Exam 2 Flashcards
Basics of Chlamydophila psittasi (Psittacosis or Ornithosis)
- obligate parasite of intestinal and respiratory tract of birds
- obligate intracellular
- gram (-)
Encounter, Pathogenesis, Damage of Chlamydophila psittasi (Psittacosis or Ornithosis)
ii. Encounter
1. asymptomatic adult bird carriers
2. doesn’t replicate in environment, but elementary bodies can persist & expose via aerosol
iii. Pathogenesis
1. local spread in intestinal and upper/lower respiratory epithelium ->
2. receptor mediated endo/phagocytosis into epithelial cells and macrophages
->
3. phagolysosomal fusion is inhibited ->
4. differentiate into elementary bodies and lyse cells releasing elementary bodies to invade new cells
iv. Damage
1. Endotoxin release -> cell lysis -> severity dependent on age of bird, species of bird, virulence of strain
Immunity against, diagnosis, treatment & prevention for Chlamydophila psittasi (Psittacosis or Ornithosis)
v. Immunity
1. Cell mediated by T cells is most important
vi. Diagnosis
1. REPORTABLE (health concern for bird owners)
2. Cloacal swab & antigen ELISA
3. Serology of antibody
4. Necropsy
vii. Treatment
1. Tetracycline!
viii. Prevention
1. Quarantine of affected birds
2. Imported birds treated prophylactically
3. sanitation
3 Types of anti-microbials
- synthetic anti-metabolites
- natural products of bacteria & fungi (bacteriocins)
- natural products of higher eukaryotes
Antibiotic Vs Antimicrobial
Antibiotics
a. substance produced by a microorganism that inhibits or kills other microorganisms, but causes little or no damage to the host
Antimicrobial
a. Any substance of natural or synthetic origin that inhibits or kills a microorganism, but causes little or no damage to the host
6 Questions to ask when selecting antibiotics
a. Is dz infectious?
b. Is dz bacteria caused?
c. Which antibiotic works for this bacteria?
d. Will the antibiotic penetrate the site of infection?
e. Is the antibiotic toxic to the patient?
f. Will antibiotic use promote development of resistance?
Bactericidal Vs Bacteriostatic antibiotics
bacteriostatic:
i. reversible inhibition of bacterial growth
bactericidal:
i. irreversible inhibition of bacterial growth (usually bacterial lysis)
Examples of Antibiotics that can be both static & cidal
a. chloramphenicol is usually bacteriostatic but is bactericidal at high doses
b. penicillin is cidal at recommended doses, but static at low doses
When are bactericidal drugs preferred
a. immunosuppressed or immunodeficient animals
b. infections such as endocarditis or meningitis where reliance on an inflammatory response can be detrimental
Why use multiantibiotic therapy?
a. Obtain synergistic effect
b. Prevent or delay emergence of persistent organisms
c. Treat polymicrobial infections
d. Treat serious infection before pathogen is identified
4 Potential effects of antimicrobial combinations:
a. indifference: combined antibiotics are no more effective than the more effective antibiotic used alone.
b. additive: combined action is equal to the sum of the actions when used alone
c. synergism: combined action is significantly greater than the sum of both effects (ideal)
d. antagonism: combination is less effective than individual
Why not to use cidal and static drugs together?
Drugs antagonize each other = less effects of both
Describe the difference between obligate parasite, obligate pathogen, opportunistic pathogen, extracellular pathogen, facultative intracellular pathogen and obligate intracellular pathogen.
Obligate parasite:
- can only persist & replicate on mucus membranes
Obligate pathogen:
- exogenous pathogen
Opportunistic pathogen:
- endogenous flora that causes disease when there is opportunity
Extracellular pathogen:
- replicates and survives outside of host cell
Facultative intracellular
- can replicate inside or outside of host cell
Obligate intracellular
- replicates and survives inside of host cell
Bordatella bronchseptica (kennel cough) Basics, entry, spread, damage, diagnosis, treatment, prevention
- Exogenous obligate pathogen
- extracellular
- gram (-)
- highly contagious (inapparent carriers)
Entry
- coughing & sneezing
- Pili attach to but don’t penetrate ciliated tracheal epithelial cells
Spread
- Localized to mucosal surface
- Cause pneumonia in cats & others but not dogs (unless underlying issue
Damage
- Endotoxin: fever
- cytotoxin (exotoxin): damages ciliary epithelium = ciliostasis = inflammation = coughing
- Adenylate cyclase (exotoxin): inhibits phagocytes = facilitates multiplication & spread
Diagnosis
Dry hacking cough
Treatment
- Usually self-limiting (IgA)
- does not require antibiotics unless pneumonia
- Supportive care
Prevention
- Improved ventilation, reduce exposure, Vx, sanitation
Vaccines available for Bordatella bronchseptica (kennel cough)
systemic bacterin:
- IgG to B. bronchiseptica
- Less protective
- included w/ vx for parainfluenza virus, adenovirus-2, & distemper
intranasal vaccine (live avirulent strain)
- elevates local IgA
- Blocks binding of bacteria to cilia
- available for cats
Basics of Bovine Shipping Fever & associated bacteria
- Growing, non-immunized calves after arrival @ feedlot
- Due to stress, mixing of cattle, poor nutrition, poor ventilation
- Many viruses + Mannheimia involved
- Mannheimia: Normal flora, extracellular, gram (-), obligate parasite (must live on mucus membrane, short survival in environment),
Entry & Spread of Bovine Shipping Fever (Mannheimia)
Entry
- Decreased immune competency due to stress (normally phagocytized)
Inhaled into trachea & bronchioles
Spread
- Gain entry to lung due to viral infection/damage
- Inhabit ventral portions of cranial lung lobes
Mannheimia Virulence 4 Factors
Fimbriae:
- enhances colonization
Polysaccharide capsule:
- Inhibits phagocytosis
Endotoxin:
- alters bovine leukocyte function
- can cause vasculitis and associated thrombosis
Leukotoxin (exotoxin):
- cell lysis of leukocytes and platelets
- destroys immune cells,-> tissue necrosis
Diagnosis of Shipping Fever
- History of exposure to stress factors and sudden onset of respiratory disease (clinical signs w/in 7-14 days after arrival in feedlot)
- Lung tissue or blood from septicemic animals
- collect Trans-tracheal wash & culture
- cytology: degenerate neutrophils w/ gram (-) rods
- bacterial culture for antibiotic sensitivity
Treatment & Prevention of Shipping Fever
Treatment
- acute pneumonia - antibiotics will reduce incidence of mortality and development of chronic pneumonia if treated early (Oxytetracycline)
- chronic pneumonia – Treatment is of little value due to permanent lung damage
Prevention
- Maximum immunity & minimum stress
- minimize multiple sources of cattle
- vaccinate 3 weeks prior to transport
- minimize transport stress
- segregate upon arrival and feed highly palatable feed
- Mannheimia (Pasteurella) bacterins are not very effective
- New bacterin/toxoid Vx effective against leukotoxin
Similar Conditions to Shipping Fever in other Species
- Canine infectious respiratory Disease Complex (CIRDC)
- Feline Lower Respiratory Tract Infection
Compare Penecillins Group 1, 3, 4, 5: Do they work on gram (-) or gram (+)? Are they resistant to β-lactamase?
Group 1 Gram (+) Not resistant
Group 3 Gram (+) resistant
Group 4 Gram (+) & Gram (-) not resistant
Group 5 Gram (-) resistant
Penicillins (Group 1): Basics
a. Bactericidal
iii. Narrow window against gram (+) anaerobes
vi. Killed by beta-lactamases & acid hydrolysis
viii. not taken up by cells
viii. New generations less susceptible to acid hydrolysis
Sites of action of antibacterial drugs
a. Inhibitors of cell wall synthesis
b. Inhibitors of protein synthesis
c. Inhibitors of nucleic acid synthesis
ß-lactam antibiotics: site of action, example drugs, bactericidal or static, structure, action
inhibitors of cell wall synthesis
a. penicillin, cephalosporins, carbapenems, monobactams
b. bactericidal
c. high therapeutic index
Structure
i. ring structure
ii. enzymes that catalyze hydrolysis of beta-lactam bond
Action
e. inhibit final cross-linking of peptidoglycan in cell wall formation
Beta-lactams (beta-lactamase inhibitors): drug examples, cidal or static, work against gram (+) or (-)
a. Cephalosporins and Cephamycins
b. Bactericidal
c. greater resistance to ß-lactamases
d. improved penetration of membranes
e. work against gram (+) and Gram (-)
f. can be used in penicillin-allergic individuals
Differences between generations of beta-lactams
1st Gen (Pen G) - gram (+)
2nd Gen - gram (-) or (+)
3rd Gen- gram (-) more than (+)
4th Gen (Beta-lactmase inhibitors) - gram (-) or (+)
Glycopeptides; drug, cidal or static, mechanism of action, gram (+) or (-)
a. Vancomycin
b. Bactericidal
c. blocks cell wall synthesis
d. effective against Gram positive bacteria
(especially cocci)
g. is not taken up by cells
h. should be reserverd for serious resistant infections in humans!!
Antibiotics that block protein synthesis
- Tetracyclines
- macrolides
- chloramphenicol
- aminoglycosides
Tetracyclines; cidal or static, mechanism, work against
i. Bacteriostatic
ii. inhibit protein synthesis
iii. broad-spectrum
iv. negative effect on normal flora
b. Can enter cells
v. resistance is widespread among bacteria due to plasmid encoded membrane pump
Aminoglycosides; cidal or static, mechanism, work against
i. Bactericidal
ii. inhibits protein synthesis
iii. aerobes
Iiii. Do not penetrate cells
iv. resistance in older aminoglycosides is widespread
Macrolides / Lincosamides; static or cidal, mechanism, drugs, active against, special treatment considerations
i. Bacteriostatic
ii. inhibit protein synthesis
iii. Erythromycin (macrolide)
iv. Clindamycin (lincosamide)
v. Gram (+), mycoplasmas, anaerobes
ix. Resistance is common
x. do not use in horses or rabbits!
xi. use for wounds, abscess, periodontal Dz
Chloramphenicols
i. Bacteriostatic
ii. inhibit protein synthesis
iii. can’t use in food animals (florfenicol can)
iv penetrates cells
iiv. broad spectrum
Antibiotics that inhibit nucleic acid synthesis
- quinolones/fluroquinolones
- sulfonamides
- trimethroprim / ormetoprim
- rifampicin
Quinolones / Fluroquinolones
i. Bactericidal
ii. inhibit nucleic acid synthesis
iii. aerobes, facultative anaerobes, rickettsia, mycoplasmas
vi. Penetrate mammalian cell
Sulfonamides
i. Bacteriostatic
iii. Inhibit nucleic acid synthesis
iv. broad spectrum
v. ineffective in the presence of pus or necrotic tissue
vi. Resistance widespread, but overcome by combining sulfonamides with trimethoprim
Trimethoprim / Ormetoprim
i. Bacteriostatic
ii. Bactericidal when combined w/ sulfonamides
Rifampicin
i. Bactericidal
ii. Inhibits nucleic acid synthesis
iii. Gram (+) bactereia
iv. Used in combo w/ others to avoid resistance
Constituative Vs Acquired Resistance
constitutive resistance:
• bacteria resistant to antibiotics because they normally lack the uptake systems or targets of the antibiotics
• not related to prior exposure to antibiotics
• ex: Penicillin G cannot enter members of the family Enterobacteriaceae
acquired resistance:
• bacteria become resistant to antibiotics by mutation resulting in alteration of uptake systems or targets of the antibiotics
• dependent on prior exposure to antibiotics
• ex: Staphylococcus aureus resistance to penicillin G (due to bacterial production of enzymes that inactivate penicillin)
3 Mechanisms of acquired resistance
Alter the target for the drug
Alter uptake of drug
Inactivate drug
Multi-antibiotic resistance Vs cross-resistance
multi-antibiotic resistance
• presence of different mechanisms of resistance
• antibiotics must be in different classes (aminoglycosides Vs penicillin)
cross-resistance
• resistance to one antibiotic implies resistance to others due to common mechanisms
• antibiotics in same class
Acquired Resistance via DNA Mutation
- Usually lethal
- When not lethal result in:
- Disadvantageous = loss of mutant from pop
- No advantage = mutant in pop in low levels
- Selective advantage = resistant to host defense & antibiotics = growth until dominant in pop
Acquired Resistance via Genetic Transfer
- Done by transduction or conjugation
- Transfer of DNA (resistance genes) between bacteria
- Responsible for multi-antibiotic resistance
Transduction
• transfer of DNA following infection with a bacteriophage
• bacteriophage inserts its genetic material into bacterial chromosome
Conjugation
• direct interbacterial transfer of DNA (plasmid) thru sex pilus
• plasmids (extrachromosomal DNA): encode mechanism of antibiotic resistance
• plasmids transferred horizontally
• plasmid transfer uncommon in gram (+)
• transfer of chromosomal genes when plasmids obtain chromosomal genes using transposons
Selecting antibiotics effective against bacteria
- Gram related spectra
- History of sensitivity
in vitro sensitivity
• shows which antibiotics not to use
• obligate anaerobes, obligate intracellular, & slow growing bacteria not suitable for routine testing
in vitro susceptibility testing
• MIC: min conc. of antibiotic that completely inhibits bacterial growth
• disk diffusion (Kirby-Bauer) test provides an estimate of MIC: the diameter of the zone of inhibition is inversely proportional to the MIC
3 categories of results for MIC
o susceptible
o moderately susceptible
o resistant
UTIs in Dogs
o Lower UTI (cystitis) most common
Most frequent pathogens • Most common (75%) • E. coli • Proteus • Klebsiella
- Less common
- Staphylococcus psuedintermedius/aureus
- Streptococcus
- Pseudomonas
- Any bacteria
- Fungus
- May see candida w/ long-term antibiotic use
UTIs in Cats (common pathogens)
o Less common than dogs
Most common pathogens • E. coli • Proteus • Staphylococcus aureus • Pasturella multocida
UTIs in Horses
o Uncommon
Most common pathogens
• E. coli
• Staphylococcus aureus
• Streptococcus
UTIs in cattle, cheep, pig
o Uncommon
o E. coli most common
periparturient cows:
o Corynebacterium pilosum & C. cystitidis
Encounter, Spread, & Immunity for UTIs
Encounter
o Normal flora of lower urinary tract (opportunistic)
Spread beyond lower urinary tract (Pyelonephritis)
• Ascend ureters & colonize renal pelvis
• = pyelonephritis (very serious condition)
• can result in renal damage & loss of function
Immunity
• Limited Ab & cell mechanisms
• No immunity following UTI
Bacterial entry & reasons for entry in UTI
o Ascending from exterior
o Colonization of urinary tract
o Usually limited to urethra & caudal bladder (uncomplicated cystitis)
Due to breakdown of urinary defenses • Urinary stasis • Mechanical block of flow • Damage to epithelial surface • Late gestation • Bacterial factors • Diseases that cause decreased osmolarity
Diagnosis of Lower UTI: tests & rule-out differentials
- Abdominal pain or painful urination
- Small firm bladder
Dysuria (frequency (pollakiuria), blood, etc)
• Blood at beginning = urethra
• Blood at end = bladder
Rule-outs
• Urethrocystitis
• Pyelonephritis
• prostatitis
Tests
• Urinalysis
• Microscopic exam
Bacteriologic culture of urine from cysto
• If UTI, will see WBCs
Most likely bacteria if acidic or alkaline urine w/ rods, cocci, or coccobacili
- Acid w/ rods = most likely E. coli
- Acidic w/ cocci = most likely strep (chains) or emterococcus
- Alkaline w/ coccobacilli = most likely proteus
- Alkaline w/ cocci = most likely staph
Diagnosis of Pyelonephritis & Prostatitis
Pyelonephritis
• systemic signs + cystitis
• may have abnormal renal function
• casts
• diagnostic methods:
o visualize kidneys
o pyelocentesis
Prostatitis
• systemic signs + cystitis
• prostate enlarged and/or asymmetrical shape
• diagnostic methods:
o prostatic aspiration w/ culture
o biopsy
How to select antibiotics for UTI & know if they are affective
Antibiotic Selection
• urinary tract is a CONDITIONALLY SUSCEPTIBLE site
• many labs test urinary isolates at levels of antibiotics expected in the urine, not blood
• bacteria resistant in blood may be susceptible in urine because antibiotic is concentrated in urine
• effective treatment may require 10-14 days (think of toxicity)
Are they effective?
• re-culture at 48 hours:
• growth = change antibiotic
• no growth = continue another 7-10 days
Recurrent cystitis & Chronic bacterial cystitis
recurrent cystitis
• sources of infection:
• relapse = infection with the same organism
• re-infection = infection with a new organism
• either case may have underlying causes
chronic bacterial cystitis
• culture at 48 hours, if no significant growth, continue antibiotics for 4- 6 weeks .
Antibiotics used for UTI & which bacteria they work for
o Ampicillin
o Chloramphenicol
o Oxytetracycline
o Trimeth sulfa (long-term use = keratoconjuctavitis)
o All work on E. coli, Klebsiella, Proteus, Staph
o Most work on Pseudomonas accept oxytetracycline
Corynebacterium renale Infection of Ruminants; basics, bacteria involved, virulence factors, spread
o Contagious cystitis and pyelonephritis in cattle and sheep
o No underlying problem needed to cause disease
Bacteria: • all normal flora • C. renale, • C. cystitidis • C. pilosum
Virulence factors:
• pili – adherence
• urease - increase pH & facilitate adherence
Spread
• Subclinically infected
• direct contact with urine or splashing of urine
• can be endemic & difficult to eradicate
Basics of Leptospira
o Order: Spirocheaetales
Families
• Leptospiraceae: Leptospira,
• Spirochetaceae: Brachyspira, Borrellia, Treponema
o Spiral shaped o Gram (-) o obligate pathogen o no replication but persists in environment o likes wet environments
Leptospira Encounter: direct v indirect encounter, maintenance v accidental hosts
- Persists in renal tubules & genital tract of carrier animals
- Infected animals shed in urine & contaminate environment
Direct:
• From infected animal to healthy via urine
Indirect:
• from contaminated env -> healthy animal
Maintenance host
• Rodents w/ icterohaemorrhagiae
• Cattle w/ hardjo
• Dogs w/ canicola
Accidental host
• Dogs, cattle, humans w/ icterohaemorrhagiae
• Humans w/ canicola
Leptospira Pathogenesis & virulence factors
- penetrate thru intact mucous membranes or abraded or water softened skin ->
- enter systemic circulation ->
- multiply rapidly & spread to many tissues
- renal colonization in most infected animals
Virulence Factors
• LPS: incites significant damage
• hemolysins: lysis of cells
• flagellum: for movement thru body
Leptospira clinical findings in dogs, cattle, horses
Dogs
Uremic type
o Inappetance, lethargy, vomiting, PU/PD, fever
o Oliguria, anuria and severe renal azotemia
o UA: gluc, prot, active sediment, granular casts
Icteric Type
o Focal hepatic necrosis
o Icterus, mild-moderate hypoalbuminemia
o Chronic active hepatitis, fibrosis, failure
o Peak signs 6-8 days post-onset (lags behind renal signs)
Cattle
• Abortion 4mo – term
• Dam: Icterus, Hemoglobinuria, fever, Mastitis
• Calf: IMHA, anemia, acute renal failure
Horses
• Recurrent uveitis
• Acute renal failure in foals
Immunity to Leptospira & what does immunity in cattle, pigs, dogs, horses, & sheep look like?
- Immunity to Lepto is conferred via Ab directed against LPS.
- Adequate Ab response within 7-10 days PI
- little cross protection across serovars but may have some
IMPORTANT:
• Cattle: subclinical w/ or w/o lepto in urine
• Pigs: infected w/ Pomona = subclinical w/ lepto in urine
• Dogs: infected w/ canicola = subclinical w/ lepto in urine
• Horses: recurrent uveitis & maybe blindness
• Sheep: infected w/ hardjo = subclinical w/ lepto in urine
Diagnosis of Leptospira
- U/A for Hematuria, pyuria, proteinuria, glucosuria
- Increased BUN and creatinine, thrombocytopenia Increased serum bilirubin, ALP (icteric form)
- Can be isolated from blood or urine
- Dark field microscopy on urine
- Microscopic agglutination test to look for Ab
- NO culture
Treatment & Prevention of Leptospira
Treatment
• Eliminate active infection and carrier state w/ antimicrobials
o Dogs – ampicillin / doxycycline
o Horses- PenG / Oxytetracycline
o Cattle – Oxytetracycline/ Dihydrostreptomycin
• Treat systemic complications
Prevention
• Bacterins
• Vaccinate in endemic areas: 2 to 3 injections, 2 or 3 weeks apart (boost every 6 to 8 months)
• Vx effective ONLY if targeting the serovars currently in the environment
Nosocomial V Iatrogenic Infections
nosocomial infection
o new infection acquired during hospitalization
iatrogenic infection
o acquired by direct action of a veterinarian (or technician)
Sources of Nosocomial Infections
o Invasive Devices
o Patient Flora
o Medical personnel
o Hospital environment
Flora Carried by Certain Species that can cause nosocomial infection
- Salmonella - horses
- Bordetella bronchiseptica - dogs
- Chlamydophila psittaci - birds
- Feline Viral Rhinotracheitis - cats
- Normal flora that gains access to a normally sterile site (E. coli pneumonia or UTI, Staph intermedius bacteremia)
Control of Nosocomial Infections; define: sterilization, disinfection, antisepsis, germicide, sanitation, decontamination, & cleaning
Sterilization
• destruction of all living organisms, including spores
• autoclave @ 121C for 15 mins; monitor w/ Bowie Dick tape test
• ethylene oxide used for heat intolerant materials
disinfection
• elimination of all vegetative organisms, but not spores from an inanimate object
antisepsis
• treatment of living tissue in an attempt to destroy all vegetative organisms
germicide
• agent that destroys vegetative organisms on either tissue or an inanimate object
sanitation
• removal of organism numbers to an acceptable level for public health standards
decontamination
• removal of pathogens to allow safe handling of material
cleaning
• removal of organic material
Basics of Postoperative Infections
o Staph aureus can invariably be isolated from operative area
o surgical procedures limit risk of surgical wound infection
o source of contamination = patient’s skin
o Surgical prepping reduces bacterial numbers on skin.
o Minimal time in surgery minimizes tissue desiccation.
o Good technique minimizes tissue damage.
o Can prescribe pre-operative or perioperative antibiotics
o Rate of infection doubles every hour patient is under
1st line V 2nd line antibiotic therapy for perioperative use
First Line • Routinely used in hospitals • Work 75-85% of the time • Older generation & low cost • Ie. Penicillin, trimethoprim/sulfa, gentamicin
Second Line • Restricted use • Work 85-95% of time • Newer more expensive drugs • Ie. amikacin, ticarcillin, imipenem, vancomycin
