Felton Bugs

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Streptococcus pneumoniae: basic

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1. diplococci
2. the most common cause of community-acquired pneumonia
3. common inhabitant of the throat and nasopharynx of healthy individuals
4. Gram-positive lancet-shaped diplococcus
5. alpha-hemolytic.
6. both smooth (encapsulated) and rough (non-encapsulated) varieties.
7. fermentative and produces lactic acid.
8. facultative; do not use oxygen during aerobic growth

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pneumococcus diagnostics

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1. Optochin sensitivity: Paper disks (P disks) impregnated with optochin; grows up a zone of inhibition (no bacterial growth and no hemolysis)
2. Bile solubility; presence of an autolytic enzyme in the cell wall of pneumococci;
a. pneumococcus the suspension will become clear,
b. viridans streptococcus it will remain turbid.

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pneumococcus: Surface Antigens

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1. Capsular Polysaccharides; capsule is the most important virulence factor of the pneumococcus; allows them to avoid phagocytosis by PMN's.
2. Non-encapsulated (rough) strains are non-virulent.
3. Homologous antibodies against capsular polysaccharide will opsonize pneumococci and render them sensitive to phagocytosis; anticapsular antibodies are protective against infection and are essential for recovery from pneumococcal infection.

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pneumococcus: Extracellular Products

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1. Pneumolysin. Pneumococci produce a hemolysin, pneumolysin O.
2. Purpura-producing principle: substance causes purpura and dermal hemorrhage in experimental animals; derived from the cell wall peptidoglycan.
3. Lipoteichoic Acid. LTA activates complement and induces inflammatory cytokine production by activating Toll-like receptors. (TLR-2)
4. IgA protease; cleaves secretory immunoglobulin IgA at the hinge region,
preparing it for further degradation by other proteases
5. Amidase; autolysin produced by S. pneumoniae. When the cell lyses it releases components that induce inflammation

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Legionella himophila: basic

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1. Gram-negative rod
2. Most species of Legionella are motile.
3. Spores are not found.
4. thin peptidoglycan layer, and cytoplasmic membrane; toxicity of its lipopolysaccharide (LPS) is significantly less than that of other Gram-negative bacteria
5. original Philadelphia strain (serogroup 1) is still the most common, and a limited number of serogroups (1 to 4) account for 80% to 90% of cases.

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Legionella (Pathogenesis and epidemiology) part 1

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1. inhaled when aerosols are created in manmade water supplies that harbor the organism in the environment
2. necrotizing multifocal pneumonia marked by headache, fever, chills, dry cough, and chest pain
3. affect the alveoli and terminal bronchioles; (image) the filling of alveoli with exudate. Some of the alveolar septa are starting to degenerate.
4. facultative intracellular pathogen; ability to survive and multiply within cells of the monocyte–macrophage series (alveolar macrophage)
5. aided by pili and outer membrane proteins (OMP), which bind complement components. Another OMP called macrophage invasion potentiator (Mip)

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Legionella pathophysiology part 2

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1. Inside the vacuole, the bacteria continue to replicate by
a. preventing phagosome-lysosome fusion and
b. avoiding the destructive acidification and enzymatic digestion found there.
2. Legionella-containing endosome recruits secretory vesicles from the endoplasmic reticulum (ER) remodeling it into rough ER.
3. use of a system that secretes proteins able to modulate host cell vesicle traffic and prevent transport into the lysosome.
4. ability to extract iron from transferrin and a peptide toxin that inhibits activation of the oxidative killing mechanisms of phagocytes; instead of being killed by the bactericidal mechanisms of phagocytes, L pneumophila multiplies freely
5. Induction of apoptosis and formation of a pore-forming toxin eventually lead to death of the macrophage; releases a new population of Legionella cells; repeat cycle
6. The multiple degradative enzymes released in this process lead to destructive lesions in the lung and a systemic toxicity that may be related to cytokine release.

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Legionella (Immunity)

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1. The high level of innate immunity to Legionella infection; brisk pattern recognition responses triggered by toll-like receptors (TLRs) in macrophages and dendritic cells.
2. These include TLRs that recognize foreign molecular patterns associated with bacteria in general (lipopolysaccharide, peptidoglycan, and others) and may also include a TLR located in endocytotic vesicles that recognizes patterns found in intracellular pathogens including viruses and some fungi
3. activation of the TH1 adaptive immune response and its associated cytokines (interferon, IL-12, IL-18) completes the process of macrophage activation and intracellular killing of the invading Legionella; Failure of this aspect of the immune response is the primary reason for most cases of progressive Legionnaires disease in the immunocompromised

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Legionella diagnostics

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1. stained with direct fluorescent antibody (DFA) and high-quality specimens such as lung aspirates, bronchoalveolar lavage, or biopsies are preferred;
2. organism may not be found in sputum.
3. (PCR) have proved to be rapid and much more sensitive than DFA.
4. A simple card-based antigenuria detection test has also proved to be sensitive for the most common L. pneumophila serogroup 1, but less so for other serogroups and Legionella species.

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Legionella TX and prevention

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1. azithromycin, respiratory fluoroquinolones
2. The prevention of legionellosis involves minimizing production of aerosols in public places from water that may be contaminated with Legionella.

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Influenza - viridae

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1. Family orthomyxoviridae
2. negative sense ss RNA viruses (Baltimore Class V).
3. RNA alone is not infectious. Capsid core contains an RNA-dependent RNA polymerase called RNA transcriptase to make + strand RNA messenger from the – ssRNA genome.
4. segmented, meaning they have multiple strands of the genome- in this case, 8 segment

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Influenza outer membranes

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1. helical nucleocapsids surrounding the RNA segments with a lipid envelope added at the cell membrane;
2. outer surface of the envelope has glycoprotein spikes-one kind being hemagglutinin (H), and the other neuraminidase (N).
3. Early synthesis of viral messenger RNA takes place in the nucleus; needs host cell factors as a primer for replication.
a. hemagglutinin spikes; attachment of the virus to the cell and infection of the cell.
b. neuraminidase spikes; enzymes which help free the newly synthesized virus from the cells.

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Members causing infection in man

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1. Influenza types A, B, and C, cause acute respiratory disease.
2. Route of infection is via aerosol droplets, (90% attack rate in close quarters).
3. Virus replicates in superficial respiratory cells, and destroys the ciliated columnar epithelium in the bronchi.
4. There are three major human influenza A hemagglutinins (H1, H2, and H3) and two neuraminidase (N1 and N2)

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Mechanisms for Variations in influenza viruses

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1. Antigenic drift- due to chance mutations, result in minor changes in the virus.
2. Antigenic shift- reassortment between strains, results in major changes in surface antigens, and may cause severe pandemics; source; to be birds, especially ducks.
a. pig supports the replication of both human and avian influenza viruses; nascent nucleocapsids are packed and bud from the cellular membrane, some avian and some human segments will be incorporated; varying percent of segments coming from avian or human viruses.

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Corynebacterium diphtheriae

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1. Gram-positive rod-shaped bacteria that resides in the pharynx and spread via respiratory droplets.
2. systemic illness by production of a protein exotoxin that spreads via the circulation
3. obligate aerobes, non-motile, and grow in clusters

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Diphtheria toxin (DT)

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1. key virulence factor; gene encoding DT is located on the genome of a lysogenic bacteriophage that is integrated into the bacterial chromosome (lysogenic conversion).
2. DT has two subunits, A and B, which stand for Active and Binding. The B subunit binds to its receptor on the target cell membrane and delivers the A subunit across the membrane into the cytoplasm.
3. The A subunit becomes an enzymatically active ADP ribosyltransferase which consumes NAD and transfers ADP ribose onto an essential component of the protein synthesis machinery; inhibiting protein synthesis and killing the intoxicated cell.
4. Local damage to the pharyngeal mucosa causes formation of a grayish pseudomembrane that is characteristic of diphtheria and may cause suffocation.

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Coccidioidomycosis: basic

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1. from inhaling the spores (arthroconidia) of the dimorphic, soil-dwelling fungi, Coccidioides
2. organisms exist as filamentous moulds; individual filaments (hyphae) elongate and branch, some growing upward
3. Alternating cells within the hyphae degenerate, leaving barrel-shaped viable elements called arthroconidia;may become airborne for extended periods; small size allows them to evade initial mechanical mucosal defenses and reach deep into the bronchial tree, where infection is initiated in the nonimmune host.

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Coccidioidomycosis: life cycle

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1. Once in a susceptible host, the arthroconidia enlarge, become rounded, and develop internal septations; spherules
2. The septations encompass uninuclear elements called endospores. Spherules may rupture and release packets of endospores that can themselves develop into spherules, thus propagating infection locally.

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Coccidioidomycosis: Host Immune Response

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1 Necrotizing granulomas containing spherules are typically identified in patients with resolved pulmonary infection.
2. polymorphonuclear leukocyte response occurs frequently
3. asymptomatic pts or in whom the initial pulmonary infection resolves, delayed-type hypersensitivity
4. most common clinical presentation is a self- limited acute or subacute community-acquired pneumonia that becomes evident 1–3 weeks after infection.
5. For such patients, symptoms—especially fatigue interfering with normal activities—may last for weeks to many months.

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Coccidioidomycosis: diagnosis

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1. Serology: Several techniques are available
2. Rising complement-fixation (CF) titers are associated with clinical progression, and the presence of CF antibody in CSF is an indicator for coccidioidal meningitis. Antibodies disappear over time in persons whose clinical illness resolves.
3. always useful to obtain samples of sputum or other respiratory fluids and tissues for culture in suspected cases. The clinical laboratory should be alerted to the possibility of this diagnosis, since Coccidioides can pose a significant hazard to laboratory workers if it is inadvertently inhaled.

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Coccidioidomycosis: TX

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1. patients with localized acute pulmonary infections and no risk factors for complications; only periodic reassessment to demonstrate resolution of their self-limited process.
2. patients with extensive spread of infection or are at high risk of complications because of immunosuppression or other preexisting factors; antifungal drug therapy, surgical debridement, or a combination of both.
3. Azoles (fluconazole and itraconazole) have replaced amphotericin B (AMB) as initial therapy for most chronic pulmonary or disseminated infections.
4. AMB is now usually reserved for patients with respiratory failure due to coccidioidomycosis, those with rapidly progressive coccidioidal infections, or women during pregnancy.