Infectious Disease Flashcards

1
Q

If an equid with corona virus becomes acutely neurologic, what might be the cause?

A

Hyperammonemia may be due to increase from or absorption from the GI tract, and may contribute to the cause of death.

10.1111/jvim.12480

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2
Q

What kind of bacteria is Corynebacterium pseudotuberculosis?

A

C. pseudotuberculosis is a gram positive bacteria and causes extern and internal abscesses, was well ulcerative lymphangitis.

10.1111/jvim.12534

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3
Q

What are the two biovars of Corynebacterium pseudotuberculosis?

A

Equis and Ovis.

The Equis biovar is nitrate (+) and the Ovis biovar is nitrate (-).

10.1111/jvim.12534

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4
Q

Clostridium botulinum causes what in horses?

A

Botulism is characterized by progressive flaccid paresis and cranial nerve deficits (dysphagia, most common).

10.1111/jvim.12502

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5
Q

What was most related to nonsurvival in horses with botulism? What are other factors?

A

Development of sustained recumbency at any point during hospitalization. Other factors related to nonsurvial were decreased rectal temp on arrival, cardiovascular compromise, dysphagia and abnormal respiratory effort.

10.1111/jvim.12502

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6
Q

What was the difference in animals that were colonized with M. haemolytica post-arrival colonization vs on arrival?

A

Recovery of M. haemolytica from 20% of cattle after arrival was higher than expected, as was the significant increase in prevalence over time. However, recovery of M. haemolytica in the second sample was not associated with increased morbidity or mortality, suggesting that post‐arrival colonization is more likely to be subclinical and may not be as great a concern for feedlot operators. In contrast, isolation of M. haemolytica on arrival was associated with a short‐term, significant increase in risk of clinical illness.

10.1111/jvim.12547

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7
Q

What are possible vectors for Corynebacterium pseudotuberculosis? What possible insect vector was seen to be able to transmit?

A

Vectors in the horse are unknown, but speculations are: horse-to-horse contact, contact with pathogen-infested soil, insect vectors.

The bacterium can penetrate through skin, through abrasions.

The house fly, Musca domestica L. was seen to transmit.

House flies are not bloodsucking flies, but may transmit the bacterium through excoriated skin via mouthparts and tarsal exoskeleton. Further investigation is warranted to determine if house flies act as mechanical vectors or amplify the bacteria, and to determine if bacteria are carried on the external or in the internal organs.

10.1111/jvim.12545

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8
Q

What is the pathogen for Lyme disease and what are some likely clinical signs? What is the vector?

A

Borrelia burgdorferi

Clinical signs in horses include shifting leg lameness, change in attitude, neurologic disease (eg, ataxia and weakness), skin lesions, uveitis, laminitis, lethargy, and hyperesthesia.

Ixodes scapularis is the vector.

10.1111/jvim.13973

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9
Q

What does bovine corona virus cause in cattle?

A

Neonatal calves - diarrhea
Adults - winter dysentery
Both - respiratory illness

Also can be isolated in healthy animals

10.1111/jvim.14811

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10
Q

What are characteristic clinical signs of Streptococcus equi ssp. equi?

A

Characteristic clinical signs include fever, accompanied by copious purulent nasal discharge, abscessation and rupture of lymph nodes in the head and neck region, followed by recovery over several weeks.

10.1111/jvim.15037

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11
Q

In a study evaluating clinical, serologic and microbiologic factors related to unexpectedly mild disease severity in weanlings, which of these factors was of value in detecting exposure to S. equi?

A

immunologically naïve foals naturally exposed to an apparently fully virulent S. equi failed to exhibit classical clinical signs of strangles. This lack of clinical disease also was associated with incomplete serological reactivity to an enhanced serologic test for exposure to S. equi. The important aspect in relation to disease containment and control during outbreaks is that clinical signs alone may be insufficient to release horses from quarantine measures if they have clear exposure risks to known infected horses, and in particular with the well‐recognized risk of persistence as clinically silent carriers.

Serodiagnosis appears to be of value in detecting exposure to S. equi even in the absence of clinical signs.

10.1111/jvim.15037

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12
Q

What are some difficulties of diagnosing neuroborreliosis?

A

Documented clinical disease is rare, whereas subclinical infection with the causative organism appears to be widespread in horses living in endemic areas.

Less severe cases might be under‐reported because of the tremendous difficulty in confirming that clinical signs in the living horse are caused by Borrelia infection and not another cause. Lack of a reliable antemortem diagnostic test is a major obstacle.

10.1111/jvim.15067

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13
Q

Since simultaneous testing of serum and CSF to calculate a CSF : serum ratio using the Lyme multiplex is not a reliable means of identifying equine neuroborreliosis cases, what criteria should be utilized for a presumptive diagnosis of neuroborreliosis in the horse?

A

First, the horse should have had possible exposure to Borrelia by residence in or travel to an endemic area.

Second, the horse should show neurologic signs for which other potential etiologies have been excluded by appropriate diagnostic testing.

These clinical signs should increase suspicion of neuroborreliosis: consistent with multifocal or diffuse nervous system involvement, often with cranial nerve involvement.

Abnormal CSF results, particularly those indicative of meningitis, with either a neutrophilic or lymphocytic pleocytosis, should increase suspicion for the disease.

Some horses with neuroborreliosis might have additional supportive evidence of nervous system infection, with either positive CSF PCR results or immunological test results suggestive of intrathecal antibody production.

10.1111/jvim.15067

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14
Q

In marine mammals with protozoan encephalitis, infection by 2 or more protozoa is linked with severity of disease. What might horses diagnosed with EPM, caused by Sarcocytis neurona, also be coinfected with?

A

Neospora hughesi or Toxoplasma gondii

10.1111/jvim.15127

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15
Q

What has Theilers or idiopathic acute hepatitis been assoc. with in horses?

A

Been described in horses after treatment with equine serum products such as: tetanus antitoxin (most common), botulinum antitoxin, S. equi, pregnant mare serum, equine plasma.

10.1111/jvim.15368

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16
Q

What three flaviviruses and other virus were identified in horses have been suggested as potential causes of serum hepatitis?

A

Equine pegivirus
Theiler’s disease-assoc. virus
Non-primate hepacivirus

Equine parvoviruses

10.1111/jvim.15368

17
Q

What is a newly identified virus that should be tested for in all horses to be used as donors, and why?

A

Equine parvovirus (EqPV-H) has been isolated in cases of serum hepatitis, or Theiler’s. Blood product manufacturers should be tested for EqPV-H.

10.1111/jvim.15368

18
Q

What does a SeM Ab titer after infection with S. equi of >/= 1:12800 indicate?

A

Prior ACVIM consensus statements have indicated that a titer of >/= 1:12800 is seen in horses with metastatic abscesses or purpura.

A more recent study has shown that a horse may have complications of strangles without a SeM antibody titer ≥1:12 800 and that a horse may have a SeM antibody titer ≥1:12 800 without complications. A convalescent SeM antibody titer ≥1:12 800 warrants additional investigation for complications or persistent GP infection but does not necessarily confirm a horse has complicated disease.

10.1111/jvim.15388

19
Q

Can horses infected with Salmonella be clinically or biochemically differentiated from horses infected with equine corona virus?

A

We observed significantly lower neutrophil counts in the ECoV population as compared with UNK horses. In addition, we found no differences in clinical or hematologic abnormalities among horses diagnosed with ECoV and Salmonella. Therefore, the results of our study suggest that ECoV should be included in the differential diagnoses for horses presenting with fever, anorexia, intestinal disease, and neutropenia. Molecular diagnostic testing for both ECoV and Salmonella should be performed to aid diagnosis and improve hospital and on‐farm biosecurity measures in these cases.

10.1111/jvim.15386

20
Q

Do systemically healthy horses and horses with GI disorders shed ECoV at the time of admission and after 48 hours of stress assoc. with hospitalization?

A

The presence of ECoV in feces of hospitalized adult horses was low. Thus, fecal samples that are PCR‐positive for ECoV in adult horses that have clinical signs consistent with this viral infection are likely to be of diagnostic relevance. The clinical relevance of the viruses observed using EM remains to be investigated.

10.1111/jvim.15449

21
Q

What are the different anatomic distributions for lymphoma in horses?

A

Alimentary
Cutaneous
Multicentric
Mediastinal

10.1111/jvim.15411

22
Q

What form of lymphoma showed a longer median survival time?

A

Horses with cutaneous lymphoma and those that achieved CR tended to have longer median survival times than those with alimentary or multicentric lymphoma and those that achieved PR.

10.1111/jvim.15411

23
Q

What are treatment options for lymphoma?

A

Surgical excision
Corticosteroids
Chemotherapy
A combination

10.1111/jvim.15411

24
Q

Tick paralysis is caused by salivary neurotoxins binding to the presynaptic NMJ, preventing release of acetylcholine. This occurs in small animals, and has been seen in large animals as well. While most clinical signs in small animal are caused by LMN dysfunction, in large animals this exact location of dysfunction has not been localized. In a study of two ponies with suspected tick paralysis, what were their clinical signs and where did these signs isolate the problem?

A

Profound weakness with intact postural reactions - LMN

Intact spinal reflexes - UMN

Decreased tongue and tail tone - LMN

Overall, profound weakness with normal proprioception is most consistent with LMN weakness despite the fact that other classic signs of neuromuscular dysfunction such as muscle trembling while standing or neurogenic muscle atrophy were not apparent in these horses.

10.1111/jvim.15540

25
Q

Considering the LMN dysfunction caused by tick paralysis, what are some differentials?

A

Botulism
Equine herpes myeloencephalitis (EHV-1)
West Nile

10.1111/jvim.15540

26
Q

What is a classical triad of clinical signs that animals with Salmonella shedding show? Does this always occur?

A

Diarrhea
Fever
Leukopenia

10.1111/jvim.15579

27
Q

Why might a vaccine not be protective?

A

The potential mechanisms of why vaccines are not protective include the targeted organism not being causal, the immunologic response not being protective, or the difficulty of inducing a protective response for bacteria.

10.1111/jvim.15633

28
Q

Lipopolysaccharide infusion causes what changes after administration?

A

Tachycardia, fever, gut hypomotility, severe decrease in WBC, and increase in serum lactate and TNFalpha. Leukocyte mRNA expression of TNFalpha, IL-1beta, IL-6 and IL-8 were increased.

10.1111/jvim.15783

29
Q

How did the administration of meloxicam, in donkeys with LPS infusions, mediate LPS’ deleterious effects?

A

Decreased and delayed onset of tachycardia. Did NOT prevent fever. Leukopenia returned to baseline more rapidly. TNFalapha concentrations decreased.

10.1111/jvim.15783