Unit 1 Flashcards
three factors that drive whether or not a pathologic agent will cause disease
- susceptible host - conducive environment - pathogen
____ is the ability of an organism to cause disease
pathogenicity
____ is the degree of pathology caused by the organism (and is dependent on conditions)
virulence
what variety of organism only invades host cells when they can gain a selective advantage in the host
facultative intracellular pathogens
list some ways pathogens can be transmitted
- animal vectors - direct contact - fomites - droplets - airborne - fecal-oral
list the general immune responses to infection in the order that a pathogen meets them
physical barriers innate immunity adaptive immunity (humoral and cellular)
____ is the ecological community of commensal, symbiotic, and pathogenic microorganisms found in and on all multicellular organisms
microbiota
what is the function of flagella and another name for them
- motility - H Antigen
what is the function of Pili/fimbriae and another name for them
- adhesion - F Antigen
Capsules
composition?
function?
composition: polysaccharide and water function: antiphagocytic and protects against complement
what is the key ingredient in bacterial cell walls
peptidoglycan cross-linked with NAM and NAG
what is the cell wall composition for gram positive bacteria
very thick peptidoglycan layer and a thin inner plasma membrane
____ and ____ guide the immune response for gram positive bacteria
teichoic and lipoteichoic acids
what is the cell wall composition for gram negative bacteria
a sandwich of outer membrane, peptidoglycan, and plasma membrane
what induces inflammation/immune response in gram negative bacteria
the Lipid A portion of Lipopolysaccharide
why are gram negative bacteria more prone to a toxic immune response
the Lipid A portion of Lipopolysaccharide isn’t “visible” until the cell lyses, and then acts as an endotoxin and triggers a cytokine storm
what is a virulence factor
any bacterial factor that enhances a bacterium’s ability to colonize, invade, replicate within, and/or damage the host
what is Koch’s postulate
that virulence factors are encoded by genes and if these genes are inactivated then the pathogen is less virulent
what process does pili/fimbriae
adhesion (enhances it)
what process do toxins and exoenzymes affect
invasion of tissues (break down barriers that hold host cells together)
what process do capsules affect
immune invasion
____ are proteins produced and secreted by bacteria with a specific activity
exotoxins
____ are part of the bacterial cell wall that is usually released when the bacterium is lysed (Lipopolysaccharide in gram negatives)
endotoxins
four ways that exotoxins can act as super antigens to cause sepsis and shock
- damage cell membrane - disrupt signaling pathways - act of extracellular tissue - cause constant immune stimulation
a ____ is an organism that grows on and derives nourishment from dead or decaying organic matter (soil)
saprophyte
fungi are known as ____ because they require external carbon
heterotrophs
what makes up a mold
mycelium made of hyphae
molds that have hyphae with septa are:
septate
molds that have hyphae without septa are:
coenocytic
molds that are pigmented are:
dematiaceous
molds that aren’t pigmented are:
hyaline
a fungi (usually pathogenic) that is a mold at room temperature and yeast at body temperature is known as a:
dimorphic
three components found in the fungal cell wall
chitin, glucans, and mannoproteins
two components of the fungal cell membrane
- phospolipid bilayer
- sterols such as ergosterol, zymosterol (not cholesterol)
spores are fungal reproductive structures that germinate and yield a new ___
mycelium
what fungal spore structure is shown?
a sporangium filled with sporangiospores
what fungal spore structure is shown?
arthrospores
what fungal spore structure is shown?
a: macroconidia
b: microconidia
what fungal spore structure is shown?
blastospores
what fungal spore structure is shown?
chlamydospores
what fungal spore structure is shown?
zygospore
list some predisposing factors to fungal invasion
- immunosuppression (stress, steroids, diabetes, autoimmune)
- prolonged antibiotic therapy
- immune defects
- immaturity, aging, malnutrition
- heavy exposure to spores
- compromized tissues
- persistently moist skin
what is the function of the polyene Amphotericin B
kills fungi by binding both ergosterol and cholesterol
can cause nephrotoxicity
what is the mechanism of action of the antifungal class: azoles
inhibit synthesis of ergosterol, which disrupts the cell membrane
fungistatic (not fungicidal) so it takes prolonged treatment because several generations have to pass
what is the mechanism of action of the antifungal class: allylamines
inhibit
allylamines are especially good for treating _____
dermatophytes
what drug would you use to treat Candida or Cryptococcus
Flucytosine
an _____ is a naturally occuring chemical, whereas an ______ is a naturally occuring or manmade chemical
an antibiotic is a naturally occuring chemical, whereas an antimicrobialis a naturally occuring or manmade chemical
four mechanisms of action of antimicrobials
1: affect cell wall/membrane integrity
2: interfere with protein synthesis
3: impede DNA repair and replication
4: block metabolic pathways
what is the mechanism of action of β-Lactams
they inhibit cell wall synthesis by binding to the enzymes involved in the production or cross-linking of peptidoglycan
three main classes of β-Lactams
- penicillins
- cephalosporins
- carbapenems
how often are carbapenems used
not often. theyre saved as the last resort antibiotics
which class of β-Lactams is known for being more resistant to β-Lactamases
cephalosporins
what is the mechanism of action of glycopeptides
inhibit cell wall synthesis (different class than beta lactams though)
what is the mechanism of action of Polymyxins
disrupt cell membrane phospholipids by binding the Lipid A region of LPS
what formulation are polymyxins usually given in and why
mostly topicals because the systemic form causes nephrotoxicity and neurotoxicity
what are some examples of drug classes that inhibit protein synthesis
- tetracyclines
- macrolides
- lincosamides
- aminoglycosides
- phenicols
three classes of drugs that affect nucleic acids
fluoroquinolones
nitroimidazoles
nitrofurans
two classes of drugs that disrupt the folic acid pathway
sulfonamides
trimethoprim
what are some good antibacterials for anaerobes
nitroimidazoles
beta-lactams
macrolides
tetracyclines
what are some bad antibacterials for anaerobes
aminoglycosides
fluoroquinolones
what would be a good antibacterial for a mycoplasma (no cell wall)
tetracyclines
macrolides
lincosamides
what is a good choice of antibacterial for intracellular bacterial
tetracyclines
phenicols
macrolides
lincosamides
what drugs would you administer to cover a four-quadrant approach
beta-lactam with metranidazole
what is a “four quadrant approach” and when is it important
a four quadrant approach affects gram positives, gram negatives, aerobic, and anaerobic organisms
important is critical situations where you cant wait for a culture result
what is intrinsic resistance
an innate ability to resist through structural or functional characteristics and not through genomic changes (these organisms have never been susceptible)
why dont aminoglycosides work on anaerobes
they lack the oxidative metabolism needed to uptake aminoglycosides
what are some characteristics/structures of biofilms that help with intrinsic resistance
- electrical charge
- efflux pumps in the slime
- slow growing cells at the bottom layer (so theyre hard to kill)
four mechanisms of antibiotic resistance
- pump out the drug (efflux pumps)
- modify/ inactivate the drug (enzymes)
- modify the drug target
- inhibit drug uptake (modified cell wall proteins)
three methods of acquired resistance
mutation of current genes
acquisition of foreign genes
combination of both
what is acquired resistance
bacteria obtains the ability to resist the activity of a particular agent to which it was previously susceptible
what is a plasmid
a circle of DNA that can move between cells
what is a transposon
small piece of DNA that moves back and forth between chromosomes and plasmids
how can bacteriophages enable horizontal gene transfer
they attack bacteria and can carry DNA from germ to germ
what are the three methods of horizontal gene transfer
transduction (movement via phages)
conjugation (germs connect directly)
transformation (genes released from nearby and picked up by another germ)
what are some ways to avoid the judicious use of antibacterials
- culture and sensitivity (low budget? gram stain)
- avoid combination therapy unless indicated
- identify compliance issues
- prevent in-house infections
four common ailments/procedures that dont call for antimicrobials
- feline lower urinary tract disease
- spay/neuter
- feline upper respiratory disease (usually viral)
- kennel cough (self-limiting)
what can you do instead of medicated milk replacer
adequate colostrum within 24 hours
husbandry and management
what can you do instead of using antibiotics for neonatal scours
rehydrate only unless systemic
colostrum management
hygiene & cleanliness
reduce stress
regulate traffic flow
vaccination protocols
what can you do instead of using antibiotics for mastitis
culture samples with high somatic cell count (number of neutrophils in the milk)
dont treat if about to cull or dry off
MANAGEMENT
How can you prevent bovine respiratory disease
wean/castrate/dehorn at least 30 days prior to shipping (stress)
parasite treatment
vaccinate
biosecurity
four instances where a four quadrant approach would be indicated
pilonephritis (kidney infection)
prostatitis
pneumonia
sepsis
Ringworm
disease name:
location on host body:
zoonotic?
Ringworm
disease name: dermatophytosis
location on host body: keratinized structures (hair, skin, nails)
zoonotic? YES, can jump species
how is dermatophytosis (ringworm) diagnosed and treated
diagnosed suggestively with Wood’s lamp (UV) and definitively with a DTM culture.
treated with topical therapy
Dermatomycosis
what pathogen:
predisposing factors:
effect of overgrowth:
Dermatomycosis
what pathogen: Malassezia pachydermatis
predisposing factors: immunosupression (normally is present in small numbers)
effect of overgrowth: dermatitis and otitis
Aspergillosis
species affected:
contracted by:
other:
Aspergillosis
species affected: birds, horses (guttural pouch mycosis), dogs (nasal aspergillosis), cattle (placentitis/abortion)
contracted by: usually inhalation of spores
other: factors into otitis, abortion, mastitis, and systemic disease
histoplasmosis
form:
found (environment and geographical):
symptoms:
histoplasmosis
form: dimorphic, soil saprophyte and yeast in body
found (environment and geographical): soil in areas with bird and bat feces. Mississippi and Ohio River Valley
symptoms: granulomatous lung lesions and possible disseminated disease
list two important pyogenic (induce pus formation) bacteria
Saphylococcus,
Streptococcus
Staphylococci
Morphology:
arrangement:
oxygen needs:
behavior:
Staphylococci
Morphology: gram positive cocci
arrangement: clusters
oxygen needs: most are facultative anaerobes
behavior: opportunistic, colonize nasal cavity, nasopharynx, skin, and mucous membranes
what is the main pathogen that causes abscesses, mastitis, dermatitis, and “bumble foot”
Staphylococcus aureus
what is the main pathogen that causes canine and feline pyoderma
Staphylococcus pseudintermedius
three main virulence factors of staphylococcus aureus
- secreted factors (toxins, enzymes, and invasins)
- membrane-bound factors (adhesins)
- capsule/slime layer
Streptococci
Morphology:
arrangement:
oxygen needs:
behavior:
other:
Streptococci
Morphology: gram positive cocci
arrangement: chains
oxygen needs: facultative anaerobes
behavior: commensal organisms of the upper respiratory mucosa and lower urogenital mucosa
other: most have capsule
list some bacteria that belong in the group Enterobacteriaceae
Escherichia coli
Salmonella
Yersinia (plague)
Enterobacter
many Enterobacteriaceae are considered Coliforms. what does this mean?
they are gram-negative rods, non-spore forming, and ferment lactose and are found in large numbers in feces of warm-blooded animals
Escherichia coli
morphology:
predisposed individuals:
general symptoms:
symptoms in freshly weaned pigs:
Escherichia coli
morphology: enterobacteriaceae so gram-negative rods
predisposed individuals: young animals without established immune system
general symptoms: neonatal sepsis and diarrhea, UTI from fecal contamination
symptoms in freshly weaned pigs: conjunctivits and ciguatoxin (bloody eyes)
Clostridium
morphology:
large, spore-forming, gram-positive rods
list two main endospore forming bacterium
bacillus and clostridium
list the four types of exotoxin driven disease caused by clostridia
- Neurotoxic (tetanus and botulism)
- histotoxic (blackleg, bacillary hemoglobinuria)
- enteropathogenic (clostridial enterocolitis)
- atypical (Tyzzer’s Disease)
what makes Mycobacterium hard to kill and stain
their cell wall is lipid rich
Mycobacterium
symptoms:
treatment issue:
zoonitic?
Mycobacterium
symptoms: chronic granulomatous lesions (macrophages)
treatment issue: multidrug resistance
zoonitic? YES, especially bovine tuberculosis
Rickettsiales
oxygen requirements:
obligate intracellular
what is the tissue target of Rickettsiaceae
vascular endothelium
what is the tissue target of Anaplasma
erethrocytes, platelets, and leukocytes
what is the tissue target of Ehrlichia
leukocytes
what is the tissue target of Neorickettsia
leukocytes
what is sepsis
sepsis occurs when an infection triggers the systemic inflammatory response system (SIRS) and the body is unable to maintain a physiological normal and leads to DIC and death
infection + SIRS = sepsis
list some common presenting clinical signs of sepsis
bounding to weak pulses,
brick red mucous membranes (dog),
pale mm (cat),
fever (dogs) or hypothermia (cats),
tachypnea,
hypotension,
lethargy
what lab abnormalities are common for an animal in sepsis
anemia (esp cats),
elevated hematocrit,
left shift and toxic change,
thrombocytopenia,
hyperlactemia,
clotting disorders
disease of what system is most likey to result in sudden death
cardiovascular
list some common bacterial causes of sudden death
anthrax, clostridial disease, anaplasmosis, salmonella, Leptospirosis, MRSA, Streptococcus equi, acute pneumonia
list some common viral causes of sudden death
Classical and African swine fever, distemper
list some common toxin-driven causes of sudden death
bracken fern, sweet clover, lead, blister beetles
list some common trauma causes of sudden death
lightnight strike, bloat, colic
Bacillus anthracis
morphology:
longevity:
oxygen requirements:
Bacillus anthracis
morphology: gram-positive spore-forming saprophyte
longevity: spores remain viable in soil for 50 years
oxygen requirements: facultative anaerobic
what are the presenting clinical signs of a ruminant with anthrax
peracute:
acute:
peracute/acute:
what are the presenting clinical signs of a ruminant with anthrax
peracute: SUDDEN DEATH
acute: high fever, weakness, convulsions, death
peracute/acute: tachycardia, tachypnea, melena, bloody milk
presenting clinical signs of a horse with anthrax
rapidly developing subcutaneous edema, fever, severe colic, bloody diarrhea, death in 2-3 days
presenting clinical signs of a dog with anthrax
pharyngeal edema, gastroenteritis
describe the lesions found during an anthrax necropsy
“blackberry jam” spleen, hemorrhages of skin and lymph nodes, bloody discharge from orifices, failure of blood to clot, delayed or incomplete rigor mortis
list three virulence factors of anthrax
capsule (inhibits phagocytosis)
tripartitie exotoxin
host macrophages (release toxic contents when they explode)
what cell recognizes and engulfs anthrax spores in the host
macrophages
describe how Tripartite Exotoxin of Anthrax works
- protective antigen forms a hole for entry of other toxins
- edema factor causes fluid release and edema
- lethal factor inhibits cytokine release
list some techniques helpful for diagnosing anthrax
paying attention to the time of year
blood smears allowed to grow
culture
PCR
what should you do for necropsy of a suspected anthrax case
collect blood with needle and syringe from ear or tail vein
do not send ears
if animal is already open, collect spleen (otherwise leave carcass closed so vegetative cells will die eithout sporulating)
how is anthrax treated
prevented
treated with penicillin, tetracyclines, and quarantine
prevented by live vaccination
Anthrax zoonosis
most common transmission route:
highest mortality rate route:
Anthrax zoonosis
most common transmission route: cutaneous (from contacting an infected carcass)
highest mortality rate route: inhalation
list four clostridial agents and the disease they cause that are associated with toxemia induced fatality
Blackleg: Clostridium chauvoei
Bacillary Hemoglobinuria: Clostridium haemolyticum
Malignant Edema: Clostridium septicum
Hemorrhagic bowel: Clostridium perfringens A
Feline Infectious Anemia
pathogen:
signalment:
signs:
transmission:
Feline Infectious Anemia
pathogen: Mycoplasma haemofelis
signalment: outdoor males
signs: weakness, pallor, tachypnea, tachycardia, collapse
transmission: fleas and bite wounds (blood contact)
Mycoplasma haemofelis
appearance on blood smear
epicellular, small gram-negative rods on the periphery of RBC
why might a cat come up positive on PCR for FIA but their blood smear was clear
FIA is cyclical anemia, the pathogen is at lowest when RBC number is lowest
how is FIA treated
supportive care (oxygen and transfusion), doxycycline, and enrofloxacin/marbofloxacin
will not be completely eliminated
is FIA zoonotic?
rarely. usually it is species specific
cat scratch fever
pathogen:
signalment:
transmission:
symptoms:
zoonotic?
cat scratch fever
pathogen: Bartonella henselae
signalment: shelter kittens, especially young or immunosupressed
transmission: fleas
symptoms: lymphadenopathy and contributes to endocarditis
zoonotic? yes, but self limiting
Bovine anaplasmosis
pathogen:
symptoms:
transmission:
Bovine anaplasmosis
pathogen: Anaplasma marginale
symptoms: progressive anemia due to extravascular destruction of erythrocytes
transmission: ticks or used needles
anaplasma marginale
morphology:
how it causes disease:
anaplasma marginale
morphology: gram-negative obligate intraerythrocytic cocci
how it causes disease: the erythrocytes get coated in antibodies that are phagocytosed by macrophages in the spleen and liver
does anaplasmosis cause hemoglobinuria?
does babesia?
does anaplasmosis cause hemoglobinuria? NO
does babesia? YES
Anaplasmosis
diagnosis:
Treatment:
prevention:
Anaplasmosis
diagnosis: cELISA is gold standard. blood smear
Treatment: tetracycline or Imidocarb
prevention: vector control and good hygiene
Canine Cyclic Thrombocytopenia
pathogen:
action:
transmission:
Canine Cyclic Thrombocytopenia
pathogen: Anaplasma platys
action: infects platelets and cause thrombocytopenia
transmission: tick vector
Bacillary Hemoglobinuria
pathogen:
primary sign:
Bacillary Hemoglobinuria
pathogen: Clostridium haemolyticum
primary sign: intravascular hemolysis causes hemoglobinuria (“red wine urine”)
Rocky Mountain Spotted Fever
pathogen:
role of ticks:
clinical signs:
Rocky Mountain Spotted Fever
pathogen: Rickettsia rickettsii
role of ticks: vector AND reservoir (must be attached for 5-20 hours)
clinical signs: vasculitis
rocky mountain spotted fever
diagnosis:
treatment:
zoonotic:
rocky mountain spotted fever
diagnosis: paired sera taken 10-14 days apart (ELISA)
treatment: doxycycline
zoonotic: yes but from ticks not dogs
describe the Ehrlichia spp. life cycle
- taken into a leukocyte
- it envades lysosomes through inhibition of phagosome-lysosome fusion and undergoes binary fission to replicate
- clusters of bacteria form morulae (like a lil pouch of bacteria)
- exit and spread through lysis and cytoplasmic projections
Canine Monocytic Ehrlichiosis
pathogen:
vector:
treatment:
Canine Monocytic Ehrlichiosis
pathogen: Ehrlichia canis
vector: brown dog tick
treatment: doxycycline for 3 weeks
Ehrlichia acute phase symptoms
fever, anorexia, occulonasal discharge, lymphadenopathy, limb edema, possible nerve deficits, thrombocytopenia
Ehrlichia chronic phase symptoms
splenomegaly, renal failure, pneumonitis, uveitis, meningitis, severe thrombocytopenia, pancytopenia, severe weight loss
four diseases tested for by the SNAP 4Dx Plus
Heartworm (Dirofilaria immitis)
Lyme Disease (Borrelia burgdorferi)
Ehrlichiosis (E. canis and E. ewingii)
Anaplasma
Canine Granulocytic Ehrlichiosis
pathogen:
vector:
symptoms:
treatment:
Canine Granulocytic Ehrlichiosis
pathogen: Ehrlichia ewingii
vector: lone star tick
symptoms: polyarthritis, lameness, joint swelling, stiff gait
treatment: doxycycline
Equine Granulocytic Ehrlichiosis
pathogen:
vector:
symptoms:
Equine Granulocytic Ehrlichiosis
pathogen: Anaplasma phagocytophilum
vector: Ixodes ticks
symptoms: necrotizing vasculitis, fever, anorexia, depression, limb edema, petechiation, icterus
how is Equine Granulocytic Ehrlichiosis
detected:
treated:
how is Equine Granulocytic Ehrlichiosis
detected: PCR, IFA
treated: oxytetracycline and tick control
Equine Monocytic Ehrlichiosis (Potomac Horse Fever)
pathogen:
causes:
vector:
Equine Monocytic Ehrlichiosis (Potomac Horse Fever)
pathogen: Neorickettsia risticii
causes: acute enterocolitis
vector: trematodes
Tularemia
Pathogen:
zoonosis:
vector:
easily confused with:
Tularemia
Pathogen: Francisella tularensis
zoonosis: very very. most common in sheep, cats, and rabbits
vector: ticks
easily confused with: plague, pseudotuberculosis, pneumonia
Francisella tularensis
morphology:
infects:
which subspecies is worse:
Francisella tularensis
morphology: gram-negative facultative intracellular coccobacillus
infects: macrophages
which subspecies is worse: Type A is highly virulent and found in NA only
three ways Tularemia can be transmitted and their resulting forms
- aerosol transmission: pneumonic form
- direct contact: ulceroglandular or occuloglandular forms
- ingestion: oropharyngeal or typhoidal form
four steps of Tularemia pathogenesis
- local ulcerative lesion
- local lymphadenopathy
- transient bacteremia
- spread to lymph nodes, liver, spleen, bone marrow, and sometimes lung
Tularemia
diagnosis:
treatment:
Tularemia
diagnosis: culture, 4-fold increase in antibody titers, lymph node aspirate/biopsy
treatment: isolation, tetracycline, streptomycin, gentamicin, fluoroquinolones
Plague
pathogen:
morphology:
zoonosis:
transmission:
Plague
pathogen: Yersinia pestis
morphology: small gram-negative coccobacillus
zoonosis: yes. rodents, humans, cats, and dogs
transmission: fleas
three forms of plague
bubonic form
septicemic form
pneumonic form
plague
diagnosis:
treatment:
plague
diagnosis: lymph node aspirates, biopsies
treatment: aminoglycosides and tetracyclines for three weeks
Glanders
pathogen:
zoonosis:
transmission:
pathogenesis:
Glanders
pathogen: Burkholderia mallei
zoonosis: yes. mostly equids but also cats and humans
transmission: ingestion of food or water contaminated with nasal discharges
pathogenesis: ulcerative nodules in nasal cavity, respiratory tract, lungs, and skin resulting in septicemia
Melioidosis
pathogen:
morphology:
species affected:
pathogenicity:
Melioidosis
pathogen: Burkholderia pseudomallei
morphology: motile gram-negative facultative anaerobe
species affected: sheep goats and pigs but zoonotic through mastitic milk
pathogenicity: suppurative or caseous lesions of lungs, liver, spleen, lymph nodes, or SQ tissue
signs of right-sided heart failure
ascites, GI congestion (causes anorexia, GI distress, and weight loss), liver congestion
signs of left sided heart failure
decreased cardiac output
pulmonary congestion
definition of endocarditis
inflammation of the inner layer of the heart (endocardium)
what are the steps that lead to vegetative lesions of the heart and what are they composed of
microbial colonization of the heart valves because of the turbulence there. microbes expose underlying collagen. platelets aggregate on collagen. coagulation cascade is activated.
vegetative lesions are aggregates of platelets, fibrin, blood, and bacteria
