non-enteric gram-negative bacteria Flashcards
neisseria species shape
diplococci
n. gonorrhoeae
gonococci
n. meningitidis
meningococci
distinguishing structural difference between n. gonorrhoeae and n. meningitidis
polysaccharide capsule on n. meningitidis
epidemiology of n. gononorrhoeae
causes gonorrhea
transmission occurs by any form of sexual conduct
newborns may acquire an eye infection from an infected mother
virulence factors of n. gononorrhoeae (FIVE)
type iv pili - mediate attachment to non-ciliated mucosal epithelium; highly variable - protection from antibody response via antigenic variation
por protein - facilitates invasion into epithelial cells; promotes intracellular survival by preventing phagosome-lysosome fusion
opa proteins (opacity proteins) - mediates attachment to host cells
igA protease - hydrolyzes IgA, which would otherwise block bacterial attachment to the mucosal surface
beta-lactamase - hydrolyzes the beta-lactam ring in penicillin
n. gononorrhoeae pathogenesis
gonococci attach to mucosal cells
penetrate into the cells and pass thourgh within a phagosome to the subepithelial space where the infection is established.
the release of LOS stimulates TNF-alpha which causes most of the symptoms associated with the disease.
gonococci are released in a PMN-rich exudate
n. gononorrhoeae disease
nearly half of infected women are asympotmatic; major reservoir to promote the spread of infection.
most men show symptoms early
infants may become infected when passing through the birth canal of an infected mother (causes an eye infection, may lead to blindness)
n. gononorrhoeae symptoms
purulent discharge where infection resides
extended infection may result in PID and subsequent sterility
anorectal gonorrhea
pharyngitis
n. gononorrhoeae disease
disseminated infection
the bacteria move from the initial site of infection through the blood to the skin or joints
characterized by fever, arthritis, and a pustular rash with an inflamed base.
n. meningitidis epidemiology
bacteria colonize the nasopharynx of healthy people but can lead to meningitis, sepsis or bronchopneumonia
carriage in transient
person-to-person spread is through aerosolization of respiratory tract secretion
n. meningitidis virulence factors (THREE)
capsule - protects from phagocytosis
type iv pili - allows colonization of nasopharynx; highly variable
LOS - endotoxin causes inflammation and mediates most clinical manifestation
n. meningitidis pathogenesis
meningococci attach to mucosal cells (mediated by pili) and are internalized in phagocytic vacuoles
migrate to subepithelial space
the release of LOS is responsible for the diffuse vascular damage (inflammation)
n. meningitidis disease
meningitis, meningococcemia, pneumonia
eikenella corrodens epidemiology/disease
colonize the human orpharynx
opportunistic pathogen - causes oral infections in the immunocompromised or those who have oral trauma (mostly seen causing disease following trauma to the mouth or bite wounds)
pseudomonas aeruginosa epidemiology
opportunist pathogen
ubiquitous in nature and environmental sites within a hospital; can transiently colonize the respiratory tract and GI tract of healthy or hospitalized patients
pseudomonas aeruginosa virulence factors (FIVE)
adhesins - flagella, type iv pili, alginate capsule
alginate capsule - mucoid polysaccharide capsule that protects from phagocytosis and antibiotics
type III secretion system - allows bacteria to inject toxins into the host cell
exotoxin A - disrupts protein synthesis in host cells; leads to hemorrhagic lesions (ecthyma gangrenosum) associated with disseminated infections
inherently antibiotic resistant - mutation of bacterial porin proteins prevents uptake of antibiotics; beta-lactamase production
pseudomonas aeruginosa pathogenesis
the bacteria generally gain access to a host via inhalation, but since the organism is ubiquitous, it may gain access through other routes
pseudomonas aeruginosa disease
can infect respiratory tract, urinary tract, skin and soft tissues, ears, eyes, blood (bacteremia), and heart (endocarditis)
pulmonary infections - colonization is typically seen in patients with chronic lung disease or cystic fibrosis
in CF patients, following colonization P. aeruginosa mutates into a mucoid variant (forms am alginate matrix) in the CF lung; once this happens patients have poor prognosis
skin and soft tissue infection - burn wounds and folliculitis
finer nail infections
UTIs
ear infection
eye infections
bacteremia - tends to occur in immunocompromosied patients
Haemophilus influenzae epidemiology
H. influenzae serotype b is most virulent
since introduction of Hib vaccine, most H. influenzae infections in the US are caused by the nonencapsulated (non-typeable) strains
H. influenzae virulence factors
type iv pili and nonpilus adhesins - allow for colonization of the nasopharynx
capsule - antiphagocytic, contains polyribitol phosphate (PRP)
igA proteases - hydrolyze IgA, which would otherwise block bacterial attachment to the mucosal surface
H. influenzae pathogenesis
the illness begins as a mild upper respiratory tract disease; indiseeminated disease the bacteria translocate from the nasopharynx across epithelial and endothelial cells where they gain access to the bloodstream
H. influenzae disease
nonencapsulated: spread locally - ears, insuses, lower respiratory tracts; disseminated disease is uncommon
encapsulated - disseminate and cause meningitis, epiglottis, cellulitis, pneumonia; primarily seen in unvaccinated people
aggregatibacter species
part of the normal oral microbiotia; a. actinomycetemcomitans and a. aphrophilus are opportunistic humsn pathogens
aggregatibacter species virulence (TWO)
leukotoxin - contributes to the killing of neutrophils and monocytes
fimbriae - attachment to various types of host cells
aggregatibacter species disease
both pathogens colonize the human mouth and are capable of participating in biofilm formations on the surface of the teeth
once the bacteria gain access to the periodontal space, disease may occur - these species are a primary cause of localized aggressive periodontitis
if either is able to penetrate through the tissues into the bloodstream, systemic infection may result - the bacteria are able to attach to damaged or artificial heart valves leading to endocarditis
Bordetella pertussis and Bordetella papapertussis disease
cause pertussis (whooping cough) in human
Bordetella species epidemiology
the mucous membranes of the human respiratory tract is the natural habitat for B. pertussis and B. parapertussis
Bordetella species virulence factors (THREE)
fibrriae - allows bacteria to bind to various host cells
pertussis toxin (only B. pertuss) - impacts cell signaling with the host cell; inhibits phagocyte killing and monocyte migration
tracheal cytotoxin - kills respiratory cells
Bordetella species pathogenesis
bacteria are inhaled, attach to the ciliated epithelial cells of the respiratory tract; in this location, the bacteria proliferate and secrete virulence factors that result in tissue damage
Bordetella species disease stages
catarrhal stage - resembles the common cold - most contagious at this stage
paroxysmal stage - repetitive coughs followed by whoops during inhalation
convalescence stage - coughing attacks gradually subside
