E.Coli

1. Description

2. Virulence Factors

3. Types of E. Coli and the Diseases they Cause

1. Resides in colon, acquires mutations and becomes pathogenic.

2. Virulence factors include: mucosal interaction with pili - colonization of intestinal epithelial cells, exotoxin production - HL/HS and shiga like toxin, endotoxin production - Lipid A portion of LPS. Plasmid determinant: K88,99, CFAI, CFAII = adherence to target epithelial cells. Heat-liable enterotoxin, heat-stable enterotoxin = activate adenylate cyclase/guanyl cyclase respectively in small bowel causing diarrhea. Hemolysin = cytotoxin.

3. ETEC: traveler's diarrhea, plasmid encoded virulence, HL (increases cAMP) and HS, colonizing factor antigens CFAs on pili. Acts in the small intestine, homology with cholera toxin. Watery diarrhea nausea, abdominal pain and low grade fever. Transmits via contaminated food or water. There is no vaccine.

EPEC: infantile diarrhea in the US and abroad. Watery diarrhea, fecal oral transmission. Virulence via bundle forming pili. It attached on the wall of epithelial cells.

EHEC: Hemorrhagic colitis. Watery diarrhea and abdominal pain. Blood diarrhea. Hemolytic uremic syndrome in 10% of the cases in children. Transmission via raw milk, hamburgers, apples, oranges or food contaminated with cattle feces. Petting zoos. Person to person can occur. Attaching and effecing lessions in large intestine. Intimin and Shiga toxin - inhibit protein synsthesis. Phage coded. Thrombocytopenia, renal faiulue and microangiopathic hemolytic anemia. Do not ferment sorbitol.

Shigella Sonnei and other Shigella

1. Description

1. Invation = induces phagocytosis by intestinal epithelial cells

Yersenia and Y. Pestis

1. Description

1. Mediates adherence to human epithelial cells and induces phagocytosis, intreacellular binding of Ca.

Bacillus Anthracis

1. Description

1. Has two large plasmids - pXO1 and pXO2, the toxin complex is composed of protective antigen,, lethal factor and edema factor. They produce edema toxin = PA + EF and lethal toxin = LF + PA. Causes anthrax, without its plasmid it's non pathpgenic

Clostridium Tetani

1. Description

1. Tetanus neurotoxin encoded by plasmid

Staphylococci

1. Characteristics

2. Examples

3. Toxins

4. Drug Resistance

5. Disease

6. Lab. Diagnostics

1. Gram +. Causes suppurative disease. Grape like clusters. Produce catalase (yellow) - used to separate them from the streptococci. Protein A - an antiphagocytic surface component.

2. Staphylococci aerous (yellow colonies, hemolytic, produces coagulase, hemolysins, and most of them ferment mannitol, phage typing used here, antiphagocytic), S. epidermidis (white colonies, non-hemolytic, non-pathogen, non-coagulase, can be opportunistic), S. saprophyticus (urinary tract pathogen).

3. Hemolysins - alpha hemolysin - exotoxic factor that has a dermonecrotic hemolytic and lethal effect, leukocidin, hyluronidase, coagulase, enterotoxins - cause food posisoning, exfoliations - scalded skin syndrome, pyrogenic toxins - toxic shock syndrome. 

4. Penicillin, they produce penicillinase which breaks beta lactam ring (beta lactamase) and inactivates the drug

5. Produce spores and abscess. Most are localized. Staphylococcal enterocolitis - infectious invasive disease. Staphylococci food poisoning - intoxication due to ingestion of preformed enterotoxin (food poisoning). Heating food will kill organism without inactivating preformed heat stable enteroxin.

6. Blood agar plates. To indicate vorulence test for coagulase and fermentation of mannitol. Enterotoxin tests are not useful. 

Streptococci and Enterococci

1. Hemolysis

2. Disease Causing

3. Characteristics

4. Resistance

5. Things to Know from Book

6. Lab. Diagnostic

1. There are three types 

a. alpha - green, incomplete

b. beta - clear, complete

c. gamma - lack of hemolysis

2. Group specific carbohydrate antigens A (Strep. pyogenes - has hyaluronic acid capsule which are antiphagocytic - have type specific M antigens and T protein), B (Strep. Agalactiae), D. A and B are the most common. Non-suppurative: acute glomerulonephritis and rheumatic fever. Penicillin is used in treating these diseases.

3. They are catalase negative. Alpha hemolytic have low degree of pathogenesity and are found as normal flora. But these can cause subacute bacterial endocarditis - SBE. Non-hemolytic have low degree of virulence, can also cause SBE. Enterococci (Strep. faecalis)  are classified as group D and can cause SBE, are alpha hemolytic. Group D is salt tolerant. Enterococci - present in urinary tract as part of normal flora. They have increased resistance to Penicillin

4. There are a few resistant strains that are called fresh eating and quickly destroy tissue.

5. Main toxins and enzymes, contribution to pathogenecity - M protein which is highly immunogenic, usefulness of detecting anti-streptolysin O antibodies in patient's serum

6. A group is sensitive to bacitracin. 

Pneumococci

(Strep. Pneumonia)

1. Description

2. Things to Know

3. Disease Causing

4. Diagnostic Test

1. Pyogenic cocci - pus producing. Invasive. Behave as extracellular parasites. Gram +. Fastidious bacteria. The most capsular material there is the most virulent the organism. Type 3 pneumococcus - largest capsule - most virulant.

2. Quelling Reaction

3. Pneumonia in adults and bacterial meningitis in children. Invasiveness accounts for virulence not the production of toxins. Treat pneumonia with Penicillin G, there is resistance - use tetracyclines or erythomycin. High incidence of healthy carriers - there are vaccines. 

4. Optichin dist P dick test to distinguish between organims 

Corynebacteria

1. Description

2. Lab. Diagnostics

3. Treatment

1. Gram + rods. Ex: C. Diphtheriae - causing diphtheria sore throat, fevel, upper respiratory infection. Toxin encoded by lysogenic bacteriophage. Can be opportunistic. Patients with intravascular cathetiers and prosthetics can get bacterimias from C. Jeikeium (JK) - only vancomycin works on this one.

Organisms found in formal flora of the skin etc. 

2. Test for exotoxin diphtheria - inhibits protein synthesis, acts on the heart and diphragm.

3. Treat with antitoxin, antimicrobial chemotherapy. Vaccination exists. Subceptible to penicillin, erythromycin, tetracycline, cephalosporins.

Gram Positive Rods

1. Examples

1. Listeria monocytogenes - associated with animals and animal by products, can cause meningitis and bacteremia.

2. Erysipelothrix rhusiopathiae - occational diseases of handlers of fresh meat and fish

Neisseria Meningitidis

(Meningococcus)

1. Description

2. Epidemiology

3. Disease

4. Pathogenesis

5. Protection

6. Virulence

7. Lab Diagnosis

8. Treatment

1. Gram negative diplococci, no flagella, non motile, grow aerobically but enhanced with 5% CO2. Has a capsule.

2. Present in casopharyngeal flora of 10% individuals, only human host, spread by inhalation, fatality is 10% treated, no very common, mostly under 2yrs and adolescents, cases declining because of the vaccine.

3. Causes meningitis - acute, purulent meningitis and or sepsis and shock, fever, stiff neck, hypotenson, purpura, petechial or small thrombi rash. Shock can occur in the absence of meningitis. Adrenal destruction - waterhouse-friderichsen syndrome due to disseminated vascular coagulation. Disease mostly causing meningitis and bacteremia. 

4. Attach by pilli to non ciliated epithelia of nasopharinx. Get blood borne and goes to the brain. You get blebbing of the outer membrane - this is toxic - outer membrane contains LOS a form of LPS that causes endotoxic shock. The symptoms are due to LOS. LOS aquire sialic acid which blocks activation of compliment. Iron binding proteins make it virulent. 

5. Ab + compliment. People with compliment deficiency especially C8 (but also 5-9) are more susceptible. Those that hace lost their spleen are also susceptible to all encapsulated organism.

6. Capsule: prevents phagocytosis, shed polysaccharides into blood or lymph to bind up antibodies. By 12yrs of age mos to of the population has acquired resistance. Common in 19-21yr because these were never exposed. The main mechanism of host protection is Ab. Group B (all classified based on their capsule) is seen as self so it hides for the host's defense. Affects a lot of children. There is no vaccine abailable for B, vaccines are for A,C,Y, and W-135 - they involve diphtheria toxin as a carrier. Vaccination for older children - 11/12 and college students.

7. Spinal tap. gram stain smear of CSF. Presence of PMN with diplococci. You can culture patechiae on Martin Lewis chocolate agar + Ab.

8. Treat with penicillin, for prophylaxis - use rifampin or ciprofloxicin.

Haemophilus Influenzae

1. Description

2. Pathogenesis

3. Treatment

1. Gram negative pleomorphic rods/cocci, non motile. Type b causes meningitis in children months to 2 years. Also sepsis, spiglottitis, pneumonia, and septic arthritis. Carried in nasopharync by healthy people. Transmitted orally. This one has capsule. Other strains can cause otitis media, sinusitis and chronic bronchitis. Requires X and V factor for growth. Blood agar doesn't supply this, use lysed RBC.

2. Capsule of type b is PRP (polyribosyribitol P). By 6 years of age, resistance develops.

3. Vaccine - conjugate vaccine is effective in infants. Protein carrier is used p diphtheria, tatanus toxoid. Incidence has been reduced by 99%. Ab promote phagocytosis by compliment fixation. Hib vaccine. Treat with 3rd generation cephalosporins.

Neisseria Gonorrhoeae

1. Description

2. Signs and Symptoms

3. Pathogenesis

4. Resistance
5. Diagnostics

6. Treatment

1. Gram negative diplococcus - causes gonorrhea. Around 400,000 cases/year in the US. Sexually transmitted human to human. Colonizes mucous membranes (UG tract, urethra and endocervix, pharynx, anus). Replicates in epithelial cells.

2. Pain on urination and purulent pus. Diplococci in PMN cellsl uppon exudate examination. Can resolve in a few weeks if not treated. Females have abdominal pain, 30% are asymptomatic - transmission. 10% of males if not treated carry organism after recovery.

3. LOS in outer membrane - endotoxic activity, can bind to sialic acid and block compliment. Pili and Opa proteins are used for attachment to non-ciliated epithelial cells and invasion. Release of peptidoglycan upon death might cause pelvic inflammation. Usually localized in mucosal tissue but can become a disseminated gonococcal infection - DGI. Gonococcal arthurus can occur if it gets into the joints of say elbows and knees. Can cause extopic pregnancy.

4. Antigenic variation of pili and opa. LOS and compliment blockage. Survive in PMN. Make catalase that interferes with peroxide mediated killin mechanisms inside of PMNs. Also make IgA protease. There is no vaccine  - too many variants. Makes you susceptible to getting HIV. Neonates - eye infection during birth.

5. Sugar fermentation distinguish GC from N. meningitidis.

6. Cephalosporins or fluoroquinolones (ciprofloxacin). Penicillin no longer used because of resistance. Doxycyline and azithromycin also treat Chlamydia trachomatis - 30% of GC patients are co infected. Ophtahlmia neonatorum treated with silver nitrate drops or tetracyclin or erythomycin ointment. 

Remember - both N. gono and N. meningitidis are gram negatice diplococci, have LOS, meningococus have capsule, gonococus does not. Fastidious. N. men. causes systemic disease. N gono remains local although it can become systemic. Both are human ti human transmission - N. men carried in nasopharynx, N gon. carried by asymptomatic females and recovering males.

Pseudomonas Aeruginosa

1. Description

2. Symptoms

3. Disease

4. Virulence

5. Treatment

1. Gram - rod with polar flagella, colonize GI tract as normal flora in about 10% people. Opportunistic pathogen. Prefers aerobic environment. No human to human transmission. Resistant to most antibiotics, colonizes in burs and cystic fibrosis.

2. Colonizes lung in children with cystic fibrosis, colonizes burns and wounds - osteomyelitis, respiratory infections, pneumonia, bacteremias, sepsis, UTI, skin infections after got tubs, keratitis and conjunctivitis, swimmer's ear.

3. Cystc fibrosis - strain produces alginate capsule that blocks phagocytosis - composed of mannuronic and glucoronic acids. Burn patients - capsule helps organism penetrate deeper into tissue and become systemic = sepsis.

4. Exotoxin A - ADP ribosylates elongation factor 2 - inhibits protein synsthesis - has the same mechanism of action as diphtheria toxin (heart receptors) but they have different receptors. Exoenzyme S - ADP ribosylates host cell G proteins. LPS. Multiple antibiotic resistance. Quorum sensing - when they reach a certain concentration colony turns on many virulant genes. They have tendency to form biofilms - ex: cystic fibrosis. 

5. Fruity odor, produce pyocyanin blue, resistant to multiple antibiotics.

Bordetella Pertussis

(Whooping Cough)

1. Description

2. Virulence

3. Immunity

4. Diagnosis

1. Gram - small coccobacillus, human host, spread by aerosol, colonizes ciliated epithelium or trachea and bronchi. Starts as catarrhal - mild coughing or sneezing. Then coughing and vomiting, convalescence. Adult and pediatric. Highly contagious. 

2. Pertussis toxin - ADP ribosylating toxin, Gi gets ribosylated, doesn't work so cAMP continues to increase. This leads to ions and water in the cell. They also have other virulence factors - fimbriae, pertactin, filamentous hemagglutinin, tracheal cytotoxin.

3. Ab and adherence factors to the pertussis toxin are protective. New vaccine acellular pertussis (aP) given with diphtheria and tetanus toxoid (DTaP) to children

4. Nasopharynx swab, culture on bordetgengou and ragan lowe agar. Look for aggluttination. Doesn't grow on blood agar.