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Chlamydiaceae family

two genera: chlamydia (C. Trachomatis) and chlamydophilia (c. pneumoniae, and C. psittaci)

obligate intracellular pathogens

originally considered viruses due to small size

reclassified as bacteria. Possess inner and outer membranes similar to gram negative bacteria (but lack peptidoglycan layer). Contain both DNA and RNA. Possess prokaryotic ribosomes. Synthesize own proteins, nucleic acids, and lipids. Susceptible to antibacterial antibiotics.

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Chlamydia: development cycle

exist in two forms. IN active infectious form (elementary bodies) and metabolically active non-infectious forms (reticulate bodies)

1. EBs infect host cell and convert to RBs.

2. RBs replicate using host cell's ATP for energy and form inclusion (phagosome with replicating RBs)

3. Reticulate bodies reorganize into EBs

4. EB's released by reverse endocytosis

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Chlamydia trachomatis

Divided into two biovars: trachoma and LGV

major outer membrane protein (MOMP) important structural component

variable regions in gene encoding momp results in 18 serologic variants or serovars

trachoma: serovars A, B, Ba, C

Urogenital tract disease: serovars D-K

Lymphogranuloma venerum: Li, L2, L2a, L2b, L3

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pathogenesis and immunity: chlamydia trachomatis

limited range of cells that can infect

receptors for EBs restricted to nonciliated columnar, cuboidal and transitional epithelial cells

Found on mucous membranes of urethra, endocervix, endometrium, falopian tubes, anorectum, respiratory tract, conjunctivae

LGV serovars more invasive due to replication within mononuclear phagocytes

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Pathogenesis and immunity: chlamydia trachomatis 2 Chlamydia

Clinical manifestation caused by: direct destruction of cells during replication. Proinflammatory cytokine response they stimulate

entry via minute abrasions or lacerations

severe inflammatory response with neutrophils, lymphocytes, and plasma cells

LGV serovars form lesions in lymph nodes with resulting granuloma formation

infection does not result in immunity

reinfection results in vigorous inflammatory response and tissue damage

results in scarring (ocular and UG), blindness, sterility and sexual dysfunction

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Epidemiology: trachoma Chlamydia

leading cause of preventable blindness worldwide

WHO estimates: 6 million blind due to trachoma. 150 million in need of treatment.

endemic in NOrth and sub-Sahara Africa, Middle east, Asia, and South America

Infections predominantly in chidlren and are chief reservoir for endemic disease

trasmitted eye to eye via droplet, hand, clothing, and eye seeking flies

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Epidemiology: Urogenital disease Chlamydia

Most common bacterial STI in US

2006 reported 1 million infections

underestimate many patiients do not seek medical care, asymptomatic disease

estimated 2.8 million new infections each year in the US

50 million new infections each year worldwide.

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Epidemiology: LGV Chlamydia

occurs only sporadically in US.

Highly prevalent in Africa, Asia, and South America

Seen more frequently in men (women with more asymptomatic disease)

recent outbreaks reported in Europe and NOrth America in MSM

HIV coinfection common

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Clinical diseases: Trachoma Chlamydia

Two phases of infection

Active Trachoma: initial infetion causes mild self limited follicular conjunctivitis. Characeristic follice on superior tarsal conjunctiva. Often Asymptomatic.

Cicatricial disease: Severity and duration of active trachoma predicts progression to cicatricial disease. Repeated episodes infection -> conjunctiva inflammation and eyelid scarring. Scarring leads to corneal abrasion and scarring and blindness.

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Trachoma Chlamydia

WHO grade TF (trachomatous inflammation, folicular). To make a diagnosis of WHO grade TF, five or more white or yellow follicles > 0.5 mm must be visualized on the upper tarsal conjunctiva

Herbert's pits are shallow pits in the cornea that form as a result of follicle rupture. They are pathogenomonic for trachoma but are not assessed in the current grading scheme.

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Trachoma 2 Chlmydia

1. Trichiasis occurs when eyelid conjunctiva scar tissue contracts, distorting the lid margin and causing the eylashes to rub on the cornea.

2. Pannus is the growth of vascular tissue over the cornea as a result of edema and ulceration due to eyelash abrasion on the cornea

3. evidence of corneal opacity blurring part of the pupil margin.

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Clinical disease: Urogenital disease in Women Chlamydia

Asymptomatic disease common in women (up to 80%)

clinical manifestations in women include bartholinitis, cervicitis, endometritis, perihepatitis, salpingitis, and urethrtis

cervicitis most common presentation in women

mucopurulent discharge, friable cervix, and cervica edema see

urethritis often accompanies cervicitis and presents with UTI like symptoms

Tishugh-curtis syndrome: perihepatitis with inflammation of liver capsule

if untreated may develop PID

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Chlamydia Cervicitis

mucopurulent discharge is visible coming from the OS in a patient with chlamydia cervicitis. The cervix is erythematous and friable.

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Clinical diseases: Urogenitcal disease in Men Chlamydia

Most infections 75% in men symptomatic.

urethral discharge and/or dysuria

Causes 35-50% of cases of NGU (non gonococcal urethritis)

Incubation period longer than N. Gonorrhoeae so consider diagnosis in patients treated for GC who present with new symptoms

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Clinical disease: Oculogentical syndromes Chlamydia

Newborn inclusion conjunctivits: acquired during passage of infant through infected birth canal. Develops in 25% of infants whose mothers have active genital infections. After incubation of 5-12 days develop swollen eyelids, hyperemia and purulent discharge

Adult inclusion conjunctivitis: Afflicts 18-20 year olds. Genital infection precedes eye involvement. Transmitted via autoinoculation or oral genital contact. Mucopurulent discharge, keratitis, corneal infiltrates and scarring.

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Clinical diseases: Reiter syndrome and infant pneumonia Chlamydia

Reiter syndrome: Uretrhtis conjunctivitis, polyarthritis, and mucocutaneous lesions. Initiated by genital infection with C. Trachomatis. Typically occurs in young men.

Infant pneumonia: Occurs 2-3 weeks after birth. Rhinitis initially hten staccato cough and tachypnea. Typically afebrile. Chest X ray shows bilateral interstitial infiltrates.

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Clinical syndromes: LGV

Primary lesion (papule or ulcer) at site of infection develops after incubation period of 1-4 weeks

lesion non painful

may be accompanied by systemic symptoms

second stage of infection with inflammation and swelling of lymph nodes that drain the site of initial infection

inguinal nodes most commonly involved become painful, fluctuant buboes that can rupture

proctitis common in women with LGV due to lymphatic spread from cervix or vagina

utreated may resolve or become chronic with fistulas, strictures, and genital elephantiasis

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Clinical syndromes: LGV parinaud oculoglandular syndrome

Caused by LGV serotypes

conjunctival inflammation with preauricular, submandibular, and cervical lymphadenopathy

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Laboratory diagnosis Chlamydia

Symptomatic easier than asymptomatic

do not culture pus: need epi cells

do culture: urethra, cervix, rectum, oropharynx, conjunctiva

do not culture vagina

cytology for inclusions, pap smears: insensitive

cultured in cell culture: process quickly, only acceptable test in criminal cases, less sensitive than nucleic acid based tests but more specific

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Laboratory diagnosis 2 Chlamydia

antigen detection: direct immunofluorescence, enzyme linked immunoassay, utilizes antibodies directed at MOMP or LPS, may cross react to LPS of other bacteria

Nucleic acid assay (NAAT): best test today. Nucleic acid probe (16s rRNA). PCR, Ligase chain rxn (LCX). Preformed on first voided urine or urethralcervical discharge

serology: limited value except in neonatal disease.

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Treatment Chlamydia

LGV: doxycycline for 21 days

erythromycin for neonatal disease.

ocular/genital disease: azithromycin or doxycycline

preventions: increased sanitation, safe sex practices

control: treatment of contacts

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FAMILY MYCOPLASMATACEAE

five species associated with human disease

most important species mycoplasma pneumoniae: important cause of respiratory disease

additional pathogens cause GU disease: mycoplasma genitalium, mycoplasma hominis, Ureaplasma urelyticum

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Mycoplasma pneumoniae: physiology and structure

smallest free living bacteria

unique because do not have a cell wall and cell membrane contains sterols

because lack cell wall are pleomorphic and cannot be classified as rods or cocci.

sterols may provide added strength/stability to membrane

unable to syntehsis sterol ring so require external source of cholesterol from serum or supplemented media

facultative anaerobes except M. Pneumoniae which is a strict aerobe

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Pathogenesis and immunity of mycoplasma pneumoniae

extracellular pathogen that adheres to respiratory epithelium via adhesion proteins

terminal adhesion protein (P1): binds glycoprotein receptors of base of cilia of epithelial cells

results in cilistastasis and then destruction of ciliated epithelial cells.

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Pathogenesis and immunity of mycoplasma pneumoniae

loss of ciliated cells interfers with clearnace of upper airways and lower respiratory tract becomes contaminated and irritated

caues the chronic cough seen in M pneumoniae infections

M pneumoniae acts as super antigen

stimulates inflammatory cells to site of infection

cytokine release of TNF alpha, IL1, and IL6

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Epidemiology of mycoplasma pneumoniae

strict human pathogen

respiratory disease due to m pneumoniae occurs worldwide throughout the year

proportionally more common during summer and fall

epidemic disease occurs every 4-8 years: usually start in the fall and persist for 12-30 motnhs

most common in 5-15 year olds

not a reportable disease so true incidence is unknown

colonizes airway and transmited vial respiratory droplets during coughing episodes.

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Clinical syndromes of Mycoplasma

Mild URTI: most common manifestation

Otitis media; can develop bullous hemorrhaic myringitis

tracheobronchitis: low grade fever, malaise, HA, and dry nonproductive cough. Symptoms develop 2-3 weeks after exposure and can persist for weeks

Pneumonia can develop in some patients. A typical pneumonia (often referred to as walking pneumonia). Patchy bronchopneumonia on chest x ray

compicatios include pericarditis, hemolytic anemia, neurologic abnormalities, encephalitis, arthritis, erythema multiforme and stevens johnson syndrome.

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Laboratory diagnosis Mycoplasma

microscopy limited value since no cell wall

culture: relatively insensitive.

Special media with serum (for cholesterol), yeast extract (nucleic acid precursors), glucose, pH indicator, penicillin

gowth indicated by metabolism of glucose and pH change

colonies with homogenous granular appearance

difficult to grow; most labs do not perform cultures

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Laboratory diagnosis mycoplasma 2

serology: enzyme immunoassays for IgM and IgG. Four fold rise in titers suggestive of infection. Commonly single serum IgM used for diagnosis results in voer diagnosis due to low specficity. Specific antibody responses may last for months so single serum sample may be misleading. Paired sera should be used to confirm diagnosis

PCR: very sensitive. variable specficity due to cross reaction with non pathogenic mycoplasma

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Tx, prevention, and control mycoplasma

sensitive to macrolides, tetracylcines, and fluoroquinolones

avoid tetracyclines and flouroquinolones in children

treatment should be reserved for more serious disease (pneumonia, steves johnson syndrome, neurologic disease.

steroids may be of benefit in servere pulmonary disase, stevens johnson syndrome, encephalitis and hemolytic anemia.

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treatment, prevention, and control mycoplasma 2

patients contagious as long as cough persists even with antibiotic therapy

isolation of hospitalized patients

no vaccine available

antibiotic prophylaxis to close contacts who are at high risk (sickle cell disase, immunosupressed) may be of some benefit.