BACTERIAL INFECTIONS

DR. MERCEDES CAETE-MUJERES

PRINCIPLESOFANTIMICROBIALTHERAPY
1.

Appropriate specimens for gm stain, culture and

sensi. test should be obtained prior to initiating
antimicrobials to isolate the etiologic agent.

2. Antimicrobial tx prior to the availability of

microbiologic exam should be on based on the
expected pathogen and its prevailing
susceptibility.

3. Definitive antibiotic txt should be

based on the isolated org. and its demonstrated
susceptibility. Failure to isolate the organism,
the most likely pathogen based on statistical
probability should be the basis for the choice .
4. The choice of the specific agent, dose, route
and duration of txt are determined by
a. spectrum of activity
b. pharmacokinetic profile in relation to the
site of infection

c. Physiologic conditons of the host in

relation to: age, pregnancy,
renal,hepatic and immune status
d. adverse reaction profile of the drug
5. The antimicrobial txt of choice should be the
most effective, specific vs the pathogen.
The least toxic, the least expensive, a narrow
spectrum is preferred to avoid superinfection
and development of resistance.

 6.Antimicrobialcombination
preventionofemergenceofresistantorganism
polymicrobialinfections
initialtherapyi.e.neutropenia
decreasedtoxicity
synergism

PHARMACOKINETICS
Concn in serum and tissues vs time
Reflects absorption, distribution, metabolism and
excretion
Use for estimating dose, frequency, adjustments
and comparison of drugs

Absorption
ORAL
Bioavailability
10-20% - PCN, erythromycin
100% - clindamycin, Metronidazole,
doxycycline, TMP-SMZ

INTRAMUSCULAR
- 100% bioavailability
- for long acting drugs procaine,
benzathine PCN, Ceftriaxone
INTRAVENOUS
- 100 % bioavailability
- adeq concn in pleural, peritoneal,
pericardial and synovial fluids

Distribution
interstitial fluid concn is similar to serum
free/unbound drug pharmacologically
active
protein binding not deleterious
i.e. Ceftriaxone high protein bound

prolongs the time the concn

remains above the MIC

Site of Infection
- major role in the choice, dose and route
- concn above the MIC at the site major
determinant of therapeutic outcome
CNS Infection
lipid soluble drugs
i.e. Chloramphenicol, Rifampicin, Isoniazid
- better CSF levels

Beta-lactams
- efficacy based on inc BBB permeability
Metronidazole
- excellent concn in abscess
Endocarditis
- vegetations protected site of infection
- drug bactericidal, high dose, parenteral,
prolonged txt
- serum level 8x > than MBC of the org

Ostiomyelitis
- resistant to opsonophagocytic activity
- Fluoroquinolones superior bone conc
Chronic Prostatitis
- most drugs do not penetrate
- ion trapped antimicrobials
i.e. TMP-SMZ, quinolones

Abscess
- poor drug penetration
- drug inactivation (i.e. aminoglycosides)
- drainage enhances efficacy
Intraocular Infection
- endophthalmitis direct administration
Foreign bodies
- serve as nidus
- production of glycocalyx slime
-interferes w/ phagocytosis, impairs
penetration

Drugsmustdistributetositeofinfection
Poor cell penetration
Beta lactams, Vancomycin, Aminoglysides
Better cell penetration
Macrolides, Tetracycline, Metronidazole,
Rifampicin, TMP-SMZ, Quinolones

Metabolism and Elimination

Bioactive metabolites
i.e. Cefotaxime, Rifampicin, Clindamycin
- contribute to efficacy
Dose adjustment when elimination
capability is impaired
a. by glomerular filtration
- drug clearance correlated with crea
clearance

b. by hepatic / biliary
- no marker
- alternative drug

ANTIMICROBIALPHARMACODYNAMICS
PHARMACODYNAMICS
- refers to the quantitative relationship
among drug concn in serum and tissues, in vitro
susceptibility and microbial response at the site
of infection.
Describesbiochemical&physiologicaleffectsofthe
drug&itsmetabolism

Pharmacokinetics
Encompassesallthewaythatthebodymanipulatesadrug,
includingabsorption,distribution,metabolism,andexcretion.

Overview of interaction of pharmacokinetics and

Pharmacodynamics
Dosage regimen
Concentration
versus time in
serum
Concentration
versus time in
tissue and other
body fluids

Concentration
vs. Time at site
of infection

Pharmacologic
or toxicologic
effect

Antimicrobial
effect versus
time

Pharmacodynamics parameters:
1. Kinetics of bacterial killing (manner in which it
kills)
a. concn-dependent drugs
- the higher concn of the drug exceeding
the minimum inhibitory concn (AUC/MIC), the
greater is the bactericidal effect
- i.e. aminoglycosides
- concn exceeding the MIC of the drug ten
fold, i.e. fluoroquinolones

- AUC/MIC > 125

- attained by less frequent dosing/once daily
dosing
b. time-dependent drugs
- the bactericidal effect is dependent on the
length of time the bacteria are exposed to the
serum conc which exceed the MIC by at least 4x

-attained by constant infusion ffg an

initial bolus dose or choosing the drug
with the longest half-life
- i.e.

B-lactams

Clindamycin

Vancomycin

Macrolides

Metronidazole

2. Post-Antibiotic Effect (PAE)

- the length of time that bacterial growth is
inhibited after conc of the drug fall below the MIC
3. Post-Antibiotic Leukocyte Enhancing Effect
(PALE)
- enhanced leukocyte phagocytosis and
intracellular killing of bacteria during the drug free
period
4. Inoculum Effect
- rate of growth of the microorg is a function of
the original inoculum size

MICROBIOLOGIC ACTIVITY

PHARMACOKINETICS

Affinity for binding sites

Critical concn to ensure maximal binding

ANTIMICROBIAL
PHARMACODYNAMICS

Duration of exposure at sites

BACTERIAL CELL DEATH

INTEGRATION OF MICROBIOLOGICAL ACTIVITY AND PHARMACOKINETICS

SEPSIS

S E P S I S
Infection
- presence of org in a normally sterile site
with of w/o an inflammatory host response
Bacteremia
- bacteria present in blood (+ bld culture)

 Systemic Inflammatory Response Syndrome

(SIRS)
- response to clinical insult
( Infectious or Non infectious)
- manifested by 2 or more of the ff:
Temp > 38 or < 36 degrees C
HR > 90 beats/min
RR > 20/min of PACO2 <32 mmHg
WBC >12,000 cells/mm or < 4000
cells/mm3 or 10% bands

Sepsis
- SIRS that has a proven or suspected
microbial etiology
Sepsis Syndrome
- Sepsis + evidence of altered organ
hypoperfusion with at least one of the ff:
hypoxemia
Increase lactate
Oliguria
Altered mentation

Severe Sepsis
- sepsis with one or more signs of organ
dysfunction, hypoperfusion, or hypotension, such
as metabolic acidosis, acute alteration in mental
status, oliguria, or adult respiratory distress
synd
Septic shock
- sepsis induced hypotension (SBP < 90
mmhg) unresponsive to 500 ml fluid challenge +
peripheral hypoperfusion

Refractory Septic shock

- Septic hock for >1 hr : does not respond
to fluid or pharmacologic intervention
Multiple Organ Dysfunction Synd (MODS)
- impaired organ function sec to sepsis
pulmonary failure; ARDS
Renal failure
Hepatic dysfxn
DIC

PATHOPHYSIOLOGY
NIDUS OF INFECTION

BACTERIAL INVASION

Release of Endotoxin (Lipid-A moiety of LPS)

Exotoxin
Trigger Humoral Enzymatic Mediators
(cytokines, peptide hormones, TNF ,
interleukins, interferons, CSF)
Acivation of complement, clotting, fibrinolytic and kinin
pathways

HALLMARK OF SEPTIC SHOCK

VASODILATATION
INCREASE VASCULAR PERMEABILITY
Decrease intravascular fluid volume

Reduction in circulation blood volume

TISSUE HYPOPERFUSION

Lactic acidosis

CELL DEATH

Etiology

1.

Gram (+) Organisms

- S. aureus
- Streptococci
- Coagulase (-) Staphylococcus

2. Gram (-) organisms

- Pseudomonas, Acinetobacter
- E. coli, Klebsiella
- Enterobacter spp.

45%(+)bloodculture

SignsandSxSuggestingaSystemic
BacterialInfectionasacauseofSepsisSyndrome
PRIMARY
- fever, chills
- hyperventilation
- hypothermia
- skin lesions
- change in mental status

SECONDARY
- hypotension
- bleeding
- leukopenia
- thrombocytopenia
- organ failure
- Lung: cyanosis, acidosis
- Kidney: oliguria, anuria,
acidosis
- liver: jaundice
- heart: congestive
failure

EFFECTSOFPROINFLAMMATORYCYTOKINETNF
Inflammation
- fever
- leukocyte mobilization
Cardiovascular
- tachycardia
- hypotension
- myocardial depression
- capillary leak
- endothelial changes

CNS
- anorexia
- fever
- headache
Metabolic Hormonal
- acidosis
- bone resorption
- catabolic state cachexia
- increase pituitary and stress hormone production

 Hematologic
- inhibition of erythropoiesis and myelopoiesis
- leukopenia
- disseminated intravascular coagulation
Renal
- oliguric renal failure
- renal cortical necrosis

CLINICALAPPROACH
HISTORY
- predisposing disorders
- previous infections and antimicrobial tx
- history of travel
PHYSICAL EXAM
MICROBIOLOGIC STUDIES
- blood culture at least 2 sets at diff. sites

FACTORSAFFECTINGOUTCOMEOFSYSTEMIC
BACTERIALINFECTIONS
UNDERLYING CONDITIONS
- neutropenia
- hypogammaglobulinemia
- diabetes
- alcoholism +/- cirrhosis
- renal failure
- respiratory failure
COMPLICATIONS OF THE INFECTIOUS EVENT AT
THE ONSET OF TREATMENT i.e. SHOCK, ANURIA

 ANTIMICROBIAL THERAPY

GRADE (SEVERITY) OF BACTEREMIA

SOURCE OF INFECTION
INTERVAL AFTER INITIATION OF THERAPY
AGE

RECOMMENDEDANTIMICROBIALREGIMENS
1. COMMUNITY ACQUIRED INFECTIONS IN THE
NON NEUTROPENIC PATIENTS (ANC >1000/MM3)
A. SUSPECTED URINARY TRACT SOURCE
- 3RD Gen Cephalosporins or
- Piperacillin or
- Ticarcillin or
- Quinolon
- ALL +/- Aminoglycoside

B. NON URINARY TRACT SOURCES

- 3RD Gen Cehalosporins + Metronidazole OR
- Ticarcillin Clavulanate OR
- Ampicillin Sulbactam OR
- Piperacillin Tazobactam OR
- ALL +/- Aminoglycoside
2. HOSPITAL ACQUIRED INFECTION, NON
NEUTROPENIC
- 3RD Gen Cephalosporins + Metronidazole OR
- Ticarcillin Clavulanate OR

- Ampicillin Sulbactam OR
- Piperacillin Tazobactam OR
- Imipenem
- ALL +/- Aminoglycoside
3. HOSPITAL-ACQUIRED INFECTION,NEUTROPENIC
- Ticarcillin Clavulanate OR
- Ampicillin Sulbactam OR
- + Aminoglycoside OR
- Imipenem +/- Aminoglycoside
- Ceftazidime + Metronidazole + Aminoglycoside

4. THERMAL INJURY AT LEAST 20% OF BODY

SURFACE AREA
- Ceftriaxone+Aminoglycoside OR
-Vancomycin+AntipseudomonalPCN+Aminoglycoside
5. ESTABLISHED OR SUSPECTED GENTAMYCIN
RESISTANCE
- use Amikacin
6. SUSPICION OF INDWELLING VASCULAR
CATHETER INFECTION
- Add Vancomycin

ADJUNCTIVEMEASURESINTHETHERAPYOFSEPSISSYNDROME
1. MAINTENANCE OF ADEQUATE TISSUE
PERFUSION WITH VOL REPLACEMENT
- Crystalloids
- Colloids
2. USE OF SYMPHATOMIMETIC AMINES
- Dopamine
- Dobutamine
- Isoproterenol
- Norepinephrine

 Anticoagulation Heparin
-Septicemia asso w/ DIC and Pulmonary Embolic
Phenomena
Platelet Transfusion
-Thrombocytopenia
Cryoprecipitate
- Hypofibrinogenemia
Fresh Frozen Plasma
- Depleted Coagulation Factors
Packed RBC of Whole Blood as indicated

3. SURGICAL INTERVENTION
- Abscess drainage
- debridement
- Removal of infected cathethers, prosthesis and
foreign bodies

2012SurvivingSepsisCampaign
InternationalGuidelinesforthe
ManagementofSevereSepsisand
SepticShock

EarlyGoalDirectedTherapy(1to3hrs)
Blood culture 2 sites
Antimicrobial administration
Lactic acid determination
Fluid resuscitation
goals:

Centralvenous pressure(CVP)812mmHg*
Meanarterialpressure65mmHg
Urineoutput0.5mL/kg/hr
Centralvenousoxygensaturation70%,ormixedvenous65%

Diagnosis
Obtainappropriateculturesbeforestartingantibioticsprovidedthis
doesnotsignificantlydelayantimicrobialadministration:
Obtaintwoormorebloodcultures(BCs)
OneormoreBCsshouldbepercutaneous
OneBCfromeachvascularaccessdeviceinplace48hours
Cultureothersitesasclinicallyindicated

Performimagingstudiespromptlyinordertoconfirmandsample
anysourceofinfectionifsafetodoso

AntibioticTherapy
Beginintravenousantibioticsin1to3hrs
Broadspectrum,activeagainstlikelybacterial/fungalpathogens
Combinationtherapynomorethan35daysanddeescalation
followingsusceptibilities
Durationoftherapytypicallylimitedto710days;longerif
responsesloworinimmunologicdeficiencies

FluidTherapy
Fluid resuscitateusingcrystalloids 30ml/kgin1to2hrs
colloids
albumin

Useafluidchallengetechniquewhileassociatedwitha
hemodynamicimprovement

Vasopressors/InotropicTherapy
MaintainMAP65mmHg
Norepinephrineordopamine centrallyadministeredaretheinitial
vasopressorsofchoice
Useepinephrineasthefirstalternativeagentinsepticshockwhen
bloodpressureispoorlyresponsivetonorepinephrineordopamine
Donotuselowdosedopamineforrenalprotection
Inpatientsrequiringvasopressors,insertanarterialcatheteras
soonaspractical
Usedobutamineinpatientswithmyocardialdysfunction

Steroids
Considerintravenoushydrocortisonewhenhypotensionresponds
poorlytoadequatefluidresuscitationandvasopressors(2C)
Hydrocortisoneispreferredtodexamethasone(2B)
Steroidtherapymaybeweanedoncevasopressorsarenolonger
required(2D)
Hydrocortisonedoseshouldbe300mg/day(1A)

BloodProductAdministration
Giveredbloodcellswhenhemoglobindecreasesto7.0g/dLto
targetahemoglobinof7.0 9.0g/dL
Ahigherhemoglobinlevelmayberequiredinspecialcircumstances
(eg:myocardialischemia,severehypoxemia,acutehemorrhage,
cyanoticheartdisease,orlacticacidosis)
Donotuseerythropoietintotreatsepsisrelatedanemia

MechanicalVentilationofsepsisinduced
AcuteLungInjury(ALI/ARDS)
Targetatidalvolumeof6mL/kg (predicted)bodyweightinpatients
withALI/ARDS
Positiveendexpiratorypressure(PEEP)shouldbesettoavoid
extensivelungcollapseatendexpiration
Maintainmechanicallyventilatedpatientsinasemirecumbent
positionunlesscontraindicated(45degrees)
UseaconservativefluidstrategyforpatientswithestablishedALI
whodonothaveevidenceoftissuehypoperfusion

MechanicalVentilationofsepsisinduced
AcuteLungInjury(ALI/ARDS)
Useaweaningprotocolandaspontaneousbreathingtrial(SBT)
regularlytoevaluatethepotentialfordiscontinuingmechanical
ventilation
BeforetheSBT/Tpiece,patientshouldbe:
Arousable
behemodynamically stablewithoutvasopressors
havenonewpotentiallyseriousconditions
havelowventilatory andendexpiratorypressurerequirement
requireFiO2levelsthatcanbesafelydeliveredwithafacemaskor
nasalcannula

GlucoseControl
UseIVinsulintocontrolhyperglycemiainpatientswithseveresepsis
followingstabilizationintheICU
Aimtokeepbloodglucose8.3mmol/L(150mg/dL)usingavalidated
protocolforinsulindoseadjustment
Provideaglucosecaloriesourceandmonitorbloodglucosevalues
every12hours(4hourswhenstable) inpatientsreceiving
intravenousinsulin

BicarbonateTherapy
Donotusebicarbonatetherapyforthepurposeofimproving
hemodynamicsorreducingvasopressorrequirementswhen
treatinghypoperfusioninducedlacticacidemiawithpH7.15

DeepVeinThrombosis(DVT)Prophylaxis
Useeitherlowdoseunfractionatedheparin(UFH)orlowmolecular
weightheparin(LMWH),unlesscontraindicated
Useamechanicalprophylacticdevice,suchascompression
stockings oranintermittentcompressiondevice,whenheparinis
contraindicated
InpatientsatveryhighriskLMWHshouldbeusedratherthanUFH

StressUlcerProphylaxis
ProvidestressulcerprophylaxisusingH2blockerorprotonpump
inhibitor
BenefitsofpreventionofupperGIbleedmustbeweighedagainst
thepotentialfordevelopmentofventilatoracquiredpneumonia

NOSOCOMIALINFECTIONS

NOSOCOMIALINFECTIONS
Definition:

- Infection acquired during or as a result of

hospitalization
- manifest after 48 hrs after admission or
discharged
- i.e. surgical wound infection developing in the
weeks after discharge

CATEGORIESOFINFECTION
1.

PNEUMONIA

- 4-7 times per 1000 hospitalization (NNIS)

- 15 cases per 1000 ventilator days
- as high as 50 % mortality
RISK FACTORS:
- intubation
- patients in ICU
- altered level of consciousnes esp with NGT
- elderly patients

- chronic lung disease

- post operative patients
- H2 blockers of antacids
- Nebulizers, humidifiers
Clues to Diagnosis
- New cough, fever, leukocytosis
- Sputum production, change in the character of
secretions
- New infiltrate on Chest X-ray
- Requirement for change in ventilation settings

MICROORGANISMS
- Pseudomonas aeruginosa
- Staph aureus; MRSA
- Klebsiella pneumoniae- ESBL
- Stenotrophomonas maltophilia
- Acinetobacter
- Legionella; adenovirus, respiratory syncytial virus

2.Bacteremia
Primary Bacteremia
- isolation of recognized pathogen frm the blood
without a infection at another site
- related to presence of intravascular device esp at
insertion site; contaminated infusates or tubings, ports,
leaking connections or hematogenous seeding of a
catheter
Organisms: Coagulase negative staph / candida spp.
S. aureus, enterococci

Clinical Diagnosis:
- fever, signs of cutaneous involvement
- erythema, induration, tenderness
- purulent discharge
- Vascular access line removed quantitative culture of
catheter tip growth of 15 colonies or more correlates
with infection of the line

3.SurgicalWoundInfection
- 1.5 13 per 100 operation rates of surgical infection
Risk Factors
- type / classification of surgical procedures clean;
clean-contaminated; contaminated; dirty-infected
- long pre-operative length of stay
- preoperative shaving of the field (esp. if preformed
24 hrs prior)
- presence of a drain
- a long duration of surgery
-presence of untreated remote infection
- the surgeon

ClinicalDiagnosis
Erythema extending more than 2 cm beyond the
margin
- Localized tenderness and induration
- Fluctuance
- Drainage of purulent material
- Dehiscence of sutures

wound

4.UrinaryTractInfection
- most common type of nosocomial infection
- least severe sequelae
Risk Factors:
- female sex
- prolonged urinary catheterization
3-5 % risk per day of catheterization
- lack of systemic antibiotic therapy
- breach of appropriate catheter care

Other Infectious Sources of Fever

- antibiotic assoc. diarrhea-Clostridium difficile,
- decubitus ulcers
- sinusitis esp in intubated patients, NGT
Non Infectious Sources of Fever
Drug Fever
-antibiotics, phenytoin, H2 blockers
Phlebitis
- bld transfusion (non hemolytic reaction)

MENINGITIS

BACTERIALMENINGITIS
Definition
- an inflammatory response to bacterial infection of piaarachnoid and CSF of the subarachnoid space
throughout the cerebrospinal axis
Epidemiology:
incidence: 3-5 per 100,000 population per year

3 Major Meningeal Pathogens Worldwide:

1. H. influenzae decrease incidence H. influenzae
conjugate vaccines
2. N. meningitidis
- the only major cause of epidemics of bacterial
meningitis
3. S. pneumoniae

ETIOLOGY
H. influenzae
- more than 90% capsular type b strains
- common under 6 years of age
- follows nasopharyngeal acquisition of virulent
strains
- predisposing factors: sinusitis, epiglotitis,
pneumonia, otitis media, head trauma with CSF
leak, DM, alcoholism, asplenia

N. Meningitidis
- most often in young children and young adults
- usually due to serogroups A and C
- isolated in 20% of all cases of bacterial
meningitis
- nasopharyngeal carriage accounts for initiation
of infection
S. Pneumoniae
- most common in adults over age of 30
- accounts 15% of cases of meningitis

- often asso with pneumonia, otitis media,

mastoiditis, sinusitis or endocarditis
- predisposing condition
= asplenic states, alcoholism, cirrhosis,
multiple myeloma, hypogammaglobulinemia
- most common meningeal isolate in head trauma
with basilar fracture and CSF leak
L. monocytogenes
- represents small minority of cases
- major agent during neonatal production
- can occur in elderly, alcoholics, diabetics, CA pts

Group B Streptococci (S. agalactiae)

- an impt cause of neonatal meningitis
- asso with premature rupture of membranes, low
birth wt
Aerobic gram (-) bacilli
- E.coli in neonates
- Klebsiella sp., E. coli, Pseudomonas aeruginosa
- isolated ff head trauma of neurological
procedures

Staphylococcus
- S. epidermidis most common with indwelling CSF
shunts
- S. aureus accounts 1-8% of cases
- 2nd most common cause of CSF shunt
infection
- asso with head trauma, neurological
procedures, abscesses in other organs,
sinusitis, osteomyelitis, pneumonia,
cellulitis, decubitus ulcers

Anaerobes
- rare, < 1% of pyogenic cases
- its recovery from CSF suggest intraventricular
rupture of a brain abscess
- may arise from secondary contiguous focus
Flavobacterium meningosepticum
- a problem in neonatal intensive care units and
nosocomial meningitis
Polymicrobial bacterium
- mostly occur in adults, asso with tumors close to
the neuroaxis

Pathogenesis
Pathogenic steps
1. Nasopharyngeal colonization
2. Nasopharyngeal epithelial cell invasion
3. bloodstream invasion
4. bacteremia with intravascular survival
- evasion of the hosts altrnative complement
pathway
- an important strategy for intravascular survival
- virulence property depends or expression of
capsular polysaccharide

Pathogenesis
5. crossing of blood-brain barrier and entry into CSF
6. survival and replication in the subarachnoid space
Hypothesis to account for observed neutropism of
meningeal pathogens and entry into the CNS:
1. Meningitis is secondary to a sustained bacteremia
that must be of sufficient duration and magnitude
2. Adhesion to critical blood-brain barrier components
- microvascular cerebral endothelial and epithelial
lining of choroid plexus and ventricles

3. Microorganisms are carried in macrophages or other

phagocytic cells which enter the CNS and replicate
inflammation of subarachnoid space
opsonic activity is undetectable even in infected
CSF
inefficient phagocytosis
Represents an infection in an area of impaired
host resistance

Pathophysiologic consequences
increase permeability of blood barrier vasogenic
cerebral edema
Cytotoxic cerebral edema swelling of brain cells
from release of toxic factors
Interstitial Cerebral Edema
- due to obstruction of normal CSF pathways with
increase in resistance to CSF outflow
Pathologic hallmark exudate in the subarachnoid
space

Clinicalmanifestation
Headache, fever, meningismus, NIV
Weakness, photophobia, myalgia
Kernigs and/or Brudzinskis sign
- absence does notruleout the diagnosis
Cerebral dysfunction declining level of consciousness
Cranial nerve palsies
Seizures

Diagnosis
Dx rests on CSF examinatin
- elevated opening pressure
- neutrophilic pleocytosis
- increase protein, hypoglycorrhachia
- bacteriology
Increase CSF conc of C-reactive protein
Increase in CSF levels of TNF
CT/MRI scans little rule in the dx; may detect
complication and/or parameningeal source of infection

Treatment
Empiricl regimens
Based primarily on the age of the host and likely
infecting pathogen
Ampicillin + 3rd Gen Cephalosporins
(Cefotaxime,
Ceftriaxone )
Penicillin G
Vancomycin if indicated

Adjunctivetherapy
Dexamethasone 0.15 mg/kg q 6 hrs x 4 days
- beneficial in children with proven or suspected
H. influenzae
- dec CSF conc of IL-1B
- to be given shortly before of simultaneously with 1st
dose of antimicrobial alternate CSF
inflammatory response
- dec incidence of moderate to severe bilateral
sensorineural hearing loss and/or overall neurologic
sequelae
.MANNITOL DECREASE ICP

PNEUMONIA

PNEUMONIA
An infection of the pulmonary parenchyma
Transmission:
1. Aspiration of Organisms
Fromoropharyngealflora
impairedlevelofconsciousness alcoholics,
strokes
swallowingdisorders
mechanicalimpediments useofNGT,ET
Patientsownstomach
inc gastricpHwithatrophicgastritisuseofH2

drugabusers,w/seizures,

blockers,antacids

PNEUMONIA
Transmission:
- use of NGT facilitates transfer
Use of contaminated resp. equipments
2. Inhalation of Infectious Aerosols
- airborne droplet nucleiparticles <3-5 um in diameter
- deposited in small bronchioles / alveoli
3. Hematogenous spread from extrapulmonary site
especially in S. aureus as in IVDU
4. Direct inoculation and contiguous spread
- from tracheal intubation; stab wounds

PNEUMONIA
Pathology (anatomic involvement)
interstitial or alveoli
- lobar entire lobe involvement
- bronchopnuemonia restricted to alveoli contiguous to
bronchi
- necrotizing multiple small cavities < 2 cm in
diameter, in one or more bronchopulmonary
segments or lobes

PNEUMONIA
Clinical Manifestations
Typical pneumonia syndrome
- sudden onset of fever, cough productive of purulent
sputum, pleuritic chest pain
-inc fremitus, dullness, egophony, rales
Atypical pneumonia syndrome
- gradual onset, dry cough
- extrapulmonary symptom headache, myalgia,
fatigue, sore throat, diarrhea, vomiting
- chest xray- abn despite paucity of p.e. findings

CriteriaforHospitalizationofPatientswith
Pneumonia
- Elderly (> 65 yrs of age)
- Significant comorbidities DM, neoplasm, immunosupp
- Leukopenia (< 5000 WBC / uL)
- S. aureus, gm (-) bacilli or anaerobe as the suspected
cause
- Suppurative complications (empyema, arthritis,
meningitis, endocarditis)
- Failure of outpatient management
- Inability to take oral medication
- Tachypnea (>30/min)

CriteriaforHospitalizationofPatientswith
Pneumonia
- Tachycardia (>140/min)
- Hypotension (< 90 mm Hg systolic)
- Hypoxemia (arterial PO2 < 60 mmHg)
- Acute alteration of mental status
- Lung abscess one or more cavities >/= 2 cm in
diameter

MicrobialPathogensThatCausePneumonia
Community Acquired
- Mycoplasma pneumoniae
- Streptococcus pneumoniae
- Haemophilus influenzae
- Chlamydia pneumoniae
- Legionella pneumophila
- Oral anaerobes
- Moraxella catarrhalis
- Staph aureus
- Nocardis spp.

- viruses
- fungi
- M. tuberculosis
-C. psittaci

MicrobialPathogensThatCausePneumonia
Hospital Acquired
- Enteric Aerobic
- Gram negative bacilli
- Pseudomonas aeruginosa
- Staphylococcus aureus
- Oral anaerobes

MicrobialPathogensThatCausePneumonia
HIV Infection Associated
- Pneumocystis carinii
- Mycobacterium tuberculosis
- Streptococcus pneumoniae
- Haemophilus influenzae

PNEUMONIA
Age and Comorbidity
an important prediction of the infecting agent
- < 6 mos C. trachomatis, RSV
- 6 mos 5 yrs H. influenzae
- young adults M. pneumoniae, C. pneumoniae
- elderly H. influenzae, L. pneumophila, M. catarrhalis
Aspiration oral anaerobes, viridans strep.
Severe hypogammaglobulinemia encapsulated bacteria,
S. pneumo, H. influenzae

PNEUMONIA
Severe neutropenia
- P. aeruginosa, S. aureus, Enterobacteriaciae
- aspergillus
Long term glucocorticoid
M.tuberculosis
Nocardia

PNEUMONIA
DIAGNOSIS
1. Radiography
- confirms presence and location of infiltrate
- assesses extent of infection
- detects pleural involvement
- gauge response to txt
- maybe N if unable to mount an inflammatory
response i.e. agranulocytosis or early stage of
infiltrative process S. aureus or PCP

PNEUMONIA
2. Sputum Exam
- Sputum gm stain: >25 PMN < 10 EC/LPF
- 62% sensitivity, 85% specificity
- mixed flora on gm stain of uncontaminated sputum
suggest anaerobic infection
- sputum stained and DFA for Legionella
3. Invasive Procedures
- Transtracheal aspiration
- Percutaneous Transthoracic lung puncture

PNEUMONIA
- Fiberoptic bronchoscopy
- open lung biopsy
4. Other tests
- blood culture
- thoracentesis
- serologic studies

if either is (+) = dxtic of the

etio of pneumonia

PNEUMONIA
TREATMENT
- Whatever regimen is chosen, antimicrobial activity
should encompass S. pneumoniae, the most common
cause of pneumonia

ClinicalFeaturesofpatientswithCAP
accordingtoriskcategories

EmpiricantimicrobialtherapyforCAP

EmpiricantimicrobialtherapyforCAP

AlgorithmforthemanagementorientedriskstratificationofCAPamong
immunocompetentadults

LUNGABSCESS
Definition :
- A suppurative pulmonary infection involving
destruction of lung parenchyma to produce one or more
large cavities with air fluid level
Predisposing Causes:
1. Aspiration
- most important factor, thus anaerobe major org
2. Periodontal disease of gingivitis
3. Bronchiectasis

LUNGABSCESS
4. Secondary infection of pulmonary embolus with
infarction septic embolization bacteremia
5. Inhalation of bacteria containing aerosols
6. Suppurative Inflammation behind a bronchial
obstruction
7. Immunosuppressive txt i.e. Nocardia

LUNGABSCESS
PATHOGENESIS / PATHOLOGIC CHARACTERISTICS
- Primary site post. Segment of the R upper lobe
- Apical segments of lower lobe horizontal/supine
- Endotracheal tubes impairs coughing impede
pulmonary clearance- leakage of oropharyngeal
secretions into the tracheobronchial tree

LUNGABSCESS
- Subdiaphragmatic infection extend to the lung via
lymphatics, defects in diaphragm, blood
- Infection may arise in behind obstruction
i.e. tumor, foreign body, enlarged LN
COMPLICATIONS
- Empyema 1/3 of cases
- Brain abscess
- localized bronchiectasis
- hepatobiliary fistula, brain abscess-amoebic

LUNGABSCESS
MICROBILOGIC CHARACTERISTICS
- Hematogenous spread to the lungs
- gm (+) cocci (S.aureus), gm (-) enteric bacilli,
anaerobes
- produces multiple abscesses
- w/ gm (-) bacilli occurs in asso w/ UTI or
manipulation, bowel surgery or nosocomial infection

LUNGABSCESS
DIAGNOSIS
Chest X-ray
Cavity with air-fluid level
Pneumonitis w/ multiple small excavations in a
dependent segment
Culture empyema fluid, blood, sputum
Transtracheal aspiration
Charcot-Leyden crystal in sputum suggestive of
amoeba

LUNGABSCESS
Differential diagnosis
- Cavitating carcinoma, tuberculosis
- infected lung cyst
Treatment
- Antimicrobial (for 2 mos-4 mos cure w/o relapse)
- Postural drainage

LUNGABSCESS
CLINICAL MANIFESTATIONS:
Anaerobic Lung Abscess
- Pneumonia first cavitation 7 days after aspiration
- (+) hx of unconsdiousness, alcoholism, deceased gums,
absence gag reflex
- foul smelling sputum

LUNGABSCESS
Anaerobic Necrotizing Pneumonia
- confined primarily to 1 pulmonary segment or lobe
- often spreads rapidly greenish discoloration of the
lung with sloughing of the tissues pulmonary gangrene
- putrid sputum
Nonanaerobic Lung abscess and Necrotizing Pneumonia
- 1 infection due to S. aureus, S.pyogenes, Nocardia,
K. pneumoniae
- E.coli, Legionella, Proteus spp., tuberculosis, fungi

LUNGABSCESS
Secondary Lung Abscess and Necrotizing Pneumonia
- due to bacteremia, endocarditis, septic
thrombophlebitis, subphrenic infection
- Abscess form w/in a necrotic pulmonary tumor or
behind an obstruction
- S. aureus bacteremia hematogenous lung abscess
- may ff Vincents angina septicemia
Amebic Lung Abscess
- Perforation of amebic liver abscess rupture thru
diaphragm
- chocolate or anchovy sauce like odorless sputum

FEVEROFUNKNOWNORIGIN

FEVEROFUNKNOWNORIGIN
Definition:
Petersdorf and Beeson:
1. temp >38.3 c (101 OF) on several occasions
2. greater than 3 weeks duration
3. failure to reach a diagnosis after 1 week of
investigation

DurockandStrut
Nosocomial

Neutropenic HIV asso

Classic

Pxs situation Hospitalized, Neutrophil ct. HIV (+)

acute, no infxn <500/Ul or
when admitted expected to
reach that
level in 1-2
days

all others
w/ fever
>/= 3 wks

Duration of
3 days
Illness while
on investigation

3 days

3days or
4 wks as
outpt

3days or 3
wks of opd
visits

Examples of
Causes

Aspergillosis
Candidiasis

TB, MAI

Infxn,
Malig.

Thrombophlebitis,
sinusitis
PMC
drug fever

FEVEROFUNKNOWNORIGIN

1.

CAUSES:
Infections (22.5% Knockaert)
a. Localized pyogenic infections
- dental abscess, sinusitis, tuboovarian abscess
b. Intravascular infections
- aortitis, infective endocarditis, IV cath infxns
c. Systemic bacterialinfections
- Typhoid fever, catscratch, Legionaires dse,
Brucellosis, Gonococcemia, Lyme dse, Lepto, SY,
rat bite fever, Listeriosis, Meliodosis, relapsing
fever

FEVEROFUNKNOWNORIGIN
d. Mycobacterial infections
- Mtb, MAI, other atypical mycobacterial infxns
e. Fungal infections
- Blastomycosis, Cryptococcosis, Aspergillosis,
Mucormycosis
f. Rickettsial infections
g. Mycoplasmal
h. Chlamydia
- LGV, Psittacosis

FEVEROFUNKNOWNORIGIN
i. Viral
- CMV, EBV, HIV
j. Parasitic
P. carinii, Amebiasis, Toxoplasmosis
k. Presumed infections
Kawasakis dse, (Mucocutaneous I.N synd)
Kikuchis dse (Necrotizing lymhadenitis)

FEVEROFUNKNOWNORIGIN
2. Neoplasms (7%)
Malignant Lymphoma, hepatoma, leukemia, colon CA,
renal CA, Hodgkins dse
Benign atrial myxoma, renal angiolipoma
3. Collagen Vascular disease (21.5%)
4. Granulomatous diseases
5. Miscellaneous Conditions (26.5%)
- gout, hematoma, thyroiditis
6. Inherited and Metabolic diseases
- adrenal insuff, familial Mediterranean fever

FEVEROFUNKNOWNORIGIN
7. Thermoregulatory disorders
- brain tumor, CVD
8. Factitious Fever ( Self induced)
9. Arebrile FUO (<38.3 C)
10. Habitual Hyperthermia
(Exaggerated Circadian Rhythm)

CausesofFUOlasting>6months
CAUSES
None identified
Misc causes
Factitious causes
Granulomatous Hepatitis
Neoplasm
Stills dse
Infection
Collagen Vascular dse
Familial Mediterranean fever
NO FEVER

% of Cases
19
13
9
8
7
6
6
6
3
27

INFECTIVEENDOCARDITIS

INFECTIVEENDOCARDITIS
- a dse that produces vegetations on the endocardium
- Heart valve usually involved
- Endarteritis infection AV shunt, coarctation of aorta
CLASSIFICATION
3 Categories:
1. Native valve endocarditis
2. Endocarditis in IVDU
3. Prostheric valve endocarditis

INFECTIVEENDOCARDITIS

Acute Endocarditis
- most often secondary to S. aureus, occurs on
normal valves, rapidly destructive, produces
metastatic foci, fatal in < 6 wks if untreated

Subacute
- viridans strep, on damaged valves, (-) metastatic
foci, 6 wks-1 yr course

= the infecting org the most impt basis for classif

NATIVEVALVEENDOCARDITIS
ETIOLOGY
Streptococci (55%)
- Viridans Strep (normal inhabitants of oropharynx)
S. mutans, mitis, mellerei
S.bovis in elderly with premalignant GI lesion
- Group A B hemolytic strep; GBS
Enterococci (6%)
- normal inhabitants of GIT, anterior urethra,
mouth (rare)
- hx of GUT manipulation, trauma, cystoscopy,
catheterization, prostatectomy, abortion, C/S

NATIVEVALVEENDOCARDITIS
Staphylococci (30%)
- S. aureus 5-10x > S. epidermidis
HACEK (Haemophilus, Actinobacillus, Cardiobacterium,
Eikenella, Kingella)
- part of oropharyngeal flora
Others: gm (-) bacilli

large emboli, atypicals

NATIVEVALVEENDOCARDITIS
EPIDEMIOLOGY
Male > Female > 50 y.o ; uncommon in children
Predisposing heart condition (60-80%)
RHD 25%, MV>AV, TV rare
CHD other than MVP 10-20 %
- PDA, TOF, VSD, coarctation of the aorta,
pulmonary stenosis
- bicuspid aortic valve, complicated ASD
Degenerative heart dse aortic stenosis, Marfans
20-70% - no underlying heart dse

ENDOCARDITISINIVDRUGUSERS
Young male
Skin source; acute in onset
S. aureus > 50%, Strep, Enterococci 20%, gm(-) bacilli,
fungi 6%
Multiple organisms-common
TV infected in 50%, AV 20%, MV 20%
Murmurs are frequently absent

PROSTHETICVALVEENDOCARDITIS(10
20%)

Males > 60 y.o.

1st year after sx 1-2%; 0.5%/yr thereafter

A.

Early onset endocarditis

- onset of symptoms within 60 days of sx; valve
contamination during op or perioperative bacteremia
- S. epidermidis > S. aureus
- aortic valve prosthesis > mitral valve infxn at suture
line

PROSTHETICVALVEENDOCARDITIS
B. Late onset endocarditis
- after 60 days, long incubation period
- from transient bacteremia
- Streptococci accounts 40%

INFECTIVEENDOCARDITIS
PATHOGENESIS
- vegetations characteristic lesions on valves
endothelium
- colonization by microorganisms of sterile vegetations
- org. of little pathogenecity i.e. Viridans Strep
implant on deformed valves
- more virulent i.e. S. aureus, S. pneumo

N valves

PATHOGENESIS OF INFECTIVE ENDOCARDITIS

Valvular endothelium

Mucous mem, other colonized tissue

Local factors

Trauma
Turbulence

Bacterial adherence

Metabolic changes

IgA protease, bacteriocins

TRAUMA

Plt fibrin deposition

Bacteremia

Non bacterial thrombotic endocarditis

Complement, antibody

ADHERENCE
COLONIZATION
Bacterial division, fibrin deposition, platelet
aggregation, Intracellular proteases, protection
from neutrophils

Mature vegetation

INFECTIVEENDOCARDITIS
CLINICAL MANIFESTATIONS
- fever > 95%
- arthralgia / myalgia
- murmur > 85% except in early acute endocarditis,
LVDU
- Splenomegaly
- Petechiae conjunctiva, palate, buccal mucosa
- Splinter hges subungual, linear, dark red streaks
- Roths spots oval retinal hmge with clear pale center

INFECTIVEENDOCARDITIS
- Oslers nodes small tender nodules on fingers, toe
pads
- Janeway lesions small hges on palm and soles
- Clubbing, embolic episodes, neurologic manifestations
LABORATORIES:
- anemia, leukocytosis, proteinuria, hematuria
(micoscopic)
- increase ESR, (+) RF, (+) circulating immune
complexes
- decrease serum complement

INFECTIVEENDOCARDITIS
- Blood culture (+) in 95 % bacteremia continuous
- Echocardiography TEE detects 1-1.5 size vegetations
90%sensitivethanTEE

- a (-)TEE strong evidence vs IE

INFECTIVEENDOCARDITIS

I.
A.

CLINICAL DIAGNOSIS OF IE

Definite : 2 major criteria or 1 major + 3 minor or

5 minor
Major Criteria
1. Isolation of viridans Strep, S. bovis, HACEK of
community acquired S. aureus, Enterococci from 2
separate blood cultures of isolation of organism
consistent with endocarditis in :
a. bld culture >12 hrs apart or
b. all of 3 or most of four or more blood
cultures with 1st and last at least q hr
apart

CLINICALDIAGNOSISOFIE
2. Evidence of Echocardiography:
- oscillating mass (intracardiac) or abscess or new
partial dehiscence of prosthetic valve or new valvular
lesions
B. Minor Criteria
1. predisposing lesion of IVDU
2. fever 38 c
3. major arterial emboli, septic pulmonary infarcts,
mycotic aneurysms, IE he, conjunctival hges,
Janeway lesions

CLINICALDIAGNOSISOFIE
4. GN, Oslers nodes, Roths spots, RF
5. (+) blood cultures not meeting the major criteria or
serologic evidence of active infection with an organism
that causes endocarditis
6. echocardiogram consistent with endocarditis but not
meeting the major criterion

CLINICALDIAGNOSISOFIE
II. Possible IE :
Findings that fall short of definite but do not fall into
rejected category.
III. Rejected:
Alternative disease or resolution of syndrome or no
evidence of IE at surgery or autopsy with 4 days of
antibiotic txt.

TREATMENTOFINFECTIVEENDOCARDITIS
Drug microbicidal, high concn (serum), long duration
to sterilize the vegetation
Bactericidal titer 1:8 indicates adequate tx.
Txt on native valve end. while awaiting culture , should
cover enterococci - more resistant than Strep.
Pen G, Cephalosporin : Cefazolin, Ceftriaxone, Vancomycin,
Ampicillin +/- Gentamycin
Duration 4-6 wks

TREATMENTOFINFECTIVEENDOCARDITIS
SURGERY indications :
- fungal endocarditis, persistent (+) blood culture during
txt
- Relapse after appropriate txt
- Recurrent emboli
- aortic valve endocarditis, with 1st / 2nd degree AV block

INFECTIVEENDOCARDITIS
PROGNOSIS: Factors predisposing to poor px:
- Non Streptococcal infec, CHF, aortic valve
involvement
- prosthetic valve infec, older age
- valve ring or myocardial abscess, embolus
- rupture of mycotic aneurysm, large vegetations
(fungi)

INFECTIVEENDOCARDITIS
ANTIMICROBIAL PROPHYLAXIS
- indic. for those w/ predisposing cardiac lesions who
are undergoing procedures known to cause bacteremia
= valvular HD
= congenital HD except uncomplicated ASD
= intracardiac prosthesis
= asymmetric septal hypertrophy
= previous IE
= MVP w/ MR
= thickened redundant mitral valve leaflets

INTRAABDOMINAL
INFECTIONS

INTRAABDOMINALINFECTIONSAND
ABSCESSES
- Secondary to disruption of normal anatomic barrier
= ruptured AP, diverticulum, ulcer, bowel wall ischemia
= inflammatory process, pancreatitis, PID
2 stages: 1. Peritonitis

in untxtd

2. Abscess

PERITONITIS
SPONTANEOUS BACTERIAL PERITONITIS / PRIMARY
- w/o an apparent source of contamination
- usually in conjunction w/ liver cirrhosis (alcoholism)
- in association w/ ascites
- sec to hematogenous spread of org. from altered
portal circulation defect in filtration fxn
- single org. E. coli most common, gm (+) cocci,
streptococci, enterococci
- anaerobes infrequent
- medical txt

PERITONITIS
SECONDARY PERITONITIS
- results from spillage of org. from intraabdominal
viscus
- mixed flora gm (-) bacilli + anaerobes E. coli,
B. fragilis
- surgery life saving
PERITONITIS IN PATIENTS undergoing CAPD
- involves skin org S. aureus (10%), coag(-) (30%)
- similar to iv cath. Infec. org migrate along the
catheter exit site infection

PERITONITIS
PERITONITIS IN PATIENTS undergoing CAPD
- usually caused by single org.
- gm (-) bacilli: fungi maybe found
INTRAPERITONEAL ABSCESS
- from SBP, infection of genital tract (female),
pancreatitis
- location omentum, mesentery, psoas muscle,
subphrenic
-Dx: U/S, CT scan
- Tx: antibiotics + drainage

VISCERALABSCESSES
LIVER ABSCESS
- solitary / multiple
- hematogenous spread
- local spread
from contigous sites
biliary
pelvis, peritoneal cavity
S/S: fever, RUQ pain/tenderness, chills, anorexia,
jaundice, 50% - asymptomatic, hepatomegaly
Organisms:
- from biliary tree enteric gm (-) bacilli, enterococci

LIVERABSCESS
- pelvic/intraperitoneal mixed flora
- hematogenous usually single org S. aureus,
strep., S. melleri, candida (neutropenic),
amebic
Dx:
- inc alkaline phosphatase = in > 90%
- CXR suggestive = elevated R hemidiaphragm, R
basilar infiltrates, pleural effusion
TX: medical, percutaneous drainage, surgery

SPLENICABSCESS
0.14% to 0.7%
- hematogenous bacterial endocarditis most
common associated infection
- on immunosuppression, hemoglobinopathies
- splenomegaly (50%), LUQ pain, fever, inc WBC
- streptococci most common, S.aureus (2nd),
gm (-) anaerobes (from UTI), Salmonella, anaerobes
(5%)
Tx: splenectomy
Antibiotics adjunct
Mortality: HIGH

TUBERCULOSIS

ANTIMYCOBACTERIALDRUGS
1. First-line essential antituberculous drugs
necessarycomponentsofshortcourseTxmost
effective
a. Isoniazid
b. Rifampicin
Firstlinesupplementaldrugs
a.Pyrazinamide
b.Ethambutol
c.Streptomycin

ANTIMYCOBACTERIALDRUGS
2. Second line antituberculous drugs
- less effective, more severe reactive
- use for either drug resistance TB or intolerant to 1st
line drugs
- when 1st line supplemental drugs not available
a. Quinolones
Ofloxacin, Ciprofloxacin
b. Capreomycin
c. Amikacin and Kanamycin
d. Para-aminosalicylate acid (PAS)
e. Thiacetazone

ANTIMYCOBACTERIALDRUGS
f. Viomycin
g. Ethionamide
h. Cycloserine
Miscellaneous Drugs
Amoxicillin / Clavulanic acid
Clofazimine, Clarithromycin
Rifamycin - rifapentine

TUBERCULOSIS
EPIDEMIOLOGY:
CDC 8.7 cases / 100,000 population
Factors responsible for the inc rates of cases:
- HIV infection
- Immigration from areas with high prevalence
- Poverty, homelessness
- drug abuse
Transmission: airborne droplet nuclei (3000 infectious
nuclei) during coughing, sneezing, talking
- thru skin of placent - rare

TUBERCULOSIS
DETERMINANTS:
- probability of contact with source case
- intimacy and duration of contact
- degree of infectiousness of the case
- environment of the contact
- sputum smear (+) highly infectious
- sputum smear (-) / culture (-) much less infectious
- culture (-) and extrapulmonary TB non infectious

TUBERCULOSIS
From Infection to Disease
Risk of developing disease depends on:
- individual innate susceptibility
- level of function of cell mediated immunity
Primary Tuberculosis
- common up to 4 yrs old
- usually not transmissible
- if acquired later temporary containment

TUBERCULOSIS
RISK FACTORS FOR ACTIVE DSE
- HIV coinfection highest risk
- Silicosis, neoplasms, hemophilia
- CRF with Hemodialysis, DM
- Immunosuppressives
- Condition assoc with malnutrition
- Old, sef-healed fibrotic TB lesions

PATHOGENESIS
Inhalation of TB Bacilli
Upper airways --- expelled
Regional LN

alveoli

(transported by macrophages
Host-bacterium Interaction (CMI)
Containment of bacillary multiplication
and phagocytosis macrophages
Production of lymphokines T.
lymphocyte
Hematogenous dissemination to
organs and tissues

Multiplication of Bacilli

2-4 wks after tissue damaging response (delayed type hypersensitivity rxn)
-Destruction of non activated macrophages that contain multiplying bacilli
-Macrophage activating response
-Killing and destruction of TB bacilli

Granuloma (tubercles) formation consists of lymphocytes macrophages

(containing TB bacilli)
- Epitheliod and giant cells

Caseous material
liquifies; further
evolution and growth

Invasion and
destruction of
bronchial walls,
bld vessels
Cavity formation
+ bacilli
multiplication

Airways
(sputum)

Caseous necrosis (soft

cheese)
(central part of granuloma)
Healing
fibrosis and
calcification
within
parenchymal
and hilt LN

PULMONARYTUBERCULOSIS
CLINICAL MANIAFESTATION
Primary TB
- initial infxn, often in children
- localized to middle and lower lung zones
- with hilar or paratracheal LAD
- lesions may heal spont small calcified nodule Ghon
lesion
- may cause pleural effusion, bronchial destruction,
hematogenous determination

PULMONARYTUBERCULOSIS
POST PRIMARY TB
- adult type reactivation or secondary TB
- results from endogenous reactivation of latent infxn
- localized to apical and post segments of upper lobes
- from small infiltrates to extensive cavity formation

EXTRAPULMONARYTUBERCULOSIS
LYMPH NODE TB ( TUBERCULOUS LYMPHADENITIS)
- most commonly involved
- painless swelliing of LN at cervical and supraclavicular
sites
PLEURAL TUBERCULOSIS
- common in primary TB
- results from penetration of few TB bacilli in pleural
space pleural effusion

EXTRAPULMONARYTUBERCULOSIS
TUBERCULOUS EMPYEMA
- less common; results from rupture of a cavity w/ large
no of org. -- bronchopleural fistula
- result in pleural fibrosis and restrictive lung dse
TUBERCULOSIS OF THE UPPER AIRWAYS
- complication of advanced cavitary PTB
- involves the larynx, pharynx and epiglottis

EXTRAPULMONARYTUBERCULOSIS
PERICARDIAL TB (TUBERCULOUS PERICARDITIS)
- direct progression of primary focus w/in the
pericardium; reactivation of latent focus; rupture of an
adjacent lymph node
- complication : chronic constrictive pericarditis w/
thickening fibrosis & calcification
GENITOURINARY TB
- 15% of extrapulmonary cases
- due to hematogenous seeding ff primary infxn
- culture (-) pyuria in acidic urine due to Dx

EXTRAPULMONARYTUBERCULOSIS
GENITAL TB
- females fallopian tubes, endometrium
- males epididymis fistula orchitis, prostatitis
SKELETAL TB
- reactivation of hematogenous foci or spread from
adjacent paravertebral LN
- spinal TB Potts dse or tuberculous spondylitis
- 2 or more vertebral bodies involved

EXTRAPULMONARYTUBERCULOSIS
SKELETAL TB
- upper thoracic spine most common site
- paraplegia abscess compressing spinal cord
- collapse of vertebral bodies Kyphosis (gibbus)
- PARAVERTEBRAL cold abscess
- may involve hips and knees
GASTROINTESTINAL TB
- swallowing of sputum w/ direct seeding of
hematogenous spread or ingestion of milk from cows
infected w/ bovine TB (rare)

EXTRAPULMONARYTUBERCULOSIS
GASTROINTESTINAL TB
- terminal ileum and cecum most common sites
- anal fistula should prompt evaluation for rectal TB
- tuberculous peritonitis ffs either direct spread from
ruptured LN or intraabdominal organs or hematogenous

EXTRAPULMONARYTUBERCULOSIS
MILIARY OR DISSEMINATED TB
- due to hematogenous spread
-either recent infection or reactivation of old
disseminated foci
- lesions yellowish granuloma 1-2 mm, resemble millet
seeds thus termed miliary
- hepatospelnomegaly, LAD
- eye choroidal tubercles- pathognomonic

EXTRAPULMONARYTUBERCULOSIS
MILIARY OR DISSEMINATED TB
- CXR miliar reticulo nodular pattern
- cryptic miliary TB chronic course characterized by
mild intermittent fever, anemia in the elderly
- non reactive miliary TB
- an acute septicemia form, massive hematogenous
dissemination

EXTRAPULMONARYTUBERCULOSIS
TUBERCULOUS MENINGITIS AND TUBERCULOMA
- 5% of extrapulmonary TB
- from hematogenous spread of primary or post primary
pulmonary
disease or from rupture of subependymal tubercle
into subarachnoid space
- evolves over 1 or 2 wks
- confusion, lethqrgy, alterd sensorium, neck rigidity
- paresis of cranial nerves (ocular nerves) frequent
finding
- (+) AFB smear/ CSF 20% of cases
- glucocoticoids useful adjunct esp with cerebral
edema

EXTRAPULMONARYTUBERCULOSIS
TUBERCULOMA
- presents as space occupying lesion
- seizures and focal signs
- scan contrast enhanced ring lesion
LESS COMMON EXTRAPULMONARY TB
- chorioretinitis, uveitis, panophthalmitis, conjunctivits
- tuberculous otitis hearing loss, otorrhea, perforation
of tympanic membrane
- cutaneous TB cold abscess, ulcers, scrofuloderma,
lupus vulgaris, miliary lesions, erythema nodosum

EXTRAPULMONARYTUBERCULOSIS
LESS COMMON EXTRAPULMONARY TB
- adrenal TB
- congenital TB transplacental spread or ingestion of
contaminated amniotic fluid
HIV ASSO. TB
- TB an impt opportunistic dse among HIV infected
patients
- HIV seropositivity several times higher among pts
with tuberculosis

TUBERCULOSIS
DIAGNOSIS:
- High Index of Suspicion
= prolonged fever, night sweats, wt loss, anorexia,
malaise, weakness, hemoptysis
- Chest Xray classic upper lobe infiltrates with
cavities; lower zone infiltrates w/o cavity atypical
finding
- AFB Mx
= Presumptive dx (+)AFB 3 early morning sputum
specimen

TUBERCULOSIS
- Mycobacterial culture
= definitive use of Lowenstein Jensen or Middlebrook
7H10 media
- PPD skin test
= limited value, low sensitivity and specificity
- Polymerase Chain Reaction (PCR)

TUBERCULOSIS
TREATMENT
Initial Phase 2 months (bactericidal phase)
= Isoniazid, Rifampicin, Pyrazinamide
+/- Ethambutol, +/- Streptomycin
Continuation phase 4 months
= Isoniazid, Rifampicin +/- Ethambutol
= Sterilizing phase : eliminate semidormant persistees
= drugs are given daily or intermittent

TUBERCULOSIS
Continuation phase 4 months
= lack of adherence / non compliance most important
impediment to cure; develop acquirted drug resistance and
relapse
- Measure for addressing non-compliance
a. direct observed treatment (DOT)
b. provision of drugs in combined formulation

TUBERCULOSIS
Monitoring Response to Treatment
Bacteriologic evaluation
Sputum AFB smear at 2,5 and 6 mos
If (+) at 5 mos
treatment failure
Sputum culture If (+) afeter 3 mos

txt failure

Chest Radiography not recommended, may lag behing

bacteriologic response
- useful for comparative purposes

TUBERCULOSIS
Drug Resistant TB
- due to spontaneous point mutations in the
Mycobacterial genome
Primary Drug Resistance
- a strain infecting a patient who has has not
previously been treated
Acquired resistance
- develops during the course of txt w/ inappropriate
regimen
Multidrug Resistant TB (MDR)
- Isoniazid-rifampicin resistance

TUBERCULOSIS
PREVENTION
BCG vaccination
= attenuated strain of M. bovis
= vary in efficacy, 0-80%
= induces PPD reactivity
= does not predict the degree of protection
= recommended for routine use at birth in countries with
high TB prevalence

TUBERCULOSIS
PREVENTIVE CHEMOTXT
- Isoniazid 5mh/Kg/day for 6-12 mos
- recommended for prophylaxis
- HIV infected person
- close contacts of TB patients
- with fibrotic lesion CXR
- recently infected person
- with high risk medical conditions

TUBERCULOSIS
Basics of Control

Promptcasedetection
Provisionofdirectlyobservedshortcoursechemotxttoallsputumsmear(+)
Maintenanceofasystemofregulardrugsupply
Systemforapatientevaluationandprogrammgt

CHOLERA

CHOLERA
- an acute severe diarrheal dse that can result in rapidly
progressive dehydration and death

Etiology:
- natural habitat costal salt waters, estuaries
- no known animal reservoir
- transmission: ingestion of water contaminated by
human feces
- infectivity is redeuced in hypochlorhydric person and
use or antacids
- susceptibility (unknwn reason)
- greatest risk bld type O
- least risk bld type AB

CHOLERA
PATHOGENESIS
Toxin Mediated dse production of cholera toxin
= potent enterotoxin elaborated by the org once it
adheres to the bowel wall of the small intestine
= stimulation of secretory mech intracellular
accumulation of cyclic AMP secretory dirrhea

CHOLERA
Clinical Manifestation:
Incubationperiodof2428hrs
Suddenonsetofpainlesswateryvoluminousdiarrheawithvomiting
Stool graynonbilouscloudyfluidwithflecksofmucusnoblood,
inoffensiveodor
Ricewaterstool
Feverusuallyabsent

CHOLERA
Clinical Manifestation:
- Symp. paralled with vol contraction weakness,
hypotension, tachycardia, weak pulses, sunken
eyeballs, dec skin turgor/ wrinkled
Washerwomans skin somnolence, coma

Volandelectrolytedepletion acutetubularnecrosis acuterenal

failure

Diagnosis:
Clinical suspicion
Culture isolation/stool use of selective medium (TCBSthiosulfate-citrate-bile salts-sucrose)

CHOLERA
TREATMENT
Rapidandadeqreplacementoffluidsandelectrolyte
Tetracycline
Decdurationofillness
Hastensclearanceoforganism

Erythromycin(alternativetoTCN) Ciprofloxacin,Ampicillin

CHOLERA
PREVENTION

Provisionofsafewatersupply
Properfacilitiesforsanitarydisposaloffeces
Properfoodpreparationandstorage
Vaccine underdevelopment

SHIGELLOSIS

SHIGELLOSIS
- an acute infectious inflammatory colitis due to one of
the members of the genus Shigella
Etiology:
- common in poor environmental sanitation
- transmission: fecal-oral route or contaminated
vectors food, water, flies and fomites
- anal-oral sexual practice in homosexuals
= asso with gay bowel syndrome
= almost always due to S.flexneri

SHIGELLOSIS
PATHOGENESIS:
- invasion of colonic epithelial cells cell to cell spread
of infection
- production of SHIGA TOXIN role in the pathogenesis
of microangiopathy, hemolytic uremic syndrome,
thrombotic thrombocytopenic purpura

SHIGELLOSIS
CLINICAL MANIFESTATION
Bacillary Dysentery
- passage of small volume stools (10-30x / day)
consisting of blood, mucus and pus
- assoc w/ abdl cramps, tenesmus painful straining
with stooling
rectal prolapse
- severe cases toxic dilatation and colonic perforation

SHIGELLOSIS
Extraintestinal complication
- Hemolytic Uremic Syndrome (HUS)

Hemorrhagiccolitis
Seizures,thrombocytopenia
Reactivearthritis(S.flexneri)
Pneumonia,meningitis,seratoconjunctivitis

DIAGNOSIS
- culture isolation

SHIGELLOSIS
TREATMENT
- Ampicillin (Amoxicillin not effective)
- TMP-SMZ
- Quinolones
- Antimotility drugs delay excretion of organism
- facilitate further invasion enhances severity of
the disease
PREVENTION
- appropriate environmental and personal hygiene
- antibiotic not indicated for asymptomatic carrier

TYPHOIDFEVER

TYPHOIDFEVER
- an acute systemic febrile infection of mononuclear
phagocytes
Etiology:
Primary Salmonella typhi
Others: S. paratyphi A and B, S. typhimorium
Epidemiology:
- most cases traced to human carriers
gallstones
(resides in bile stone)
intermittently reaches bowel
lumen
stool

TYPHOIDFEVER
PATHOGENESIS:
- fecal oral route
- 105 microorganism required for infection
- Salmonella pass on the distal ileum and colon
penetrate mucosal barrier
bacterial invasion asymp bacteremia
ingested by mononuclear phagocytes
(intracellular multiplication)

persistent bacteremia (persistent fever)

invasion GB and Peyers patches
(inflamm response to tissue invasion
cholecystitis, intestinal perforation)

Regain entry into bowel lumen

Stools (beginning 2nd week)

TYPHOIDFEVER
CLINICAL MANIFESTATION
- incubation period 3 to 60 days
- fever hallmark; prolonged, persistent (4-8 weeks)
steplike daily increase
- constipation, diarrhea, abdl pain, hepatosplenomegaly
- bradycardia; epistaxis (early)
- Rose spots small pale red blanching raised macules on
chest, abdomen during 1st week
- anorexia, wt loss, sensorial changes
- complications: hepatitis, meningitis, nephritis,
myocarditis, pneumonia, arthritis, osteoyelitis, parotitis,
orchitis, necrotizing cholecystitis, GI bldng, perforation

TYPHOIDFEVER
DIAGNOSIS
- Leukopenia and neutropenia
- Culture isolation
Blood (+) in 90% 1st week
Bone marrow (+) 100%
Stool 75% 3rd wk; 1/3 -1/2 (+) one year
TREATMENT
- Chloramphenicol
- Ceftriaxone, TMP-SMZ, Ampicillin, Qinolones,
Cefotaxime
- Dexamethasone x 24-48 hrs; w/severe ty: CNS Mx, DIC,
hpn, GI bleed, perforation

TYPHOIDFEVER
Chronic carrier:
- esp with gallstones, (+) stool culture for 1 year
- TMP-SMZ + Rifampicin x 6 wks
Ampicillin or Amoxicillin + Probenecid x 6 wks
Quinolones for 4 wks
PREVENTION
- environmental and personal hygiene
- precaution in food handling by carriers and disposal
of stools
- Live oral vaccine (Ty 21a) x 3 doses

NONTYPHOIDALSALMONELLOSIS
- infection caused by Salmonella organism other than S.
typhi (paratyphi, enteritidis, cholerasuis, typhimurium,
schoffmuelleri and others)
Epidemiology:
- a dse of industrialized world
- org found in processed foods, milk-chocolate products,
dried/frozen foods, eggs
- other sources: chicks, ducks, turtles, medical products of
animal origin i.e. Bile salts, pancreatin

NONTYPHOIDALSALMONELLOSIS
CLINICAL MANIFESTATION
Gastroenteritis
- incubation period of 24-48 hrs
- fever, diarrhea, abdl cramps, nausea, vomiting
- S/E: many leukocytes
Localized of Systemic Infection
Arterial infection
- usu. ffs Intestinal infection
- preexisting arteriosclerotic infrarenal aortic
aneurysm

NONTYPHOIDALSALMONELLOSIS
Arterial infection
- S. typhimurium 25%, inc prevalence in GI
Salmonellosis
- S. cholerasuis 20% of cases
- Suspected in elderly with prolonged fever assoc. with
back, abdominal or chest pain ffg Gastroenteritis
Cholecystitis, splenic abscess
- most common localized infrarenal abnormality

NONTYPHOIDALSALMONELLOSIS
Urinary Tract Infection
- with urolithiasis, structural abnormality
- co-exist with renal TB or S. haematobium
Pneumonia or empyema
- rare, with preexisting abnormality
Meningitis
- most prevalent in infants and young children

NONTYPHOIDALSALMONELLOSIS
Septic arthritis
- asso with immunosuppressive, prosthesis, sickle cell dse
Osteomyelitis
- Salmonella infetion of long bones predictably asso with
sickle cell dse
- occurs in young patients
Bacteremia
- gen w/o prior diarrhea, more acute onset
- intermittent symptomatic bacteremia seen in
hepatosplenic or urinary schistosomiasis

NONTYPHOIDALSALMONELLOSIS
TREATMENT
- Ampicillin 6-12 gm/dl; Ceftriaxone, Chloramphenicol
- Gastroenteritis antibiotics inc duration of
convalescent carriage; do not shorten illness
- Asymptomatic Salmonella stool (+) (except S.typhi)
= should not receive antibiotic
= active dse may be provoked
= generally self-limiting

NONTYPHOIDALSALMONELLOSIS
PREVENTION
- vigilance in food prep
- during outbreaks foodhandlers should be kept away
from work until 3 stool cultures are negative
Other measures:
- hydration, restriction, physiotherapy, anticoagulation,
bowel, blader and renal function care, prevent GI bleeding
and decubitus ulcres, treatment of intercurrent infectiond

LEPTOSPIROSIS

LEPTOSPIROSIS
- a dse by leptospires characterized by a broad
spectrum of clinical manifestations
Etiology : Leptospira interogans pathogenic
- with 23 serogroups, 200 serovar
- Leptospira biflexa freeliving
- this coiled motile org with hooked ends with flagella
- enable them to burrow into tissues
Epidemiology
- rodents most impt reservoir
- can persist in renal tubules for years

LEPTOSPIROSIS
TRANSMISSION
- direct contact with urine, blood or tissue from
infected animal
- exposure to contaminated environment
(water impt.vehicle)
- recreational exposure with domestic animal contact
PATHOGENESIS
- enters the host thru abrasions in the skin or intact
mucous membrane conjunctiva, oro-nasopharynx

LEPTOSPIROSIS
PATHOGENESIS
- multiply in bld and tissues
1st 4-10 days (+) bld culture CSF and blood
- damage to capillary endothelium vasculitis
- Kidneys: interstitial nephritis & tubular necrosis
- Liver: centrilobular necrosis w/ proliferation of
Kupffer cells
- pulmonary hges but no inflam.
- skeletal muscle invasion: swelling, vacuolation of
myofibrils, focal necrosis
- vasculitis impair microcirculation & inc.
capillary
permeability --fluid leakage --hypovolemia

LEPTOSPIROSIS
Presence of Leptospires in the CSF
- does not cause damage w/ the CNS
- rise in Ab coincides w/ development of meningitis
immunologic mech.
CLINICAL MANIFESTATION
- incub period: 1-2 wks (2-26 days)
- 15-40% cases inapparent infection

LEPTOSPIROSIS
ANICTERIC LEPTOSPIROSIS
Leptosperemic Phase
- fever, chills, NIV, intense headache, photophobia
- myalgia impt feature, esp in calf muscles, back &
abdomen
- conjunctival suffusion, pharyngeal injection
- rash, hepatosplenomegaly
Immune Phase
- coincides w/ devt of antibodies
- less severe, may persist for wks
- devt of aseptic meningitis w/ symptoms disappear
within a few
days

LEPTOSPIROSIS
Severe Leptospirosis (WEILS SYNDROME)
- most severe form; characterized by jaundice, renal
dysfunction, hgic. diathesis w/ high mortality
- jaundice profound orange cast to the skin
- renal failure with oliguria or anuria dialysis may be
required
- hgic. manifestations epistaxis, purpura, ecchymoses
- rhabdomyolisi, myocarditis, pericarditis
- congestive heart failure

LEPTOSPIROSIS
DIAGNOSIS
Definitive :Culture isolation (EMJH media/Fletcher
medium)
Blood CSF 1st 10 days
Urine one week after
Seroconversion
1. Rise in Ab titer microscopic agglutination titer (MA+)
> 1:100 days
2. (+) macroscopic slide agglutination test in the presence
or compatible clinical illness

LEPTOSPIROSIS
- Used for screening, not specific
- ELISA, PCR
- Dark field exam results in misdiagnosis, should not be
used
TREATMENT
- PCN for 7 days
- Doxycycline, Ampicillin, Amoxicillin, Erythromycin
PREVENTION
- Chemoprophylaxis-Doxyxycline 200mg p.o. once/wk
- avoidance of exposure
- Rodent control

TETANUS

TETANUS
Definition:
- neurologic disorder characterized by inc. muscle
tone & spasm caused by tetanospasmin
Etiology: Clostridium tetani
- anaerobic gm (-) rod terminal spore ---- tennis
rocket/drumstick
- found in soil, feces, inanimate objects
- spores may survive for years, resistant to
disinfectant and boiling for 20 minutes
- tetanospasmin formed in vegetative cells

TETANUS
Epidemiology:
- affects nonimmunized, partially immunized, fully
immunized persons but fail to maintain adequate immunity
w/ booster doses
- common in males
- follows: acute injury, laceration, abrasion
- may complicate skin ulcers, abscesses, gangrene
- asso w/ burns, frost-bite, middle ear infection,
surgery, abortion, childbirth, drug abuse
- rarely no injury or portal of entry is identified

PATHOGENESIS
TETANOSPASMIN
(Germination and toxin production in wounds with low oxidation-reduction
petential i.e. devitalized tissues, foreign bodies, active infection)

Toxin release

Binds to peripheral motor neurons

Enters axons

Retrograde intraneural transport

Nerve cell body or brain stem and spinal cord

Migrates to presynaptic terminals

Blocks the release of inhibitory neurotransmitters

(GABA and lysine)

Loss of inhibition

Inc alpha neuron

activity

RIGIDITY, SPASMS

Affect preganglionic
sympathetic

Sympathetic
hyperactivity

May block neurotransmitter release at neuromuscular

junction
weakness and paralysis

TETANUS
CLINICAL MANIFESTATIONS:
Generalized tetanus
- most common; onset time- 7 days (3-14 days)
- toxin released in wounds enters lymphatics & blood
stream -- spread to distant nerve terminals
- intraneural transport time is equal for all nerve
terminals
short nerves affected before long
nerves
sequential involvement of nerves of the
head, trunk and extremities

TETANUS
Generalized tetanus
- trismus/lockjaw inc tone of masseter muscle
- dysphagia, stiffness, pain in neck, shoulder and back
muscles
- risus sardonicus grimace/sneer due to sustained
contraction of facial muscle
- opisthotonus arched back back muscle contraction
- paroxysms of beneralizes muscle spasms
spontaneous and provoked by stimulation
- repititive spasms impaired ventilation, apnea or
laryngospasm
- may be febrile; mentation is unimpaired

TETANUS
Grading and severity:
MILD muscle rigidity, few or no spasm
MODERATE trismus, dysphagia, rigidity, spasm
SEVERE frequent explosive paroxysms
Autonomic dysfunction:
Labile/sustained hypertension, tachycardia, arrhythmia,
hyperpyrexia, profuse sweating, peripheral
vasoconstriction, increase catecholamines

TETANUS
Complications:
- pneumonia, muscle rupture
- fractures, decubitus ulcer
- deep vein thrombophlebitis
- pulmonary emboli
- rhabdomyolysis

TETANUS
Neonatal Tetanus
- occurs during 1st 2 weeks of life
- born to inadequately immunized mothers, unsterile
treatment of umbilical cord
- poor feeding, rigidity, spasms
Local Tetanus
- uncommon, restricted to muscles near the wound
- excellent prognosis

TETANUS
Cephalic Tetanus
- follows head injury or ear infection
- trismus, dysfunction of one or more cranial nerve esp
CN VII
- high mortality

TETANUS
DIAGNOSIS
- base entirely on clinical findings
- isolation of C.tetani may be found in patient w/o
tetanus
- serum antitoxin level of 0.01 unit/ml or more
- tetanus unlikely
DIFFERENTIAL DIAGNOSIS
- alveolar abscess, strychnine poisoning, dystonic drug
reaction, hypocalcemic tetany, encephalitis, rabies

TETANUS
TREATMENT
General Measures: goals of therapy
- eliminate source of toxin
- neutralize unbound toxin
- prevent muscle spasms
- provide support esp respiratory
Antibiotic therapy to eradicate vegetative cells
Penicillin 10-12 million units/day x 10 days
Metronidazole 2 gm/day

TETANUS
Antitoxin
- neutralize circulating and unbound toxin
- does not affect toxin already bound to neural tissue
- tetanus immunoglobulin (TIG) 500 unit (3000, 6000
units)
- equine tetanus antitoxin up to 100,000 units IM,
IV

TETANUS
Control of Muscle Spasm
Benzodiazepine Diazepam (up to 250 mg/d), lorazepam,
midazolam
Barbiturates, chlorpromazine
Dantrolene, baclofen
Respiratory care intubation or tracheostomy
Autonomic dysfunction
Labetalol alpha and Beta adrenergic blocker
Esmolol

TETANUS
PREVENTION
Active immunization
Primary 3 doses 1st and 2nd 4-8 wks apart
Booster dose every 10 years
Wound Management
- Local wound care: wash with soap and water thoroughly
- Antibiotic prophylaxis: PCN VK 500 mg QID x 5 days
- Active immunization and passive immunization as
indicated

TETANUS
Wound Classification
- Non-tetanus prone: < 6 hrs, < 1 cm, no devitalized tissue
and contaminants from glass or knife
- Tetanus prone: > 6 hrs, > 1 cm, presence of
devitalized
tissue and contaminants, missile, crush, burn, frostbite

IMMUNIZATION SCHEDULE

TYPE OF
INJURY

History of
Vaccination:
None, incomplete, or
doubtful

Vaccination
History
Confirmed:
Booster > 10 yrs

Vaccination
History
Confirmed:
Booster < 10 yrs

Non tetanus
prone wound

DT/DPT, start active

immunization series

Tetanus toxoid

None

Tetanus prone
wound

DT/DPT + TIG

Tetanus toxoid

>5 yrs: Tetanus

toxoid
<5 yrs: none

Neglected
wound

DT/DPT + TIG

Tetanus toxoid +
TIG

Tetanus toxoid +
TIG

SYPHILIS

SYPHILIS
(Treponemapallidum)
Transmission
Sexual Contact most infectious early in the dse
Chancre, mucous patch, condyloma
Congenital (placenta) passing thru birth canal
Kissing/touching with active lesions
Transfusion
Accidental direct inoculation
Incubation period: 3-90 days
Directly proportional to size of the inoculum
spirochetes can establish an infection

few to 4

SYPHILIS
STAGES ( CLINICAL FEATURES)
FIRST STAGE CHANCRE
- at site of inoculation, occurs 21 days after
- may go unnoticed, its absence is common
- painless single lesions can occur (esp in HIV)
- spirochetes are easily demonstrated
- heals spontaneously in 2-8 wks without a trace or
with a thin atrophic scar

SYPHILIS
SECONDARY STAGE SECONDARY SYPHILIS /
DISSEMINATED FORM
- occurs 2-8 wks after chancre ( or even if chancre
still persist)
- multiplication and dissemination of the organism
- high antigen load, greatest number of Treponemes
Skin all different rashes present at one time
- involves entire bodly ( trunk
extremities)
including palms and soles
- macular, maculopapular, papular, pustular pinkish to
reddish, pruritus

SYPHILIS
- condyloma lata
- mucous patches in the tongue, silver gray,
superficial erosion with red periphery
- enlargement of epitrochlear lymph nodes
always suggest the diagnosis
- maybe asso with fever, malaise, pharyngitis,
laryngitis, generalized lymphadenopathy
CNS 40% involvement, headache, meningismus, diplopia,
vertigo, tinnitus
RENAL immune complexes glomerulonephritis
- nephrotic syndrome

SYPHILIS
GIT Hepatitis
Arthritis, Osteitis, Periostitis, Uveitis
LATENT SYPHILIS
- subclinical infection, asymptomatic
- detected by serology
a. early latent
- 1st 4 years
- relapse may occur, 75% within the 1st year as
mucocutaneous relapses
b. late latent
- relapse unlikely

SYPHILIS
LATE / TERTIARY SYPHILIS / THIRD STAGE
- progressive dse affecting any organ
Neurosyphilis
- chronic meningitis, involving every portion of CNS
- asymptomatic (+) CSF abnormality
(+) VDRL
- lumbar puncture is necessary
- symptomatic meningovascular (endarteritis) of
blood vessels, parenchymatous involvement

SYPHILIS
- Personality disorders, Affect, Reflexes, Eye, Sensorium,
Intellect, Speech
Cardiovascular Syphilis GUMMA
- indolent, tumor like masses mucocutaneous skin punch
out ulcers with local destruction skin, bone
Charcots joints trophic degenerative dse

SYPHILIS
CONGENITAL SYPHILIS
- occurs during early stage
- mothers treated within 1st 4 months of pregnancy
fetus not infected
- rhinitis, snuffle earliest sign
- saddle nose, saber skin
- necrotizing funisitis (pathognomonic)
- clutton joints (knee effusion atrophy)
- Hutchinsons teeth

SYPHILIS
DIAGNOSIS
- Darkfield microscopy
- Biopsy
- Serology
a. non specific VDRL, RPR
b. specific FTA-Abs, TPHA, TPI
TREATMENT
- PCN, doxycycline, ceftriaxone

GONORRHEA

GONORRHEA
Sexual transmission from asymptomatic individual or who
have the symptoms, ignore/discount or dont cease
sexual activity
Female to male: 20% risk/intercourse
60-80% after > 4 exposures
Male to female: 50% risk/contact
90% after > 3 exposures

GONORRHEA
CLINICAL FEATURES
Male: Acute Urethritis
- most common, incub period: 2-5 days (1-10 days)
- scanty, mucoid discharge purulent meatal erythema
- dysuria w/ or w/out frequency, urgency
- complications: epididymitis, penile edema,
lymphangitis, periurethral abscess, acute prostatitis
Female: mostly asymptomatic
Endocervicitis mucopurulent discharge, endocervical
bleeding

GONORRHEA
Anorectal: 40% of cases
pruritus, tenesmus, purulent discharge, rectal
bleeding
Pharyngeal : oral genital sexual exposure major risk
- mostly asymptomatic
- transmission from pharynx uncommon
- pharyngitis, cervical lymphadenopathy
Pelvic Inflammatory Disease
- endometritis, salphingitis, tuboovarian abscess, pelvic
peritonitis

GONORRHEA
Perihepatitis (Fitz Hugh - Curtis Syndrome)
- direct extension from fallopian tubes to the liver, or
lymphangitis, bacteremia
- occurs with overt PID
Disseminated Gonococcal Infection
- 0.5-3.0% of cases
- septic arthritis / polyarthritis migratory
- dermatitis most common, papules, pustules, ecthyma
gangrenosum

GONORRHEA
In pregnancy
- inc risk of abortion, premature labor, perinatal
mortality
- risk of disseminated infection
Opthalmia neonatorum
- acquired either in utero, during delivery or post
partum
- develops within a week (2-3 days) after delivery
DIAGNOSIS
- Culture isolation
- Gram stain: gram negative intracellular diplococci

CHLAMYDIA
TRACHOMATIS
INFECTIONS

CHLAMYDIATRACHOMATISGENITAL
INFECTIONS
Non gonococcal urethritis (NGU)
- C. trachomatis accounts 20-40% of cases
- S/s of urethritis, (-) for gonorrhea on exam
Post Gonococcal Urethritis (PGU)
- NGU developing 2-3 wks after treatment for GU
Epididymitis
- accounts 70% of cases
- scrotal pain, epididymal tenderness and swelling,
fever

CHLAMYDIATRACHOMATISGENITAL
INFECTIONS
Reiters syndrome
- conjunctivitis, urethritis/cervicitis, arthritis,
mucocutaneous skin lesion
Proctitis
- in homosexual practicing receptive anorectal
intercourse
- rectal pain with mucous discharge, tenesmus, bleeding
Mucopurulent Cervicitis

CHLAMYDIATRACHOMATISGENITAL
INFECTIONS
Pelvic Inflammatory Disease
- ascending spread from lower genital tract
- endometritis, endosalphingitis, pelvic peritonitis
- infertility asso w/ fallopian tube scarring
Urethral Syndrome in Women
- dysuria, frequency, pyuria
Inclusion conjunctivitis of the newborn
- profuse mucopurulent discharge of the eye

VENEREALWARTS(CONDYLOMATAACUMINATA)(HumanPapilloma
Virus)
- Manifested as anogenital warts umbilicated papules on
exposed epithelial surfaces of the skin and mucous
membrane of the external genitalia and perianal areas
- May spread to the urethral meatus, vagina and cervix
DIAGNOSIS
- thru physical exam
- Papanicolaou smear
- PCR

VENEREALWARTS
(CONDYLOMATAACUMINATA)
TREATMENT
- CO2 laser ablation
- Cryotherapy, application of caustic agents
- Electrodessication
- Surgical excision

LYMPHOGRANULOMAVENEREUM(LGV)
- caused by C. trachomatis strains of L1, L2, L3 serovars
1st stage papule (herpetiform ulcer) heals
spontaneously without scarring, some with
urethritis
2nd stage inguinal lymphadenopathy fluctuant
inflammation (bubo)
(rupture and drain thick yellow purulent
discharge)
3rd stage esthiomene hypertrophic chronic
granulomatous enlargement with ulceration
genitalia (vulva / scrotum)

of

LYMPHOGRANULOMAVENEREUM(LGV)
DIAGNOSIS
- culture and non culture test
- urine PCR (polymerase chain reaction) or
- LCR (ligase chain reaction)
- serology

GENITALHERPES
(HerpesSimplexVirus1&2)
PRIMARY GENITAL HERPES
- 70-95% HSV
- incubation period 2-7 days
- vesicles at glans, shaft, vulva, perineum
- rapidly ulcerate with pain and burning senasation asso
with inguinal lymphadenopathy
RECURRENT HERPES GENITALIS
- occurs in 20-40 %
- less severe vesicular lesions, slow viral shredding

GENITALHERPES
RECURRENT HERPES GENITALIS
- precipitating factors stress, local trauma, fever,
sunlight menstruation
more of HSV 1
DIAGNOSIS
- VIRUS ISOLATION
- Tzanck smear
- Serology

CHANCROID(SoftChancre)
(Haemophilusducreyi)
- more in uncircumcised males
- IP 5-7 days
- Tender erythematous papules pustule-ulcer with
exudates, bleeds easily asso with tender Inguinal
lymphadenopathy
- male single lession; female multiple lesions

PREVENTIONANDCONTROLOFSTDs
ABSTINENCE
- use of safer sexual parctices; use of condoms and
spermicides
- early detection and curative or suppressive treatment
of cases
- partner notification and treatment
- all patients with STDs or at high risk or even pregnant
patients should routinely encourage to undergo serologic
testing for Syphilis and infection with appropriate
counselling before and after testing

PREVENTION ANDCONTROLOFSTDs
- Screening of sexually active persons
- Use of vaccine ie. Hep B immunization, HPV vaccine
- Reporting of cases
- Public education and personal counselling