Proliferative Disorders of the Lymphoid and Myeloid System Flashcards
What characterizes bovine lymphoma?
- Frequency of occurrence
- Age at onset
- Organ involvement
- Etiologic agent
4 forms of sporadic lymphoma
- Calfehood (juvenile)
- Thymic (Adolescent)
- Cutaneous
- Multicentric (Atypical)
Etiology of sporadic lymphoma in calfhood
- Unknown cause, rare
- NOT ASSOCIATED with BLV
- Age of onset is 3-6 months
Prognosis of sporadic lymphoma in calfhood
- Grave
History of sporadic lymphoma in calfhood
- Slight depression, weight loss, weakness, lymphadenopathy
- Less common signs are fever, ruminal tympany, enlarged liver, ataxia, and diarrhea
PE of sporadic lymphoma in calfhood
- generalized bilateral enlargement of lymph nodes
- Pale mucous membranes
- Tachycardia
- Hyperpnea
- Cough
Etiology of thymic sporadic lymphoma
- very rare
- Calves 6-24 months old (newborns up to 4 years)
- Not associated with BLV
Prognosis of thymic sporadic lymphoma
- 2-9 week course of disease
- Fatal, and most patients die from bloat (vagal indigestion or bloat from impingement on the esophagus)
Clin path of thymic sporadic lymphoma
- Generally unremarkable
Etiology of cutaneous sporadic lymphoma
- Not associated with BLV
- 1-3 years of age (tends to be younger)
Dfdx for cutaneous sporadic lymphoma
- Squamous cell carcinoma
History of cutaneous sporadic lymphoma
- Cutaneous swellings around anus, vulva, shoulders, and flank
- 1-3 month periods
- SIgns may regress and reoccur
Clinical signs and presentation of cutaneous sporadic lymphoma
- Raised or ulcerated lesions
- Associated with other organ involvement (e.g. cardiac insufficiency, brisket edema, jugular pulse)
- Enlarged lymph nodes
Atypical sporadic lymphoma - how common?
- SUPER rare
- may be associated with BLV
Bovine leukosis virus other name
- Enzootic bovine leukosis
Etiology of bovine leukosis virus
- Causes adult lymphoma
- Most common neoplastic disease of cattle
What type of virus is bovine leukosis virus
- Oncogenic retrovirus
Epidemiology of bovine leukosis virus
- Herd size positively correlated with rate of disease
- Infection more common than disease
How old are most cattle that show clinical signs of bovine leukosis virus associated disease?
- > 2 years
Economic losses of bovine leukosis virus
- Heavy!
Transmission of bovine leukosis virus
- Horizontal
Clinical signs of BLV
- History: loss of condition, drop in milk production
- Diarrhea, ataxia, paresis, ketosis
- Infertility
- Enlarged lymph nodes
- Exophthalmos
- Partial to complete anorexia
PE of BLV
- Reflects organ system failure from tumor involvement
- Cardiac dysrhythmia, tachycardia, tachypnea, hyperpnea
- Often peripheral lymph node and internal iliac lymph node enlargement
Common tumor sites of BLV
- Heart, Uterus, Lymph nodes, Abomasum
- Also rumen/reticulum, kidney, spinal cord, retrobulbar space
Clinical signs if GI involvement with BLV
- Scant pasty feces or melena
CBC of BLV
- Unremarkable
- May be microcytic hypochromic anemia if GI hemorrhage
- +/- Elevated fibrinogen
- Only 30% of infected cows develop lymphocytosis
Cytology of BLV vs biopsy in terms of sensitivity
- FNA of PLN has low sensitivity (41$)
- Biopsy of PLN has high sensitivity (100)%
Diagnosis of BLV
- Serology for ELISA of blood or milk
- PCR for BLV nucleic acid (don’t do by itself)
- ELISA + PCR has increased sensitivity
What is ELISA for BLV looking for?
- Antibodies to 51-kD envelope glycoprotein (gp51)
- Presence of antibodies does not equal disease or mean that they will get sick
- If they have signs of lymphoma, they are guaranteed to have a high titer if positive
- If they’re not showing signs, no guarantees that they’ll test positive even if infected
Treatment of BLV
- No curative treatment
Control BLV
- reduce blood transmission (donors, needles, etc.)
- Reduce physical contact among infected and non-infected (more practical in smaller herds)
- Colostrum from BLV positive dam may be protective**
- Fly control may help
What is BLADs?
- Bovine leukocyte adhesion deficiency
Inheritance pattern of BLADs?
- Autosomal recessive
- Heterozygous carriers are clinically normal
% of Holstein calves impacted by BLADs?
- 6% in the US
Signs of BLADs
- Chronic bacterial infections
- Can’t fend off invaders like normal
Pathophysiology of BLADs
- Leukocytes lack surface glycoproteins called Beta-integrins
- Without surface proteins, adhesion and migration to chemotactic factors is inhibited
- Basically leukocytes continue to roll and can’t extravasate
Clinical signs of BLADs
- Infectious processes
- Calf diarrhea
- Pneumonia
- Hyperplastic lymph nodes
Clin path of BLADs
- Mature neutrophilia (>40,000/L) without significant left shift, lymphocytosis, and monocytosis
- Hypoalbuminemia, hypoglobulinemia
- Low serum creatinine, BUN, glucose
How to test for BLADs?
- Holstein Association of America
Anthrax - where is it?
- Endemic
- Worldwide
- Texas and Plains region in the US
Etiology of anthrax
- Bacillus anthracis
- vegetative cells in tissue
- Will form spores when conditions limited
What determines sporulation of anthrax?
- Oxygen!
- SPores thrive in high pH with high levels of calcium and magnesium
- Often outbreaks are seen following earth-disturbing activities
Spread of anthrax
- blood sucking insects (Tabanid flies)
- Scavenging animals
- Carcasses of infected wildlife can be a source too
Three routes of anthrax transmission KNOW THESE
- Ingestion
- Cutaneous
- Inhalation
Which route of anthrax transmission is most common in cattle?
- Ingestion
Pathogenesis?
- bacteria produce dormant spores that can live in environment for awhile
- When spores get into the body of an animal or person, they can be activated and turn into active growing cells
- When active, the bacteria can multiply, spread out in the body, produce toxins, and cause severe illness and death
What are the four main virulence factors in anthrax?
- Capsule
- Protective antigen
- Lethal factor
- Edema factor
Capsule purpose
- Survives in macrophages, which cannot kill it
Protective antigen role
- Makes pores to enter cells
Lethal factor and edema factor roles
- Cell lysis, inflammation, prevent clotting
- This is what prevents signs of rigor
Clinical signs of anthrax
- Depends on route of infection
- Fever, depression, respiratory distress, congestion of mucous membranes (due to lethal factor) and convulsions
- May see bloody diarrhea, hematuria, and localized tissue swelling
Diagnosis of anthrax
- DO NOT open carcasses of suspect animals
- THis is reportable and zoonotic
- Microscopic smears of blood or tissues and bacterial cultures
- YOU MUST ALWAYS notify the lab if you suspect anthrax
Which tissues to submit to a lab fo ranthrax?
- make sure you CALL the state vet if you suspect
- Submit unclotted blood, intact eye, and regional lymph node
Appearance of anthrax on a slide
- Boxcar look
Treatment of anthrax
- Grave prognosis
- Often unrewarding
- Penicillin and tetraycline for minimum of 5 days
One main feature on necropsy of animals with anthrax
- Rigor doesn’t seem to set in
Control and prevention of anthrax
- REPORTABLE!
- DO not open the carcass
- Quarantine if outbreak and psosibly vaccinate
- Pasture management
How to manage an outbreak of anthrax?
- Quarantine
- Vaccinate normal animals prophylactically
- Insect control
Vaccination of anthrax
- Prophylactic vaccination in some endemic areas
Public health and anthrax
- Zoonotic disease
- Humans develop 3 forms
- Cutaneous, inhalational, GI
- Rare in US - cutaneous most common
- Vets are an at risk group
What causes caseous lymphadenitis
Corynebacterium pseudotuberculosis
- 2µm, gm positive, intracellular, nonmotile, pleomorphic, rod-shaped facultative anaerobe
When to assume caseous lymphadenitis?
- In any small ruminant with a bump until proven otherwise
Which species gets nitrate positive CL vs nitrate negative CL?
- Nitrate positive in horses
- Nitrate negative in Small ruminants (thick capsules)
- Both in cattle
CL epidemiology - where does it come from?
- Soil borne organism
- Can last for several months ot years in the soil
Seasonality of CL
- Not seasonal
Transmission of CL
- Direct contact, insects, and fomites
Incubation period of CL
- Long
prevalence of CL
- up to 5-10%
Pathophys of CL
- Organism gains access via wound or abrasion and spreads to SQ or submucosal lymphatics to macrophages
- Organism survives intracellularly due to high lipid content
- Replicates in phagolysosomes
Virulence factors of CL
- Exotoxins
- Phospholipase D and Sphingomyelinase
- Corynomycolic acid + PLD
Role of PLD and sphingomyelinase in CL
- Hydrolyze and degrade cell wall
- Increase vascular permeability
- Help it extravasate
- PLD helps form the capsule too
Corynomycolic acid and phosphlipase D role
- Induce inflammation, edema, pain
What happens when an abscess ruptures with CL?
- Organisms released into the environment
Signs of CL in sheep and goats
- Poor performance
- External abscesses
- Internal abscesses
- Parotid LN often but al others too
Dfdx for CL
- Trauma, seroma, hematoma, FB, injection reaction, tumor
Clin path of CL
- Anemia of chronic disease
- Leukocytosis with neutrophilia
- Elevated fibrinogen (internal abscesses more likely)
Diagnosis of CL
- ELISA
- Synergistic hemolysin inhibition test (SHI)
- Definitive diagnosis is isolation of organisms
SHI or synergistic hemolysin inhibition test
- Measures IgG response to exotoxin in patient’s serum
- More helpful in a high prevalence herd
- SErial testing on a herd level basis is most helpful
Treatment of CL
- Drainage would be contamination of environment
- Complete excision of abscess preferred
- Antibiotics are usually unrewarding
- Large operations may cull, but that’s pretty expensive
Prevention of CL
- isolation of infected animal, fly control, good sanitation, and careful disposal of bedding
- Immunization
