1
Approach to Infectious Diseases and their prevention
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2
Antibiotic stewardship practices
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3Community-Acquired Infections
4
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Health Care?Associated Infections
5
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Gram-Positive Bacteria (part-1)6
Gram-Positive Bacteria (part-2)
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7
Gram-Negative Bacteria (part-1)
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8Gram-Negative Bacteria (part-2)
9
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Spirochetal Diseases
10
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Diseases Caused by Atypical/Miscellaneous Bacterial Infections11
Revision-cum-exam on bacteria (Must to know type)
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1
12
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Infections Due to DNA Viruses13
Infections Due to RNA Viruses (part 1)
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14
Infections Due to RNA Viruses (part 2)
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15HIV/AIDS ? part 1
16
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HIV/AIDS ? part 2
17
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Fungal Infections18
Parasitic Infections (part 1)
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19
Parasitic Infections (part 2)
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20Revision-cum-exam on Virus, Fungal, and Parasite (Must to know type)
Streptococcal Infections
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Pneumococcal Infections
Staphylococcal Infections
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Enterococcal InfectionsStreptococcal Infections
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Streptococcus, from the Greek streptos, meaning "twisted," and kokkos,meaning "berry"
Normal flora colonizing the human respiratory, gastrointestinal, and
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genitourinary tracts
Facultative anaerobes, although some are strict anaerobes, are Fastidious and
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grow best in 5% CO2Respiratory droplets are the usual mechanism of spread, although other routes,
including food-borne outbreaks been described
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GROUP A STREPTOCOCCI (GAS)
Elaborates a number of cell-surface components (M protein, Polysaccharide
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capsule) and extracellular products (streptolysins S and O, streptokinase,
DNAses, SpyCEP, several pyrogenic exotoxins)
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Differential diagnosis of streptococcal pharyngitis includes many, however,Symptoms and signs suggestive of viral infection to be ruled out (conjunctivitis,
coryza, cough, hoarseness, or discrete ulcerative lesions of the buccal or
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pharyngeal mucosa)
The throat culture remains the diagnostic gold standard (properly collected, by
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vigorous rubbing of a sterile swab over both tonsillar pillars)A rapid diagnostic kit for latex agglutination or enzyme immunoassay of swab
specimens is a useful adjunct with >95% specificity
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Treatment is given primarily to prevent suppurative complications and ARF AND
requires 10 days of penicillin treatment
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Complications
1. Suppurative complications result from the spread of infection from the pharyngeal
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mucosa to deeper tissues by direct extension or by the hematogenous or lymphaticroute and may include cervical lymphadenitis, peritonsillar or retropharyngeal
abscess, sinusitis, otitis media, meningitis, bacteremia, endocarditis, and pneumonia
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2. Local complications, such as peritonsillar or parapharyngeal abscess formation,
3. Nonsuppurative complications include ARF and PSGN
ARF is not a sequela to streptococcal skin infections, although PSGN may follow either skin
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or throat infection. The reason for this difference is not known.
One hypothesis is that the immune response necessary for development of ARF occurs only
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after infection of the pharyngeal mucosa.In addition, the strains of GAS that cause pharyngitis are generally of different M protein
types than those associated with skin infections.
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up to 20% of individuals in certain populations may have asymptomatic pharyngeal
colonization
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When a carrier is transmitting infection to others, attempts to eradicate carriage arewarranted, but no specific treatment/guidelines
Pneumococcal Infections
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Belongs to the -hemolytic group, but growth is inhibited in the presence of
optochin (ethylhydrocupreine hydrochloride), and bile soluble
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Rapid and dramatic changes in the epidemiology of during the past decadeafter routine childhood vaccine (PCV)
Not all pneumococcal serotypes are equally likely to cause disease; serotype
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distribution varies by age, disease syndrome, and geography
Intermittent inhabitants of the healthy human nasopharynx and are transmitted
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by respiratory dropletsSpread either via the bloodstream to distant sites or locally to mucosal surfaces
In children, nasopharyngeal ecology varies by geographic region,
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socioeconomic status, climate, degree of crowding, and particularly intensity ofexposure to other children
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Invasive pneumococcal disease (IPD)Pathophysiology of severe pneumococcal pneumonia among adults reflects a
rapidly progressive cascade of events that often unfolds irrespective of
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antibiotic administration
Rates of pneumococcal disease vary by season, by sex, and by risk group
Local cytokine production after a viral infection is thought to upregulate
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adhesion factors
Delayed ontogeny of capsule-specific IgG in young children is associated with
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susceptibility to infectionThere is no pathognomonic presentation of pneumococcal disease
The suspicion should be in differential diagnosis of
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pneumonia,otitis media,
fever of unknown origin, and
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meningitis
Clinical syndromes
Classified as noninvasive (e.g., otitis media and nonbacteremic pneumonia) or
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invasive (e.g., bacteremic pneumonia)
The presentation of pneumococcal pneumonia does not reliably distinguish it
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from pneumonia of other etiologiesThe differential diagnosis includes
Cardiac conditions such as myocardial infarction and heart failure with atypical
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pulmonary edema;
Pulmonary conditions such as atelectasis; and pneumonia caused by viral pathogens,
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mycoplasmas, Haemophilus influenzae, Klebsiel a pneumoniae, Staphylococcusaureus, Legionel a, or (in immunocompromised hosts) Pneumocystis
Cholecystitis, appendicitis, perforated peptic ulcer disease, and subphrenic abscesses
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Pneumonia
The gold standard for etiologic diagnosis of pneumococcal pneumonia is
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pathologic examination of lung tissueGram's staining and culture of sputum
Chest radiography helps in diagnosis, but an infiltrate can be absent either early
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in the course of the illness or with dehydration; upon rehydration, an infiltrateusually appears
The appearance varies; lobar or segmental or patchy consolidation
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Parapneumonic effusions are more common than empyemaPleural fluid with frank pus, bacteria, or a pH of 7.1 indicates empyema
Blood cultures are positive in a minority (<30%)
Urinary pneumococcal antigen assays; important among whom
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nasopharyngeal colonization is relatively lowMeningitis
Pneumococcal meningitis typically presents as a pyogenic condition that is
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clinically indistinguishable from meningitis of other bacterial etiologiesDefinitive diagnosis of pneumococcal meningitis rests on CSF examination
(1) evidence of turbidity (visual inspection);
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(2) elevated protein level, elevated white blood cel count, and reduced glucose
concentration (quantitative measurement); and
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(3) specific identification of the etiologic agent (culture, Gram's staining, antigentesting, or polymerase chain reaction [PCR])
Blood culture or detection of antigen in urine is considered highly specific
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Mortality rate for pneumococcal meningitis is ~20%Other Invasive Syndromes
Primary bacteremia without other sites of infection (bacteremia without a
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source; occult bacteremia),
Osteomyelitis
Septic arthritis
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EndocarditisPericarditis
Peritonitis
The essential diagnostic approach is collection of fluid from the site of infection
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by sterile technique and examination by Gram's staining, culture, and--when
relevant--capsular antigen assay or PCR
Noninvasive Syndromes
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Otitis media is the most common pneumococcal syndrome and most often
affects young children
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Sinusitis presents with facial pain, congestion, fever, and-- in many cases--persistent nighttime cough
Treatment
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Meningitis: Vancomycin (adults, 30?60 mg/kg per day) and cefotaxime or
ceftriaxone (adults, 4 g/d in 1 dose or 2 divided doses)
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If hypersensitive to -lactam agents, rifampin (adults, 600 mg/d) can besubstituted
A repeat lumbar puncture should be considered after 48 h
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if the organism is not susceptible to penicil in and information on cephalosporin
sensitivity is not yet available,
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if the patient's clinical condition does not improve or deteriorates, orif dexamethasone has been administered and may be compromising clinical
evaluation.
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When antibiotic sensitivity data become available, treatment should bemodified accordingly
Glucocorticoids significantly reduce rates of mortality, severe hearing loss, and
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neurologic sequelae in adults and should be administered to those with
community-acquired bacterial meningitis
FOR INVASIVE INFECTIONS (EXCLUDING
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MENINGITIS)
For Noncritical illness, ceftriaxone, 50?75 mg/d (doses 12?24 h apart)
For critically illness, including those who have myocarditis or multilobular
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pneumonia with hypoxia or hypotension, vancomycin may be added if the
isolate may possibly be resistant to -lactam drugs, with its use reviewed
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once susceptibility data become availableFor outpatient management, amoxicillin (1 g every 8 h) may be given
The optimal duration of treatment for pneumococcal pneumonia is
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uncertain, but its continuation for at least 5 days once the patient becomesafebrile appears to be a prudent approach
Amoxicillin (80?90 mg/kg per day) is recommended for acute otitis media or
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sinusitis
Prevention
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1. Vaccination against S. Pneumoniae and influenza viruses,2. Reduction of comorbidities that increase the risk of pneumococcal disease,
3. Prevention of antibiotic overuse
PPSV23 for all persons 65 years of age and for those 2?64 years of age who
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have underlying medical conditions that put them at increased risk for
pneumococcal disease or, if infected, disease of increased severity
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It does not induce an anamnestic response, and antibody concentrations waneover time; thus revaccination is particularly important
PCV13 followed by a dose of PPSV23 is now recommended for all
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immunocompromised children and adults
Staphylococcal Infections
S. aureus is a pluripotent pathogen (both a commensal and an opportunistic),
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causing disease through both toxin- and non-toxin-mediated (pyogenic)mechanisms
Leading cause of health care?associated infections
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Approximately 30% of healthy persons are colonized with S. aureus, with a smallerpercentage (~10%) persistently colonized
The rate of colonization is elevated among insulin-dependent diabetics, HIV-infected
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patients, patients undergoing hemodialysis, injection drug users, and individuals with
skin damage
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More infections also with neutropenic patients, those with chronic granulomatousdisease, and those with Job's or Chediak-Higashi syndrome
The anterior nares and oropharynx are frequent sites of human colonization,
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although the skin (especially when damaged), vagina, axilla, and perineum may
also be colonized
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Transmission of S. aureus most frequently results from direct personal contact, rarely inaerosols
In recent outbreaks for CA-MRSA, Risk factors common to these outbreaks include
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poor hygienic conditions, close contact, contaminated material, and damaged skin
Pathogenesis
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1. Contamination and colonization of host tissue surfaces,2. Breach of cutaneous or mucosal barriers,
3. Establishment of a localized infection,
4. Invasion
5. Evasion of the host response; an antiphagocytic polysaccharide microcapsule and
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intracel ular survival including host response
6. Metastatic spread
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It produces three types of toxin:cytotoxins,
pyrogenic toxin superantigens, and
Exfoliative toxins.
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Antitoxin antibodies are protective against illness in TSS, staphylococcal food
poisoning, and staphylococcal scalded-skin syndrome (SSSS), however, Illness
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develops after toxin synthesis and absorption and the subsequent toxin-initiated hostresponse
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Diagnosis
Gram's stain and microscopic examination of abscess contents or of
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infected tissueRoutine culture of infected material and blood cultures (S. aureus is rarely a
blood culture contaminant)
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Uniformly positive blood cultures suggest an endovascular infection such as
endocarditis
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Polymerase chain reaction (PCR)?based assays have also been applied tothe rapid diagnosis
Treatment
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Surgical incision and drainage of all suppurative collections, and device
removal constitute the most important therapeutic intervention
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Prolonged (4?6 weeks) antibioticsPrevention and other staphs
1. Primary prevention of S. aureus infections in the hospital setting involves hand
washing and careful attention to appropriate isolation procedures
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2. Decolonization strategies, using both universal and targeted approaches with
topical agents
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3. "Bundling" for nosocomial infections4. Immunization strategies failed
Less virulent than S. aureus, CoNS are among the most common causes of
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prosthetic-device infectionsStaphylococcus epidermidis is found on the skin as well as in the oropharynx
and vagina
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Staphylococcus saprophyticus is a common pathogen in UTIs
Staphylococcus lugdunensis and Staphylococcus schleiferi, produce more
serious infections (native valve endocarditis and osteomyelitis)
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Only 10?25% of blood cultures positive for CoNS reflect true bacteremia
Enterococcal Infections
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Normal inhabitants of the large bowel of human adults, two species, E. faecalis andEnterococcus faecium
Originally classified as streptococci but Only after DNA hybridization studies and later 16S rRNA
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sequencing enterococci grouped as a genus distinct
They hydrolyze esculin in the presence of 40% bile salts and grow at high salt concentrations
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(e.g., 6.5%) and at high temperatures (46?C)Main reason for Increased gastrointestinal colonization by enterococci is the administration of
antimicrobial agents, In particular, that are excreted in the bile and have broad-spectrum
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activity
Second most common organisms (after staphylococci) isolated from hospital associated
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infections in the United StatesThe most important factors associated with VRE colonization and persistence in the gut include
1. Prolonged hospitalization;
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2. Long courses of antibiotic therapy;3. Hospitalization in long-term-care facilities, surgical units, and/or intensive care units;
4. Organ transplantation;
5. Renal failure (particularly in patients undergoing hemodialysis) and/or diabetes;
6. High acute physiology and chronic health evaluation (APACHE) scores;
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7. Physical proximity to patients infected or colonized with VRE or these patients' roomsCLINICAL SYNDROMES
Urinary tract infection and prostatitis
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Bacteremia and endocarditisMeningitis
Intraabdominal, pelvic, and soft tissue infections
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Neonatal infections, including sepsis (mostly late-onset), bacteremia,
meningitis, pneumonia, and UTI
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TreatmentIntrinsically resistant and/or tolerant to several antimicrobial agents
Tolerance defined as lack of killing by drug concentrations 32 times higher
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than the minimal inhibitory concentration [MIC])Combination therapy with a cell wall?active agent and an aminoglycoside
has been the standard of care
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The treatment of E. faecalis dif ers substantial y from that of E. faecium,
mainly because of differences in resistance profiles
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Thank you