egg" colonial
appearance
* Hard to detect contaminants of cell culture
* Adhere to the epithelium of mucosal surfaces in the
respiratory and urogenital tracts
* Not eliminated by mucus secretions or urine flow
* Susceptible to adverse environmental conditions such as
heat and drying
136
Transmission can occur via direct sexual contact, mother to
child during delivery or in utero or by respiratory secretions
or fomites in cases of
MYCOPLASM
137
Causes bronchitis, pharyngitis and common respiratory
infection known as primary atypical pneumonia (PAP) or
walking pneumonia
m oneumoniae
138
symptoms resemble those of Chlamydophila pneumoniae
* milder, not seasonal and has higher incidence in young
adults
mYCOPLASMA PNEUMONIAE
139
ost common presentation is OF MYCOPLASMA PNEUMONIAE
ost common presentation is tracheobronchitis often
accompanied by pharyngitis
140
early symptoms are non-specific headache, low grade
fever, malaise, anorexia, sore throat, dry cough and ear
ache
MYCOPLASMA PNEUMONIAEW
141
implicated as a co-infection or cofactor in epidemic group A
meningococcal meningitis (Neisseria meningitidis) and
infant pneumonitis.
PMYCPLASMA PNEUMONIA
142
INFECTIONS CAUSED BY M HOMINIS
* Do not cause vaginitis OR NGU (Nongonococcal
urethritis)
* Associated with infections of the urogenital tract and might
play a role of bacterial vaginosis
and cause
salpingitis, pyelonephritis, PID or post-partum fevers
143
M HOMINIS LOCATION
* Found in the lower genitourinary tract of approximately 50%
of healthy adults
* Organisms may invade the upper GUT
144
Ureaplasma urealyticum
* Associated with infections of the urogenital tract and might
play a role of bacterial vaginosis
* Do not cause disease in the female lower genital tract
(vaginitis)
* Associated with approximately 10% of cases of NGU in men
as well as upper female GUT disorders
* Associated with reproduction disorders, chorioamnionitis,
congenital pneumonia and the development of chronic lung
disease in premature infants (also M. homini
* Has been reported to cause chronic inflammatory disease
such as arthritis and cystitis in hypogammaglobulinemic
patients
145
Has been recovered from more than 60% of normal sexually
active females
* Common organism isolated from tracheal aspirates of low
birthweight infants with respiratory disease
* Infections usually occurs in utero and not during passage
through the birth canal
Ureaplasma urealyticum
146
Has been linked to respiratory distress in premature infants
UREAPLASMA PARVUM
147
first isolated in 1980, has been
associated with NGU, cervicitis, endometriosis, and PID.
Mycoplasma genitalium,
148
mycoplasma genitalium
- LINKED TO TUBAL STERILITY
149
Primarily a resident of the gastrointestinal tract that occurs
secondarily in the genitourinary or respiratory tracts
Mycoplasma genitalium
150
Found more frequently in urethral samples taken from men
with acute NGU than in those from men without urethritis
association has been found between M. genitalium and
individuals with HIV
mycoplasma genitaliuym
151
has been reported more frequently in the
urethra and rectum of homosexual men with HIV infection.
M. hominis
152
* Detected in throats of patients with lower respiratory tract
infection, isolated from tissue in patients with and without
AIDS
* Isolated from synovial fluid of patients with rheumatoid
arthritis.
Mycoplasma fermentans and Mycoplasma
penetrans
153
has been demonstrated in urine of
homosexual males with HIV-associated disease
M. penetrans
154
specimen and collection for mycoplasm
* Specimens include body fluids, sputum, blood, synovial
fluid, CSF, amniotic fluid, urine wound aspirates,
nasopharyngeal swab, cervicovaginal swab and tissues
* Extremely sensitive to drying and heat
* Specimens should be inoculated at bedside or be delivered
immediately to the lab in a transport medium
o SP4 (sucrose phosphate buffer, Mycoplasma
base, horse serum [20%], and neutral red) or
Shepard 10B broth or 2SP, which are designed for
Mycoplasma.
* Cotton-tipped swabs and wooden shafts should be avoided
because of inhibitory effects
* Swab should be made of Dacron polyester or calcium
alginate with aluminum or plastic shaft and should be
removed after it is placed in the transport medium
* On arrival in the lab, specimens should be frozen at -70C if
immediate plating cannot be done within 24 hours
155
direct examniation of mycoplasm
* Direct examination by DNA fluorescent stain (acridine
orange)- not specific for mollicutes
* Usually by serology (acute and convalescent sera, 2-3
weeks apart to demonstrate 4-fold rise antibody titer)
* PCR has been used but difficult to interpret
156
read culture and serology of mycoplasm
157
treatment in mycoplasm
* Sensitive to Tetracycline, newer fluoroquinolones and
macrolides
* M. hominis is usually resistant to Erythromycin; sensitive
to clindamycin and lincomycin
* Ureaplasma is resistant to clindamycin and lincomycin;
sensitive to erythromycin
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