HACEK Pathogens Flashcards

1
Q

What are the HACEK pathogens?

A

Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella

Normal part of the oral-pharyngeal microbiota

Most common gram-negative cause of endocarditis among people who do not use IV drugs

Treatment choice is cephalosporin and ceftriaxone

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2
Q

Describe Haemophilus Influenzae

A

Colonizes URT in the first few months of life

Requires blood factors for growth

Capsulated or Uncapsulated

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3
Q

Which strains of H. influenzae cause mucosal surface infections?

A

Uncapsulated or non-typable

Localized infections
OM, sinusitis, bronchitis and pneumonia

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4
Q

Which strains of H. influenzae cause invasive disease?

A

Encapsulated strains - composed of polyribitol phosphate (PRP)

Can express one of six polysaccharide capsules

H. influenzae type B acocunts for 95% of all strains that cause invasive disease

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5
Q

How does H. influenzae overcome nonspecific mucociliary defenses?

A

OMP P2 and P5 promote binding to mucous

LPS - damages ciliated cells

Adhesins and Pili

IgA proteases

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6
Q

How do uncapsulated strains of H. influenzae cause disease?

A

Direct movement of organisms to the site of infection.

E.g. sinuses, eustachian tubes, bronchi

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7
Q

How is H. influenzae transmitted?

A

Person to person through respiratory droplets

Children 6-18 months are highest risk

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8
Q

How is a H. influenzae infection diagnosed?

A

Blood culture in children with suspected disease

CSF, pleural fluid, and sputum cultures

Gram stain - gram negative

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9
Q

What is H. influenzae treated with?

A

Third generation cephalosporins

Conjugated PROP vaccine

Antibiotic prophylaxis for close contacts with rifampin

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10
Q

What are the three general mechanisms of antibiotic resistance?

A

Decreased entry

Altered target

Destroy antibiotic

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11
Q

What is the major mechanism of antibiotic resistance in gram-negative pathogens?

A

B-Lactamases

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12
Q

What are the main types of B-lactamases?

A

Penicillinases

Extended-spectrum B-lactamases - inactivates most except carbapenems

Carbapenemases

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13
Q

What are three characteristics of all Clostridium?

A

Spore forming

Obligate anaerobes

Form toxins

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14
Q

What is the mechanism of C. tetani toxin?

A

Travels to spinal cord and blocks glycine and GABA release by inhibitor neurons

Acts on Renshaw cells

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15
Q

What are the symptoms of C. tetani infection?

A

Spasm, muscle contraction, rigidity

Classic: Lockjaw, Risus sardonicus (forced grin)

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16
Q

What is the treatment for C. tetani?

A

Wound debridement

Metronidazole

Tetanus immune globulin

Benzos or NM blockers until toxin wears off

17
Q

What is the mechanism of Botulinum toxin?

A

Works at NMJ

Prevents ACh release, inhibiting muscle contraction

Results in flaccid paralysis

18
Q

What are the three types of botulism?

A

Food - toxin ingestion, undercooked food

Infant - spores, growth in infant intestine (contaminated honey)

Wound - infection with C. botulinum

19
Q

How does Botulism present?

A

Symptoms appear 12-48hrs after ingestion

3 D’s: Diplopia, dysphagia, dysphonia

20
Q

What is the treatment for botulism?

A

Antitoxin to block circulating toxin

Can’t block toxin already in nerves

Supportive care, toxin washout

21
Q

What is C. perferingens?

A

Widespread in nature/soil

Infects dirty wounds and causes food poisoning

Causes gas gangrene (clostridial myonecrosis)

Traumatic wound with vascular compromise

22
Q

What is alpha toxin?

A

Produced by C. perferingens

Destroys muscle tissue and causes hemolysis

Phospholipase that acts on lecithin and degrades cell membrane

23
Q

What is myonecrosis?

A

Necrotizing infection of muscle

Most often due to C. perfringens, C. speticum, C. histolyticum or C. sordellii

Usually associated with local trauma

Gas is always found in the skin

24
Q

How does myonecrosis present?

A

Severe pain at injury site within 24hrs

Skin tense and tender, fever, hypotension, shock

Diagnosis: gas at injury site on imaging, crepitus

Treatment: Surgical debridement plus BS antibiotics

25
What differentiates food poisoning by C. perferingens and S. aureus/B. cereus?
Ingested spores of C. perferingens produce toxin, causing late onset (8-22 hours) S. aureus has preformed toxin, early onset
26
What is C. difficile?
Ubiquitous spores in nature Ingestion not harmful with normal GI flora Causes antibiotic-associated colitis - antibiotics alter normal gut flora Non invasive disease via toxin
27
What two toxins are produced by C. diff?
Toxin A - enterotoxin, watery diarrhea Toxin B - Cytotoxin, cell necrosis/fibrin deposition Both bind to GI cells and are internalized
28
What is the presentation, diagnosis, and treatment for C. diff colitis?
Massive watery diarrhea Stool detection of toxin A and B Treat with metronidazole and oral vancomycin
29
What is Listeria?
Found in soil Facultative intracellular organism Move from cell to cell to avoid extracellular response In adults, from contaminated food In neonates, transplacental or vaginal transmission
30
What does Listeria cause?
Gastroenteritis - usually self limited Meningitis - elderly or newborns Infection in pregnancy causes bacteremia in 3rd trimester
31
What is granulomatosis infantiseptica?
Severe in utero infection from Listeria Disseminated abscesses and/or granulomas Multiple organs affected Most babies stillborn or dies soon after birth