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
Photochromogen: slow growing, and produce a yellow-orange pigment when exposed to light.
Causes chronic pulmonary infection involving upper lobes of the lungs, resembles Mtb clinically
Tap water major reservoir
ID by DNA probe
Responds quickly to antimicrobial therapy
Slow growth
Acid-fast aka Ziehl–Neelsen stain
M. kansasii
Photochromogenic
Cutaneous infection associated with exposure to salt/freshwater following trauma
Causing “swimming pool granuloma” or “fish tank granuloma” (salt water)
Most common in southern coastal states
Grows slowly at 30 ⁰C (no growth at 37 ⁰C)
ID: biochemical/molecular
Acid-fast aka Ziehl–Neelsen stain
M. marinum
Scotochromogen (produces pigmentation in the dark or the light)
Most commonly recovered non pathogenic microbe of its class (no treatment needed)
Found in soil and water
Colonizes respiratory tract
Long, wide, branching, beaded Acid fast bacilli
DNA probe for ID
M. gordonae
Acid fast
Scotochromogen
Causes chronic pulmonary disease in adults with underlying lung disease (COPD, bronchiectasis)
Grows best at 42C, found in hot water systems
Rare, extrapulmonary disease in immunocompromised
Biochemical/Molecular ID
M. xenopi
Acid fast
Usually non-chromogenic:
This class is comprised of three dominant species: M. avium, M. intracellular, M. paratuberculosis
Most commonly isolated Mycobacterium spp.
Environmental reservoir
Slow growth
ID by DNA probe
Important pathogen in immunocompromised (disseminated disease) AND immunocompetent hosts (pulmonary infection, lymphadenitis)
Mycobacterium avium Complex (MAC)
Growth in <7 days (Rapid growing mycobacteria )
Post-traumatic, post-surgical, post-injection wound infections
Chronic pulmonary infections
Grow optimally at lower temps (30C)
Short, non-branching Acid fast bacilli in clusters, appear as Gram Positive on Gram stain
Arylsulfatase positive
Often drug resistant, difficult to treat
M. abscessus
Cannot be cultivated in vitro (armadillo animal model)
Spread from person-person, most likely via nasal secretions
Long incubation
Causes single, multiple or widespread anaesthetic skin lesions
M. leprae
Curved rods - *comma shaped
Polar flagella
Oxidase positive
Positive TCBS Agar - can survive in bile while most Gram negative can’t
Vibrio cholerae
Adds ADP-ribose group to Gs protein
Permanently actives Gs > adenyl cyclase Gas canister on that guy,
High cAMP causes high chloride transport
Transporter is CFTR - defective in cystic fibrosis. Some evidence that CF heterozygotes are more resistant to diarrhea.
High salt concentration in intestinal lumen produces osmotic inflow of water
Water flow leads to diarrhea
What toxin?
Cholera Toxin
Require NaCl for culture (= halophiles)
• Grow on TCBS medium (thiosulfatecitrate-bile salts)
• Diarrhea from eating raw fish & shellfish
• Wound /soft tissue infections
Non-inflammatory enteritis
Non-cholera Vibrios
Two exotoxins, distinguished by heat sensitivity:
• Labile Toxin (LT) resembles cholera toxin, produced in lower amounts, increases cAMP
• Stable Toxin (ST) structural analogue of gut peptide hormone, stimulates guanyl cyclase -coupled receptor, increases cGMP
• Elevated cAMP or cGMP produces diarrhea as in cholera – less toxin, less severe disease, watery diarhea, not bloody like EHEC
Enterotoxigenic E. coli [ETEC]
Type III secretion system: exports proteins to cytosol, causing cytoskeletal rearrangement
One protein inserts into enterocyte plasma membrane and allows tight binding.
‘Pedestal’ that cups bacterium produced
Brush border disappears (“attaching and effacing lesion”)
Enteropathogenic E. coli [EPEC]
Sorbitol negative (nonfermenters) Predominant serotype: O157:H7 Toxin: Verotoxin inflammatory enteritis, HUS - hemolytic uremic syndrome Bloody diarrhea
Shiga toxin producing E. coli (STEC)
Transcytosis by M cells
Invade enterocytes via basolateral surface & induce phagocytosis by Type III system
Type III also secretes inflammatory cytokines
Turkey baster
Lyse phagocytic vacuole: bacteria enter cytosol
Proteins on bacterial surface induce actin polymerization
Actin ‘tail’ pushes bacteria through plasma membrane into adjacent cells (like lysteria)
Toxin:
Induces damage in endothelial cells
AB5 structure
A subunit cleaves RNA of large ribosomal subunit at specific position
Attacks 60S portion, Ribosome inactive
Isolates without toxin produce dysentery but less severe
Shigella
Gastroenteritis (=Enterocolitis)
Non-bloody diarrhea, fever, nausea, vomiting,
Exit lumen via M cells, invade enterocytes, multiply locally
• Induce apoptosis in macrophages via Type III system
Non-typhoidal Salmonella
Clinical manifestation
Guillian Barre syndrome-”guy and the bears”: ascending paralytic disease due to antibodies directed toward the nervous tissue - demyelination of peripheral nerves
Gastroenteritis - bloody diarrhea - red stools
Reactive arthritis - cAMPY infection
Campylobacter jejuni
Stool antigen assays
Treatment: Escapes stomach acid:
Resides below mucus layer
Urease positive: converts urea to ammonia (basic) - **crucial
• Chronic infection/inflammation: stomach cancer, gastric lymphoma
Virulence:
Type IV secretion system exports cytotoxin
Campylobacter Helicobacter
Grow at 4 degrees C [refrigerated foods: milk, blood products, etc.] - like lysteria
-primarily transmitted through puppy’s feces
From Intestine travels to local lymph nodes
Bloody diarrhea- red stool
Local inflammation, most often in children
Enteropathogenic Yersinia
Early: Diarrhea (bacteria in small intestine) - pea soup
Later: Systemic febrile illness (bacteria invade/exit large intestine)
Penetrate intestine via M cells
Do not cause macrophage apoptosis
Typhoidal Salmonella
anaplasma phagocytophilum, lets talk about it
A useful diagnostic feature is that it forms morulae in neutrophils.
It will have mild to severe fever, and unlikely to have rash. It is obligate intracellular as all ricketssia are. And transmitted by ticks as all rickettsia except for coxiella is.
Ehrilichia chaffeensis
It is obligate intracellular as all ricketssia are. And transmitted by ticks as all rickettsia except for coxiella is.
infects monocytes and macrophages however morulae are rare and not a good diagnostic feature.
Loss of platelets and loss of leukocytes are characterstic diagnostic features.
Characterized by fever, headache and myalgia
Ricketsia typhi
It is an infection of endothelial cells and is predominant in tropical and subtropical seaboard regions. Rat is reservoir where infections are asymptomatic and long lasting
It is obligate intracellular as all ricketssia are. And transmitted by ticks as all rickettsia except for coxiella is.
It is pretty mild and always has fever.
Rickettsia akari
The target is macrophages and monocytes, same as ehrlichae.
It is obligate intracellular as all ricketssia are. And transmitted by ticks as all rickettsia except for coxiella is.
Key feature is at site of inoculation, a papule forms which ulcerates and forms a dark eschar. Infection disseminates into fever but appears along with generalized rash.
Rickettsia prowazekki
It is obligate intracellular as all ricketssia are. And transmitted by ticks as all rickettsia except for coxiella is.
It is the only Rickettsia able to cause devastating epidemics..wow. Enter the bloodstream through endothelial cells, induce phagocytosis, escape phagosome, proliferate until it bursts. Anyways, the louse POOPs. and you scratch it into your skin. Severe headache, fever,, myalgia and rash - spreads from trunk to extremities but spares the face palms and soles.
What are the three exotoxins produced by Bacillus anthracis
- Edema factor: activates calmodulin activated adenylate cyclase which increases levels of cAMP. The edema helps the anthrax because it prevents host defenses from reaching the sites and prevents phagocytosis.
- Lethal toxin: which causes necrosis, responsible for the black eschar due to the loss of growth signal. The protease cleaves a protein kinase involved in signaling.
- Protective antigen: allows it to enter cells
Inhalation of spore of this microbe can lead to hemorrhagic lymphadenitis!
Bacillus anthracis.
Gram positive Rod
Beta hemolytic
Catalase positive.
Has a tumbling motility
Lysteria monocytogenes.
Which microbes are spore forming? 5 things
Clostridium perfinges Bacilllus anthracis Clostridium dificil Clostridium botulinum Clostridium tetani
Clostridium perfinges secretes exotoxins, enterotoxins, and hydrolytic enzymes, what are they?
Exotoxin: alpha toxin aka phospholipase C. It lyses WBCs, platelets, RBCs, endothelial cells (tomatoes)
Enterotoxin, compromises the cell membranes, ion transport leading to loss of fluid and proteins. Also gives it heat invulnerability
Hydrolytic enzymes: DNAse, collagenase, proteases, hyaluronidase
Attempts to ID a microbe has shown large, rod shaped, non motile bacteria which are gram positive rods. It was cultured anaerobically on blood agar showing double zone of hemolysis. What is it?
Clostridium perfringes:
- double zone of hemolysis (double fine zone)
- Gram positive rod
- obligate anaerobe
You see racquet shaped bacilli and you know immediately, this is cool.
C. tetani.
What is the diagnostic test for detecting C. difficile?
Enzyme immunoassay for C. difficile toxins A and B. Stool culture is a sensitive test but it is slow results.
The toxins are what causes the damage, not C.difficile
Catalase and urease negative. It is gram positive rod that is non-hemolytic on plate and forms rhyzoids. The plate has to be set up in an anaerobic environment.
C. dificile
So you know the exudate has gram positive cocci and gram negative rods but when you do an aerobic culture, you find enterococci only. What was likely the gram negative rod?
Bacteroides fragilis
You take a culture of bacillus anthracis and gram stain it. You see many gram positive but also some stain pink. What is responsible for the minority of pink staining cells?
Hydrolysis of peptidoglycan.
It will also show up bamboostick appearance due to its central or subterminal spores
A patient had a crushing injury and soon it became swollen and painful, which steadily became more severe. x ray showed gas in tissue. Fluid from blister was found to be large gram positive rods.
Clostridium perfringens
A pregnant female develops infection of the membranes around the fetus. Bacteroides fragilis is recovered. Which route is this organism most likely to have reached the fetus
Bacteroides fragillis and all other Gram negative anaerobic rods are normal flora in the large intestines. It likely spread from the large intestine to the genitourinary tract
How does tetanus toxin antibodies work?
They neutralize the protein exotoxin of C.tetani
Aerobic culture of the microbe leads to nonhemolytic colonies. The ulcer surrounded by redness the man got becomes a thick black scab. What is the likely culprit
Bacillus anthracis
A patient has an abscess with Bacteriodes fragilis. What allowed this infection to occur?
Tissue ischemia.
What is the mode of action of fluoroquinolones?
ex. ciprofloxacin, lomefloxacin, levofloxacin.
- Inhibits topo II, DNA gyrase. So you can’t relax the positively supercoiled bacterial DNA for replication
- Inhibits topo IV, which prevents the separation of chromosomal DNA into respective daughter cells during division.
The most popular choice for UTIs, and anthrax (ciprofloxacin) and (levofloxacin, gemifloxacin and moxifloxacin are used increasingly for treatement of upper and lower tract infections
Student develops nausea and vomiting a few hours after eating fried rice. What is the classic microbe.
Bacillus cereus.
What are the two diagnostic tests for latent tuberculosis
- Mantoux test: tuberculin or PPD is injected intradermally. The ring of induration is measured in 48-72 hours. Greater 5mm is positive for high risk individuals, 10 mm is positive for moderate and over 15 is positive for everyone
- IGRA- tests for the presence of gamma interferon that is produced by T lymphocytes which recruits macrophages. You run 3 tests, whole blood alone (baseline), whole blood with mitogen (show WBCs produce IFN) and whole blood with the Mtb peptide.
What are fast tests for active Tb? (mention preparation)
- Specimens
-bronchoalveolar lavage or gastric lavage
-urine
-blood
Stool - Specimen from non-sterile sites need to be decontaminated before further analysis - NALC (N-acetyl cysteine, naOH)
- Direct detection: acid fast stain and look for chording
- Fluorochrome stain - but needs to be confirmed with acid fast stain - NAAT:
- Perform an antimycobacterial susceptibility testing
In the lab, a microbe was found to be gram negative , polar flagella.
Also produced pyoverdin (siderophores) rod with pili, LPS, exotoxin A and type 3 secretion system. On agar plate there were no acids and color was yellow. Person had cystic fibrosis What was the agent?
P. aeruginosa
What is the diagnostic test for Y. pestis and what are the 3 virulence factors
Diagnosis is mostly made by NAAT. On Wayson stain, it has a safety pin appearance (baby has safety pin)
- paralyzes phagocytes
- Acquires iron
- Capsule
What is transmitted by fleas?
Yersinia pestis.
N. gonorrhoeae and Chlamydia What are similar between their symptoms, what is different
They both feature urinary tract infections. If in women, the primary concern is the development of PID which can lead to infertility.
The difference is that while N. gonorrhea always shows acute symptoms, the symptoms of chlamydia are mild or absent
GORPS, what does this acronym refer to?
Gonorrhoeae
Genitourinary tract infections (most important)
Opthalmia neonatorum (conjunctivitis occurring in the first 28 days)
Rectal infection
Pharyngitis
Septic arthritis, scattered skin lesions’
Which microbes are diplococci?
S. pneumonia
N. gonorrhoeae
N. meningitidis
What is the special culture for Gonnorhea and the diagnostic test for it?
Special culture: Thayer-Martin which contains antimicrobial agents to kill normal flora
NAATs: primary method.
(chlamydia often copresents with gonnorhea and chlamydia cannot be cultured because it is obligate intracellular).
What is exfoliatin toxin?
Thick exfoliates which get rid of dead skin cell. Produced by S. aureus, it induces blisters (bullae) which causes bullous impetigo, and then desquamation of the epidermis.
“Scalded Skin Syndrome”
What are the general characteristics of mycobacteria
- thin, slightly curved, beaded bacilli
- obligate aerobe
- non motile
- cell wall contains N-glucolylmuramic acid and has very high lipid content
- acid fast
- slow growing
Which nontuberculoid Mycobacteria are ID’d by DNA probe vs biochemical/molecular methods?
What special test of abscessus?
DNA probe
M. kanseii
M. gordonae
MAC
Biochemical/molecular methods
M. marinum
M. xenopi
M. Abscessus
Abscessus
-species level ID and antibiotic susceptibility tests are important
M.leprae cannot be cultured in vitro
What are the virulence factors for N. gonorrhoeae?
POLI
Pili (facilitate attachment to mucosa and epithelium)
Opa (opacity proteins aka PII which are important for ce.l interactions
LOS (a shorter and more branched side chain of LPS
IgA protease.
These are all heterogeneous antigenically
What is Fulminant Septicemia aka Meningococcemia
It is an LOS mediated septic shock frequently seen in infants
It shows large purplish blotchy hemmorhages (petechial rash) that leads to disseminated intravascular coagulation (DIC)
And adrenal collapse.
Describe the vaccine of meningococci
Capsular polysaccharides bound to diptheria toxoid
