Article Review: Ocular lesions associated with systemic hypertension in dogs: 65 cases (2005–2007)

The first of a bunch of articles I recently picked out of JAVMA was interesting because while I never got any readings without some form of anesthesia, I imagine that hypertension was extremely common in many of the dogs I saw at Lapaw Animal Hospital. Whether it’s a result of obesity, illness, or hospital stress, systemic hypertension is usually an indicator of some other problem, and therefore important in the analysis of the patient.

Image from Conrad Weiser Animal Hospital

The article is a bit confusing, because it goes into great detail the different potential causes of both hypertension and ocular lesions, and the significance of the data based on which was diagnosed first with each case. I began to lose track when on one hand they would mention that the data may be too biased to determine a cause and effect relationship between the two symptoms due to a preexisting condition, but then also said that those preexisting conditions had such a relationship.  It does seem clear that ocular lesions are promoted by the presence of hypertension in both dogs and cats, while the disagreements in the literature are mainly in how much one is indicative of the other. The relationship of hypertension correlating with ocular lesions in cats has varied from 50-100%, which tallied with the frequency of 62% in this case review. While these frequencies don’t prove any sort of direct relationship, they do support the evidence we do have that hypertension can lead to ocular lesions, and that if one is discovered in a patient, it’s worth looking for the other.

This is the first case study I’ve looked at in detail, and I’ll certainly be reading more as I move into veterinary medicine. It was really interesting to me how they selected cases, and how thoroughly they reviewed the significance of possible bias in each case. I absolutely understand why it’s so important, and the way each patient is presented changes how each symptom is portrayed in relation to the others, which makes the range of values for this specific correlation so understandable. Owners are much more likely to bring their dog into the clinic when seeing a clouded or irritated eye

Image from Bass Lake Pet Hospital

than hypertension would be found during a routine exam. Then you have to examine old clinic notes to see if other conditions led to either event, or to see if the veterinarian made the assumption that they were related, and though the situation was resolved, no lab work supports their theory. Some of the limitations  mentioned in the study were the fact that they lad a low sample of normotensive dogs with ocular lesions, and that diagnosis of hypertension is difficult due to situational stress interpretation in the face of blood pressure values and varied measurements within the “grey area” of test results. They also did significant analysis within the cases that took into account patients that were taking anti-hypertensive drugs for other conditions, but mention that those patients might have skewed the data, because there is no way to ensure that there was owner compliance in administration.

An interesting note is that all 5 dogs in the study that were currently taking Phenylpropanolamine either acutely or chronically were all hypertensive, supporting anecdotal evidence that it can promote hypertension. This makes sense to me, as PPA is controlled due to its potential use in creating amphetamine, and its inclusion in many prescription stimulants (Adderall, etc.).

All in all, a good article, and a good look at the relationship between ocular findings and hypertension. Though a large part of me does feel for those research assistants at the University of Wisconsin School of Veterinary Medicine who combed through thousands of patient files to find these 65 cases.

ResearchBlogging.orgLeblanc NL, Stepien RL, & Bentley E (2011). Ocular lesions associated with systemic hypertension in dogs: 65 cases (2005-2007). Journal of the American Veterinary Medical Association, 238 (7), 915-21 PMID: 21453181

Newsworthy: Vaccine linked to “bleeding calf syndrome”

When I first started working in an actual clinic, I was blown away with the education I received in vaccine administration. Before at the shelter my instruction included solely how to administer them and not to be bitten while doing so. Spending a minute to educate clients on vaccine reactions, the steps we took to prevent them from happening, and the importance of the proper scheduling of a series were all new to me, and considering how seriously we took all these things, it vastly contrasted with my training at the shelter. How vaccines work has always been interesting to me, and the immunology involved isn’t terribly complicated on the surface. Even if the mechanisms escape me, I can still visualize the flowchart (something I wish I could consistently do with G-proteins, a crucial topic but one I constantly have to review).

Image from Veterinary Laboratories Agency

Anyway, the point is I was really interested in this article. Bleeding calf syndrome is technically called bovine neonatal pancytopenia (BNP), but is probably still a frightening thing to see. It actually only emerged in 2007. The characteristic bleeding is caused by thrombocytopenia after the calf’s bone marrow becomes compromised. The lack of platelets causes the appearance of bleeding through the skin the name refers to. A group of doctors in Germany were able to determine the etiology of the condition (which has a calf mortality rate of 90%). Based on another study, they knew that the colostrum given to affected calves could also induce the symptoms in other unrelated calves, and after not finding evidence from pathogenic or genetic causes looked at an “immune mediated process” (Deutskens, 2011).

What they found was that there was a correlation between cows vaccinated for Bovine Viral Diarrhea Virus (BVDV) and calves suffering from BNP. After a lot of spectroscopy and protein identification, they found that the vaccine actually was the cause. What the issue was, is that the BVDV vaccine is made using kidney cells from cows, instead of another species (for example many human vaccines are cultured in pig cells). Here’s how that works: there is a specific protein “map” coating all nucleated cells that the immune system uses to identify which team they play for. Anything with a different protein coat is assumed to be foreign, and is attacked. This is the major reason why donated organs are rejected, because the donor has a slightly different “map” than you and your immune system assumes it’s trying to hurt you. With the vaccine grown in bovine cells, remnants or copies of this Major Histocompatability Complex (MHC, the “map”) are introduced to the mother, who has an immune response to them.

This is where it gets interesting, the antibodies the mother makes to attack this are called alloantibodies, and they don’t hurt the mother. They just become another antibody she reserves along with the ones that attacked the rest of the BVDV vaccine. None of her cells have that foreign “map”, so none of her cells need to worry about that extra antibody she created. However, the alloantibody gets stowed away in the colostrum along with all the others just before partuition, still ready to attack the MHC the vaccine was made with. If by coincidence the MHC of the calf is the same as the one in the vaccine cultures, then those alloantibodies given to the calf through the dam’s colostrum will attack cells within the calf, starting with blood cells and moving to the bone marrow. Making it technically not an auto-immune response, because it comes from a foreign immune system, but still a case of friendly fire. Those alloantibodies in the colostrum treat every calf cell featuring that MHC as if it’s an infection.

It should be noted that other vaccines for BVDV that are grown using non-bovine cultures do not cause these problems. This is because if the mother creates antibodies for the MHC of another species, there is no way that the calf can be affected by them. The authors of both the news article and the journal article mention that this serves as an example why same-species vaccine cultures and formation of alloantibodies should be avoided.

Check out the journal article for yourself, the introduction and discussion are well written and interesting. There’s also a similar alloantibody caused disease in humans called Neonatal Alloimmune Thrombocytopenia that’s interesting, the major difference being that the alloantibodies are introduced through the placenta instead of ingested through colostrum.

ResearchBlogging.orgDeutskens F, Lamp B, Riedel CM, Wentz E, Lochnit G, Doll K, Thiel HJ, & Rumenapf T (2011). Vaccine-induced antibodies linked to Bovine Neonatal Pancytopenia (BNP) recognize cattle Major Histocompatibility Complex class I (MHC I). Veterinary research, 42 (1) PMID: 21878124

Article Review: Effects of intravenous administration of Lactated Ringer’s solution on hematologic, serum biochemical, rheological, hemodynamic, and renal measurements in healthy isoflurane-anesthetized dogs

Well, it’s about time I mentioned an article I didn’t particularly enjoy on here. It’s not like I think it’s a waste of paper, it’s an important topic, but it does nothing creative and does little to contribute to the understanding of the subject. The article looks at the effects of different rates of Lactated Ringers Solution administered while under isoflurane anesthesia. It uses healthy animals, discusses well documented effects in humans, and just reinforces common practice.

Lactated Ringers is the most frequently prescribed fluid for maintenance of homeostasis in surgery and pretty much any other health stress event. I know when any patient wasn’t feeling well from any situation at my clinic, we always administered LRS either through a catheter or subcutaneously for outpatients, the dosage based on weight and severity of condition. We know how to use it, and it’s gotten a proven history of effectiveness in both humans and animals. The article justifies itself by saying that fluid therapy in dogs is largely based on human evidence, and that the formulas we use to determine rates have not been thoroughly investigated. Yet throughout the article they repeatedly compare their results to similar studies, and make no conclusions that aren’t already accepted in human and animal medicine. Additionally, the gaps in the literature they identify can’t even be answered using the methods and results of this study, so you can’t use them to justify its existence.

So the big conclusions they determined were that providing LRS increased plasma volume and cardiac output, didn’t increase urine production, and appears to leave the blood volume and remain in extracellular space. These are important points, but they were accepted unanimously without the presence of this study. Further, if their goal was to confirm these assumptions, their results are pretty much irrelevant with a sample size of only 8 animals, all in perfect health, similar size (26-41 lbs isn’t a lot of variance in the world of dogs), and undergoing no medical stress other than common anesthesia and mechanical ventilation.

My impression after finishing the paper was that the people at QTest labs (associated with Ohio State University College of Veterinary Medicine) needed a study to do, needed to get a grant proposal ready, and did enough research on the subject to sell this trial. It’s well written and the authors do a great job of placing their results in context of the literature, mostly because it all agrees. But it can’t hide the fact that it does nothing revolutionary other than providing history on the subject, and giving an excellent account of the methods used in the study. With such great, specific, and controlled procedures, this facility could be solidifying other theories that have conflicting data, if they’d use a sample size large enough.  I’m sure that they don’t always do milk run trials such as this one, and I look forward to seeing their name again in future articles.

ResearchBlogging.orgWilliam W. Muir III, Anusak Kijtawornrat, Yukie Ueyama, Steven V. Radecki, & Robert L. Hamlin (2011). Effects of intravenous administration of lactated Ringer’s solution on hematologic, serum biochemical, rheological, hemodynamic, and renal measurements in healthy isoflurane-anesthetized dogs JAVMA, 239 (5), 630-637

Article Review: Animal Play and Animal Welfare

Today’s article comes again from sciencedirect, and it’s the last literature review I’ll do for a while. It discusses play as an indicator for good welfare in captive and production animals. The challenges associated with understanding the motivations of play, and a brief history of landmark studies concerning play behaviors.

Temple Grandin writes that play in dogs may be training for different social situations. She supports this because dominant animals will change roles to a subordinate position and vice versa. In this way dogs and others would be ready to handle new situations outside of their norm. One benefit of play the article mentions supports this theory, that it’s sheer variability and fluidity may prepare animals for the unexpected. While the rest of their survival and social behaviors are predictable and procedural, play constantly creates new challenges and situations to react to that aren’t life or death. I think this makes sense, but I also think it’s even broader than Grandin puts it. Playful bucking and jumping by cattle, goats, sheep, and horses doesn’t seem to be play behavior related to dominance or social skills. To address this, the article lists several schools of thought as to the main purpose of play.

The first category believes in long-term benefits resulting from play. This includes benefits such as somatic development (differentiating muscle fibers, motor skills, etc.), proficiency in species specific behaviors (hunting, sex behaviors, etc.), and general improved physical and emotional flexibility across novel situations (social changes, new environments, anything new). There’s a lot of research supporting this school, but it doesn’t completely answer the question. Adult animals still play, even those that have sexual experience or have no need to hunt. This thinking largely explains why we see so much more expression of playing behaviors in juvenile animals, and is well supported. This sometimes doesn’t pan out well welfare wise, as experience with sexual or aggressive behaviors may not benefit say, your neutered indoor cat.

The second category is more recent, and proposes that play provides primarily immediate benefits to the animal. The first idea is that play provides/communicates information about the immediate environment it finds itself in. This may be information concerning other group members, its effectiveness physically in that situation, or its current level of development. Another idea is that play is self medicating; as it’s been proven that play releases natural opioids (Pellis & Pellis, 2009). Finally, play may be used for social communication. An animal can reinforce its status, reduce tension, or “break the ice” with a strange animal. I like this theory, but just like the other one, it doesn’t provide a complete picture. It sounds like a cop-out, but I think the reality is a mixture of the two thoughts. Behavior is rarely black and white, and I’m convinced by the research on both sides of the debate. What will be interesting is when we single out species specific behaviors and determine if they reflect the immediate benefits as opposed to the long term benefits. Dogs aren’t a good model because the pedomorphism nature of their evolution makes them predisposed to juvenile play their entire lives.

The bulk of the article relates all of the information to the use of play as an indicator of good welfare. It’s not a new idea, and the article provided a very comprehensive pros and cons list. The pros being that play is contagious, it releases opioids, it doesn’t occur in depressed or ill animals, and animals appear to enjoy it. The cons being that it’s extremely variable between species and individuals, and that occasionally it can increase in frequency to respond to stress (lending evidence in support of the second theory). Eventually, play is identified as a decent indicator of good welfare, and promoter of animal contentment. I agree with the conclusion, and also with the final statement that we have many questions left to ask.

Suzanne D.E. Held, & Marek Spinka (2011). Animal Play and Animal Welfare Animal Behaviour (81), 891-899

Article Review: A review of the causes of poor fertility in high milk producing dairy cows

The more I read, the more I’m extremely grateful for the rigor that my reproduction class required. None of this would have made sense to me last year, and it’s amazing how many of the details I’ve been able to keep in my conscious memory. I’m sad that I’m missing the advanced repro course offered in the fall, but hopefully the experience I’m gaining here will be just as valuable, and I can continue applying what I’ve learned so that I don’t lose the knowledge.

I was extremely impressed with this article. It felt like a lecture rather than a textbook, and as a reader it was easy to finish, but still full of great content. The focus is on how while our dairy cows have been engineered to crank out milk, we’ve seen a dramatic drop in their reproductive success which hurts the efficiency of dairy operations.

Pretty amazing what selective breeding can do. But we knew that, we managed to make dachsunds from wolves.

The article explains that rather than a minimalist approach that looks at only one factor (such as inadvertent selection for poor reproductive fitness) to correct the problem, a more inclusive or holistic approach is needed. I learned a lot more about common problems such as lameness, mastitis, metritis, and poor BCS and how they relate specifically to resumption of estrus after parturition and zygote viability. I’m always amazed how farmers can actually succeed at maintaining herd numbers when conception and birth rates are so low.

There was a lot written about heat stress, and that always seems obvious when it gets over any comfortable temperature. But heat and other environmental stressors are actually a lot more dangerous to reproductive health than I was aware. According to the article, “exposure of ovarian oocytes to unfavorable physiological events during follicle development from primadorial to pre-ovulatory stage may result in the ovulation of defective oocytes up to three months after the insult (Britt, 1992; Fair, 2010).” When you have 60-90 days to breed your cattle to stay on schedule, this is extremely influential to your breeding program. This also makes the situation down in Texas more dangerous in that, with the dry weather during their normal wet season, any excess stress surrounding parturition could delay or destroy what’s left of their breeding program. Once they can’t even breed replacement heifers, its all over.

So, after looking at multiple conditions that hurt reproductive efficiency and discussing their prevention. The article sums itself up with a nice poster identifying the key areas they covered.

(Walsh, 2011)

For the causes and preventative measures covering these you can check out the article. It finishes up by making the point that we can’t just develop a new antibiotic for metritis or mastitis, but we need to reevaluate our genetic selection and more importantly, our management strategies to ensure as many of these factors are met as possible.

Walsh SW, Williams EJ, & Evans AC (2011). A review of the causes of poor fertility in high milk producing dairy cows. Animal reproduction science, 123 (3-4), 127-38 PMID: 21255947

Article Review: Leptospira and Leptospirosis

In my latest ScienceDirect purge, I came across this article covering Leptospirosis. I had no idea it would be such a dense read, figuring it would be a simple review of the disease with emphasis on new discoveries. I ended up using a lot of immunology references and Google searches. This article isn’t just an entry from the Merck manual.

The article does a very good job of covering Lepto microbiology, but I was especially impressed with the point they made to identify everything we don’t know. Indeed that was the emphasis of the article, that lepto contains so many pathways unique to it as a bacterium that we don’t know nearly as much about it as we do something like E. Coli. Additionally, Lepto is extremely hard to culture, as you end up with non-virulent colonies. They identify and isolate the virulent daughters by inoculating lab animals.

You might assume that immunity to Lepto is a simple thing, given how prevalent Lepto vaccination is due to the zoonotic risk. However the article makes the point multiple times that immunity to one Lepto serovar does not grant immunity to others, though occasionally it can help grant passive immunity or resistance across different species. While the exchange of genetic material between parent and daughter lepto colonies is not well understood, it appears to be slow mutating, which is interesting given how unique the antigens between serovars seem to be.

There’s a lot of complicated immunology discussed in the article that I don’t feel qualified to comment on, but it’s very interesting, and I recommend glancing through. The more microbiology I learn the more I understand that 99% of the workings of the cell happen on membranes (a statement that probably produces a loud “duh” from any student, biologist, or doctor). For a more clinical discussion of Lepto, a simpler reference like Merck or Blackwells will help, as well as several peer-reviewed sources that the article itself recommends for information on clinical presentations.

Adler, B., & de la Peña Moctezuma, A. (2010). Leptospira and leptospirosis Veterinary Microbiology, 140 (3-4), 287-296 DOI: 10.1016/j.vetmic.2009.03.012

Article Review: Sources of Stress in Captivity, Part II

Took me forever to get around to reading the rest of this article, this last term was pretty heavy. But nonetheless I haven’t forgotten about this thing, and it’s not like I have to keep an update schedule for my breathlessly waiting readers on here. So with that, let’s get back into it.

The second half of the article focused on more biotic and behavioral stressors, still mostly from a zoo perspective. This half was much more interesting, as the abiotic factors discussed in the first half were pretty simple. That’s not to say that they weren’t well explored and there wasn’t any new information presented, but I’m pretty sure it wasn’t hard for them to come to the conclusion that if we cook our captive animals on concrete on a hot day that it’ll cause stress. One of the neatest things when they were examining behavioral stress was that they always identified when a certain stressor was used as the definition of stress in other studies. Things such as separation from conspecifics and invasive handling were not only examined, but identified as the state of being “stressed” in other studies.

Both at the beginning and the end of this section they really hit the nail on the head for stress in capitivity.

“…the primary difference between such stimuli in nature and the same stimuli in captivity is in the animal’s ability to control it’s exposure to these stimuli…confinement in captivity brings with it a host of other potential stressors, largely in the form of restricted choice” (Morgan and Tromberg, 2007)

Like in The Matrix, it’s a problem of choice. Whether that’s removal of the choice to retreat from people or animals, of feeding time and meal composition, of which animals it shares space with, of mate selection, and obviously of home range/habitat selection. That’s the reason for stress in captivity as broadly defined as it can be. It makes sense, but they touch upon it again later when they discuss the roles of predictability for environment enrichment. Animals when given a choice will chose a predictable schedule over unpredictability, but there are conflicting results as to which one provides more benefits. Novelty  has been shown to be necessary for environmental enrichment: the provision of toys in stall horses greatly reduces stall vices/stereotypies such as cribbing and swaying. Stereotypies are also reduced in pigs with long pieces of straw to chew (see Grandin for perspective on this behavior). Novelty comes up in the article when discussing controlled things such as feeding and cleaning times, and uncontrolled factors like the number and behavior of visitors to zoos.

Human contact is discussed thoroughly as a stressor and enrichment. Social and domesticated species have been shown to benefit greatly from human contact, however other species display obvious detrimental effects.

“In one review of black rhinocerous breeding success in US zoos, animal mortality was positively correlated with the degree of public access to the animals.” (Morgan and Tromberg, 2007)

The only real trend is that the effect of human contact creates wildly different effects based on its nature. If the contact is social or feed associated, it can be great, but across the board, negative contact whether in treatment, handling, or painful/invasive medical procedures will make future contact with people a negative and stressful experience. The article does take a moment to clarify what they thought created a pleasant experience.

“Part of what pleasant handling appears to involve is meeting the animal on its own terms.” (Morgan and Tromberg, 2007)

Grandin talks about this a lot with how animals approach novelty with caution. They enjoy novelty because it turns on the SEEKING blue ribbon emotion, but if that novelty moves beyond what they’re ready to explore, they crank on the FEAR emotion and the novel thing becomes stressful.

So, given everything examined, how do we fix it? That depends on your goals. If you want to create a zoo/farm that keeps the animals at the same stress level as them living in the wild, you better work at Yellowstone (and even then!). It’s really not going to happen. So let’s say we set some reasonable goals, like wanting to reduce pacing stereotypies in our larger animals. So, how do we identify the stressors in those enclosures?

“Many of the stressors reviewed above produce the same or very similar effects on animals…This ambiguity makes such behavioral and physiological responses unreliable symptoms for troubleshooting a given captive situation” (Morgan and Tromberg, 2007)

All we get is that something is wrong, but have no idea what. It’s like saying a person or animal has nausea, diarrhea, and fever. Helpful, we now know it could be one of a thousand issues that all cause those symptoms, more information is needed to make an appropriate diagnosis. In all honesty, other than some simple species specific observations, it comes down to individuals. Some will do better in captivity than others, and some will respond to changes you make to minimize stress better than others. The article mentions that if your goal is a conservation effort, captivity can promote learned helplessness, which results in the loss of adaptive coping strategies. There’s a lot of issues with conservation efforts: loss of genetic diversity (cheetahs), over-success (grey wolves), and loss of natural adaptability and wild behaviors (pandas). Learned helplessness can be useful or at least non-detrimental with respect to domesticated species, but anything you intend on reintroducing to the wild may have issues.

Perhaps (unless it’s a conservation effort) we should just resign ourselves to the fact that when we put animals in a zoo, we are domesticating them. Part of the lure of the zoo is to see wildlife in a controlled setting, but there’s an oxymoron there. Wildlife is out of our control, deer that have problems giving birth die, and predators won’t discriminate between a keystone species and other food options (oh if only we could keep all the salmon to ourselves). Maybe the new direction should be not to impersonate nature, but promote behaviors that inherently make zoo life less stressful for those animals. The article briefly mentions “contrafreeloading” behavior, in which animals will choose to work for a food reward even when it is offered freely. I want to bring up circus animals and how, even though many inhumane techniques have been used to teach them the tricks they do, many of them have been selected for their willingness to do a shapeable behavior or to work with items. We could be selecting our zoo animals for their willingness to participate with handlers and items, and we could provide enrichment through allowing them to work for their rewards. This is accepted with marine mammal exhibits where wild whales, dolphins, sea lions, and anything else we can seemingly fit in a tank receives enrichment in this way (not to say that swimming stereotypies still don’t exist). You can’t argue that we’re attempting to keep their wild habitat and behaviors with three shows a day jumping through hoops. I would need to read more on the subject to provide a supported discussion, but that’s my feeling. And that’s the end of that article, I highly recommend reading through it, but be prepared for a grind, it’s a long one.

Article Review: Sources of Stress in Captivity, Part I

I’ve been hanging onto this review of literature for a long time, it’s about 40 pages long, so I’ve slowly gotten about half way through in my spare time. I’ve decided to break down my thoughts into two posts, not only for the length of the article, but so that I don’t have to essentially write an essay all at once.

Most of the article is written from a zoo perspective, but they do take time to review bits of literature pertaining to domestic livestock. One of my favorite things about this article so far is how they chose to define stress and stressors.

“Stress will be defined as the experience of having intrinsic or extrinsic demands that exceed an individual’s resources for responding to those demands.”

“A ‘stressor’ is anything that challenges homeostasis…in this case may be an actual physical challenge to homeostasis (such as exposure to a sudden change in temperature, physical restraint, or combat) or the threat of such a challenge (such as a direct stare from a more dominant individual, or the approach of a human with handling gloves). In either case, stressors result in a cascade of physiological events designed to prepare the body for homeostatic challenge – the so-called ‘fight or flight’ response.”

I immediately read that first definition of stress and said to myself “yes, that’s what it is”. Mostly in terms of whenever I want to define how I feel stressed. But in reality, I was much more impressed with the definition provided because “stress” is such a catch all term for essentially anything wrong with an animal or it’s environment. I remember working at the animal shelter and being told that most of the diarrhea we saw in healthy cats and dogs in the shelter was a result of “stress.” While that may have been true in many cases, the employees, myself included, used the word stress to essentially explain any question proposed by visitors regarding abnormal behavior from the animals. We gave them the assumption that we knew something they didn’t, and usually the issue was dropped. Without a clear definition of what exactly “stress” meant to those shelter animals though, we had no way of asking the important question, what is causing this animal to be stressed?

We never thought, other than taking basic care of these animals to maintain health, hygiene, and human contact; about what we should be doing to keep them mentally sound. With all the behavior and minor health issues we crossed off as stress induced, we never made an attempt to cure that. It’s not that we didn’t care, but in hindsight it’s just something that wasn’t explored or audited. When I think about it now there was probably a lot of little things that we could have been done if we had just asked the question, instead of just assuming that all stress was inevitable.

I bring this up because I’m sure that other organizations, whether they be animal shelters, veterinary clinics, small farms, or large animal production facilities might have that same oversight. Just providing yourself with a concrete, identifiable definition of stress causes you to move onto the next big one, what are the stressors?

So far in the article I’ve read the sections on abiotic stressors, which included lighting, ambient temperature, sound (ranges and pressure), odors, and tactile interaction with the environment. These are actually harder to work with in my opinion, biotic factors are easier for us to understand and study from a physiological standpoint. Figuring out the umwelt of different species is something that Temple Grandin says she does by thinking in pictures, but I think it goes beyond that. The sheer amount of Olfactory cues that we can only observe animal reactions to tell me that the sensory overload our livestock animals receive every day is beyond something as simple as changing the lighting alone. It’s like explaining the instant assailment of information that flows into your mind when you look at a classroom. Or trying to explain how (literate) people can see words on highway signs and with a single look compute the meaning of those specific shapes. How can we get into the head of a cow and understand how that whiff of estrus urine translates into information?

Anyway, some of the bigger problems noted in the article were flicker rates in florescent lighting that animals can see, extremely high sound pressure in zoo and agricultural settings from both machinery and people (that doubles what would be found in a natural setting), and problems associated with the materials used to create habitats or bedding. As a potential start to a solution, at the end of the abiotic section they make recommendations on what sort of equipment (and where to get it) should be used to measure these factors and potential stressors. Identification of what we know is the first step, so that new options and unforeseen stressors become more obvious.

I’ll have much more to say on this article in part II, but I’ll leave these preliminary thoughts for now. Look for more on this from me soon.

Article Review: Effects of acclimation to human interaction on performance, temperament, physiological responses, and pregnancy rates of Brahman-crossbred cows

Came across this article when searching for stress studies in cattle. I’ve been more and more interested in examining behavior and stress as I’ve read more Temple Grandin. I think it’s a field I can explore as I look for things I want to do with my DVM. Don’t get me wrong, I love working with clients and animals in a clinic setting, but I don’t see myself as a business owner, and I really want to look at what else is out there. Options I’ve been exploring are USDA jobs, lab work, and of course research through the college and elsewhere. Anyway, Giovanna Rosenlicht got me into the habit of reading journal articles in my spare time, which is great and actually really interesting….I am a nerd.

Anyway I don’t have too much to say about this article, the methods are sound and thorough, 395 animals used is a sample size I can get behind. Too many studies especially with companion animals have pitiful sample sizes of like 20 animals. Anyway, following reading the discussion, the dramatic difference I expected to see in the people acclimated group was not present. However there was a final statement that acclimation did have an inconsistent positive effect on reproduction success.

I have a vested interest in animal welfare, and I strongly support an approach that helps the industry see benefit, rather than dig trenches. Studies like this are the only way non-radical, educated, and effective welfare decisions can be made. What happens when people try to make knee-jerk responses to animal welfare? Look at the ban on horse slaughter and the subsequent problems associated with that piece of feel-good legislation.

Anyway, I get sidetracked, this post was supposed to be concerning the article. One of the main points that is crucial to the focus of the study was the correlation with excitable temperament (as often seen in Bos Indicus ancestry cattle) and elevated cortisol concentrations; which are detrimental to multiple physiological systems in the body, and result in “subclinical health disorders that negatively affect cattle reproduction, such as lethargy, lameness, and immunosuppression.” With cortisol levels (along with epinephrine and many other endocrine secretions that are a result of handling and housing stress) being a quantitative measure of animal health and contentment, this data will add onto the already large stack of evidence that the better we treat our meat/eggs/milk, the better product we receive.

It’s unfortunate that a larger and more consistent correlation was not found within the study, but the data is still sound, and definitely leaves room for further study in specific age groups, species and breeds, and other acclimation techniques.

It is also worth mentioning that this research was carried out in Florida, but one of the authors is now doing research at the Oregon State Burns research station. I’ll be looking for and have found many related articles from that location/author and will be discussing more of those in the future.