TL;DR: The role of the Clinical Microbiology Laboratory in Nosocomial and Community Infections and Antimicrobial Agents and Susceptibility Tests, Quality Control, Media, Reagents and Stains is examined.
Abstract: General Issues in Clinical Microbiology Diagnostic Technologies in Clinical Microbiology Nosocomial and Community Infections: the Role of the Clinical Microbiology Laboratory Bacteria Fungi Parasites Viruses Rickettsiae and Chlamydiae Antimicrobial Agents and Susceptibility Tests Quality Control, Media, Reagents and Stains.
TL;DR: General techniques laboratory safety collection and submission of diagnostic specimens essential equipment and reagents for a veterinary diagnostic microbiology laboratory diagnostic applications of immunological tests
Abstract: General techniques laboratory safety collection and submission of diagnostic specimens essential equipment and reagents for a veterinary diagnostic microbiology laboratory diagnostic applications of immunological tests bacterial pathogens - microscopy, culture and identification the isolation and identification of viral pathogens antimicrobial agents bacteriology staphylococci streptococci corynebacteria and rhodococcus equi actinomycetes, myobacteria, listeria species erysipelothrix species bacillus species clostridia non spore-forming anaerobes enterobacteriaceae pseudomonas species aeromonas and plesiomonas species actinobacillus species pasteurella species francisella tuiarensis brucella species moraxella species miscellaneous non-fermenters spirochaetes miscellaneous gram-negative bacteria chlamydiae rickettsiae mycoplasma species mastitis food poisoning mycology - general aspects dermatophytes aspergillus species pathogenic yeasts dimorphic fungi zygomycetes miscellaneous pathogenic fungi mycotoxicoses virology viral diseases unconventional viruses (prions) kit-set tests available for virology zoonoses control of infectious diseases a systems approach to infectious diseases of domestic animals.
TL;DR: It is concluded that Legionnaires' disease is caused by a gram-negative bacterium that may be responsible for widespread infection.
Abstract: To identify the etiologic agent of Legionnaire's disease, we examined patients' serum and tissue specimens in a search for toxins, bacteria, fungi, chlamydiae, rickettsiae and viruses. From the lungs of four of six patients we isolated a gram-negative, non-acid-fast bacillus in guinea pigs. The bacillus could be transferred to yolk sacs of embryonated eggs. Classification of this organism is incomplete. We used yolk-sac cultures of the bacillus as antigen to survey suspected serum specimens, employing antihuman-globulin fluorescent antibody. When compared to controls, specimens from 101 to 111 patients meeting clinical criteria of Legionnaires' disease showed diagnostic increases in antibody titers. Diagnostic increases were also found in 54 recent sporadic cases of severe pneumonia and, retrospectively, in stored serum from most patients in two other previously unsolved outbreaks of respiratory disease. We conclude that Legionnaires' disease is caused by a gram-negative bacterium that may be responsible for widespread infection.
TL;DR: Analysis of the genome of Coxiella burnetii, Nine Mile phase I RSA493, a highly virulent zoonotic pathogen and category B bioterrorism agent, was sequenced by the random shotgun method, suggesting that the obligate intracellular lifestyle of C. burningetii may be a relatively recent innovation.
Abstract: The 1,995,275-bp genome of Coxiella burnetii, Nine Mile phase I RSA493, a highly virulent zoonotic pathogen and category B bioterrorism agent, was sequenced by the random shotgun method. This bacterium is an obligate intracellular acidophile that is highly adapted for life within the eukaryotic phagolysosome. Genome analysis revealed many genes with potential roles in adhesion, invasion, intracellular trafficking, host-cell modulation, and detoxification. A previously uncharacterized 13-member family of ankyrin repeat-containing proteins is implicated in the pathogenesis of this organism. Although the lifestyle and parasitic strategies of C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures differ considerably in terms of presence of mobile elements, extent of genome reduction, metabolic capabilities, and transporter profiles. The presence of 83 pseudogenes displays an ongoing process of gene degradation. Unlike other obligate intracellular bacteria, 32 insertion sequences are found dispersed in the chromosome, indicating some plasticity in the C. burnetii genome. These analyses suggest that the obligate intracellular lifestyle of C. burnetii may be a relatively recent innovation.
TL;DR: If IFN-gamma causes similar events to occur in vivo, then persistently infected cells could augment the pathogenesis of the chronic inflammatory sequelae that follow chlamydial infection by serving as depots of antigen capable of stimulating a sustained inflammatory response.
Abstract: An in vitro cell culture system was used to study the effect of interferon gamma (IFN-gamma) on Chlamydia trachomatis growth and differentiation. The effect of IFN-gamma on chlamydiae was dose-dependent. IFN-gamma at 2 ng/ml completely inhibited chlamydial growth and differentiation; however, persistent infection was established when chlamydiae were cultured with IFN-gamma at 0.2 ng/ml. Persistent infection was characterized by the development of noninfectious atypical chlamydial forms from which infectious progeny could be recovered only when IFN-gamma was removed from the culture system. Analysis of persistently infected cells by immunofluorescent microscopy and immunoblotting with specific antibodies revealed that the atypical chlamydial forms had near-normal levels of the 60-kDa heat shock protein, an immunopathologic antigen, and a paucity of the major outer membrane protein, a protective antigen. Furthermore, steady-state levels of other outer membrane constituents, such as the 60-kDa cysteine-rich outer membrane protein and lipopolysaccharide, were greatly reduced. If IFN-gamma causes similar events to occur in vivo, then persistently infected cells could augment the pathogenesis of the chronic inflammatory sequelae that follow chlamydial infection by serving as depots of antigen capable of stimulating a sustained inflammatory response.