Microbiology Flashcards
list the nonspecific defenses of the skin
physical barrier to infection! cool ~pH 5 mostly dry sweat glands salty sebaceous glands fatty acids, wax esters β-defensins lysozyme neutrophils, langerhans cells (epidermal macrophages) normal microbiota
identify the two leading agents of soft tissue and bone infection
staphylococcus aureus and streptococcus pyogenes
Both Gram + cocci
Staph.aureus tends to form abscesses (which can necrose, or become gangrenous)
Strep. pyogenes tend to spread through tissues
briefly describe cellulitis: specifically 1) how it usually develops 2) common regions of formation and age of infected individuals 3) risk factors for acquiring it, and cellulitis as a risk factor for other ailments 4) common symptoms and 5) diagnosis and treatment
acute, spreading infect. deeper dermis and subcutaneous fat
*Streptococcus pyogenes, *Staphylococcus aureus, other streptococci, Gr-bacilli (more common in immunocompromised)
usually originates from superficial skin lesions or following trauma
more common lower extremities
usually middle aged, elderly
E.g. risk factors: diabetes, varicella, impaired peripheral circulation, chronic steroid use
most common
pain, erythema, edema, warmth
indistinct border
possibly
may progress to sepsis w/in 24-48 hrs
can lead to necrotizing fasciitis, osteomyelitis
Diagnosis is rapid esp with s. pyogenes.
Treat with antibiotic
Describe the defining feature of MRSA
Defining feature is the staph cassette chromosome mec (SCCmec) encodes the mecA gene
Imparts broad spectrum B-lactam resistance, and is thus resistant to all penicillin like drugs.
Panton-Valentine leukocidin (PVL) virulence factor which destroys Neutrophils (forms pores in them)
briefly describe the symptoms and diagnosis of cutaneous nocardiosis and actinomycosis
a
characterize the normal environment, structure, morphology, biochemistry, virulence factors and growth requirements of Staphylococcus aureus,
Staph. aureus
normal environment- anterior nares, mucous membranes,
structure- G+
morphology-cocci clusters, non-motile
biochemistry-facultative anaerobes, coagulase +, catalase +
virulence factors- capsule, cytolytic exotoxins, protein A antiphagocytic Fc binder, enzymes, Fibronectin-binding protein (bind to mucosal cells).
growth requirements- high salt MSA. MSA-selective for staph, differential for mannitol fermentation (aureus does)
characterize the normal environment, structure, morphology, biochemistry, virulence factors and growth requirements of Pseudomonas aeruginosa,
Pseudomonas aeruginosa
normal environment-in immunocompromised, health care associated infection HAI, ubiquitous (in nature)
structure- G-
morphology-baccilus/non-enteric rods
biochemistry-oxidase +(cytochrome oxidase), strick areobe
virulence factors-pili, capsule (alginate), spreading factors: collagenase, elastase, B-hemolysis, protease.
growth requirements-minimal nutrients, MacConkey agar, blood agar. Some produce pigments: pyocyanin (blue) attracts PMNs, pyoverdin (green) is a siderophore
characterize the normal environment, structure, morphology, biochemistry, virulence factors and growth requirements of Haemophilus influenzae
Haemophilus influenzae
normal environment- human reservoir URT
structure- G-
morphology
biochemistry
virulence factors-encapsulated (PRP, polyribitol phosphate capsule) more likely to cause cellulitis and osetomyelitis, (Hib), LPS, IgA1 protease,
growth requirements-chocolate agar (needs X factor; hemin, and V factor NAD)
Quellung reaction-Ab binds capsule to make it more visible
characterize the normal environment, structure, morphology, biochemistry, virulence factors and growth requirements of Eikenella corrodens
Eikenella corrodens
normal environment- normal in mouth,GU, bowel
structure-G-
morphology-Rod
biochemistry- Facultative anaerobe, oxidase +
virulence factors-
growth requirements-fastidioius: blood, chocolate agar, pits agar, bleach like odor
human bit and clenched fist injury infections
characterize the normal environment, structure, morphology, biochemistry, virulence factors and growth requirements of Nocardia spp.
Nocardia spp. (type of actinomycetes)
normal environment-soil/gardening
structure- G+
morphology- filamentous bacillus
biochemistry- aerobes to strict anaerobes, some acid fast (beaded) on staining*
virulence factors- facultative intracellular
growth requirements- slow growing
Nocardiosis- characterized by necrosis, absecess formation and granulomas. Primary skin -lungs secondary reverse.
pulmonary, cutaneous, mycetoma,
characterize the normal environment, structure, morphology, biochemistry, virulence factors and growth requirements of Actinomyces israelii
Actinomyces israelii- non acid fast normal environment- mouth, GU, intestines structure G+ morphology biochemistry virulence factors growth requirements- fastidious
actinomycosis- Actinomyces plays lead role
CoNS
coagulase negative staph.
Staph aureus is the only coagulase positive staphloccoci
What is the catalase activity of strep and staph bacteria? Don’t get this confused with coagulase!
Staphlococcus catalase +
Steptococcus catalase -
IgA1 protease can cause mucosal infections. Which three bacteria are known for this?
Nice strip of Ham
Neisseria (gonorrhoeae, meningitidis)
Streptococcus pneumoniae
Haemophilus influenzae
Actinomyces and nocardia have what morphologic structure?
Rods
The Hib vaccine targets what part of the bacterium? Why are non-typeable strains unaffected?
PRP capsule, non-typeable strains lack this
Describe the diseases, source of human infection and mode of transmission of Pasteurella multocida.
Disease: cellulitis, osteomyelitis, URT infection
Source: cats and dogs
Transmission: bite, lick, scratch
How do you get Bartonella quintana?
AKA Trench fever is transmitted by body louse/lice. More common cause of bacillary angiomatosis than B. henselae.
Describe Bartonella henselae
Picmonic-pleomorphic gram - rod. Source cat scratches causing fever and bacillary angiomatosis in the immunocompromised (though it’s benign). Mimics Kaposi sarcoma (also in the immunocompromised) which presents with purple bumps on the skin. This bacteria also causes reactive arthritis and a non-caseating granuloma.
Describe Brucella
Picmonic- gram - cocci/rod. Usually transmitted by unpasteurized cows milk or goat cheese. The obligate intracellular bacterium likes to infect macrophages and can cause lymphandenopathy (likes to be where phagocytes congregate;spleen etc). Sometimes these tissues are walled off by granulomas. Additonally, an undulating fever is sometimes present. Treatment includes doxycycline and gentimicin.
Not mentioned-osteomyelitis and septic arthritis is a common complication.
Define pyomyositis, and the common culprits
Purulent infection of skeletal muscle usually with abscess formation. (cubby knee)
Common culprits-Staph. Aureus, clostridium perfringins
Define Osteomyelitis, its two types, and describe diagnosis and treatment.
Bone infection-
Hematogenous: kids long bones, 1 bug, capillary corner stuck.
Contiguous: Staph A, Strep. P, in acute soft tissue infections that spread to bone.
Diagnose- will not bear weight on extremity, recent trauma
Treat with antibiotics following bone biopsy.
Other microbes mentioned: Brucella, and Pasteurella multocida.
Define necrotizing fascitiitis
How does it usually begin?
What are some hallmarks of the condition?
3 fasciitis terms to know
deep-seated infection of subcutaneous tissue that results in progressive destruction of fascia and fat, but may spare the skin
Usually begins with cellulitis. Spreads along fascial planes and the underlying destruction is more widespread than the skin lesion
Pain is disproportionate to the apparent severity of the lesion
1) bullae-blisters
2) crepitus- crackly
3) fluctuance-moveable or compressible (gas/pus, or both)
How do you diagnose necrotizing fasciitis?
May suspect when patient fails to respond to broad spectrum IV antibiotics (lack of debridment), or when they you can see cutaneous manifestations.
Often misdiagnosed as cellulitis, abscess, or septic arthritis
What are the symptoms and diagnosis of gas gangreen?
Usually a traumatic wound with muscle damage. Usually clostridium perfingens
Symptoms-
sudden onset severe pain at site injury
↓
rapid progression edema, tenderness, pallor
↓
discoloration, hemorrhagic bullae, foul-smelling discharge
↓
crepitus subcut. tiss., muscle
↓
systemic findings of toxicity
↓
shock
↓
multiorgan failure
↓
death usually w/in 48 hrs onset symptoms
Diagnosis
pain at site traumatic injury, signs of systemic toxicity, gas in soft tissue
can confirm w/ Gram stain, anaerobic culture
abundant rectangular Gr+ rods, absence inflammatory cells (lysis by toxins!)
double zone hemolysis on blood agar
lec-ithin-ase activity on egg yolk agar
