Microbiology: Gram Negative Cocci Flashcards
1
Q
Niesseria Gonorrhoeae
A
- 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
Q
Pathogenesis of N gonorrhoeae
A
- 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
Q
Gonococcemia
A
- 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
Q
Epidemiology of Gonorrhoeae
A
- 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
Q
Diagnosis of Gonorrhoeae
A
- 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
Q
Treatment of Gonorrhoaea
A
- 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
Q
Neisseria meningitidis
A
- 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
Q
Pathogenesis of meningitidis
A
- 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
Q
Meningococcemia
A
- 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
Q
Acute bacterial meningitis
A
- 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
Q
Epidemiology of meningitidis
A
- 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
Q
Diagnosis of meningitidis
A
- 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
Q
Tx of meningitidis
A
- 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)