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Bacteriology
Pathogen parade
| Term | Definition |
|---|---|
| The structural and biological characteristics of N. meningitidis. | Non-motile, Gram-negative diplococci with fastidious growth requirements and a polysaccharide capsule |
| N. meningitidis Diseases | Meningococcal Meningitis; occasionally septicaemia in absence of meningitis |
| N. meningitidis transmission | From person-to-person through droplets of respiratory or throat secretions, such as kissing, sneezing or coughing on someone and sharing eating or drinking utensils with infected person. |
| N. meningitidis important virulence factors. | The polysaccharide capsule is antiphagocytic; Endotoxin, IgA protease, Pili and outer membrane proteins are also implicated. |
| N. meningitidis cell/tissue tropism | Epithelial cells in the human pharynx |
| N. meningitidis replication (intra and/or extracellular) | Intracellular |
| N. meningitidis immune escape mechanism(s) | Sialic acid polysaccharide antigen in their LOS, allows evasion of complement since bacteria coated with sialic acid mimics the host cell surface. They also secrete IgA protease, they are intracellular and the polysaccharide capsule is antiphagocytic |
| N. meningitidis antibiotic resistance and transmission | There is very little antibiotic resistance, there is no current concern |
| N.meningitidis treatment and prevention strategies (vaccine available?) | Treatment are Penicillin and Chloramphenicol or cephalosporin (penicillin allergies). "Kissing contacts use Rifampicin prophylaxis. Tetravalent vaccine available (types A, C, Y, W135), but NOT for type B. |
| N. meningitidis pathogenesis | The bacteria attach to and multiply in epithelial cells of the nasopharynx, then penetrates the mucosal cells and enters the bloodstream. The organism crosses the blood–brain barrier into the cerebrospinal fluid and causes purulent meningitis |
| The structural and biological characteristics of N. gonorrhoeae. | Gram-negative, aerobic, non-motile, non-spore-forming diplococcus and NO capsule |
| N. gonorrhoeae Diseases | Gonorrhoea; urethritis (males), Cervicitis, Pelvic Inflammatory Disease, infertility (females)and ophthalmia neonatorum in infected infants |
| N. gonorrhoeae transmission | Transmission is by sexual contact (anal, vaginal, and oral sex) or through vertical transmission |
| N. gonorrhoeae important virulence factors (7). | Pilus, Por proteins, Opa proteins, LOS, Rmp proteins, IgA protease and capsule. |
| N. gonorrhoeae cell/tissue tropism | N. gonorrhoeae may be carried in genital tract, nasopharynx and anus. |
| N. gonorrhoeae replication (intra and/or extracellular) | They replicate intracellularly, inside endocytic vesicles |
| N. gonorrhoeae antibiotic resistance and transmission | Tetracycline, penicillin and fluoroquinolones acquired by spontaneous chromosomal mutations, plasmid-mediated transfer or DNA transformation and recombination |
| N.gonorrhoeae treatment and prevention strategies (vaccine available?) | Treated for Gonorrhoea and Chlamydia. Antibiotics are: ceftriaxone (cyclosporins)and doxycline (tetracyclin) Prevention: No vaccine and prophylactic use of antibiotics does not help |
| N. gonorrhoeae pathogenesis | N.gonorrhoeae does not produce exotoxin, thus damage to the host results from inflammatory responses elecited by the organism (e.g. LOS) |
| N. gonorrhoeae immune escape mechanism(s) | It has a capsule, antigenic variation of pilus, LOS and Opa, produces IgA protease and attaches sialic acid to its LOS to inhibit complement activation. |
| Streptococcus pneumoniae treatment and prevention strategies (vaccine available?) | Penicillin remains the antibiotic of choice. Heptavalent protein conjugate pneumococcal vaccine for children from 2-23 months of age and 24-59 months at high risk. 23-valent polysaccharide vaccine is available for children older than 5 years of age |
| Streptococcus pneumoniae antibiotic resistance and transmission | Resistance primarily against beta-lactams (penicillin) and macrolides. Mutant strains must arise, that have mutations on one or more genes that express the PBPs and alteres the target site |
| Streptococcus pneumoniae replication (intra and/or extracellular) | replicates outside of cells |
| Streptococcus pneumoniae cell/tissue tropism | Normal habitat is the human respiratory tract; Human Nasopharyngeal Epithelial Cells |
| Streptococcus pneumoniae pathogenesis and important virulence factors | It has two: polysaccharide capsule and IgA protease |
| Streptococcus pneumoniae transmission | Normal habitat is the human respiratory tract; ca. 5% of population may carry in small numbers. Transmission via droplet spread. |
| Streptococcus pneumoniae immune escape mechanism(s) | Capsule protects the organism from phagocytosis and IgA protease degrade IgA |
| The structural and biological characteristics of Streptococcus pneumoniae | Gram-positive diplococcus, non-spore-forming, non-motile, capsulated; capable of aerobic and anaerobic respiration |
| Streptococcus pneumoniae Diseases | Pneumococcal meningitis |
| Staphylococcus aureus Diseases | Boils; skin sepsis; postoperative wound infection; scalded skin syndrome; catheter-associated infection; food-borne infection; septicaemia, endocarditis; toxic shock syndrome; osteomyelitis; pneumonia |
| Staphylococcus aureus pathogenesis | pathogenesis is multifactorial, so it is difficult to determine precisely the role of any given factor. |
| The structural and biological characteristics of Staphylococcus aureus | Gram-positive coccus; Some strains produce capsules. Non-fastidious; capable of aerobic and anaerobic respiration; |
| Staphylococcus aureus immune escape mechanism(s) | protein A interacts with IgG opsonization; PV Leukocine causes pore formation in leukocytes; coagulase clots plasma and coats bacterial cell with fibrin to prevent phagocytosis; |
| Staphylococcus aureus transmission | Spread is by contact and airborne routes. Organism survives drying; tolerant of salt and nitrites. |
| Staphylococcus aureus important virulence factors | All strains: mucopeptide and coagulase. Some strains: capsule, protein A, enterotoxins (protein exotoxin), leukocidin (PVL) |
| Staphylococcus aureus cell/tissue tropism | Normal habitat: humans (and animals associated with them); skin, especially nose and perineum (carriage rates higher in hospital patients and staff) |
| Staphylococcus aureus replication (intra and/or extracellular) | intracellular |
| Staphylococcus aureus antibiotic resistance and transmission | Resistant against Beta-lactams, vancomycin (plasmid-mediated), methicillin. S aureus develop drug resistance: mutation in chromosomal genes and acquisition of resistance genes as plasmids, transducing particles, transposons |
| Staphylococcus aureus treatment and prevention strategies (vaccine available?) | In susceptible isolates, antibiotics of choice are penicillins; Mupirocin can be used for topical treatment of carriage. Prevention of spread by isolation and/or treatment of carriers in high-risk areas in hospital. No vaccine available. |
| Staphylococcus Epidermidis treatment and prevention strategies (vaccine available?) | Treatment: remove or replace the infected implant; drug of choice is often vancomycin, to which rifampin or aminoglycoside can be added. Prevention: catheter care; no vaccine available. |
| Staphylococcus Epidermidis antibiotic resistance and transmission | Often multiresistant,including penicillin and methicillin. |
| Staphylococcus Epidermidis replication (intra and/or extracellular) | intracellular |
| Staphylococcus Epidermidis cell/tissue tropism | Normal habitat: skin |
| Staphylococcus Epidermidis pathogenesis and important virulence factors | The organism produces slime layers, which forms a hydrophobic biofilm on plastic implants allows other bacteria to colonize, creating a multilayer biofilm |
| Staphylococcus Epidermidis transmission | Spread by contact with self, other patients or hospital personnel. Almost all infections acquired in hospital, but may be endogenous. Survives drying; salt tolerant. |
| Staphylococcus Epidermidis immune escape mechanism(s) | ------- |
| The structural and biological characteristics of Staphylococcus Epidermidis | Gram-positive coccus; Some strains produce capsules. Non-fastidious; capable of aerobic and anaerobic respiration; |
| Staphylococcus Epidermidis Diseases | Opportunist pathogen associated with device-related sepsis (e.g. catheter-related sepsis; prosthetic valve endocarditis; infection of artificial joints; shunt infections); urinary tract infection; sternal wound osteomyelitis. |
Created by:
Beantha
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