Diabetic Infections Flashcards
Key terms for fungal infections
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
How does DM lead to increased risk of infections
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
Broad catagories of infections associated with DM
UTIs
- fungal and bacterial
Pyomyosisits and foot infections
Necrotizing fasciitis
Malignant external otitis
Superifical fungal infections
Murcomycosis
Emphysematous UTIs
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
Most common UTI pathogen?
Klebsiella pneumoniae
- gram (-) anaerobic rod
- *species is heavily associated with alcoholics and diabetics
- casues UTIs and pneumonia
Produces “current jelly” sputum
What is the #1 cause of all UTIs (even in diabetics)
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
University of Texas wound classification
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
What is the time for healing in a non complicated ulcer?
Decreases 1-2% in size per day
Infection in foot ulcers
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
Malignant external otitis
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
Fungi general physiology
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
What is the most common superficial DM mucoses
Onychomycoses
- usually caused by trichophyton rubrum
Treatment = “azoles”
Most common opportunistic infections
Candida, aspergillus, cryptococcus, mucor, pneumocystis
candida especially with DM since there is glucose-inducible proteins which promotes adhesion to buccal or vaginal epithelium
Candida facts
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
Diagnosis of candida
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”
Mucormycosis
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
What are organisms in superfical skin infections
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
What is the most common cause of cellulitis
Idiopathic or not cleaning wounds
Does cellulitis include muscle infection?
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
Necrotizing fasciitis
Commonly caused by GAS and clostridium perfringens
Common predisposing factors
- bacterial super infections
- burns
- bites
- deep wounds
- excessive NSAID use
3 types of necrotizing infections
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
Fournier gangrene
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
Fusobacterium
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
Bacteroides fragilis
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
Prevotella
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
Strep pyogenes virulence factors
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
Treatment for gangrene
usually clostridium septicum or perfringens
Surgical debridement and IV antibiotics
Also hyperbaric oxygen chamber**
Infectious myositis
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
