https://www.osmosis.

org/learn
/Rickettsia_rickettsii_(Rocky_
Mountain_spotted_fever)_and
_other_Rickettsia_species
Summer 2020
Week 9
• Murray’s Medical Microbiology Chapter 33, 34, 35
https://www.osmosis.org/lear • Jawetz’s Medical Microbiology Chapter 26, 27, 28
https://www.osmosis.org/lear
n/Mycoplasma_pneumoniae n/Mycoplasma_pneumoniae • Kaplan Medical- Immunology & Microbiology-
Chapter-2, Page 251-257

Rickettsia, Mycoplasma, & Chlamydia

Unusual bacteria

1
Learning objectives
By the end of today’s class, you should be able to:
1. Associate Rickettsia, Ehrlichia, Anaplasma and Coxiella infections with their vectors; associate virulence
mechanisms with symptoms
2. Identify host cells for intracellular Gram-negative pathogens and describe mechanisms that allow
intracellular growth
3. Identify intracellular growth of bacteria as protective against beta-lactam antibiotics
4. Identify mycoplasmas and chlamydiae as bacteria lacking any peptidoglycan
5. Identify cell-wall-lacking bacteria as obligately intracellular
6. Identify niches in the human body habitually occupied by call-wall-lacking bacteria
7. Compare and contrast Chlamydia trachomatis and Neisseria gonorrheae based on pathogenesis,
symptoms, patient demographics, and plausible treatments
Facultative vs Obligatory Intracellular
Bacteria
Facultative intracellular bacteria
• Invade host cells when they can gain a selective
advantage in the host.
• Bacteria that can enter and survive within
eukaryotic cells are shielded from humoral
antibodies.
• Once inside host cells, bacteria must utilize
specialized mechanisms to protect themselves from
the harsh environment of the lysosomal enzymes
encountered within the cells.
• Could be cultured in artificial media in laboratory.
• Examples-
• Legionella
• Francisella
• Brucella
• Salmonella
Obligate intracellular bacteria
• Cannot live outside the host cell.
• Unable to carry out energy metabolism
• Lack many biosynthetic pathways
• Entirely dependent on the host cell to supply them
with ATP and other intermediate molecules.
• Cannot be grown in artificial media (agar
plates/broths) in laboratories
• Require viable eukaryotic host cells (e.g., cell
culture, embryonated eggs, & susceptible animals).
• Examples-
• Chlamydia spp
• Coxiella burnetii
• Rickettsia spp
Rickettsiaceae Family
• Family Rickettsiaceae- All are aerobic, gram
negative rods
• Members- Rickettsia, Orientia, Ehrlichia,
Anaplasma and Coxiella
• Obligate intracellular parasites
• Transmitted by arthropod vectors (ticks, mites,
fleas)
• Exception- Coxiella (causes Q fever) primarily
airborne; sometime tick bite
Rickettsiae: Overview
• Obligate intracellular parasites- by Giemsa stain.
• LPS – weak endotoxin activity
• Cell wall proteins– OmpA/OmpB- basis of typing.
• Grow in different parts of the host cell:
• Typhus group- preferably in cytoplasm
• Spotted fever group- preferably in the
nucleus
• Growth is enhanced in presence of sulfonamides.

Transovarian
transmission in ticks

Two cell types designated large and small cell variants

(LCV and SCV). - Both types are infectious.
R. rickettsii: Rocky Mountain Spotted Fever
Wild rodents and ticks
• Most RMSF cases seen during April to September are the reservoirs
• Incubation: Average 7 days
• High fever (1020F) , severe headache, myalgias, nausea, vomiting
• A macular rash develops in 90% of patients (3-5 days)  Rash may become the spotted (petechial) form
• Centripetal spread - initially on the wrists, arms, and ankles,  then spreads to the trunk
• Spotted rash may precede neurological manifestations, pulmonary failure, kidney failure, and cardiac
abnormalities
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Rickettsia: Pathogenesis
• A predilection for endothelial cells and thus can infect most host
tissues

• Rickettsiae enter host endothelial cells by stimulating endocytosis

- R. rickettsii uses OmpA for adherence

• After engulfment, these bacteria degrade the phagosomal

membrane - Phospholipase

• Bacteria replicate in the cytoplasm & nucleus of endothelial cells

resulting into vasculitis

• Can lead to massive necrosis

Obligate intracellular parasites, grow and replicate in

cytoplasm of eukaryotic host cells (typically endothelial cell)
R. rickettsii: Laboratory diagnosis
• Giemsa or Gimenez staining (Gram stain NOT effective)
• Serology- Weil felix test (cross reaction of Rickettsia antigens with Proteus
strains) – no longer recommended (BUT still asked)
• Microimmunoflouroscence (MIF)
• ELISA - Detects the antibodies directed against OMP and LPS
• Nucleic acid-based - PCR

• Culture- grown in tissue culture system

• Mouse fibroblast, HeLa and Hep2 cell lines

Besides cell culture , R. rickettsii grows in yolk sac of

embryonated eggs, and laboratory animals.
Treatment, prevention & control
• Doxycycline Transmission of R. rickettsii:
• American dog tick (Dermacentor
variabilis)
• Avoiding exposure to ticks is the best protection
measure.
• Wear protective clothing while handling • Rocky Mountain wood tick
animals/outdoor activities. (Dermacentor andersoni)
• Immediately remove the ticks if notice nearby.

• Brown dog tick (Rhipicephalus

sanguineus) 
 R. prowazekii: Epidemic Typhus
• Humans are main reservoir

• Human body louse is vector (Pediculus humanus)

• Flying squirrel as non-human reservoir

• Epidemiology
• Worldwide but more in Central and South America, Africa

Recurrent infection with R. prowazeki: Brill-Zinser disease

 R. prowazekii: Epidemic Typhus
• Clinical manifestations - high fever, intense headache, chills, and myalgia (8 day incubation period)
• Characteristic rash - fourth to seventh day of disease
• Centrifugal - First appears on the upper trunk and then becomes generalized- Opposite of RMSF
• Involves the whole body except the face, palms, and soles
• Disease progression  encephalitis, meningoencephalitis  significant alterations of mental status
• ~20% fatality, if untreated
• Recrudescent (recurring) disease - years after infection (Brill-Zinsser disease)
• Host defense low - organisms multiply - disease generally milder than first disease

• Diagnosis- Lab - MIF Treatment/Prevention:

• Tetracyclines
• Louse eradication
• Vaccine no longer in use
R. typhi - Endemic Typhus
• Gulf states
• Rodents are the primary reservoir
• Transmitted by rat/cat flea
• Rash develops in 50% late in illness - chest and abdomen
• Diagnosis- Indirect fluorescence assay
• Treatment - tetracycline
• Generally resolves in
3 weeks without treatment
Xenopsylla cheopis Ctenocephalides felis
R. akari: Rickettsial pox
• Causes rickettsial pox
• Biphasic
1. One week- Papule develops at bite site  ulceration  eschar formation
2. 9-14 days later- abrupt high fever, severe headache, sweats, myalgia, and photophobia
 Then papulovesicular rash (vesicles form, crust over)
Pox like
• Can get confused with anthrax (rash distinguishes it as rickettsial pox) progression of the
• Mites – for transmission of infection rash
• Heals without treatment but doxycycline speeds recovery
Orientia tsutsugamushi: Scrub typhus
• Causes scrub typhus
• Severe headache, fever, and myalgias
• In <50%, macular to papular rash develops on trunk and spreads centrifugally to extremities
• Central nervous system issues and heart failure
• Lacks cell wall and LPS
• Transmitted by mites
• Treated with doxycycline
Ehrlichia/Anaplasma
• General • Pathogenesis
• Gram negative bacilli - Obligate intracellular • Intracellular
• Divide in monocytes (Ehrlichia) or
granulocytes (Anaplasma) in phagosomes • Lab Diagnosis
(form aggregates called morulae) • PCR
• Causes (ehrlichiosis/anaplasmosis) • Blood film for morulae

• Transmission • Treatment
• Ehrlichia - lonestar tick (Southeastern US.) • Doxycycline
• Anaplasma - black legged tick (Upper
Midwest)
NO Transovarian
transmission in ticks
• Disease
• High fever, fatigue, headache (like RMSF E. chaffeensis Human monocytic ehrlchiosis
without rash) E. ewingii Human granulocytic ehrlichiosis
• Leukopenia Human granulocytic anaplasmosis
Coxiella burnetti
• Gram negative bacilli – intracellular- can survive in
environment and milk
• Q (Query) Fever
• 2 variants- small cell & large cell variants
• 2 phases of LPS- Phase-I (intact LPS) Coxiella arrest
the process of phagocytic killing
• Transmission- Arosols of catle/sheep amniotic fluid
Consumption of unpasteurized milk
• Wide host range- mammals, birds, ticks
• Clinical diseases:
• Flu-like symptoms
• pneumonia
• Hepatitis
Refer Table-34-2
• Isolated fever Murray’s Text book of Medical
• Endocarditis- especially suspected when culture is Microbiology 8th Edition
negative
Q.
• A 40-year-old man comes to the office because of chills and a headache. His temperature is 39°C (102.2°F),
pulse is 85/min, respirations are 18/min, and blood pressure is 120/80 mm Hg. He has an erythematous
maculopapular eruption that he says began on his trunk and spread to his arms and legs. Ten days ago, he
returned from working in a clinic in Algeria. His infection is determined to be caused by a microbe closely
related to mitochondria. Which of the following is the most likely causative agent?
A. Rickettsia rickettsii
B. Ureaplasma parvum
C. Mycoplasma hominis
D. Rickettsia prowazekii
E. Treponema pallidum
Mycoplasma & Cell wall-less or
defective bacteria • It can pass through filters typically
used to remove bacteria.

Unlike bacteria : they lack cell wall

Unlike viruses : they do not need a host cell for replication
Mycoplasma: the pleuropneumonia organism
• Lacking a rigid cell wall during their entire life cycle, also much smaller than conventional bacteria.
• The first organism of this type was associated with pleuropneumonia of cattle- PPO or PPLO
• Associated with mucosal surfaces, residing extracellularly in the respiratory and urogenital tracts.
• Cell wall-free bacteria - 15 species are from human origin- rest all are from animal origin.
• Clinically important species:
• M. pneumoniae
• M. hominis
• M. genitalium Replication controversial
• Ureaplasma species
More similar to that of animal cells than
that of bacterial cells because of sterols
present in the membrane.

Unlike bacteria : they lack cell wall

Unlike viruses : they do not need a host cell for replication
Electron micrograph of Mycoplasma pneumoniae
cells. The arrows indicate the attachment organelles.
Mycoplasma: Cultural characteristics
• Requires sterols for growth, can be grown on • It is also intrinsically resistant to antimicrobials,
laboratory media like beta-lactams, that work by targeting the cell
• Most are facultatively anaerobic wall.
• Exception M. pneumoniae – strictly aerobic • Resistant to antibiotics that interfere with the
integrity of cell wall; penicillins, cephalosporins,
• Generation time 1-6 hours- Needs 10-14 days to
vancomycin, bacitracin
observe visible growth.
• Susceptible to tetracycline, erythromycin
• Fastidious- Requires L-cysteine and iron in the culture
medium.

• M. pneumoniae cultures use specialized media:

• Buffered charcoal yeast extract agar
• Tyrosine buffered yeast extract agar
• Feeley Gorman agar
• PPLO agar medium

Growth on PPLO agar medium

Mycoplasma pneumoniae: Pneumonia
Eaton agent

• A wide spectrum of clinical symptoms / disease manifestations.

• A type of atypical bacterial pneumonia.
• Magnitude of this health issue in the USA- 2 million cases of M. pneumoniae infections occur each year.
• 1 - 10 in every 50 cases of community-acquired pneumonia
• Due to its lack of a cell wall - extremely susceptible to desiccation.
• Transmission from person to person by airborne droplets only occurs through close contact.

Because these bacteria lack cell

walls entirely, they don’t have
regular shapes and must live in a
very osmotically-stable
environment.
M. pneumonia: Pathogenesis
• Mycoplasma pneumoniae is the #1 cause of
“atypical” or “walking” pneumonia and is also
frequently carried asymptomatically.

• M. pneumoniae binds to ciliated respiratory epithelia

via “P1 adhesin” on pilus surface,  ciliostasis and
IL-1, TNF, and IL-6 secretion  lung infiltration
‘Adhesins’ are secreted at the attachment organelle.
• Extra pulmonary complications involving all of the
major organ systems.
M. pneumoniae: Pathogenesis
• The CARDS toxin - a unique virulence factor:
• Community Acquired Respiratory Distress Syndrome (CARDS) toxin.
• Most likely aids in the colonization  leading to inflammation  airway dysfunction.

• Primarily lives on the surface of the respiratory epithelial cells  invade tissues and replicate intracellularly.

• The endocytosis of M. pneumoniae by the host cells could:

• Aid in the establishment of a latent or chronic disease state
• Facilitate the bacterium in evading an immune response
• Interfere with the efficacy of certain drug therapies

• ADP-ribosylating and vacuolating cytotoxin - Elicits extensive vacuolization and ultimate cell death of
mammalian cells, including distinct and progressive patterns of cytopathology in tracheal rings.
Mycoplasma pneumoniae: Diagnosis
• Serology tests for M. pneumoniae
• Antibodies directed against M. pneumoniae - complement fixation test
• Enzyme immunoassays for the detection of IgM and IgG
• Sera needs to be collected early in infection and then after 3 – 4 weeks to demonstrate a rise in
antibody levels
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• Serology has been the most common means for laboratory

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detection of M. pneumoniae infection due to the slow growth

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• Newer diagnostic methods utilizing nucleic acid

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Mycoplasma pneumoniae: Treatment
• Erythromycin – Ureaplasmas (resistant to tetracyclines)
• Doxycycline & fluoroquinolones – Mycoplasmas

• Prevention of disease is problematic.

Other mycoplasmas and Ureaplasma
• M. hominis and M. genitalium and U. urealyticum can colonize the genitourinary tract.
• M. hominis is associated with pyelonepritis, postpartum fevers, and systemic infections in immunocompromised
patients.
• M. genitalium is associated with nongonococcal urethritis and pelvic inflammatory disease.
• U. urealyticum is associated with nongonococcal urethritis, pyelonephritis, miscarriage and premature birth.

• Because the genitourinary tract is colonized with other Mycoplasma species and Ureaplasma, it is difficult to
determine the role of these organisms in disease in individual patients.
• The evidence implicating the organisms in these diseases is based on:
(1) recovery of the bacteria from specimens from infected patients,
(2) a serologic response to the organism,
(3) clinical improvement after treatment with specific antibiotics,
(4) demonstration of disease in animal models, or
(5) a combination of these findings.
Non-gonococcal urethritis
Pathogen Species

Bacteria
Chlamydia trachomatis
Ureaplasma urealyticum
Mycoplasma hominis
Mycoplasma genitalium
Protozoa
Trichomonas vaginalis
Viruses
Genital Herpes virus
Adenovirus
Learning Objectives
• Identify chalmydiae as bacteria lacking any peptidoglycan
?
• Identify cell-wall-lacking bacteria as obligate intracellular
• Identify niches in the human body habitually occupied by call-wall-lacking bacteria
• Compare and contrast Chlamydia trachomatis and Neisseria gonorrhea based on pathogenesis, symptoms,
patient demographics, and plausible treatments
• Differentiate Chlamydophila pneumoniae infection from other pneumonias based on patient characteristics
and presentation
• Identify risk factors for serious disease caused by Chlamydophila psittaci
• Recommend diagnostic techniques and treatments for infections caused by cell-wall lacking bacteria
 A major cause of disease
Chlamydia trachomatis: Overview globally - Top 1 notifiable
diseases in U.S.

• Obligate intracellular parasite – Can NOT make their own ATP – mucosal infections
• Invades non-ciliated columnar, cuboidal, and transitional epithelial cells

β-lactam antibiotics are NOT

• Plasma membrane and outer membrane but NO classical peptidoglycan layer a suitable treatment for
- NO or reduced muramic acid chlamydial infections

• The cell wall resembles the cell wall of Gram (-) bacteria with a relatively high lipid content
• Has LPS with weak endotoxin activity
• MOMP – Major Outer Membrane Protein- 18 serological variants - serovars

• Visualized upon Giemsa/immunofluorescence stainings- Gram staining NOT useful

Chlamydia trachomatis: Biology/ Two
morphological forms
• Elementary body (EB)- Smaller
• Electron dense core, rigid- Resistant to harsh
environmental conditions (like spore) RB replicate
• Extracellular & Infectious, but can NOT replicate
EB infect
• Reticulate body (RB) – Larger - metabolically active
• Fragile pleomorphic morphology
• Replicates inside vesicles - Inclusion bodies
• ONLY intracellular; NOT infectious

Metabolically A single mature inclusion

containing RBs and Ebs
• After 18-24 hours RBs reorganize to EBs and 24-48 hours active RBs in an
early inclusion
later the cell ruptures and releases infective EBs
Chlamydia trachomatis: Developmental
Cycle & Pathogenesis
• Receptors for EBs - primarily restricted to
nonciliated columnar, cuboidal, and transitional
epithelial cells.

• Infection is initiated by
• attachment of EBs to epithelial cells
• found on the mucous membranes of the
urethra, endocervix, endometrium, fallopian
tubes, anorectum, respiratory tract, and
conjunctivae

• Ability to replicate in mononuclear phagocytes

(LGV biovariant)

← Chlamydia developmental cycle

EB: elementary body

RB: reticulate body
Chlamydia trachomatis: Pathogenesis
The clinical manifestations are caused by: Clinical forms of chlamydiasis:
Trachoma (chronic
• Direct destruction of cells during replication conjunctivitis)
• Proinflammatory cytokine response Urogenital diseases
Pneumonia
Lymphogranuloma venereum
• Trachoma – leading cause of preventable blindness - predominantly (LGV)
in children- Africa
• Urogenital infections - Untreated  severe reproductive
Burning during urination (white,
complications 
cloudy discharge)
• PID, infertility (70% due to tubal factor)
• Ectopic pregnancy (35% of cases)
• 50%-75% of passing rate of infection from mother to fetus
• 30-50% of newborns develop conjunctivitis
Chlamydia trachomatis: Urogenital Disease
• Transmitted mainly during vaginal, anal, or oral sex

• Initially infects the single-cell columnar epithelial layers

• Endocervix - female, Urethra - male

• Multiply and spread to surrounding tissues

• Intense inflammation, redness, edema and discharge
• Mucopurulent cervicitis - female
• Non-gonococcal urethritis - male
• These conditions are often sub-clinical

• Infection common in women - 20%- 40% of untreated women

• Mostly asymptomatic – ≥75% of infected women, 25%-50% of men
Chlamydia trachomatis: Urogenital Disease
• Only symptoms - Burning during urination or an unusual discharge (white,
cloudy discharge)

• Infection ascends along the endometrial epithelium to the fallopian tubes

• Persistent infection
• Scarring of the fallopian tubes, sterility, infertility, ectopic pregnancy, or
chronic pelvic pain
• Pelvic Inflammatory Disease (PID)
• Fitz-Hugh−Curtis (FHC) syndrome
• most common is C. trachomatis and second is N. gonorrohoeae

• Transmission-
• Vaginal passage  neonatal inclusion conjunctivitis  leads to blindness
• Respiratory droplets
• Fecal contamination

♂ Epididymitis, prostatitis, proctitis, non-

gonococcal urethritis (NGU)

♀ Cervicitis, salpingitis, PID, infertility, and ectopic

pregnancy
Chlamydia trachomatis: Urogenital Disease
Disease - Lymphogranuloma venereum (LGV)

• Serovars L1, L2, L2a, and L3

• Chronic STD endemic in Africa, Asia, and S. America

• 1° - painless papule or ulcer on genitals, heals rapidly

• 2° - inflammation and swelling of regional lymph nodes
forming buboes; can rupture and form fistulas,
strictures, lymphatic obstruction leading to genital
elephantiasis (3°)

• Proctitis is common with LGV

• Progression to systemic: fever, chills, anorexia,

headache, myalgias, and arthralgias
Chlamydia trachomatis: Trachoma
(keratoconjunctivitis)
• #1 cause of blindness in the world

• Endemic in Middle East, North Africa, South Asia and

South America

• Predominantly in children
• Serovars A, B, Ba, and C
• Transmitted eye-to-eye by droplets, hands,
contaminated clothing, and flies; also aerosol
droplets or fecal contamination
• Begins with follicular conjunctivitis  corneal
ulceration and scarring with in-turned eyelashes 
blindness
Chlamydia trachomatis: Additional Diseases
• Adult conjunctivitis
• Preceded by genital infection
• Autoinoculation and oral genital contact
• Pulmonary disease (infant pneumonia) in newborns 2-3 weeks after birth
(rhinitis, bronchitis with characteristic staccato cough)
• Fitz-Hugh-Curtis syndrome (perihepatitis) is a rare complication of PID that
is 5 times more likely to be caused by Chlamydia than by N gonorrhoeae
• Reiter’s syndrome (Reactive arthritis – inflammatory reaction to infection)
• Autoimmune disorder caused by cross-reactive Abs
• Initiated by genital infection with C. trachomatis
• Urethritis, polyarthritis, and mucocutaneous lesions
• Conjunctivitis
• Most common 20-40 y.o.; males > females
• HLA-B27
Fitz-Hugh-Curtis syndrome
Chlamydia trachomatis: Immunity
• Long lasting immunity after infection is limited
• Reinfection is usually less aggressive
• However, may cause aggressive inflammatory response and tissue damage in immune privileged sites:
• Vision loss with ocular infections
• Scaring, sterility, sexual dysfunction with genital infection
Chlamydia trachomatis: Diagnosis
• Cytoplasmic inclusions seen on Giemsa-, iodine-, or fluorescent antibody stained smear or scrapings
• Direct fluorescent antibody technique , ELISA for chlamydial ag (MOMP/LPS) – present in cytoplasmic
inclusions
• Appropriate sample collection is critical
• Must get into appropriate epithelial layers to get intracellular organisms
• Nucleic acid probe (rRNA) & PCR (NAAT)
• Culture in tissue culture cells, embryonated eggs
• Most specific method of diagnosis
Chlamydia trachomatis: Treatment

• For all chlamydia

• Tetracycline derivatives are primary drug choice
• Doxycycline
• Or Macrolide, azithromycin
• For LGV, use doxycycline, Topical application

Why not penicillins, cephalosporins?

• Antibiotics are only effective against the Reticulate bodies
 Chlamydia trachomatis: Summary
General: Disease:
• Obligate intracellular parasite (can't make ATP) • Trachoma keratoconjunctivitis (blindness)
• Lack pf classic peptidoglycan layer (reduced muramic acid) • Fitz-Hugh−Curtis syndrome
• Gram stain not useful • Reiter's syndrome
• Sexually transmitted diseases
• STD in women (asymptomatic in ~75%)
Transmission: • Cervicitis, salpingitis, PID, infertility, & ectopic
• Sexual
pregnancy
• Two biovariants - Trachoma and LGV (lymphogranuloma
• STD in men (asymptomatic in ~40%)
venereum) • Epididymitis, prostatitis, proctitis, non-gonococcal
urethritis (NGU)
Pathogenesis:
• Two morphological forms: • Lymphogranuloma venereum (LGV)
• Elementary body: resistant to harsh conditions, small, • 1° - painless papule or ulcer on genitals, heals rapidly
infectious, cannot replicate, infects mononuclear • 2° - inflammation & swelling of regional lymph nodes
phagocytes forming buboes; can rupture and form fistulas,
• Reticulate body: replicates by binary fission inside strictures, lymphatic obstruction leading to genital
inclusion bodies, larger, metabolically active elephantiasis (3°)
• Invades nonciliated epithelial cells • Proctitis is common with LGV

Lab Diagnosis Treatment

• ELISA, cytoplasmic inclusions, NAAT, cell culture • Tetracycline, macrolides
Ex
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Chlamydia

Age specificity and other risk
Newborns (birth – 6 weeks)
Children (6 weeks-18 years)
Adults (40-65 years)
Elderly (>65 years)
Nosocomial (Hospital
acquired)
Immunocompromised
Special risks
Intravenous
Postviral (secondary infection)
Neutropenia
Chronic steroids , MS,
*Tuberculosis may manifest in either immunocompetent or immunocompromised (HIV) host (Previous lecture)
Pneumonias
Infection agents
Group B streptococcus
E. coli
Viruses (e.g., RSV, influenza), Mycoplasma pneumoniae, Chlamydophila
pneumoniae, Streptococcus pneumoniae
M. pneumoniae , C. pneumoniae, S. pneumoniae, viruses (adenovirus,
VZV)
S. pneumoniae , Viruses, anaerobes, H. Influenza,
Gram negative rods; Entereobacteiaceae and Pseudomonas
Gram negative rods; Klebsiella pneumoniae, Pseudomonas aeruginosa
Staphylococcus aureus (drug resistant)
Gram negative rods; Klebsiella pneumoniae, Pseudomonas aeruginosa
S. pneumoniae, Fungi, Filamentous bacteria (e.g Nocardia)
Pneumocyststis jiroveci, Viruses (e.g. CMV)
S. aureus
S. aureus
Aspergillus and others fungi.
Nocardia, Moraxella, H influenza, etc
 Biovarian Serovaria Disease Syndromes
Species
t nt
A-C Trachoma (conjunctivitis)
Trachoma STD - genital chlamydia,
Chlamydia
D-K infant conjunctivitis,
trachomatis
pneumonia
LGV L1-L3 Lymphogranuloma venereum
Chlamydophila Pneumonia, upper respiratory
pneumoniae disease, arthritis
Chlamydophila
Psittacosis, abortion, heart
psittaci
tissue damage, arthritis
(pr. sit-eh-cee)

Chlamydophila pneumoniae
Chlamydophila pneumoniae: Disease
• Transmitted person to person by respiratory droplets
• Mostly asymptomatic or cause mild bronchitis  causing a persistent
cough, sinusitis, malaise  more severe infections  pneumonia
(atypical pneumonia) or Walking pneumonia
• typically involve a single lobe of the lung.
• It was known as the Taiwan acute respiratory agent (TWAR) from the
names of the two original isolates – TW-183 & AR-39.
• Epidemiology
• 300,000 cases/year reported from the United States of America.
• 10-20% of community-acquired pneumonia cases among adults
• More common in males (60-90%)
• School-aged children at greatest risk

• Treatment:
• Doxycycline, or levofloxacin
• Macrolides (erythromycin, azithromycin, & clarithromycin)
http://www.nature.com/nrmicro/journal/v2/n1/fig_tab/nrmicro796_F1.html
Chlamydophila psittaci: Disease
• A zoonotic disease - Psittacosis or Parrot fever
• Transmission - by inhalation of dust contaminated with respiratory secretions or
feces of infected birds especially parrot.
• Influenza like symptoms- bronchitis or pneumonia (atypical pneumonia)
• Hepato/splenomegaly

Treatment:
• Doxycycline
• Macrolides
(erythromycin,
• The criteria for the diagnosis of acute  C. pneumoniae and psittaci  infection – azithromycin, &
• A single IgM titer of >1:16 or a 4-fold increase in IgG titer (on a repeat clarithromycin)
 Sexually Transmitted Infections (STIs)
Bacteria Virus Others (Fungi & Parasites )
Transmitted in adults predominantly by sexual intercourse
Neisseria gonorrhoeae HIV (type 1 and 2) Trichomonas vaginalis (protozoa)
Chlamydia trachomatis HTLV-1 Phthirus pubis (ectoparasite)
Treponema pallidum HSV-2
Haemophilus ducreyi HPV
Klebsiella HBV
Ureaplasma urealyticum Mollusum contagiosum virus
Mycoplasma genitalium
Sexual transmission repeatedly described but NOT well defined or NOT the predominant mode
Mycoplasma hominis CMV, Candida
Gardnerella vaginalis HTLV-2 Sarcoptes scabie (ectoparasite)
Group B streptococcus HCV
Mobiluncus spp HSV-1
Helicobacter cinaedi, fennelliae EBV
HHV-8
 Sexually Transmitted Infections (STIs)
Type of infections Infectious agents
Genital Ulcers (Non-exudative infections)
Herpes HSV-2>>HSV-1
Syphilis Treponema pallidum
Lymphogranuloma venereum (LGV) Chlamydia trachomatis
Genital warts (condylomata Human papillomavirus (HPV)
acuminata)
Sexually transmitted systemic infections
AIDS HIV-1, HIV-2
Pelvic inflammatory disease (PID) Chlamydia trachomatis , Neisseria gonorrhoeae, Gardnerella vaginalis,
Haemophilus, and anaerobes such as Peptococcus and Bacteroides species.
Laparoscopic studies have shown that in 30-40% of cases, PID is
polymicrobial.
Cancer (neoplasia)
Cervical carcinoma HPV
Gardnerella vaginalis: "Minor" STI or STD
• Gram-variable – staining, facultative anaerobic, Diagnosis:
non-spore forming, non-motile coccobacilli
•  frothy gray or yellow-green vaginal discharge,
• Bacterial vaginosis in some women as a result of a pruritus
disruption in the normal vaginal microflora
• "amine whiff test“ – 10% KOH is added to the
• May be asymptomatic or will include vaginal discharge, a fishy smell is produced
discharge, vaginal irritation, and a "fish like" odor
Treatment:
• CDC: Unclear if Gardnerella is STD
Metronidazole or clindamycin, oral or topical
gel/cream

Differential:
• Trichomonas vaginalis and Gardnerella vaginalis have similar clinical presentations – we will discuss
further in Block 5
• Wet mounts: Gardnerella shows classic "clue cell" under the microscope – bacteria adhering to the surface
of squamous epithelial cells
Gardnerella vaginalis: STD

clue cell

- Gram stains of vaginal fluid from patients with bacterial vaginosis

- Note the clue cells - epithelial cells whose surface is covered with Gram-variable bacteria (Gardnerella
vaginalis), making the epithelial cells appear purple
Zoonotic bacterial infections

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