Bacteria Flashcards
Gram negative structure
outer membrane containing Lipopolysaccharide (LPS)= endotoxin- induce septic shock
much thinner peptidoglycan with periplasmic space
beta lactamases are plasmid derived enzymes that chew up antibiotics in Gram Neg
gram neg lose the stain
Gram positive structure
- Thick multilayered peptidoglycan sheath outside of cytoplasmic membrane
- penicillin binding proteins found in both and strengthen peptidoglycan
Bacterial morphology
shape and arrangement
Cocci in clusters
* staphylococcus
Cocci in chains
* streptococcus
Coccis in pairs with pointed ends
* streptococcus pneumoniae
Cocci in pairs with kidney bean shape
* Neisseria
Rods (bacilli) with square ends
* bacillus
Rods with rounded ends
* salmonella
Rods with club shaped
* Corynebacterium
Rods fusiform
* Fusobacterium
Rods comma shaped
* Vibrio
Rods short pleiomorphic
* Hemophilus
Spirochetes- spiral shape with relaxed coil
* Borrelia
Spirochetes- spiral shape with tight coil
* Treponema
Microbiome
Distinctmicrobial communities that inhabit different host environments-> normal flora
established= permanent residents of associated body sites
Normal flora can cause disease when they gain access to other sites
Principles of pathogenesis
not all microorganisms are pathogens
Opportunistic pathogens-> usually normal flora /environmental organisms that do not cause disease except
* immunosuppression
* imbalance
Virulence- how many organisms does it take to cause disease
* letal dose vs infectious dose
* lower #= higher the virulence
terms related to infection
- Colonization- presence of a new organism that is neither normal flora nor the cause of disease
- Carrier individual colonized with potential pathogen in significant #s
- Inoculum- # of organisms to which a person is exposed
- Communicable/contagious- able to be spread form host to host
- Infection- invasion of tissues by microorganism that causes disease
Bacterial major mechanisms
1. Toxin producing-> exotoxins (secreted proteins), endotoxins (LPS in cell wall of G-), Superantigen (kind of exotoxin cuases release of larger amounts of cytokines from helper t and macrophages)
2. Invasion and inflammation-> enzymes (collagenase, hyaluronidase), virulence factors -> leads to inflammatory respons (erythema, edema, warmth, and pain)
Stages of infection
- Transmission from external source through a port of entry
- Evasion of innast host
- Adherence to mucous membranes
- Colonization by bacteria
- Disease symptoms caused by toxin or invasion inflammation
- Host responses innate and adaptive thru 3-5
- Progression or resolution of disease
Cant be seen in gram stain
MR CLMT
- Mycobacterium-> M. tuberculosis, ACID FAST STAIN
- Treponema pallidum-> DARK FIELD MICROSCOPY OR FLUORSCENT ANTIBODY
- Mycoplasma pneumoniae
- Legionella pneumophila-> prolonged counterstain
- Chlamydiae-> C. Trachomatis-> inclusion bodies in cytoplasm
- Rickettsiae-> Giemsa stain
role of oxygen
Obligate aerobes- pseudomonas aeruginosa
facultative anaerobes- e. coli
aerotolerant organisms- clostridium
microaerophiles-= campylobacter jejuni and h pylori
obligate anaerobes- Bacteroides fragilis
Medically important normal flora
LESS SAVE BB
- staphylococcus epidermis-> S. aureus, pseudomonas aeruginosa, propionibacterium, candida= skin
- Staphylococcus aureus-> nose
- Viridans streptococci-> eikenella corrodens= mouth
- Streptococcus mutans-> prevotella= dental plaque
- Anaerobes and Bacteroides-> gingival crevices
- V. streptococci= throat
- E. coli-> bifidobacterium, lactobacillus, enterococcus faecalis, clostridium= colon
- lactobacillus, e coli, group b strep-> c. albicans= vagina
- s. epidermis= urethra
exo vs endotoxin
Exo
* from gram +/-
* secreted from cell
* polypeptide
* highly toxic
* various clinical effects
* high Abs called antitoxins
* toxoids used as vaccines
* diseases: tetanus, botulism, diptheria
Endotoxin
* cell wall of negative
* not from cell
* lipopolysaccaride
* less toxic
* fever and shock clinical
* poor antigenic
* no toxoids and no vaccine
* diseases: meningococcemia, sepsis by gram negative rods
Superantigens (SAgs)
Causes:
1. massive proliferation of T cells
2. massive cytokine release
Results: fever, shock and death
SAgs bind to class 2 MHCs ag on APCs which bind a large subset of TcRs in a non specific manner
Lab cultures
Culture and sensitivity: blood, throat, sputum, csf, stool, urine, genital, wound, abscess
incubate in or without oxygen to detect aerobes vs anaerobes
Sensitivity testing-? MIC
Molecular tests:
Nucleic acid amplification test NAATs or PCR (gold standard and preferred)
Serologic tests:
Direct antigen detection-> F-AB
IgM, IgG
gram + cocci
staphylococcus and streptococcus
- S. aureus (+ coagulase)
A. toxigenic superantigen- food poisoning,
B. pyogenic- abscess= SSTI,
C. Local- skin and soft tissue,
D. Disseminated - sepsis, endocarditis, osteomyelitis, septic arthritis - S. Epidermidis (- coagulase)- frequent culture contaminant
- S. Saprophyticus (-)- UTI
Catalase test= btwn staph + or strep -
Colagulase= between aureus vs epi
Staph skin infections
impetigo
hidradenitis suppurativa
cellulitis
necrotizing fasciitis
furuncle
paronychia
felon
carbuncle
blepharitis
folliculitis
bullous impetigo
abscess
mastitis
MRSA
Methicillin Resistant S. Aureus
Mech: mutation in penicillin binding protein
weird spider bite with necrosis
#1 cause of abscesses
Staphylococcal Scalded Skin Syndrome
Superantigen
- Exfoliatin exotoxin= protease that targets desmoglein (intracellular adhesion protein)
perioral crusting and conjunctivitis
Toxic shock syndrome TSS
superantigen
Sx:
* fever
* rash- erythroderma
* mucosal involvement
* hypotension
* multi organ disease
* desquamation a= 2 weeks later
causes
* menstrual= tampons
* Non= postsurgical wounds, post partum, nasal packing
* pediatric skin lesions
- Staph auresu= TSS and enterotoxins; superantigens
- Group A strep-> streptococal pyogenic exotoxin A, B, both
TX
REMOVE FB
Streptococcus species
gram +
- S. pyogenes= A lancefield= Beta
- S. agalactiae= B lancefield= Beta
- S. pneumoniae= NA= Alpha
lancefield groups
based on antigenic cell wall polysaccharides
- Group C & G= asym colonizers and normal flora of upper airway= cause disease in immunosuppressed or chronically ill patients
- Group F= asym colonizers of oropharynx or gi cause severe suppurative infections including deep tissue abscesses, bacteremia, endocarditis
Group A- Streptococcus pyogenes
Group B- Streptococcus agalactiae
Group D- Enterococci, streptococcus bovis
Strep groups
S. pyogenes (PIT)
1. pyogenic
a. Local= IMPETIGO, CELLULITIS, PHARYNGITIS/TONSILLITIS
b. Disseminated= SEPSIS
2. Toxigenic= SCARLET FEVER TOXIC SHOCK
3. Immune mediated = RH & AGN
S. agalactiae (group b)= pyogenic= neonatal sepsis & meningitis
E. facalis (group d)= pyogenic= UTI, endocarditis
S. Bovis= pyogenic= Endocarditis
S. pneumoniae= pyogenic= pneumonia, otitis media, meningitis, sinusitis MOPS
Viridans strep= pyogenic= endocarditis
Toxigenic manifestation of Group A strep
Scarlet fever aka scarlatina
Day 1: flushed cheeks, rash in axilla and groin, pastia’s lines, coated whitish tongue sandpaper rash- erythrogenic toxin
Day 3: Circumoral pallor, strawberry tongue, + blanching test
desquamation
Necrotizing fasciitis
Action of hyaluronidase and exotoxin B
enzyme and toxin that breakdown hyaluronic acid