Chlamydiaceae
The genus chlamydia is in the family chlamydiaceae, only three species are pathogen to human: Chlamydia trachomatis, Chlamydophila pneumonia, Chlamydophila psittaci.Chlamydia trachomatis
Chlamydophila pneumonia Chlamydophila psittaciChlamydiaceae
Trachoma
Lymphogranuloma venereum (LGV)
Nongonococcal Urethritis (NGU)
Chlamydiaceae
Comparative Properties of MicroorganismsChlamydiaceae
obligate intracellular parasites small enough to pass through 0.45-μm filters possess inner and outer membranes similar to those of gram-negative bacteriacontain both DNA and RNApossess prokaryotic ribosomessusceptible to antibiotics. The life cycle two distinct forms:1- Elementary body (EB) (Infectious)2- Reticulate body (RB)Chlamydiaceae
Resemble bacteria except it cannot multiply outside living cells/ tissues (like viruses)Cannot synthesize ATP – depends on host cell for energy & nutrient sources. Hence, called Energy Parasites.All are non-motile, gram negative.Antigenic Properties
Three major Antigens Genus specific Ag: heat stable, common to all Chlamydiae, a lipopolysaccharide resembling LPS of GNB. Present in all stages. Species specific protein Ags: present at the envelope surface, help in classifying chlamydia into species Ag for Intraspecies typing: found only in some members of a species, located on major OMP (MOMP), demonstrated by micro- IF. Classifies species into serovars/ serotypes
Chlamydiaceae
Pathogenesis:The growth cycle begins when small EB. infects the host cell, (non ciliated, columnar or transitional) epithelial cells, that line the conjunctiva, respiratory tract, urogenital tract & rectum.During the next 8 hours they organize into larger, less dense RBsHost cells synthesizing functions to their own metabolic needs & begin to multiply by binary fission.In 24h. after infection, & then the dividing organism begin reorganizing into infective EB (Elementary Body).At about 30h. multiplication stopped & the 35-40h. Disrupture of host cells……………….(continning the cycle). Which divertLife cycle of Chlamydia
Life Cycle of ChlamydiaThin section electron micrograph
In McCoy cells and stained with iodine.
In McCoy cells stained with a fluorescein-labeled antibody against it
Chlamydiaceae
Pathogenesis: The Elementary Body (EB) the outer membrane similar to that of many gram negative bacteria, the most prominent component of this membrane is the major outer membrane protein (MOMP). That contain specific & subspecific epitopes that can be defind by monoclonal antibodies. The Chlamydia outer membrane that also contain LPS.metabolically inactive infectious forms (elementary bodies [EBs]). metabolically active, noninfectious forms (reticulate bodies [RBs]). EBs are resistant to many harsh environmental factors. bacteria lack the rigid peptidoglycan layer. surrounded by a cytoplasmic membrane and a double-layer outer membrane.
Chlamydiaceae
Chlamydiaceae
Chlamydia trachomatis: Trachoma serovar A, B, Ba, C eye infection trachoma Trachoma sevovar D, Da, K, Ia, Ja associated with inclusion conjunctivitis, milder eye infection and urogenital infections. Trachoma serovar L1, L2, L2a, L2b, L3 Lymphogranuloma venereum (LGV) & invasive urogenital tract disease.
Chlamydiaceae
Infection does not confer long-lasting immunity; rather, reinfection characteristically induces a vigorous inflammatory response with subsequent tissue damage. This response produces the vision loss in patients with chronic ocular infections, and scarring with sterility and sexual dysfunction in patients with genital infections.Clinical Diseases
Trachoma: Initially, patients have a follicular conjunctivitis, The conjunctivae become scarred as the disease progresses.Greek word trakkus – rough (roughness of conjunctiva)Adult Inclusion Conjunctivitis: The infection is characterized by mucopurulent discharge, keratitis, corneal infiltrates, and occasionally some corneal vascularization. “Swimming Pool Conjunctivitis” – associated with bathing in community swimming pools contaminated with chlamydia from genital secretions.If infection left untreated infection generally ends in blindness in adults.Clinical Diseases
Conjunctival scarring and hyperendemic blindness caused by Chlamydia trachomatis in ocular infections.Inguinal swelling and lymphatic drainage
Lymphogranuloma venereum (LGV). It is sexually transmitted disease (STD), patients have inguinal and anorectal symptoms, the bacteria enter the lymph nodes near the genital tract and lead to produce astrong inflammatory response that often result in bubo formation. Subsequent rupture of the lymph node. Some times caused the disease Nongonococcal Urethritis (NGU), Epididymitis & prostatitis. Infection in adult women include urethritis, follicular cervicitis, endometritis, salpingitis, Pelvic Inflammatory Disease (PID).
Clinical Diseases
Lymphogranuoma venereum: Genital tract infection with C. trachomatis serovars L1, L2, L2a, L2b, L3 may present as lymphogranuloma venereum. Commonest in the tropics, this condition is occasionally seen in developed countries. It usually begins with a genital ulcer followed by lymphadenopathy of the regional lymph nodes. Buboes are seen if infection persist, can spread to the gastrointestinal and genito-urinary tracts, causing strictures and, in rare cases, peno-scrotal elephantiasis.
Patient with lymphogranuloma venereum causing unilateral vulvar lymphedema and inguinal buboes.
Clinical Diseases
Reiter Syndrome ureyhritis, conjunctivitis, polyarthritis in adult belived to be caused by Chlamydia trachomatis. Salpingitis can lead to scarring & dysfunction of the oviductal transport system leading to infertility of ectopic pregnancy.
Clinical Diseases
Chlamydia infection in the newborns Neonatal conjunctivitis During pass from birth canal, infants can be infected with Chlamydia Spp. Characterized by a mucopurulent discharge. incubation period about 14 days after birth. The disease presents as a swelling of the eyelids and orbit, hyperaemia and a purulent infiltration of the conjunctiva. Acquired from the mother during birth. If untreated the infection usually resolves, but a substantial proportion of these infants develop chlamydial pneumonia about 6 weeks after birth
Clinical Diseases
Neonatal conjunctivitis due to chlamydial infection.
Clinical Diseases
Fluorescent-stained elementary bodies (arrows) in a clinical sampleChlamydophila pneumoniae
C. pneumoniae was first isolated from the conjunctiva of a child in Taiwan no animal reservoir has been identified. C. pneumoniae is a human pathogen that causes sinusitis, pharyngitis, bronchitis, and pneumoniaRespiratory secretions, No animal reservoir, Human pathogen, Bronchitis, pneumonia, and sinusitis, 50% of people have serologic evidence, A significant cause of acute exacerbations of asthma, Atypical pneumonias,
Chlamydophila pneumoniae
Chlamydophila pneumoniae detection from direct sputum smear using fluorescent-labeled monoclonal antibody, highlighting cytoplasmic inclusion
Chlamydophila psittaci
The cause of psittacosis-parrot fever, Ornithosis, Human infections may be asymptomatic or mild, Exposure to an infected bird may not be suspected, Convalescent serum may not be collected so that the clinical diagnosis can be confirmed, Antibiotic therapy may blunt the antibody response,
Usually transmitted to humans through the inhalation of dried excrement, urine, or respiratory secretions Occupational disease Person-to-person transmission is rare
Chlamydophila psittaci
The incubation period is about 10 days Ranges from an 'influenza-like' syndrome, with general malaise, fever, anorexia, sore throat, headache and photophobia, to a severe illness with delirium and pneumonia.
Chlamydophila psittaci
Diseases caused by Chlamydophila psittaci and Chlamydophila pneumoniae.
Chlamydophila4 approaches available: Microscopic demonstration of inclusion or elementary bodies. Isolation of chlamydia. Demonstration of chlamydial Ag. Demonstration of Abs or hypersensitivity.
Laboratory Diagnosis
MicroscopyGram negative but stained better by Giemsa, Castaneda or Machiavello stains.Giemsa Stain: Elementary body & the Reticulate body stains blue in cytoplasmLugol’s iodine: rapid & simple screening method for ocular infections, stains glycogen matrix of C. trachomatisImmunoflurescence staining: more sensitive & specific, by using monoclonal Abs. Identifies inclusion bodies as well as extracellular elementary bodies. Used for ocular, cervical or urethral specimens. Laboratory Diagnosis
CultureYolk sac of 6 - 8 days old chick embryo.Tissue culture – McCoy, HeLa cell lines Laboratory Diagnosis
A monolayer of tissue culture cells has been exposed to cells of chlamydia trachomatis. Infected cells within the cell sheet have a cytoplasm with a granular appearance.
Laboratory Diagnosis
Demonstration of antigens:Micro – IF : infected ocular or genital samples are stained with fluorescent conjugated AbELISA: best for screening large number of specimens, detects LPS AgMolecular methods: PCR Laboratory Diagnosis
Laboratory Diagnosis
C. trachomatis can be demonstrated in clinical material by several direct procedures and by culturing in human cell lines. Samples, particularly from the urethra and cervix in GU infection and conjunctivae in ocular disease, should be obtained by cleaning away overlying exudate and gently scraping to collect infected epithelial cells. Direct tests: Microscopic examination using direct fluorescent antibody staining reveals characteristic cellular cytoplasmic inclusions. C. trachomatis infections can be detected with high sensitivity and specificity using DNA amplification performed on urine specimens. This permits cost-effective screening of large numbers of individuals without the need for access to a medical clinic and a pelvic examination.Culturing methods: C. trachomatis can be cultivated by tissue culture in several human cell lines. In the standard procedure using McCoy cells, addition to the culture medium of a eukaryotic metabolic inhibitor, such as cycloheximide, enhances growth of the parasite. The presence of chlamydial inclusions can be demonstrated after 2 to 7 days of incubation. Detection of serotypes: Serotypes of C. trachomatis can be determined by immunofluorescence staining with monoclonal antibodies. However, the procedure is not widely used because it adds little to clinical impressions. Serologic testing for specific antibodies is similarly not helpful except in suspected LGV, in which a single high-titer response is diagnostic.
Laboratory Diagnosis
Treatment and prevention
Chlamydiae are sensitive to a number of broad-spectrum antibacterials. Azithromycin and Tetracycline are currently the drugs of choice. Resistant strains have not been reported in the clinical setting. Erythromycin should be used in small children and pregnant women because of the effects of tetracyclines on teeth and bones. The only recommended treatment for a concurrent gonococcal infection is with Ceftriaxone. A topical ocular preparation containing erythromycin provides moderately effective prophylaxis in newborns.RICKETTSIA
RICKETTSIA
Rickettsia have the structural features of typical prokaryotic cells. They are small, rod like or coccobacillary shaped. have a typical double-layered, gram-negative cell Wall but they stain poorly The best visualized under the light microscope with one of the polychrome stains, such as Giemsa or Macchiavello. Obligate intracellular bacteria (do not make sufficient ATP for independent life) Rickettsia contain a number of antigens that convey both group and species specificity.
Electron micrograph of Rickettsia prowazekii in experimentally infected tick tissue.
RICKETTSIA
Species of Medical Importance Rickettsia rickettsii Rickettsia prowazekii Rickettsia typhiRICKETTSIA
Pathogenesis Rickettsia are transmitted to humans by arthropods, such as fleas, ticks, mites, and lice (arthropods can serve as reservoirs of infectious organisms). Rickettsia species have an affinity for endothelial cells located throughout the circulatory system Following a bite by an infected arthropod, the organisms are taken into cells by a process similar to phagocytosis. They multiply in both the nucleus and cytoplasm of host cells.RICKETTSIA
Infections Caused by Rickettsiae and Close RelativesRICKETTSIA
Rickettsia rickettsii Reservoir: small wild rodents and larger wild and domestic animals (dogs) Transmission: hard ticks: Dermacentor (also reservoir hosts because of trans-ovarian transmission) Pathogenesis: invade endothelial cells lining capillaries, causing vasculitis in many organs including brain, liver, skin, lungs, kidney, and GI tractRICKETTSIA
Disease: Rocky Mountain spotted fever (RMSF)Headache, fever (102°F), malaise, myalgias, toxicity, vomiting, and confusion.Rash (maculopapular → petechial) starts (by day 6 of illness) on ankles and wrists and then spreads to the trunk, palms, soles, and face (centripetal rash).Ankle and wrist swelling also occur.Diagnosis may be confused by GI symptoms, periorbital swelling, stiff neck, conjunctivitis, and arthralgiasRICKETTSIA
Child’s right hand and wrist displayingthe characteristic spotted rashwith raised or palpable purpura,which is pathognomonic of vasiculitis(the fundamental lesion of RockyMountain spotted fever). Spotted fevers caused by Rickettsia.