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Oral Carriage & Suffering of

Staphylococcus Aureus


ii

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iii

Oral Carriage & Suffering

of Staphylococcus Aureus Oral Infection & Staph.Aureus

AUTHOR

Dr. Biswajit Batabyal

EDUCREATION PUBLISHING (Since 2011)

www.educreation.in


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Content List ______________________________________________________

S. No. Content Page

Abbreviations

Abstract

1. Introduction 1

1.1. Microbiology 2

1.2. Role in disease 3

1.3. Atopic dermatitis 4

1.4. Toxic shock syndrome and food

poisoning

4

1.5. Mastitis in cows 4

1.6. Reproduction 4

1.7. Virulence factors 5

1.8. Role of pigment in virulence 6

1.9. Classical diagnosis 7

1.10. Rapid diagnosis and typin 7

1.11. Treatment and antibiotic resistance 8

1.12. Antibiotics 9

1.13. Penicillin Group 9

1.14. Cephalosporins Group 15

1.15. Macrolide Antibiotics Group 16

1.16. Lincosamides Group 18

1.17. Rifamycins 19

1.18. Linezolid 20


vi

1.19. Quinolones (Fluoroquinolones) 21

1.20. Vancomycin 22

1.21. Carbapenems Group 23

1.22. Mechanisms of antibiotic resistance 24

1.23. MRSA in oral cavity 27

2. Literature Review 30

3. Aims & Objectives 43

3.1. Importance of the Study 43

3.2. Aims of the Study 43

3.3. Objectives of the Study 44

4. Research Methodology 45

4.1. Study Period & Study Setting 45

4.2. Study patients and participants 45

4.3. Collection and processing of the samples 46

4.4. Identification of isolates 48

4.5. Mannitol salt agar 48

4.6. Gram Technique 50

4.7. Catalase test 52

4.8. Coagulase test 53

4.9. DNase test 56

4.10. Sensitivity testing using Disc Diffusion

technique

58

4.11. Tryptone soya broth 63

4.12. Mueller Hinton agar 63

4.13. Methicillin Resistant Staph. aureus

detection

64

4.14. List of materials used for the study 65

4.15. Control strain 68

4.16. Maintenance of isolated strains 69

5. Results 70


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6. Statistical Analysis 84

7. Discussion 92

8. Conclusion 105

9. Bibliography 108


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ix

ABBREVIATIONS ______________________________________________________

AMX : Amoxicillin

AMP : Ampicillin

AMC : Amoxicillin/clavulanic acid

AS : Ampicillin/sulbactam

ABST : Antibiotic sensitivity test

ATCC : American Type Culture Collection °C : Degree centigrade

CPS : Coagulase positive Staphylococcus

CLSI : Clinical Laboratory Standard Institute

CPD : Cefpodoxime

CD : Clindamycin

CIP : Ciprofloxacin

CV : Crystal violet

DNA : Deoxyribonucleic acid

DNase : Deoxiribonuclease

EF : Exfoliative

E : Erythromycin

EDTA : Ethylenediaminetetraacetic acid

Gm : Gram

GPC : Gram positive cocci

GNB : Gram negative bacilli

GDA : Group-D Assistant

H2O2 : Hydrogen per oxide

HCl : Hydrochloric acid

hr : Hour

Ig : Immunoglobulin


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IPM : Imipenem

IS : Intermediate Sensitive

LZ : Linezolid

MRSA : Methicillin resistant Staphylococcus aureus

MSSA : Methicillin sensitive Staphylococcus aureus

MDR : Multi drug resistant

mg : Milligram

MW : Molecular weight

MRP : Meropenem

MSA : Mannitol salt agar

MHA : Mueller Hinton agar

mm : Millimeter

ml : Milli litre

mcg : Microgram

min : Minute

NEG : Negative

Nacl : Sodium chloride

NCCLS : National committee for clinical laboratory

standards

OX : Oxacillin

OF : Ofloxacin

OS : Oral Surgery

OPD : Outdoor patients department

OP &

OM

: Oral Pathology & Microbiology

OT : Operation theater

ORSA : Oxacillin resistant Staphylococcus aureus

OSSA : Oxacillin sensitive Staphylococcus aureus

PI : Piperacillin

PIT : Piperacillin/Tazobactam

POS : Positive

PBP : Penicillin-binding protein

PCR : Polymerase chain reaction


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PVL : Panton-valentine leukocidin

R : Resistant

RNA : Ribonucleic acid

rRNA : Ribosomal Ribonucleic acid

RIF : Rifampicin

S : Sensitive

SA : Staphylococcus aureus

SSSS : Staphylococcal scalded skin syndrome

Scc mec : Staphylococcal cassette chromosome mec

Sec : Second

SSIs : Surgical Site infections

TSS : Toxic shock syndrome

TI : Ticarcillin

TCC : Ticarcillin/clavulanic acid

TSB : Tryptone soya broth

V : Volume

VA : Vancomycin

VRSA : Vancomycin-resistant Staphylococcus aureus

VISA : Vancomycin Intermediate Staphylococcus

aureus

W : Weight

WHO : World Health Oraganisation

μg : Microgram

μl : Micro liter

*****


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ABSTRACT ______________________________________________________

The oral cavity carriage and antibiotic susceptibility patterns of

Staphylococcus aureus in Dental hospital staff and healthy general

population were determined. Oral cavity swabs were taken from

113 healthy general population and 90 health care workers.

Antibiotic disc susceptibility testing was conducted following the

CLSI method. Staphylococcus aureus carriage was noted in 28.3%

of healthy general population and 38.9% of health care workers.

Resistance to commonly used oral antibiotics of healthy general

population & health care workers, ampicillin 93.8% & 97.2%,

amoxicillin/clavulanic acid 84.4% & 77.2%, amoxicillin 43.8% &

57.2%, ciprofloxacin 53.2% & 57.2% and ofloxacin 37.5% &

42.9%, respectively. 5.7% methicillin resistant Staphylococcus

aureus was detected among the hospital personnel from isolated

strain. The MRSA isolates showed multiple drug resistance

(MDR), except imipenem. Hospitals should assess the advantages

and disadvantages of routinely culturing personnel, however, in

outbreak situation hospital personnel especially young persons

may be sources of nosocomial infection.

Staphylococcus aureus is a well recognized pathogen

associated with a variety of clinical syndrome. The role of Staph.

aureus in some types of oral disease may be more important than

previously recognized. The present study was designed to

investigate the prevalence of Staphylococcus aureus, MRSA and

their rate of resistance to different anti staphylococcal antibiotics.

For this study, Gurunanak Institute of Dental Science & Research

(Kolkata), selected patients who were suffering from

Staphylococcus aureus oral infection. Isolated Staphylococcus

aureus was tested for Oxacillin (1 mcg) sensitivity and their

antibiotic susceptibility was investigated by using eighteen

antibiotics followed by Disk diffusion technique following CLSI

method. Out of the 223 specimens collected, 109 (48.8%) were


xiv

isolated. All the 109 (48.8%) specimens were studied in detail.

5.5% of the isolates were shown to be methicillin resistant Staph.

aureus (MRSA). Percentage (%) of resistance in commonly used

oral antibiotics are ampicillin 98.1%, amoxycillin/clavulanic acid

73.3%, amoxycillin 44.9%, ofloxacin 48.6% and ciprofloxacin

41.2%. The MRSA isolates showed multiple drug resistance

(MDR), except linezolid and imipenem. In line with more recent

surveys, this retrospective study suggests that Staph. aureus may

be more frequent isolate from the oral cavity than hitherto

suspected. The role of Staph. aureus in several diseases of the oral

mucosa merits further investigation.

The problem of infection has been persistent in the surgical

world even after the introduction of antibiotics. Pathogens that

infect surgical site can be acquired from the hospital environment

or other infected patients. A total of 66 pus samples from post-

operative oral & maxillofacial surgical infections were received in

the Department of Microbiology, Gurunanak Institute of Dental

Science & Research, Panihati, Kolkata, over a period of one year.

The isolates were identified using standard laboratory procedures.

All the isolates were tested for susceptibility to various commonly

used antibiotics and screened for oxacillin susceptibility according

to CLSI guidelines. Out of 66 pus samples received, 34(51.5%)

were culture positive for Staph. aureus. Methicillin resistance was

documented in 14 (41.2%) of the Staph. aureus isolates. Highest

efficacy was observed with linezolid (97.0%). All MRSA isolates

were 100% sensitive to linezolid. The hospital acquired surgical

site infection is alarming. Hospital disinfection and treatment

protocols should be practiced.

*****


Oral Carriage & Suffering of Staphylococcus Aureus

1

INTRODUCTION ______________________________________________________

Staphylococcus aureus literally the “golden cluster seed” or “the

seed gold” and also known as golden staph and Oro staphira is a

facultative anaerobic, Gram-positive coccus and is the most

common cause of staph infections. It is frequently part of the skin

flora found in the nose and on skin. About 20% of the human

populations are long term carriers of Staph. aureus [1]. The

carotenoid pigment staphyloxanthin is responsible for Staph.

aureus characteristic golden color, which may be seen in colonies

of the organism. This pigment acts as a virulence factor with an

antioxidant action that helps the microbe evade death by reactive

oxygen species used by the host immune system. Staph organisms

which lack the pigment are more easily killed by host defenses.

Staph. aureus can cause a range of illnesses from minor skin

infection, such as pimples, impetigo, boils (furuncles), cellulitis

folliculitis, carbuncles, scalded skin syndrome, and abscesses, to

life-threatening diseases such as pneumonia, meningitis,

osteomyelitis, endocarditis, toxic shock syndrome (TSS), chest

pain, bacteremia, and sepsis. Its incidence is from skin, soft tissue,

respiratory, bone, joint, endovascular to wound infections. It is still

one of the five most common causes of nosocomial infections,

often causing postsurgical wound infections. Abbreviated to Staph.

aureus or Staph. aureus in medical literature, Staph. aureus should

not be confused with the similarly named and similarly dangerous

(and also medically relevant) species of the genus Streptococcus.

Staph. aureus was discovered in Aberdeen, Scotland in 1880

by the surgeon Sir Alexander Ogston in pus from surgical

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abscesses [2]. Each year, some 500,000 patients in American

hospitals contract a staphylococcal infection [3].

1.1. Microbiology

Staph. aureus is a facultative anaerobic, Gram-positive coccus,

which appears as grape-like clusters when viewed through a

microscope and has large, round, golden-yellow colonies, often

with hemolysis, when grown on blood agar plates [4]. The golden

appearance is the etymological root of the bacteria’s name;

“golden” in Latin. Staph. aureus is catalase-positive (meaning that

it can produce the enzyme, “catalase”) and able to convert

hydrogen peroxide (H2O2) to water and oxygen, which makes the

catalase test useful to distinguish staphylococci from enterococci

and streptococci. A small percentage of Staph. aureus can be

differentiated from most other staphylococci by the coagulase test:

Staph. aureus is primarily coagulase positive (meaning that it can

produce the enzyme “coagulase”) that causes clot formation,

whereas most other Staphylococcus species are coagulase-negative

[4]. However, while the majority of Staph. aureus are coagulase-

positive, some may be atypical in that they do not produce

coagulase(the most common organism in patients with nosocomial

bacteremia is coagulase-negative staphylococcus) [5]. Incorrect

identification of an isolate can impact implementation of effective

treatment and /or control measures [6].

Fig.1.1.Grampositive cocci in cluster



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Fig.1.2. Staph. aureus Electron micrograph

1.2. Role In Disease

Staph. aureus are responsible for food poisoning through the

production of an enterotoxin and pathogenicity is also associated

with coagulase positivity. Staph. aureus may occur as a

commensal on skin; it also occurs in the nose frequently (in about a

third of the population) [7] and throat less commonly. The

occurrence of Staph. aureus under these circumstances does not

always indicate infection and, therefore, does not always require

treatment (indeed, treatment may be ineffective and re-colonization

may occur). It can survive on domesticated animals such as dogs,

cats, and horses, and can cause bumble foot in chickens. It can

survive for hours to days, weeks, or even months on dry

environmental surfaces depending on strain [8]. It can host phages,

such as Panton-Valentine leukocidin, that increase its virulence.

Staph. aureus can infect other tissues when barriers have been

breached (e.g. skin or mucosal lining). This leads to furuncles

(boils) and carbuncles (a collection of furuncles). In infants Staph.

aureus infection can cause a severe disease staphylococcal scalded

skin syndrome (SSSS) [9].

Staph. aureus alv infections can be spread through contact

with pus from an infected wound, skin-to-skin contact with an

infected person by producing hyaluronidase that destroys tissues,

and contact with objects such as towels, sheets, clothing, or athletic

equipment used by an infected person. Deeply penetrating Staph.

aureus infections can be severe. Prosthetic joints put a person at

particular risk for septic arthritis, and staphylococcal endocarditis



4

(infection of the heart valves) and pneumonia, which may be

rapidly spread.

1.3. Atopic Dermatitis

Staph. aureus is extremely prevalent in atopic dermatitis patients,

who are less resistant to it than other people. It often causes

complications. The disease is most likely found in fertile active

places including, the armpits, hair, and scalp. The large pimples

that appear in those areas may cause the worst of the infection if

popped. This can lead to scaled skin syndrome. A severe form of

this is Ritter’s disease seen in neonates.

1.4. Toxic Shock Syndrome And Food Poisoning

Some strains of Staph. aureus, which produce the exotoxin TSST-

1, are the causative agents of toxic shock syndrome. Some strains

of Staph. aureus also produce an enterotoxin that is the causative

agent of Staph. aureus gastroenteritis. The gastroenteritis is self-

limiting, with the person recovering in 8-24 hours. Symptoms

include nausea, vomiting, diarrhea, and abdominal pain.

1.5. Mastitis In Cows

Staph. aureus is one of the causal agents of mastitis in dairy cows.

Its large polysaccharide capsule protects the organism from

recognition by the cow’s immune defenses [10].

1.6. Reproduction

Staph. aureus reproduces asexually. It starts this process by

reproducing its DNA. The membrane stretches out and separates

the DNA molecules. The cells from a hollow space that eventually

divides out into two new cells. The new cell wall does not fully

separate from the existing cell wall, which is why the cells are



5

observed in clusters. This cell will eventually reproduce and cells

will attach onto it [11].

1.7. Virulence Factors

Toxins

Depending on the strains, Staph. aureus is capable of secreting

several toxins, which can be categorized into three groups. Many

of these toxins are associated with specific diseases.

Super antigens

PTSAgs have super antigen activities that induce toxic shock

syndrome (TSS). This group includes the toxin TSST-1, which

causes TSS associated with tampon use. The staphylococcal

enterotoxins, which cause a form of food poisoning, are included

in this group.

Exfoliative toxins

EF toxins are implicated in the disease staphylococcal scalded-skin

syndrome (SSSS), which occurs most commonly in infants and

young children. It also may occur as epidemics in hospital

nurseries. The protease activity of the exofoliative toxins causes

peeling of the skin observed with SSSS.

Other toxins

Staphylococcal toxins that act on cell membranes include alpha-

toxin, beta-toxin, delta-toxin, and several bicomponent toxins. The

bicomponent toxin Panton-Valentine leukocidin (PVL) is

associated with severe necrotizing pneumonia in children. The

genes encoding the components of PVL are encoded on a

bacteriophage found in community-associated methicillin-resistant

Staph. aureus (MRSA) strains.

Protein A

Protein A is a protein that is anchored to staphylococcal

peptidoglycan pentaglycine bridges (chains of five glycine

residues) by the transpeptidase Sortase A [12]. Protein A is an IgG-

binding protein that binds to the Fc region of an antibody. In fact,



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studies involving mutation of genes coding for protein A resulted

in a lowered virulence of S. aureus as measured by survival in

blood, which has led to speculation that Protein A contributed

virulence requires binding of antibody Fc regions[13]. Protein A in

various recombinant forms has been used for decades to bind and

purify a wide range of antibodies by immune affinity

chromatography. Transpeptidases such as the sortases that are

responsible foranchorning factors like Protein A to the

staphylococcal peptidoglycan are being studied in hopes of

developing new antibiotics to target MRSA infections [14].

1.8. Role Of Pigment In Virulence

Some strains of Staph. aureus are capable of producing

staphyloxanthin-a carotenoid pigment that acts as a virulence

factor. It has an antioxidant action that helps the microbe evade

death by reactive oxygen species used by the host immune system.

Staphyloxanthin is responsible for Staph. aureus characteristic

golden color [15]. When comparing a normal strain of Staph.

aureus with a strain modified to lack staphyloxanthin, the wild

type pigmented strain was more likely to survive incubation with

an oxidizing chemical such as hydrogen peroxide than the mutant

strain was. Colonies of the two strains were also exposed to human

neutrophils. The mutant colonies quickly succumbed while many

of the pigmented colonies survived. Wounds on mice were

inoculated with the two strains. The pigmented strains created

lingering abscesses. Wounds with the unpigmented strains healed

quickly.

These tests suggest that the staphyloxanthin may be key to the

ability of Staph. aureus to survive immune system stacks. Drugs

designed to inhibit the bacterium’s production of the

staphyloxanthin may weaken it and renew its susceptibility to

antibiotics [16]. In fact, because of similarities in the pathways for

biosynthesis of staphyloxanthin and human cholesterol, a drug

developed in the context of cholesterol-lowering therapy was

shown to block Staph. aureus pigmentation and disease

progression in a mouse infection model [17].



7

1.9. Classical Diagnosis

Depending upon the type of infection present, an appropriate

specimen is obtained accordingly and sent to the laboratory for

definitive identification by using biochemical or enzyme-based

tests. A Gram stain is first performed to guide the way, which

should show typical gram-positive bacteria, cocci, in clusters.

Second, the isolate is culture on mannitol salt agar, which is a

selective medium with 7-9% NaCl that allows Staph. aureus to

grow, producing yellow-colored colonies as a result of mannitol

fermentation and subsequent drop in the medium’s pH.

Furthermore, for differentiation on the species level, catalase

(positive for all Staphylococcus species), coagulase (fibrin clot

formation, positive for Staph. aureus), DNAse (zone of clearance

on nutrient agar), lipase (a yellow color and rancid odor smell),

and phosphatase (a pink color) tests are all done. For

staphylococcal food poisoning, phage typing can be performed to

determine if the staphylococci recovered from the food to

determine the source of infection.

1.10. Rapid Diagnosis And Typing

Diagnostic microbiology laboratories and reference laboratories

are key for identifying outbreaks and new strains of Staph. aureus.

Recent genetic advances have enabled reliable and rapid

techniques for the identification and characterization of clinical

isolates of Staph. aureus in real-time. These tools support infection

control strategies to limit bacterial spread and ensure the

appropriate use of antibiotics. These techniques include real-time

PCR and quantitative PCR and are increasingly being employed in

clinical laboratories [18, 19].



8

1.11. Treatment And Antibiotic Resistance

The treatment of choice for Staph. aureus infection is penicillin;

but, in most countries, penicillin-resistance is extremely common

and first-line therapy is most commonly a penicillinase-resistant

beta-lactam antibiotic (for example, oxacillin or flucloxacillin).

Combination therapy with gentamicin may be used to treat serious

infections like endocarditis [20, 21], but its use is controversial

because of the high risk of damage to the kidneys [22]. The

duration of treatment depends on the site of infection and on

severity.

Antibiotic resistance in Staph. aureus was uncommon when

penicillin was first introduced in 1943. Indeed, the original petri

dish on which Alexander Fleming of Imperial College London

observed the antibacterial activity of the penicillium fungus was

growing a culture of Staph. aureus. By 1950, 40% of hospital

Staph. aureus isolates were penicillin-resistant; and, by 1960,this

had risen to 80% [23]. Researchers from Italy have identified a

bacteriophage active against Staphylococcus aureus, including

methicillin-resistant strains (MRSA), in mice and possibly humans

[24].

Methicillin-resistant Staphylococcus aureus (MRSA) is a

bacterium responsible for several difficult-to-treat infections in

humans. It is also called multidrug-resistant Staphylococcus aureus

and oxacillin-resistant Staphylococcus aureus (ORSA). MRSA is

any strain of Staphylococcus aureus that has developed resistance

to beta-lactam antibiotics, which include the penicillins

(methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the

cephalosporins. Strains unable to resist these antibiotics are

classified as methicillin-sensitive Staphylococcus aureus, or

MSSA. The development of such resistance does not cause the

organism to be more intrinsically virulent than strains of

Staphylococcus aureus that have no antibiotic resistance, but

resistance does make MRSA infection more difficult to treat with

standard types of antibiotics and thus more dangerous. MRSA is

especially troublesome in hospitals and nursing homes, where

patients with open wounds, invasive devices, and weakened


http://en.wikipedia.org/wiki/Bacteria

http://en.wikipedia.org/wiki/Infection

http://en.wikipedia.org/wiki/Staphylococcus_aureus

http://en.wikipedia.org/wiki/Antibiotic_resistance

http://en.wikipedia.org/wiki/Beta-lactam_antibiotics

http://en.wikipedia.org/wiki/Penicillin

http://en.wikipedia.org/wiki/Methicillin

http://en.wikipedia.org/wiki/Dicloxacillin

http://en.wikipedia.org/wiki/Nafcillin

http://en.wikipedia.org/wiki/Oxacillin

http://en.wikipedia.org/wiki/Cephalosporin


9

immune systems are at greater risk of infection than the general

public.

1.12. Antibiotics

The word antibiotic [25] is derived from Greek stems that mean

“against life”. In 1889, the French researcher Paul Vuillemin

coined the term to describe a substance he isolated some years

earlier from Pseudomonas aeruginosa. The substance, called

pyocyanin, inhibits the growth of other bacteria in test tubes, but it

was too toxic to be useful in disease therapy. Vuillemin’s term has

survived to the current era. Antibiotics are now considered to be

chemical products or derivatives of microorganisms that are

inhibitory to other microorganisms.

Scientists

are uncertain as to how the ability to produce

antibiotics arose in living things, but it is conceivable that random

genetic mutations were responsible. Clearly, the ability to produce

an antibiotic conferred an extraordinary evolutionary advantage on

the processor in the struggle for survival. In this section we shall

discuss the sources of antibiotics-which are used in this study, their

modes of action, and side effects, and how they are used by

physicians to control infections disease.

1.13. Penicillin

Since the 1940s, Penicillin [25] has remained the most widely

used antibiotic because of its low cost and thousands of

derivatives. Penicillin G, or Benzyl penicillin, is currently the

most popular penicillin antibiotic and is usually the one intended

when doctor prescribe “Penicillin”. Other types are Penicillin F

and Penicillin V, all with the same basic structure of a beta-lactam

nucleus and several attached groups.

The Penicillins are active against a variety of Gram-positive

bacteria, including Staphylococci, Streptococci, Clostridia, and

Pneumococci. In higher concentrations, they are also inhibitory to

the Gram-negative diplococci that cause gonorrhea and

meningitis, and they are useful against syphilis spirochetes.


http://en.wikipedia.org/wiki/Immune_system

http://en.wikipedia.org/wiki/Nosocomial_infection


10

Penicillin functions during the synthesis of the bacterial cell wall.

It blocks the cross-linking of carbohydrates in the peptidoglycan

layer during wall formation.

Antimicrobial Activity [26]:

The initial step in Penicillin action is binding of the drug to cell

receptors. These receptors are PBPs, at least some of which are

enzymes involved in transpeptidation reactions. From three to six

(or more) PBPs per cell can be present. After penicillin molecules

have attached to the receptors, peptidoglycan synthesis is

inhibited as final transpeptidation is blocked. A final

bacterialcidal event is the removal or inactivation of an inhibitor

of autolytic enzymes in the cell wall. This activates the autolytic

enzymes and results in cell lysis. Organisms with defective

autolysin function are inhibited but not killed by Beta-lactam

drugs, and they are said to be “tolerant”.

Since active cell wall synthesis is required for penicillin

action, metabolically inactive microorganisms are not susceptible.

Penicillin G and Penicillin V are often measured in unit (1 million

Units=0.6 gm), but the semi synthetic penicillins are measured in

grams. Whereas 0.002-1microgm/ml of Penicillin G is lethal for a

majority of susceptible gram positive organisms, 10-100 times

more is required to kill gram negative bacteria(except Neisseriae).

Resistance

Resistance to penicillins falls into several categories:

1. Production of Beta-lactamases by Staphylococci, gram

negative bacteria, haemophili, gonococci, and others. More

than 50 different Beta-lactamases are known, most of them

produced under the control of bacterial plasmids. Some Beta-

lactamases are inducible by the new cephalosporins.

2. Lack of penicillin receptors (PBPs) or altered PBPs (e.g.,

Pneumococci, enterococci) or inaccessibility of receptors

because of permeability barriers of bacterial outer membranes.

These are often under chromosomal control.



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