MMSC 428 FINAL QUESTIONS AND ANSWERS
2025
Staphylococcus aureus - CORRECT ANSWER --gram positive cocci in clusters
-facultative aerobe (prefers O2)
-halo tonic
-ferment mannitol (yellow on MSA plate)
-catalase +
-*coagulase +*
-clumping factor +
-medium sized b-hemolytic white colonies
-serological tests for TSST-1 and DNA probes are the best diagnosis methods
-most clinically significant staphylococcus
-important cause of nosocomial infection
staphylococcus aureus virulence mechanisms - CORRECT ANSWER --protein A:
virulent cell wall protein that binds to IgG antibodies and prevents them from being
active
-hemolysis: produce B-hemolysis of RBCs
-exfoliating: causes epidermal layer of skin to peel off
-pyrogenic toxin: causes fever
-toxic shock syndrome toxin 1 (TSST-1): super antigen over stimulates the T cells and
produces cytokine storm
-Panton valentine leucocidin (PVL): lyses WBCs, platelets and RBCs
-staph coagulase: activates fibrin to cause clotting and prevent WBCs from reaching the
bacteria
-hyaluronidase: breaks down hyaluronic acid in tissue to spread bacteria
-lipases & proteases: destroy host tissues and spread bacteria
staphylococcus aureus clinical manifestations - CORRECT ANSWER --furuncle: large
raised supportive dome shaped boil due to infection of oil gland or hair follicle
-carbuncle: a furuncle that progresses and infects a deeper level of the skin, infection
causes systemic symptoms of fever and chills
-impetigo: bullous (>5 mm) domed fluid filled pustules surrounded by zone of erythema,
mainly seen in children
-cellulitis: inflammatory infection of connective tissue
-staphylococcal scalded skin syndrome (SSS): release of exfoliating exotoxin causes
exfoliate dermatitis with red peeling skin that resembles a burn, mainly in children and
newborns
,-toxic shock syndrome (TSS): release of TSST-1 and enterotoxin B cause systemic
symptoms including fever, liver and kidney damage, vomiting, diarrhea, muscle aches
and rash, menstrual and non-menstrual forms
-endocarditis
-intoxication food poisoning: food is contaminated with enterotoxins (no actual bacteria)
and causes vomiting and diarrhea
-nosocomial infections: wound infections, osteomyelitis, biofilm on body implants
-childhood infections: SIDS, head and neck infection
staphylococcus aureus drug resistance - CORRECT ANSWER --penicillin resistant due
to acquiring beta-lactamase genes
-MRSA: methicillin resistant staphylococcus aureus
-VISA: vancomycin intermediate staphylococcus aureus
-VRSA: vancomycin resistance staphylococcus aureus
staphylococcus epidermidis - CORRECT ANSWER --gram positive cocci in clusters
-nontitle
-facultative anaerobe (prefer O2)
-smooth, round, non-hemolytic white colonies on BSA
-staph coagulase - (indicated by the fact that it is no hemolytic)
-clumping factor -
-PYR -
-ODC d+
-is part of the normal biota, only causes opportunistic infections
-hospital acquired infections: biofilms, septicemia, osteomyelitis, catheter associated
UTI
staphylococcus lugdunensis - CORRECT ANSWER --gram positive cocci in clusters
-staph coagulase -
-clumping factor d+
-PYR +
-*ODC +* (very strong and fast)
-mannitol -
-no hemolytic
-oxacillin resistant (mea gene)
-highly virulent
-equally clinically significant as Staphylococcus aureus, just isolated less frequently
-community and hospital acquired infections: skin abscess, meningitis, septicemia,
septic shock, UTI
-endocarditis: very aggressive and fatal
,staphylococci characteristics - CORRECT ANSWER --gram positive cocci that grow in
clusters
-*catalase +* (good to differentiate from streptococcus)
-non-motile, lack flagella
-facultative anaerobes (prefer O2)
-lysostaphin sensitive
-glucose fermentation +
-modified oxidase test -
-bacitracin resistant
-produce a sticky glycocolyx that allow them to establish a biofilm
-important causes of hospital acquired infections
micrococcus - CORRECT ANSWER --gram positive cocci in pairs, tetrads or clumps
-related to staphylococci, but less clinically significant
-*lysostaphin resistant* (would only be able to lyse staphylococcus cells)
-glucose fermentation -
-modified oxidase (cytochrome C oxidase) +
-bacitracin sensitive
streptococcus pyogenic (group A strep) - CORRECT ANSWER --gram positive cocci in
chains
-Lancefield group A cell walls antigens
-aero tolerant anaerobe (fermentation only)
-modified oxidase test -
-catalase -
-*PYR +* (the only B-hemolytic strep that is)
-B-hemolytic
-bacitracin sensitive
-fastidious
-requires blood to be cultured
-small, transparent, dry colonies
-the most virulent streptococci
-usually detected using antigen detection or serology
streptococcus pyogenic (group A strep) virulence mechanisms - CORRECT ANSWER -
-streptomycin O: hemolysis that is active in anaerobic conditions, produces B-hemolysis
-streptomycin S: hemolysis that is active in aerobic conditions, produces B-hemolysis
-M protein: virulent protein that aids attachment to host cells and evades WBC
phagocytosis
, -hyaluronic acid capsule: weakly immunogenic, body does not fight it off
-pili: adhesion
-streptokinase: anti-clotting factor that breaks down clots so bacteria can spread
-hyaluronidase: breaks down skin and allows more bacterial spreading
-streptodornoase: breaks down extracellular DNA from lysed host cells and uses it to
make its own nucleic acids
streptococcus pyogenic (group A strep) clinical manifestations - CORRECT ANSWER --
pharyngitis: strep throat with malaise, fever, headache, nausea and vomiting, mainly
seen in children under 15 due to protective M-protein antibodies that adults have
-scarlet fever: untreated strep throat leads to release of erythrogenic toxins and breaks
down RBCs causing rash and damage to blood vessels that causes "strawberry
tongue", mainly seen in developing countries where strep does not get treated
-purpura fever (child bed fever): infection of infant that is inoculated with bacteria during
birth and leads to bacteremia/ sepsis
-impetigo: no bullous (<5 mm) lesions that leak and then crust over, mainly seen on the
face of children
-erysipelas: infection of dermis and subcutaneous tissue that causes inflamed lesions
on the skin, mainly in elderly individuals
-necrotizing fasciitis: "flesh eating bacteria" skin infection that rapidly progresses to
inflammation and necrosis of skin, fat and fascia membrane around muscle
-wound and burn infections, cellulitis
-streptococcal toxic shock syndrome: cold like symptoms progress to flu-like symptoms
and a fatal pneumonia
-sinusitis and OME common in children
streptococcus pyogenic culture - CORRECT ANSWER --throat swab for sample
-techniques are not well standardized between clinics
-SBA: can be used but normal biota would over populate
-selective strep agar (SSA): inhibits normal biota
Post-streptococcal sequelae (streptococcus pyogenic/ group A strep) - CORRECT
ANSWER --acute glomerulonephritis: antibodies bind to streptococcus pyogenic in the
blood and form large immune complexes which become trapped in the small vessels of
the kidneys, body attempts to clear out the immune complexes using complement,
WBCs, etc. and causes a type 3 hypersensitivity response that damages the kidneys
-acute rheumatic fever: body produces antibodies against M proteins that cross react
and attack antigens on the heart, leading to a type 1 hypersensitivity response that
causes valve damage
-both treated with penicillin
2025
Staphylococcus aureus - CORRECT ANSWER --gram positive cocci in clusters
-facultative aerobe (prefers O2)
-halo tonic
-ferment mannitol (yellow on MSA plate)
-catalase +
-*coagulase +*
-clumping factor +
-medium sized b-hemolytic white colonies
-serological tests for TSST-1 and DNA probes are the best diagnosis methods
-most clinically significant staphylococcus
-important cause of nosocomial infection
staphylococcus aureus virulence mechanisms - CORRECT ANSWER --protein A:
virulent cell wall protein that binds to IgG antibodies and prevents them from being
active
-hemolysis: produce B-hemolysis of RBCs
-exfoliating: causes epidermal layer of skin to peel off
-pyrogenic toxin: causes fever
-toxic shock syndrome toxin 1 (TSST-1): super antigen over stimulates the T cells and
produces cytokine storm
-Panton valentine leucocidin (PVL): lyses WBCs, platelets and RBCs
-staph coagulase: activates fibrin to cause clotting and prevent WBCs from reaching the
bacteria
-hyaluronidase: breaks down hyaluronic acid in tissue to spread bacteria
-lipases & proteases: destroy host tissues and spread bacteria
staphylococcus aureus clinical manifestations - CORRECT ANSWER --furuncle: large
raised supportive dome shaped boil due to infection of oil gland or hair follicle
-carbuncle: a furuncle that progresses and infects a deeper level of the skin, infection
causes systemic symptoms of fever and chills
-impetigo: bullous (>5 mm) domed fluid filled pustules surrounded by zone of erythema,
mainly seen in children
-cellulitis: inflammatory infection of connective tissue
-staphylococcal scalded skin syndrome (SSS): release of exfoliating exotoxin causes
exfoliate dermatitis with red peeling skin that resembles a burn, mainly in children and
newborns
,-toxic shock syndrome (TSS): release of TSST-1 and enterotoxin B cause systemic
symptoms including fever, liver and kidney damage, vomiting, diarrhea, muscle aches
and rash, menstrual and non-menstrual forms
-endocarditis
-intoxication food poisoning: food is contaminated with enterotoxins (no actual bacteria)
and causes vomiting and diarrhea
-nosocomial infections: wound infections, osteomyelitis, biofilm on body implants
-childhood infections: SIDS, head and neck infection
staphylococcus aureus drug resistance - CORRECT ANSWER --penicillin resistant due
to acquiring beta-lactamase genes
-MRSA: methicillin resistant staphylococcus aureus
-VISA: vancomycin intermediate staphylococcus aureus
-VRSA: vancomycin resistance staphylococcus aureus
staphylococcus epidermidis - CORRECT ANSWER --gram positive cocci in clusters
-nontitle
-facultative anaerobe (prefer O2)
-smooth, round, non-hemolytic white colonies on BSA
-staph coagulase - (indicated by the fact that it is no hemolytic)
-clumping factor -
-PYR -
-ODC d+
-is part of the normal biota, only causes opportunistic infections
-hospital acquired infections: biofilms, septicemia, osteomyelitis, catheter associated
UTI
staphylococcus lugdunensis - CORRECT ANSWER --gram positive cocci in clusters
-staph coagulase -
-clumping factor d+
-PYR +
-*ODC +* (very strong and fast)
-mannitol -
-no hemolytic
-oxacillin resistant (mea gene)
-highly virulent
-equally clinically significant as Staphylococcus aureus, just isolated less frequently
-community and hospital acquired infections: skin abscess, meningitis, septicemia,
septic shock, UTI
-endocarditis: very aggressive and fatal
,staphylococci characteristics - CORRECT ANSWER --gram positive cocci that grow in
clusters
-*catalase +* (good to differentiate from streptococcus)
-non-motile, lack flagella
-facultative anaerobes (prefer O2)
-lysostaphin sensitive
-glucose fermentation +
-modified oxidase test -
-bacitracin resistant
-produce a sticky glycocolyx that allow them to establish a biofilm
-important causes of hospital acquired infections
micrococcus - CORRECT ANSWER --gram positive cocci in pairs, tetrads or clumps
-related to staphylococci, but less clinically significant
-*lysostaphin resistant* (would only be able to lyse staphylococcus cells)
-glucose fermentation -
-modified oxidase (cytochrome C oxidase) +
-bacitracin sensitive
streptococcus pyogenic (group A strep) - CORRECT ANSWER --gram positive cocci in
chains
-Lancefield group A cell walls antigens
-aero tolerant anaerobe (fermentation only)
-modified oxidase test -
-catalase -
-*PYR +* (the only B-hemolytic strep that is)
-B-hemolytic
-bacitracin sensitive
-fastidious
-requires blood to be cultured
-small, transparent, dry colonies
-the most virulent streptococci
-usually detected using antigen detection or serology
streptococcus pyogenic (group A strep) virulence mechanisms - CORRECT ANSWER -
-streptomycin O: hemolysis that is active in anaerobic conditions, produces B-hemolysis
-streptomycin S: hemolysis that is active in aerobic conditions, produces B-hemolysis
-M protein: virulent protein that aids attachment to host cells and evades WBC
phagocytosis
, -hyaluronic acid capsule: weakly immunogenic, body does not fight it off
-pili: adhesion
-streptokinase: anti-clotting factor that breaks down clots so bacteria can spread
-hyaluronidase: breaks down skin and allows more bacterial spreading
-streptodornoase: breaks down extracellular DNA from lysed host cells and uses it to
make its own nucleic acids
streptococcus pyogenic (group A strep) clinical manifestations - CORRECT ANSWER --
pharyngitis: strep throat with malaise, fever, headache, nausea and vomiting, mainly
seen in children under 15 due to protective M-protein antibodies that adults have
-scarlet fever: untreated strep throat leads to release of erythrogenic toxins and breaks
down RBCs causing rash and damage to blood vessels that causes "strawberry
tongue", mainly seen in developing countries where strep does not get treated
-purpura fever (child bed fever): infection of infant that is inoculated with bacteria during
birth and leads to bacteremia/ sepsis
-impetigo: no bullous (<5 mm) lesions that leak and then crust over, mainly seen on the
face of children
-erysipelas: infection of dermis and subcutaneous tissue that causes inflamed lesions
on the skin, mainly in elderly individuals
-necrotizing fasciitis: "flesh eating bacteria" skin infection that rapidly progresses to
inflammation and necrosis of skin, fat and fascia membrane around muscle
-wound and burn infections, cellulitis
-streptococcal toxic shock syndrome: cold like symptoms progress to flu-like symptoms
and a fatal pneumonia
-sinusitis and OME common in children
streptococcus pyogenic culture - CORRECT ANSWER --throat swab for sample
-techniques are not well standardized between clinics
-SBA: can be used but normal biota would over populate
-selective strep agar (SSA): inhibits normal biota
Post-streptococcal sequelae (streptococcus pyogenic/ group A strep) - CORRECT
ANSWER --acute glomerulonephritis: antibodies bind to streptococcus pyogenic in the
blood and form large immune complexes which become trapped in the small vessels of
the kidneys, body attempts to clear out the immune complexes using complement,
WBCs, etc. and causes a type 3 hypersensitivity response that damages the kidneys
-acute rheumatic fever: body produces antibodies against M proteins that cross react
and attack antigens on the heart, leading to a type 1 hypersensitivity response that
causes valve damage
-both treated with penicillin
