INTERMEDIATE MICROORGANISMS

Dr. Rose Elaine D. Tan Disease : Rickettsiosis

• zoonotic disease which infects primarily wild animals
• human are accidental host
• arthropod-borne
• acquired through bite of infected arthropods: lice, tick, flea, &
mite
o except Q fever (C. burnetti) which is acquired by
inhalation
• 4 groups of diseases:
o Spotted fever group
o Typhus group
o Scrub typhus group
o Others:
 Q fever
 Trench fever
 Sennetsu Rickettsiosis
• Characterized by fever, headache and generalized skin rashes
• except Q fever - no rashes

RICKETTSIA

CLASSIFICATION OF THE RICKETTSIA

Order: Rickettsiales
Family: Rickettsiaceae
Tribe: Rickettsieae
Genus Rickettsia
Species: R. rickettsii
R. akari
R. conori
R. prowazekii
R. typhi
R. tsutsugamuchi
R. australis
R. siberica
Genus Rochalimaea
Specie: R. Quintana
Genus Coxiella
Specie: C. burnetti

GENERAL CHARACTERISTIC OF RICKETTSIA:

 Small gram negative pleomorphic rods or coccobacilli
 filterable, size 0.3 – 0.6µm W X 0.8 – 2µm L
 obligate intracellular
 cannot synthesize their own AMP
 cell wall structure same with gram ( - ) bacteria
 contains both RNA and DNA
 replicate freely in the cytoplasm
 has tropism for endothelial cell that lines the blood vessel
causing vasculitis
 Genus Rickettsia are unstable extracellularly under ordinary
environmental conditions
 C. burnetti – resistant to heat and drying

TREATMENT : DOXYCYCLINE, TETRACYCLINE, CHLORAMPHENICOL

LABORATORY DIAGNOSIS :
1. Direct demonstration of organism from clinical material
•
•
multiply & reproduce by binary fission
difficult to stain
2. Isolation of organism from animal model
• Infected whole blood inoculated intra-peritoneally to
• stain used for demonstration/visualization
male guinea pig
1. Gimenez – pink – red
• R. rickettsii – testicular swelling
2. Machiavello – red
3. Giemsa – blue • R. prowazekii – no testicular swelling
4. Castañeda – blue 3. Serological
• growth is inhibited by antimicrobials
Serologic Diagnosis
• susceptible to Chloramphenicol & Tetracycline
 specific antibodies develop in response to rickettsial infection
• require living cells for growth
 demonstration of an immune response during convalescence
• can be cultured using living cell medium:
 is the most widely used method of confirming clinical diagnosis
1. Yolk sac developing chick embryo
 Complement-fixing antibodies are useful in identifying infection
2. Live animal ( mice / male guinea pig )
due to Rickettsiae in different genera and groups
3. Tissue culture
 serologic procedures:
• except for R. quintana which can grow in artificial media
o microagglutination
containing blood with specific nutritional requirement
o indirect hemeagglutination
o Microimmunoflourescent antibody test
 more sensitive and specific
 detect specific antibodies
 used for confirmation of disease
  Treatment
 Drug of choice – Chloramphenicol

Weil-Felix Reaction  Prevention

Use preventive clothing, boots and leggings
 Based on the cross reaction between antigens in the rickettsial
o
o Use forceps for removal of ticks
organism and Proteus polysaccharide O antigen
o Care should be taken during removal to prevent
 antibodies to the rickettsial organism will agglutinate certain
crushing the ticks and contaminating the fingers
non-motile strains of Proteus (0X-19, 0X-2 & OX-K)
because both tick tissues and tick flees are highly
 presumptive
infectious
 low sensitivity and specificity o NO vaccine available
 only 17% had been confirmed by this test B. Rickettsial Pox
 Proteus agglutinins usually do not appear until after a week of • agent: R. akari
illness, thus limits their usefulness in early diagnosis

 False positive: Proteus bacterial infections

• mite vector: Liponyssoides sanguineus
(formerly Allodermanyssus sanguineus)
( UTI, bacteremia, wounds)
• incubation period: 9-14 days
 most widely used test in US
• Clin. Mx:
o reddish macular rash develops at the site of the mite
bite and subsequently develops an eschar which
roughly coincides with the appearance of fever,
headache, chills, rigors, profuse sweating, myalgias,
rhinorrhea, cough, sore throat, nausea, vomiting,
and abdominal pain
o regional lymphadenopathy
o a papulovesicular rash (blister) that bursts and
crusts over develops 1-10 days after the eschar
appears and lasts for several wks

Rickettsialpox Chickenpox
• Common in adult • Common in children
• associated with primary eschar • Lacks a primary lesion
I. SPOTTED FEVER GROUP
– A red papule with a vesicle in • The papule turns into a vesicle
 basic pathologic process is a widespread vasculitis involving the center dries and forms a
black eschar with surrounding
on an erythematous base and
the skin, with production of a rash resembles a "dew drop on a rose
induration
 more severe disease can lead to dessiminated intravascular petal“
• The cutaneous vesicles are
coagulopathy with petechial and purpuric skin manifestation surrounded by papular rings • The rash begins on the head and
a. Rocky Mountain Spotted fever progresses to the trunk, arms,
(papulovesicular rash) is usually on
b. Rickettsial Pox the trunk and extremities; the and then legs
c. Other Tick-borne Diseases palms, soles, and oral mucosa may
• resemble RMSF also be involved.
• Boutonneuse fever – R. Conorii
• North Asian tick Typhus – R. sibirica  Pathogenesis:
• Queensland tick typhus – R. australis o Microscopically, the maculopapular rash shows a
• Japanese spotted fever – R. japonica mononuclear perivascular infiltrate and necrosis of
epithelial cells that result in intraepidermal vesicles
A. Rocky Mountain Spotted fever
 aka: Tick-borne typhus
 Lab dx:
o isolation of organism ( blood & vesicular fluid)
 transmission: bite of a tick infected w/ R. rickettsii o Weil-Felix antibodies does not appear after infection with
 accounts for >95% of reported cases in the US R. akari
 common among children and adults
 incubation period: 3-12 days
 Clinical manifestation:  TREATMENT: CHLORAMPHENICOL AND TETRACYCLINE
1. cardinal features: headache, fever, diffuse myalgia,
rash C. Other Tick-borne Diseases
2. rash appears 2-4 days after onset • Found in several continents
maculopapular petechial hemorrhagic • Cause sporadic cases of mild clinical pattern
• resemble RMSF
3. Gastrointestinal complaints, arthalgia, conjunctivitis, • North Asian tick Typhus – R. sibirica (central Asia, Mongolia,
stiff neck, Siberia)
periorbital edema • Queensland tick typhus – R. australis (Australia)
4. splenomegaly
• Japanese spotted fever – R. japonica (Japan)
5. hyponatremia, thrombocytopenia
6. severe disease leads to DIC with petechial & purpuric • Boutonneuse fever – R. conorii (Mediterranean, Africa, India)
rashes (aka: African tick fever, Kenya tick typhus, Indian tick
7. vasculitis involving viscera (brain, heart, kidneys) can typhus)
produce • Humans are accidental hosts
significant complications • Arthropod vectors: Ixodid ticks
• MOT: tick bite
 Fatality Rate if Untreated 20-25%
 Pathogenesis • incubation period varies from 6-10 days
o R. ricketsii produces widespread endothelial damage that • triad of symptoms are most characteristic:
results in occlusion of small vessels, microthrombi, o fever, headache, and malaise
microhemorrhages, secondary fluid and electrolyte o erythematous papules appears on days 3-5 of the
changes, and in severe cases, necrosis, shock and death illness w/c spreads from the extremities to the trunk,
o Kinins play a role in pathophysiology of the vasculitis and neck, face, palms, and soles
DIC o Disease is characterized local eschars or skin lesions
at the site of the tick bite
 Lab Diagnosis:
1. Initial diagnosis and treatment should be based on • BOUTONNEUSE FEVER
clinical grounds
2. Isolation – rarely done o is transmitted by the dog tick Rhipicephalus
3. Weil-Felix sanguineus
4.
5.
Microimmunoflourescent Antibody test
ELISA
o has a characteristic rash and a distinct mark:
6. PCR

 tache noire (eschar or cutaneous
necrosis ) at the site of the tick bite
caused by rickettsial vasculitis ("black
spot") is pathognomonic
 heals slowly over 10-20 days without
leaving a scar
c. Murine typhus
• aka: endemic typhus, flea-borne typhus, rat typhus
• etiologic agent: R. typhi
• man is infected when, by scratching, he introduces the feces or
contents of a crushed rat-flea, Xenopsylla cheopis, which has
fed on infected rat
• similar to louse-borne typhus but tends to have a milder and
shorter course

• Clin. Mx: mild; Fatality Rate if Untreated 1-2 percent

o Incubation period: 1-2 weeks
o fever is less pronounced and remittent, headache is
less severe
o rash is less extensive,
o headache, malaise, myalgia,

• Lab. Diagnosis: Serology

o Weil-Felix Reaction

• Treatment: Tetracycline, Chloramphenicol

II. TYPHUS FEVER

• Is a louse-bourne disease
• Typhus-group organisms are characterized by intracytoplasmic
growth and a common, soluble, group-specific, complement-
fixing antigen
a. Epidemic Typhus
b. Brill-Zinsser Disease
c. Murine Typhus

a. Epidemic typhus
• Aka: Louse-bourne Typhus
• etiologic agent: R. prowazekii
• transmitted by infected feces of the louse usually through
scratching the skin, or sometimes by bite
o Pediculus humanus corporis - body louse
o Pediculus humanus capitis – head louse
• During each blood meal, the feeding process is irritating and
scratching by the host produces minor excoriations that
function as portals of entry for the rickettsia in the louse feces
• Clin Mx:
o incubation period: 10-14 days
o severe frontal headache, fever, malaise
o skin rash (hallmark) 4-7 days after onset, noted at
the trunk spreading to the extremities (centrifugal
spread)
o Rash usually spares the palms, soles and face
o patchy cutaneous erythema  maculpopapular
 hemorrhagic
o 2nd week of illness the CNS becomes involved and
apathy and dullness, delirium and coma
• Fatality Rate if Untreated 30%
III. SCRUB TYPHUS
• aka: Chigger-borne typhus; Tsutsugamushi disease
• etiologic agent : R. tsutsugamushi
• endemic in Australia, Japan, Korea, India and Vietnam
• vector: trombiculid mites
• Larval stage of mite (chigger) – stage that feeds on vertebrae
• 3 major antigenic type (Karp, Gilliam, Kato)
• Clin. Mx:
o incubation period 1-3 weeks after bite of a chigger
o sudden onset of chills, HA, fever, cough, nausea,
vomiting, myalgia
o the site of the mite bite develops a necrotic black
scab (eschar), becomes indurated and covered by a
scale
o Lymphadenopathy proximal to the eschar
o gen. maculopapular rash appears 5-8days after
o deterioration of mental status, pneumonia,
circulatory failure
• Diagnosis: Serology
o Weil-Felix Reaction

• lab dx:
 Agglutinins to Proteus OX-K antigen appear in
the convalescent sera of many but not all
o isolation of organism patients with scrub typhus
o serologic test
o Weil-Felix reaction • Treatment: Tetracycline, Chloramphenicol
o PCR
• Prevention:
• Treatment:
o Tetracycline, Chloramphenicol o Prevent chigger bites
o Patients who develop circulatory and renal  Wear protective clothing
complications before receiving antibiotics may die  Insect repellents
despite therapy o Control of mite population
 Insecticides
b. Brill – Zinsser disease  Clearing of vegetation
• aka: relapsing louse-borne typhus  Chemical treatment of the soil
• secondary to recrudescent R. prowazaki
• the organisms appear to lie dormant, most likely in the cells of
the reticuloendothelial system, until they are reactivated by an IV. Q FEVER
unknown stressor, multiply and cause another acute but milder • etiologic agent: Coxiella burnetti
infection • Q from the word “querry”
• Arthropod vector: ticks
• Clin. Mx: • worldwide distribution
o milder than epidemic typhus
• resistant to desiccation and exposure to light or temperature
o Shorter duration of the disease (less than 2 weeks)
extremes
o skin rash rarely seen
o headache, malaise, myalgia • Human outbreaks 2° to:
o Consumption of infected milk
• Lab. Diagnosis: o handling of contaminated wool or hides
o microimmunofluorescent test using IgM and IgG o soil contaminated by infected animal feces
antibody o infected straw
o Weil-Felix agglutinins usually do not develop o dusty clothing
 Modes of transmission:
o through the skin – contaminated minor abrasions
o through the lungs – inhalation of infectious aerosols
o through the mucus membrane – conjunctival contact
with infectious materials
o through the GIT – ingestion of contaminated raw milk
 Clin Mx:
o incubation period ranges from 2-6 weeks
o can manifest various signs
o no one classic presentation exists
o inapparent infection, influenza-like illness,
Pneumonia, endocarditis, hepatitis
o Usually begins with sudden onset of chills, HA, fever,
myalgia
o Characteristically, rash is absent
o Fatality Rate if Untreated 2.4 %for the acute form;
60 % if chronic endocarditis
develops
• obligate intracellular
• Although capable of synthesizing macromolecules, they have
no system for generating energy
o NO ATP (no energy - yielding enzyme)
o the host cell's energy system fuels the chlamydial
metabolic processes
• contain both RNA & DNA
• rigid cell wall that resemble gram (-) bacteria
o due to disulfide bond cross-linking among the major
outer membrane proteins (MOMP)
• lack peptidoglycan layer and muramic acid, not susceptible to
lysozyme
• has tropism for columnar epithelial cells lining the mucous
membrane
• sensitive to antibiotics
• reproduce and multiply binary fission

 Lab. Dx:
o Most definitive – isolation of C. burnetii from clinical
specimens
o Can be accomplished by intraperitoneal inoculation
of guinea pigs, mice or embryonated hens’ egg
o Serology – Complement-fixation test
o Weil-Felix antibodies are not elicited in response to
infection with C. burnetii

 Treatment:
o Tetracycline - preferred drug of choice 2 distinct morphologic forms:
o Chloramphenicol 1. ELEMENTARY BODY ( EB )
o Pts do not uniformly respond and as quickly • small, dense spherical body measuring 0.2 -0.4 µ
compared to other rickettsial disease • found extracellularly (outside of cell)
• infectious form
 Prevention:
• capable of extracellular survival
o Identify and decontaminate affected areas
o Milkbourne transmission – prevented by • has rigid outer membrane
pasteurization
2. RETICULATE BODY (RB)
• reproductive form of organism
• size 0.7 - 1.0 µ (larger than EB)
• Found intracellularly
• non-infectious
• grow only within host cell
• incapable of survival outside cell
• metabolically active form

V. TRENCH FEVER
• aka: Shinbone fever

• etiologic agent: Rochalimaea quintana (Bartonella quintana)

• Arthropod vector: Body louse (Pediculus humanus corporis)

• transmitted by inoculation of the organism in louse feces
through a skin break or a louse bite
• R. quintana – the only rickettsia that can be grown on cell-free
media Life Cycle:
• Reservoir: Human only 5 MAJOR PHASES:
1. Attachment and penetration of EB
• Clin. Mx: 2. Transition of metabolically inert EB into metabolically active
o diverse clinical presentations RB
o Ranges from asymptomatic to a persistent fever 3. Division of RB and production of many progeny
lasting months 4. Maturation of the non-infectious RB into EB
o incubation period is 5-20 days 5. Release of EB from the host cell (after 48 hours)
o Fever, HA, malaise, chills, myalgia, maculopapular
rash
o Bone pain - tends to occur in the shin (tibia), neck,
and back; worsens during subsequent attacks

• Lab. Diagnosis:
o Xenodiagnosis
 Feeding of uninfected lice on an infected
patient and the later demonstration of
rickettsia in the louse tissue
o Primary isolation on enriched-blood agar media
o Like other Rickettsia, can also be grown in yolk sacs
of embryonated hens’ eggs
o Serology
 CFT
 Indirect immunoflourescent antibody test

• TREATMENT: TETRACYCLINE, CHLORAMPHENICOL

• Prevention: control human louse infestation

CHLAMYDIA
• small round → oval/ovoid-shaped cell
• non-motile
 • Trachoma – leading cause of preventable blindness in the world
• leading cause of neonatal ocular disease USA
• leading cause STD in USA and Europe
o men: begins as urethritis and spread to epididymis
o women: begins in the cervix, uterus, fallopian tubes
and can result in PID and infertility
• the presence of basophilic intra-cytoplasmic, iodine-staining
inclusion bodies (Halberstadter-Prowazek bodies) is specific for
C. trachomatis
• inclusion bodies of the other species of chlamydia do not
contain glycogen and do not stain with iodine

Chlamydia trachomatis

Serovar Disease Distribution

A B Ba C Trachoma Asia and Africa

Disease of eye and

genitals:
Conjunctivitis
D- K Urethritis World wide
Cervicitis
Lab diagnosis Respirtaory System:
1. direct microscopic examination of clinical specimen for Infant pneumonia
chlamydial inclusion bodies
• very hard to stain
• for visualization: Machiavello and Giemsa stain
LGV1 LGV2 Lymphogranuloma
Worldwide
2. isolation of the organism LGV3 venerium (LGV)
• can be cultures only using living cell media :
1. yolk sac of 6-8 day chick embryo
(observed characteristic inclusion 1. Trachoma
body can be found) • most common cause of chronic infection of the conjunctiva
2. live laboratory animal inoculation ( mice ) that is currently the leading cause of preventable blindness
3. tissue culture (Hela cells, McCoy cells) throughout the world
• MOT
3. detection of specific antibodies against these bacteria serologic 1. Transplacental transmission mother →
test: infant
• CF 2. Contaminated eye-to-hand-to-eye
• micro-immunoflourescence technique 3. Fomites (infected towel rub to eye)
• ELISA • Pathogenesis:
o C. trachomatis replicates preferentially on mucosal
Antigenic Composition: surfaces within squamocolumnar epithelial cells
3 MAJOR GROUPS OF ANTIGEN HAVE BEEN IDENTIFIES: o They stimulate a brisk infiltration of polymorphonuclear
1. Genus-specific Ag cells; esp. early in infection
• heat stable o Submucosal lymphocytic infiltration leads to lymphoid
• LPS with an acidic polysaccharide as the antigen
follicle formation and fibrotic changes

determinant • Clinical Manifestations:

o MacCallan Classification of Trachoma
2. Species-specific Ag  Stage 1 – (Incipient Trachoma)
• found on or near the envelope surface - maybe asymptomatic, with little if any
• protein antigen are shared by all members of the conjunctival exudates
specie - minimal keratitis is usually present
• trachomatis (18); C. psittaci (15)  Stage 2
- established trachoma with follicular and
3. Serotype-specific Ag papillary hypertrophy
• common only to certain isolate within the specie - Trachomatous pannus accompanies
• C. trachomatis subdiv. into 2 biovars : corneal infiltration
o Trachoma – 12 serovars  Stage 3
- includes cicatricial complications with
o LGV – 3 serovars
scarring of the conjunctiva; trichiasis,
entropion and further pannus develop
 Stage 4
- healed trachoma without evidence of
active inflammation
- maybe asymptomatic if with no
complications develop

CHLAMYDIA TRACHOMATIS
• human only known host
• primarily involves the eyes and genital tract

Stage 2 - Follicular trachomatous inflammation is the presence of
5 or more follicles (each at least 0.5 mm in diameter) on the
central part of the upper tarsal conjunctiva
Stage 2 - Intense trachomatous inflammation is pronounced
inflammatory thickening of the upper tarsal conjunctiva that
obscures more than one half the normal deep tarsal vessels
Stage 3 -Trachomatous conjunctival scarring (TS) is the
presence of easily visible scars in the tarsal conjunctiva
Stage 3 - Trachomatous trichiasis (TT) is defined as the presence
of at least 1 eyelash rubbing on the eyeball or evidence of recent
removal of in-turned lashes
Stage 3 - Easily visible corneal opacity over the pupil; it is so
dense that at least part of the pupil margin is blurred when viewed
through the opacity
• lab dx:
o PCR – method of choice
o direct fluorescein-labeled monoclonal antibody
o enzyme immunoassay (EIA)
o Direct microscopic examination
 the presence of glycogen-containing,
iodine-staining intracellular microcolonies
or inclusion bodies (Halberstadter-
Prowazek bodies) is specific for C.
trachomatis
• WHO recommends 2 antibiotics:
o oral azithromycin or Doxycycline or Tetracycline
o tetracycline eye ointment
• Good standards of hygiene
2. Inclusion Conjunctivitis
• Caused by C. trachomatis serotypes D through K
• acute infection of conjunctiva among neonates
o acquired from genital tract during passage thru an
infected birth canal of mother with genital chlamydia
o Characterized by inflammation of the conjunctiva
accompanied w/ purulent yellowish discharge which
usually occurs 5 - 12 days after birth
o Vulvovaginitis, ear infection, and mucopurulent
rhinitis may accompany ocular disease
• Adult inclusion conjunctivitis
o Is a sexually transmitted disease
o but also contamination from unchlorinated
swimming pools
o presents as a unilateral (or less commonly bilateral)
red eye with mucopurulent discharge, marked
hyperemia, papillary hypertrophy, and a
predominant follicular conjunctivitis
• Lab. Diag. :
o Microbiological - conjunctival scrapping
↓ (specimen)
Yolk sac / Hela cell
 demonstrate basophilic intra-cytoplasmic
inclusion body (Halberstadter Prowazek
inclusion body)
o Serological
 Direct Fluorescent antigen staining - 90%
sensitive
 ELISA
 CF
3. Lymphogranuloma venereum ( LGV )
• aka: Lymphogranuloma inguinale, climatic bubo, tropical bubo,
• Caused by C. trachomatis biovar LGV; serovar LGV 1, 2, 3
• sexually acquired
• common among sexually active young adults 15-40 years
• More recognized among males than in females
• All patients with LGV should be thoroughly examined for
evidence of other STDs
• LGV replicates preferentially on the regional lymph nodes
o Autopsies of patients with chronic LGV infection
reveal lesions of the lymph node composed of
aggregates of large mononuclear cells forming
abscesses surrounded by epithelial cells
• heal with scarring
CLINICAL MANIFESTATIONS:
• First stage (primary LGV)
o occurs 3-30 days after inoculation
o The primary lesion begins as a small, unnoticed
painless papule or pustule that may erode to form a
small, asymptomatic open sore (ulcer) that usually
heals rapidly without scarring within a week
o men: coronal sulcus, prepuce, glans, and scrotum
o women: posterior vaginal wall, posterior cervix,
fourchette, and vulva
• Second stage (secondary LGV)
o begins 2-6wks after the primary lesion
o Early symptoms of fever, headache and myalgia
o consists of painful regional lymphadenopathy
(usually in the inguinal and/or femoral lymph
nodes)
o About 1/3 of infected people develop a "groove
sign" caused by pressure from the tight ligament
separating the groin lymph nodes
o These nodes join together to form
"buboes,“(abscesses) which may split open and
drain and form sinus tracts, or they may become
hard and then slowly heal on their own
o Women may not have any visible lymph node and
have only mild back or belly pain
• Third stage (tertiary LGV)
o termed genitoanorectal syndrome
o rectal involvement is more common in men who
have sex with men and in women who practice anal-
receptive intercourse
o Patients initially develop proctocolitis and later may
present with pain on defecation, deep boils
(abscesses), perirectal fistulas, strictures, rectal
stenosis and scarring
o hyperplasia of intestinal and perirectal lymphatics
forming lymphorrhoids
o women: this stage may be the first time symptoms
are seen as enlargement, thickening, and fibrosis of
the labia (lymphatic obstruction can lead to
elephantiasis of the vulva – “esthiomene”)
o men: chronic lymphatic obstruction leading to
elephantiasis
 Penile and scrotal edema and distortion
have been termed “saxophone penis”
LAB DX:
• compatible clinical Manifestations
• recovery of the organism from site of infection and
identification of C. trachomatis, biovar LGV
• Demonstration of risinf antibody titer of LGV by
microimmunoflourescent antibody titer
• Frei test
• intradermal skin test previously used to diagnose LGV
• indicative of delayed hypersensitivity to chlamydial antigens
• not specific
Antibiotic regimens:
• Doxycycline 100 mg PO bid for 21 d
• Erythromycin • Pneumonia in young adults (most char. presentation)
• Tetracycline
• Sulfadiazine CLIN MX:
• Fever in the first few days
4. Chlamydial urogenital infections
• Caused by C. trachomatis serotype D through K
• Pharyngeal erythema without exudate occurs in various
• occurs in men with history of other venereal disease and atypical pneumonias
promiscuity and frequently in the consorts of women with • Rhonchi and rales are present even in mild dse
cervical chlamydia infection
• Males: LAB. DIAG:
o most common manifestation is nongonococcal • PCR/ Isolation/ CFT/ MIFT
urethritis
o develop a white, cloudy or watery discharge from Treatment: Erythromycin and Tetracycline
the tip of the penis
• Females:
o chronic cervicitis and urethritis
o characterized by mucopurulent cervical discharge,
erythema, and inflammation

Reiter’s Syndrome
• now referred to as reactive arthritis
• triad of recurring symptoms including:
o conjunctivitis/iridocyclitis
o Polyarthritis
o Genital inflammation
 Males: non-gonococcal urethritis
associated with reactive arthritis may be
postdysenteric or postvenereal, with
frequency, dysuria, urgency, and urethral
discharge
 Females: Cervicitis within 1 month of the
arthritis
• 50-65% of pts have C. trachomatis genital infection

5. Neonatal Pneumonia
• Prevalent cause of pneumonitis in infants
• Characteristically becomes ill 4-16wks of age with prominent
respiratory symptoms of wheeze and cough and lack systemic
findings of fever and toxicity
• Chlamydial neonatal conjunctivitis often precedes the onset of
pneumonia

CHLAMYDIA PSITTACI
• etiologic agent of Psittacosis, an infection of birds & mammals MYCOPLASMA
that is transmissible to humans • smallest & simplest procaryote capable of self - replication
• can cause a pneumonia-like illness
• cell wall-less (absence of cell wall)
• the respiratory tract is the main portal of entry o lack of a reaction to Gram stain
• acquired by inhalation of infectious dropping from: o lack of susceptibility to antimicrobial agents,
o birds, parrot, parakeets = Psittacosis including beta-lactams
o turkey, duck, chicken = Ornithosis • originally called PPLO (Pleuropneumonia like organisms)
• other source of material: blood, tissue, excreta, feathers • frequent causative agent of primary atypical pneumonia
• usually associated with mucosal surfaces, residing
GENERAL CHARACTERISTICS OF C. PSITTACI:
extracellularly in the respiratory and urogenital tracts
• The intracellular microcolonies contain little glycogen and do
not stain recognizably with iodine • Species of Medical importance :
• The inclusion bodies are more diffuse and irregular in shape o Mycoplasma pneumoniae
and do not indent the nucleus of the host cell o Mycoplasma hominis
• These inclusions (( Levinthal - cole - lillie bodies) stain with o Ureaplasma urealyticum
Giemsa and Macchiavello stain
• The development of inclusions is not inhibited by sulfadiazine o
or cycloserine

CLINICAL MANIFESTATIONS:
• Onset of fever, severe frontal headache, myalgia
• Followed by pulmonary manifestations: non-productive cough,
rales, and consolidation
• X-ray suggests bronchopneumonia or atypical pneumonia

LAB. DIAG. :
1. Direct microscopic examination
2. Detection of inclusion body (levinthal - cole - lillie
body) 3. Serological
 CF test ( non-specific )

 Immunoflourescent AB test GEN. CHARACTERISTICS:

(more sensitive & • extremely pleomorphic cells (no definite morphologic form)
confirmatory) can appear as spherical, ovoid or pear-shaped to filamentous
• size 0.2 - 0.8 µm in diameter x 8 - 10 nm thick
Treatment: Tetracycline, Erythromycin • filtrable (can pass thru bacteriological filters of 450nm pore
size)
CHLAMYDIA PNEUMONIAE • reproduce by binary fission
• 1986 – new strain of C. psittaci (TWAR strain) • facultative anaerobe
Gen. Charac: • motile → gliding motility 2O to specialized tip structure which
• more homogenous than other chlamydia serves as attachment and movement site of
• EB is pear shaped the cell
• human pathogen • stain poorly with gram stain but are ( gram - )
• MOT • Dienes stain for visualization of the organism
o inhalation of aerosolized droplets • Phase-contrast microscopy & Darkfield microscopy – are
recommended for microscopic examination
o person-to-person transmission by resp. secretions
CULTURAL CHARACTERISTICS:
• have a unique requirement for cholesterol and related sterol
for membrane synthesis
• lack enzymatic pathways for purine and pyrimidine synthesis
• can be cultured on non-living cell media
• requires complex culture media for growth such as:
o beef-heart infusion broth (BHIB) supplemented with
horse serum, yeast extract and nucleic acid
o solid media (beef-heart infusion agar BHIA) → dome-
shaped colony with a dense central core “fried egg
appearance”
Mycoplasma hominis
• most frequently isolated mycoplasmas from the urogenital
tract
• M. hominis – a large colony-forming mycoplasma 200-300µm in
diameter with a characteristic fried egg appearance
• M. hominis and Ureaplasma species are common commensal
inhabitants of the lower genitourinary tract in adolescents and
adult men and women who are sexually active
• 20% of healthy sexually active women carry M. hominis in their
vagina
• Implicated in post-partum fever, post-abortal fever, PID and
pyelonephritis
• Recent isolate M. genitalium
o isolated from urethral specimens of patients with
nongonococcal urethritis
o Shares extensive serologic cross-reactivity with M.
pneumoniae
o Has attachment mechanism and surface protein similar
with M. pneumoniae
Ureaplasma urealyticum
• most frequently isolated mycoplasmas from the urogenital
tract
• U. ureatycum were originally referred to as T-strain
mycoplasma (T for Tiny) because of the small
colonies (15-60µm) produced
• They also differ from other mycoplasmas because of their
unique ability to metabolize urea with the production of
ammonia
• Ureaplasma causes nonchlamydial nongonococcal urethritis
• Ureaplasma species are common commensal inhabitants of
the lower genitourinary tract in adolescents and adult men and
women who are sexually active
• 60% of healthy sexually active women carry U. urealyticum in
their vagina
• Play a role in perinatal mortality
MYCOPLASMA PNEUMONIAE
• number one cause of bacterial bronchitis and pneumonia in
young adult
• responsible for 20% of all cases of community acquired
pneumonia
• Reimann described the 1st cases of mycoplasmal pneumonia
o Reimann coined the term "primary atypical
pneumonia" after observing 7 patients in
Philadelphia with marked constitutional symptoms,
upper and lower respiratory tract symptoms, and a
protracted course with gradual resolution
• Peterson discovered the phenomenon of cold agglutinin in
1943, where high titers were seen among pts with M.
pneumoniae
• in 1944, Eaton was credited with discovering a specific agent,
coined Eaton's agent, as the principal cause of primary
atypical pneumonia
o First thought to be a virus, Eaton's agent was proved
to be a Mycoplasma species in 1961
PATHOPHYSIOLOGY
• M. pneumoniae is a surface parasite colonizing the epithelial
lining in the mucosa of the respiratory tract
• the prolonged paroxysmal cough seen in this disease is
thought to be due to the inhibition of ciliary movement
• The organism has a remarkable gliding motility and specialized
filamentous tips end that allows it to burrow between
cilia within the respiratory epithelium, eventually causing
sloughing of the respiratory epithelial cells
• 2 properties correlated with its pathogenicity in humans:
o selective affinity for respiratory epithelial cells
 organism attaches to respiratory epithelial
with the help of protein P1 (adhesin)
o ability to produce hydrogen peroxide, which is
thought to be responsible for much of the initial cell
disruption in the respiratory tract and for damage to
erythrocyte membranes
Disease: Primary Atypical Pneumonia (Walking Pneumonia)
• found worldwide
• Common among healthy patients younger than 40 years, with
the highest rate in 5- to 20-year olds
• MOT: acquired by aerosol droplets
• incubation period 2-3 weeks
• Pneumonia is generally mild and self-limited
• M. pneumoniae is perhaps best known as the cause of walking
or atypical pneumonia characterized by gradual onset of
fever, malaise, headache, sore throat and persistent dry,
hacking non-productive cough for as long as a month
• the most frequent clinical syndrome caused by this organism is
tracheobronchitis or bronchiolitis, often accompanied by upper
respiratory tract manifestation
Lab Studies
• WBC count generally is not helpful, since results may be
normal or elevated
• Sputum Gram stains and cultures usually are not helpful, since
M pneumoniae lacks a cell wall and cannot be stained
• Elevated ESR may be present but are nonspecific
Imaging Studies
• Radiographic findings are variable, but abnormalities are
usually more striking than the findings on PE
o Bronchopneumonia often involves a single lower
lobe
o Reticulonodular or interstitial infiltrates, primarily in
the lower lobes, may resemble other diseases with
granulomatous pathology, such as tuberculosis,
mycoses, and sarcoidosis
o Hilar adenopathy sometimes is mistaken for
malignancy
Diagnosis:
1. Early stage of infection → based on clinical manifestations
2. Culture - specimen: sputum / throat swab
o difficult to culture and requires 7-21 days to grow
→ “fried - egg” colonies with a small zone of
hemolysis
3. Cold Agglutination test
o a nonspecific test for M pneumoniae, but findings
are positive in 50-70% of patients after 7-10 days of
infection
o measures the titer of cold agglutinins (antibodies) in
patient serum during acute and convalescent phase
4. Complement Fixation
o Patient serum + glycolipid antigen  fourfold rise in
antibody titer
(diagnostic)
5. Elisa, PCR
Treatment: Tetracycline and Erythromycin
Prevention:
• No vaccine available
• Avoid close contact with acutely ill patient
bajah-bajah16.08.08