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
Q

What differentiates food poisoning by C. perferingens and S. aureus/B. cereus?

A

Ingested spores of C. perferingens produce toxin, causing late onset (8-22 hours)

S. aureus has preformed toxin, early onset

26
Q

What is C. difficile?

A

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
Q

What two toxins are produced by C. diff?

A

Toxin A - enterotoxin, watery diarrhea

Toxin B - Cytotoxin, cell necrosis/fibrin deposition

Both bind to GI cells and are internalized

28
Q

What is the presentation, diagnosis, and treatment for C. diff colitis?

A

Massive watery diarrhea

Stool detection of toxin A and B

Treat with metronidazole and oral vancomycin

29
Q

What is Listeria?

A

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
Q

What does Listeria cause?

A

Gastroenteritis - usually self limited

Meningitis - elderly or newborns

Infection in pregnancy causes bacteremia in 3rd trimester

31
Q

What is granulomatosis infantiseptica?

A

Severe in utero infection from Listeria

Disseminated abscesses and/or granulomas

Multiple organs affected

Most babies stillborn or dies soon after birth