Diabetic Infections Flashcards

1
Q

Key terms for fungal infections

A

Budding = common mode of asexual reproduction from yeasts
- fungal cells can produce multiple buds and these buds contain progeny nuclei

Conidia = asexual reproductive structures contained in yeast or hyphae cells.
- can be conidiophores (specialized hyphae), microconidia (small conidia) and macrocondia (larger conidia)

Arthrocondida = conidia produced from fragmented hyphae cells

Blastoconidia = conidia produced from budding yeasts

Chlamydospores = spherical conidia produced from terminal intercalary hyphal cells

Phialoconidia = conidia that are produced by vase-shaped conidiogenous cells called phi Alice

Dematiaceous fungi = fungi that contain melanin (brown/black pigments)

Dimorphism fungi = fungi hat can alter back and further between mold and yeast based on temperature/environment

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2
Q

How does DM lead to increased risk of infections

A

Neuropathy = can lead to skin ulcers that go unnoticed and leads to foot infections
- also casues urinary retention which produces UTIs

Peripheral artery disease = decreases blood flow and diminishes oxygen delivery tot he tissues
- this increases growth of anaerobes, makes it harder for immune cells to get to the site and act as well as induces ischemia

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3
Q

Broad catagories of infections associated with DM

A

UTIs
- fungal and bacterial

Pyomyosisits and foot infections

Necrotizing fasciitis

Malignant external otitis

Superifical fungal infections

Murcomycosis

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4
Q

Emphysematous UTIs

A

UTIs of the lower or upper urinary tract that also forms gas

UPEC and K. Pneumoniae species account for over 70%

Shows all UTI symptoms except also:
- * diffuse abdominal pain

Commonly forms in diabetes (usually women) with UTI

Highest mortality rates**

  • class 3 = extension of gas or abscess in the perinephric or pararenal space
  • class 4 = involvement of both kidneys or a solitary functioning kidney
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5
Q

Most common UTI pathogen?

A

Klebsiella pneumoniae
- gram (-) anaerobic rod

  • *species is heavily associated with alcoholics and diabetics
  • casues UTIs and pneumonia

Produces “current jelly” sputum

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6
Q

What is the #1 cause of all UTIs (even in diabetics)

A

UPEC species

Gram (-)
Lactose fermenting
Urease (-)
Nitrate (+)

  • *gets even stronger with diabetes mellitus**
  • produces advanced glycation end products (AGEs) accumulate in diabetics overtime. These enhance binding of UPEC isolates to bladder urothelium and make it even harder to fully kill
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7
Q

University of Texas wound classification

A

Gives grade and stage of a foot ulcer in diabetics

Grade:
0 = pre-postulcerative (hasent gotten through full thickness of dermis
1 = full thickness ulcer not involving tendon/capsule or bone
2 = tendon and capsular involvement without bone
3 = bone is present in the ulcer

Stage:
A = noninfected 
B = infected 
C = ischemic 
D = both infected and ischemic
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8
Q

What is the time for healing in a non complicated ulcer?

A

Decreases 1-2% in size per day

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9
Q

Infection in foot ulcers

A

Superficial infections
- usually gram (+) cocci

Polymicrobial infections in deep ulcers

  • enterococcus
  • enterobacteriaceae
  • P. Aeruginosa
  • anaerobes

Gangrene and necrotic infections

  • anaerobic streptococcus
  • bacteroides species
  • clostridium species

all antibiotic regiments should be as targeted as possible since most diabetic ulcer infections are highly antibiotic

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10
Q

Malignant external otitis

A

Invasive infection of the external auditory canal and skull base

Typically found in elderly patients with DM that have

  • recent ear surgery or hearing aid irritation
  • immunocompromised
  • become HIV positive
  • *almost always P. Aeruginosa**
  • can also be aspergillus, candidia, S. Aureus, Proteus, Klebsiella (only immunocompromised)

Symptoms

  • intense otalgia and pain with chewing
  • excessive drainage of the ear (otorrhea)
  • if advanced = cranial and facial nerve palsies
  • if untreated = fatal CNS complications

Diagnosis

  • elevated ESR/CRP
  • culture and gram stain of ear drainage

Treatment
- systemic antimicrobials

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11
Q

Fungi general physiology

A

Cell walls
- composed of glucan and chitin molecules

Cell membrane
- composed of ergosterol

Contains true nucleus and organelles (eukaryotic)

Non motile

Reproduce by budding or mitosis

require neutrophils and T-lymphocytes are critical to control infections

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12
Q

What is the most common superficial DM mucoses

A

Onychomycoses
- usually caused by trichophyton rubrum

Treatment = “azoles”

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13
Q

Most common opportunistic infections

A

Candida, aspergillus, cryptococcus, mucor, pneumocystis

candida especially with DM since there is glucose-inducible proteins which promotes adhesion to buccal or vaginal epithelium

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14
Q

Candida facts

A

Always on skin and GI tract

Is a budding yeast with pseudohyphae and germ-tubes

In immunocompetent

  • oral thrush
  • vulvovaginitis (very common in DM women also)
  • diaper rash

In immunocompromised

  • esophagitis
  • skin infections
  • disseminated infections and sepsis
    • endocarditis (if IV drug user usually)

disseminated Candida bloodstream infections are also common in hospitalizations

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15
Q

Diagnosis of candida

A

Scrap and stain with Periodic Acid-Schaff (PAS) or Gomori Methenamine Silver (GMS)
- shows budding yeasts and pseudohyphae

  • also grows on Sabouraud agar*
  • C albicans = green colonies
  • C tropicalis = blue colonies
  • C. Krusei = light pink colonies

Treatment of all species = “azoles”

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16
Q

Mucormycosis

A

Include Mucor and Rhizopus species
- are broad a septae hyphae with irregular right angles.

Causes devastating rhino-orbital-cerebral infections

  • also pulmonary infections
  • often are inhaled spores and cross into Brian via cribiform plate
  • These organisms possess ketone reductase enzymes*
  • which allows them to thrive in high glucose/acidic conditions

common appears in immunocompromised, diabetics, neutropenia, burns, metabolic acidosis

Symptoms:

  • headaches, CN nerve involvement, necrosis and painful periorbital/facial swelling
  • if it has crossed into the CNS = black eschar is the hallmark

Prognosis = poor
- stain with methenamine sliver and look for broad aseptate hyphae with right angles and irregular branching

Treatment = surgery, control DM and antifungals

17
Q

What are organisms in superfical skin infections

A

S. Aureus (Purulent) and GBS (non-Purulent)

Superfical examples

  • cellulitis
  • folliculitis
  • erysipelas

Deep localized

  • furunclosis
  • hidradenitis
  • skin abscesses

Deeper
- multiple different ones but usually require hospitalization

**necrotizing fasciitis = GAS

18
Q

What is the most common cause of cellulitis

A

Idiopathic or not cleaning wounds

19
Q

Does cellulitis include muscle infection?

A

NO

Cellulitis is only skin/ dermis

All cellulitis shows

  • erythema
  • edema
  • warmth
  • diffuse tenderness
  • lymphadenopathy

Should get the following serology to differentiate

  • anti-Streptolysin O
  • Anti-DNase B
  • anti-hyaluronidase
20
Q

Necrotizing fasciitis

A

Commonly caused by GAS and clostridium perfringens

Common predisposing factors

  • bacterial super infections
  • burns
  • bites
  • deep wounds
  • excessive NSAID use
21
Q

3 types of necrotizing infections

A

Type 1:

  • polymicrobial
  • often in head and neck
  • **is associated with DM

Type 2:

  • typically GAS or strep pyogenes
  • No cormorbitides present usually

Type 3:
- typically vibrio species and other marine bacteria

22
Q

Fournier gangrene

A

Perineum necrotizing fasciitis

Way more common in men

Casued usually by facultative organisms
- E. Coli, Klebsiella, enterococci

Can be caused by anaerobes

  • bacteroides
  • fusobacterium
  • clostridium
23
Q

Fusobacterium

A

Gram (-) rods

  • non spore forming
  • anaerobic
  • upper respiratory and GI bacteria usually colonized (not normal flora)
  • is assocaited with mouth infections and bites
  • has potent endotoxin LPS
24
Q

Bacteroides fragilis

A

Gram (-) rods

  • non spore forming
  • microareophilic
  • non-motile
  • GI bacteria
  • Polysaccharide capsules
  • *contains B-lactamase
    • is the leading casue of all intraabdominal abscesses**
  • shows deep diaphragm tenderness and high fever
25
Q

Prevotella

A

Gram (-) rods

  • non-spore forming
  • anaerobic

Always presents with foul-smelling discharge and always produces gas

  • will show negative aerobic cultures*
  • require complex media to grow

Commonly present in

  • periodontal abscesses
  • PID or ovarian abscesses
  • pneumonia
  • Brian abscesses
26
Q

Strep pyogenes virulence factors

A

Exotoxins A/B/C

  • produce mass cytokines
  • produces scarlet fever and TSS (A)
  • produces necrotizing fasciitis (B)

Streptolysin O and S

  • damages mammalian cells and lysis them
  • produces hemolysis

Streptokinase
- converts plasminogen to plasmin and prevents clotting

C5a peptidase
- inactivates C5a

Streptodornases
- DNAses that degrease viscous DNA In necrotizing tissues

Hyaluronidase
- disrupts organization of ground substance which promotes hematogenous spread

27
Q

Treatment for gangrene

A

usually clostridium septicum or perfringens

Surgical debridement and IV antibiotics

Also hyperbaric oxygen chamber**

28
Q

Infectious myositis

A

Usually S. Aureus (90%)

Is always polymicrobial in diabetics

3 stages:

1) local muscle pain, fever mild leukocytosis
- immediate
- can be treated just antibiotics

2) increased muscle tenderness, edema, Purulent abscesses, marked leukocytosis
- usually 10-20 days after stage 1

3) systemic toxicity, fluctuate muscles, bacteremia/septicemia symptoms
- anytime after stage 2

2/3 treatment = antibiotics and abscess drainages