Staphylococcus simulans is a coagulase-negative staphylococcus (CoNS) typically found in animals rather than humans. It is an opportunistic pathogen, especially among farm or domesticated animals such as cows, goats, and horses. One of the most common illnesses produced by S. simulans is bovine mastitis, a swelling of the udder in cows. Â
Although S. simulans seldom colonize human skin, it can cause diseases in humans, especially in those with diseases in humans, especially in those intimate contact with sick animals. Personnel employed by equine facilities or with a history of contact with farm animals may be more susceptible to illness.Â
On the other hand, S. simulans, a widespread mammalian pathogen, is rarely detected in human tissue and is typically recovered in 0.4%-2.1% of urinary samples. Healthcare professionals, veterinarians, and those working in agricultural fields may be more susceptible to S. simulans infestations. Â
simulans brings uncertainty to veterinary care and infects farm livestock, dogs & cats with illnesses. Bovine mastitis is an expensive illness for the dairy business; S. aureus intramammary invasions are common, and ruminant-associated modular complex strains are typically involved. Antibiotic-resistant Staphylococcus strains, both coagulase-positive & coagulase-negative, have become more common during the past few years, creating a severe challenge for both human and animal therapy.
Kingdom: BacteriaÂ
Phylum: BacillotaÂ
Class: BacilliÂ
Order: BacillalesÂ
Family: StaphylococcaceaeÂ
Genus: StaphylococcusÂ
Species: Staphylococcus simulansÂ
Staphylococcus simulans is a gram-positive bacterium that belongs to the Staphylococcus genus. Like other staphylococci, it is spherical and occurs in grape-like clusters. It typically ranges in size from 0.5 to 1.5 µm in diameter. Â
The bacterium has a cell envelope composed of multiple layers, including the cytoplasmic membrane, peptidoglycan layer, and an outer layer called the capsule or glycocalyx.Â
The cell wall consists of a mesh-like network of glycan chains cross-linked by peptide bridges, providing rigidity and shape to the cell.Â
The cytoplasmic membrane acts as a selective barrier, regulating the transit of nutrients out and in of the cell; it primarily comprises phospholipids.Â
Specific information regarding the antigenic types of S. simulans needs to be better studied, and the available literature needs to describe distinct serotypes or antigenic variations of S. simulans extensively.
Research in this area is relatively limited compared to other Staphylococcus species, such as Staphylococcusaureus. The literature does not provide comprehensive details on specific serotypes or antigenic variations within Staphylococcus simulans.Â
The exact pathogenesis of Staphylococcus simulans is not as well-characterized as that of Staphylococcus aureus, but several factors contribute to its potential to cause disease:Â Â
Autolysins, such as Atl (autolysin) and Sle1 (surface protein E), play essential roles in the pathogenesis of S. simulans; Atl promotes biofilm formation, which is a critical factor in Staphylococcussimulans virulence. It contributes to the attachment and accumulation of bacteria on surfaces, leading to the development of biofilms; Atl can degrade host antimicrobial peptides and modify the surface of Staphylococcus aureus, helping the bacteria evade immune recognition and clearance. Â
Sle1 (Surface Protein E) contributes to the development of biofilms on medical devices, which can lead to persistent infections. It can promote antimicrobial resistance. Â
Staphylococcus simulans can produce cytolytic toxins that can lyse host cells. Alpha-toxin, also known as alpha-hemolysin, is a pore-forming toxin; it can form pores in the membranes of host cells, leading to cell lysis and tissue damage. Â
Beta-toxin, also called sphingomyelinase C, is another cytolytic toxin produced by some strains of S. simulans. It hydrolyzes sphingomyelin, a significant component of cell membranes, disrupting cell integrity and lysis.Â
Lysozyme, an enzyme in various bodily secretions such as tears, saliva, and mucus, plays a crucial role in human defense against Staphylococcus simulans. Lysozyme catalyzes the hydrolysis of the glycosidic bonds in the peptidoglycan structure, disrupting and degrading the S. simulans cell wall. Â
Antimicrobial peptides (AMPs): These are small peptides integral to the innate immune system’s response to S. simulans. These peptides have broad-spectrum antimicrobial activity,Â
Psoriasin, or S100A7, is an AMP predominantly expressed in the skin and mucosal tissues. It can disrupt the bacterial cell membrane and induce S. simulans‘ death. Â
Dermcidin is an antimicrobial peptide primarily found in human sweat. Eccrine sweat glands produce it, which has been shown to have antimicrobial activity against S. simulans. Dermcidin has been found to inhibit biofilm formation by interfering with the initial attachment of bacteria to surfaces and disrupting the biofilm matrix. Â
Histatins possess immunomodulatory properties that can influence the host’s immune response against S. simulans. Histatins are a family of antimicrobial peptides primarily found in human saliva. They can regulate the production of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). By influencing the levels of these cytokines, histatins can help regulate the magnitude and duration of inflammation during S. simulans infections.Â
Host defense against S. simulans involves a complex interplay between pro-inflammatory signals and the adhesion and extravasation of neutrophils across capillary endothelial. Pro-inflammatory signals, such as cytokines and chemokines, induce the upregulation and activation of endothelial receptors, including P-/E-selectins, ICAM-1 (intercellular adhesion molecule-1), and hyaluronan. These receptors interact with specific ligands present on the surfaces of neutrophils, such as PSGL-1 (P-selectin glycoprotein ligand-1), LFA-1 (lymphocyte function-associated antigen-1), Mac-1 (Macrophage-1 antigen), and CD44. Â
These reciprocal interactions facilitate neutrophil adhesion to the endothelial cells lining blood vessels and subsequent extravasation into the infected tissues. Once extravasated, neutrophils can phagocytose and kill S. simulans through various mechanisms, including releasing antimicrobial substances and forming neutrophil extracellular traps (NETs). This coordinated response involving pro-inflammatory signals, endothelial receptors, and neutrophil ligands is essential for effective host defense against Staphylococcus infections.Â
Osteoarticular Infections: Staphylococcus simulans can cause bone and joint infections, leading to osteomyelitis (bone infection) or septic arthritis. These infections can result in localized pain, swelling, limited motion, and other signs of inflammation.Â
Native Valve Endocarditis:S. simulans has been associated with infective endocarditis, particularly involving native heart valves. Native valve endocarditis is an infection of the inner lining of the heart & heart valves. Symptoms may include fever, fatigue, heart murmur, and signs of systemic infection.  Â
Diabetic Osteitis: In individuals with diabetes, S. simulans cause osteomyelitis, explicitly affecting the foot or other bones. Diabetic osteitis refers to bone infection associated with diabetic foot ulcers or other diabetic-related complications.Â
Gram Staining: A Gram stain is performed on the isolated colonies to determine their Gram reaction. Under the microscope, Staphylococcus simulans appear as Gram-positive cocci in clusters resembling grapes. Â
Culture method: The Baird Parker medium is a selective and differential culture method used to diagnose Staphylococcus simulans. It typically consists of a selective agent called lithium chloride, which inhibits the growth of Gram-negative bacteria and egg yolk and tellurite, which help differentiate S. simulans from other Staphylococcus species. S. simulans colonies may appear as large, gray to black colonies with a glossy appearance. Â
Biochemical test: A coagulase test is performed for Staphylococcus simulans; since it is a coagulase-negative staphylococcus (CoNS), it does not produce the coagulase enzyme in the coagulase test, plasma is added to a bacterial culture, and if the bacteria produce coagulase, it will cause clotting of the plasma. Since S. simulans is coagulase-negative, it will not cause clotting, distinguishing it from coagulase-positive staphylococci like Staphylococcusaureus.Â
Practicing good hygiene is essential to control the spread of S. simulans. It includes regular handwashing with soap and water or using alcohol-based hand sanitizers. Proper hand hygiene should be followed by healthcare workers, individuals working with animals, and those in close contact with infected individuals.
In animal settings, proper animal management practices, including regular veterinary care, hygiene protocols, and isolation of infected animals, can help prevent the transmission of S. simulans. Good husbandry practices and appropriate sanitation measures are essential to minimize the risk of infection.Â
Staphylococcus simulans is a coagulase-negative staphylococcus (CoNS) typically found in animals rather than humans. It is an opportunistic pathogen, especially among farm or domesticated animals such as cows, goats, and horses. One of the most common illnesses produced by S. simulans is bovine mastitis, a swelling of the udder in cows. Â
Although S. simulans seldom colonize human skin, it can cause diseases in humans, especially in those with diseases in humans, especially in those intimate contact with sick animals. Personnel employed by equine facilities or with a history of contact with farm animals may be more susceptible to illness.Â
On the other hand, S. simulans, a widespread mammalian pathogen, is rarely detected in human tissue and is typically recovered in 0.4%-2.1% of urinary samples. Healthcare professionals, veterinarians, and those working in agricultural fields may be more susceptible to S. simulans infestations. Â
simulans brings uncertainty to veterinary care and infects farm livestock, dogs & cats with illnesses. Bovine mastitis is an expensive illness for the dairy business; S. aureus intramammary invasions are common, and ruminant-associated modular complex strains are typically involved. Antibiotic-resistant Staphylococcus strains, both coagulase-positive & coagulase-negative, have become more common during the past few years, creating a severe challenge for both human and animal therapy.
Kingdom: BacteriaÂ
Phylum: BacillotaÂ
Class: BacilliÂ
Order: BacillalesÂ
Family: StaphylococcaceaeÂ
Genus: StaphylococcusÂ
Species: Staphylococcus simulansÂ
Staphylococcus simulans is a gram-positive bacterium that belongs to the Staphylococcus genus. Like other staphylococci, it is spherical and occurs in grape-like clusters. It typically ranges in size from 0.5 to 1.5 µm in diameter. Â
The bacterium has a cell envelope composed of multiple layers, including the cytoplasmic membrane, peptidoglycan layer, and an outer layer called the capsule or glycocalyx.Â
The cell wall consists of a mesh-like network of glycan chains cross-linked by peptide bridges, providing rigidity and shape to the cell.Â
The cytoplasmic membrane acts as a selective barrier, regulating the transit of nutrients out and in of the cell; it primarily comprises phospholipids.Â
Specific information regarding the antigenic types of S. simulans needs to be better studied, and the available literature needs to describe distinct serotypes or antigenic variations of S. simulans extensively.
Research in this area is relatively limited compared to other Staphylococcus species, such as Staphylococcusaureus. The literature does not provide comprehensive details on specific serotypes or antigenic variations within Staphylococcus simulans.Â
The exact pathogenesis of Staphylococcus simulans is not as well-characterized as that of Staphylococcus aureus, but several factors contribute to its potential to cause disease:Â Â
Autolysins, such as Atl (autolysin) and Sle1 (surface protein E), play essential roles in the pathogenesis of S. simulans; Atl promotes biofilm formation, which is a critical factor in Staphylococcussimulans virulence. It contributes to the attachment and accumulation of bacteria on surfaces, leading to the development of biofilms; Atl can degrade host antimicrobial peptides and modify the surface of Staphylococcus aureus, helping the bacteria evade immune recognition and clearance. Â
Sle1 (Surface Protein E) contributes to the development of biofilms on medical devices, which can lead to persistent infections. It can promote antimicrobial resistance. Â
Staphylococcus simulans can produce cytolytic toxins that can lyse host cells. Alpha-toxin, also known as alpha-hemolysin, is a pore-forming toxin; it can form pores in the membranes of host cells, leading to cell lysis and tissue damage. Â
Beta-toxin, also called sphingomyelinase C, is another cytolytic toxin produced by some strains of S. simulans. It hydrolyzes sphingomyelin, a significant component of cell membranes, disrupting cell integrity and lysis.Â
Lysozyme, an enzyme in various bodily secretions such as tears, saliva, and mucus, plays a crucial role in human defense against Staphylococcus simulans. Lysozyme catalyzes the hydrolysis of the glycosidic bonds in the peptidoglycan structure, disrupting and degrading the S. simulans cell wall. Â
Antimicrobial peptides (AMPs): These are small peptides integral to the innate immune system’s response to S. simulans. These peptides have broad-spectrum antimicrobial activity,Â
Psoriasin, or S100A7, is an AMP predominantly expressed in the skin and mucosal tissues. It can disrupt the bacterial cell membrane and induce S. simulans‘ death. Â
Dermcidin is an antimicrobial peptide primarily found in human sweat. Eccrine sweat glands produce it, which has been shown to have antimicrobial activity against S. simulans. Dermcidin has been found to inhibit biofilm formation by interfering with the initial attachment of bacteria to surfaces and disrupting the biofilm matrix. Â
Histatins possess immunomodulatory properties that can influence the host’s immune response against S. simulans. Histatins are a family of antimicrobial peptides primarily found in human saliva. They can regulate the production of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). By influencing the levels of these cytokines, histatins can help regulate the magnitude and duration of inflammation during S. simulans infections.Â
Host defense against S. simulans involves a complex interplay between pro-inflammatory signals and the adhesion and extravasation of neutrophils across capillary endothelial. Pro-inflammatory signals, such as cytokines and chemokines, induce the upregulation and activation of endothelial receptors, including P-/E-selectins, ICAM-1 (intercellular adhesion molecule-1), and hyaluronan. These receptors interact with specific ligands present on the surfaces of neutrophils, such as PSGL-1 (P-selectin glycoprotein ligand-1), LFA-1 (lymphocyte function-associated antigen-1), Mac-1 (Macrophage-1 antigen), and CD44. Â
These reciprocal interactions facilitate neutrophil adhesion to the endothelial cells lining blood vessels and subsequent extravasation into the infected tissues. Once extravasated, neutrophils can phagocytose and kill S. simulans through various mechanisms, including releasing antimicrobial substances and forming neutrophil extracellular traps (NETs). This coordinated response involving pro-inflammatory signals, endothelial receptors, and neutrophil ligands is essential for effective host defense against Staphylococcus infections.Â
Osteoarticular Infections: Staphylococcus simulans can cause bone and joint infections, leading to osteomyelitis (bone infection) or septic arthritis. These infections can result in localized pain, swelling, limited motion, and other signs of inflammation.Â
Native Valve Endocarditis:S. simulans has been associated with infective endocarditis, particularly involving native heart valves. Native valve endocarditis is an infection of the inner lining of the heart & heart valves. Symptoms may include fever, fatigue, heart murmur, and signs of systemic infection.  Â
Diabetic Osteitis: In individuals with diabetes, S. simulans cause osteomyelitis, explicitly affecting the foot or other bones. Diabetic osteitis refers to bone infection associated with diabetic foot ulcers or other diabetic-related complications.Â
Gram Staining: A Gram stain is performed on the isolated colonies to determine their Gram reaction. Under the microscope, Staphylococcus simulans appear as Gram-positive cocci in clusters resembling grapes. Â
Culture method: The Baird Parker medium is a selective and differential culture method used to diagnose Staphylococcus simulans. It typically consists of a selective agent called lithium chloride, which inhibits the growth of Gram-negative bacteria and egg yolk and tellurite, which help differentiate S. simulans from other Staphylococcus species. S. simulans colonies may appear as large, gray to black colonies with a glossy appearance. Â
Biochemical test: A coagulase test is performed for Staphylococcus simulans; since it is a coagulase-negative staphylococcus (CoNS), it does not produce the coagulase enzyme in the coagulase test, plasma is added to a bacterial culture, and if the bacteria produce coagulase, it will cause clotting of the plasma. Since S. simulans is coagulase-negative, it will not cause clotting, distinguishing it from coagulase-positive staphylococci like Staphylococcusaureus.Â
Practicing good hygiene is essential to control the spread of S. simulans. It includes regular handwashing with soap and water or using alcohol-based hand sanitizers. Proper hand hygiene should be followed by healthcare workers, individuals working with animals, and those in close contact with infected individuals.
In animal settings, proper animal management practices, including regular veterinary care, hygiene protocols, and isolation of infected animals, can help prevent the transmission of S. simulans. Good husbandry practices and appropriate sanitation measures are essential to minimize the risk of infection.Â
Staphylococcus simulans is a coagulase-negative staphylococcus (CoNS) typically found in animals rather than humans. It is an opportunistic pathogen, especially among farm or domesticated animals such as cows, goats, and horses. One of the most common illnesses produced by S. simulans is bovine mastitis, a swelling of the udder in cows. Â
Although S. simulans seldom colonize human skin, it can cause diseases in humans, especially in those with diseases in humans, especially in those intimate contact with sick animals. Personnel employed by equine facilities or with a history of contact with farm animals may be more susceptible to illness.Â
On the other hand, S. simulans, a widespread mammalian pathogen, is rarely detected in human tissue and is typically recovered in 0.4%-2.1% of urinary samples. Healthcare professionals, veterinarians, and those working in agricultural fields may be more susceptible to S. simulans infestations. Â
simulans brings uncertainty to veterinary care and infects farm livestock, dogs & cats with illnesses. Bovine mastitis is an expensive illness for the dairy business; S. aureus intramammary invasions are common, and ruminant-associated modular complex strains are typically involved. Antibiotic-resistant Staphylococcus strains, both coagulase-positive & coagulase-negative, have become more common during the past few years, creating a severe challenge for both human and animal therapy.
Kingdom: BacteriaÂ
Phylum: BacillotaÂ
Class: BacilliÂ
Order: BacillalesÂ
Family: StaphylococcaceaeÂ
Genus: StaphylococcusÂ
Species: Staphylococcus simulansÂ
Staphylococcus simulans is a gram-positive bacterium that belongs to the Staphylococcus genus. Like other staphylococci, it is spherical and occurs in grape-like clusters. It typically ranges in size from 0.5 to 1.5 µm in diameter. Â
The bacterium has a cell envelope composed of multiple layers, including the cytoplasmic membrane, peptidoglycan layer, and an outer layer called the capsule or glycocalyx.Â
The cell wall consists of a mesh-like network of glycan chains cross-linked by peptide bridges, providing rigidity and shape to the cell.Â
The cytoplasmic membrane acts as a selective barrier, regulating the transit of nutrients out and in of the cell; it primarily comprises phospholipids.Â
Specific information regarding the antigenic types of S. simulans needs to be better studied, and the available literature needs to describe distinct serotypes or antigenic variations of S. simulans extensively.
Research in this area is relatively limited compared to other Staphylococcus species, such as Staphylococcusaureus. The literature does not provide comprehensive details on specific serotypes or antigenic variations within Staphylococcus simulans.Â
The exact pathogenesis of Staphylococcus simulans is not as well-characterized as that of Staphylococcus aureus, but several factors contribute to its potential to cause disease:Â Â
Autolysins, such as Atl (autolysin) and Sle1 (surface protein E), play essential roles in the pathogenesis of S. simulans; Atl promotes biofilm formation, which is a critical factor in Staphylococcussimulans virulence. It contributes to the attachment and accumulation of bacteria on surfaces, leading to the development of biofilms; Atl can degrade host antimicrobial peptides and modify the surface of Staphylococcus aureus, helping the bacteria evade immune recognition and clearance. Â
Sle1 (Surface Protein E) contributes to the development of biofilms on medical devices, which can lead to persistent infections. It can promote antimicrobial resistance. Â
Staphylococcus simulans can produce cytolytic toxins that can lyse host cells. Alpha-toxin, also known as alpha-hemolysin, is a pore-forming toxin; it can form pores in the membranes of host cells, leading to cell lysis and tissue damage. Â
Beta-toxin, also called sphingomyelinase C, is another cytolytic toxin produced by some strains of S. simulans. It hydrolyzes sphingomyelin, a significant component of cell membranes, disrupting cell integrity and lysis.Â
Lysozyme, an enzyme in various bodily secretions such as tears, saliva, and mucus, plays a crucial role in human defense against Staphylococcus simulans. Lysozyme catalyzes the hydrolysis of the glycosidic bonds in the peptidoglycan structure, disrupting and degrading the S. simulans cell wall. Â
Antimicrobial peptides (AMPs): These are small peptides integral to the innate immune system’s response to S. simulans. These peptides have broad-spectrum antimicrobial activity,Â
Psoriasin, or S100A7, is an AMP predominantly expressed in the skin and mucosal tissues. It can disrupt the bacterial cell membrane and induce S. simulans‘ death. Â
Dermcidin is an antimicrobial peptide primarily found in human sweat. Eccrine sweat glands produce it, which has been shown to have antimicrobial activity against S. simulans. Dermcidin has been found to inhibit biofilm formation by interfering with the initial attachment of bacteria to surfaces and disrupting the biofilm matrix. Â
Histatins possess immunomodulatory properties that can influence the host’s immune response against S. simulans. Histatins are a family of antimicrobial peptides primarily found in human saliva. They can regulate the production of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). By influencing the levels of these cytokines, histatins can help regulate the magnitude and duration of inflammation during S. simulans infections.Â
Host defense against S. simulans involves a complex interplay between pro-inflammatory signals and the adhesion and extravasation of neutrophils across capillary endothelial. Pro-inflammatory signals, such as cytokines and chemokines, induce the upregulation and activation of endothelial receptors, including P-/E-selectins, ICAM-1 (intercellular adhesion molecule-1), and hyaluronan. These receptors interact with specific ligands present on the surfaces of neutrophils, such as PSGL-1 (P-selectin glycoprotein ligand-1), LFA-1 (lymphocyte function-associated antigen-1), Mac-1 (Macrophage-1 antigen), and CD44. Â
These reciprocal interactions facilitate neutrophil adhesion to the endothelial cells lining blood vessels and subsequent extravasation into the infected tissues. Once extravasated, neutrophils can phagocytose and kill S. simulans through various mechanisms, including releasing antimicrobial substances and forming neutrophil extracellular traps (NETs). This coordinated response involving pro-inflammatory signals, endothelial receptors, and neutrophil ligands is essential for effective host defense against Staphylococcus infections.Â
Osteoarticular Infections: Staphylococcus simulans can cause bone and joint infections, leading to osteomyelitis (bone infection) or septic arthritis. These infections can result in localized pain, swelling, limited motion, and other signs of inflammation.Â
Native Valve Endocarditis:S. simulans has been associated with infective endocarditis, particularly involving native heart valves. Native valve endocarditis is an infection of the inner lining of the heart & heart valves. Symptoms may include fever, fatigue, heart murmur, and signs of systemic infection.  Â
Diabetic Osteitis: In individuals with diabetes, S. simulans cause osteomyelitis, explicitly affecting the foot or other bones. Diabetic osteitis refers to bone infection associated with diabetic foot ulcers or other diabetic-related complications.Â
Gram Staining: A Gram stain is performed on the isolated colonies to determine their Gram reaction. Under the microscope, Staphylococcus simulans appear as Gram-positive cocci in clusters resembling grapes. Â
Culture method: The Baird Parker medium is a selective and differential culture method used to diagnose Staphylococcus simulans. It typically consists of a selective agent called lithium chloride, which inhibits the growth of Gram-negative bacteria and egg yolk and tellurite, which help differentiate S. simulans from other Staphylococcus species. S. simulans colonies may appear as large, gray to black colonies with a glossy appearance. Â
Biochemical test: A coagulase test is performed for Staphylococcus simulans; since it is a coagulase-negative staphylococcus (CoNS), it does not produce the coagulase enzyme in the coagulase test, plasma is added to a bacterial culture, and if the bacteria produce coagulase, it will cause clotting of the plasma. Since S. simulans is coagulase-negative, it will not cause clotting, distinguishing it from coagulase-positive staphylococci like Staphylococcusaureus.Â
Practicing good hygiene is essential to control the spread of S. simulans. It includes regular handwashing with soap and water or using alcohol-based hand sanitizers. Proper hand hygiene should be followed by healthcare workers, individuals working with animals, and those in close contact with infected individuals.
In animal settings, proper animal management practices, including regular veterinary care, hygiene protocols, and isolation of infected animals, can help prevent the transmission of S. simulans. Good husbandry practices and appropriate sanitation measures are essential to minimize the risk of infection.Â
Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.
Digital Certificate PDF
On course completion, you will receive a full-sized presentation quality digital certificate.
medtigo Simulation
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.
medtigo Points
medtigo points is our unique point redemption system created to award users for interacting on our site. These points can be redeemed for special discounts on the medtigo marketplace as well as towards the membership cost itself.
Community Forum post/reply = 5 points
*Redemption of points can occur only through the medtigo marketplace, courses, or simulation system. Money will not be credited to your bank account. 10 points = $1.
All Your Certificates in One Place
When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.
