non-enteric gram-negative bacteria Flashcards

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1
Q

neisseria species shape

A

diplococci

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2
Q

n. gonorrhoeae

A

gonococci

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3
Q

n. meningitidis

A

meningococci

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4
Q

distinguishing structural difference between n. gonorrhoeae and n. meningitidis

A

polysaccharide capsule on n. meningitidis

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5
Q

epidemiology of n. gononorrhoeae

A

causes gonorrhea
transmission occurs by any form of sexual conduct
newborns may acquire an eye infection from an infected mother

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6
Q

virulence factors of n. gononorrhoeae (FIVE)

A

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

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7
Q

n. gononorrhoeae pathogenesis

A

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

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8
Q

n. gononorrhoeae disease

A

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)

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9
Q

n. gononorrhoeae symptoms

A

purulent discharge where infection resides

extended infection may result in PID and subsequent sterility

anorectal gonorrhea

pharyngitis

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10
Q

n. gononorrhoeae disease

A

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.

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11
Q

n. meningitidis epidemiology

A

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

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12
Q

n. meningitidis virulence factors (THREE)

A

capsule - protects from phagocytosis

type iv pili - allows colonization of nasopharynx; highly variable

LOS - endotoxin causes inflammation and mediates most clinical manifestation

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13
Q

n. meningitidis pathogenesis

A

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)

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14
Q

n. meningitidis disease

A

meningitis, meningococcemia, pneumonia

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15
Q

eikenella corrodens epidemiology/disease

A

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)

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16
Q

pseudomonas aeruginosa epidemiology

A

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

17
Q

pseudomonas aeruginosa virulence factors (FIVE)

A

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

18
Q

pseudomonas aeruginosa pathogenesis

A

the bacteria generally gain access to a host via inhalation, but since the organism is ubiquitous, it may gain access through other routes

19
Q

pseudomonas aeruginosa disease

A

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

20
Q

Haemophilus influenzae epidemiology

A

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

21
Q

H. influenzae virulence factors

A

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

22
Q

H. influenzae pathogenesis

A

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

23
Q

H. influenzae disease

A

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

24
Q

aggregatibacter species

A

part of the normal oral microbiotia; a. actinomycetemcomitans and a. aphrophilus are opportunistic humsn pathogens

25
Q

aggregatibacter species virulence (TWO)

A

leukotoxin - contributes to the killing of neutrophils and monocytes

fimbriae - attachment to various types of host cells

26
Q

aggregatibacter species disease

A

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

27
Q

Bordetella pertussis and Bordetella papapertussis disease

A

cause pertussis (whooping cough) in human

28
Q

Bordetella species epidemiology

A

the mucous membranes of the human respiratory tract is the natural habitat for B. pertussis and B. parapertussis

29
Q

Bordetella species virulence factors (THREE)

A

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

30
Q

Bordetella species pathogenesis

A

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

31
Q

Bordetella species disease stages

A

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