- Streptococcus - Staphylococcus - NGA Strep - NGB Strep

1. Stapylococcus Strep Pneumonia NGA Strep NGB Strep
Gram +ve Bacteria
Staphylococcus
Group 5: ClinMed /21
“I’m OK on your skin, but
please DON’T let me in”

2. - Gram positive
- Cocci (spherical)
- Aerobic
- Grow in pairs n clusters
- Normal flora in humans (ubiquitous)
- Coagulase +/-
- Resistant to heat n dryng
• Mainly found on the skin n nares
• Most clinically significant strain
• Common cause of skin n soft tissue
pyogenic infectn
• Coagulase +
• Beta-hemolysis (complete) on blood agar
• Some are MRSAs [Methicillin-resistant
S.aureus] => Beta-lactam antibiotics
resistant
STAPHYLOCOCCUS | DEFINITION
Attributes S. aureus

3. Contributing Factors
• Colonization: colonizes skin n mucous
memb
• Skin trauma: entry of bact. Into the body
• Weakened immune system: bact.
Overgrowth
• HAI: invasive procedures, or surgical site
contamination
• CAI: sharing personal items, contact sports,
direct contact
Causes  virulence factors
• Capsule: Some strains produce a
polysaccharide capsule/slime layer,
interfering with opsonophagocytosis.
• Clumping Factor and Coagulase: interfere
with phagocytosis and promote clotting,
aiding in abscess formation.
• Protein A: Interacts with immunoglobulin G
(IgG), preventing antibodies from acting as
opsonins.
• Enzymes: catalase (inactivates hydrogen
peroxide), penicillinase /β-lactamase
(inactivates penicillin), n lipase (assoc w skin
infctn).
• Hemolysins: e.g α-toxin, β-hemolysin, δ-
hemolysin, n Panton-Valentine leukocidin,
cause tissue necrosis n increase permeab.
of leukocytic cell memb, leading 2 cell death.
ETIOLOGY

4. • Exotoxins: e.g exfoliatins (cause skin
separation), enterotoxins (cause food
poisoning), n toxic shock syndrome toxin-1
(associated with toxic shock syndrome).
Intrinsic Factors:
• Teichoic Acid: Mediates adhesion to
mucosal cells.
• Proteins: Promote adhesion to various
human proteins.
• Antibiotic Resistance Mechanisms:
productn of penicillinase n altered penicillin-
binding proteins (PBPs), leading to
methicillin-resistant S. aureus (MRSA).
• Colonization: starts w colonization of S.
aureus on the skin or mucosal surfaces.
• Skin Disruption: such as wounds, burns,
eczema, or medical procedures like
ventriculoperitoneal shunts or catheter
insertions, provides entry points for S.
aureus.
• Toxins n Enzymes: produces toxins n
enzymes that invade tissues or cause injury,
thus disease manifestation.
Risk Factors
• Corticosteroid treatment, malnutrition,
ETIOLOGY Ct.
Pathogenesis

5. azotemia (BUN, Cr), n antibiotic therapy w
drugs to which S. aureus is resistant
• Viral RTIs (influenza) – predispose to
secondary staph infect
• Immune Dysfunction: defective
phagocytosis and killing; Pts with HIV
infection
• Skin infections: Impetigo (cantagiosa n
bullous); Furuncles (boils); abscess;
cellulitis; SSS n SSF
Rubor et tumor cum dolore et pus
• RTIs: Otitis media, sinusitis, suppurative
parottitis } => rare
• Pneumonia: High fever; tachypnea,
dyspnea, cough; abdominal pain
• Sepsis: Fever, chills, nausea, myalgia,
tachycardia, hypotension, confusn; Vegetatn
depositn in valves, lungs, joints
• Muscle infections: Pyomyositis (muscle
abscesses)
• Bone n jt. Infectn: Osteomyelitis,
suppurative arthritis
• TSS [Toxic Shock Syndrome]: Fever,
shock, scarlet fever-like rash
• Food poisioning: Nausea, vomiting;
Diarrhea, abdominal cramps
• Others: meningitis; endocarditis; peritonitis
Pathogen. Ct.
Clinical feat

6. Lange: Review of Medical Microbiology and
Immunology -- Levinson

7. • KS has no known etiology, however
presents with features similar to toxic
shock syndrome
• KS is a “vasculitis involving small, n
medium sized arteries, esp coronary
arteries” (Levinson, n.d)
Clinical feat
• High fever of at least 5dys
• Bilateral nonpurulent conjunctivitis
• Lip and oral mucosa lesions (strawberry
tongue)
• Diffuse erythematous maculopapular
rash
• Hands n feet edema
• Cervical lymphadenopathy
Characteristic clinical finding
• Cardiac involvement: myocarditis,
arrhythmias, regurgitatn (mitral n aortic)
Main cause of morbidity n mortality
• Aneurysm of Coronary arteries
Other facts
• Common in children < 5years
Therapy | Mx
• High dose IVIgG => reduce fever
• Aspirin
Staph. Aurues: Kawasaki Syndrome

8. • Samples: cellulitis aspirates, abscess
cavities, blood, bone/joint aspirates
• Culture
• Identification: Gram stain and tests for
coagulase, clumping factor, and protein A
reactivity. Assess antimicrobial susceptibility
patterns
• Diagnostic Methods: selective media,
latex agglutination, or molecular
techniques(PCR)
• Incision n drainage of purulent material
• Removal of foreign bodies
• Antibiotics: basis: site, severity, pt
response, and susceptibility
- Initial Rx for MSSA: semisynthetic pen. Or
1st gen cephalosporins
- Vancomycin: MRSAs or pen.-allergics
- Clindamycin 4 MSSA/CAI MRSA strains
susceptible to it
- Monitor serum vanco levels
- Linezolid, daptomycin => resistance
- Rifampin n Genta => synergy in
endocarditis
EVALUATN | Mx
Evaluation
Management

9. - AKA Pneumococcus
- Gram positive
- Cocci (spherical)
- Leading cause of bacterial pneumonia
- Colonizes upper respiratory tract
• Transmitted via respiratory droplets from
infected person
• Usually colonizes URT of healthy
individuals, esp children
• Host factors: extremes of age; immune
def; chronic diseases [Diabetes, lung];
smoking; RTIs
• Virulence Factors: disease causing
factors =>
- Polysaccharide capsule: host immune
defense evasion
- Pneumolysin: cell damaging toxin
- Surf proteins: attachment n invasion
DEFINITION
STREPTOCOCCUS PNEUMONIAE
Etiology

10. • First the bacteria colonize the upper
respiratory tract
• Evade the host's immune defenses by
producing factors such as capsules which
inhibit phagocytosis
• Invade bloodstream or adjacent tissues ,
causing infection such as pneumonia
meningitis or otitis media
• Pneumococcal toxins can contribute to
tissue damage and inflammation, further
exacerbating the infection
• Otalgia [ear pain]
• Sinusitus: headche and facial tenderness
• Occult bacteremia-Fever without a
localizing source in children aged 2-
24months
• High fever: 102F ([c * 9/5] + 32)
• Signs of pneumonia: cough, chest pain,
SOB, Malaise, poor appetite etc
• Meningitis or other CNS infection
Clinical Feat
PATHOGENESIS

11. • Culture: gold std
• Identification: Gram staining;
Pneumococcal latext agglutination test
• Diagnostic Methods: selective media,
latex agglutination, or molecular
techniques(PCR)
• Pen. Derivatives: ampicillin; amoxicillin
- Amoxicillin: 1st line for previously healthy ppl
- Ampicillin/pen. G: fully immunized infants n
n school going children
- Empiric therapy with 3rd gen parenteral
cephalosporin: Ceftriaxone => pen.
Resistance
- Non-beta-lactam agents => less effective
than 3rd gen ceph
- Clindamycin, erythromycin or related
macrolides e. g Azithromycin provide good
alternative therapy to susceptible strains.
- Due to resistance, empirical treatment of
pneumococcal infections should be based
on knowledge of susceptibility patterns in
specific communities
Management
Evaluation
EVALUATION | Mx

12. • Involves strep species other than Group
A streptococcus (Strep. pyogenes)
• Cause infections such as RTIs, skin n
soft tissue infections, UTIs, bacteremia,
n endocarditis
• GBS: significant cause of neonatal
sepsis, pneumonia, n meningitis esp in
newborns
• Strep pneumonia: causes RTIs
[pneumonia, sinusitis, otitis media],
bacteremia, n meningitis
• Enterococcus spp: normal GIT flora but
can cause UTIs, endocarditis
• Virulence factors: polysaccharide
capsule, enzymes, adherence factors
• Host factors: age, immunity, recent
antibiotic use
• Transmssn: resp droplets, direct contact
DEFINITION
ETIOLOGY
Non Group A Streptococcus

13. • Adherence to host tissue n the ECM
components using pili and adhesins.
• Colonization n proliferation in host tissues
causing localized infections n invasion to
deeper tissues causing systemic infections
• Toxins and enzymes like hemolysins that
lyse RBCs n aid in tissue destruction n
proteases n hydraluaninases that facilitate
tissue penetration and degradation
• Immune evasion thro mechanisms that
inhibit phagocytosis by neutrophils n
macrophages n factors that interfere with the
complement system n components of the
innate and adaptive immunity like the
Streptococcus Inhibitor of Complement
(SIC).
• Biofilm formation enhances bacteria survival
and resistance to antibiotics
• Fever
• Cough, tonsillar exudates, sore throat
• Bleeding gums, bad breath
• Bacteremia, UTI symptoms
• Pre-term labor, uterine tenderness
• Skin rash
Clinical Feat
PATHOGENESIS

14. CLINICAL ASSESSMENT
• Hx taking
• Physical exam
LABS
• Throat swabs
• Urine cultures
• CSF cultures
• CSF cultures
• PCR
• Pen
• Cephalosporins: ceftriaxone; cefotaxime
• Macrolide: erythromycin, clarithromycin,
azithromycin
• Clindamycin
• Vanco
• Linezolid => drug resistant strains
• Tetracyclines: doxycycline => some
activity agnst
Evaluation
EVALUATION | Mx
Management

15. - Involves strep species other than Group B
streptococcus (Strep. Agalactiae)
• Other Strep Species: NGB strep include:
Strep viridans, Strep bovis, n Strep
anginosus. Often part of the normal flora of
the oral cavity, GIT, or GUT but can cause
infections when they breach the body's
defenses or when the host's immune
system is compromised.
• Virulence factors: polysaccharide
capsule, enzymes, adherence factors
• Host factors: age, immunity, recent antib.
use
• Transmssn: resp droplets, direct cont,
fecal-oral route
• NGA and NGB Strep are other strep colony
species bearing groups C and G Lancefield
antigens
?? Good to know ??
• Are commonly referred to S. dysgalactiae,
equisimilis subspecies
DEFINITION
ETIOLOGY
Non Group B Streptococcus

16. • Colonization: colonizes the GI and GU
tracts of women, esp during pregnancy.
• Capsule: Have encapsulated structure rich
in sialic acid, which mimics host cell
sugars, aiding in immune evasion n
infection.
• Immune Evasn: resistnce 2 phagocytosis
n modulatn of immune signaling pathwys.
• Toxins: GA Strep produces toxins, eg
streptolysins, streptokinase, n exotoxins eg
streptococcal pyrogenic exotoxin (SPE)
and streptococcal superantigen. These
toxins contribute to tissue damage,
inflammation, n systemic manifest. such as
TSS n necrotizing fasciitis.
Pneumolysin is a key toxin produced by S.
pneumoniae, which contributes to cell
damage and inflammation. Inflammatory
responses, including cytokine release,
contribute to the pathology of pneumococcal
infections.
• Pharyngitis; Endocarditis; Osteomyelitis;
septic arthritis; Fever; chills [sepsis]; UTIs
• Confusion; headache; Dyspnea; cough
[pneumonia]
• Red, tumens et dolens cutem [Red, swollen
n painful skin]
Clinical Feat
PATHOGENESIS

17. • Samples: Sputum, throat swabs, bal,
blood, skin/wound swabs, urine
• Gram stain: Gram-positive cocci arranged
in pairs/chains = Strong indication of a
streptococcal infection
• Culture: std blood agar used. Alpha-
hemolysis (greenish discoloration);
Gamma-hemolysis (no change on the agar)
• Biochem tests: catalase [all strep are -ve];
Bile Esculin Agar [for enterococci] optochin
sensitivity[S.pneumoniae]; bacitracin
sensitivity [S. pyogene => Group A]
• Advanced dx tools: MALDI-TOF MS; PCR
• Ampicillin / Pen
• Vanco
• Erythromycin / Clindamycin
• Cephalosporins: Cef;
Evaluation
EVALUATION | Mx
Management

18. • SSS: Scalded Skin Syndrome
• SSF: Staphylococcal Scarlet Fever
• HAI: Hospital Acquired Infection
• CAI: Community Acquired Infection
• MSSA: Methicillin susceptible S.aureus
• MRSA: Methicillin Resistant S.aureus
• Vanco: Vancomycin
• Genta: Gentamycin
• Pen: penicillin
• Nelson Textbook of Pediatrics, 2-Volume
Set
• Review of Medical Microbiology and
Immunology, 12eds
Glossary | References
Glossary References

19. Staphylococcus
• Faith Chebet
• Ouma Winnie
• Nancy Jepkemoi
• Ann Kezziah
Strep Pneumonia
• Catherine Boke
• Daphine Benson
• Mary Gatwiri
• Tabitha Maina
NGA-Strep
• Shiphrah Waw
• Emmanuel Kipkogei
• Tony Mutugi
• Sharon Karambu
NGB-Strep
• Clive Kamanu
• William
• Siraj
TABs | The Amazing Brains

20. Thanks for being attentive as
hawks
GOODBYE