Microbiology: Gram Negative Cocci Flashcards Preview

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Flashcards in Microbiology: Gram Negative Cocci Deck (13):
1

Niesseria Gonorrhoeae

-Aerobic diplococci (in pairs) that are oxidase and catalase positive
-Produces acids by oxidation of glc
-Grows on chocolate agar, but not blood agar, dry conditions, or FAs
-Pili mediate attachment to cells, transfer of genetic material, and mobility (all pathogenic, virulence factor)

2

Pathogenesis of N gonorrhoeae

-Acquired by sexual contact (obligate human pathogen), infects sub-epithelial cells in mucous membranes of urethra in men and endocervix in women
-Pili, PorB, Opa, LOS (lipo-oligosaccharide, endotoxin) stimulate IgG3 production and facilitate penetration and binding (except LOS, instead stimulates inflammation/TNF-a release)
-Can avoid degradation if internalized
-Meningococcal disease occurs in absence of specific Abs directed against the capsule
-High prevalence, low mortality rates (can lead to corneal scarring)
-Both genders experience purulent discharge from genitals, dysuria
-Organism cannot infect squamous epithelial vagnial cells in post-pubescents
-Females may develop ascending genital infections (salpnigitis, tubovarian abscesses, pelvic inflammatory disease)

3

Gonococcemia

-Gonococcal bacteremia leads to disseminated gonococcal infections
-Often affects skin and joints, can cause numerous untreated asymptomatic infections
-Manifestations are fever, migratory arthralgias, arthritis, purulent rash/skin lesions
-Peri-hepatitis, pharyngitis
-Purulent conjunctivitis may affect newborns especially during delivery
-Anorectal gonnorhea in homosexual men

4

Epidemiology of Gonorrhoeae

-Only occurs in humans (no reservoir except asymptomatic infected persons)
-Most men are initially symptomatic, half of women have mild or asymptomatic infections
-2nd most common STI after clap, higher rates in poorer regions, in black people, and people w/ multiple sexual encounters
-Women at 50% risk on exposure, men at 20% risk on exposure
-Symptoms may clear in a few weeks and asymptomatic carrier can be established

5

Diagnosis of Gonorrhoeae

-Gram stain is sensitive for testing purulent exudates
-Must be confirmed by culture of exudate (chocolate agar, selective media) that contains cysteine and energy source (glc, lac, pyr)
-Use selective media and non-selective media since vancomycin in selective media kills some strains of gonorrhoeae
-Blood cultures only effect during 1st week of gonococcemia
-Oxidase positive, definitive identification guided by pattern of oxidation of carbs (glc)

6

Treatment of Gonorrhoaea

-Penicillin not used due to B-lactamase, PBP2, cell wall changes
-Now also resistant to tetracycline, erythromycin, aminoglycosides
-Some are resistant to fluoroquinolones and ciprofloxacin
-Tx is combination of ceftriaxone or ciprofloxacin plus doxycycline
-No vaccine available, prophylaxis for exposed adults and newborns available. Condoms too

7

Neisseria meningitidis

-Aerobic diplococci, oxidase and catalase positive
-Acids produced by oxidation of glc and maltose
-Pili mediate attachment to cells, transfer of genetic material, and mobility (all pathogenic, virulence factor)
-2nd most common cause of community-acquired meningitis in adults, can cause fatal sepsis and bronchopneumonia
-12 serogroups based on Ag differences of capsules
-Por B interferes w/ degranulation of neutrophils, LOS has endotoxin activity
-Fe is essential for growth/metabolism

8

Pathogenesis of meningitidis

-Infection by aspiration of infective particles, which attach to epithelial cells of mucosal surfaces and enter bloodstream (usually through naso/oropharyngeal)
-Blood borne bacteria may enter CNS if not treated
-Are internalized by phagocytosis and avoid intracellular death (via capsule), replicate, and migrate to sub-endothelial spaces causing diffuse vascular damage from LOS endotoxin
-Can only infect patients who lack Abs against capsule or non-capsular Ags, or patients that have late-acting complement)
-low prevalence but high mortality, begins often w/ skin lesions (small to larger ones)

9

Meningococcemia

-With or without meningitis is life-threatening
-causes thrombosis of small vessels and multi-organ involvement, bilateral destruction of adrenal glands
-May present as chills, fever, malaise, headaches
-Milder and chronic form can occur: fever, arthritis, skin lesions
-Possible pneumonia, is usually preceded by resp. tract infections. Symptoms are cough, chest pain, rales, fever

10

Acute bacterial meningitis

-Abrupt headache, meningeal signs (cervical rigidity, thoracolumbar rigidity hamstring spasm, exaggerated reflexes), fever
-High mortality untreated, low mortality treated
-Incidence of neuologic sequelae is low (just hearing deficits and/or arthritis
-Children may show non-specific signs such as fever and vomiting

11

Epidemiology of meningitidis

-Humans are only carriers
-Almost all infections caused by serogroups A, B, C, Y, and W135 (Y and W135 most associated w/ pneumonia)
-Serogroups B, C, and Y in Europe and America
-Serogroups A and W135 in developing countries
-Transmitted by respiratory droplets, higher rates in low SES (socioeconomic setting) populations
-Asymptomatic carrier occurs from 1-40%. Oro/nasopharyngeal carriers common in children
-Most outbreaks caused by A, sporadic cases by B, C, and Y

12

Diagnosis of meningitidis

-Most characteristic symptom is skin rash (usually petechiae lesion)
-Once septic the bacteria can be seen in WBCs from blood samples when gram stained
-Culture methods: it is inhibited by toxic factors in media, anticoagulants in blood
-Oxidative positive diplococci that grows on chocolate agar or selective media
-Definitive ID from pattern of oxidation of carbs

13

Tx of meningitidis

-Susceptible to penicillin (occasional low levels of resistant)
-If patient can't take penicillin, cephalosporin or chlormamphenicol are recommended
-Prevention includes prophylaxis by antibios
-Conjugate vaccine is available for children
-Group B has weak immunogen and doesn't provide immunity response (no vaccine has B parts)
-Vaccination w/ suspension of serogroup A can be used to control outbreaks and for those at risk of getting the disease (complement deficiency)