Download MBBS (Bachelor of Medicine, Bachelor of Surgery) General Medicine 2022 PPT 1 Gp Infections Part I Lecture Notes
Infectious diseases
4/5th Semester Classes on Infectious Diseases, 8-9AM, Tuesdays (LT-1)
Topics
1
Approach to Infectious Diseases and their prevention
2
Antibiotic stewardship practices
3
Community-Acquired Infections
4
Health Care?Associated Infections
5
Gram-Positive Bacteria (part-1)
6
Gram-Positive Bacteria (part-2)
7
Gram-Negative Bacteria (part-1)
8
Gram-Negative Bacteria (part-2)
9
Spirochetal Diseases
10
Diseases Caused by Atypical/Miscellaneous Bacterial Infections
11
Revision-cum-exam on bacteria (Must to know type)
1
12
Infections Due to DNA Viruses
13
Infections Due to RNA Viruses (part 1)
14
Infections Due to RNA Viruses (part 2)
15
HIV/AIDS ? part 1
16
HIV/AIDS ? part 2
17
Fungal Infections
18
Parasitic Infections (part 1)
19
Parasitic Infections (part 2)
20
Revision-cum-exam on Virus, Fungal, and Parasite (Must to know type)
Streptococcal Infections
Pneumococcal Infections
Staphylococcal Infections
Enterococcal Infections
Streptococcal Infections
Streptococcus, from the Greek streptos, meaning "twisted," and kokkos,
meaning "berry"
Normal flora colonizing the human respiratory, gastrointestinal, and
genitourinary tracts
Facultative anaerobes, although some are strict anaerobes, are Fastidious and
grow best in 5% CO2
Respiratory droplets are the usual mechanism of spread, although other routes,
including food-borne outbreaks been described
GROUP A STREPTOCOCCI (GAS)
Elaborates a number of cell-surface components (M protein, Polysaccharide
capsule) and extracellular products (streptolysins S and O, streptokinase,
DNAses, SpyCEP, several pyrogenic exotoxins)
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
pharyngeal mucosa)
The throat culture remains the diagnostic gold standard (properly collected, by
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
Treatment is given primarily to prevent suppurative complications and ARF AND
requires 10 days of penicillin treatment
Complications
1. Suppurative complications result from the spread of infection from the pharyngeal
mucosa to deeper tissues by direct extension or by the hematogenous or lymphatic
route and may include cervical lymphadenitis, peritonsillar or retropharyngeal
abscess, sinusitis, otitis media, meningitis, bacteremia, endocarditis, and pneumonia
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
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
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.
up to 20% of individuals in certain populations may have asymptomatic pharyngeal
colonization
When a carrier is transmitting infection to others, attempts to eradicate carriage are
warranted, but no specific treatment/guidelines
Pneumococcal Infections
Belongs to the -hemolytic group, but growth is inhibited in the presence of
optochin (ethylhydrocupreine hydrochloride), and bile soluble
Rapid and dramatic changes in the epidemiology of during the past decade
after routine childhood vaccine (PCV)
Not all pneumococcal serotypes are equally likely to cause disease; serotype
distribution varies by age, disease syndrome, and geography
Intermittent inhabitants of the healthy human nasopharynx and are transmitted
by respiratory droplets
Spread either via the bloodstream to distant sites or locally to mucosal surfaces
In children, nasopharyngeal ecology varies by geographic region,
socioeconomic status, climate, degree of crowding, and particularly intensity of
exposure to other children
Invasive pneumococcal disease (IPD)
Pathophysiology of severe pneumococcal pneumonia among adults reflects a
rapidly progressive cascade of events that often unfolds irrespective of
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
adhesion factors
Delayed ontogeny of capsule-specific IgG in young children is associated with
susceptibility to infection
There is no pathognomonic presentation of pneumococcal disease
The suspicion should be in differential diagnosis of
pneumonia,
otitis media,
fever of unknown origin, and
meningitis
Clinical syndromes
Classified as noninvasive (e.g., otitis media and nonbacteremic pneumonia) or
invasive (e.g., bacteremic pneumonia)
The presentation of pneumococcal pneumonia does not reliably distinguish it
from pneumonia of other etiologies
The differential diagnosis includes
Cardiac conditions such as myocardial infarction and heart failure with atypical
pulmonary edema;
Pulmonary conditions such as atelectasis; and pneumonia caused by viral pathogens,
mycoplasmas, Haemophilus influenzae, Klebsiel a pneumoniae, Staphylococcus
aureus, Legionel a, or (in immunocompromised hosts) Pneumocystis
Cholecystitis, appendicitis, perforated peptic ulcer disease, and subphrenic abscesses
Pneumonia
The gold standard for etiologic diagnosis of pneumococcal pneumonia is
pathologic examination of lung tissue
Gram's staining and culture of sputum
Chest radiography helps in diagnosis, but an infiltrate can be absent either early
in the course of the illness or with dehydration; upon rehydration, an infiltrate
usually appears
The appearance varies; lobar or segmental or patchy consolidation
Parapneumonic effusions are more common than empyema
Pleural 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
nasopharyngeal colonization is relatively low
Meningitis
Pneumococcal meningitis typically presents as a pyogenic condition that is
clinically indistinguishable from meningitis of other bacterial etiologies
Definitive diagnosis of pneumococcal meningitis rests on CSF examination
(1) evidence of turbidity (visual inspection);
(2) elevated protein level, elevated white blood cel count, and reduced glucose
concentration (quantitative measurement); and
(3) specific identification of the etiologic agent (culture, Gram's staining, antigen
testing, or polymerase chain reaction [PCR])
Blood culture or detection of antigen in urine is considered highly specific
Mortality rate for pneumococcal meningitis is ~20%
Other Invasive Syndromes
Primary bacteremia without other sites of infection (bacteremia without a
source; occult bacteremia),
Osteomyelitis
Septic arthritis
Endocarditis
Pericarditis
Peritonitis
The essential diagnostic approach is collection of fluid from the site of infection
by sterile technique and examination by Gram's staining, culture, and--when
relevant--capsular antigen assay or PCR
Noninvasive Syndromes
Otitis media is the most common pneumococcal syndrome and most often
affects young children
Sinusitis presents with facial pain, congestion, fever, and-- in many cases--
persistent nighttime cough
Treatment
Meningitis: Vancomycin (adults, 30?60 mg/kg per day) and cefotaxime or
ceftriaxone (adults, 4 g/d in 1 dose or 2 divided doses)
If hypersensitive to -lactam agents, rifampin (adults, 600 mg/d) can be
substituted
A repeat lumbar puncture should be considered after 48 h
if the organism is not susceptible to penicil in and information on cephalosporin
sensitivity is not yet available,
if the patient's clinical condition does not improve or deteriorates, or
if dexamethasone has been administered and may be compromising clinical
evaluation.
When antibiotic sensitivity data become available, treatment should be
modified accordingly
Glucocorticoids significantly reduce rates of mortality, severe hearing loss, and
neurologic sequelae in adults and should be administered to those with
community-acquired bacterial meningitis
FOR INVASIVE INFECTIONS (EXCLUDING
MENINGITIS)
For Noncritical illness, ceftriaxone, 50?75 mg/d (doses 12?24 h apart)
For critically illness, including those who have myocarditis or multilobular
pneumonia with hypoxia or hypotension, vancomycin may be added if the
isolate may possibly be resistant to -lactam drugs, with its use reviewed
once susceptibility data become available
For outpatient management, amoxicillin (1 g every 8 h) may be given
The optimal duration of treatment for pneumococcal pneumonia is
uncertain, but its continuation for at least 5 days once the patient becomes
afebrile appears to be a prudent approach
Amoxicillin (80?90 mg/kg per day) is recommended for acute otitis media or
sinusitis
Prevention
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
have underlying medical conditions that put them at increased risk for
pneumococcal disease or, if infected, disease of increased severity
It does not induce an anamnestic response, and antibody concentrations wane
over time; thus revaccination is particularly important
PCV13 followed by a dose of PPSV23 is now recommended for all
immunocompromised children and adults
Staphylococcal Infections
S. aureus is a pluripotent pathogen (both a commensal and an opportunistic),
causing disease through both toxin- and non-toxin-mediated (pyogenic)
mechanisms
Leading cause of health care?associated infections
Approximately 30% of healthy persons are colonized with S. aureus, with a smaller
percentage (~10%) persistently colonized
The rate of colonization is elevated among insulin-dependent diabetics, HIV-infected
patients, patients undergoing hemodialysis, injection drug users, and individuals with
skin damage
More infections also with neutropenic patients, those with chronic granulomatous
disease, and those with Job's or Chediak-Higashi syndrome
The anterior nares and oropharynx are frequent sites of human colonization,
although the skin (especially when damaged), vagina, axilla, and perineum may
also be colonized
Transmission of S. aureus most frequently results from direct personal contact, rarely in
aerosols
In recent outbreaks for CA-MRSA, Risk factors common to these outbreaks include
poor hygienic conditions, close contact, contaminated material, and damaged skin
Pathogenesis
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
intracel ular survival including host response
6. Metastatic spread
It produces three types of toxin:
cytotoxins,
pyrogenic toxin superantigens, and
Exfoliative toxins.
Antitoxin antibodies are protective against illness in TSS, staphylococcal food
poisoning, and staphylococcal scalded-skin syndrome (SSSS), however, Illness
develops after toxin synthesis and absorption and the subsequent toxin-initiated host
response
Diagnosis
Gram's stain and microscopic examination of abscess contents or of
infected tissue
Routine culture of infected material and blood cultures (S. aureus is rarely a
blood culture contaminant)
Uniformly positive blood cultures suggest an endovascular infection such as
endocarditis
Polymerase chain reaction (PCR)?based assays have also been applied to
the rapid diagnosis
Treatment
Surgical incision and drainage of all suppurative collections, and device
removal constitute the most important therapeutic intervention
Prolonged (4?6 weeks) antibiotics
Prevention and other staphs
1. Primary prevention of S. aureus infections in the hospital setting involves hand
washing and careful attention to appropriate isolation procedures
2. Decolonization strategies, using both universal and targeted approaches with
topical agents
3. "Bundling" for nosocomial infections
4. Immunization strategies failed
Less virulent than S. aureus, CoNS are among the most common causes of
prosthetic-device infections
Staphylococcus epidermidis is found on the skin as well as in the oropharynx
and vagina
Staphylococcus saprophyticus is a common pathogen in UTIs
Staphylococcus lugdunensis and Staphylococcus schleiferi, produce more
serious infections (native valve endocarditis and osteomyelitis)
Only 10?25% of blood cultures positive for CoNS reflect true bacteremia
Enterococcal Infections
Normal inhabitants of the large bowel of human adults, two species, E. faecalis and
Enterococcus faecium
Originally classified as streptococci but Only after DNA hybridization studies and later 16S rRNA
sequencing enterococci grouped as a genus distinct
They hydrolyze esculin in the presence of 40% bile salts and grow at high salt concentrations
(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
activity
Second most common organisms (after staphylococci) isolated from hospital associated
infections in the United States
The most important factors associated with VRE colonization and persistence in the gut include
1. Prolonged hospitalization;
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;
7. Physical proximity to patients infected or colonized with VRE or these patients' rooms
CLINICAL SYNDROMES
Urinary tract infection and prostatitis
Bacteremia and endocarditis
Meningitis
Intraabdominal, pelvic, and soft tissue infections
Neonatal infections, including sepsis (mostly late-onset), bacteremia,
meningitis, pneumonia, and UTI
Treatment
Intrinsically resistant and/or tolerant to several antimicrobial agents
Tolerance defined as lack of killing by drug concentrations 32 times higher
than the minimal inhibitory concentration [MIC])
Combination therapy with a cell wall?active agent and an aminoglycoside
has been the standard of care
The treatment of E. faecalis dif ers substantial y from that of E. faecium,
mainly because of differences in resistance profiles
Thank you
This post was last modified on 05 April 2022