micro lecture 14 Flashcards

1
Q

is Campylobacter G+ or G-

A

IT IS G-

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2
Q

list facts about Campylobacter

A

Curved, spiral or S-shaped rods

Single flagellum (motile)

Microaerophilic

Don’t ferment carbohydrates

Infect intestine (jejunun, ileum, colon)

Bacteraemia possible though rare (extremes of age, co-morbidity)

Widely distributed in nature

Fowl (major reservoir) and Mammals

Faecal / oral route transmission

Cause intestinal disease – rarely extra-intestinal

99% of infections are C. jejuni species

Linked to subsequent Guillain-Barre syndrome

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3
Q

describe the common infection caused by Campylobacter jejuni?

A

Acute enteritis:

1-7 days incubation
Self-limiting (but several weeks)
Systemic symptoms: Fever, headache, myalgia
Intestinal symptoms: cramps, diarrhoea

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4
Q

what are the prevention and treatments for Campylobacter jejuni?

A
Thorough cooking (esp BBQ chicken), 
milk pasteurisation, disinfect surfaces

Fluid and electrolyte balance often sufficient

Antibiotics if needed (start early & if severe):
erythromycin / clarithromycin (resistance?)
ciprofloxacin

3rd generation cephalosporin if very severe

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5
Q

describe the implications Shigella?

A

Shigellosis (bacterial bacillary dysentery)

Most common in young children

Non-motile, unencapsulated,
does not ferment lactose (Lac-)

Person-to-person, contaminated stools

Also: flies, food, water

Low infectious dose (10 - 200 organisms)

Invade and destroy mucosa of large intestine

Shigatoxin – enterotoxic, cytotoxic

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6
Q

list major groups of Shigella?

A

Group A: S. dysenteriae (most severe)

Group D: S. sonnei

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7
Q

Shigella causes Bacillary dysentery

what are the features of Bacillary dysentery?

A

Diarrhoea with blood, mucous and painful abdominal cramps

Severe in children and elderly

Malnourished: dehydration and death

Resolves in 1 week (if survived)

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8
Q

what is the treatment for Shigella

A

Antibiotics reduce duration and shedding

Widespread resistance

ciprofloxacin, ceftriaxone or azithromycin

Vaccine in development (NB many serotypes)

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9
Q

describe Vibrio species

A

Short, curved rod-shaped

Single polar flagellum

Facultative anaerobes

Require NaCl – waterborne organisms, so seawater / estuaries

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10
Q

describe Vibrio cholerae

A

Transmitted via food and water

No known animal reservoirs or vectors

Carriage in humans uncommon

Associated with raw seafood

Outbreaks – poor sanitation of water supplies

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11
Q

what are the implication of Vibrio cholerae

A

Severe disease occurs in about 5% of cases:

If untreated: 50% death within hrs

Treatment: <1% death

Aggressive replacement of fluid & electrolytes

Antibiotics decrease duration and shedding

Tetracyclines, macrolides, quinolones

Public health measures to reduce faecal water contamination.

WHO vaccine programme

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12
Q

what are the three species of Yersinia

A

Y. enterocolitica (enterocolitis)

Y. pseudotuberculosis (enterocolitis, despite name)

(Y. pestis – bubonic plague)

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13
Q

describe the implication of Yersinia enterocolitica

and what is used in treatment

A

Contaminated food (abattoirs, raw meat)

Lesions in ileum, enlargement of lymph nodes

Enterocolitis: fever, abdominal pain, diarrhoea, right lower quadrant tenderness
(pseudoappendicitis)
Resolves in 2-3 weeks

May → Polyarthritis, pharyngitis, septicaemia

treatment

ciprofloxacin,
trimethoprim-sulphamethoxazole

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14
Q

what are the features of Helicobacter pylori

A

Curved or spiral organisms,
closely related to Campylobacter

Multiple polar flagellae (corkscrew motility)
Produces urease (urea to ammonia, protects against acid)
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15
Q

what are the implications of Helicobacter pylori

A

World-wide distribution, very common

Person-to-person transmission

“Never” isolated from food or water

Untreated: chronic life-long condition

Colonises stomach, duodenum, oesophagus

Survives in mucus layer coating epithelium

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16
Q

how does Helicobacter pylori colonizes the colon and causes ulcer

A

Urease -> ammonia ions -> neutralises acid -> allows colonisation/multiplication

Ammonia ions
cytotoxin = low-grade destruction of mucous producing cells, exposing connective tissues to acid

17
Q

what are Helicobacter pylori tendencies ?

A

Initial infection
1 week
Gastritis, diarrhoea

Chronic
Superficial gastritis, ulcers

Risk of carcinoma, B-cell lymphoma

18
Q

what is the treatment for Helicobacter pylori?

A

Elimination requires combination therapy
Readily develops resistance,
always multiple agents
Proton pump inhibitor, amoxicillin, clarithromycin, metronidazole, …

19
Q

what are the resistance mechanisms of Gram-negative organisms?

A

β-lactamases. Multiple variants, including activity against extended-spectrum agents (3rd , 4th gen cephalosporins, carbapenems). Efficacy much increased by outer membrane “holding” the enzyme near to the drug’s site of action in the periplasmic space

(also enzymes to deactivate aminoglycosides)

Porins. Selection of porin-poor strains can limit penetration of otherwise effective drugs

Efflux pumps. Active removal from within the cell. Better to pump it right out, rather than periplasmic space

Binding site mutation (common for quinolones)