Antibiotics Classifications, Microbiology, Antibiotic Spectrum, Pathogenesis

1. MICROBIOLOGY-
ANTIBIOTICS
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 Microbiology is the science of studying the microbes
 Variety in the genes of microbes explain behavior as well
as how microbes are helpful and/or problematic to us
 These teeny, tiny dots that we may not even be able to
see with the highest power of our microscopes, are
sometimes able to kill us
 Keep in mind that humankind has also been able to
harness the power of the microbial world for our benefit
using their versatility and success at adaptation
MICROBIOLOGYMICROBIOLOGY
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MICROBIOLOGYMICROBIOLOGY
BACTERIA:
 Microscopic living organisms
 Vary in size, shape, metabolic processes, and genetic
characteristic
 Certain common structures in them
 Highly differentiated class of organisms in between the
plant and animal kingdom
 Contain both RNA and DNA, complete enzyme, system
and are cell like in structure
 Have cell wall and are multiplied by self-disunion
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STRUCTURESTRUCTURE OFOF THETHE
BACTERIALBACTERIAL CELLCELL
Two different ways of grouping bacteria.
Response to gaseous oxygen:
 Aerobic bacteria
 Anaerobic bacteria
 Facultative anaerobes
Energy Sourcing
 Heterotrophs; depend on other preformed sources
 Autotrophs; Prepare their own energy
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STRUCTURESTRUCTURE OFOF THETHE
BACTERIALBACTERIAL CELLCELL
The bacterial cell consists of various structural
elements these elements are as follows:
 Capsule
 Cytoplasm
 Cell wall
 Nucleoid
 Cytoplasmic membrane`
 Spores (resting forms of certain bacteria) www.seas9.com

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HETROTROPHIC BACTERIA
SAPROPHYTES COMMENSALS SYMBIONTS PARASITES
( LIVE ON (TABLE COMPANION PERFORMS (LIVE AT THE
DEAD ORGANIC PRESENT IN GIT FUNCTION EXPENSE OF
SUBSTANCES) VAGINA & R.TRACT) BENEFICIAL THE
HOST).
FOR THE
HOST E.G.
INTESTINAL
FLORA
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STRUCTURESTRUCTURE OFOF THETHE
BACTERIALBACTERIAL CELLCELL
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BACTERIALBACTERIAL REPRODUCTIONREPRODUCTION
 Bacterial reproduction is highly efficient process
 Some bacteria can double their number in only 20
minutes Most common method is binary fission
 Two identical daughter cells are formed from the
original Binary fission is asexual as no male and
female gamete are involved
 New cells are simply copies of the original.
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8. GENERATION TIME
THE INTERVAL OF TIME BETWEEN BACTERIAL DIVISIONS
IS CALLED THE GENERATION TIME. THIS INTERVAL VARIES
AMONG BACTERIAL SPECIES. MYCOBACTERIUM
TUBERCULOSIS, FOR EXAMPLE, HAS A GENERATION TIME
OF 18 HR. IN CONTRAST, THE GENERATION TIME OF
ESCHERICHA COLI IS 20 MIN. OF COURSE, GENERATION
TIMES ARE CALCULATED ACCORDING TO BACTERIAL
GROWTH UNDER IDEAL CONDITIONS.
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BACTERIALBACTERIAL REPRODUCTIONREPRODUCTION
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BACTERIALBACTERIAL REPRODUCTIONREPRODUCTION
GROWTH CURVE:
During cultivation, cells undergo a number of phases
that are collectively referred to as the growth curve. The
growth curve is generally considered a laboratory
phenomenon. Not something that occurs in the body.
The curve is usually divided into four phases;
 LAG
 logarithmic
 stationary
 death
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BACTERIALBACTERIAL REPRODUCTIONREPRODUCTION
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BACTERIALBACTERIAL
REPRODUCTIONREPRODUCTION
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13. 1. GENUS AND SPECIES
2. SHAPES AND ARRANGEMENTS
3. STAINING PROPERTIES OF BACTERIAL CELLS
4. BIOCHEMICAL PROPERTIES
5. OXYGEN REQUIREMENT, ETC.
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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14. COCCUS
CAN BE AS SINGLE CELL, IN
PAIRS (DIPLOCOCCI), IN THE
FORM OF CHAIN
(STREPTOCOCCI) OR IN
CLUSTER FORM
(STAPHYLOCOCCI).
EXAMPLES ARE S.
PNEUMONIAE AND S.
AUREUS.
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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15. BACILLUS
ROD SHAPE IS CALLED
BACILLUS.
TWO BACILLI TOGETHER -
DIPLOBACILLI
CHAINS OF BACILLI ARE
CALLED STREPTOBACILLI
PALISADES –
RODS SIDE BY SIDE OR
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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16. VIBRIO
COMA SHAPED ORGANISMS
BEST-KNOWN SPECIES OF
VIBRIO IS V. CHOLERAE WHICH
CAUSES CHOLERA, A SEVERE
DIARRHOEAL DISEASE
RESULTING FROM A TOXIN
PRODUCED BY BACTERIAL
GROWTH IN THE GUT.
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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17. SPIRAL
COILED BACTERIA AND ARE USUALLY SINGLE
THESE BACTERIA INCLUDE THE SPIROCHAETES, SUCH AS
TREPONEMA PALLIDUM WHICH CAUSES SYPHILIS.
HOWEVER SPIROCHAETES HAVE A DIFFERENT TYPE OF
MOTILITY FROM THAT OF THE COMMON SPIRAL BACTERIA.
SPIRILLIUM IS RIGID
SPIROCHETE FLEXIBLE AND UNDULATING
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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18. STAINING PROPERTIES:
GRAM’S STAIN IS COMMONLY USED DEPENDING ON THEIR BACTERIAL
CELL WALL PROPERTIES THEY ARE EITHER STAINED PINK (GRAM – VE)
OR PURPLE (GRAM + VE) BACTERIA.
GRAM POSITIVE ORGANISMS HAVE A THICK PEPTIDOGLYCAN (MUREIN)
LAYER AND 2 CLASSES OF TEICHOIC ACIDS. LIPOTEICHOIC ACID WHICH
IS ON THE SURFACE, EMBEDDED IN THE PEPTIDOGLYCAN LAYER AND IS
LINKED TO THE CYTOPLASMIC MEMBRANE. WALL TEICHOIC ACID IS ON
THE SURFACE AND IS LINKED TO ONLY THE PEPTIDOGLYCAN LAYER.
TEICHOIC ACID IS RESPONSIBLE FOR THE ANTIGENIC DETERMINANT OF
THE ORGANISM.
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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19. STAINING PROPERTIES:
GRAM POSITIVE CELL WALL
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA

20. STAINING PROPERTIES:
GRAM NEGATIVE HAVE A THIN PEPTIDOGLYCAN (MUREIN)
LAYER WITH AN OUTER MEMBRANE ATTACHED TO THE
PEPTIDOGLYCAN LAYER BY LIPOPROTEINS. THE OUTER
MEMBRANE IS MADE OF PROTEIN, PHOSPHOLIPID AND
LIPOPOLYSACCHARIDE. IN THE LIPOPOLYSACCHARIDE, THE
LIPID PORTION IS EMBEDDED IN THE PHOSPHOLIPID AND THE
O ANTIGEN POLYSACCHARIDE IS ON THE SURFACE. THE LIPID
IS CALLED LIPID A AND IT IS TOXIC, BUT THE WHOLE
LIPOPOLYSACCHARIDE IS CALLED AN ENDOTOXIN. THE CELL
WALL HAS CHANNELS CALLED PORINS FOR THE TRANSPORT
OF LOW MOLECULAR WEIGHT SUBSTANCES. BETWEEN THE
CYTOPLASMIC MEMBRANE AND THE CELL WALL IS A
PERIPLASMIC SPACE WITH HYDROLYTIC ENZYMES, ANTIBIOTIC
INACTIVATING ENZYMES AND TRANSPORT PROTEINS.
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA
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21. STAINING PROPERTIES:
GRAM NEGATIVE CELL WALL
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CLASIFICTION OF BACTERIACLASIFICTION OF BACTERIA

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PATHOGENECITYPATHOGENECITY
Pathogenicity is the ability to destroy tissue and cause
a physiological or anatomical change and, eventually
disease.
MECHANISMS OF PATHOGENESIS
Microorganisms cause disease by certain basic
mechanisms:
 Invasion of tissue
 Production of toxins
 Virulence www.seas9.com

23. ORGANISMS DISEASE
GRAM-POSITIVE COCCI
STAPHYLOCOCCUS AUREUS BOLUS, FOOD POISONING
STREPTOCOCCUS PNEUMONIA PNEUMONIA
STREPTOCOCCUS PYOGENES PHARYNGITIS,RHEUMATIC FEVER
STAPHYLOCOCCUS EPIDERMIDIS SKIN INFECTIONS
GRAM-POSITIVE BACILLI
AEROBIC
LISTERIA MONOCYTOGENES MENINGOENCEPHALITIS
CORNYEBACTERIUM DIPHTHERIAE DIPHTHERIA
BACILLUS SPECIES
ANAEROBIC
CLOSTRIDIUM PERFRINGENS GAS GANGRENE
CLOSTRIDIUM TETANI TETANUS
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PATHOGENECITYPATHOGENECITY
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24. ORGANISMS DISEASE
GRAM-NEGATIVE BACILLI
AEROBIC
ESCHERICHIA COLI ENTERITIS, UTI
BORDETELLA PERTUSSIS WHOOPING COUGH
RICKETTSIA RICKETTSII ROCKY MOUNTAIN
SPOTTED FEVER
KLEBSIELLA PNEUMONIAE PNEUMONIA
SHIGELLA DYSENTERIAE DYSENTERY
HAEMOPHILUS INFLUENZAE PNEUMONIA
SAIMONELLA ENTERITIDIS ENTERIC FEVER OR
TYPHOID
FOOD POISONING
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PATHOGENECITYPATHOGENECITY
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25. ORGANISMS DISEASE
GRAM-NEGATIVE BACILLI
ANAEROBIC
BACTEROIDES FRAGILIS ULCER, SEPTICEMIA,
ENDOCARDITIS
SPIROCHETES
TREPONEMA PALLIDUM SYPHILIS
BORRELIA RECURRENTIS RELAPSING FEVER
ATYPICAL BACTERIA
MYCOPLASMA PNEUMONIAE PNEUMONIA
CHLAMYDIA PNEUMONIAE
LEGIONELLA PNEUMOPHILA
UREAPLASMA
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PATHOGENECITYPATHOGENECITY
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BACTERIALBACTERIAL INFECTONSINFECTONS
 A complex interaction b/w bacteria & host
 Bacteria must overcome obstacles before disease occurs
 They must enter the host successfully and colonize
tissue and then damage host tissue, and grow in that
location Microorganisms can enter the body at various site
 Microorganisms enter the body, for example, through
respiratory tract, cuts or wounds, insect bites and
consumption of contaminated food.
 Additionally, hospital procedures involving catheters,
intravenous therapy or transplantation increase the
chances of microorganisms entering a patients body.
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BACTERIALBACTERIAL INFECTONSINFECTONS
DEFENSE MECHANISM OF THE HUMAN BODHY
The body resists infection and disease in a number of ways
through nonspecific responses and specific responses.
Four nonspecific defenses in the body
 Skin
 Mucous membranes
 Phagocytosis
 Inflammation
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BACTERIALBACTERIAL INFECTONSINFECTONS
DEFENSE MECHANISM OF THE HUMAN BODY
HUMORAL IMMUNITY
 Antibodies which are highly specific protein molecules
 Antibody mediated defenses include:
 Antitoxins, bacteriolytic antibodies, antibodies plus
complement, opsonizing antibodies
CELL – MEDIATED IMMUNITY
 Specific immune response provided by T-lymphocytes
 Cell-mediated defenses include:
 Cytotoxic T-lymphocytes, K & NK cells, activated macrophageswww.seas9.com

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BACTERIALBACTERIAL RESISTANCERESISTANCE
For treatment purposes, resistance to a specific anti-biotic
mean that bacteria are not inhibited by doses of the drug
which are both tolerable and safe for the average patient.
Some bacteria, by means of complex genetic and
biochemical mechanisms acquire resistance to the drug.
The resistance can be
 Intrinsic
 Acquired
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BACTERIALBACTERIAL RESISTANCERESISTANCE
INTRINSIC RESISTANCE
Chromosome determines this type of resistance
Is a stable inheritable (genetic) characteristic
ACQUIRED RESISTANCE
Bacteria have the ability to acquire resistance to antibacterial agents
by several mechanisms that alter their genetic material. Acquired
resistance is the alteration in the genetic material
This is achieved by:
 Transposition
 Conjugation
 Transduction
 Transformation
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BACTERIALBACTERIAL RESISTANCERESISTANCE
THE CLINICAL IMPLICATIONS OF RESISTANCE
Three approaches to limiting bacterial resistance are;
 Appropriate antibiotic used by the physician
 Reduction of selective pressure of antibiotic use
 Development of new antibiotics.
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32. INHIBITION OF CELL WALLS SYNTHESIS DAMAGING OF
CYTOPLASMIC MEMBRANE
PENCILLINS AMINOGLYCOSIDES
CEPHALOSPORINS POLYMYXIN B
FOSFOMYCIN
INHIBITION OF PROTEIN BIOSYNTHESIS
AMINOGLYCOSIDES INHIBITION OF NUCLEIC
LINCOSAMIDES ACID SYNTHESIS
MACROLIDES
TETRACYCLINES RIFAMPICIN (RNA)
CHLORAMPHENICOL FUSIDIC ACID (DNA)
FUSIDIC ACID) QUINOLONES (DNA)
FOLIC ACID ANTAGONISTS B-LACTAMASE INHIBITION
SULFONAMIDES CLAVULANIC ACID
TRIMETHOPRIM SULBACTAM
CO-TRIMOXAZOLE TAZOBACTAM
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ANTIMICROBIAL ACTIVITYANTIMICROBIAL ACTIVITY
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InspirationInspiration ExpirationExpiration
RESPIRATION -RESPIRATION -
PHYSIOLOGYPHYSIOLOGY
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Definition:
Infection of one or more para-nasal sinuses is called sinusitis
Incidence:
 Common, in adolescents and adults
 Associated with DNS, adenoids, nasal polyp, tumours,
denture abnormalities, pressure changes.
 Change in weather especially high humidity, common cold,
measles, trauma etc are also predisposing factors for this
condition.
SINUSITISSINUSITIS
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SINUSITIS - ORGANISMSSINUSITIS - ORGANISMS
S. pneumoniae 31% (20-35%)
H. influenza 21% (6-26%)
Anaerobes 6% (1-10%)
M. catarrhalis 2% (2-10%)
S. aureus 4% (0-8%)
GNR 9% (0-24%)
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SINUSITISSINUSITIS
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43. DEFINITION:
INFECTION/INFLAMMATION OF THE PHARYNX AND TONSILS.
INCIDENCE:
COMMON INFECTION, USUALLY IN CHILDREN, VIRAL
(USUALLY SELF LIMITING) BUT CAN BE BACTERIAL.
PHYSICAL OR CHEMICAL STIMULI, AND NASAL DISEASES
ALSO PREDISPOSE TO THIS INFECTION. OVERWORK,
COMMON COLD, CHANGE OF SEASON, OPERATION ON
NASAL CAVITY ETC. PREDISPOSE TO TONSILLITIS.
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PHARYNGITIS & TONSILLITISPHARYNGITIS & TONSILLITIS
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44. INFLAMMATION OF LARYNX IS CALLED LARYNGITIS.
VIRAL (E.G., PARAINFLUENZA OR MEASLES VIRUS) OR
BACTERIAL INFECTIONS, PHYSICAL AND CHEMICAL
STIMULI E.G. EXCESS SMOKING OR STRAINING OF VOCAL
CORDS CAN ASLOS LEAD TO LARYNGITIS.
DRYNESS AND SORENESS OF THE THROAT, DRY AND
HACKING COUGH, DYSPHONIA AND A CHANGE IN VOICE.
VOCAL REST, REMOVAL OF OFFENDING AGENTS AND
TREATMENT OF INFECTION WITH ADMINISTRATION OF
ANTIBIOTIC SYSTEMATICALLY.
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LARYNGITISLARYNGITIS

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46. INFLAMMATION (INFECTION) OF THE MIDDLE EAR CAVITY,
USUALLY CAUSED BY BACTERIA IS CALLED OTITIS MEDIA.
ACUTE OTITIS MEDIA, SUDDEN ONSET, ASSOCIATED WITH
SEROUS EFFUSION, CAN TURN INTO PUSY DISCHARGE
SUPPURATIVE OTITIS MEDIA
CHRONIC OTITIS MEDIA, PERSISTENCE OF THE INFECTION IN
INCOMPLETELY TREATED PATIENT, OCCURS IN THOSE WITH
BLOCKED TYMPANIC TUBE, PERFORATED EAR DRUM, OR IN
PATIENTS WITH CHRONIC/RECURRENT THROAT INFECTION.
WHEN THERE IS CHRONIC DISCHARGE OF PUS IT IS CALLED
CHRONIC SUPPURATIVE OTITIS MEDIA (CSOM).
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OTITIS MEDIAOTITIS MEDIA
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47. DEFINITION:
INFLAMMATION /INFECTION OF THE MUCUS MEMBRANE
LINING OF THE BRONCHUS.
CHRONIC BRONCHITIS;
PRESENCE OF COUGH FOR PERIOD OF THREE MONTHS
FOR TWO CONSECUTIVE YEARS. CHRONIC BRONCHITIS IS
USUALLY CAUSED BY CIGARETTE SMOKE, CHEMICALS,
GASES ETC.
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BRONCHITISBRONCHITIS
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48. ACUTE ON CHRONIC BRONCHITIS; (ABECB)
WHEN THERE IS AN ACUTE ATTACK OF INFECTION
(BRONCHITIS) ON UNDERLYING CHRONIC
BRONCHIATIC PATIENT
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BRONCHITISBRONCHITIS
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49. INCIDENCE:
USUALLY VIRAL, PRIMARY BACTERIAL IN DEBILITATED
PATIENTS, USUALLY SECONDARY INFECTION BY BACTERIA.
CHRONIC BRONCHITIS; CIGARETTE SMOKE, CHEMICALS,
GASES ETC
BACTERIOLOGY:
S. PNEUMONIAE, S. PYOGENES, H. INFLUENZAE,
M. CATARRHALIS, S. AUREUS (IN ELDERLY) ETC.
H. INFLUENZAE AND M. CATARRHALIS ARE MAJOR
PATHOGEN IN INFECTIVE EXACERBATION OF CHRONIC
BRONCHITIS, AND PENETRATE WELL INTO SPUTUM AND
BRONCHIAL MUCOSA.
GRAM-NEGATIVE ENTERIC BACILLI ARE LESS FREQUENTLY
INVOLVED
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BRONCHITISBRONCHITIS
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50. It is now evident that many exacerbations in COPD, as in asthma,
are due to upper respiratory tract viral infections (such as
rhinovirus infection) and to environmental factors, such as air
pollution and temperature.
There is an increase in neutrophils and in the concentrations of
interleukin-6 and interleukin-8 in sputum during an exacerbation,
and patients who have frequent exacerbations have higher
levels of interleukin-6, even when COPD is stable.
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ACUTE EXACERBATIONACUTE EXACERBATION
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51. Bronchial biopsies show an increase in eosinophils during
exacerbations in patients with mild COPD but there is no increase
in sputum eosinophils during exacerbations in patients with severe
COPD.
 An increase in markers of oxidative stress and exhaled nitric
oxide, presumably reflecting increased airway inflammation, is
observed during exacerbations.
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ACUTE EXACERBATIONACUTE EXACERBATION
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52. SPUTUM PATHOGENS IN AECB
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50%50%
19%19%
17%17%
14%14%
H. influenzae
S. pneumonia
M. catarrhalis
Other
PATHOGENESIS OF COPD:PATHOGENESIS OF COPD:
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53. SYMPTOMATOLOGY:
PRODUCTIVE COUGH, FEVER, DYSPNOEA, CHEST PAIN
MALAISE, BODY ACHES. A SCANTY AND WATERY SPUTUM IS
INDICATIVE OF VIRAL OR MYCOPLASMA INFECTION.
ACUTE ON CHRONIC BRONCHITIS (AECB) IS USUALLY
DIAGNOSED WHEN THE CONTINUED SYMPTOMS WORSENS,
SUCH AS INCREASE IN COUGH, SPUTUM PRODUCTION WITH
PUS AND EVEN BLOOD, AND DYSPNOEA.
COMPLICATIONS:
EMPHYSEMA, RESPIRATORY FAILURE,
CARDIAC FAILURE (COR-PULMONALE).
DIAGNOSIS:
SPUTUM FOR C/S, X-RAY CHEST, RESPIROMETRY
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BRONCHITISBRONCHITIS
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54. INTRODUCTION:
IT IS WELL RECOGNIZED THAT COMMUNITY ACQUIRED
PNEUMONIA (CAP) PLAYS A HUGE BURDEN UPON HEALTH
CARE SYSTEM.
THIS CONDITION HAS A HIGH MORBIDITY AND MORTALITY.
A LARGE NUMBER OF PATIENTS ARE ADMITTED IN
HOSPITAL WITH
THIS CONDITION.
THE OUTCOME DEPENDS ON OPTIMIZATION OF THERAPY,
AGE OF THE PATIENT, LENGTH OF STAY, AND OTHER CO-
MORBID CONDITIONS.
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PNEUMONIAPNEUMONIA
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55. DEFINITION:
INFLAMMATION / INFECTION OF THE LUNG PARENCHYMA ALONG
WITH ITS TERMINAL BRONCHIOLES IS CALLED PNEUMONIA OR
PNEUMONITIS.
INCIDENCE:
PNEUMONIA OCCURRING IN AN OTHERWISE HEALTHY PERSON
IS LABELED AS COMMUNITY ACQUIRED PNEUMONIA (CAP).
IN HOSPITAL SITUATION IT IS CALLED HOSPITAL ACQUIRED
(NOSOCOMIAL PNEUMONIA) LIKELY TO RUN A MORE SEVERE
COURSE.
EXTREMES OF AGE,
DEBILITATING CONDITIONS,
WEAK DEFENSE MECHANISM
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PNEUMONIAPNEUMONIA
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56. BACTERIOLOGY:
COMMUNITY ACQUIRED
S. PNEUMONIAE, H. INFLUENZAE,
M. CATARRHALIS, L. PNEUMOPHILA,
M. PNEUMONIAE, C. PNEUMONIAE
HOSPITAL ACQUIRED
K. PNEUMONIAE, H. INFLUENZAE PROTEUS SPP, E. COLI
S. AUREUS, PSEUDOMONAS AERUGINOSA.
L. PNEUMOPHILA, AND M. PNEUMONIAE.
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PNEUMONIAPNEUMONIA
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PNEUMONIA – CLINICALPNEUMONIA – CLINICAL
CLASSIFICATIONCLASSIFICATION
Typical
Community Acquired
Hospital Acquired Atypical
 Recurrent
 Aspiration
 Opportunists(immuno-compromised
Host)
Unusual (Geographical)
Unresolved
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PNEUMONIA – COMMONPNEUMONIA – COMMON
ETIOLOGYETIOLOGY
Streptococcus pneumoniae
 Streptococcus pyogenes
 Haemophilus influenzae
 Klebsiella pneumoniae
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PNEUMONIA – LESS COMMONPNEUMONIA – LESS COMMON
ETIOLOGYETIOLOGY
Legionella spp.
 Mycoplasma pneumioniae
 Pseudomonas aeruginosa
 Chalamydia trachomatis
 Coxiella burnetii
 Anaerobic bacteria
 Mycobacteria
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S. pneum oniae
H. inf l enzae
Inf luenza
Legionella
Chlam ydia
GNEB
P. aeruginosa
Mycoplasm a
Coxiella
27%27%
11%11%
22%22%
10%10%
8%8%
6%6%
5%5%
6%6%
5%5%
Ruiz,AJRCCM 1999; 160:397
u
PNEUMONIA - COMMUNITYPNEUMONIA - COMMUNITY
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Streptococcus pneumoniae
Staphylococcus aureus
Morexalla catarrhalis
Enterococcus sp.
Hemophilus influenzae
Klebsiella pneumonia
Escherichia coli
Serratia sp.
Providencia sp.
Enterobacter sp.
Pseudomonas aeruginosa
Legionella pneumophila
Mycobacterium tuberculosis
Influenza virus
El-Solh,AJRCCM 2001; 163:645 (Buffalo NY)
45%
13%
10%
6.5%
PNEUMONIA - NOSOCOMIALPNEUMONIA - NOSOCOMIAL
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62. BACTERIOLOGY:
COMMUNITY ACQUIRED
FOR THOSE REQUIRING ADMISSION, THE NUMBER
ONE CAUSE IS S. PNEUMONIAE, FOLLOWED BY M.
CATARRHALIS, AND C. PNEUMONIAE.
AMONGST PATIENTS WHO ARE SERIOUS ENOUGH
REQUIRING ICU CARE S. PNEUMONIAE IS ON TOP.
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PNEUMONIAPNEUMONIA
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63. SYMPTOMATOLOGY:
CLINICAL SYMPTOMS VARY ACCORDING TO CAUSATIVE
ORGANISMS. IN BACTERIAL PNEUMONIA THE ONSET OF
DISEASE IS SUDDEN WITH CHILLS, HIGH GRADE FEVER,
TACHYPNOEA (INCREASE IN RESPIRATORY RATE), PAIN
IN CHEST, AND PURULENT AND COPIOUS SPUTUM. IN
VIRAL AND MYCOPLAMA INFECTION THE ONSET IS
GRADUAL AND SYMPTOMS ARE MILDER.
HOSPITAL ACQUIRED PNEUMONIA, AND PNEUMONIA AT
EXTREMES OF AGE RUNS A MORE RAPID COURSE
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PNEUMONIAPNEUMONIA
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PNEUMONIAPNEUMONIA
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PNEUMONIAPNEUMONIA
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URINARY TRACTURINARY TRACT
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67. INFECTIONS OF URINARY TRACT ARE COMMON.
MOST COMMON INFECTION OF THE URINARY TRACT IS CYSTITIS.
CAN SPREAD UPWARDS TO CAUSE PYELONEPHRITIS
THE SUSCEPTIBILITY OF URINARY TRACT FOR INFECTION
INCREASES WITH CERTAIN ANATOMICAL (ENLARGED
PROSTATE), FUNCTIONAL (VESICOURETERIC REFLUX), OR
OBSTRUCTIVE (STONE) IN THE URINARY PASSAGE.
INSTRUMENTATION AND PREGNANCY FURTHER PREDISPOSE TO
INFECTIONS
67
URINARY TRACT INFECTIONURINARY TRACT INFECTION
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68. ACUTE GLOMERULONEPHRITS
ACUTE PYELONEPHRITIS
BACTERIA CAUSING PYELONEPHRITIS INCLUDE E. COLI,
KLEBSIELLA SPP, AND PROTEUS SPP, LESS COMMONLY
SERRATIA SPP, PSEUD. AERUGINOSA, ENTEROBACTER SPP.,
AND S. SAPROPHYTICUS.
CHRONIC PYELONEPHRITIS
CONCURRENT HYPERTENSION IS COMMON.
URETERITIS
ACUTE CYSTITIS
DUE TO SPREAD OF COLIFORM MICROBES (E. COLI, S.
FAECALIS, KLEBSIELLA SPP, PROTEUS SPP., AND P.
PYOCYANEA)
CHRONIC CYSTITIS
URETHRITIS
68
URINARY TRACT INFECTIONURINARY TRACT INFECTION
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69. 69
CYSTITIS
Infection with coliform bacteria
Women > men (short urethra!)
Predisposing factors
Pregnancy
Calculi
Medical procedures (e.g catheter)
Diabetes
Chemotherapy
Tumors
URINARY TRACT INFECTIONURINARY TRACT INFECTION
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70. PELVIC INFLAMMATORY DISEASE (PID)
USUALLY BEGINS AS VULVOVAGINITIS. UPWARD SPREAD IS
COMMON COMPLICATIONS;
INFERTILITY, PERITONITIS, INTESTINAL OBSTRUCTION,
BACTERAEMIA
GONORRHEA
COMMONLY OCCURRING VENEREAL DISEASE
CAUSED BY NEISSERIA GONORRHEA
SUPPURATIVE URETHRITIS; INFECTION MAY SPREAD TO
PROSTATE GLAND, EPIDIDYMIS AND TESTES.
SYPHILIS
CAUSED BY TREPONEMA PALLIDUM
THREE STAGES SEEN; PRIMARY SORE (CHANCRE),
SECONDARY LESIONS (CONDYLOMATA LATA) TERTIARY
LESIONS (GUMMAS)
GENITAL TRACT INFECTIONSGENITAL TRACT INFECTIONS
70
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71. TRICHOMONAS VAGINALIS
THESE PROTOZOA CAUSE ACUTE VULVOVAGINITIS. IT IS
USUALLY SEXUALLY TRANSMITTED AND IS COMMONLY
PRESENT IN WOMEN WITH GONORRHEA.
DISORDERS OF THE BODY OF THE UTERUS
(A) ACUTE ENDOMETRITIS
(B) CHRONIC ENDOMETRITIS
DISORDERS OF THE UTERINE TUBES AND OVARIES
ACUTE SALPINGITIS
GENITAL TRACT INFECTIONSGENITAL TRACT INFECTIONS
71
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72. SECONDARY:
-CUTS & BURNS
-BITES
-BED SORES
-SURGICAL WOUNDS
-DIABETES MELLITUS
SKIN & SOFT TISSUE INFECTIONSSKIN & SOFT TISSUE INFECTIONS
72

73. THE TERM ‘OSTEOMYELITIS’ INDICATES INFLAMMATION OF THE
BONE CAUSED BY INFECTIVE ORGANISMS. THIS CAN BE CAUSED
BY THE FOLLOWING TYPES OF ORGANISMS.
NON-SPECIFIC PYOGENIC ORGANISMS LIKE STAPHYLOCOCCS
AND STREPTOCOCCUS.
SPECIFIC ORGANISMS CAUSING TUBERCULOUS
OSTEMYLITIES,
SYPHILITIC OSTEOMYELITIS, TYPHOID AND PARTATYPHIOD
OSTEOMYELITIS.
MYCETOMAL (FUNGAL) INFECTIONS CAUSING ‘ACTINOMICOSIS’
OR
MADURAMYCOSIS.
PARASTIC INFECTION - HYDATID CYST.
OSTEOMYELITISOSTEOMYELITIS 73
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74. PYOGENIC OSTEOMYELITIS:
INFECTION CAN REACH THE BONE BY THE FOLLOWING
ROUTES:
A. THROUGH THE BLOOD STREAM FROM A FOCUS OF
INFECTION ELSEWHERE (HAEMATOGENOUS).
B. DIRECT INVASION FROM THE ATMOSPHERIC AIR AS
IN OPEN FRACTURES.
C. SPREAD FROM A NEIGHBOURING FOCUS E.G.
MASTOIDITIS FROM MIDDLE EAR INFECTION,
OSTEOMYELITIS OF MANDIBLE FROM DENTAL
ROOT ABSCESS.
OSTEOMYELITISOSTEOMYELITIS 74
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75. CLINICAL TYPES OF PYOGENIC OSTEOMYELITIS:
CLINICALLY PYOGENIC OSTEOMYLITIES CAN
PRESENT AS FOLLOWS:
ACUTE OSTEOMYELITIS.
CHRONIC OSTEOMYELITIS.
PRIMARY SUB-ACUTE OSTEOMYELITIS.
ACUTE FLARE UP OF CHRONIC OSTEOMYELITIS.
OSTEOMYELITISOSTEOMYELITIS 75
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76. WHAT IS TUBERCULOSIS?
TUBERCULOSIS IS A BACTERIAL DISEASE USUALLY
AFFECTING
THE LUNGS (PULMONARY TB). OTHER PARTS OF THE
BODY
CAN ALSO BE AFFECTED, FOR EXAMPLE, LYMPH NODES,
KIDNEYS, BONES, JOINTS, ETC. (EXTRA-PULMONARY TB).
WHO GETS TUBERCULOSIS?
TUBERCULOSIS CAN AFFECT ANYONE OF ANY AGE.
IMMUNOCOMPROMISED INDIVIDUALS SUCH AS THOSE
WITH AIDS (OR THOSE INFECTED WITH THE HUMAN
IMMUNODEFICIENCY VIRUS - HIV) ARE AT INCREASED
RISK.
TUBERCULOSISTUBERCULOSIS 76
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77. TUBERCULOSISTUBERCULOSIS 77
AN ISSUE IN EVERY REGION OF THE GLOBE:
• Hot spots* • Outbreaks
*At least 4% of
TB cases are
MDR strains
(Data provided
by WHO)
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78. 5. Host factors. Patients who have neutropenia or other impairments of host
defense mechanisms generally need combinations of bactericidal drugs at dosages
that achieve high serum levels. Drug allergies and underlying illnesses, especially
renal or hepatic dysfunction, often influence antimicrobial selection.
6. Indications for combinations of antibiotics.
7. Clinical pharmacology (e.g., dosage, routes of administration, adverse
reactions, drug interactions, and serum levels).
8. Appropriate duration of therapy. (Extensive data on which to base
decisions are often lacking, but some empirical guidelines are available for certain
types of infection.)
9. Public health considerations in a closed community
(e.g., a hospital). The widespread use of certain antibiotics may select out a
highly resistant flora that poses a threat of nosocomial infection. In many hospitals,
the administration of certain antimicrobial agents is limited to very specific
indications.
10. Cost. The price of antimicrobial agents varies widely, and new drugs are often
much more expensive than older agents. If the efficacy and toxicity of two or more
agents are equal, the least expensive one should be selected.
78SELECTION OF ANTIMICROBIALSELECTION OF ANTIMICROBIAL
DRUGSDRUGS
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79. 79
 β -Lactams : Penicillins,
 Cephalosporins ; cephradine, cefaclor, cefixime
 Monobactam; aztreonam
 Aminoglycosides; gentamycin, kanamycin
 Tetracyclines;
ANTIMICROBIAL AGENTSANTIMICROBIAL AGENTS
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80. β -Lactam / β Lactamase inhibitors; clavulunate
Carbapenems; meropenem
Glycopeptides; tiecoplanin (Targocid)
Macrolides; erythromycin, clarithromycin
Quinolones; ofloxacin, ciprofloxacin
80
ANTIMICROBIAL AGENTSANTIMICROBIAL AGENTS
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81. Penicillins
Fermentation products of Penicillium mold
B-lactam nucleus attached to thiazolidine ring
Changing the ring changes spectrum and resistance
Mechanism of action
Interferes with final step of cell wall synthesis
Static or -cidal depending on bacterial enzymatic
regulatory system (deregulated by penicillin)
Clinical Pharmacology
Eliminated via kidney, almost unchanged--Probenecid
Stomach acid destroys most penicillins
Wider uptake with inflammation (CSF, Middle ear, etc)
81
ANTIMICROBIAL AGENTSANTIMICROBIAL AGENTS
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82. Antistaphylococcal Penicillins
Methicillin, Oxacillin, Cloxacillin, Dicloxacillin, Nafcillin
Used for penicillin-resistant Staph infections.
Dicloxacillin achieves the highest serum levels. All should be given in
fasting state.
Less efficacy than natural penicillin for PCN-sensitive microbes.
82
ANTISTAPHYLOCOCCAL PENICILLINSANTISTAPHYLOCOCCAL PENICILLINS
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83. Ampicillin, Amoxicillin, Bacampcillin
More rash (especially with Mono)
H. influenzae showing 5-55% resistance
Spectrum
Strept., pneumococci (except highly-resistant), H. influenzae,
Proteus, many E. Coli.
Inactivated by B-lactamases (including penicillinase) therefore
less effective against Staph.
Ampicillin destroyed by acid, Amoxicillin and Becampicillin may
be taken at mealtime—serum and middle ear levels higher than
with Ampicillin.
83
AMINO-PENICILLINAMINO-PENICILLIN
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84. Amoxicillin + clavulanate, Ampicillin + sulbactam, Ticarcillin +
clavulanate, Piperacillin + tazobactam
Clavulanic acid irreversibly binds B-lactamase enzyme
Spectrum: reverses resistance trends in H. Infl, M. cat., S. aureus,
B. fragilis. Timentin & Zosyn add psuedomonal coverage.
No change in effectiveness for pneumococci
84
AUGMENTED PENICILLINAUGMENTED PENICILLIN
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85. Ticarcillin, Mezlocillin, Piperacillin
Less active than the amino-penicillins against gram positives
Inactivated by B-lactamases therefore no advantage over other
penicillins for nonpseudomonal infection.
Synergistic against P. aeruginosa when combined with
aminoglycosides (should always treat with two agents)
85
ANTIPSEUDOMONAS PENICILLINANTIPSEUDOMONAS PENICILLIN
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86. Toxicity:
 Rash (5%)—can be treated with antihistamines, but
drug usually stopped. Recurs in only 50% with
repeated exposure. PCN/Mono rash does not
preclude future use. Only 5% cross reactive with
Cephalosporins.
 Anaphylaxis (1/10,000)—more often with IV doses.
Can desensitize. Do not use any B-lactam
antibiotic
(may use Azobactam).
 GI, Salt load, Platelet dysfunction (ticar)
86
PENICILLINSPENICILLINS
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87. Resistance:
Intrinsic resistance (inability to bind or penetrate)
B-lactamases & penicillinases hydrolyse b-lactam ring
H. influenza, M. catarrhalis, S. aureus, many anaerobes, gram
negative organisms
Either plasmid or chromosomally mediated
S. aureus releases penicillinase into milieu destroying drug before contact
with cell (doesn’t inactivate semisynthetic (oxacillin) or cephalosporins)
S. pneumo resistance is entirely different –mediated by alterations in
binding sites—moderate resistant strains still sensitive to higher doses.
87
PENICILLINSPENICILLINS
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88. Semisynthetic B-lactam derived from Cephalosporium acremonium
Mechanism: Same mechanism as PCN
Resistance: Mediated by B-lactamase enzymes
Clinical pharmacology: Wide distribution, but poor CSF penetration
even with inflammation.
Metabolism: Liver, Probenecid useful to increase levels.
“Generations” groups according to spectrum
88
CEPHALOSPORINSCEPHALOSPORINS
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89. First Generation
Cefadroxil (Duricef), Cefazolin (Ancef), Cephallexin (Keflex)
Spectrum: Most gram positive cocci (GAS, S. pneumo, S. aureus
(except MRSA—resistant to all cephalosporins), E. coli, Proteus,
Klebsiella. Does not cover P. aeruginosa or H. influ.
Use: S. aureus infection, surgical prophylaxis
89
CEPHALOSPORINSCEPHALOSPORINS
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90. Second Generation
Cefuroxime (Ceftin/Zinacef)-- effective against common
OM/sinusitis bacteria, including amp-resistant H. influenzae, good
CSF penetration, active against intermediate- resistant S.
pneumoniae
2nd
generation equivalents—Cefpodoxime (Vantin), Cefdinir
(Omnicef) activity equal to Ceftin—used as alternative to
Augmentin
Spectrum: more gram negative coverage, valuable in treatment of
H. influenzae. Not as effective against S. aureus as 1st
generation.
90
CEPHALOSPORINSCEPHALOSPORINS
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91. Third Generation
Spectrum: gram negative > gram positive. Good for identified B-
lactamase + H. influenzae, or M. catarrhalis, N. Gonorrhoeae, N.
meningitidis
Ceftriaxone (Rocephin), Cefotaxime (Claforan) effective against
S. pneumoniae (even intermediate and high resistance), H.
influenzae, N. meningitidis. Used for high-level, multi-drug resistant
pnuemococcal infections with Vancomycin. Single dose IM can
be effective for OM.
Ceftazidime (Fortaz) has best effectiveness against Pseudomonas
of all B-lactams (alternative to Gentamycin)
91
CEPHALOSPORINSCEPHALOSPORINS
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92. Produced by Streptomyces erythreus (erythromycin is natural
product)
Mechanism: bind to 50s subunit of bacterial ribosomes and block
protein synthesis
Resistance: target site alteration, antibiotic alteration, altered
transfer
Distribution: good penetration into oropharyngeal secretions.
92
MACROLIDESMACROLIDES
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93. Spectrum: effective against atypicals (Chlamydia, Mycoplasma),
Staph.(MRSA is resistant), Strep., Bordetella pertussis, H. influ, M.
catarrhalis.
ENT indications: Failed treatment of GAS in pharyngitis, resistant S.
pneumo, H. influ., and M. catarrhalis in AOM (Bactrim/
Clarithromycin/ Azythromycin), Sinusitis (Clarithromycin equal to
Augmentin, Azythromycin 500mg qDx3d =Augmentin x10 days)
Toxicity: generally considered safe—side effects are rare.
Ototoxicity (dose-dependant, peak)
93
MACROLIDESMACROLIDES
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94. Derived from Streptomyces lincolnensis
Mechanism: Inhibits protein synthesis by binding to the 50s ribosome.
Distribution: Poor CSF penetration, but excellent bone, oropharyngeal
secretion levels.
Spectrum: gram +, anaerobes. No activity against gram -.
Resistance is mediated via decreased membrane permeability and
alteration of 50s binding site.
Toxicity: nausea/vomiting, C. difficile colitis
94
CLINDAMYCINCLINDAMYCIN
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95. Glucopeptide produced by Streptomyces orientalis
Mechanism: bacteriocidal via inhibition of cell wall replication
PO dosing has no systemic uptake
Spectrum: gram +, MRSA. Vanc + Gent shows synergy against
mixed infections.
Toxicity: red man syndrome, phlebitis
ENT uses: MRSA, severe infections with resistant gram + organisms
95
VANCOMYCINVANCOMYCIN
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96. Bacteriocidal via production of DNA toxic substances within the
cell
Distribution: nearly all tissues, including CSF, saliva, bone,
abscesses.
IV=PO
Spectrum: active vs. anaerobes, parasites
ENT uses: C. difficile, anaerobic infections (abscesses)
Toxicity: disulfram reaction, others are rare
96
METRONIDAZOLEMETRONIDAZOLE
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97. Produced by Streptomyces and Micromonospora
Mechanism
Bind to ribosomes and interfere with protein
synthesis
Bacteriocidal
Clinical pharmacology
PO poor absorption; IM or IV best
Distribution: hydrophillic, poor CSF, cross placenta
Metabolism
Excreted unchanged, special dosing for renal
failure
97
AMINOGLYCOSIDESAMINOGLYCOSIDES
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98. Spectrum
Gram-negative bacilli, P. aeruginosa (use with anti
pseudomonas penicillins)
Resistance
Antibiotic modifying agents cause antibiotics to be unable to
bind to the ribosome
Toxicity
Nephrotoxic (trough)
Ototoxic (concentrated in perilymph, corresponds with
prolonged therapy and peak levels)
Neuromuscular blockade (think of this in Myasthenia Gravis)
98
AMINOGLYCOSIDESAMINOGLYCOSIDES
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99. Spectrum includes H. influenzae, M. catarrhalis. Generally not
effective vs. other microbes.
Mechanism: acts on protein synthesis chain
Combined with erythromycin (Pediozole) it is as effective as
ampicillin in treating AOM.
Sulfonamide + Trimethoprim (Bactrim) is alternate 1st
line agent for
AOM. Both drugs act on protein chain—synergistic. Effective vs.
beta-lactamase producing bacteria.
Sulfa allergies can result in life-threatening TEN.
99
SULFONAMIDESSULFONAMIDES
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100. Derivative of previous earlier antibiotic (nalidixic acid)
Mechanism of action: Inhibits DNA gyrase (bacteriocidal)
Resistance is mediated by gyrase mutations and efflux mechanisms
(drug permeation)
100
FLOUROQUINOLONESFLOUROQUINOLONES
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101. Spectrum: Broad coverage. Effective vs. gram +, gram -,
atypicals, and Pseudomonas.
Respiratory quinolones (levofloxacin): active vs. GAS, S. pneumo
(including penicillin-resistant forms), S. aureus (including MRSA), H.
influ., and M. catarrhalis (including penicillin-resistant strains).
Antipseudomonas quinolones (ciprofloxacin): effective vs.
Pseudomonas and gram-negative bacteria.
New floxins (Gati, Moxi, Gemi): similar to respiratory quinolones but
less activity vs. Pseudomonas and addition of anerobic activity
101
FLOUROQUINOLONESFLOUROQUINOLONES
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102. Bioavailability: IV = PO. Once/day dosing. Wide distribution (CSF,
saliva, bone, cartilage).
Toxicities: drug interactions (cations), tendon toxicity, ?bone
growth impairment. Ototopicals show no ototoxicity
Gatifloxacin $2 cheaper/pill (retail) than Levo.
102
FLOUROQUINOLONESFLOUROQUINOLONES
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103. ENT uses: Necrotizing OE, Auricular perichondritis (or in
procedures involving cartilage), Chronic ear disease, Sinusitis,
Pharyngotonsillitis.
103
FLOUROQUINOLONESFLOUROQUINOLONES
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104. VISIT WWW.SEAS9.COM
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