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Cardiology.CV.hemolymph > ch.37SmithContinued > Flashcards

ch.37SmithContinued Flashcards

1
Q

What near-terminal event has been reported in horses with the acute or chronic liver failure?

A

fulminant intravascula rhemolytic syndrome

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2
Q

In hemoytic syndrome in horses with liver failure what is the pathogenesis?

A

+/- rbc fragility
** copper does not play a role

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3
Q

What is seen at necropsy in horses with hemolytic syndrome?

A

Widespread hemorrhagic lesions that resemble those described for DIC

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4
Q

Congenital erythropoietic porphyria has been reported in what spp?

A

Holstein cattle

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5
Q

Congenital erythropoietic porphyria is commonly referred to as?

A

pink tooth

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6
Q

Clinical signs of congenital erythropoietic porphyria

A

slow growth rates in calves
photosensitization
exfoliation of nonpigmented skin when exposed to sunlight
reddish-brown teeth
modest anemia

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7
Q

congenital erythropoietic porphyria: how is the disorder inherited in cattle?

A

autosomal recessive

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8
Q

congenital erythropoietic porphyria: disease pathogenesis?

A

metabolic defect is a herediatry deficiency fo the enzyme uroporphyrinogen III syntehase (UROS) which catalyzes an esential setp in syntehsis of the porphyrin structure of hemoglobin

–> resluts in accumulation of urorophoryn and coproporphyrin which deposit in teh teeth, where they are concentrated in the dentin, bones and other tissues

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9
Q

The reduced IV red cell lie span seen in congenital erythropoietic porphyria is due to

A

high concentration of uroporphyrin and coproporphyrin with in the cells

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10
Q

congenital erythropoietic porphyria consequence of porphyrs

A

may induce hemolysis and ldeay red cell series maturation in the bone marrow

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11
Q

Is there treatment for congenital erythropoietic porphyria?

A

No, however these cattle do reasonable well if housed indoors out of direct sunlight

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12
Q

What is the principle differential for congenital erythropoietic porphyria?

A

chronic flourosis– also produces brown discoloration of the theeth

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13
Q

Porphyria has been reported in what other spp, that has no health effects but causes a reddish brown discoloration?

A

Swine

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14
Q

Animals may develop acquired toxic porphyrias, with what substances?

A

heavy metal poisonings– principally lead

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15
Q

Pathogenesis of lead in the development of porphyria?

A
  1. inhibit several key enzymes of heme synthesis
    -inhibition of aminolevulinate dehydrase leads to accumulation of aminolevulinic acid & decreased aminolevulinate dehdyrase activity
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16
Q

Depression anemia can be caused by:

A
  1. deficiencies of vitamins and minerals essential for RBC production
  2. systemic disease processes that interfere with normal erythropoiesis
  3. processes that damage or displace normal bone marrow elements
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17
Q

List nutritional deficiency’s as causes of depression anemia

A

Iron deficiency
Copper deficiency
cobalt deficiency
vitamin B12 deficiency
Folic acid deficiency

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18
Q

List anemias of inflammatory disease (depression anemia)

A

chronic infection
chronic inflammation
fractures and severe trauma
neoplasia

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19
Q

List anemia seondary to organ dysfunction

A

chornic liver disease
chronic kidney disease
chronic GI disease
parasitism (trichostrongylosis)

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20
Q

List causes of bone marrow damage/dysplasia that cause depression anemia

A

myeloid and megakaryocytic bone marrow hypoplasia in Standardbred horses
Bracken fern poisoning
Congenital dyserythropoiesis and keratosis in polled Hereford calves
Trichloerthlene-extracted soybean meal toxicity
Myelophthisic disorders (myeloproliferative disease, lymphoma)
aplastic anemia

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21
Q

In neonates what is the major source of iron?

A

colostrum

**as well as soil, dam’s feces, and milk

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22
Q

A modest anemia is anticipated in what cattle?

A

veal calves

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23
Q

Iron deficiency anemia has been documented in which spp?

A

calves and piglest housed exclusively indoors or in hatches with no access to soil

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24
Q

What in the body, account sfor 2/3rds of the total iron reserves found in teh body?

A

circulating erythrocytes

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25
Q

Where is 1/3 of the iron stored in the body?

A

liver
spleen
bone marrow

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26
Q

With chornic blood loss anemia, iron depletion is first indcated by what source?

A

decreased marrow iron
– seen with Prussian blue stain for iron

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27
Q

When is the typical microcytic, hypochromic erythrocytes seen in what stage of iron deficiency anemia?

A

In the late stages

**dec PCV, hgb concen, MCV, MCHC

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28
Q

The observed red cell abnormalities (echinocytosis, keratocytosis, schistocytosis, acanthocytosis, ovalcotosis) seen with Fe deficiency anemia are thought to be associated with:

A

oxidative damage

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29
Q

What is the treatment of Fe def anemia?

A

Dep on the cause and corection or resolution fo hte process responsibel for chornic blood loss

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30
Q

Iron dextran intended for use in baby pigs can cause anaphylaxis in what spp?

A

horses and cattle

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31
Q

Copper deficiency can occur as a primary problem in what animals?

A

milk fed animals or
pastured animals in copper deficient areas

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32
Q

More commonly than primary copper deficiency, it occurs secondary to

A

-imbalances in other trace minerals (dietary molybdenum excess, sulfur content or zinc)

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33
Q

Copper is an essential cofactor for:

A

a wide variety of enzymatic reactions

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34
Q

Clinical signs of copper deficiency are most prominent in what age group?

A

young, growing animals

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35
Q

Clinical signs of copper deficiency

A

reduced growth rate
rough and depigmented hair
diarrhea
osteoporosis with spontaneous fractures and anemia

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36
Q

In lambs copper deficiency can cause what syndrome?

A

swayback or enzootic ataxia

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37
Q

What role does copper play in iron metabolism

A

-important in iron transport from gut to marrow
-incorporation of iron into the heme moiety

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38
Q

What mineral deficiency anemia closely resembles iron deficiency anemia?
microcytic , hypochromic anemia?

A

Copper deficiency anemia

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39
Q

If sideroblasts are seen on bone marrow biopsy, what do they mean?

A

Problem in the incorporation of iron into the erythrocyte hemoglobin rather than actual deficiency of iron
ie: copper deficiency

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40
Q

How is copper deficiency detected?

A

measuring serum copper as ceruloplasmin, erythrocyte superoxide dismutase or copper content of hair, liver or kidney

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41
Q

In ruminants and horses only deficiency of what vitamin can lead to the development of anemia?

A

Vitamin B12 and folate

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42
Q

Which vitamins play an essential role in DNA synthesis?

A

vitamin B12 and folate

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43
Q

In ruminants, what has vitamin B12 deficiency been associated with?

A

grazing cobalt deficient pastures

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44
Q

Anemia resulting from chronic inflammatory occurs because of what mechanisms

A

-chronic release of inflammatory mediators (Interleukins) and release of acute phase proteins from the liver
–>sequestering iron from the circulation into storage forms (primarily liver and bone)

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45
Q

Myeloid and megakaryocytic bone marrow hypoplasia has been reported in what spp?

A

8 standardbred horses– all sired from the same stallion

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46
Q

aplastic anemia is a stem cell disorder characterized by:

A

reduced bone marrow production of all blood components in the absence of ta primary disease process infiltrating the bone marrow or suppressing hematopoiesis

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47
Q

What is usually the first indicator of aplastic anemia?

A

hemorrhagic diathesis caused by thrombocytopenia
– manifested as epistaxis, mucosal petechiae, or prolonged hemorrhage after trauma or injections

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48
Q

The diagnosis of aplastic anemia is based upon?

A

peripheral pancytopenia
bone marrow hypoplasia with fatty replacement

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49
Q

What toxicosis in ruminants resembles clinical signs of aplastic anemia?

A

bracken fern toxicosis

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50
Q

Clinical signs of bracken fern toxicosis

A

fever
melena
epistaxis
hematuria
mucosal petechiae
hyphema
bleeding from eyes and vagina

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51
Q

What is the major toxic factor in bracken fern?

A

ptaquiloside

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52
Q

Paradoxical erythroid hypoplasia is caused by

A

use of recombinant human erythropoietin (rhEPO) in race horses
**treated with steroids and returned to racing

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53
Q

Absolute erythrocytosis (polycythemia) definition

A

caused by an increase derythropoiesis that creates a circulating erythrocyte mass above nromal for the species

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54
Q

What must be ruled out with suspicion of Absolute erythrocytosis ?

A

relative erythrocytosis– caused by hemoconcentration, endotoxemia or splenic contraction (horses)

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55
Q

Absolute erythrocytosis diagnosis is based on

A

persistently elevated PCV
hemoglobin
erythrocyte count w/o clinical evidence of shock or dehydration
** and without response to IV fluid therapy

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56
Q

all disorders characterized by Absolute erythrocytosis share clinical manifestations caused by:

A

expanded blood volume &
increased viscosity

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57
Q

Besides humans familial erythrocytosis is described in what spp?

A

cattle

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58
Q

Familial erythrocytosis is caused by

A

autonomous erythropoietin produciton without demonstrable lesion

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59
Q

What should be ruled out when considering congenital erythrocytosis as a diagnosis?

A

-chronic hypoxia (r/o by measuring arterial O2 concentration)

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60
Q

Define polycythemia vera

A

idiopathic myeloproliferative disorder characterized by excessive proliferation of erythroid, myeloid and megakaryocytic elements, without an increasein plasma erythropoietin
**rare in animals

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61
Q

In domestic animals, absolute erythrocytosis is usually secondary to

A

chronic disease that produce tissue hypoxia
-ie: residence at high altitude, congenital heart defects that produce right to left shunting, chronic pulmonary disease

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62
Q

The partial pressure of oxygen (Po2) in capillaries must be maintained close to what level to ensure adequate off-loading of oxygen to tissues?

A

40 mmHg

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63
Q

In regards to the effects of high altitude, which spp are most susceptible and resistant?

A
  1. Cattle- most susceptible (1800 m above sea level) & sheep
  2. Horses (>2200 m above sea level)
  3. Goats
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64
Q

Is RAO/equine asthma able to cause hypoxemia sufficient to induce erythrocytosis?

A

No

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65
Q

When erythrocytosis not a in response to an appropriate phsyiologic stimulus, what is the recommended treatment?

A

phlebotomy to keep PCV below 50%
**controls hypervolemia and blood hyperviscosity

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66
Q

At what level of PCV is oxygen carrying capacity impaired?

A

> 60%

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67
Q

What are the forms of bovine lymphoma:

A
  1. sporadic bovine lymphoma:
    - calf or juvenile form
    -thymic or adolescent form
    -cutaneous form
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68
Q

Lymphoid tumor’s of cattle with sporadic bovine lymphoma are typically of what cell lineage?

A

B and T cell

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69
Q

The msot common form of lmypom ain cattle occurs when and is associate dwith?

A

-adult cattle >2 yrs of age
- assoc with bovine leukemia virus

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70
Q

What cell lineage are BLV associated lymphomas of adult cattle?

A

B-cell lineage

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71
Q

BLV is an oncogenic type C retrovirus classified in what genus, subfamily and family?

A

genus: Deltaretrovirus
subfamily: Orthoretrovirinae
family: Retroviridae

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72
Q

What is the prevalence of juvenile lymphoma?

A

unknown
**but its rare

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73
Q

Common clinical signs of juvenile lymphoma

A

enlarged nodes (smooth, not hot or painful)
bloat
dyspnea
–pale mm (anemia), tachycardia, tachypnea, hyperpnea, cough, harsh lung sounds, fever, ruminal tympany enlarged liver, ataxia diarrhea

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74
Q

Prognosis for calf or juvenile lymphoma?

A

rapidly progressive– usually fatal w/in 2 to 8 wks of onset

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75
Q

Is the juvenile form of lymphoma associated with BLV?

A

Does not appear to be associated

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76
Q

The thymic form of bovine lymphoma is rare and seen in what age group?

A

typically 6 to 24 months fo age

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77
Q

C/S of thymic lymphoma

A

**signs of space occyping lesions in the neck
brisket enlargement
pitting edema
loss in bbody condition
rumen tympany
dysphagia

+/- bloat

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78
Q

With thymic lymphoma, what lymph nodes tend to be enlarged?

A

enalrge dsuperficial cervical and prescapular nodes

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79
Q

Why is fever a common clinical finding in bovids with thymic lymphoma?

A

unknown
– tumor necrosis, inflammatory medaitors, and/or secondary resp infections

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80
Q

Thymic lymphoma is often fatal because of:

A

bloat

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81
Q

Is thymic lymphoma associated with BLV?

A

No

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82
Q

Bovine immunodeficiency virus has been associated with what condition?

A

a lymphoproliferative condition associated with hemonode enlargement and some generalized lymphadenopathy

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83
Q

BIV belonges to what genus,subfamily, family?

A

genus: Lentivurs
subfamiliy: Orthoretrovirinae
family: Retroviridae

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84
Q

BIV infected calves develop what C/S

A

enlarged superficial nodes (hemonodes)– cervical region anterior and dorsal to the prescapular lymph node , over the spine of the scapula, in the paralumbar fossa and dorsal to the sub iliac (prefemoral) lymph node

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85
Q

What is the most common neoplastic disease of cattle?

A

adult (enzootic) form of lymphoma caused by BLV infection

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86
Q

A 2007 USDA national Animal Health Monitoring System study estimated that what percentage of dairy herds are infected with BLV?

A

84%

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87
Q

BLV forms of transmission

A

Horizontal: transfer of blood form an infected cattle to susceptible
Iatrogenic (needles, ear tatto pliers, etc.)
Tabanids (horse flies)
+/-nasal secretions
vertical transmission (dam to fetus)
Colostrum contains BLV

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88
Q

Can BLV be spread through nasal secretions?

A

Thought to be considered possible

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89
Q

What are factors that are considered to be associated with high rates of BLV infection in herds?

A

-Herd size positively correlated
-Close contact and heavy stocking/comingling
-presecne of persistent lymphocytosis

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90
Q

In regards to BLV, what is persistent lymphocytosis?

A

PL is an absolute lymphocyte count at least three standard deviations above the normally mean count that persists for at least 3 consecutive months
**increased the chances of horizontal transmission

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91
Q

BLV typical age of presentation

A

older than 4 years of age
** as young as 2 years

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92
Q

Common presenting clinical signs/history with cattle infected wiht BLV

A

-history of loss in condition
-abrupt drop in milk production (over a few days)-enlarged peripheral nodes
-exophthalmos
-partial to complete anorexia
-other signs: diarrhea, ataxia, paresis, ketosis, infertility

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93
Q

Whwat are common sites of lymphoid tumor predilection in adult lymphoma?

A

heart (r-atrium)
abomasum
uterus
kdiney
spinal cord (epidural sapce)

Other sites: retrobulbar space, rumen/reticulum

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94
Q

When is pitting edema seen with lymphoma?

A

When supramammary lymph nodes or cervical lymph nodes are involved

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95
Q

What peripheral lymph nodes are typically enlarged with lymphoma?

A

prescapular
subiliac
supramammary nodes

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96
Q

Which lymph nodes in cattle with lymphoma adominal tumors are involved?

A

internal iliac nodes

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97
Q

What percentage of cattle with BLV develop persistent lifelong lymphocytosis? and of which cell line?

A

approximately 30%

**mostly B cell lines

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98
Q

Melena in cases of BLV can be seen when?

A

When abomasal wall lymphoma ulceration with bleeding– melena, +/- anemia with GI hemorrhage

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99
Q

In a retrospective study on antemortem diagnosis for BLV, what were the findings?

A

lymph node needle biopsy to be 100% sensitivty while fine needle aspirate was only 41% senstive

100
Q

What serologic tests are available for diagnosis of BLV?

A

agar gel immodiffusion (AGID)
enzyne linked immunosorbent assay (ELISA)

101
Q

What is considered a cost effective tool in BLV control programs?

A

p24 antigen and whole BLV antibodies by ELISA compared to realtime PCR methods

102
Q

Novel quantitative real-time PCR methods to measure proviral loads of known and novel BLV variants using what primers, are found to be more sensitive than some of the more traditionally real-time PCR methods and antibody based methods to detect BLV?

A

Coordination of Common Motifs (CoCoMo) primers

103
Q

Are there vaccines for BLV that offer effective protection from BLV infection and control?

A

No

104
Q

Is there evidence of BLV in semen?

A

no– transmission via insemination artificially has not been shown

105
Q

What is the most common occurring hematopoietic neoplasia in horses?

A

lymphoma

106
Q

What is one of the most common malignant neoplasms in the horse?

A

lymphoma

107
Q

Clinical signs of lymphoma

A

nonspecific lethargy
weight loss
pyrexia
lymphadenopathy
–dep on location of tumor: diarrhea, colic, neuro signs, lameness, soteolysis, pathologic fractures

108
Q

What are paraneoplastic conditions seen with lymphoma in horses?

A

pruritus and alopecia
hypercalcemia
IMHA
IMTP

109
Q

In a retrospective study of classifying 203 cases of equine lymphoma, characterized lymphoma as:

A

multicentric (involving at least 2 organs excluding regional LN)
GI
cutaneous
bone marrow
nodal
splenic
hepatic
mediastinal
heart
ocular/orbital
CNS
oral cavity
nasal

110
Q

In a retrospective study of classifying 203 cases of equine lymphoma, what were the most common anatomic locations identified?

A

Multicentric (83%)
cutaneous (19%)
Gastrointestinal (11%)

111
Q

What is the diagnostic sample of choice for lymphoma?

A

biopsy of affected lymph node or organ

112
Q

Morphologically lymphocytes are classified as small cell type if?

A

their nuclear diameters are 1.5 times the diameter of erythrocytes or less

113
Q

Morphologically lymphocytes are classified as large if?

A

their nuclei average 2 times or more the diameter of erythrocytes

114
Q

Small cell lymphoma is classified under what conditions?

A

if 60% or more small cells

115
Q

Large cell lymphoma is classified under what conditions?

A

if 60% or more large cells

116
Q

What has been identified as the most common subtype of lymphoma in the horse?

A

T cell rich B cell lymphoma

117
Q

Immunohistochemical classification to determine the cell lineage is performed using monoclonal antibodies such as, which for B cell lymphomas and which for T cell lymphomas?

A

B cell lymphomas: CD79a, CD20
T cell lymphomas: CD3, CD8

118
Q

Define multicentric lymphoma

A

lymphoma that involves two organ systems, excluding the regional lymph nodes, or involves multiple lymph nodes at distant anatomic locations

119
Q

In which location of the gastrointestinal tract, where does lymphoma most commonly occur?

A

within the small intestine

120
Q

What neoplasia is the most common in the intestinal tract in horses?

A

lymphoma

121
Q

What breed is intestinal neoplasia most common?

A

Arabians with intestinal lymphoma

122
Q

Lymphoma of the gastrointestinal tract, arised from where?

A

lymphocytes of the lamina propria of the intestinal tract–> results in diffuse or segmental thickening, focal masses or scattered crater-like ulcers with raised margins on the intestinal wall

123
Q

Clinical signs associated with intestinal lymphoma

A

hypoalbuminemia– PLE
weight loss
edema
abdominal effusion
mild recurrent colic
diarrhea

124
Q

Alimentary or intesitnal lymphoma glucose or xylose absorption tests?

A

frequently abnormal, indicating small intestine malabsorption

125
Q

Results of abdominocentesis in alimentary lymphoma?

A

abdominal fluid was diagnostic in 38% of cases

126
Q

What is the prevalence of mediastinal lymphoma?

A

varies from 4.5 to 29 % of all forms of lymphoma

127
Q

What is the predominant subtyp eof cutaneous lymphoma?

A

T cell rich, large B cell (TCRBCL)

128
Q

Is it alright to leave cutaneous lymphoma untreated?

A

risk of cutaneous lymphoma metastasizing ot internal organs or result in paraneoplsatic syndromes

129
Q

Define angiotrophic lymphoma

A

lymphoma of the small blood vessels that spares the surroundign tissues

130
Q

Define angiotrophic lymphoma

A

lymphoma of the small blood vessels that spares the surrounding tissues

131
Q

Define leukemia

A

rare neoplasia co the hematopoietic sys that originates form the bone marrow (primary leukemia)

132
Q

Characeristics of Luekoemic leukemia

A

increase in cell numbers in peripheral blood

133
Q

define subluekemia leukemia

A

an increase in abnormal blast cells in blood, with a total whit ecell count w/in reference range or low

134
Q

aleukemic leukemia characteristics

A

presence of abnormal cells in the bone marrow but not in peripheral blood

135
Q

What is a consistent finign on bloodwork with leukemia in horses?

A

hyperproteinemia– due to hyperlgobulinemia

136
Q

Define myeloma

A

neoplastic proliferation of plasma cells that primarily originates in the bone marrow but may have an extramedullary source

137
Q

Define extramedullary plasmacytoma

A

accumulation of neoplastic plasma cells outside the marrow

138
Q

Plasmacytomas can form in several organs and tissues, including the skin. what are the most commone extraosseous sites in horses?

A

lymph nodes
kidneys
spleen
liver

139
Q

In secretory myelomas, neoplastic plasma cells are responsible for overproduction of what?

A

monoclonal Ig called M protein or paraprotein

140
Q

Why are multiple bone marrow aspirates required for diagnosis of plasmacytosis?

A

because plasma cells are sparse in normal bone marrow

141
Q

Define lymphangioma

A

tumor that originates from lymphatic vessels
**rare in hroses

142
Q

What is the etiologic agent of anthrax?

A

Bacillus anthracis

143
Q

Bacillus anthracis characteristics

A

large, rectangular shaped gram pos rod

144
Q

In the vegetative form, Bacillus anthracis is most commonly found in

A

tissues of ifnected animals

145
Q

When does Bacillus anthracis produces spores?

A

Under nutritionally limiting circumstances–> facilitating survial in harsh enviornmental conditions, cinldugin ehat, dryign and chemical tratments
**oxygen depdent process

146
Q

Bacillus anthracis: entry into mammalian hosts can occur through which routes:

A

inhalation
ingestion
cutaneous routes

147
Q

Bacillus anthracis: what is the most common route of entry in animal species?

A

ingestion

148
Q

Can omnivores and carnivores become infected with Bacillus anthracis after eating meat form infected animals?

A

Yes

**less susceptible

149
Q

Bacillus anthracis: what are the key plasmid encoded virulence factors that enables its survival in the host?

A

polyD-glutamic acid capsule necoded by pXO1
3 component toxicin encoded by pXO2

150
Q

Besides the plasmid encoded virulence factors, what helps Bacillus anthracis evade the host’s immune system?

A

capsule

151
Q

Bacillus anthracis: pathogenesis at the cellular level:

A

-lethal factor and edema toxin bind to protective antigen component on host cells
PA oligomerized ot induce endocytosis
-PA creates a stable pore LF and EF enter cytoplasma
–> both toxins interfere with cell signal transduction pathways–> dsuprte innate immuen cell functions, block inflamm cyotkine responses

152
Q

Bacillus anthracis lethal factor and edema factor bind what to form lethal toxin and edema toxin?

A

protective antigen (PA)

**on host cells

153
Q

In the United States Bacillus anthracis occurs frequently ine stbalished “zones” of which states?

A

Texas
Montana
Minnesota
North and South Dakota

154
Q

What are environmental factors that are favorable to maintaining anthrax spores?

A

-soils with elevated pH
-hihg concentrations of selceted cations (Ca, MN)
_rich in organic material

155
Q

What weather changes typically precede an outbreak of anthrax?

A

droughts followed by heavy rainfall or flooding

or earth disturbing activities like excavations

156
Q

Bacillus anthracis outbreaks usually occur during what times of year?

A

During the warmer months of the year

157
Q

Bacillus anthracis Transmission can occur via

A

access to blood or tissues form ifnected animals

bites from blood sucking insects (contirbutes in an outbreak)

wildlife carcasses

158
Q

Bacillus anthracis animal susbceptibility to infection is dependent on

A

individual animal spp and route of infection

159
Q

Which spp are most susceptible to peracute infections of Bacillus anthracis?

A

Ruminants: cattle, sheep, goats

160
Q

Bacillus anthracis forms seen in horses?

A
  1. acute intestinal form: colic, diarrhea, cyanosis, fever and depression followed by fatal septicemia
  2. localized form: massive edema in neck region, progress to dependent edema involving thorax, abdomen, prepuce or mammary gland
161
Q

Which spp is less susceptible to anthrax?

A

Swine

162
Q

Necropsy of animals who died of anthrax

A

-bloody exudates from body orifices (that does not clot)
-incomplete rigor mortis
-rapid autolysis
-spleen: back berry jam consistency

163
Q

Definitive diagnosis of Bacillus anthracis is base don:

A

microscopic exam of blood or tissue smears (collected w/in 24 hours of death)

bact cultures

164
Q

what are samples that can be collected in cases where anthrax is suspected, without contaminated the environment (minimally)?

A

-unclotted blood collected form superficial veins

-ocular fluid collected in a sterile syringe using a large guage needle

-removal of an intact eye

165
Q

Gram stains of Bacillus anthracis

A

large, gram positive, sqaured ended rods found singly or in chains of two to four cells

166
Q

What stain confirms Bacillus anthracis capsule

A

polychrome methylene blue (m”faydean) stain

167
Q

Appearance of typical Bacillus anthracis colonies in culture media

A

large, gray-white in color, have a rough, dry texture and usu non hemolytic

168
Q

What is the appearance of gram stains of young Bacillus anthracis colonies?

A

long chains (10 or more cells) of large, square ended, gram-positive rods
**appearance of a row of “railway boxcars”

169
Q

Verification of Bacillus anthracis isolates is done by

A

lack of motility
capsule production on specialized media
lysis of specific bacteriophage (gammaphage)
confirmatory PCR for toxin and capsule genes

170
Q

Field isolates of Bacillus anthracis are usually susceptible to which antibiotics?

A

penicillin
tetracycline

171
Q

What is critical in controlling anthrax outbreaks?

A

carcass management
-not opened
-burn or deep burial

172
Q

prophylactic vaccination for prevention of Bacillus anthracis is usualy performed when?

A

annually 4 weeks before turning animals onto pastures where outbreaks have occurred

173
Q

Preventative measures for Bacillus anthracis

A

-ensuring pastures of good quality– grazing close to soil is avoided to minimize exposure to spores
- avoid rough feed– reduce traumatic mucosal surfaces
-**do not recommend use of lime or other calcium containing products that alkalinize the soil
- avoid grazing animals on pastures altogether

174
Q

What form of anthrax is common in humans?

A

cutaneous form

*inhalational is rare d/t high LD50 req for infection

175
Q

Lyme’s disease causative agent

A

Borrelia burgdorferi

176
Q

Borrelia burgdorferi ntramission

A

ticks belonging to Ixodes ricinus complex

177
Q

based on geographic location within the US, what ticks transmit Borrelia burgdorferi

A

east coast: ixodes scapularis most common vector
West coast: ixodes pacificu (western black legged tick)

178
Q

Ixodes scapularis larval ticks princpally acquire Borrelia burgdorferi spirochete from what animL?

A

Peromycus leucopus, the white footed mouse

179
Q

What life stage of the Ixodes tick are the major transmitters of Borrelia burgdorferi to humans and animals?

A

nymphal stages

180
Q

What are likely the enzootic reservoirs of Borrelia burgdorferi for Ixodes pacfiicus?

A

California kangarooo rate, Dipodomys californicus
Duskey footed wood rate, Neotoma fusicipes

181
Q

What are the most common clinical signs of Borrelia burgdorferi in horses?

A

lameness and hyperestehsia

182
Q

Diagnosis of recent or active Borrelia infection has been based on

A

high ELISA titers
psoitve Western blot
PCR

183
Q

Because of similar vectors, what other organism can cause infection in horses with Borrelia burgdorferi?

A

Anaplasma phagocytophyllum

**Ixodes ticks

184
Q

what are proposed antimicrobial agents for Borrelia burgdorferi

A

tetracycline
doxycyline
ceftiofur

**for 3 to 4 weeks

185
Q

Francisella (Pasteurella) tularensis describe the organism

A

factulatative, intracellular, nonspore forming , gram netative coccobacillus

186
Q

Francisella (Pasteurella) tularensis can survive longer than a year under what conditions?

A

frozen or in mud and water

187
Q

What species are most commonly infected with Francisella (Pasteurella) tularensis

A

sheep, along with dogs, cats and humans

188
Q

Humans experience what symptoms and how are they infected with Francisella (Pasteurella) tularensis?

A

plague like illness

bitten by infected ticks, fleas or insects when handling infected rabbits or hares

189
Q

Francisella (Pasteurella) tularensis clinical signs

A

acute septicemia with localization and lymphadenopathy and granulomatous lesions in the organs (particularly liver and spleen)

otherwise nonsp signs: fever, anorexia, lethargy etc. etc.

190
Q

Francisella (Pasteurella) tularensis Diagnosis

A

culture of organism from blood or organs

– BSL-3 level lab

–IFA testing, PCR or ELISA

191
Q

fetal lesions from abortions caused by Francisella (Pasteurella) tularensis

A

multiofcal pinpoint necrosis of liver, spleen and lung

192
Q

Differentials for Francisella (Pasteurella) tularensis include other bacteremias such as

A

Mannheimia (Pasteurella) haemolytica– sheep
Histophilus somni– cattle
mycoplasma mycoides subsp mycoides– goats
anthrax– all livestock

193
Q

What lesions does Corynebacterium pseudotuberculosis cause and in what spp?

A

Sheep and goats: external/internal caseous lymphadenitis

Cattle: cutaneous excoriated granulomas and mastitic, visceral or mixed infections

Horses: external and internal abscesses

194
Q

Corynebacterium pseudotuberculosis bacteria

A

gram positive, intracellular, nonmotile, pleomorphic, rod-shaped facultative anaerobe

195
Q

What component of Corynebacterium pseudotuberculosis may account for its survival within macrophages?

A

high lipid content within the bacterial cell wall
**particularly corynomycolic acid

196
Q

Strains of Corynebacterium pseudotuberculosis have been identified based on nitrate reduction and DNA fingerprinting techniques, which spp have which strains?

A

Small ruminants: nitrate negative
Horses: Nitrate positive
Cattle: Both

197
Q

Is there natural cross spp transmission of Corynebacterium pseudotuberculosis between small ruminants and horses?

A

has not been reported

198
Q

Corynebacterium pseudotuberculosis produces what exotoxins:

A

phospholipase D (PLD)
sphingomyelinase
inhibitory factor of staphylococcal Beta-hemolysin
hemolysis factor
dermanecrtoxins
mouse lethality toxins

199
Q

Which exotoxins are important the pathogenesis of Corynebacterium pseudotuberculosis?

A

phospholipase D–> hydrolyzes lysophosphatidylcholine

sphingomyelinase–> hydrolyzes sphingomyelin

-enable degradation of the endothelial cell wall and INC vascular permeability

200
Q

The SHI (synergistic hemolysis inhibition test) measures what?

A

IgG to phospholipase D exotoxin
–> synergism with R equi in lysing RBCs in agar forms the basis of the test

201
Q

Corynebacterium pseudotuberculosis small ruminant C/S:

A

supuration and necrosis of lg superficial lymph nodes

202
Q

Corynebacterium pseudotuberculosis where are external abscesses most commonly seen in sheep and goats?

A

mandibular
parotid
preformoral
prescapular

203
Q

Differential diagnosis for Corynebacterium pseudotuberculosis in sheep and goats

A

abscesses caused by other organisms
trauma
seroma
hematoma
foreing body
injection reactoin
tumors

204
Q

What is the most common presenting complaint for Corynebacterium pseudotuberculosis in sheep and goats?

A

chronic weight loss

205
Q

What is the estimated prevalence of Corynebacterium pseudotuberculosis in large breeding operations in sheep and goats in endemic areas?

A

5% to 10%

206
Q

What is the most common clinical form Corynebacterium pseudotuberculosis in cattle?

A

cutaneous excoriated granulomas

other forms: mastitis, visceral, mixed infections

207
Q

Corynebacterium pseudotuberculosis lesions in cattle

A

ulcerative, exuding granulomatous lesions as large as 20 cm in diameter with necrotic areas that are easily surgically removed, leaving granulation tissue underneath

208
Q

Do lesions caused by Corynebacterium pseudotuberculosis in cattle typically require treatment?

A

usually spontaneously heal in 2 to 4 weeks

209
Q

Corynebacterium pseudotuberculosis ulcerative lymphangitis in horses differentials:

A

blutn trauma
fracture
foreign body
uncture wounds
nonseptic cellutis
staph cellulitis
other septic cellulitis

210
Q

describe Corynebacterium pseudotuberculosis ulcerative lymphangitis lesions

A

severe cellulitis, lymphatics affected in one more more limbs , with multiple draining ulcerative lesions

211
Q

Ulcer lymphangitis lesions often become chronic with what clinical signs?

A

limb edema
lameness
weakness
weight loss

212
Q

What are the dfiferential diagnosis for Corynebacterium pseudotuberculosis in horses?

A

blunt trauma
fracture
foreign body
puncture wounds
nonseptic cellulitis
staphylococcal cellulites
other septic cellulitis

213
Q

Corynebacterium pseudotuberculosis external abscessation is referred to as

A

pigeon fever

214
Q

IN a large study of Corynebacterium pseudotuberculosis infection in horses, what percentage of horses developed internal abscesses (538 horses)

A

63% of horses

215
Q

Corynebacterium pseudotuberculosis most common clinical signs of internal abscessation in horses

A

anorexia
fever
letarhgy
tachycardia
modest weight loss

216
Q

Corynebacterium pseudotuberculosis most commonly affected anatomic location in horses caused internal abscessation?

A

liver
mesentary
mediastinum
lungs
kidneys
diaphragm
spleen
pericardium
blood
uterus

217
Q

Corynebacterium pseudotuberculosis internal abscessation differential diagnosis

A

streptococcus
Actinomycoses
Staphylococcus
R equ in in foals
Coccidoides immitis
anaerobes
neoplasia
other causes of weight loss

218
Q

Corynebacterium pseudotuberculosis presentation in humans?

A

occurs as a subacute to chornic lymphadenitis and pneumonia

219
Q

Corynebacterium pseudotuberculosis human infections occur as a result from

A

consumption of unpasteurized infected milk or milk products
continued close contact with infected animals
handling contaminated equipment
exposure to wounds with exudates

220
Q

Corynebacterium pseudotuberculosis spread from horses to humans?

A

Not reported

221
Q

Corynebacterium pseudotuberculosis common clinical pathological abnormalities

A

anemia of chronic disease
inflammatory leukogram

222
Q

What percentage of hosres with abdominal abscesses had abnormal peritoneal fluid?

A

93%

223
Q

Of the percentage of horses with abdominal abscess caused by Corynebacterium pseudotuberculosis, with normal peritoneal fluid, where was the abscess located?

A

retroperitoneally (involving the kidneys)

224
Q

Reasons for lack of culture results in Corynebacterium pseudotuberculosis peritoneal fluid

A

retroperitoneal locations
sequestered w/in a thick capsule
suppressed by local factors or nucleated cells

225
Q

Bacterial culture is the preferred method of diagnosis for external infection, but horses without external abscesses what diagnostic test imay be useful?

A

SHI: synergistic hemolysis inhibition (SHI) test increased titers greater than 1280 are significantly assoc with internal infections

226
Q

Corynebacterium pseudotuberculosis defintiive diagnosis

A

isolating the organism from abscesses or draining wounds
**grows well in blood agar 24 to 48 hours

227
Q

When are Corynebacterium pseudotuberculosis infections most commonly seen in hroses

A

during fall and ealry winter months
**high incedence in September, October and November

228
Q

What are insect vectors involved in transmission of Corynebacterium pseudotuberculosis in horses?

A

H. irritans (horn fly)
Stomoxys calcitrans
Musca domestica
**biting insects

229
Q

Corynebacterium pseudotuberculosis disease transmission

A

biting insects (vector brone routes)
direct contac twith exduates or contaminated soil

230
Q

Corynebacterium pseudotuberculosis incubation period in hroses

A

3 to 4 weeks

231
Q

Risk factors for Corynebacterium pseudotuberculosis in hroses

A

young adult horses (<5 years of age)
horses housed otuside or with access to an outside paddock
Or in contact iwht other horses on pasture compared to stable dhroses

232
Q

Corynebacterium pseudotuberculosis disease in sheep and goats, transmission

A

contact with exudate from draining abscess from animal to animal
or contaminated equipment

233
Q

Corynebacterium pseudotuberculosis sheep that acquire the organism orally or from shearing wounds tend to have lesions lcoated whre?

A

parotid
submandibular
preformal
thoracic abscesses

234
Q

IN sheep and goats Corynebacterium pseudotuberculosis incubation period?

A

variable, long
experimentally 2 weeks to sveral months

235
Q

Corynebacterium pseudotuberculosis pathogenesis in horses

A

**speculative
-enters through skin or mucous membrane abrasion or wounds
-spread through lymphatics
-macrophages phagocytose and migrate to invasion site to engulf them
corynebacterium replicates in phagolysosome

236
Q

Why does Corynebacterium pseudotuberculosis survive intracellularly?

A

-its high lipid ocntent (corynomycolic acid, resisting the action of lysosomal enzymes

237
Q

What virulence factor of Corynebacterium pseudotuberculosis increased vascular permeability, causing spread of organism regionally and systemically

A

PLD toxins
phospholipase D

238
Q

Important features to consider when treating external abscesses caused by Corynebacterium pseudotuberculosis

A
  1. allow the abscess to mature
  2. establish drainage
  3. collect and properly dispose of the infective exudate
  4. lavage the wound with an antiseptic solution
  5. apply insect repellant oinemtns and othe rmeasure of gly control
239
Q

Corynebacterium pseudotuberculosis if antimicrobials are indicated (internal abscesses or ulcerative lymphangitis) what is necessary in their use?

A

long term (min 4 to 6 weeks)

240
Q

Corynebacterium pseudotuberculosis antimocrbial susceptibliity

A

-TMS
-PPG
0mino
docy
0kpen
rfampin

241
Q

Prognosis for horses with Corynebacterium pseudotuberculosis ulcerative lymphangitis and internal abscesses

A

guarded– improves if detected early an dlong-term therapy administered

242
Q

Corynebacterium pseudotuberculosis treatment of choice in small ruminants

A

copmlete surgical removal of affected lymph nodes

243
Q

Corynebacterium pseudotuberculosis small ruminants farms morbidity

A

can reach 100%
– depopulation mbeing the most ecnomic option

244
Q

Corynebacterium pseudotuberculosis problem with enviornmental contamination

A

can survie in soila dn on formites

245
Q

Corynebacterium pseudotuberculosis problem with enviornmental contamination

A

can survive in soil and on fomites

Cardiology.CV.hemolymph (6 decks)

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