Microbial agents Flashcards
(81 cards)
Gram stain: Gram positive cocci in clusters
Culture: Golden yellow colonies
Catalase-positive
Coagulase positive
Staphylococcus aureus
Clinical manifestations
SSTI (skin and soft tissue infections)
Cellulitis: Deep skin infection
Impetigo: Spreading, crusted skin infection
Furuncles: small pus filled local infections
Carbuncles: Larger skin abscesses
Infections of other tissues (possible metastasis of superficial infections)
Osteomyelitis – S. aureus most common cause of bone infections in children
Septic joint (infective arthritis): esp in children
Pneumonia: commonly in hospitalized patients
Acute Endocarditis: frequently associated with IV drug abuse
Bloodstream infections: Bacteremia and Septicemia
Toxinoses
Toxic Shock Syndrome from TSST-1: exotoxin results in high fever, sunburn-like rash and multi-organ failure
“Food poisoning” or Gastroenteritis from enterotoxins - ingestion of heat stable enterotoxins formed directly on contaminated food; acute onset of GI distress
Scalded Skin Syndrome – exfoliatin toxin induced bright red flush, blisters (bullae)
Treatment:
Surgically debridement is usually required in addition to systemic antibiotic treatment for abscesses.
Penicillinase resistant penicillins such as nafcillin
Clindamycin
Vancomycin although resistance is emerging
Staphylococcus aureus
Staphylococcus aureus
Gram stain: Gram positive cocci in clusters
Culture: Golden yellow colonies
Catalase-positive
Coagulase positive
Virulence factors:
Cell surface (protein A, adhesins, microcapsule)
Protein A - anti-opsonin effect by binding Fc region of antibodies
Capsule - antiphagocytic polysaccharide “microcapsule”
Adhesins - facilitate attachment to host cells/connective tissue
Hemolysin - lyse erythrocytes
PVL (Leukocidin) (Panton-Valentine Leukocidin) lyse PMNs
Superantigen Toxins
Massive systemic immune response, overproduction of cytokines Severe clinical symptoms
Toxic shock syndrome toxin (TSST-1)
Enterotoxins (“food poisoning”)
Exfoliatin (“scalded skin syndrome”)
Tissue “invasin” enzymes (staphylokinase)
enzymes that facilitate penetration through extracellular tissue
Clinical manifestations
SSTI (skin and soft tissue infections)
Cellulitis: Deep skin infection
Impetigo: Spreading, crusted skin infection
Furuncles: small pus filled local infections
Carbuncles: Larger skin abscesses
Infections of other tissues (possible metastasis of superficial infections)
Osteomyelitis – S. aureus most common cause of bone infections in children
Septic joint (infective arthritis): esp in children
Pneumonia: commonly in hospitalized patients
Acute Endocarditis: frequently associated with IV drug abuse
Bloodstream infections: Bacteremia and Septicemia
Toxinoses
Toxic Shock Syndrome from TSST-1: exotoxin results in high fever, sunburn-like rash and multi-organ failure
“Food poisoning” or Gastroenteritis from enterotoxins - ingestion of heat stable enterotoxins formed directly on contaminated food; acute onset of GI distress
Scalded Skin Syndrome – exfoliatin toxin induced bright red flush, blisters (bullae)
Treatment:
Surgically debridement is usually required in addition to systemic antibiotic treatment for abscesses.
Penicillinase resistant penicillins such as nafcillin
Clindamycin
Vancomycin although resistance is emerging
Gram stain: Gram positive cocci in clusters
Catalase-positive
Coagulase negative (distinguishes from aureus)
S. epidermis
Virulence factors (relatively less virulent)
Produces cell surface polysaccharide “slime” that adheres to bioprosthetic materials and acts as a barrier to antibiotics
Most are highly resistant to penicillins and “methicillins”
Clinical manifestations
Frequently involved in nosocomial and opportunistic infections – Catheters or Medical Devices, IV lines
UTIs
Treatment:
Vancomycin
S. epidermis
S. epidermis
Gram stain: Gram positive cocci in clusters
Catalase-positive
Coagulase negative (distinguishes from aureus)
Virulence factors (relatively less virulent)
Produces cell surface polysaccharide “slime” that adheres to bioprosthetic materials and acts as a barrier to antibiotics
Most are highly resistant to penicillins and “methicillins”
Clinical manifestations
Frequently involved in nosocomial and opportunistic infections – Catheters or Medical Devices, IV lines
UTIs
Treatment:
Vancomycin
part of normal vaginal flora Gram stain: Gram positive cocci in clusters Catalase-positive Coagulase negative *Novobiocin resistant
S. saprophyticus
S. saprophyticus
Gram stain: Gram positive cocci in clusters Catalase-positive Coagulase negative *Novobiocin resistant (distinguishes from epidermis) No virulence factors Clinical Manifestation UTIs Cystitis in women Treatment: Penicillin G
Gram stain: Gram positive cocci in chains
Catalase negative
B-hemolytic
Bacitracin Sensitive
Group A Streptococci (GAS): S. pyogenes
Virulence factors
M-protein
Streptolysin
Pyrogenic superantigen exotoxins
Streptokinase
Common clinical manifestations
Pharyngitis: purulent inflammation in the pharynx
Scarlet fever: a toxin mediated skin rash
Skin Infections (necrotizing fasciitis)
Streptococcal toxic shock syndrome: Superantigen pyrogenic exotoxin (SPE) mediated shock and multi-organ failure
Post-infection sequelae
Rheumatic fever (M protein molecular mimicry)
2-3 weeks after pharyngitis, myocarditis • arthritis • fever • chorea
Glomerulonephritis (Type III hypersensitivity)
1-2 weeks after pharyngitis or skin infection
• hematouria (cola-colored urine) • oliguria (↓urine production) • Proteinuria (↑ protein in urine) • fluid retention (hypervolemia)
Treatment
Penicillin G
If skin infection, penicillinase resistant penicillins (oxacillin) since it may be staphylococci
Group A Streptococci (GAS): S. pyogenes
Group A Streptococci (GAS): S. pyogenes
Gram stain: Gram positive cocci in chains
Catalase negative
B-hemolytic
Bacitracin Sensitive (Group A vs Group B)
Virulence factors
M-protein
Streptolysin
Pyrogenic superantigen exotoxins
Streptokinase
Common clinical manifestations
Pharyngitis: purulent inflammation in the pharynx
Scarlet fever: a toxin mediated skin rash
Skin Infections (necrotizing fasciitis)
Streptococcal toxic shock syndrome: Superantigen pyrogenic exotoxin (SPE) mediated shock and multi-organ failure
Post-infection sequelae
Rheumatic fever (M protein molecular mimicry)
2-3 weeks after pharyngitis, myocarditis • arthritis • fever • chorea
Glomerulonephritis (Type III hypersensitivity)
1-2 weeks after pharyngitis or skin infection
• hematouria (cola-colored urine) • oliguria (↓urine production) • Proteinuria (↑ protein in urine) • fluid retention (hypervolemia)
Treatment
Penicillin G
If skin infection, penicillinase resistant penicillins (oxacillin) since it may be staphylococci
Gram positive
Catalase negative
B-hemolytic
Bacitracin Resistant
Group B Streptococci (baby) Agalactiae
Clinical manifestation Neonatal Meningitis Neonatal pneumonia Neonatal Sepsis Treatment Penicillin G
Group B Streptococci (baby) Agalactiae
Gram stain: Gram positive diplococci Catalase negative alpha -hemolytic Optochin and Bile sensitive Positive Quelling Reaction: the antibodies present in the sera will bind to the polysaccharide antigens of the pneumococcal capsule and the capsule will appear more opaque and swollen
S. pneumoniae
Virulence factors
• Polysaccharide capsule
heavily encapsulated forms are more frequently associated with severe, invasive disease
• Antiphagocytic and antigenic
• Over 85 capsule serotypes
Clinical manifestations
Lobar pneumonia • Pneumococci are aspirated into the lungs where they multiply and induce an overwhelming inflammatory response \
Otitis media • Gains access to middle ear by way of eustachian tube • Most frequent bacterial ear infection in children
Meningitis • A common cause of adult bacterial meningitis • Characteristic nuchal rigidity
Bacteremia and Sepsis
• High mortality rates in adults up to 60% in elderly
• Young children, elderly, immune compromised, alcoholics, those with other lung diseases or viral infections, smokers, Asplenic patients particularly susceptible
Treatments
Penicillin G
Cefotaxime and Ceftriaxone
Vaccines: PPV and PCV13
S. pneumoniae
Gram positive Catalase negative alpha-hemolytic Optochin resistant No virulence factors Common clinical manifestations Subacute endocarditis Dental Caries Penicillin G
Viridians
Viridians
Gram positive Catalase negative alpha-hemolytic Optochin resistant No virulence factors Common clinical manifestations Subacute endocarditis Dental Caries Penicillin G
E. faecalis & E. faecium
Gram positive
y-hemolytic (nonhemolytic or alpha hemolytic)
Enterococci grow both in: i. 40% bile ii. 6.5% NaCl
No virulence factor, not very virulent, more common in hospital setting
Clinical manifestations
Biliary tract infections
*Urinary Tract infections (esp enterococci)
Intra-abdominal abscesses
Endocarditis or bacteremia
Treatment
Ampicillin + gentamycin
Resistant to Penicillin G
Resistance to vancomycin (the 2nd option) on the rise
Gram positive y-hemolytic (nonhemolytic or alpha hemolytic) Nonenterococci grow only in: 40% bile No virulence factor, not very virulent, more common in hospital setting Clinical manifestations Biliary tract infections Urinary Tract infections Intra-abdominal abscesses Endocarditis or bacteremia Treatment Ampicillin + gentamycin Resistant to Penicillin G Resistance to vancomycin (the 2nd option) on the rise
S. bovis
Gram stain urethral pus: Gram negative diplococci often within PMNs
Culture on Thayer-Martin selective media
Modified Thayer-Martin medium contains antimicrobial agents to suppress normal flora
Oxidase positive
Use only glucose for culture
N. gonorrhoeae
Virulence factors:
Pili (facilitate attachment to host mucosa/epithelia)
Opa (opacity proteins formerly called PII proteins are important for host cell interactions)
LOS (endotoxin like LPS, but shorter and more branched side chains)
IgA protease (help infect mucosa)
express proteins that can extract iron from host iron proteins (such as transferrin and lactoferrin).
Clinical manifestation
Genitourinary tract infections
• Urethritis in men and women
• Cervicitis in women can lead to PID or salpingitis − Infertility due to salpinigitis in 20%
Pharingitis and rectal infections
Opthalmia neonatorum
Bacteremia that can cause disseminated infection
• Rare because gonococci multiply poorly in bloodstream (unlike meningococci)
• Could result in septic arthritis or scattered skin lesions
Treatment
3rd gen cephalosporin (ceftriaxone) {+doxycycline to cover Chlamydia and syphilis}
For opthalmia neonatorum: IV ceftriaxone
*Widespread resistance to penicillin, tetracycline, quinolones
N. gonorrhoeae
Gram stain CSF/blood: Gram negative diplococci often within PMNs
Culture on Thayer-Martin selective media
Oxidase positive
Use glucose and maltose
N. Meningitidis
Virulence factors
*Antigenic capsule – 13 serogroups, with serogroups A, B, C, Y and W-135 causing most infections • Serogroup B most common in US
Vaccine against capsule serotypes provides immunity
Pili
Opa
LOS (endotoxin)
IgA protease
Iron extraction system
Clinical manifestation
Meningococcemia • Petechial rash
Meningitis • Stiff neck and headache • Altered mental state • Sensitivity to light
Fulminant meningococcemia • Large purplish blotchy hemorrhages • Disseminated intravascular coagulation (DIC
Treatment
Ceftriaxone
Large IV dose Penicillin G and ampicillin
Prophylaxis rifampin treatment of family members, medical personnel, or children in close contact with patient
N. Meningitidis
Patient comes with with complaints of inflamed throat and nasopharynx along with swollen cervical nodes.
upon inspection you find a gray layer of pseudomembrane. The patient also has cardiovascular and brain issues. He was not vaccinated. You culture the microbe on a tellurite plate and saw black colonies with halos. What is it?
Corynebacterium diphtheriae