DWT Exam 1 Flashcards
Reticulocytes in cat
Aggregate and punctate
Increased nucleated RBCs is called
Metarubricytosis
Normal regenerative Reticulocytes numbers <dog></dog>
Dog >800000
Cat >600000
Horse none
Appropriate metarubricytosis
Is when there is also Reticulocytosis regeneration so bone marrow releases both
Inappropriate metarubricytosis -bone marrow and spleen
Bone marrow cant hold nRBC and usually nRBCs removed by the spleen
Mean corpuscular volume
The size change in of the cell - micro or macrocytosis
What do you use to determine anemia
Hct or PCV
What increases bilirubin in circulation/ blood?
Hemolysis
Fasting hyperbilirubinemia
Functional Cholestasis
Obstruction Cholestatis
Enzootic or endemic
Continuous transmission -disease presence in location multiple times
En=on going
Epizoonotic
Peaks in baseline (endemic damage); high damage here
World wide epidemic
Pandemic
Isatrogenic and Nosocomical infections are similar because
They happen under care of veterinarians
Recrudescence defined
Is when the latent virus flares up with stress
Vertical transmission
Virus embedded in genome and passed through the germ line- this happens with retrovirus which wont shed
Susceptible vs permissive
Susceptible = able to be infected
Permissive = able to create viral progeny
What determines the host range for a pathogen?
The glycoproteins on the host
The process of viral infection :
1 attachment is no energy
2 penetration
3 uncoated to release genome into cytoplasm
4 mRNA translation
5 dna/rna replication
6 Maturation and assembly [intracellular, at PM, or at nuclear membrane]
Disease is in __
Cytopathic Effect is in ___
Define CPE
Disease in Vivo
CPE in vitro (synctia, inclusion bodies [think nuclear inclusion bodies in herpes], lysis, rounding
CPE is the morphological changes that happen to virus infected cell
There are 3 mechanisms by which virus spread to organs (systemic spread)
Name the most efficient
Viremia (hematogenous spread ) most efficient
Lymphatic spread
Neural spread- cns
Saprophyte
Lives on decaying organic matter and can sometimes cause disease (parasite but not usually a pathogen)
Parasite
A general term that is an organism that lives on or with another which it gets sustenance from
Have the potential to be a pathogen
Susceptibility vs permissive -virus
Pathogenicity vs virulence -bacteria
Infectivity
Susceptible= ability to enter and infect host
Permissive = ability to make new viral progeny in the cell
Pathogenicity = ability of bacteria to cause disease
Virulence = the variation in the ability; how much disease caused by bacteria
Infectivity = bacterias ability to enter tissue and multiple and infect
Define and which is more common: obligate pathogens and opportunistic pathogens
saprophytes are which?
Opportunistic pathogens- bacteria that is normal flora and cause disease when something changes in host
What is the most common reason the host lets in less virulent pathogen?
Bc of tissue damage and lower host innate defense mechanisms
NOT immunocompromised
High or low virulent bacteria: which are opportunistic pathogens?
Note: they are also commonly isolated from infection= highly virulent
Need less host tissue compromise and less numbers of bacteria
When biofilm act as organism
Quorum sensing
Name host predisposing factors: 3 of them
1 innate factors (age species sex)
2 Internal factors - Internal damage
3 External factors -nutrition environment
Define fomite
A source of bacteria
It is an inanimate object that has bacteria residing on it
The process of bacterial infection
Attachment
Penetrate
Evade host mechanism
Ability to multiply and cause damage to host= virulence factors
Highly virulent bacteria :
S. Aureus, E. Coli, Streptococci
Low virulent bacteria:
S. Epidermidis, Norcordia spp.
Hypertrophy
When the size increases but the number of cells does not increase
Hyperplasia
Increase in the number of cells that results
Still increase size of tissue
Difference between hyperplasia and neoplasia
Hyperplasia is controlled and neoplasia is uncontrolled by stimulus
Atrophy
When tissue fully developed
Had all these cells originally but now they have gone away
Hypoplasia - is when the tissue is not fully developed from immunological standpoint but there is fewer cells
Mechanisms of cell injury (different from causes)
Atp depletion
Gene destruction
Membrane disruption
Metabolic disturbance
Etiologic
The cause of the disease
Causes of cell injury
Oxygen loss [hypoxia, ischemia]
Physical destruction
Genetic damage
Workload imbalance [like w hypertrophy- just making cells bigger]
Nutrition
Age
Immune disfunction
Toxins
Connect infarction, hypoxia, and ischemia
Ischemia means there is less blood flow to a tissue
Which results in hypoxia where the tissue is not oxygenated enough
If it gets really bad then it becomes an infarction where the tissue becomes necrotic
Reversible cell injury
Hydropic degeneration leads to sodium and water in cell which causes cytoplasmic vacuoles
Ischemia -reperfusion injury
This is when there is low blood flow then there is blood flow and oxygen which leads to ROS production which furthers tissue damage
Pyknosis
Necrotic cell is shunk, round, dark
Karyorrhexis
Nuclear fragmentation
Karyolysis
Nuclear dissolution ; pale nucleus
Heinz bodies
Aggregates of hemoglobin due to oxidative injury
Different types of hemolytic anemia
Immune mediated hemolytic anemia ; bilirubin [extravascular], sphereocytes [extravascular], ghost cell [intracellular membrane attack complex], agglutinations
Infectious hemolytic anemia
Oxidative hemolytic anemia - chocolate blood; iron loss= methemoglobinemia, globin loss= heinz bodies, membrane destroyed= eccentrocytes
Fragmentation hemolytic anemia
Oxidative hemolytic anemia clinical signs:
Toxin ingestion
Empirical therapy:
administration of therapy based on previous experience
Aetiological diagnosis or definitive diagnosis
Specific identification of bacteria causing disease
Identify the bacteria definitively by…
Collecting a sterile sample and culturing
Finding antibody
Finding antigen
DNA detection of the bacteria
Site with normal flora need to see:
Pathogens that are not a part of the normal flora of that region that can cause disease
OR an increased amount of the normal flora that can cause disease
Bacterial infection determination
- Is it bacteria- pathognomic evidence?
- Presumptive [empirical therapy] or definitive analysis
- Which test [collect sample, antibody, antigen, genetic]
- Where to collect sample
- Time to collect sample [disease shed, antibiotics,
- Specific location localized
- Is this a sterile site
- are strict anaerobes involved?
- How to collect bacteria
- Sampling site
- Evaluate collected sample
- Stable transport to lab
Is a draining tract the site of infection?
NO
Where does the fat go
Bone marrow
Heart
Around kidney
Mesentery
Subcutaneous
What are the 5 gross patterns of necrosis
Coagulation necrosis where blood is cut off
Casseous necrosis- leukocytes [leuk its cheese]
Liquificaitive necrosis
Gangrenous necrosis- localized
Fat necrosis - sopinification of fat
Compare contrast necrosis and apoptosis
Necrosis the cell expands and there is inflammatory response ->pyknosis, karyorrhexis, karyolysis.
Apoptosis. The cell shrinks -> apoptotic bodies that macrophages eat
- no inflammatory response
What activates the caspase cascade
Apoptosis signals:
Intrinsic -mitochondrial membrane damage which leads to proapoptosis chemical cytochrome C release
Extrinsic - which is the FAS receptor TNF receptor family
Dystropic calcification vs metastatic calcification
Dis trap house - in the trap house that the necrosis happened at - locally at the site is calcium released into mitochondria
Metastatic- calcium in the blood circulation
- renal failure ; Vit D inc; increased parathyroid hormone ; bone destruction
Cells getting old leads to…
Less oxidative phosphorylation
Less nucleic and protein synthesis
Shorter telomeres - less replication
Intracellular accumulation…
Abnormal cell metabolism
Lipids
- hepatic lipidosis : too much fat as triglycerides going to liver-> liver overworked OR decreased metabolism of fat [if losing weight then the fat needs to be broken down right]
Glycogen
Pigment - melanin /tattoo ink
Enveloped or non enveloped associated with seasonal disease?
Enveloped
Composition of virus
Viral genome -DNA or RNA not both
Viral protein:
Structural protein : the virion (viral attachment protein)
Spike protein
Non-structural- enzymes for replication/ polymerases
[esp in rna virus that replicates in cytoplasm]
Lipid
DNA virus is shaped …
Icosahedral
Viral incubation period >< generation time
Incubation period is from the point of getting infection to showing signs
Generation time is point of getting illness to spreading infection
I > G
Bovine respiratory disease complex (2 virus) family? Name? Which is more severe?
Bovine parainfluenza 3 BI3
Bovine Respiratory Synactia Virus BRSV- more severe
Both not immunogenic and from the paramyxovirus
Bovine papular stomatitis vs vesicular stomatitis virus
Both affect mucosa of bovines
Bovine papular stomatitis is a dsDNA virus in the pox virus family so it is enveloped with intracytoplasmic inclusion bodies
Bovine Vesicular stomatitis is a ssRNA virus in the Rhabdovirus family that subclinical and endemic
Negri body
Intracytoplasmic inclusions of the rabies vaccine - part of the rhabdovirus
Antigenic shift vs antigenic drift
Antigenic shift is the ability to combine segmented DNA to create a new strain via recombination - othomxyoviridae, reovirus, bunyavirus all have segmented genomes
Cause of diarrhea in young pigs and calves
Bovine Viral Diarrhea Virus [ssRNA] - pestivirus
Bovine coronavirus - coronavirus
Pigs: Transmissible Gastroenteritis coronavirus
and Porcine epidemic diarrhea virus - something else
Virulence factors for bacteria
Villi for attachment, slime capsule for evading host phagocytosis, survival within cells (facultative intracellular parasite), iron sequestering, survival in protected site, toxin to cause tissue damage
Acid fast bacteria
Is least affected by detergents and exists within cells
Gram Positive is more affected by detergents than gram negative
Microcytic and hypochromic are indicative of
Iron deficiency
ITAM
In t and B cells - are attached to the alpha and beta receptors and help transduce the signal of the antigen binding into the cell
- a continuation of the TCR
- on side of Immunoglobulin with Ig a and Ig b
Which t cell helps kill intravescular pathogens? ( different from cell death)
CD4 which brings in the macrophages, B cells, ETC after binding to the MHC class 2
Erythrocytosis is induced by ___ growth factor
Erythropoietin is what is released from the kidneys
which is a growth hormone that drives RBC formation
- decreased erythropoietin leads to selective erythroid hypoplasia due to chronic kidney disease
- increased erythropoietin leads to Absolute secondary erythrocytosis (appropriate or inappropriate)
Features of epitopes recognized by B cells
4 functions of antibody
Neutralization _-toxins
Opsinization extra cellular - think going on OPPs is extra
Complement activation leads to lysis and ingestion ‘
Adcc -antibody dependent cellular toxicity when antibody is on target cell it binds Fc gamma and attracts nk (natural killer)
Mast cell activation
Uses IgE and Fc epsilon to bind to mast cell and real ease histamine granules that lead of allergic response
Most abundant immunoglobulin
IgA
Urticaria
Hives
Neonatal Isoerythrolysis in Horses
Type 2 hypersensitivity have different erythrocyte antigens so the mares colostrum is going to have antibodies that are going to attack the fools erythrocytes and that’s going to cause hemolysis
Autoimmune diseases are wit which hypersensitivity?
Type 3 immunocomplex
Arthus reaction
(Cutaneous vasculitis)
IgG binds the antigen and makes a immunocomplex
this immunocomplex attracts complement
Then binds to FC receptors in leukocytes and mast cells and creates permeability and a local inflammatory response
Immune mediated glomerulonephrititis
Type 3 hypersensitivity where the filtration is compromised because of immunocomplex is that happened there
Contact dermatitis happens with which type of hypersensitivity
Contact dermatitis happens with hypersensitivity four because it’s going to be the one that happens delayed for example with poison ivy where TH1 release is IS gamma and results in a localized skin bump and redness
Hypersensitivity versus auto immunity
They are both inappropriate immune responses
Hypersensitivity is against an allergen or antigen an auto immunity is against self
Interferons type 1
Antiviral and promote inflammation and stop the virus from replicating
Recruits macrophages and T cells
Bad in diabetes type 1 where it’s autoimmune and targeting pancreaTic beta cells
Diabetes type l mechanism
PRR activated which induces type l interferon which attracts macrophages and t cells to the pancreatic bata cell, it also increases the mhc1 class on the cell which makes the CD8 t cell kill it
The broken down beta cell pieces will be presented by APC to CD4 T cells and macrophages too
T cell will make cytokines the that will be picked up by nearby beta cell
Increase inflammation w MHC class one antigen presenting cells PRR T cells macrophages MHC2
Systemic lupus enythematus
Nets bind nuclei acid and nuclei acid binds autoantibody → complexactivates dendrite cell →interferon type l→ increases TH2 which increases the bee cells and TH 17 which increases NETs
Celiac’s disease
The auto immune disease might be type one or type four
Uses T cells and macrophages it attacks the villi of the gastrointestinal tract and reduces absorption
True or false a robust normal response to self is good
F should have a deficient response to self otherwise it is auto immunity
Central tolerance
When B cells and T cells are removed from the thymus or bone marrow before they are sent to peripheral organs if they are auto immune
Peripheral tolerance
When T and B cells that recognize cells are removed from peripheral organs like the spleen So depletion after it’s already gone to peripheral Oregon
True or false too much TH 17 will result in auto immunity
True- we want self tolerance not inflammation
Primary hemostasis
Positive acute phase protein
Increases with inflammation -hepcin and fibrinogen
Prednisone and prednisolone : which is the prodrug?
PREDNISONE IS PRODRUG
Converted to prednisolone
Glucocorticoids
Hepatomegaly and splenomegaly can happen with hemolytic anemia
The macrophages are eating the RBC in the spleen and there will be lymphocytes too contributing to it- the liver and the spleen will be enlarged
Ghost cells argue for___hemolysis
Intervascular hemolytic anemia
IMHA
PRIMARY
SECONDARY- associative process: hemoparasites
- Carprofen can lead to secondary IMHA
Hienz body, pkycnocytie, eccentrocytes are pathognumonic
Oxidative hemolytic anemia
Prions are have a long or short incubation period
Long incubation period
-a normal glycoprotein misfolded so they are not immunogenic
-vacoulation of neurons and neurophils
Discuss TSE= BSE and Scarpie, Chronic wasting disease
Scrapie is in sheep- no inflammation just vacoulation
It jumped to BSE because of eating the brains and spinal cord of sheep
CWD is the TSE in deer and elk
Scrapie and CWD spread via pasture
Which viruses have no proofreading ability and have ran dependent DNA polymerase
Retroviruses which include Feline leukemia and Bovine leukemia
What are the two components in corticosteroids
Glucocorticoids and Mineralocorticoids
What do glucocorticosteroids do (2 things)
Transactivation of anti inflammatory response and trans repression of pro inflammatory response
Acetate and acetonide esters
are insoluble GLUCOCORTICOIDS and are given IM, SQ, IA.
act w time
Succinate and phosphate esters
soluble GLUCOCORTICOIDS given IV
Cox 1 and Cox 2 function
Which one is a coagulant?
Cox 1 - GI tract cytoprotective - decrease acid and increase mucus ; coagulation
Cox 2- Inflammatory response with fever and heat and pain [if there are 2 cox then its gonna be more painful] ;anti coagulation
- help with healing and in kidney
Natural Prostaglandins
PGI1
TXA2
PGE2
PGF2a
PGI1 : Platelet gets it - antiplatelet vasodilation
TXA2: Ticket X accepted : pro platelet vasoconstriction
PGE2: please get eradicated: pro inflammatory
PGF2a: no inflammatory response
T/F cox 2 specific NSAID induce thrombosis
True because they are naturally anticoagulation factors
NSAID effects
Analgesia for pain and Antipyresis [antifever], can also be given for endotoxins, they can be anticoagulant [COX2 blocked thrombosis], Immune suppression, Kidney issues, GI ulcers, hemorrhage, IMHA and pancytopenia [ bone marrow failure], clostridium myositis
Which drug causes laminitis in horses
Glucocorticoids
Solutions go in
Aqueous suspensions go in
IV or IM
IM or SQ
Determinant etiological factor
Directly related to the cause of the disease
Intrinsic would be genetic changes
Extrinsic would be Biological- bacteria/virus, Physical- Mechanical, and Chemical - toxin
Cells that go through…
Hypertrophy
Skeletal muscle, cardiac muscle
Cells that go through…
Hyperplasia
Epithelial, bone marrow [ie. lactation mammary gland gets more cells]
CANT: cardiac muscle, neurons
Metaplasia is _cell differentiation or cell replacement__
REPLACEMENT
Microaerophile
low amount of o2 needed and come co2
T/F bacteria in sterile site transitorily do not cause inflammation because they are cleared out
True - host defense mechanisms
If highly virulent pathogen and little host tissue compromise what to treat bacteria or host?
treat bacteria
Are virulence factors of bacteria expressed constitutively?
No they are expressed as needed
Endogenous vs exogenous bacterial infection
Endogenous infection comes from the bacteria on the skin/mucous membrane and as commensals
Exogenous is from environment
How to sample uterus for bitch
guarded swab
Sample mare uterus
Guarded swab
Horse: sterile caudal to the larynx
True ; includes trachea which is sterile
First thing to see with bacterial culture
Inflammation
Followed by any pathogen, and if its a mixed infection
4 components of a virus
Viral genome
Structural and non structural proteins
Spike protein
Lipids
4 Point rule for sterile site
Is there inflammation on the isolate
Is it collected from the proper site
Is there bacteria in the sample
Will the bacteria cause disease
All DNA viruses replicate in nucleus except
Poxvirus
All RNA virus replicate in cytoplasm except
Coronavirus (Alphacprona- FIP, canine corona, TGE/ Porcine epidemic diarrhea virus Gammacoronavirus- Bovine coronavirus), orthomyxovirus (influenza), retrovirus (FeLV, BLV)
All RNA virus replicate in cytoplasm except
Coronavirus (Alphacprona- FIP, canine corona, TGE; Gammacoronavirus- Bovine coronavirus), orthomyxovirus (influenza), retrovirus (FeLV, BLV)
Effect of virus on cell metabolism
Inhibit
Cellular transcription
RNA processing pathways
Cell translation
DNA synthesis
Basically when virus invades it hijacks the genome
CPE of virus
syncytia, cell lysis. cell rounding, inclusion bodies
Where is herpes latent?
trigeminal ganglia
