3. Staphylococca
l infections
• Gram positive cocci
• Staph aureus – coagulase positive
• Colonizes the nares/axilla/perineum
• Staph saprophyticus/epidermidis –
coagulase negative (CONS)
• Mode of spread is usually direct
contact or by fomites
5. Clinical
feature
s
Usually skin infections are the commonest
Furuncles, impetigo, carbuncles, abscesses and cellulitis
Invades the fascia causing necrotizing fasciitis
Staphylococcal scalded skin syndrome is caused by S.
aureus toxins, leads to massive desquamation and
denudation
Sinusitis, otitis media, pneumonia, lung abscesses
and
empyema
6. • Acute infective endocarditis – S.
aureus is the most common
• Usually if using prosthetic valves
• Sometimes no risk factors!
• Rapidly progressive and locally
destructive
• Musculoskeletal infections
• Osteomyelitis
• Septic arthritits
• Pyomyositis
7. Toxic shock
syndrome
(TSS)
• Locally invasive toxigenic strain of S.
aureus
• Fever
• Shock
• Skin rash
• Hepatic derangement
• Sensorial changes
• High mortality
8. CONS
• Lower virulence than S. aureus
• Skin colonisers
• Usually contaminants when taking
blood samples
• LBW babies
• Central venous catheters
• Dialysis catheters
• Prosthetic joints
• UTI
• Post op surgical site infections
9. Treatmen
t
• Surgical drainage
• Antibiotics
• 90% are resistant to penicillin
• Most are resistant to penicillinase
resistant penicillin's like cloxacillin and
methicillin
• Use vancomycin and linezolid, if MRSA
12. Streptococcus
• GAS , S.pyogenes:
one of the most common bacterial
infections of school-age children, post
infectious syndromes of ARF and PSGN.
• GBS, S. agalactiae:
cause of bacterial sepsis and meningitis
in newborns
• Viridans streptococci:
are the most common cause of
bacterial
endocarditis
• Enterococci:
E. faecalis, E. faecium
14. Pharyngiti
s
• The incubation period is 1–4 days
• Symptoms include:
• Sorethroat
• Fever andchills
• malaise
• sometimes abdominal complaints
and vomiting, particularly in
children
• Symptoms are mild tosevere
14
15. Diagnosi
s
• The throat culture remains the
diagnostic gold standard
• Vigorous rubbing of a sterile swab
over both tonsillar pillars
• Rapid diagnostic kits generally are
>95% specific
• A negative result should be confirmed
by throat culture
15
19. Early-
onset
infect
ions
Occur within the first week of life
Acquired from the colonized
maternal
genital tract
Prematurity and maternal risk factors
(prolonged labor
, obstetric complications,
and maternal fever)
Presentation of neonatal
sepsis
Pneumonia, respiratory
distress
Lethargy
Hypotension
Bacteremic
Meningitis
20. Late-onset
infections
occur in infants 1 week to 3 months old
acquired during delivery or during later
contact witha colonized mother
, nursery
personnel, or another source
Meningitis is the most common
manifestation
fever
, lethargy or irritability
, poor feeding,
and
seizures
Bacteremia, osteomyelitis, septic
arthritis, and facial cellulitis,
submandibular or preauricular adenitis
21. Prevention
Identification of high-risk carrier mothers
and treatment with antibiotic or
immunoprophylaxis
Screening for anogenital colonization at
35–37 weeks of pregnancy by a swab
culture of the lower vagina and anorectum
Risk factors: preterm delivery, early rupture
of membranes (>24 h before delivery),
prolonged labor, fever, or chorioamnionitis
Vaccine may be for future
22. Pertussi
s
Bordetella pertussis
Infancy and early childhood
Intense spasmodic cough
Prevalence has reduced worldwide following aggressive vaccination
Spreads via aerosol droplets
Attack rates are almost 100% in susceptible children
Adults are usually the reservoir for B.pertussis
23. Pertussis
Incubation period – 7-14 days
Clinical picture in 3 phases
Catarrhal phase - 1-2 weeks
Paroxysmal phase - 2-6 weeks
Convalescent phase - 1-4 weeks
24. Catarrha
l phase
• Most infectious period
• Present like an URI
• But, cough increases in severity
• More at night
25. Paroxysma
l phase
• Cough progresses to episodic spasms
• Increasing intensity
• Culminates in a high pitch inspiratory
whoop
• Thick mucus secretion
• Infants may present with cyanosis
and
apneic spells
27. Complications
Respiratory – otitis media, pneumonia, emphysema,
atelectasis
Neurological – seizures, encephalopathy
Bleeding episodes – epistaxis, sub
conjunctival/retinal hg
Poor feeding leading to acute malnutrition
Flare up of TB
28. Diagnosis
USUALLY CLINICALLY LOW ESR MAY BE
PRESENT
LYMPHOCYTIC
LEUKOCYTOSIS
NASOPHARYNGEAL
SWAB TO IDENTIFY
THE ORGANISM
BORDET GENGOU
MEDIUM
USUALLY POSITIVE IN
THE CATARRHAL
AND PAROXYSMAL
STAGE
31. Leptospirosis
• Spirochetes
• Usually tropical and sub tropical
countries
• World wide distribution
• Rats are usually the principal reservoirs
• Shed via urine
• Can live in soil for weeks if moist
• Common during flooding
32. Pathogenesis
Leptospira enter the body via cuts and
abrasions
Hematogenous spread
Endothelial lining of blood vessels are
damaged
Hemorrhage and ischemic damage occurs
33. Clinical
feature
s
Varies from asymptomatic infection to MODS (usually
fatal)
70% present with anicteric febrile illness
20% present with aseptic meningitis
5-10% present with Weil disease
Incubation period is 1-2 weeks
Illness has a biphasic course
Septicemic phase
Leptospiruric phase
35. Septicemic
phase, cont
Photophobia Orbital pain
Conjunctival
effusion
Generalized
lymphadenopathy
Hepato
spenomegaly
Transient
maculopapular rash
in 10% of cases
In some cases acute
respiratory distress
occurs
But most children
are
asymptomatic
36. Leptospiruri
c phase
• In some children,
• Due to: leptospira localizes to specific
tissues
• Organism persists in tissues like kidney
and aqueous humor
Children can develop
• Uveitis, aseptic meningitis with
recurrence of fever
• Encephalitis, paralysis etc are rare
37. Weils disease
(Icteric
leptospirosis)
• After the initial phase of fever, severe
hepatic and renal dysfunction
occurs
• Jaundice with hepatomegaly
• 20% will have splenomegaly
• Renal failure can develop during the
second week
• Patients will have hematuria,
proteinuria and casts in urine
• Oliguria/anuria is common
• Mortality is 5-15%
38. Diagnosis
CBC: Anemia, leukocytosis with polymorphs
predominantly and thrombocytopenia
Liver enzymes are elevated with SGOT more than SGPT
CPK is high
Elevated serum creatinine, deranged coagulation
parameters and direct jaundice
Gold standard for serologic assessment is the
Microscopic agglutination test (MAT)
IgM ELISA can be done after 5 days of illness
39. Leptospirosi
s treatment
As early as possible!
Oral antibiotic treatment – amoxicillin and
doxycycline in children more than 8 yrs of
age
IV penicillin (6-8 million units) q4 for 7
days is the drug of choice
IV ceftriaxone is a viable alternative
40. Preventio
n (lepto)
Avoid exposure to
contaminated water
Single dose of doxycycline after
exposure can prevent illness
but is not recommended
41. Enteric fever
• Typhoid fever – salmonella enterica var
typhi
• Paratyphoid fever – S. enterica var
paratyphi A, B, C
• 20 % of all cases of enteric fever caused by
paratyphi group
• Spread is via feco oral route
• Most common cause of fever lasting more
than 7 days in india
• Gram negative, non lactose fermenting
flagellate bacterium
42. Enteric fever,
cont
• In the intestines the organism
penetrates the mucosa and infects the
lymphoid follicles, liver and spleen
• Multiplies in the reticuloendothelial
system
• Incubation period is 7-14 days
• Then disseminates into the blood
stream
• This spillage brings about the clinical
features
43. Enteric fever
clinical
features
Low grade fever
in a step ladder
pattern
Peaks to high
grade fever by
end of first week
With fever there
will be,
Headache Malaise Anorexia
Abdominal pain Diarrhea
Constipation is
rare in
children
45. Complication
s
• Intestinal complications like bleeding or
perforation mostly in adults
• Severe enteric fever is when,
neurological complications are present
• Delirium
• Coma
• Stupor
• Shock
• Mortality rates are as high as 50%
47. Enteric fever,
relapse
• Occurs in 5-15% of cases
• Usually a milder illness
• Usually depends on the drugs used
to treat the initial illness
• Carrier state
• 5-10% of adult patients can shed
salmonella in stool for 90 days
• 1-4% of them can shed up to a year
• In children usually not seen
48. Diagnosis
Low to normal leucocyte counts with neutrophilic predominance
Anemia and thrombocytopenia in advanced cases
Mild elevation of liver enzymes
High CRP
Gold standard is by blood culture
Bile broth medium or BACTEC gives better recovery of organisms
Bone marrow will give higher pathogen yield
49. Widal test
• Detects the presence of IgG and IgM
antibodies to ,
• H (Flagellar antigen) of S. typhi and para
typhi A & B
• 0 (Somatic antigen) of typhi and para typhi
• Single titer of 1:160 for both O and H is
considered positive
• Sensitivity and specificity of the test is low
50. Treatmen
t
Ceftriaxone
and cefixime
are the first
line drugs
Azithromyci
n is also
used as an
alternative
agent
Dose of
cefixime is 20
mg/kg/day
Azithromyci
n dose is 10-
20
mg/kg/day
