W1 Flashcards
The most abundant organisms on Earth comprise of:
- Acellular organisms (viruses)
- Unicellular organisms without a nucleus (prokaryotes/bacteria)
- Unicellular organisms with a nucleus (eukaryotes/fungi and some parasites)
- Multicellular organisms all have nuclei (eukaryotes/parasites)
Viruses: alive or dead?
dead. they are an obligate parasite, they use our hosts to survive
Prokaryote Morphology
Coccus (pl. cocci)
- Spherical shape
Bacillus (pl. bacilli)
- Rod shape
Sphirochete (pl. spirocheta/ spirochetes [eng])
- Cork-screw shape
Vibrio (pl. vibriae)
- Comma shape
Difference between
a. Coccus
b. Diplococci
c. Streptococci
d. Staphylococci
Coccus: single ball shape
Diplococci: two ball shapes
Streptococci: balls in a line
Staphylococci: like a bundle of grapes
staphyl: means grapes
Escherichia coli
- morphology
aka e.coli, lives in your gut
common cause of UTI’s in many people
bacilli shaped
Syphilis Bacteria’s name
- type
Treponema Pallidum
spirochete/cork screw
Helicobacter Pylori
common cause of gastritis, peptic ulcers
Eukaryote
- some examples
Single or multi-cell organisms
- With a nucleus, mitochondria, and membrane-bound organelles
Fungi, Plants, Parasites, Animals, Us
Plasmodium Falciparum
ONe agent of malaria
Candida Albicans is what type of eukaryote?
YeasT
Which eukaryote makes up mould?
commonly it is: Aspergillus Fumigatus
black you’d see in shower tubs or kitchen
What is the smallest microbe organism
VIRUSES are the smallest
Reproduction in Prokaryotes
Binary fission
- No mitosis
- asexual
Clonal expansion
if they mutate with resistance, all the clones following that will have that resistance
Reproduction of Viruses
Fission
- Asexual
- Use host apparatus to reproduce
Clonal expansion
more infectious than variant forming
Reproduction in Eukaryotes
Binary fission
- Yeasts and some protozoa
- Clonal expansion
Sexual reproduction
- Not clonal expansion
- Mitosis occurs
Reproduction in Bacteria
Bacterial conjugation
Occurs commonly, through the use of pili
There is no production of “daughter cells” per se
Transfer of genetic material
Eg. Plasmids
Eg. Transmission of antimicrobial resistance
Plasmids live outside of the nucleus just floating in the cell, they contain antibiotic resistance genes that are passed through the pilus into another bacteria.
Nomenclature of Microbes
Genus is umbrella, the under it there are types of Species
i.e.
Staphylococcus = Genus
Aureus and epidermis = different species
Slamonella, Bacillus, Streptococcus, Plasmodium, Candida = different GENUS
Key divisions of Bacteriology
GRAM STAIN
there’s also
- pathogens vs non pathogens vs opportunistic pathogens
- aerobes vs anaerobes vs facultative anaerobes
Gram’s stain
Concept is:
What colour are the individual bacteria under a microscope?
The use of 2 dyes:
- Crystal violet (BLUE – PURPLE)
- Iodine fixator
- Acid alcohol or acetone decolorization - Safranin (RED – PINK)
Cell wall of bacteria
- how is it created
- What is it made up of
called Peptidoglycan
created using penicillin binding protein
Made up of: NAG, NAM, and oligopeptides
Named penicillin binding protein because this is the target of penicillin used to create a whole in the bacteria and weaken the wall
Gram + means
It binds to the blue/purple dye because it has a THICK cell wall, and you can’t decolourize it (the step before putting the red dye)
it has a SINGLE cell membrane
the cell wall is thick and above the cell membrane
Gram - means
- What are the layers of the wall in order
That the cell wall is thin so the blue dye got removed with the de-colouring agent and allowed for the red dye to bind
it has a DOUBLE cell membrane, space between = periplasm
layers from outer to inner:
a. outer membrane
b. cell wall with peptidoglycans
c. periplasms
d. inner membrane
Most POSITIVE gram (blue staining) have masculine sounding names EXCEPT for the following three
Listeria spp
Nocardia spp
Gemella spp
typical gram negative bacteria:
Staphylococcus spp
mycobacterium spp
streptomyces spp
Most gram NEG (pink staining) have feminine names EXCEPT for those with the following suffix
- monas
- PHilus
- bacter
these all sound masculine but they are
Negative/PINK/FEMININE
examples of typical gram negative names (most end with an -a or other vowel)
Pasteurella spp,
Moraxella spp,
Escherichia
Providencia
What are examples of Bacteria without cell walls
- What colour do they stain?
They don’t stain because they don’t have a wall for the stain to attach too*
Examples:
Mycoplasma spp
- Mycoplasma pneumoniae
- Mycoplasma hominis
Chlamydia spp
- Chlamydia trachomatis
Chlamydophila spp
- Chlamydophila pneumonia
- Chlamydophila psittaci
Bacterial physical defence barriers and adherence
Capsule
- fatty coat
eg. Streptococcus pneumoniae
Biofilms
- where they live, hang out in possies, barf on each other, forming a sticky matrix that antiboitics don’t penetrate well
i. e. catheters, deep central lines. The plastic ends form a biofilm that can cause an infection - Walking on river and slipping on the gooey rock = biofilms
eg. Staphylococcus epidermidis
Fimbriae
- little hairs that make it stick on to a surface- nOT a pilus, a pilus is longer
eg. Escherichia coli
Lipopolysaccharide
another bacterial virulence factors
Lipopolysaccharide: Outer cell wall of Gram negative bacteria Endotoxin Leads to immune response - Cytokine release - Fever - Shock
Toxins
Bacterial virulence factor
They can work systemically or locally (G, CNS, resp)
Toxin induced systemic effects
Superantigens
- Activate about 10% of lymphocyte pool
- Directly bind MHCII presenting cells and T cells
Toxic shock syndrome
TSST-1
- S. aureus
- S. pyogenes
Toxins that induce GI distress
Shigatoxin
- Shigella dysenteriae
- E. coli O157:H7
Shiga-like (vero)toxin
- E. coli O157:H7
Toxins A and B
- C. difficile
Cholera toxin
- V. cholerae
Food poisoning:
- Staphylococcal enterotoxin
S. aureus
- CPE enterotoxin
Clostridium perfringens
Neurotoxin Examples
Botulinum toxin (Botox) -Paralysis “Sausage toxin” C. botulinum Tetanospasmin Tetanus C. tetani Shigatoxin seizures
Neurotoxin Examples
Botulinum toxin (Botox)
-Paralysis
- “Sausage toxin”
C. botulinum
Tetanospasmin
- Tetanus
C. tetani
Shigatoxin
- seizures
Toxins that induce respiratory distress
Diphtheria toxin
- Upper respiratory tract illness
- Respiratory obstruction
C. diphtheriae
Pertussis toxin
- Insulin-induced hypoglycemia
- Whooping cough(?)
B. pertussis
Botulinum toxin
- Through paralytic effect
Necrotizing pneumonia
- Panton Valentine Leukocidin
- S. aureus
Toxins that induce Tissue changes
Tissue changes
Alphatoxin
- Gas gangrene
- C. perfrigens
Anthrax toxin
- Edema factor
- B. anthracis
Exfoliatin
- Staphylococcal scalded skin -syndrome
- S. aureus
Panton Valentine Leukocidin
- Leukocyte and epithelial cell lysis
Community-acquired MRSA
Pyogenic exotoxin
- Superantigen
-Necrotizing fasciitis
S. pyogenes
Toxins that induce Renal Failure
- Shiga-like toxin
- Verotoxin
- Hemolytic Uremic Syndrome
Hemolysis
Bloody diarrhea
Thrombocytopenia
Renal failure
- E. coli O157:H7
Enterohemorrhagic E. coli
Listeriolysin O
gram positive bacterial toxin
Causes lysis of phagosomes
Allows the bacterium to replicate intracellularly
Allows the bacterium to evade the immune system
- L. monocytogenes
Antimicrobial Resistance
Resistance to antibiotics in the bacterial world all has to do with the concentration of the antibiotic that you can get into a specific tissue in order to overcome the minimum inhibitory concentration of that antibiotic for that particular bacterium
Minimum Inhibitory Concentration (MIC)
The lowest concentration of an antibiotic needed to prevent or inhibit the growth of a microorganism in the laboratory
Must be able to correlate this clinically
- Can we safely achieve such a concentration in a specific tissue?
What 2 factors limit ability to overcome antibacterial resistance
a. Antibiotic Bioavailability
b. Antibiotic Toxicity
Where do bacteria contain resistance genes?
In their:
Chromosomes AND on their plasmids
These genes can be transferred from bacteria to baceries
e.g. plasmids during bacterial conjugation
resistance genes give rise to proteins which:
- Are secreted and cleave antibiotics
- Beta-lactamases, cephalosporinases
- S. aureus, N. gonorrheae, Enterobacteriaceae (beta-lactamases, ESBL) - Form mutated binding sites for antibiotics
Decrease antibiotic binding where they are supposed to act
a. Mutated penicillin-binding proteins
- S. pneumoniae and beta lactams
- MRSA and all beta-lactams/cephalosporins/carbapenems
b. Mutated cell wall
- Vancomycin resistant enterococci
c. Mutated gyrase enzyme
- Ciprofloxacin resistance
d. Mutated ribosomes
- Aminoglycoside (eg. Gentamicin) resistance
- Don’t allow antibiotics (that act on ribsosomes or DNA) to enter the bacterium
a. Mutates Porin proteins
- Fluoroquinolone resistance
b. Efflux pumps
- Erythromycin resistance
Two Major Divisions of Fungi
They are either Yeast OR Mould
Yeasts (examples include):
Candida spp
Moulds (examples include):
Aspergillus spp
Rhizopus spp
Some fungi are dimorphic
Yeast at 37oC AND mould at 25oC
Histoplasma spp.
Coccidioides spp
How is fungal cell wall different from bacterial wall?
Contains CHITIN
Polymer of N-acetylglucosamine
Insects,crustaceans, mollusks, squid, and octopi also contain chitin
Plants have cellulose instead- completely different
Thus, Antibiotics would NOT work, because they target peptidoglycans specifically. you need anti-fungals
Viruses
- relative size
- How do they survive?
What are the two major divisons
Not free living organisms Smallest of the micro-organisms Need a living host to replicate Use the host’s cellular machinery to replicate Host’s enzymes Host’s ribosomes etc
there are two major divisions
DNA vs RNA viruses
What are examples of DNA Viruses
Herpes virus group HSV 1 and 2 EBV, CMV. VZV HHV-6, 7, 8 Adenovirus Hepatitis B virus Human papilloma virus Parvovirus Poxvirus
What are examples of RNA viruses
Hepatitis A virus Hepatitis C virus Rhinovirus Measles virus Mumps virus Rubella virus Influenza virus Human Immunodeficiency Virus Enteroviruses Poliovirus Coronaviruses
Among many others
How long do Viruses last in our bodies?
Many viruses cause chronic infections
HIV, Hepatitis B, Hepatitis C, Human papilloma virus, HSV 1 and 2
Some viruses are never cleared from the human host
Herpes group (HSV 1 and 2, EBV, VZV, HHV-6 etc)
Adenovirus
HIV
Most of the viruses that remain in humans are DNA viruses
Please note: HIV while an RNA virus initially, becomes a DNA virus once inside cells
DNA viruses NEVER leave our bodies. They integrate into our own DNA
i.e. chicken pox as a kid can become shingles later on
Herpes comes back every time you’re stressed or immune system goes down.
HPV: cervical cancer, anal warts/cancer
RNA viruses are usually transient visitors EXCEPT HIV because it is a RETROVIRUS
Retrovirus
RNA viruses are usually transient visitors EXCEPT HIV because it is a RETROVIRUS, that translates RNA into DNA and acts as a DNA virus that never leaves us.
This is possible because it has an enzyme: reverse transcriptase
Viruses and Cancer
Some viruses cause cancer By integrating into our DNA By disrupting oncogenes - Hepatitis C - HIV - EBV - HPV - HHV-8 (Kaposi’s sarcoma virus)
Among others
SAR-2 Coronavirus
Coronavirus group of viruses
- Family of animal RNA viruses discovered in the 1930s (named in 1968)
- Human coronaviruses discovered in the 1960s
Name derives from the protein spikes it has on surface
- Attachment to ACE receptors
- Looks like a crown
Latin: corona (“crown, “wreath”)
Transmission of COVID
Like most respiratory viruses Large droplets (2 m or 6 feet away)
BUT:
Aerosols (potential for airborne spread) Aerosol generating procedures (AGP) CPAP Intubation/extubation Deep tracheal suctioning Open circuit suctioning (ventilated patients) Drilling Endoscopy with biopsy Flushing a high efficiency toilet Singing? Talking? Laughing? Shouting? Stool
Know you COVID-19 Tests: RATs
Rapid Ag Tests (RATs)
50% sensitive when asymptomatic
70-80% sensitive when symptoms for more than 24 hours
Repeat testing (12-48 hours later) needed if negative and you’ve tested “early”
Close to 100% specific
Isolation time for COVID
- what is the area first infected by COVID
10 days* to reduce your transmissibility
- throat is the first area that gets infected
Know your COVID-19 Tests: PCR
NP (and throat) PCR is gold standard
Almost 95% sensitive ( depends on a Cycle threshold)
100% specific
- COVID infects throat area first so best to swab the throat, not nasal
What’s different about Omicron
significantly more infectious
Multiple mutations in the spike protein
Seems to have originated in parallel to other mutants
Huge replication in throat and trachea
Massive viral load in upper respiratory tract (main symptoms are sore throat and headache)
Less predilection for lung tissue (not too much cough)
Ro (R not) which was 2-3 for original wuhan virus has come up to 30!!! for omicron
How to calculate the percentage of population that needs to be vaccinated
It’s a mathematical equation:
1 – (1/R0) X 100% = “Herd immunity” calculation
Then divide by vaccine efficacy (%) = TOTAL (not just eligible) population needed to be vaccinated in order to achieve said “herd immunity”.
Wuhan ancestral strain (R0 2.5) = 63% (remember that number?) Aα, Bβ variants (R0 4) = 79% Δδ variant (R0 8) = 97% Oo variant (R0 32) = 100%
This means young children (about 12% of Quebec population) need to be vaccinated, irrespective of whether the virus is “deadly” for them.
Treatment for viral infection/COVID
there is no cure or treatment however STEROIDS (anti-inflammatory) helps to suppress CYTOKINE STORM
Multisystem Inflammatory Syndrome in Children/Adults aka Paediatric/Adult Inflammatory Multisystem Syndrome
Rare but serious syndrome <2% of children infected with COVID-19 (risk about 1 in 3,500)
Mortality: <1%
It occurs 4-6 weeks after (even from an asymptomatic) infection.
Decreased by 90% after vaccinations
What are the two types of parasites
There are two types:
Protozoa vs Multi-Celled Organisms
Atabrine
anti-malaria drug
don’t take it = become a skull
Protozoa
- give examples
Single celled organisms Examples include: Plasmodium spp Entamoeba spp Dientamoeba spp Cyclospora spp Isospora spp Toxoplasma spp
Multi-celled organisms
Worms (examples include): - Nematodes/Roundworms Ascaris spp - Platyhelminths/Flatworms and Flukes Tinea spp Schistosoma spp Echinococcus spp
pregnancy and vaccination
Increased risk of miscarriages, pre-term births, and maternal morbidity/mortality with COVID-19.
Anti-COVID-19 vaccines have been approved and recommended for use in pregnancy (all trimesters) and for breastfeeding women. They are safe and effective and provide transfer of antibodies to the newborn.
Vaccines and menstruation changes? Study showed ½ day change only Other vaccines (and viral illnesses) can do this too.
Vaccines and infertility?
Normal Microbial Flora
- When is it acquired, how?
- how does it maintain an equilibrium?
- what are some risks?
Start to acquire as soon as we are born
After vaginal birth, neonate’s flora emulates maternal perineal flora; after C-section delivery, neonate’s flora emulates maternal cutaneous flora
Quickly establish sites of colonization, especially after cessation of breast feeding
There may be a role for the appendix as a source to colonize/repopulate the large bowel
Flora maintains an equilibrium
- Occupies binding sites, reduces available free nutrients
- Contributes to host metabolism, provides host access to nutrients and vitamins
In some circumstances, the flora can become opportunistic pathogens and contribute to disease.
Good Flora
Good = Commensal organisms
Contribute to a stable ecosystem microflora which varies according to the site on or in the body
Composition of the microbial flora is influenced by host microenvironments (nutrient availability, adhesion molecules, physical environment, atmosphere, etc)
In a normal commensal state, interaction between the organisms and the host may or may not elicit a form of (protective) immune response
Bad Flora
Bad: Opportunistic pathogens
In situations of tissue breakdown, an otherwise benign member of the microflora may exploit the impaired defenses or upregulate virulence factors that result in disease pathogenesis
What are some growth characteristics and/or virulence factors that facilitate pathogenic organisms
Evolved growth characteristics and/or virulence factors that facilitate: Adherence Invasion Immune evasion Tissue destruction Cellular dysfunction
Often result in an inflammatory response and upregulated immune response
Sterile Organs include:
CNS / PNS / ANS Lungs Heart Liver Spleen Pancreas Kidneys Uterus, ovaries, testicles
Sterile Connective Tissue includes
Blood
Bone
Muscle
Tendons, ligaments
Sterile Body Fluids include:
Pleural fluid Synovial fluid Peritoneal fluid Cerebrospinal fluid (Urine)
NB urine can become colonized, this does not necessarily represent an infection or disease state.
What are sites of colonization
Skin (and its appendages) Sites of heavy colonization Conjunctiva Nose Mouth / Gums Pharynx Large bowel Vagina Anterior urethra (Bladder / urine)
What are some examples of our normal cutaneous microbial flora?
Coagulase negative staphylococci
- Staphylococcus epidermidis
Corynebacterium spp.
To a lesser extent
- Viridans streptococcus
- (much lesser extent) Beta hemolytic streptococci
- (much lesser extent) Staphylococcus aureus
Normal microbial flora of human mouth, Gram positive:
Gram positive cocci:
Viridans streptococci
Coagulase negative staphylococci
Others, including Stomatococcus (Rothia) mucilaginosa
Normal microbial flora of the human mouth, gram negative bacilli:
Aerobic: Pseudomonas aeruginosa
Facultative anaerobic: E. coli, K pneumoniae, E cloacae
Capnophilic: Capnocytophyga, Haemophilus, Neisseria
Anaerobic: Fusobacterium, Prevotella, Leptotricha
Others: HACEK, spirochetes
Normal pharyngeal microbial flora
Neisseria spp
Coagulase negative staphylococci
Viridans streptococci
Haemophilus spp.
Normal Enteric Microbial Flora
99.9% Anaerobes – 1011 /g feces
Bacteroides spp, Clostridium spp, Lactobacillus spp, Peptostreptococcus spp, Peptococcus spp.
Spirochetes
Aerobes / facultative anaerobes
108 /g feces – E coli
105-106 /g feces – Klebsiella spp, Proteus spp, Enterococcus spp, other Enterobacteriaciae
Opportunistic Pathogens
Normal flora resist colonization by pathogens, protect the balance
Normal Microbial flora of the vagina
Lactobacillus spp
Coagulase negative staphylococci
To a lesser extent: Streptococcus agalactiae (group B streptococci) Streptococcus spp. Mycoplasma Enteric gram negatives anaerobes
The Modern Paradigm Shift
Advanced technologies and computational power has contributed to a new deeper understanding about the microbial flora
We continue to learn about the intricacies of the microbial flora, and what can be cultured and identified (microbiota) and what makes up the entirety of the microbial genetic diversity whether it can be cultured or not (microbiome)
Sites once considered “sterile” have been shown to have elaborate microbial ecosystems i.e urologic system, respiratory system
Understanding the microbiome provides opportunities for basic research and even therapeutics
Important test used for Molecular Pattern identification
MALDI: cornerstone for microbiology, MALDI: uses mass spectrometry. specimen is crystalized then hit with a lazer in a vaccum tube that is chilled. Ions fly to sensor, depending on mass to charge ratio. Generates a spectrum and compared to the digital library to identify it.
Which scheme would provide the most accurate identification?
A. Gram stain of an isolate
B. Culture and biochemical analysis of an isolate
C. MALDI-TOF analysis
D. Amplification and sequencing of 16S rRNA genes
D is most ACCURATE
however it is no readily available it most labs
Which scheme would provide the most commonly used in labs for identification purposes?
A. Gram stain of an isolate
B. Culture and biochemical analysis of an isolate
C. MALDI-TOF analysis
D. Amplification and sequencing of 16S rRNA genes
C.
Which scheme is sufficient in most cases to guide appropriate empiric therapy?
A. Gram stain of an isolate
B. Culture and biochemical analysis of an isolate
C. MALDI-TOF analysis
D. Amplification and sequencing of 16S rRNA genes
Answer A, i.e its enough to allow us to treat and give antibiotics
At least with broad spectrum antibacteria
How to remember which colour stain is gram positive vs negative:
Positive is Purple/blue = masculine
Negative is Red/pink= feminine
Which two categories of bacteria are the most medically important?
Gram positive cocci
and Gram negative bacilli
The three medically important gram positive cocci
- Staphylococcus spp
- Streptococcus spp
- Enterococcus spp
The two medically important gram negative bacilli
- Enterobacteriaceae/ Eneterobacteriales
2. Haemophilus spp
Exceptions to the rule for bacteria detection: what are their characteristics
Intracellular organisms minimal or NO cell wall Bizarre morphologies Difficult to culture Difficult to stain
i.e. chlamydia
Rickettsia
Mucoplasma
Anaplasma
What are 4 types of gram positive tests
a. Catalase test: to see if it can utilize hydrogen peroxide at a high concentration to see if it will cause it to bubble
catalyse positive = staphlococcus
catalyase negative = streptoccus
b. Coagulase Test: determines whether it can form a clot.
This test helps define staphylococcus aureus
c. Table top coagulase: also shows where the glutinase forms clumps
d. Hemolysis: the degree to which an organism is able to completely lyse RBC
Alpha = organisms that can partially lyse RBCs
Beta = ‘’ ‘’ complete lyses
Gamma = nil
Staphylococcus spp
- What is it
- able to colonize through
- related to what kinds of infection
s. aureus is a gram POSITIVE (purple, thick cell wall)
it is a facultative anaerobe
- colonization due to Fibronectin binding proteins
- MSCRAMMs : marker molecule
- NEVER consider this a contaminant
infection:
pyogenic (pus producing)
- cellulitis, Furuncles, Abscesses, Osteomyelitis, endocarditis
Colonization vs infection
Implies it is occupying an area, but not necessarily causing any important disease or inflammation
low levels + intact skin = colonization
high levels + break in skin = infection
Staph aureus releases 5 main SUPERANTIGENs
- what are they and how do they work?
what are two other things they release?
TSST (Binds MCHII on APCs making them release proinflammatory cells= cytokine storm) leads to Toxic Shock Syndrome
Exfoliatin Toxin causes SSSS(Staph scalded skin syndrome)/ Ritter’s disease: painful, blistering red skin: self limiting
Enterotoxin: on food, leads to food poisoning. In blood stream can =>TSS ^^
Hemolysins- attack RBC releasing Fe
Leukocidin - attack leukocytes/WBC
Two other things:
- it also releases coagulase, which is able to form clots
- Protein A: anchors antibodies inversely so it can’t opsonize/compliment system neither.
What test helps you identify
a. general staph infection
b. specifically staph aureus infection
a. staph are catalase positive: test that foams up confirms it is staph
b. staph aureus is coagulase positive
Staph Resistance and their general mechanisms
These mutations progressively get worse and worse. People who frequently use antibiotics/develop greater resistance will have something lower on the list.
the SA at the end is for Staph Aureus first S = sensitive I = intermediate R = resistant M = Methacilin V = vancomycin
MSSA: penicillinase expression, Majority. 50% of cellulitis pts have MSSA, s for sensitivity. Penicilin gets degraded
MRSA: expression of PBP-2a, mutation = resistance to B lactams used in AB
VISA [Vancomycin sensitive]: Super bulky peptidoglycan wall, decoy targets
VRSA: acquisition of vanA, genetically acquired, completely resistant to vancomycin
MIC creep
the degree to which we need AB to overcome resistance is increasing
Coagulase Negative Staphylococcus spp
s. epidermis
- common skin flora
- opportunistic pathogen- varied severity of disease
- implant/foreign body biofilms [Forms biofilms on foreign bodies like catheters ]
S. saprophyticus
- fairly common agent of urinary tract infection
S. Lugdunensis/ S. Schleiferi
- potentially aggressive disease, including endocarditis
Hospital vs Community Acquired resistance/staph infections
In hospital settings, patients are a group of people who are perscribed more antibiotics thus increased resistance levels: THUS increased virulence, multi-drug resistance will be seen
Community acquired: PVL expression [?] tends towards cutaneous abscesses, some aggressive manifestations (pulmonary), stereotypical resistance pattern) so more options to treat with AB
Group A streptococcus
These are the Beta-hemolytic strep
They are catalase NEGATIVE (positive for staph*)
organized as cocci in chains
ex. steptococcus pyogenes leads to strep throat.
Two types of diseases caused by Streptococcus pyogenes
- what group does this belong too?
This is a GROUP A STREPTOCOCCUS
Suppurative Diseases
- pus forming
Involve tissue, invasion damage and pus formation as opposed to
i.e. Meningitis, Sinusitis, Pharyngitis, Tonsilitis, Pneumonia, Skin (Impetigo, Erysipelas, Cellulitis), Necrotizing Fasciitis, Myositis
Non-suppurative Diseases
- does not produce puss
Non-suppurative complications occur after a latency period of a few weeks and include acute rheumatic fever, scarlet fever, streptococcal toxic shock syndrome, acute glomerulonephritis, and pediatric autoimmune neuropsychiatric disorder associated with group A streptococci
Meningitis
is an inflammation (swelling) of the protective membranes covering the brain and spinal cord. A bacterial or viral infection of the fluid surrounding the brain and spinal cord usually causes the swelling. However, injuries, cancer, certain drugs, and other types of infections also can cause meningitis.
Cellulitis
is a common bacterial skin infection that causes redness, swelling, and pain in the infected area of the skin. If untreated, it can spread and cause serious health problems. Good wound care and hygiene are important for preventing cellulitis.
Often Unilateral and lower extremities (athelete with swollen foot example in class)
Erysipelas:
is an infection of the upper layers of the skin (superficial). The most common cause is group A streptococcal bacteria, especially Streptococcus pyogenes. Erysipelas results in a fiery red rash with raised edges that can easily be distinguished from the skin around it.
Necrotizing Fascitis
aka flesh eating disease. s a rare bacterial infection that spreads quickly in the body and can cause death. Accurate diagnosis, rapid antibiotic treatment, and prompt surgery are important to stopping this infection. Cuts blood circulation which is what can lead to skin death
What is the primary reason to treat group A streptococcus Pharyngitis
A. Prevention of Parapharyngeal Abscess
B. Prevention of bacteremia
C. Prevention of Rheumatic heart disease
D. Prevention of post-streptococcal acute glomerular nephritis
E. Prevention of tonsillectomy
C!
we are aggressive in treating step so we see less rhematic heart disease
if not, can lead to RHD^
D. CAN’T be prevented with treatment. it will happen regardless.
Group A streptococcus Virulence Factors
ADHESION:
- Lipoteichoic acid/Protein F
- M protein
> adhesive, anti-compliment, MOLECULAR MIMICRY* [bases for RHD]
ANTIPHAGOCYTIC
- Hyaluronic acid capsule
ENZYMES:
- DNase, Hyaluronidases, streptolysin
SUPERANTIGENS
- Toxic shock Syndrome
Group B Streptococcus
Responsible for which infections?
- which is the most common type?
which age group is at GREATEST RISK** High index of suspicion
This is also a Beta Hemolytic Strep group
most commonly: stepcocc agalactiae
Neonatal Sepsis
Neonatal Meningitis
Prenatal Screening programs
Diabetic Wound infections
Steptococcus Pneumoniae
- what type is it
- Diseases associated with it
This is an ALPHA hemolytic strep
Diseases:
- Pneumonia: common agent of community-acquired
- Bacteremia
- Meningitis
- Sinusitis/ Acute Otitis media
Asplenic host, antibody deficiences people are more susceptible
Steptococcus Pneumoniae
- Virulence factors
- Invasive strains/ Resistance strains
- micro morphology
Virulence factors:
- H2O2 production, pneumolysin, autolysin
- most importantly: capsule, helps it avoid things
Invasive strains/ Resistance strains
- PRSP
- 19 A
Morphology
- diplococci
Viridans Streptococcus
Alpha hemolytic (some beta) Usually less virulent, can be members of the normal flora
Viridans Streptococcus
- Associated Diseases
- specific examples
Disease:
Dental Caries, Bacteremia, Endocarditis, Abscesses
S anginosus -> deep tissue abscesses
- can mimic group A streptococcus but smaller colonies
S mutans/ S Sanguis -> dental plaque and carries
Enterococcus
- type
- Where is it found
- Two medically important species
Gram positive
Non hemolytic [ but does group with the Lancefield group D]
Normal Flora of the GI tract and biliary tract
- Bile resistance, growth in high sodium content
Two medically important species
- E faecalis: LESS resistant
- E faecium: Relatively quite resistant [IV therapies only mostly]
Enterococcus
- Diseases
- Therapeutics
- VRE
Disease:
often a bystander- you don’t need to treat it directly, treat everything else and it will go away
UTIs, wound infections, intra-abdominal abscesses, cholangitis
Bacteremia, endocarditis
Therapeutics:
Minimal number of oral agents with good activity
Can employ syngergistic combinations
Decreasing number of active agents
VRE = Vancomycin Resistant Enterococcus
- plasmid mediated resistance- vanA [gene]
- Serious nosocomial [originating in hospitals] implications: wounds, lines, transfer or resistance genes
Listeria spp
- main mode of transmission
- types of disease it causes
- virulence factor
gram positive bacilli, spore forming
Major food born illness
Disease INVASIVE: - Meningitis - chorioamnionitis -Granulomatous infantiseptics - Bacteremia, endocarditis
NON-INVASIVE
- febrile diarrhea syndromes [culture negative]
Listeria spp
- virulence factors
- often confused for?
Listerolysin, ActA
- intracellular parasitism immune evasion
by hijacking transport mechanism of host cell and pushing the organism into neighboring cells
Difficult to diagnose in some cases
- often confused for Corynbacteria in CSF** if you see coryn, think of LISTERIA as possibility*
Corynebacteria
- where is it found
- diseases, key species [?]
Normal skin flora - rarely causing disease
A few important pathogens:
C diptheriae
- toxin mediated- disruption of translational elongation
- upper resp psuedomembrane
- Multiorgan involvement - myocarditis, peripheral neuropathy, cutaneous lesions
C urealyticum
- renal disease/ calculi
C Jeikeium
- multiresistant, bacteremia
Bacillus spp
- type
- diseases, and their agents
Gram positive and spore forming^
Disease
B cereus
- toxin mediated food poisoning (bad rice)
- Immunocompromised infections
B anthracis
Antharaz
- zoonoses/ Cat A biological weapon
- subterminal/ central spore
- non motile
- stereotypical appearance
- White tenacious colonies, "snowy peaks", medusa heads
Enterobacteriaceae
- where are they found
- general characteristics
- safe, dangerous?
Larger family representing the gram negative rods that are commonly found in animal intestinal tracts
General characteristics
- gram NEGATIVE bacilli
- oxidase NEG, catalase POS,
- they FERMENT GLUCOSE*, reduce nitrate
Vast majority are commensal organisms, some are opportunistic pathogens, some are virulent organisms unlikely to be found in abundance in a normal host
- enteric pathogens, urinary pathogens, blood stream infection
List common Enterobacteriaceae
Escherichia coli Klebsiella pneumoniae Salmonella enterica Enterobacter cloacae Shigella dysenteriae
How do you categorize enterobacteriaceae
All ferment glucose, but you can distinguish between them by
a. Lactose fermenters
b. Lactose non-fermenters
List the lactose fermenting Enterobacteriaceae
Klebsiella spp
E coli
Enterobacter
Serratia spp
(think Keys, KEES)
List the NON fermenters of Enterobacteriaceae
Salmonella spp
Shigella spp
Yersinia Enterocolitica
E coli and Klebsiella species are major urinary pathogens, how would a MacConkey plate help?
A. It would promote growth of Gram positive organisms and help isolate urinary pathogens
B. It would help differentiate lacotose fermenters from other pathogens
C. It selects for coliforms/ Gram negative rods
D. It provides a colourful alternative to sheep blood agar
E. B and C
E?
MacConkey Agar
Helpful to identify
“coliforms”/gram neg rods and lactose fermentation
to distinguish between different enterobacteriaceae
Salmonella and Shigella species are major enetric pathoens, how would a MacConkey plate help?
A. It would promote growth of Gram positive organisms and hlep isolate enteric pathoens
B. Translucent colonies could be further analysed
C. Pink colonies could be further analyzed
D. It is impossible to tell what is growin in stool as it is a 20% solution of bacteria
E. This is a useless test, let me do a PCR
B. because these are lactose NON FERMENTING so it will remain clear/yellow
Escherichia coli
- type
-
The prototypical gram negative rod
Primary culprit of urinary tract infections
- Adhesion molecules, pili
Can cause intra-abdominal infection, bacteremia and seed other sites
Majority of E coli live in harmony with the colonic flora and immune system
Some strains can make you very sick
What is the pathogenesis of Cholera and ETEC
ETEC = enterotoxigenic E coli
Causes intraluminal accumulation of Na+ and water = dehydrated type of diarrhea
Treatment is rehydrate
ETEC
= enterotoxigenic E coli
Diarrhea*
Enterotoxigenic Escherichia coli (E. coli), or ETEC, is an important cause of bacterial diarrheal illness. Infection with ETEC is the leading cause of travelers’ diarrhea and a major cause of diarrheal disease in lower-income countries, especially among children. ETEC is transmitted by food or water contaminated with animal or human feces. Infection can be prevented by avoiding or safely preparing foods and beverages that could be contaminated with the bacteria, as well as washing hands with soap frequently.
has the same pathogenesis of cholera
Treatment: rehydrate
Zoonosis
A zoonosis is an infectious disease that is transmitted between species from animals to humans
E coli O157: H7
- infective modality
- Toxin mechanism
Zoonosis
Not the only EHEC strain
Shigatoxin like toxin production
- Reactivation of lytic phage carrying toxin gene by physiologic stress (antibiotics) can enhance production and exposure
- Damage to endothelium, glomerulus, CNS endothelium
- TTP in adults, HUS in children (severe vascular outcomes)
Majority are SORBITOL non- fermenting
- use special SORB- MacConkey for diarrhea ( but may miss some!)
Salmonella/Shigella
Disease
Salmonella species
- Gastroenteritis
- Infection of vascular endothelium
- Infection of organ systems i.e osteomyelitis
- Typhoid fever
Shigella species
Has two mechanisms of disease:
a. Direct invasion → apoptosis [bloody diarrhea]
b. Shigatoxin → mucosal endothelial cell damage, Na disruption and intraluminal fluid accumulation
Pathogenesis of Typhoid Fever
- clinical symptoms
ingested into Small Intestine -> mesenteric lymph nodes -> Transient Bacteremia -> Multiplication in macrophages [liver, spleen, bone marrow]
leads to
a. Septicemia: Fever, kidney and other organs infected
b. through bile into gall bladder -> cholecystitis, carrier state
c. through bile into small intestine -> inflammation and ulceration of peyers patches -> diarrhea, hemorrhage, perforation
This comes in WAVES, the different symptoms comes and goes and gets worse
Vibrio Cholerae
Curved Gram negative rod
Epidemic / Pandemic
Toxin mediated disease
Acquired from contaminated water, shellfish
Profuse watery diarrhea
Rehydration is most critical therapy
Not distinctive on typical media for diarrhea
Pseudomonas
- what type
- where are they commonly found
- Significant subtype, characteristic features
Gram negative bacilli
- slightly thinner and longer than E coli
Most commonly encountered “glucose non-fermenter” (NOT under enterobacteriaceae)
Multiple species
Soil and water pathogen
P aeruginosa
- Metallic sheen, smells of grapes
- may express multiple important virulence factors
- Characterized by green appearance → expression of pyocyanin and pyoverdin (these are both virulence factors)
Can express a mucoid exopolysaccharide
Can form BIOFILM- gel for organisms to exist in a metabolic state, difficult for AB to penetrate
Biofilm formation
- triggers
- significance
Biofilms are a collective of one or more types of microorganisms that can grow on many different surfaces. Microorganisms that form biofilms include bacteria, fungi and protists. One common example of a biofilm dental plaque, a slimy buildup of bacteria that forms on the surfaces of teeth
Biofilm Formation Process. Bacteria form biofilms in response to environmental stresses such as UV radiation, desiccation, limited nutrients, extreme pH, extreme temperature, high salt concentrations, high pressure, and antimicrobial agents.
Pseudomonas
- where is infection likely
- what are some severe manifestations in altered immunity
- Diseases
Important nosocomial [hospital acquired] pathogen
Severe manifestations in altered immunity
- Febrile neutropenia, burns, cystic fibrosis patient
Disease includes
- Complicated urinary tract infections, ventilator associated pneumonia, line associated infections
- Necrotizing otitis externa, “hot tub” folliculitis
- Bacteremia, endocarditis, septic arthritis, osteomyelitis
- Post surgical infection
wide spectrum of disease seen^
Pseudomonas
- Virulence factors
- Quorum Sensing
- MDR (Multi- Drug Resistant)
Virulence factors
- Pili, flagella, LPS, Exotoxin A, Proteases, Phospholipases
- Alginate → antiphagocytic, biofilm formation
Quorum Sensing
- Autoinducers → “power in numbers”
- like a pheromone system: send molecules into environement and other cells nearby will start to activate genes in concert to form biofilm, virulence, resistance factors etc.
MDR – Pseudomonas aeruginosa. Occurs due to: - Rapid acquisition of resistance genes - Alteration of outer membrane permeability - Limited therapeutic options
Major Gram Negative Non- Fermenters
- Pseudomonas
- Stenotrophomonas maltophilia
- ICU VAE/VAP
3. Acinetobacter baumanii MDR Returned from Iraq ?via Germany ?via medical vessel
Neisseria
- what type is this
- name an important subtype, describe it
Gram negative diplococcus (paired-cocci)
Obligate human pathogens
Increased susceptibility in hosts with terminal complement cascade deficiencies, and humoral immune deficiencies
Meningococcus (N meningitidis)
- Agent of meningitis, meningococcemia → sepsis, shock, DIC
- 5-10% asymptomatic nasopharyngeal carrier rate
- Encapsulated
- Multiplication in the blood stream
vaccine preventable; YES vaccine for B
extreme outcome: necrosis of tissue
Gonoccus
This is a subtype of Neisseria/ (N gonorrhoeae)
Agent of gonorrhea, PID, epididymitis, infertility
Evade immune system by
- phase variation – genetic mechanisms that facilitate oscillation between expression and repression of adhesion virulence factors
- antigenic variation – genetic recombination resulting in altered pili expression
Gonococcemia
- Dermatitis-arthritis syndrome, bacteremia
Increasing antibiotic resistance (British “super” GC)
PID
Pelvic inflammatory disease is an infection of a woman’s reproductive organs. It is a complication often caused by some STDs, like chlamydia and gonorrhea. Other infections that are not sexually transmitted can also cause PID
Haemophilus
- type
- Disease
Gram negative small coccobacilli (coccoid-rods)
Opportunistic pathogen
Encapsulated – serotype a-f
Disease
- Classically Hib [heamo^ influenza b] associated with epiglotitis
- Encapsulated → septicemia, meningitis
- All → Pneumonia*, otitis media, conjunctivitis, sinusitis, osteomyelitis, skin infections
Vaccination has protected most individuals from aggressive forms of disease
Septicemia
Septicemia, or sepsis, is the clinical name for blood poisoning by bacteria. It is the body’s most extreme response to an infection.
Haemophilus
- morphology under microbe
put staph and this together on a plate:
- Demonstrates “satellitism”
- Growth around a streak of S aureus
Identify different species given dependence
on growth supplements and hemolysis on a QUAD plate
X – (unknown X-factor) hemin
V – (vitamin) NAD
Examples of Encapsulated Organisms
Neisseria meningitidis
Haemophilus influenzae
Streptococcus pneumoniae
There are others... However: there are vaccines available to protect against these specifically for people with: Hematologic disorders Splenectomy
“Fastidious” (or not) Gram negative bacilli
HACEK agents of endocarditis: Aggrigatibacter (Haemophilus) aphrophilus Aggrigatibacter actinomycetemcomitans Cardiobacterium hominis Eikenella corodens Kingella kingae (Bartonella henselae → “?BAACEK” )
Bites
- common animals and their bacteria’s
Cat
Pasteurella multocida
- Rapidly progressive extreme cellulitis
Dogs
Capnocytophyga canimorsus
Capnocytophyga cynodegnmi
- these are problematic for people who are Asplenic, immunocompromised → shock, DIC
Human bite
Eikenella corrodens
- Severe suppurative infection, septic arthritis, endocarditis
Bordetella pertussis
- common disease
- what are the three stages
- symptom
- Virulence factors
Disease Whooping cough - Catarrhal stage - Paroxysmal stage - Recovery stage
Chronic cough
Virulence factors
- Pertussis toxin (cAMP modulator), tracheal cytotoxin (murein analog), LPS, pili, filamentous hemagglutinin
Extremely contagious, vaccine preventable
Non- Invasive Bacterial Disease
A few select examples of agents that mediate disease by toxin:
B pertussis
C diphtheriae
V cholarae
C difficile, C tetani, C botulinum
Anaerobes
- Where can they be found
- more or less than E.coli?
- What type of infections do they lead to
- these do not need oxygen at all.
Normal microbial flora of colon
In colon, outnumber E coli 1000 to 1
Some species found in oral pharynx, gums, deep structures of skin
Often participate in polymicrobial infections
Pulmonary abscess, peritonitis/abdominal abscess
Pelvic infections
Upper respiratory infections
Anaerobes
& b-lactamases
Anerobes below the diaphram have B-lactamases but they don’t above the diaphragm
Clostridiodes Difficile
Spore forming, Gram positive anaerobic bacilli
Risk factors for serious infections:
Antibiotic use
Clindamycin, cephalosporins, fluoroquinolones
Immunocompromised
Elderly, cancer patient, low antibody levels
?Use of proton pump inhibitors
Use of NG tube
Clostridioides Difficile
- 2 active toxins
- One known dangerous strain
- Treatments
Has 2 active toxins – TcdA and TcdB (A and B)
Has a secondary binary toxin – cdtA and cdtB
Treatments:
Metronidazole, oral vancomycin, fidaxomicin, taper therapy, pulse therapy, IVIg, stool transplant (FMT)**
Mechanism of action of Clostridium difficile
- C. Difficile vegetative cells produce toxins A and B and hydrolytic enzymes.
- Local production of toxins A and B leads to production of tumour necrosis factor-alpha and pro-inflammatory interleukins, increased vascular permeability, neutrophil and monocyte recruitment
- Then the opening of epithelial cell junctions and epithelial cell apoptosis
- Local production of hydrolytic enzymes leads to connective tissue degradation, leading to colitis, pseudomembrane formation
and - WATERY DIARRHEA
Bacteroides
- where are they most commonly found
- characteristic of their survival
- Antibiotic response
The most prevalent bacterial component of the colonic flora
Opportunistic pathogen once breach in colonic mucosa
Minimal oxygen tolerance – upregulation of genes to defend against oxidative stress
Antibiotic resistance and transmission of resistance elements by conjugative transposons
- Clindamycin - >40% resistance (go to for above the diaphragm)
- Metronidazole - almost all susceptible (go to for below the diaphragm)
Where else are bacteroides found?
Oral spirochetes
Fusobacterium necrophorum
- Lemierre’s disease
- Septicemia, jugular vein thrombosis, metastatic abscesses
Aspiration resulting in anaerobic lung abscesses, empyema
- Risk factors: Seizures, alcoholics, poor dentition
Agents of Bacterial “Atypical Pneumonia”
Chlamydophila pneumoniae, Chlamydophila psitacci, Coxiella burnetti, Mycoplasma pneumoniae, Legionella pneumophilia, Mycobacterium tuberculosis
“walking pneumonia”: don’t make people super sick
Difficult to culture
- It’s a problem when TB is the most likely organism to grow
Molecular and serologic testing available
- upper and lower respiratory tract discordance can occur with samples
for molecular analysis
Legionella urinary antigen can be performed
- Only detects serovar 1
Which of the following is most correct concerning Mycobacteria?
- Tuberculosis is caused by a complex of Mycobacteria species, NTM cause similar pulmonary disease
- Leprosy is caused by Mycobacteria leprae
- Individuals with AIDS are susceptible to a systemic infection with M avium-intracellularae or MAC/MAI
- Non tuberculous mycobacteria are acid fast, and are ubiquitous in nature
- All of the above
Which is false concerning Chlamydia?
- Can lead to pelvic infection, remote peri-hepatic inflammation
- Can manifest as different STIs dependent on serotype
- Usually requires prolonged course of treatment
- Can lead to ocular disease
- Can result in asymptomatic carriage
- is false, one course is enough
everything else is true
Legionella
- type of bacteria
- two forms
- cause of symptoms
- known illness form it…
Gram negative rod
Associated with contaminated water systems in homes and institutions
Acquisition via infectious aerosols and microaspiration
Survives phagocytosis by immune phagocytes
There are two forms:
Replicative form ↔ transmissible form
Immune response to virulence factors (flagellin) mainly responsible for signs and symptoms
Pontiac fever- without the liver dysfunction and pneumonia
What is the parasite name for guinea worm
Draculunculus Medinensis
