Bacterial Infections

(Part 1)

Ma. Anna P. Bañez, M.D.

Department of Child Health

Staphylococcus Staphylocccus aureus

• Classified • Virulence Factors
– Cell wall Components
– Coagulase positive • Peptidoglycan Clumping factor
• Staphylococcus aureus • Teichoic acid Fibronectin binding
• Slime (coagulase- negative) PBP2a
– Coagulase negative • Capsule Protein A
• Staphylococcus epidermidis, S. saprophyticus, S. – Toxins
haemolyticus • Catalase Hemolysin
• Coagulase Lipase
• Leukocidin ß- Lactamases
– Enzymes
• Enterotoxins A, B,C,D, E
• Exfoliatin A,B
• TSST-1

Relationship of Virulence Factors to

diseases associated with S. aureus
Epidemiology
• Most neonates are colonized within the 1st week of
Staphylococcus aureus life
Multiple strains
• 20-30% of normal individuals are colonized with S.
aureus in the anterior nares
Localizing Strain
Toxin Producing Strains • Other sites of colonization:
TSST 1 enterotoxin exfoliatin axilla,perineum,vagina ,rectum
Coagulase • Transmission: direct contact or droplet spread
Clumping factor
Protein A
TSS Food SSS • Handwashing between patients contacts decreases
Bacteremia poisoning
the transmisssion
Focal
Infection

Boil
Disseminated
Infection Abscess
Sinusitis

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 Epidemiology
• Factors that increase the likelihood of infection
– defects in mucocutaneous barriers
– congenital or acquired defects in
complement,phagocytosis,chemotaxis (Job,Chediak-
Higashi,Wiskott-Aldrich)
--corticosteroid treatment
– acidosis
– azotemia
– viral Infections ( measles, influenza)
Staphylococcal Scalded Skin Syndrome
Abortive type:
(+)generalized scarlatiniform rash
w/o blister
w/ facial crusting and fissuring
Ritter Disease: generalized exfoliation in the newborn
Bullous Impetigo: localized type of SSSS
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Clinical Manifestations
Staphylococcal Scalded Skin Syndrome
• Secondary to exfoliative toxins A&B
• Affects infants and children <10 y/o
• Rash preceded by malaise,fever, irritability,exquisite skin
tenderness
• (+)brightly erythematous skin become wrinkled;if severe,(+)
generalized ,sterile, flaccid bullae->large sheets of
epidermidis peel away->moist,glistening denuded areas->dry
quickly & heal by desquamation w/in 2-3days
• Prominent radial crusting and fissuring around eyes,mouth
and nose
Staphylococcal Scalded Skin Syndrome
Diagnosis:
Clinical
Skin biopsy: site of blister
cleavage is granular layer
Culture:>90%(+) culture np
<10%(+) culture
skin/blood
Treatment: anti-staphylococcal antibiotic

Toxic Shock Syndrome
Secondary to TSST-1 that causes massive fluid loss from
IV space directly or thru IL-1 & TNF
Epidemiology:
Patients at risk:
-menstruating women using vaginal
tampons/other vaginal devices
-non-menstrual cases:infected wound, nasal
packings,sinusitis,tracheitis,pneumonia,abscess,
burns,etc
Staphylococcal Toxic Shock
Syndrome
Clinical manifestations
• Abrupt onset w/ high fever,vomiting &
diarrhea,sorethroat,headache,myalgias
• Diffuse macular rash appears w/in 24 hrs,w/ straw-
berry tongue,hyperemia of pharyngeal,conjunctival
& vaginal mucosa
• (+)altered sensorium,oliguria,hypotension->shock
,DIC,ARDS, heart/renal failure
• Recovery w/in 7-10days w/ desquamation of
palm/soles; hair/nail loss after 1-2 months

Diagnostic Criteria of Staphylococcal TSS

Diagnosis
Major Criteria (All Required)
•Acute fever, temp >38.8
• Based on clinical manifestations
•Hypotension (orthostatic or Shock)
•Rash (erythroderma with late desquamation) • No specific laboratory tests; appropriate
Minor Criteria (Any 3) selective tests show multi- organ system
•Mucous membrane inflammation •Muscle abnormalities involvement
•Vomiting, diarrhea •CNS abnormalities
•Thrombocytopenia
• Bacterial culture of the associated focus
•Liver abnormalities
(vagina, abscess)
•Renal abnormalities
Exclusionary Criteria
•Absence of another explanation
•Negative blood CS (except for S. aureus)

Treatment Staphylococcal Food Poisoning

• B-lactamase resistant anti-staph +/-
clindamycin (unresponsive cases)
• Drainage of the vagina, removal of retained
tampons and focally infected site
• Fluid treatment
• Steroids & IVIg for severe cases
• Secondary to Enterotoxin
• Epidemiology:
-ingestion of toxin-contaminated food:pastries
custards, salad dressing, sandwich, poultry, sliced
meat/meat products
-involve uncooked food in contact w/ food
handler’s hand or inadequately heated/refrigerated
food.
-food left in room temperature permit multiplication
of organism and release of pre-formed, heat stable
toxin

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 Staphylococcal Food Poisoning
Clinical Manifestation
• Skin infections: S.aureus the most common cause of pyogenic skin
infection
Clinical Manifestations A. Impetigo
-incubation period: 30 minutes-8 hrs(2-4 hrs) -non-bullous
-abrupt onset of severe nausea, abdominal cramps, -bullous impetigo:always caused by S.aureus
vomiting & prostration-> watery diarrhea B. Folliculitis
C. Hydradenitis
-normal to low grade fever D. Furuncles
-last only 1-2 days F. Carbuncles
Diagnosis: G. Cellulitis: suppurative; may appear late or prevented by early
tx; maybe external manifestations of underlying
-epidemiologic considerations bone/joint infection
-isolation from stool/vomitus, toxin-testing H. Breast abcess
Treatment: -Wound infection
-Tropical pyomyositis: subacute ,not septic ,
Fluid and electrolyte replacement muscle pain,single or multiple

Clinical manifestations
• Eye Infection
• Purulent conjunctivitis
• Hordeolum or Stye
–Involve sebaceuos gland/ eyelash follicles
–Well localized or w/ eyelid cellulitis
• Pre-septal /Orbital cellulitis
• Cavernous sinus thrombophlebitis
–2/3 of cases due to S.aureus
–Periorbital swelling and inflammation + CN
paralysis (III,IV,VI), proptosis, retinal venous
obstruction,aute visual deteriotation

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 Clinical Manifestations Clinical Manifestations

Sepsis Purulent Pericarditis

-bacteremia& sepsis may be associated w/ -Rare, serious complication after bacteremia
any localized infection -Usually with associated illness(respiratory
tract/bone/skin infection)
-maybe acute w/fever, chills, -S.Aureus,most common followed by hib,
nausea,vomiting, myalgia
meningococci,pneumococci,gram(-) enterics
-unrecognized until w/ secondary -Fever,respiratory distress,chf
hematogenously disseminated -(+/-) Pericardial friction rub
focus(lungs,heart,joint/bones,brain) -Diagnosis: CXR (cardiomegaly), 2d echo
-Treatment: pericardiocentesis,pericardiectomy

Clinical Manifestations
Clinical manifestations -Osteomyelitis
Endocarditis -Primarily caused by S.Aureus
-Occur in patients w/ no heart disease, w/ congenital or rheumatic -By hematogenous route or contiguous focus
lesions,after cardiac surgery -Infants: minimal toxicity;no localsigns,pseudo- paralysis, multiple
-S. aureus,common cause of acute, virulent endocarditis on native -Older children: either acutely w/ fever & toxicity or subacutely w/ local
valves complaints
-Fever, lethargy w/ rapid disease progression -PPE: marked tenderness over involved bone; (+) local swelling/redness
when infection spread out from metaphysis to subperiosteal space
-Frequent cardiac decompensation causing secondary soft tissue infection
-Serious symptoms & rapid progression recognized early before -Diagnosis:
embolic phenomena /chronic changes Blood culture (+) 50-57% of cases
occur(anemia,splenomegaly,splinter/conjunctival hemmorhage Needle aspirate of bone pus: best specimen
& janeway spots)
Bone x-ray: destructive changes seen in 10-16 days radionuclide
-Diagnosis: blood CS, 2d-echo scan/MRI
ESR, CRP & WBC count monitor course & response

Clinical manifestations Clinical Manifestations

Septic arthritis
Deep Tissue Abscesses
Common pathogens according to age:
-in the course of bacteremia, staphylococci may establish
Neonate: S.Aureus multiple, metastatic foci:
2 months-4 years old: hib, S.Aureus Liver abscess:
Beyond 4 years old: S.Aureus - S.aureus, gram (-) enterics & anaerobes are the most common
-Maybe hematogenous, by contiguous spread or direct inoculation isolates
-PPE: redness,swelling skin/soft tissue + painful joint w/ decrease -fever, abdominal pain & hepatomegaly
range in motion -Diagnosis: ultrasound
-Diagnosis: Renal Abscess:
Blood culture -S. aureus most common
Need aspirate of joint fluid: best specimen -fever,costovertebral pain & tenderness
X-ray: joint space widening & soft tissue swelling Splenic Abscess:
ESR, CRP & WBC count monitor course & response to TX -polymicrobial : S. aureus, Streptococci,Enterobacteriaciae

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 Clinical Manifestations
Staphylococcal Enterocolitis
-follow overgrowth of normal flora by staphylococcus
after use of broadspectrum antibiotics DIAGNOSIS:
-bloody, mucoid diarrhea presumptive: gram(+) cocci in grapelike
Staphylococcal Peritonitis clusters
-in patients w/ CAPD definitve: isolation by culture
-catheter tunnel usually involved

Meningitis
-S. aureus, unusual cause
-occurs in patients w/ cns abnormalities/head trauma

Treatment:
-Incision and drainage
Treatment
-Removal of foreign bodies
-Antibiotics Skin and Soft Tissue infections
Serious infections: -oral: BLR B-lactam(cloxacillin)
-Intravenous therapy:
first/second gen cephalosporins
B-lactamase resistant b-lactam: oxacillin
B-lactam/B-lactamase inhibitor
-Other drugs: Clindamycin
First/second generation cephalosporins Erythromycin
B-lactam/b-lactamase inhibitor, clindamycin(except Co-trimoxazole
endocarditis,cns infections) -localized/superficial infections
- Strains resistant to BLR b-lactam ab(mrsa/ ORSA) topical mupirocin,fusidic acid
vancomycin
- Rifampicin or gentamycin provide synergism if combined w/
BLR b-lactam

Coagulase – Negative Staphylococci

Prevention
Handwashing is the most effective measure
for preventing the spread of staphylococci
from one individual to another
- normal inhabitants of human skin,throat, mouth,vagina & urethra
Staphylococcus epidermidis
-most common & persistent species
-infection preceded by colonization or direct inoculation during
surgery
-produces an exopolysaccharide (slime) that enhances adhesion to
foreign surfaces,resist phagocytosis & impair penetration to foreign
surfaces
-originally avirulent, now a nosocomial pathogen:
- in patients with indwelling foreign devices
-surgical trauma
-immunocompromised states( malignancy, neonates)

-Low virulence usually requires presence of another factor (immune

compromised state /foreign body) for development of infection

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 Clinical Manifestations Clinical Manifestations
Bacteremia CSF Shunt Infection
- indolent, not associated with overwhelming shoc -S. eidermidis ,common pathogen in CSF shunt meningitis
- S. epidermidis , the most common cause of late-onset sepsis among -usually introduced during surgery
prematures & nosocomial bacteremia in all ages
- also in patient w/ malignancy and bone marrow transplantation -70-80% within 2 months of operation: meningeal irritation,
fever, increased ICP &/or peritonitis
Endocarditis
-infection of native heart UTI:
valves w/ or w/out CV catheter -S.eidermidis causes asymptomatic UTI among catheterized
-S.epidermidis, a common cause of prosthetic valve endocarditis pts.,after renal surgery/transplant
-S.saprophyticus causes symptomatic UTI in previously healthy
Central Venous Catheter Infection sexually active teenage girls
-exit site & subcutaneous tunnel become infected->direct path to
bloodsream
-common due to high rate of colonization Peritonitis:
-line sepsis: fever, tenderness/erythema at exit or along tunnel, -S.epidermidis, most common pathogen in CAPD_associated
catheter peritonitis
thromboses, leucocytosis
-abdominal pain,fever, >100 wbc/mm3, (+) gs/culture

Diagnosis Treatment
True bacteremia should be suspected;
-BLR B-lactam antibiotic (Oxacillin)
– when blood cs grow rapidly CONS (1st 24 hours)
– 2 or more blood culture is positive with the same CONS -for MRSE or ORSE: Vancomycin
– When the peripheral venous blood CS has quantitative
colony count comparable to that drawn from central -addition of gentamicin or rifampicin
venous catheter
– when clinical and laboratory S and S compatible with may increase antimicrobial efficacy
CONS sepsis are present and subsequently resolve with -removal of foreign bodies (CSF shunt,
appropriate therapy
prosthetic heart valves)
No blood CS that is positive for CONS in a neonate or
patient with IV catheter should be considered
contaminated without careful assessment and
examination of patient

Clinical Manifestations

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 Streptococcal Pharyngitis
-GABS,major cause of bacterial pharyngitis
-Highest in children > 3y/o (5-15 y/o)
-Fever,headache,abdominal pain,vomiting
-Sorethroat soon after initial complaint; slight to severe
-(+) Early, tender anterior cervical adenitis
-Physical findings suugestive of streptococcal infection:
diffuse redness of tonsils /pillars
Petechial mottling of soft palate w/ or w/o exudate
-Features suggestive of viral infection: ( + 2 or more)
Conjunctivitis,rhinitis,cough, hoarseness
-Clinical judgement not predictive
-Toddlers with GABS respiratory infection: protracted fever w/
fever, irritability,anorexia,seromucoud rhihitis, nasal
excoriation

Streptococcal Pharyngitis Streptococcal Pharyngitis

– Treatment
• Early antibiotic therapy will hasten recovery by 12-24 hr
• Primary benefit of treatment is prevention of RF (almost
successful it given within 9 days of illness)
– Diagnosis
• Reduce transmission of infection to others
• Throat culture • Penicillin : drug of choice; 10 day TX
• Serology: rapid, high specificity – Pen V
<60 lbs: 250 2-3x /dy
>60 lbs: 500 2-3x/dy
– Amoxicillin
– benzathine penicillin single IM dose
» <27 kg 600,000 U
» 1.2 Million U for larger children and adult
– Erythromycin estolate / ethyl succinate (allergy to
penicillin)
» 30-40 mg/kg/day tid or qid

Scarlet Fever

• Uncommon < 3y/o

– Caused by pyrogenic exotoxin (erythrogenic toxin)
• Acute onset of fever, vomiting,toxicity,chills and pharyngitis
followed by rash 12-46 hrs

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 Vaginitis

• Common cause of pre- pubertal vaginitis

• Serous discharge with marked erythema and
irritation of vulvar area
• Dysuria and discomfort in walking

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 Severe Invasive Disease
Hypotension plus two or more
• Toxic Shock syndrome
Renal Impairment
– occurrence of shock, Coagulopathy
multiorgan system Hepatic involvement
failure early in the ARDS
course of infection Scarlet fever rash
– (+)soft tissue Soft tissue necrosis
infection(cellulitis,absc Definite case
ess,necrotizing Clinical criteria plus group A
fasciitis)w/ increasing streptococcus from a normally
pain sterile site
Probable case
Clinical criteria plus group A
streptococcus from a non strerile
site

Severe Invasive Disease

• Focal and systemic infections that do not meet the

criteria for TSS and necrotizing fasciitis
– Meningitis
– BPN
– Peritonitis
– Puerperal sepsis
– Osteomyelitis
– Suppurative arthritis
– Myositis
– Surgical wound infection

Suppurative Complications Non-suppurative complications

Secondary to local inflammation: Rheumatic Fever:

peritonsillar abscess -associated w/ serotypes M1,2,5,6,18,24
retropharyngeal abscess -follows a streptococcal pharyngitis
Direct extension: -abnormal host immnue response to an undefined component
otitis media of GABS->immunologic damage
sinusitis -latent period: 1-3 wks support immunologic tissue damage
Lymphatic spread:
lymphadenitis
Glomerulonephritis:
Bacteremia:
sepsis -acute nephritic syndrome 1-2 wks after a streptococcal
pharyngitis or skin infection
osteomyelitis
pneumonia -probably immune complex –mediated (depressed C3)

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 Non-suppurative Complications
Poststreptococcal Reactive Arthritis:
-acute arthritis after a streptococcal pharyngitis but does not
fulfill Jones criteria
-unknown whether a distinct syndrome or a manifestation of RF
-large joints,non-migratory
-latent period :<10 days
-doesn’t dramatically respond to aspirin/NSAID
-observe for subsequent carditis
Laboratory Diagnosis
Microscopy: gram (+) cocci in pairs/chains
Culture: gold standard
Antigen detection:
EIA or latex agglutination
-very specific, low sensitivity
-confirm negative test by culture
Antibody detection:
Antibody to Streptolysin O (ASO)
-measured 3-4 wks after infection
->166 Todd units in 80% of untreated
streptococcal pharyngitis
-modified or abolished by antibiotic Tx
-high titers in RF; variable response in
AGN
-weakly (+) or normal in
pyodermas(streptolysin inactivated by
skin lipids)
Prevention
• Primary Prevention
– Appropriate antibiotic Route Antibiotic
therapy instituted
before the 9th day of
symptoms of acute IM
group A Streptococcal
pharyngitis
• Secondary Prevention
– Prevent group A Oral
Streptococcal
pharyngitis in patients at
substantial risk of
recurrent acute RF
Non-suppurative Complications
Pediatric Autoimmune Neuropsychiatric Disorders Associated
with Streptococcus pyogenes (PANDAS)
-sudden onset of obsessive-compulsive &/or Tic disorders
-patients w/ Sydenham’s chorea frequently have obsessive-
compulsive symptoms & a subset of patients w/ obsessive-
compulsive & tic disorders will have chorea as well as acute
exacerbations following grp A streptococcal infection
-(+)autoimmune antibodies in response to GAS infection that
cross-react w/brain tissue
Treatment
Anti-Deoxyribonuclease Streptococcal Pharyngitis:
-best serologic test for strep
pyodermas Phenoxymethyl Pen: 10 day- treatment
-rise seen 6-8 wks after
<60 lb :400,000(250) 2-3x a day
infection
-(+) in streptococcal pharyngitis >60 lb :800,000(500) 2-3x a day
Nonspecific Findings
increased or normal WBC count Other Drugs: erythromycin,amoxycillin,cefalexin,
increased ESR,CRP clindamycin
Severe Streptococcal Infections
Pen G Na : 250,000-400,000 u/k/day, in 4-6 doses
x 2-6 weeks
Streptococcal Impetigo
Topicals( bacitracin or mupirocin)
Oral antibiotics if with multiple lesions
Group B Streptococcus
( Streptococcus agalactiae)
Secondary Prevention of RF
Dose Frequen • Major cause of neonatal bacterial sepsis
cy
• Facultative anaerobic gram positive cocci form
Benzathine
Pen G
1.2 M u Every 3-
4 weeks
chain or diplococci
• 9 serotypes Ia,Ib,II,III,IV,V,VI,VII, VIII
Pen V 250 mg BID
Sulfadiazine 500-1000mg OD
Erythro- 250 mg BID
mycin
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 Group B Streptococcus
Clinical manifestations
( Streptococcus agalactiae)
• Vaginal or rectal colonization occurs in approx 30% of Parturient mother:
pregnant women ( usual source for GBS transmission infants)
• Risk for early onset sepsis • -GBS a major cause of:
– Prolonged rupture of membrane >18 hours endometritis
– Intrapartum fever
– Prematurity(<37 wks) amnionitis
Maternal bacteremia during pregnancy
–
UTI

Clinical manifestations

Newborns – infants </= 3 months

Clinical manifestations

Early Onset infection Late onset infections

-occurs from 0-6 days
-ranges from asymptomatic bacteremia to septic shock -bacteremia without focus 55%
-in-utero infection may result in fetal asphyxia, coma ,shock
-meningitis 35%
-w/ prominent respiratory symptoms:
tachypnea,apnea,grunting,retractions,cyanosis -osteoarthritis
CXR findings: -soft tissue infections
reticulogranular pattern 50%
patchy pneumonia 30% Presenting signs: fever , lethargy
pleural effusion,pulmonary edema,cardiomegaly,increased
pulmonary markings
-Bacteremia or sepsis w/out localization 30-40%
-Meningitis (10%)

Group B Streptococcus Group B Streptococcus

( Streptococcus agalactiae) ( Streptococcus agalactiae)
Diagnosis : • Treatment Treatment Duration
Presumptive: – Penicillin is the drug of Bacteremia 10 days
gram stain: gram(+) cocci choice without a focus
latex agglutination:detection of GBS in serum, csf or urine – 450,000-500,000 meningits 2-3 weeks
U/kg/24 hr
Definite: – Ampicillin 300-400 ventriculitis 4 wks
isolation of GBS from blood/sterile fluids mg/kg/24 hour
osteomyelitis 4 wks

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 Prevention Other B-hemolytic Streptococci

Selective intrapartum chemoprophylaxis • Lancefield groups C-H, K-V

-decreased incidence of early onset disease
-Pen G or Ampicillin given immediately to selected women at • Groups C & G most frequent cause of human infections
onset of labor or PROM is anticipated
-maternal chorioamnionitis: important indication
• Colonize intact body surfaces( pharynx, skin, GIT, GUT)
-all infants whose mothers received SIC should be observed for
48 hrs for signs of infection; diagnostic evaluation and
treatment for symptomatic infants • Wound infections, puerperal sepsis, cellulitis,
sinusitis,endocarditis, brain abscess, sepsis, nosocomial
infections,opportunistic infections

Enterococcus
Clinical Manifestations
-Normal inhabitants of the GIT of humans & animals
• Neonatal Infections
-oral secretions & dental plaque, upper respiratory tract, – 15% of all neonatal bacteremia and septicemia
skin & vagina may also be colonized – Early onset sepsis (< 7 days)
mimic early onset GBS infection in healthy FT
babies, milder
-E.faecalis, predominant organism
– Late onset infection( >/= 7 days)
Risk Factors
-Risk Factors: • Extreme prematurity
breakdown of normal physical barriers (GIT,skin, UT) • IV catheter
prolonged hospitalization • NEC
intravascular catheters • Follows intra-abdominal surgical procedure
prior use of antibiotics – Meningitis
compromised immunity

Treatment
Clinical Manifestations
Immunocompetent with localized infection
• Infection in older children -ampicillin alone
– 15% of nosocomial UTI in children and adult Invasive infection sepsis, meningitis and
– Intraabdominal infections following intestinal endocarditis
-Penicillin/Ampicillin + aminoglycoside
perforation and surgery
-Vancomycin + aminoglycoside if with allergy to
– nosocomial bacteremia and endocarditis, less penicillin
common in children than in adults
Vancomycin-resistant Enterococcus
- Linezolid, Quinupristin-dalfopristin

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 Alpha- hemolytic Streptococcus

• S. bovis, S.mitis, S.mutans, S.sanguis

• Normal flora of the pharynx,nose,skin, GUT
• Common human diseases: dental caries,sub-
acute endocarditis, human bite infections,
suppurative intra-abdominal infections

Epidemiology Epidemiology

• Before the advent of effective conjugate vaccine (1988), Hib • Increased incidence of invasive disease:
responsible for >95% of invasive diseases in children Alaskan eskimos, Apaches, Navajos &
• 90% occurred in children <5y/o; majority in <2y/o
blacks
• Incidence presently varies in different populations,countries
• From 1989-1997, incidence of Hib disease in children <5 yrs, • Mode of transmission: droplet
in the US declined by 99% • Attack rate for secondary Hib cases in
• Non-typable strains: common etiologic agents of otitis
media, sinusitis,chronic bronchitis in adults, invasive disease
household contacts
in neonates & immunocompromised children <24 months: 3.2%
>47 months: <0.2%

Clinical Manifestations Clinical manifestations

Acute epiglottitis
Meningitis -Acute onset; (+) sorethroat->rapidly progressive
-clinically indistinguishable to meningitis due to respiratory distress(hoarseness,stridor, irritability,
S.pneumoniae or N.meningitides restlessness)->complete obstruction->death
-maybe complicated by other foci of -patient insists on sitting, leaning forward w/ extended
infection(lungs, joints, bones or pericardium) neck to maximize airway
Pneumonia -laryngoscopy:large,swollen cherry red epiglottis
-signs and symtoms indistinguishable from -warrants emergency intubation/tracheostomy
pneumonia due to other organisms
Septic Arthritis
-Hib & S.pneumonia, the most frequent isolates
from lung aspirate/ blood in children 2 months- -s/sx indistinguishable from those due to other organism
5 y/o w/ bacterial pneumonia(WHO) -most common cause among children 2months- 5y/o

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 Clinical Manifestations

• Cellulitis
– Often have antecedent URTI
– No history of trauma
– Represent seeding to the involved soft tissues during
bacteremia
- most common sites of involvement:head &neck
especially cheek & preseptal region
– Buccal cellulitis: erythematous with a violaceous hue
– Preseptal or orbital cellulitis
-clinically indistinguishable from other causative
agents: S.pneumoniae, S.aureus, GAS
_S. aureus or GAS more likely if w/ skin breaks & no
fever

Clinical Manifestations of
Clinical Manifestations Non-typable H.influenzae

Pericarditis Otitis media/Sinusitis

Occult Bacteremia -Non-typable H.influenzae are common pathogens together
-bacteremia w/o a focus in 3 months-3 y/o with S.pneumoniae and M. catarrhalis
-non-toxix looking -drug of choice: oral ampxycillin
-risk factors: Conjunctivitis
temperature >/=39 C -non-typable H.influenzae, S.pneumoniae & S.aureus are
WBC ct:>/=15,000 cells important pathogens beyond neonatal period
-Hib accounts for 5% of cases(10-25% prevaccine era) Invasive Disease in neonates
-risk of subsequent meningitis: 10-15% -occur in association with maternal chorioamnionitis or PROM
-include bacteremia with sepsis, pneumonia,RDS with shock,
conjunctivitis, scalp abscess, cellulitis, meningitis

Diagnosis Treatment

• B-lactamase-producing H.influnzae isolates identified in 1974

• Culture: blood, CSF, synovial and pleural fluid
and middle ear aspirates
• Gram stain:gram(-) coccobacillus presumptive
diagnosis
• Latex particle agglutination of csf: detection of
type b capsular antigen
• US: 36.5% isolates beta-lactamase-producing
• Philippines: <5% isolates beta-lactamse producing
• Hib Meningitis/Invasive Diseases
Ampicillin
Chloramphenicol
3rd gen cephalosporin:Ceftriaxone/Cefotaxime
Non-invasive Diseases
Amoxycillin
alternative drugs:2nd or 3rd gen cephalosporin,beta-lactam-
beta lactamse inhibitor,clarithromycin

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 Prevention
H. influenza: chemoprophylaxis
• For all household contacts in the ff circumstances:
Vaccine product Total No. of Recommended
– Household with at least 1 unimmunized/incompletely
at initiation Doses to be Regimen immunized contact <4yrs old
administered – Household with a child <12mos old without 1 ºseries
HbOC(diptheria CRM 3 doses at 2 mo – Household with immunocomp. child w/ or w/o immn
197 protein conjugate) intervals initially; 4th
or 4 dose at 12-15 mo of • For nursery school and child care contacts regardless of
PRT-T (tetanus toxoid age; any conjugate age, when 2 or more cases of Hib invasive dse has
conjugate) vaccine for dose 4 occurred within 60 days
PRP-OMP(outer 2 doses 2 mo apart; 3rd
membrane dose at 12-15mo of • For index case, if younger than 2 yrs old or member of a
protein,N.meningitides 3 age; any conjugate household with a susceptible contact & treated with a
vaccine for dose 3 regimen other than cefo or ceftri, prophylaxis is provided
just before discharge

H. influenza: chemoprophylaxis

• Prophylaxis:

• rifampicin: 20 mg/kg p.o. once a day for 4 days

– maximum dose: 600 mg

• Infants younger than 1 month old: dose not

established but some experts recommend lowering
the dose to 10 mg/kg

Serotype distribution of Invasive S.pneumoniae in Filipino

children(2000-Aug.2005)
Capeding et al RITM

6* 20%
18* 17%
14* 13.3%
5 13.3%
9* 10%
20 10%
1 3.3%
2 3.3%
4* 3.3%
19* 3.3%
38 3.3

*7 valent types=67%

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Increased incidence and severity in patients w/
the following diseases:
Diagnosis
• Congenital/acquired humoral immunodeficiency • Recovery of S. pneumoniae from site of
• HIV infection
• Asplenia
infection or the blood
• Nephrotic syndrome • Can be identified in body fluids as gram
• Chronic renal failure positive lancet shaped diplococci
• Organ transplant
• Diabetes mellitus
• Chronic pulmonary disease
• Congestive heart failure
• Csf leaks

Clinical Manifestations
Clinical Manifestations
• Peritonitis
• Most frequent bacterial cause of community-acquired
• Laryngotracheobronchitis
pneumonia, otitis media, sinusitis
• Osteomyelitis
• With Hib vaccination, pneumococcus & meningococcus
have become the 2 most common cause of meningitis in • Suppurative arthritis
infants and young children • Brain abscess
• the most common cause of meningitis in the elderly • HUS
• Account for majority of Occult bacteremia in infants and • Empyema
young children; risk of subsequent meningitis: 1-6% • Pericarditis
• Mastoiditis
• Epidural abscess

Treatment
Prevention
Penicillin G is the drug of choice for penicillin susceptible strain
– Minor infections • Immunization
• oral penicillin v 50-100 mg/kg/24 hr q6-8 hours Purified polysaccharide of 23 pneumococcal serotypes
– Bacteremia or BPN
• Pen G 200-250,000 u/kg/day q4-6 hour
-Poorly immunogenic in children<5 y/o
– Meningitis
• Pen G 200-300,000 u/kg/day q4-6 hour
For serious infections w/ intermediately R strain (MIC 0.1-1mg/L) -for children at risk of severe disease
or highly R strain (MIC>/=2mg/L)
– Vancomycin 60 mg/kg/day q6 PCV7 (conjugate vaccine with 7 serotypes)
– Rifampicin maybe added in severe and unresponsive cases -4,6B,9V,14,18C,19F,23F
-highly recommended for routine immunization
3rd generation cephalosphorins
starting 6-8 wks of life q 2 months x 3 doses,
-maybe added or substituted for vancomycin for booster 12-15 months
intermediately R strain
Ceftriaxone 100mg/k/day q 12
Cefotaxime 225-300 mg/k/day q 8

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 Prevention

• Prophylaxis

– Recommended for children with asplenia and

sickle cell disease

• Phenoxymethyl penicillin

– <5 y/o 125 mg BID

– >/=5 y/o 250 mg BID

Serogroups
• 13
• A, B and C most common causes of
invasive disease worldwide
• A - most common cause of epidemics
• B - most common cause of sporadic
disease
• Y may cause primary pneumonia
• Others: D, H, I, K, L, X, Z, W-135, 29E

Recent meningococcal disease: Epidemiology

Philippines -Asymptomatic colonization of the upper respiratory
• 1 Oct 2004 to 28 Jan 2005: 98 cases tract is frequent; may lead to immunity
(Baguio City 74, Mt.Province 22, Ifugao 2) -mode of transmission: droplet
• Case fatality ratio 33% -risk factors:
close contact
• 11 cases laboratory-confirmed
terminal complement component deficiency(C5-9)
properdin deficiency
functional/anatomic asplenia
-incubation period: 1-10 days (4days)
WHO

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 Clinical Presentation
*asymtomatic transient bacteremia to fulminant sepsis
resulting to death only a few hours after onset

Occult bacteremia

-N.meningitides account for 1% of cases

-non-toxic child w/ fever & (+) blood culture
- w/ upper respiratory or GI or maculopapular rash
-spontaneously recover or go on to have meningitis
-risk of subsequent meningitis: 30-70%

Meningococcemia
-Abrupt onset with upper respiratory symptoms,fever,chills,
myalgia weakness, headache, and a hemorrhagic rash
-Skin manifestations develop early:
-diffuse mottling to extensive purpura
-1st sign to clinical suspicion
petechiae 50-60%
purpura(microvascular dermal thromboses) 16-24%
-seen in fulminant cases(50% mortality)
maculopapular 13%
no rash 1-2%
* presence of hemorrhagic rashes w/ acral distirbution
suggestive of meningo or infectious vasculitis
-with widespread hematogenous dissemination->rapid
progression to septic shock (hypotension,DIC,adrenal
hemorrhage, renal/myocrdial failure)

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 Meningitis (w/ or w/ meningococcemia) Uncommon manifestations

• Suspected if with fever, CNS manifestations + • Endocarditis

hemorrhagic rash
• Purulent pericarditis
• Pneumonia
• Patients with meningitis have a better
• Septic arthritis
prognosis than those with meningococcemia
alone • Endopthalmitis
- a function of virulence of organism or ability of • Osteomyelitis
immune system to contain infection • Chronic meningococcemia

Case Definition (CDC) Treatment

• Confirmed: isolation of N. meningitidis from a sterile • Penicillin G IV 250,000 units/kg/day
site (e.g. blood, CSF, synovial fluid, pleural fluid, (maximum 12 million units) divided q 4 -6
pericardial fluid, petechia or purpura) in a person
with clinically compatible illness hrs x 5-7 days
• Presumptive: gram-negative diplococci from sterile ` Alternative drugs:
fluid or petechial scraping
Cefotaxime
• Probable: + antigen test in absence of + culture in Ceftriaxone
CSF or purpura fulminans in absence of + blood
culture Chloramphenicol

Isolation of hospitalized patient Prevention

• Standard precautions • Careful observation of exposed people
• Droplet precautions till 24 hours after • Chemoprophylaxis
initiation of effective antibiotic therapy • Meningococcal vaccine
• Reporting
• Counseling and public education

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 Who should receive prophylaxis? High
Chemoprophylaxis risk contacts
Age Dose Duration Efficacy
Rifampin • Household contacts esp. young children
• Child care or nursery school contact during 7 days
<= 1 mo 5 mg/kg q 12 hr 2 days 72-90% before onset of illness
10 mg/kg max 600 • Direct exposure to index patient’s secretions thru kissing,
>1 mo mg) q 12 , oral sharing toothbrushes or utensils during 7 days before
onset of illness
Ceftriaxone • Mouth-to-mouth resuscitation; unprotected contact
<=15 y 125 mg IM Single dose 97% during incubation during 7 days before onset of illness
>15 y 250 mg IM • Frequently slept or ate in same dwelling as index patient
during 7 days before onset of illness
Ciprofloxacin • Index patient if treated with penicillin; not ceftriaxone
>= 18 y 500 mg, oral Single dose 90-95%

Low risk contacts: chemoprophylaxis not

recommended Meningococcal vaccine
• Casual contact: no history of direct exposure to MPSV4-Tetravalent meningococcal polysaccharide
index patient’s oral secretions (school mate or vaccine(A,C,Y,W135)
work mate) -for high risk children >/=2yo
• Indirect contact: only contact is with high-risk -not routine: infection rate in general population is low,
contact not immunogenic,
• Health care professionals without direct
-adjunct to chemoprophylaxis during outbreaks
exposure to patients oral secretions

MCV4-tetravalent meningococcal conjugate

In outbreak or cluster, chemoprophylaxis for people vaccine(A,C,Y,W135)
other than those at high risk should be administered
only after consultation with local health authorities -in US, for routine use among adolescents at the 11-12
years old visit

Tetanus
• Typical situations associated with tetanus:
deep puncture wounds,burns,blast injury,iatrogenic cases
ear infections,tatooing

• Incubation period: 2days to months

– In neonates: 5-14 days

• Diagnosis is made clinically by excluding other causes

of tetanic spasms
– Hypocalcemia, phenothiazine reaction, strychnine
poisoning, and hysteria

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 Clinical Manifestations Generalized tetanus

Generalized Tetanus B. Non- neonatal tetanus

A. Neonatal tetanus -progressive increase in stiffness in voluntary
muscles:trismus, risus sardonicus, opisthotonus,
-secondary to unhygienic delivery & lack of boardlike abdomen, flexed arms, extended legs,
maternal immunization laryngeal spasm
-begin w/in 3-10 day of life -painful spasms precipitated by touch, bright
light,noise,etc.
-difficulty in sucking/swallowing, excessive
-intact sensorium
crying, decreased movement, stiffness
-accumulation of secretions->aspirate
to touch, opisthotonus
-duration of illness: 2 weeks

Treatment

A.Neutralization of unbound toxin

Human Tetanus IG: singlel dose of 500 units, IM for all ages
Equine tetanus antitoxin:Anti-tetanus serum(ATS):
10,000 u IM, 10,000 u IV ANST
B.Elimination of exotoxin production
-Wound Care: clean and debrid
-Antibiotic:
Metronidazole:30 m/k/dy q6h x 10 days
PenG 100,000U/k/dy q4-6h x 10 days

Treatment
Supportive management

C.Prevention & Control of spasms & convulsion • Maintenance of airway

1.Benzodiazepines • Nutrition
Valium: 0.3-0.5 mg/k IV q 2- 4 hrs max: 20-40mkdy • Fluid & electrolyte balance
• Good nursing care
Midazolam: 0.05-0.15 m/k/dose IV q 1-2 hrs or
• Rehabilitation
infusion
• Anticipation and prevention of complications
2.Neuromuscular blocking agents: in addition to
• During convalescence,active immunization
benzodiazepines for intractable seizures
pancuroniun, vencuronium
3.Control of seizures
phenobarbital, phenytoin

22 | B a c t e - P e d i a
 Tetanus prophylaxis in routine Tetanus prophylaxis in routine
wound management wound management
History of Clean, minor All other History of Clean, minor All other wounds
absorbed TT wounds wounds absorbed TT wounds Td TIG
(doses) (doses) Td TIG
Td TIG Td TIG
=3 No* no No+ no

< 3 or Yes no Yes Yes

unknown If only 3 doses: give a fourth dose
*give tetanus toxoid if >/= 10 yrs since last TT-containing vaccine dose
+give tetanus toxoid if >/= 5 yrs since last TT-containing vaccine dose

Corynebacterium diptheriae

• Pathogenesis
– Major virulence: (+) 62kd polypeptide EXOTOXIN,-
> inhibits protein synthesis and causes local tissue
necrosis->pseudomembrane

-local effect of the toxin: paralysis of palate &

hypopharynx
-toxin absorption can lead to necrosis of kidney
tubules, thrombocytopenia, cardiomyopathy and
demyelination of nerves ( occur 2-4 weeks after
mucocutaneous infection)

23 | B a c t e - P e d i a
 Clinical Manifestation
• Cutaneous Diphtheria
– Indolent, non progressive superficial, ecthymic, non
healing ulcer with a gray brown membrane
– Extremities are more often affected than the trunk or
head
– pain, tenderness, erythema and exudate are typical
– Respiratory tract colonization, symptomatic infection and
toxic complication occur in minority of patients
Complications
Cardiomyopathy
– Occurs in approx. 10-25%
– Responsible for 50-60% of deaths
– occurs 2nd to 3rd week of illness but can appear acutely as
early as first week or insidiously as late as 6th weeks
– Tachycardia out of proportion with fever;s/sx of CHF
– ECG changes:prolonged P-R interval, ST-T wave changes,
heart blocks, arrythmias
– Echocardiogram: dilated/hypertropic cardiomyopathy
Diagnosis
• culture: nose, throat,other mucocutaneous lesions
• Portion of the membrane should be removed and
submit with underlying exudate
24 | B a c t e - P e d i a
Clinical Manifestation
• Infection at other sites
– Ear (otitis externa), eye( purulent or ulcerative
conjunctivitis), genital tract (purulent and
ulcerative vulvovaginitis)
– Rare cases of septicemia
– Sporadic cases of endocarditis, pyogenic arthritis
Complications
• Toxic Neuropathy
-Parallel the extent of primary infection
-multiphasic ; acutely or 2-3 weeks after onset of
oropharyngeal inflammation
-Hypesthesia and local paralysis of soft palate occur commonly
-Weakness of posterior pharyngeal, laryngeal and facial nerves
may follow causing a nasal quality in the voice, difficulty in
swallowing and risk of death due to aspiration
-cranial neuropathy on 5th wk:oculomotor & ciliary paralysis
(starbismus,blurred vision,difficultty accomodation)
-symmetric polyneuropathy on 10th day-3rd month after
infection;primary motor deficiency w/ dec DTRs
-clinical & CSF fx indistinguishable to GBS
-complete recovery is likely
Treatment
• Antitoxin : mainstay of therapy
– Administered as empirical dose 20,000-
120,000 U based on degree of toxicity, site and
size of membrane and duration of illness
– Given early, immediately after clinical
diagnosis
– Not recommended for asymptomatic carriers
 Treatment Prevention
Antimicrobial therapy • Asymptomatic Case Contacts
• halt toxin production, treat localized infection, and prevent – Household contacts and with intimate respiratory or
transmission of the organism to contact
habitual physical contact with patient are closely
Aqueous Penicillin G monitored for illness through the 7 day incubation period
• 100,000-150,000 u/kg/24 hr divided q5 hr IV or IM
– Cultures of the nose, throat and skin lesions are performed
Erythromycin
40-50 mg/kg24 hours q6 PO – Antimicrobial prophylaxis is given regardless of
immunization status
-Therapy is given for 14 days
-Cutaneous diptheria : 7-10 days • erythromycin 40-50 mg/kg/24 hour qid po x 7 days
• Procaine penicillin G 600,000 U IM <30 kg
-Elimination of the organism should be documented by at least two 1.2 U IM for > 30 kg
successive cultures from the nose and throat obtained 24 hour apart
after completion of therapy – Diptheria toxoid vaccine is given to immunized individual
-Treatment with erythromycin is repeated if the culture result is positive who have not received booster dose within 5 years
-respiratory isolation until after cessation of TX – Children without booster dose should be vaccinated

Prevention Pertussis (intense cough)

• Asymptomatic carriers
– Antimicrobial prophylaxis is given for 7 days • Whooping cough
– Age appropriate preparation of diptheria toxoid is • Etiologic agents:
administered immediately if a booster has not been
given for 1 year 1. Bordetella pertussis (95%)
2. Bordetella parapertussis (less frequent)
– respiratory isolation or contact isolation until at least
two subsequent cultures obtained 24 hour apart after • Etiologic agents of pertussis-like illness:
cessation of therapy are negative
1. adenoviruses
Repeat cultures are performed = 2 weeks after 2. Chlamydia trachomatis
completion of therapy for cases and carriers; 3. Mycoplasma pneumoniae
- if (+) an additional 10 day course of oral
erythromycin should be given and follow up
cultures performed

Pertussis (intense cough) Pertussis

• highest risk: infants & young children
• Antigenic & Biologically active components of
Bordetella pertussis – pertussis in adults – imp’t source of infection in
unimmunized or partially immunized children
– fimbriae (pili)
– filamentous hemagglutinin (FHA) • transmission: droplet
– Pertussis Toxin: subunit A(enzymatically active) & subunit – transmissibility is greatest early in the illness
B (binding portion) during the catarrhal phase
– Adenylate Cyclase Toxin
• Incubation period: 6-21 days, usually 7-10
– Lipo-oligosaccharide (LOS)
– Tracheal Cytotoxin
days
– Pertactin

25 | B a c t e - P e d i a
 Diagonosis

Clinical
- suspected if predominant complaint of cough in the absence
of: fever,malaise,myalgia,exanthem,
enanthem,sorethroat,hoarseness,wheezes,rales
- clinical case definition:
cough>/= 14 days, w/ a least either paroxysms, whoop or
post-tussive vomiting
sensitivity:81% specificity:58%
- clues in infant<3 months: apnea or cyanosis before
appreciation of cough

Diagnosis Diagnosis
• Culture of nasopharynx: gold standard
Leucocytosis (15,000-100,00 cells.mm3)
- due to absolute lymphocytosis
-seen in the catarrhal stage • DFA: useful in with previous antibiotics
-severe course & death are correlated w/ extreme
leucocytosis n thrombocytosis • PCR : not widely available
Chest X-ray
-perihilar infiltrate or edema(sometimes,butterfly-like) • Antibody detection: not readily available
and variable atelectasis
-consolidation suggests secondary bacterial infx

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 Complications Treatment
Apnea /bradycardia
-secondary to laryngospasm or vagal stimulation before cough, Drug of choice: Erythromycin estolate
obstruction durind episode, or hypoxemia after episode -children: 50 mg/kg q 6h x 14days
Secondary infections: -abortive or attenuating only if given during
Otitis media
pre-paroxysmal stage
Bacterial pneumonia: most common cause of death
Physical sequelae of forceful coughing: -reduces communicability at any stage
-conjunctival/scleral hemorrhage • Alternative agent:
-petechiae on upper body – Cotrimoxazole
-epixtaxis
– Newer macrolides: azithro or clarithromycin
-seizures:secondary to hypoxemia, hemorrhage, hyponatremia,
alkalosis from vomiting
-subcutaneous emphysema
-pneumotharax
-umbilical /inguinal hernias

Prevention

Droplet precaution for 5 days after Erythromycin

Chemoprophylaxis:
-Erythromycin: 40-50mkd po in QID x 14 days
-Given to household and close contacts regardless of age or
immunization status
Active Immunization
-80% protective efficacy with household exposure w/ at least
3 doses
-whole cell vaccine (DTP)
-Acellular vaccine (DTaP)

Clinical Manifestations Clinical Manifestations

-biphasic course -most cases are subclinical or very mild; inapparent infection
Septicemic phase: common in high-risk occupational groups
- (+) leptospires from blood, csf, pther tissue
-initial symptoms last x 2-7 days -Symptomatic infection:
- may be followed by abrief period of well being
acute febrile illness w/ nonspecific signs/symptoms: 70&
Immune phase:
aseptic meningitis: 20%
-appearance of antibodies,(-) leptospires from blood, csf, (+)
hepatorenal dysfunction: 10%
localized signs & symptoms
-may persist in kidneys, urine & aqueous humor
-lasts for several weeks
-typically sudden onset, usually biphasic

27 | B a c t e - P e d i a
 Clinical manifestations
2 clinical syndromes: Clinical manifestations
2 clinical syndromes
1. Anicteric Leptospirosis
Anicteric Leptospirosis
-Septicemic phase:
-self-limited systemic illness abrupt, fever,chills, lethargy, severe, debilitating myalgia,
extreme muscle tenderness(lower extremities, lumbosacral
spine, abdomen), conjunctival suffusion w/photophobia &
-more common; 85-90% of cases orbital pain w/o disharge, generalized lymphadenopathy
hepatosplenomegaly, truncal rash (maculopapular, urticarial ,
hemorrhagis, desquamating)
-usually biphasic
-less common:pharyngitis, pneumonitis, athritis, carditis,
cholecystitis, orchitis

Clinical manifestations Clinical manifestations

2 clinical syndromes 2 clinical syndromes
Anicteric Leptospirosis 2. Icteric leptospirosis
Immune phase: -severe form in <10% of patients
-may follow a brief asymptomatic interlude -septicimic phase similar to anicteric type
-characterized by recurrence of fever & aseptic meningitis ; -immune phase characterized by clinical/laboratory evidence of
abnormal csf profiles( mod inc in pressures, pleocytosis w/ hepatorenal dysfunction
PMNs,slightly inc protein, normal sugar) in 80% of pts,only -hepatic manifestations: RUQ pain,hepatomegaly, jaundice,
50% modest increase in liver enzymes
w/ meningeal signs,resolve spontaneously w/in -renal manifestations: common, may dominate clinical
a week picture; all w/ renal abnormalities(hematuria,
-uveitis,unilateral or bilateral proteinuria,casts),azotemia w/ oliguria/anuria
-ARF in 16-40% 0f cases, principal cause of death
-hemmorrhage and CV collapse in fulminating cases

Diagnosis
Microcapsular agglutination test
Serology:
-usual basis for diagnosis -utilizes chemically stable microcapsules instead of sheep
Microscopic agglutination test ethrocytes
-appear by 12th day, maximum at 3rd week -detects IgM antibodies
-serogroup specific assay, using live antigen suspensions of -with greater specificity, higher titers and more sensitive in
leptospiral serovar
earlier stages
-read by darkfield microscopy for agglutination; titers are
determined <5 days of illness 33%
-definite:(>/=)fourfold rise in titer in paired`sera 6-7 days of illness 83%
-probable:single specimen >/=1:1600 >7 days of illness 96%

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 Treatment Supportive Management

‐initiation of treatment before 7th day will probably  • Fluid and electrolyte blance

shorten clinical course and decrease severity • Ensure adequate renal perfusion and fluid 
administration to prevent acute renal failure
Drug of choice: • (+) pre‐renal azotemia, diuress with fluids or 
Pen G Na  6‐8 million U/m2/24 hrs q 4 x 7 days colloids to establish volume
‐Mild disease: • If no response to diuresis wth fluids/ colloids, 
Doxycycline (not for pregnant women and children <  possible ATN‐> fluid restriction + diuretics & 
8 yrs old) 10‐20 mg/k/day PO q 6 for 7 day dopamine
• With severe prolonged azotemia: dialysis

Prevention and Control

1. Hygienic conditions in slaughter houses, farm 
yards, bathing pools
2. Avoidance of exposure to urine and tissues from 
infected animals
The End
3. Vaccination of animals • 
4. Rodent control Lord, thank you for everything,
I can’t name them all but it all comes from You,
5. Chemoprophylaxis everyday I am very grateful for everything!
Doxycycline: 200 mg 1x a week for people with 
significant short term exposure in environments 
w/ risk factors for transmission to humans

Edited by: K.D. Espino, 2009

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