APP 1 Chapitre

Question 1

True or false

Answer 1

Staphylococci are Gram-positive cocci that form grapelike clusters. They include Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus saprophyticus (which almost exclusively causes urinary tract infections), and numerous others.

Question 2

Encounter with staph?

Answer 2

Organisms grow on the surface of humans and survive on inanimate surface. During a lifetime, ~90% of humans are colonized at some point with S aureus in their external nares or skin.

Question 3

Entry of staph?

Answer 3

Carriage of staphylococci usually occurs after direct, skin-to-skin contact with another carrier. Infection may also occur after penetration of a contaminated object through the skin.

Question 4

Spread and Multiplication of staph?

Answer 4

Commensal staphylococci (eg, S epidermidis) are colonizers of normal skin and rarely cause deeper infection unless they are physically introduced into deeper tissues in association with an intravenous catheter or other artificial device. Virulent staphylococci (ie, S aureus) may cause skin and mucous membrane infections, from which organisms may disseminate to almost any organ or tissue.

Question 5

Damage of S aureus?

Answer 5

S aureus is pyogenic (“pus forming”), except in toxic shock syndrome, which may occur with nonpyogenic infection. Staphylococci cause skin and soft tissue infections (such as furuncles, abscesses, and necrotizing fasciitis), pneumonia, food poisoning, and toxin-induced diseases (toxic shock and scalded skin syndromes). If the organisms enter the bloodstream, they may cause osteomyelitis, kidney abscesses, or endocarditis.S aureus produces microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), including peptidoglycan, teichoic acids, protein A, clumping factor, and others. They also secrete virulence factors such as hemolysins, leukocidins, superantigens, and other exotoxins.

Question 6

Diagnosis of staph?

Answer 6

Staphylococci have a characteristic appearance on Gram stain, and they are easily isolated on most laboratory media.

Question 7

Treatment of staph?

Answer 7

Most strains produce β-lactamase (an enzyme that breaks down penicillin). Consequently, antistaphylococcal penicillins or cephalosporins are used. However, some strains express penicillin-binding protein 2a, which also makes the organism resistant to the above-mentioned agents (methicillin-resistant S aureus or MRSA). Drainage of abscesses and supportive therapy for hypotension and shock are also critical, nonantimicrobial elements of care.

Question 8

Prévention staph?

Answer 8

There is no vaccine against staphylococci.

Question 9

What is staph aureus?

Answer 9

STAPHYLOCOCCUS AUREUS (Gram-positive cocci) are the most common of the pyogenic, or pus-producing, bacteria that cause human diseases. They colonize the anterior nares of 30%-40% of individuals and may be present on other mucous membranes and the skin.

Question 10

Diseases caused by staph aureus?

Answer 10

Skin and soft tissue infections
Furuncles, carbuncles, paronychia (nail infections)
Wound infections (traumatic, surgical)
Cellulitis
Impetigo (also caused by streptococci)

Bacteremia (frequently with metastatic abscesses)

Endocarditis

Central nervous system infections
Brain abscess
Meningitis (rare)
Epidural abscess

Pulmonary infections
Embolic
Aspiration

Musculoskeletal infections
Osteomyelitis
Arthritis

Genitourinary tract infections
Renal abscess
Lower urinary tract infection

Toxin-related diseases
Toxic shock syndrome
Necrotizing pneumonia
Scalded skin syndrome
Extreme pyrexia syndrome
Food poisoning (gastroenteritis)

Question 11

Why can staph aureus survive in almost any environnement?

Answer 11

Staphylococcus aureus is a large (1 μm in diameter) Gram-positive coccus that grows in grapelike clusters. It is one of the hardiest of the non–spore-forming bacteria and can survive for long periods on dry, inanimate objects. It is also relatively heat resistant. These properties permit S aureus to survive in almost any environment in which humans coexist.

Question 12

Staphylococcus epidermidis

Answer 12

The most ubiquitous Staphylococcus species is Staphylococcus epidermidis, which is found on the skin and mucous membranes of most people and only infrequently causes disease in healthy individuals. This organism causes numerous infections in hospitals and in patients with implanted artificial devices (eg, -intravenous catheters, vascular grafts, and artificial joints).

Question 13

S aureus

Answer 13

S aureus generally causes more serious infections, including pneumonia, bone and joint infections, endocarditis, sepsis, and severe life-threatening TSS. The species name aureus means “golden” and refers to carotenoid pigmentation of S aureus colonies (other species colonies are white, but occasionally, S aureus colonies are also white)

Question 14

Staphylococcus saprophyticus

Answer 14

Staphylococcus saprophyticus is unique in that it causes only urinary tract infections.

Question 15

Staphylococcus lugdunensis,

Answer 15

A fourth species, Staphylococcus lugdunensis, is an uncommon cause of aggressive endocarditis. The genus Staphylococcus contains other species that occasionally cause disease; those species are described in standard microbiological texts.

Question 16

Caracteristics (coagulase and colonies and common) of 4 species of staph?

Answer 16

Question 17

2 tests to identify strains?

Answer 17

Within a species of staphylococci, individual strains can be identified by differences in their resistance to a panel of antibiotics and by using a procedure called phage typing or, more commonly, pulsed field gel electrophoresis. Phage typing, which is rarely done today, involves determining the sensitivity of a strain to a variety of standard bacteriophages. Pulsed field gel electrophoresis involves isolating staphylococcal DNA, treating the DNA with restriction enzymes that cut the DNA only rarely, and then resolving those DNA fragments in agarose gels. The newer molecular techniques for typing staphylococci based on the DNA sequence of the bacterial chromosome provide greater discrimination than phage typing between outbreak-related and non–outbreak-related strains and, as shown in the cases cited in this chapter, showed the relatedness of the organisms.

Question 18

Where are staph found?

Answer 18

Staphylococci share their environment with that of human beings. They live on people and survive on inanimate objects and surfaces (fomites), such as bedding, clothing, and doorknobs. Humans are the major reservoir for S aureus. The organisms frequently colonize the anterior nares and are found in ~30% of healthy individuals. However, studies of individuals over time have found that up to 90% of people are eventually colonized in the nares with S aureus at some point in their lives. The organisms can also be found transiently on the skin, oropharynx, and vagina and in feces. Staphylococci are well equipped to colonize the skin because they grow at high salt and lipid concentrations. They make enzymes, referred to as lipases and glycerol ester hydrolases, that degrade skin lipids.

Question 19

Cell surface proteins for staph aureus?

Answer 19

The ability of S aureus to colonize the skin and mucosal surfaces has been associated with bacterial cell surface proteins—the MSCRAMMs (microbial surface components recognizing adhesive matrix molecules)—that bind to a variety of host extracellular matrix proteins. Fibronectin-binding proteins (FnbpA and FnbpB) have been identified on the surface of S aureus. Fnbp’s allow the bacteria to invade epithelial and endothelial cells and to attach to exposed fibronectin in wounds, which may make FnbpA and FnbpB important virulence factors for the invasion of deeper tissues. S aureus also has MSCRAMMs for collagen binding, called CNAs. They are important components of connective tissue, bones, and joints. Other MSCRAMMs, called clumping factors A and B, are present for fibrinogen binding and experimentally have been shown to be important in clot formation and endocarditis. These proteins are responsible for the clumping seen in the slide coagulase test.

Question 20

Who gets more staph aureus?

Answer 20

Staphylococci spread from person to person, usually through direct contact or aerosols associated with upper respiratory viral or bacterial infections. It is important to remember that S aureus is an important secondary pathogen associated with patients recovering from influenza and parainfluenza (croup) infections. Infants may become colonized with S aureus shortly after birth, acquiring the organism from people in their immediate surroundings. Some people will become carriers for prolonged periods, while others will harbor the organisms only intermittently. For unknown reasons, people in certain occupations, including physicians, nurses, and other hospital workers, are more prone to colonization. Also, certain patient groups, including diabetics, patients on hemodialysis, and chronic intravenous drug abusers, have a higher carriage rate than does the general population.

Question 21

Entry?

Answer 21

S aureus and most other bacteria do not usually penetrate into deep tissues unless the skin or the mucous membranes are damaged or actually cut. Skin damage may be caused by burns, accidental wounds, lacerations, insect bites, surgical intervention, or associated skin diseases. If present in very large numbers, some bacteria, including S aureus, are able to enter spontaneously and cause disease. This scenario occurs in cases of poor hygiene or prolonged moisture of the skin, which permits the growth of large numbers of organisms. It is not known if these infections are caused by spontaneous penetration or if the organisms enter through inapparent cuts and abrasions.

Question 22

Spread and multiplication?

Answer 22

The survival of S aureus in tissues depends on several factors: the number of entering organisms, the site involved, the speed with which the body mounts an inflammatory response, and the immunological status of the host. When the inoculum is small and the host is immunologically competent, infections by these and other organisms are usually stopped. Nonetheless, staphylococci possess a particularly complex but effective pathogenic strategy, and even healthy persons may be unable to combat S aureus. Luckily, the area of inflammation most often remains localized, and the organisms can be contained.

Question 23

True or false most local staphylococcal infections lead to the formation of a collection of pus called an abscess. Abscesses in the skin are called boils or, in medical parlance, furuncles. Multiple interconnected abscesses are called carbuncles. Alternatively, staphylococci can spread in the subcutaneous or submucosal tissue and cause a diffuse inflammation called cellulitis. In most cases, these skin infections are caused by S aureus and not by the other staphylococcal species.

Answer 23

True

Question 24

How does an abcess develop?

Answer 24

The development of an abscess is a complex process that involves both bacterial and host factors (Fig. 11-4). The early events are characteristic of an acute inflammatory reaction, with a rapid and extensive influx of leukocytes (eg, neutrophils). Chemotactic factors, derived both from bacteria and complement, are made in large amounts. However, some staphylococci not only survive this onslaught but are even capable of killing and lysing many of the neutrophils that have entered the infection area by the production of cytolysins. The lysed neutrophils pour out large amounts of lysosomal enzymes, which damage surrounding tissue.

The development of an abscess is a complex process that involves both bacterial and host factors. S aureus infections cause a rapid and extensive influx of leukocytes (eg, neutrophils). Chemotactic factors, derived both from bacteria and complement, are made in large amounts. S aureus secretes coagulase that causes formation of clots. Protein A is released where it may bind antibodies reducing opsonization. S aureus lyse neutrophils and red blood cells that have entered the infection area by the production of cytolysins (leukocidins and hemolysins). The lysed neutrophils pour out large amounts of lysosomal enzymes, which damage surrounding tissue.

Question 25

Formation of capsule of abcess?

Answer 25

The combination of MSCRAMMs and an intense host response to the organisms results in the area being surrounded with a thick-walled fibrin capsule. The center of the abscess is usually necrotic and contains debris consisting of dead neutrophils and epithelial cells, dead and live bacteria, and edema fluid. An abscess, then, is a well-defined area in tissue that contains pus. From the point of view of the host, it represents a containment of invading organisms in one site. However, from the point of view of the staphylococci, it represents a walled-off site protected from the host immune attack. The site may also be the source of toxins produced and secreted by the organism such as TSST-1, staphylococcal enterotoxins, and staphylococcal enterotoxin–like molecules, which can result in TSS.

Question 26

Role of neutrophiles in S aureus?

Answer 26

Staphylococcal infection involves a massive struggle between the white blood cells and the invading organisms (see Fig. 11-4). Despite an impressive array of virulence factors, S aureus does not always win the struggle; neutrophils usually gain the upper hand. The importance of neutrophils in containing staphylococcal infections is evident in children with the hereditary defect in phagocyte function called chronic granulomatous disease. This potentially fatal disease is characterized by frequent and serious infections with S aureus. Neutrophils of these patients are unable to make sufficient hydrogen peroxide to set off the oxidative killing pathway. In these children, the balance between staphylococci and phagocytes is clearly shifted toward the microorganisms.

Question 27

How do they avoid neutrophiles?

Answer 27

First, the cell surface of staphylococci plays an important defensive role. More than 90% of S aureus strains that cause disease are surrounded by a capsule that may inhibit phagocytosis, but its role in virulence is far less clear than the capsules of meningococcus or pneumococcus. By far the most common capsular serotypes are 5 and 8. Staphylococci also make a slime layer that provides protection from host neutrophils. Peptidoglycan in the cell wall of S aureus activates complement by the alternative pathway, thus contributing to the inflammatory response. Lipoteichoic acid in peptidoglycan also interacts with toll-like receptors (particularly toll-like receptor 2) on the surface of macrophages, causing these phagocytic cells to release proinflammatory cytokines. Note that in this regard, staphylococcal lipoteichoic acid resembles the endotoxin of Gram-negative bacteria. Endotoxin activates the alternate pathway of complement and interacts with toll-like receptor 4 on macrophages to cause proinflammatory cytokine release. Lipoteichoic acids and teichoic acid are polymers of ribitol and glycerophosphates (see Chapter 3), which also appear to be involved in complement activation and possibly in the adherence of these organisms to mucosal cells.

Question 28

Protein A?

Answer 28

A fourth wall component, protein A, has an unexpected property: it binds to the Fc terminus of immunoglobulin G. This binding incapacitates the antibody function of these molecules because their antigen-binding end, the Fab portion, is dangling away from the surface of the organisms. As a result, the number of Fc residues available for attachment to phagocytes is reduced, thereby reducing opsonization. Protein A is also released into the environment surrounding bacterial growth, where it may bind free antibodies in the same manner

Question 29

Role coagulase and catalase?

Answer 29

In addition to these components, S aureus secretes many enzymes and toxins that are almost certainly directed toward the struggle with phagocytes. Catalase converts hydrogen peroxide to water and may help counteract the neutrophils’ ability to kill bacteria by the production of oxygen free radicals. Coagulases convert fibrinogen to fibrin and may help prevent the organisms from being phagocytized, since white cells penetrate fibrin clots poorly.

Question 30

Toxins?

Answer 30

Several pore-forming toxins are important virulence factors of S aureus. The molecules damage not only phagocytic cells but also other cells (eg, vascular endothelium, renal endothelium, neurons, and myocardial cells). These toxins exert their effect by creating channels in cell membranes that significantly disturb cellular homeostasis. The α-, γ-, and δ-toxins have been traditionally referred to as hemolysins (cytolysins) because they lyse red blood cells contained in blood agar plates. However, this effect on red cells does not appear to play a role in human infection. α-Toxin, γ-toxin, and a related toxin called Panton-Valentine leukocidin are particularly effective in damaging neutrophils. Another non–pore-forming hemolysin is called β-toxin; this protein toxin is a sphingomyelinase (also called hot-cold hemolysin) that prepares red blood cells at 37 °C for lysis at 4 °C. The role of β-toxin in human disease is unclear but appears to be important in biofilm formation, sometimes called biofilm ligase, especially during endocarditis.

Question 31

Other virulence factors?

Answer 31

Several other proteins made by S aureus probably enhance its virulence by damaging tissues. Many strains make a hyaluronidase, which hydrolyzes the matrix of connective tissue and perhaps facilitates bacterial spread along tissue planes. Most strains also make lipases, proteases, deoxyribonucleases (DNases), and other enzymes that may also act as virulence enhancers.

Question 32

Resistance to antibios?

Answer 32

In addition to tissue-damaging factors, S aureus produces substances that make them difficult to treat with antibiotics. Two highly clinically significant examples of these substances are β-lactamase, a powerful enzyme that hydrolyzes the classical penicillins, and production of penicillin-binding protein 2a (PBP2a), which confers resistance to all penicillin- and cephalosporin-class antibiotics. The bacteria carrying PBP2a are referred to as methicillin-resistant S aureus or MRSA. β-Lactamase is found in about 90% of S aureus strains and is responsible for the resistance to penicillins that was identified in the late 1940s and spread rapidly around the world. PBP2a mediates continued peptidoglycan synthesis in the presence of all types of penicillin and cephalosporin antibiotics as a result of an alteration in the binding site and decreased affinity for these antibiotics. Today, up to 70% of hospital-associated S aureus strains and 30% of community-associated strains may be methicillin resistant owing to PBP2a. Currently, PBP2a is encoded by as many as eight different staphylococcal cassette chromosome methicillin resistance (mec) DNAs contained within the chromosome.

Question 33

Mestases of staph aureuses?

Answer 33

Most local staphylococcal diseases are self-limiting by spontaneously draining through the skin; they do not typically result in metastatic infections. In healthy individuals, organisms that escape from a local abscess are usually destroyed by the clearance mechanisms of the blood and the lymphatics. When staphylococci become implanted in deep tissues, they tend to colonize tissues that have been previously damaged by physical trauma, disease, or surgical intervention. Otherwise, the site of metastatic infection seems random and is probably dictated by the clearing capacity of the organ and the amount of blood flowing through it. The main sites of metastatic abscesses are the highly vascularized organs: bones, joints, lungs, and kidneys. Immunocompromised patients frequently have multiple staphylococcal metastases, which can lead to serious and often fatal diseases.Once implanted in deep tissue and able to survive, S aureus elicits an inflammatory reaction similar to that of a skin abscess. In the words of Pasteur, osteomyelitis is a “boil of the bone.” The consequences of abscess formation in deep sites depend on their location. Nowhere is it more devastating than in the heart, lung, or brain. However, if the function of the organ is not directly compromised, staphylococcal abscesses can persist for a considerable period and cause relatively mild symptoms. These symptoms may tax the diagnostic acumen of the physician.

Question 34

Damage of S epidermidis

Answer 34

However, infections with S epidermidis and other coagulase-negative staphylococci are found with increasing frequency in patients with implanted artificial devices, such as prosthetic joints or intravenous catheters. When defense mechanisms are impaired, S epidermidis can cause serious infections, like septicemia and endocarditis. A potential virulence factor of these organisms is the peptidoglycan, and the same exopolysaccharide slime layer that is present in S aureus has been found in more than 80% of disease-causing isolates of S epidermidis. It is thought that this slime layer allows the organisms to stick to the surface of plastics used in various implanted medical devices.

Question 35

Damage of S saprophyticus,

Answer 35

another coagulase-negative organism, may be the most highly specialized of the staphylococci in terms of pathogenicity because it is almost entirely associated with urinary tract infections, particularly cystitis in young women.The reason for this specialization is not yet known, but it seems likely that this organism has unique properties that allow it to bind the epithelium of the urethra or the bladder.

Question 36

SSSS?

Answer 36

The symptoms of each of these diseases are clearly caused by toxins, even in the absence of bacteria. The first disease is called staphylococcal scalded skin syndrome (SSSS), a life-threatening disease that mainly affects neonates. SSSS is characterized by extensive sloughing of the skin. Two exotoxins, known as exfoliative toxins A and B, cause these symptoms. Their role in human disease has been clearly established because the administration of specific antitoxin prevents the skin lesions in humans or mice. Exfoliative toxins are highly tissue-specific serine proteases that cause separation of the layers of the epidermis at the desmosomes. Exfoliative toxin production by S aureus does not contribute to systemic infections by the bacteria.

Question 37

TSS?

Answer 37

second disease definitively caused by exotoxins, called toxic shock syndrome (TSS), is characterized by fever, skin rash, hypotension, peeling of the skin on recovery, and the dysfunction of several essential systems as was the case in Ms. G’s illness (see Fig. 11-3). However, TSS can occur in the absence of one or more of those defining symptoms. The disease was originally associated with the use of highly absorbent tampons, which appear to introduce oxygen into the vagina and stimulate toxin production by the organisms. Oxygen is absolutely essential to the production of TSS-inducing toxins, and the vagina in the absence of tampons is anaerobic. TSS still occurs in association with tampon use, though less frequently as a result of the use of lower-absorbency tampons, but also commonly follows staphylococcal infections of any other type, and it occurs in men as well as women. Ms. G presented with the typical signs of TSS; she was of menstrual age and also used tampons. However, her case of TSS was associated with an abscess associated with recent arthroscopic knee surgery. Of particular importance is the increasing association of TSS with lung infections and necrotizing pneumonia, particularly in strains of bacteria that are methicillin resistant.

Question 38

What toxins TSS?

Answer 38

The exotoxins involved in TSS include toxic shock syndrome toxin-1, the cause of all menstrual TSS cases and one-half of nonmenstrual cases, and staphylococcal enterotoxins, particularly enterotoxin serotypes B and C. These three exotoxins are produced by the bacteria in high concentrations, and that may be why they cause TSS. The toxins have been referred to as superantigens because of their novel way of interacting with T lymphocytes and macrophages (see Fig. 8-3). Superantigens cross-link one chain (β-chain) of the T-cell antigen receptor with major histocompatibility complex class II molecules on macrophages. The effect of this interaction is a massive release of cytokines from macrophages and T cells that mediate TSS. For example, interleukin-1 (endogenous pyrogen) released from macrophages causes the fever of TSS. Tumor necrosis factor-α released from macrophages and tumor necrosis factor-β released from T cells cause capillary leak and therefore hypotension. Finally, interferon-γ and interleukin 2 release from T cells accounts for the rash of TSS patients. It is also important to remember that the massive release of interferon-γ in TSS appears to prevent formation of protective neutralizing antibodies against the superantigens. Thus, TSS patients mostly remain susceptible to recurrent TSS, particularly women who continue to use tampons after TSS episodes. In addition, superantigens appear to subvert the formation of inflammation through an undefined mechanism when the organism is in abscesses. Thus, for example, surgical incision sites may not show the characteristic inflammation associated with staphylococcal infections. The staphylococcal superantigens are structurally related to the streptococcal scarlet fever toxins, which also cause TSS.

Question 39

Extreme pyrexia syndrome?

Answer 39

Recently, a new syndrome has been described and is associated with a superantigen related to TSST-1. This illness called extreme pyrexia syndrome is characterized by acute onset of fevers exceeding 108 °F. Because of the exceptionally high fevers in spite of heroic efforts to reduce body temperature, all patients thus far described have succumbed. The high fevers in these patients are consistent with the exceptional pyrogenicity of this and other superantigens

Question 40

Enterotoxins A throug E and I?

Answer 40

Finally, staphylococcal enterotoxin serotypes A through E and I are major causes of food poisoning when ingested. These exotoxins can cause disease even in the absence of the organism. They cause intensive intestinal peristalsis, apparently by working directly on the vomiting control center of the brain. They are heat stable, resist proteases, and are not necessarily destroyed by cooking, even though the staphylococci that produced them are killed. These toxins cause signs and symptoms that mimic the disease when administered to laboratory animals. Note that the same strain of S aureus can cause several of the diseases mentioned.

Question 41

Diagnosis?

Answer 41

Recognizing staphylococcal infections is not usually a difficult diagnostic problem, and they are among the most frequent infections seen both in the community and in the hospital. A localized abscess in a seriously ill patient should be aspirated and the contents examined by Gram stain and culture to identify the staphylococcal species as well as the antibiotic susceptibility patterns. Clusters of large Gram-positive cocci point to staphylococcal infection. The patient’s blood should also be cultured to determine if the organisms have invaded the bloodstream. Both S aureus and coagulase-negative staphylococci are commonly isolated in blood cultures; however, the latter is most often a contaminant and is considered pathogenic only under special circumstances. The coagulase test serves to distinguish the two species.

Question 42

MRSA antibiotics to use?

Answer 42

Infections with MRSA require treatment with vancomycin, which until recently was the last available drug for some highly resistant strains. Other antibiotics active against MRSA include aminoglycosides, macrolides, clindamycin, daptomycin, linezolid, doxycycline, tigecycline, trimethoprim/sulfamethoxazole, and the only β-lactam antibiotic with activity against MRSA, ceftaroline.

Question 43

True or false One antibiotic that deserves special mention is clindamycin. This inhibitor of protein synthesis has become a useful antibiotic in the treatment of exotoxin diseases of staphylococci because of its ability to prevent exotoxin synthesis prior to inhibiting the growth of the organisms. The choice of drugs should be based on the antibiotic sensitivity of the infecting strain and the special characteristics of the patient.

Answer 43

True

Question 44

VRSA?

Answer 44

Vancomycin-resistant S aureus (VRSA) has acquired the genes that encode vancomycin resistance from resistant Enterococcus species in patients infected with both pathogens. Newer antimicrobial agents, such as linezolid, and daptomycin, generally have activity against staphylococci that are resistant to multiple antibiotics. These newer antibiotics are generally reserved for such cases and when vancomycin cannot be used. Nevertheless, if multidrug-resistant staphylococci emerge as major clinical entities, we may one day face the daunting problem of common and potentially dangerous staphylococcal infections with no effective antibiotics at our disposal.

Question 45

TSS treatment?

Answer 45

Some physicians have advocated the use of intravenous immunoglobulin in the treatment of superantigen-mediated TSS. These antibody preparations are obtained from large pools of human volunteers, many of whom have preexistent antibodies to superantigens. There is published evidence of reductions in fatality rates with the use of intravenous immunoglobulins for the treatment of streptococcal TSS.

Question 46

True or false?

Answer 46

The bacteria will probably be resistant to penicillin but sensitive to semisynthetic penicillins, such as nafcillin—that is, methicillin-sensitive S aureus (MSSA). Semisynthetic penicillins and cephalosporins that are resistant to staphylococcal β-lactamase will kill these bacteria.

Question 47

Antibio à utiliser?

Answer 47

Answer 48