Inspired by table salt – cyanide poisoning

Hi Readers,

I was eating my dinner early this week and I noticed on the salt bottle that an anticaking agent called ‘potassium ferrocyanide’ was used. I began to wonder, as I remembered learning in biology that cyanide is a competitive inhibitor, what the “ferro-” prefix signified and how the “ferro-” prevents it from inhibiting our enzymes.

After carrying out some online research I found that the ferrocyanide has its cyanide ions very tightly bound to the iron atom and stays with the iron right through the digestive system. The ferrocyanide cannot freely pass through the plasma membrane.

Nitrites can be used to treat for cyanide poisoning. The nitrites oxidise some of the haemoglobin’s iron converting the haemoglobin into methemoglobin. This releases more cytochrome oxidase enzyme (more of the enzyme which is being inhibited by the cyanide, which is preventing cellular respiration).

Cyanide binds to methemoglobin, forming cyanmethemoglobin. Treatment with nitrites is not really safe as methemoglobin cannot carry oxygen, and severe methemoglobinemia may occur and needs to be treated in turn with methylene blue (which used to be used to directly treat cyanide poisoning). Sodium nitrite is rapidly effective but can cause life-threatening toxicity (methemoglobinemia), whereas sodium thiosulfate – which can also be used to treat cyanide poisoning – has a delayed effect but is far safer.

I decided to look into cyanide poisoning in cattle, and the most frequent cause of acute and chronic cyanide poisoning in livestock is ingestion of plants that either contain cyanogenic glycosides (young plants, new shoots, and regrowth of plants after cutting often contain the highest levels of cyanogenic glycosides) or are induced to produce cyanogenic glycosides and cyanolipids.

Treatment

The affected cattle should be treated immediately by drenching with sodium thiosulphate. 60 g should be given in 600 ml of water. This can then be repeated hourly until the animal recovers.

The most effective treatment for cyanide poisoning is an intravenous injection of sodium thiosulphate. This is best administered by a vet at a dose rate of 660 mg/kg as well as oral/intraruminal doses of 30 g in 100 ml of water. The animals may require repeated intravenous doses if they relapse.

Sodium thiosulphate in a high dose can be effective when given up to 30 minutes after the ingestion of a toxic dose of cyanide, but it must be given as soon as possible.

Symptoms may include:

  • rapid laboured breathing
  • irregular pulse
  • frothing at the mouth
  • dilated pupils
  • muscle tremors
  • staggering

The mucous membranes are bright red in colour due to oxygen saturation of the haemoglobin.

If large quantities of cyanide are absorbed rapidly enough, the animals detoxification mechanisms will be overwhelmed and the animal will soon die. Affected animals rarely survive more than 1-2 hours after consuming the lethal quantities of cyanogenic plants and usually die within 5-15 minutes of developing clinical signs of poisoning.

Again, as I regularly mention, PREVENTION IS BETTER THAN A CURE! In order to prevent possible cyanide poisoning:

  • Graze sorghum, sorghum crosses, or john-songrass plants only when they are at least 18-24 inches tall.
  • Do not graze plants during drought periods when growth is severely reduced or the plant is wilted or twisted.  Slowed growth and the inability of the plant to maturefavours the formation of cyanogenic compounds in the leaves.
  • Do not graze potentially hazardous forages when frost is likely (including at night). Frost allows conversion to hydrogen cyanide within the plant. It is best not to allow ruminants to graze after a light frost as this is an extremely dangerous time and it may be several weeks before the cyanide potential subsides.
  • Do not allow access to wild cherry leaves.

Have any of you ever seen this in real life? I look forward to hearing any thoughts!

Sol

References

https://en.wikipedia.org/wiki/Ferrocyanide

https://www.quora.com/How-dangerous-is-E536-anti-caking-agent-potassium-ferrocyanide-on-salt

http://emedicine.medscape.com/article/814287-treatment https://www.daf.qld.gov.au/animal-industries/animal-health-and-diseases/protect-your-animals/poisonings-of-livestock/cyanide-and-nitrate-poisoning/treating-cyanide-and-nitrate-poisoning

http://www2.ca.uky.edu/agcomm/pubs/ID/ID220/ID220.pdf

“Fixing a broken heart”

Hi Readers,

Following a talk I recently had at school on UCAS applications as I start to think about applying to university, an interesting point was raised as a side topic by our guest speaker. He mentioned that zebrafish, a fish of no economic value to commercial fisheries, might help to extend our generations’ lifetime by almost 20 years.

The zebrafish is a special animal to biologists because its body is transparent. Therefore zebrafish are transparent early in their life cycle, so it is easy for researchers to see their hearts and blood vessels grow. Their hearts begin to develop after just 12 hours, and they reach adult size – about 3cm long – in about three months. They can provide research results barely three days later. If researchers modify the fish’s genotype at the egg stage, they can see a change in organ shape or dynamics very quickly.

In this 30-hour-old zebrafish embryo, you can observe developing organs like the retina (R), the brain (B), spinal chord (SC), the muscle (M) and the heart (H).

Heart tissue damage may occur when a person has suffered from a heart attack which affects their quality of life. Understanding what proteins allow human heart cells to multiply and regenerate, as they do in these fish, could help develop drugs that help our hearts to heal themselves.

If a person has a heart attack, the heart tissue lacks blood and therefore oxygen, causing it to become damaged or dead. Zebrafish can repair their hearts, unlike humans – heart muscle cells near the damaged area lose their muscle properties and revert back to stem cells. Scientists know that a protein called Mef2 is needed to turn zebrafish stem cells into heart muscle cells.

Dr Yaniv Hinits and colleagues believe that zebrafish muscle cells near wounds are able to turn Mef2 on and off – turning Mef2 off to revert to stem cells, before growing and turning Mef2 back on to repair the heart. Their team has been awarded a grant to find out if controlling Mef2could be used to treat damaged human heart tissue. They will study Mef2 in detail, find out if it can heal the heart after injury, and test if other proteins thought to influence recovery after heart attack are working through Mef2.

From my understanding, the grant was for three years and started 1st July 2014. I hope we hear some results in a few months time from this promising experiment.

Sol

https://www.bhf.org.uk/get-involved/mending-broken-hearts/research/zebrafish—do-they-hold-the-secret-cure

https://www.sciencedaily.com/terms/danio_rerio.htm

http://www.giraldezlab.org/Zebrafish.html

 

The impact on the Farming Community and Vets alike post Brexit

Hi Readers,

With the recent news of the General Election being brought forward, I thought I’d share what I have been told by farmers on how Brexit will have an impact on them as well as the veterinary community.

Speaking to a dairy farmer his comments were:

  • He was in favour of brexit
  • The control of TB can be managed without being banned from vaccination under EU law
  • Currently if vaccinations we administered to the cattle, the EU would bar imports of British beef – which he feels would not be a bad thing as it would mean we wouldn’t need to import beef either from the EU
  • If we didn’t import so much from the EU we can produce our own beef and control numbers without being told how much to import/export
  • He hopes that a vaccination programme could eradicate bovine TB in Britain within a decade

Another beef farmer I spoke to has concerns that as a cause of Brexit, TB testing costs will have to be covered more by farmers, and testing may be forced to occur more frequently

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An article I found by Philip Case on Farmer’s Weekly had some interesting points. These outlined the effects on different areas of farming.

Subsidy reform beyond the CAP (Common Agricultural Policy which implements a system of subsidies and other programmes)

“As things stand, the EU contributes £2.9bn to the UK via the CAP and its related subsidies, yet our estimated net contribution is more than three times that, at £9.8bn. Thus, unconstrained by EU rules, the government will now be in a position, if appropriate, to increase rural payments.”

Labour

“There are an estimated 67,000 seasonal workers of non-UK origin, chiefly from eastern European countries inside the EU, in UK agriculture. Owen Paterson says UK government must reintroduce a seasonal agricultural workers’ scheme post Brexit

Combating animal and plant disease

“By retaking control of our borders, we can implement a system with the kind of rigour found in Australia and New Zealand, to the benefit of our animal and plant health. This will ensure the safety of British trees, plants and animals for generations to come.”

This is one of the areas that may affect vets and vets of the future.

A Farmer’s Weekly Reporter writes:

FUW president Glyn Roberts said: “We have long been calling for the creation of a post-Brexit UK agricultural framework, and discussions between UK and Welsh government have been frustratingly slow.

The NFU said it would use the next seven weeks in the run-up to the general election to ensure that all parties engaged with the food and farming community.

Jeremy Corbin has said he will raise minimum wage to £10 an hour but with farmers already struggling, as we are not ‘Buying British’ is this going to be possible? Having a strong insight into the hard work that goes on in this community, these workers must be there to ensure the farms function properly. If farmers are paying their workers more, will they be forced to make cuts to veterinary costs (e.g. Health Clubs) that they know are causing their farms to grow and perform better?

One thing is certain with the whole Brexit process…no one is sure what is going to happen! Young farmers and aspiring large animal vets are all concerned what will happen to our field of interest but it seems the Farming community is doing all they can. My frustration is, although we understand the benefits and drawbacks of Brexit, young people my age cannot vote to get their opinions across in such as important topic – one which will massively impact our future!

https://en.wikipedia.org/wiki/Common_Agricultural_Policy

http://www.fwi.co.uk/news/owen-paterson-spells-out-vision-for-farming-post-brexit.htm

http://www.fwi.co.uk/news/brexit-key-general-election-issue-say-farm-leaders.htm

https://www.visavet.es/bovinetuberculosis/bovine-tb/diagnosis.php

Bovine Coccidiosis

Hi Readers,

Many who know me are aware that my passion for animals stemmed from growing up on a sheep and cattle farm, which has hugely influenced my career choice. This week I thought I’d write about a disease in my favourite animal, as I’ve always been interested in pathology especially in cows.

Bovine Coccisiosis is my chosen disease for this week, a disease caused by single celled protozoa (from the genus Eimeria). Their complex lifecycle involves asexual and sexual reproduction and know for the damage they do to intestinal mucosa. There are more than a dozen species of coccidia, however only three (E.bovis, E. zuernii and E. alabamensis) are thought to be clinically significant.

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The signs of infection are dependant on factors such as age, immune status and level of challenge. The signs however include: diarrhoea (which could contain blood), tenesmus (straining to empty the bowel without success); in more chronic and subclinical forms, an appearance of a ‘poor doer’, stary coat, pasty faeces, reduced appetite and poor growth rate.

The following is a flow chart of the life cycle of this protozoa that I made to help me understand it:

Screen Shot 2017-04-08 at 20.10.25

(click to enlarge)

Faecal oocyst counts are frequently recommended for confirming a diagnosis of coccidiosis. Many samples should be taken from in contact as well as affected calves and all should be examined.

(Oocyst is the encysted zygotic stage in the life cycle of some sporozoans (a protozoan of the phylum Sporozoa))

There are some treatments for Coccidiosis are available. These include decoquinate (Deccox) – in feed, diclazuril (Vecoxan) and toltrazuril (Baycox) – all anticoccidials, two given by a drench. Sulphonamide drugs can also be used and proper nursing is also important (with oral electrolyte fluid being given if diarrhoea is causing dehydration).

Again, as I have mentioned many times, PREVENTION IS BETTER THAN A CURE! So the following measures should be in place to prevent this infection reaching and affecting a herd. It has been found in 50% of dairy herds visited by XLVets and problems are also being seen in suckling beef calves. Those affected are mostly between 2-3 months old.

  • An ‘all in, all out’ policy – allowing pens to be thoroughly cleaned between loads
  • Disinfectant may help – but most coccidial oocysts are highly resistant to most disinfectants
  • Pens should be well bedded – to keep pens clean
  • Good drainage and ventilation – to keep pens dry
  • Feed should be in troughs off the floor and clean (free from faecal contamination) as well as water troughs
  • Scouring calves should be isolated – for treatment and reducing risk of transmission to other animals
  • Strategic dosing (in feed or via drench) if time of challenge and disease can be predicted (weaning time/ when weaned calves are grouped in rearing sheds)

Other top tips include:

  • Minimise stress at all times by avoiding mixing (especially when weaning)
  • Avoid overstocking
  • Early diagnosis and treatment is essential

 References:

Alan Walker XLVets Fact sheets

Alpaca Mating

Hi Readers,

Back in October, I did some alpaca work experience and was lucky enough to be involved in testing to see if the female alpacas were pregnant. I hadn’t heard much about alpaca breeding and was interested to see how different it is to calving and lambing that I have much more experience in.

When the hembra was pregnant and so had a functional corpus luteum, she would aggressively refuse the male’s efforts to mount ie. She would try to run from the stud alpaca, with ears down, and spitting. If the female was not pregnant and had not ovulated, she would sit for remating.

This indication of pregnancy is seen if he is reintroduced over 15 days after the initial breeding. A functional corpus luteum is present 2–3 days after ovulation.

The corpus luteum develops on the ovary at the site of ovulation and produces progesterone (the pro-gestational hormone) to maintain the foetus for the entire pregnancy as well as for implantation. If a female ovulates but fails to conceive, she will become receptive again approximately 12-14 days after the failed mating.

The fertilised secondary oocyte is usually found in the uterus by day 7 after mating, with implantation occurring after around 30 days of gestation.

Ovulation in a female alpaca usually occurs as a result of ‘copulation’ (alpacas are “induced ovulators” rather than having oestrus cycles like we do).  Females can ovulate as a result of the stimulation of being near to a mating pair. When the female is ready for mounting she will sit in a “cush” position. The male vocally “orgles” (a type of mating call) as he mounts her.

Gestation is usually around 11.5 to 12 months.

I enjoy learning more about what I see on work experience as there isn’t always time to explain what is happening. However, my favourite part on this farm was bottle feeding the crias, they are not as keen to suck as lambs are though!

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Has anyone else done any alpaca or even llama experience? I look forward to hearing from you!

Sol

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References

http://www.msdvetmanual.com/exotic-and-laboratory-animals/llamas-and-alpacas/reproduction-of-llamas-and-alpacas

http://criagenesis.cc/wp-content/uploads/2015/11/CriaGenesis-Paddock-mating1.pdf

https://www.thealpacaplace.co.nz/articles/breeding-and-reproduction/breeding-alpacas/

Strangles in Horses

Hi Readers,

So after a recent outbreak of Strangles very close to home, I thought I would research this disease in greater detail. Having been aware of the disease for many years now, the necessity of knowing its whereabouts is crucial when caring for my horse.

IMG_3883

 

My biggest fear when hearing about a recent Strangles case is always how contagious it is. As a young child I was always told not to go on public bridle paths when the yard nearby has a case of strangles. However, Strangles is not actually airborne unlike equine flu so I am not sure how effective this piece of advice actually was.

It is a respiratory infection caused by Strep. Equi, which causes depression, loss of appetite/difficulty eating, raised temperature, cough, nasal discharge, swollen glands in throat and rupture of glands with pus visible as symptoms. The disease can be diagnosed by a blood test; some issues with detecting Strangles include its tendency to be mistaken by the common cold or allergies. In severe cases, Strangles can be fatal in 1% of cases when abscesses develop in other body organs which grow and rupture, a form known as ‘bastard strangles’. Another life threatening complication is “Purpura hemorrhagica”. This is widespread small bleeding along with fluid accumulation of the limbs, eyelids and gums. The outer accumulation of fluid can be so extreme that circulatory failure and death can occur.

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From seminars I have attended in farm animal health, the concepts are near enough always the same. If you go out of your way, speaking to the yard owner and educating people on the yard, to prevent the disease entering and infecting your animals in the first place, the hard decisions that come when the disease gets very severe will not have to be made. Prevention is always better that a cure! To try to prevent the disease from infecting an animal a number of precautions can be taken:

  • Avoid contact/sharing tack or equipment with horses whose health status you do not know (e.g at shows)
  • Don’t overcrowd a yard – diseases spread more easily
  • Quarantine horses that come on the yard, care should be taken with who comes into contact with the new arrival and what other animals they have to attend to  
  • If people have arrived from an affected yard, their movement should be restricted
  • Horses should be up to date with their vaccinations

There is also a vaccine to prevent Strangles. The Equilis StrepE is a vaccine that contains the active substance live deletion mutant Streptococcus equi bacteria. This is the first vaccine to be licensed for horses in the EU against strangles. All members should follow a vaccination schedule on a yard to be sure this vaccine is effective and to prevent the closure of a yard.

I would be really interested in any experience you have had with the disease. Feel free to comment below!

Sol

References

http://www.equine-strangles.co.uk/disease-control.aspx

http://www.theodora.com/drugs/eu/equilis_strepe_veterinary.html

http://www.equine-strangles.co.uk/about-strangles.aspx

 

 

 

Foot Rot in Sheep

Hi Readers,

Firstly, apologies for not updating my site recently; as I’m sure most of you are aware it’s lambing season, so I am currently balancing studying and lambing shifts! One of the things I’ve managed to do a lot of this season is foot trimming the ewes before we turn them out with their lambs. I’ve realised how much physical strength is required in order to turn the ewes over – a couple of bruises later, and I think I’m getting the hang of it!

What I wanted to look into on this post, is the reason I’ve found some ewes with bad feet who have clearly suffered from foot rot. This means I’ve injected quite a few ewes intramuscular with Alamycin – another skill I’m quickly getting the hang of!

Scald and footrot are caused by the bacterium “Dichelobacter nodosus”. This is contagious and can be passed onto other sheep especially in the UK climate – very damp and perfect temperature. It causes 90% of lameness in sheep in the UK. It may also be on set during lambing time, when the ewes are in for lambing and the straw becomes wet and warm.

The interdigital skin in the feet becomes red and swollen and covered by a thin layer of white exudate (a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation). I treated any ewes that I found with this condition using blue spray, alamycin if very bad (to the point where there was a very strong smell) and leaving it untrimmed. We will move these ewes into a separate paddock to reduce risk of infection to other sheep and so they can be treated again in a few weeks. When I was trimming feet during pre lambing checks we used a foot bath which also proved very effective in helping to heal the interdigital dermatitis.

16936048_1831553067099793_1811578445_o

Sol

References

http://www.nadis.org.uk/bulletins/lameness-control-in-sheep.aspx

Ethics on the topic of dissections in schools

Hi Readers,

After doing a number of dissections this week while studying the respiratory system of different species, one of the questions I needed to answer for a core practical was “Describe the approaches that were taken to ensure the ethically responsible use of animals in this practical activity”.

This got me thinking on what the different opinions were on dissections from an animals-rights activist’s point of view as well as those in favour of the dissections.

When doing some research I found a PETA article called “Dissections: Lessons on Cruelty”. It talks about the different animals that are commonly dissected, such as frogs and mice. It also mentions the methods in how the animals are obtained for dissection, implying that escaped cats, for example, were in fact stolen from their homes by suppliers of dissection animals. The article claims “Classroom dissection desensitizes students to the sanctity of life. Research has shown that a significant number of students at every educational level are uncomfortable with the use of animals in dissection and experimentation.” After seeing some of my peers uncomfortable with the dissection, I spoke to one of them about what exactly made them uncomfortable when watching/carrying out these practicals especially the compulsory core ones. She said: “I think sometimes it’s wasting animals. The core practical we did was dissecting a locust, which I was more comfortable with as insects are annoying. Also, if the animal is already dead then I don’t mind as much, for example, if it comes from a butcher’s. If it was a full cow on the other hand, I wouldn’t be okay with killing it just for dissecting. It could be used to feed a lot of people so dissecting it is just a waste. If a laboratory had to kill a healthy cow to do research I’d understand that but not for a school dissection as this is just to see what’s inside. I don’t really like the smell during these practical activities either, or the sight of blood.” Another peer commented that he was “just afraid of rats” so didn’t want to watch the dissection I was chosen to do in front of the class.

After reading another article, I read a statement that I found very concerning. Heidi Blake writes for the telegraph (2010) “Schools are abandoning the practice of cutting up frogs, rats and animal organs which has been a mainstay of biology lessons for generations, out of concern for squeamish pupils and fears that they could turn their scalpels on each other.” The article was based on the reduction of dissections taking place now due to health and safety concerns and that most of these practicals are now being replaced by videos or the teacher’s are carrying out demonstrations. The violent element of this statement surprised me as only a few generations before my own would claim that they remember hating biology due to having to capture their own and then dissecting the animal (mostly frogs). It leaves me with a few questions: is there more crime occurring now? Is it more between young people? Do we just hear about incidents more because of social media/ the news on national and international television?

In my opinion, I think by commercially killing animals to be eaten we are doing just as much harm as if we killed them for these practicals. We are claiming it is fine to kill them in order to fulfill a basic human need, but not fulfill the need of potential future scientists – this practice may influence a person to follow this career path who could go on to cure a human disease. This forms a cycle – treatment from disease is also a basic human need. In my experience, I have enjoyed dissections and recall wanting to dissect any animal as soon as I moved up to secondary school in order to learn more about how my own body functions as well as that of different animals. I have learned valuable skills such as accuracy, patience and steadiness. I also think diagrams of these animals usually don’t help at all and oversimplify structures; in a locust for example the spiracles are not obvious dots and if I hadn’t done the dissection myself I wouldn’t have understood fully the structure of the chitin supporting the tracheae, having not seen it under the microscope.

I have seen that many A level students are also currently carrying out these practices and would be very interested in hearing your views.

Sol

 

References

http://www.peta.org/issues/animals-used-for-experimentation/animals-used-experimentation-factsheets/dissection-lessons-cruelty/

http://www.telegraph.co.uk/education/educationnews/7668210/Schools-abandon-dissection-in-Biology-lessons-over-health-and-safety-fears.html

Respiratory Systems – Chickens vs. Sheep

Hi Readers,

This week I thought I’d investigate different respiratory systems, and the problems that can occur with them, in two different species in particular after a topic I covered in biology. I wanted to see the differences between mammals and birds.

Sheep

All mammals have the same respiratory system but adapted to their size and shape. The equation for respiration is:

oxygen + glucose -> carbon dioxide + water (+ATP)

Gas Exchange

Diffusion is when molecules move from an area of high concentration to an area of low concentration. The experiment below shows a container separated with a semipermeable membrane, dividing an area with a high concentration of a molecule (red dots) from an area with lower concentration. The membrane allows the molecules to move from one side to the other. Over time, the molecules will move from the area of high concentration to the area of low concentration. They do this until the overall net movement is equal. It reaches equilibrium.

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This happens during respiration – oxygen and carbon dioxide are often highly concentrated on opposite sides of a cell membrane. Diffusion allows gas exchange to occurIn animals with a closed circulatory system (both chickens and sheep) – gas exchange takes place across capillaries.

Unlike humans who have two lungs – the left divided into two and the right into three lobes, sheep have highly segmented lungs consisting of two lobes in the left lung and four lobes in the right lung with the bronchus of the right cranial lobe coming directly from the trachea.

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Sheep airways are similar to humans’ in terms of where epithelial cell and mast cells (type of white blood cell) are found. The sheep lungs have a significant population of pulmonary intravascular macrophages that are important in engulfing foreign particles and pathogens.

Inside the nasal cavity of mammals are ciliated epithelial cells, which are used to waft any bacteria and unwanted foreign bodies down the throat to the stomach. The stomach acid and digestive enzymes then kills them. There are also goblet cells, which are used to produce mucus. This catches the unwanted microbes; the moist and warm conditions make it even stickier to ensure the microbes do not enter and grow in the body.

Sheep are obligate nasal breathers, meaning they mostly breathe through their nose but do possess the ability to occasionally breathe through their mouths. It has been suggested that obligate nasal breathing is an adaptation very useful in prey species, as it allows an animal to keep eating, especially as sheep are grazing animals so preserve their ability to detect predators by scent. Humans however, breathe via either mouth or nose. The advantage of breathing through the nose is there is less chance of an infection as there are no ciliated epithelial cells or goblet cells, making mucus, in the mouth for protection.

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In mammals, the trachea splits off into two bronchi, which then break off further to form bronchioles. The bronchioles have alveoli attached to the end of them which is where gas exchange occurs. There are many adaptations of the alveoli that allow it to exchange gases efficiently. These include:

  • Lining of the lung and capillaries only one cell thick – so gases only have to diffuse over a short distance
  • Large surface area – lots of oxygen can diffuse into blood stream at once
  • Good blood supply – oxygen is carried away to the cells as soon as it has diffused
  • Liquid surfactant – gases must diffuse in liquid to be able to diffuse into the blood
  • Phagocytic white blood cells – engulfs bacteria to help protect the body
  • High concentration gradient – gases can diffuse in and out of the alveoli quickly due to the concentration gradient (blood has high concentration of CO2 produced by respiration but not much O2; lungs have high concentration of O2 but not much CO2

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Ventilation movements also maintain the concentration gradients because air is regularly moving in and out of the lungs.

Inspiration:

  • The diaphragm muscles contract and the diaphragm flattens and moves down
  • The intercostal muscles contract, which makes the ribs move up and out
  • The volume of the thorax increases. As the volume increases the pressure decreases
  • Air flows in down a pressure gradient
  • Oxygen diffuses into alveoli along the concentration gradient. In the alveoli, oxygen dissolves in liquid, which then diffuses the short distance into the blood capillaries

Expiration:

  • The diaphragm muscles and the intercostal muscles relax
  • Lungs return to normal size (recoils)
  • Ribs move in and down and the diaphragm moves upwards
  • Volume of the thorax decreases and the pressure increases
  • Air moves out of the lungs and out of the body down a pressure gradient

Chickens

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The openings to the nasal cavity (nares) are on the top beak. Within the cavity are:

  • Squamous epithelium – a single layer of flattened cells
  • Ciliated epithelium – cube shaped cells with cilia or hairs that trap foreign bodies (dust/bacteria)
  • Olfactory membrane – gives the sense of smell

The epithelium of the nasal cavity is covered in mucosal glands, which produce mucus that helps to keep foreign material from entering the body through the respiratory system.

Oropharynx (mouth and pharynx)

The oropharynx consists of the mouth and the pharynx (the cavity behind the nose and mouth, connecting them to the oesophagus). Behind the base of the tongue is the rima glottidis  (opening into the larynx). There are no vocal cords, epiglottis or thyroid cartilages that are normally found in mammals.

Trachea

Held open permanently by 108 to 125 cartilaginous rings. The trachea is lined with mucociliary epithelium where the hair-like cilia move foreign materials, such as dust, up and out of the trachea. Numerous mucous secreting glands are also found in the tracheal lining.

Bronchi

The trachea divides at the syrinx (found at the end of the trachea) into the left and right bronchi. The cartilaginous rings of the bronchi extend from the syrinx to where the bronchi enter the lungs. Ciliated epithelium with numerous mucous glands lines the bronchi. Some are lined with squamous epithelium.

Gas exchange

Leading off from the bronchi in the lungs are a large number of extremely small air capillaries that are interlocked with the capillaries of the lung circulatory system. These interlocked capillaries are the lungs’ gas exchange system and are very thin. The cell layers that separate the two systems (the blood circulatory system and the air supply system of the lungs) are:

  • Single cell epithelial wall of the air capillary
  • Base membrane one cell thick
  • Single cell epithelial wall of the blood capillary

Lungs and Air Sacs

Fowls do not actually have a diaphragm unlike the respiratory system in mammals. The chicken lung is also much denser than a mammals’. Unlike other species, the avian lung has very little elasticity.

The air sacs are very thin walled coming off of the bronchi (NOT FOUND IN THE LUNGS LIKE MAMMALS!). Some of these sacs also connect to many of the larger long bones to form the pneumatic bones. These make the bones lighter and are an advantage for flight.

It is very difficult to see the air sacs in a bird because they are so thin and transparent. It is believed the walls are lined with simple squamous epithelium although there is some ciliated epithelium in some areas. There are very few blood vessels present which indicates that these sacs play no part in gas exchange. The air sacs provide a very high volume of air for use by the lungs on inspiration and expiration. Therefore the lungs, with help from the air sac system, supply the oxygen necessary to fly. The air sac system permits the bird to change its center of gravity, which also aids flight.

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Inspiration, Expiration and Movement of the Body Wall

Respiration is the result of movement of the body external wall that either causes an increase or decrease in the volume of the cavity – this is because, as I mentioned earlier, fowls do not have a diaphragm. These changes in volume cause changes in pressure inside of the lungs and this causes air to either enter or leave the system.

Inspiration

  • Ribs are drawn forward
  • Sternum pulled downwards
  • Volume increases
  • Pressure decreases
  • Size of the cavity increases crosswise and from front to back

The increase in size and volume lowers the pressure in the lungs and air sacs and results in air from outside being drawn in to equalise the pressure. Inspiration occurs as the air moves into the lungs and air sacs.

Expiration

  • Muscles contract
  • Ribs and sternum return to their original position
  • Volume of the cavity reduces
  • Air pressure in the system increases

This decrease in size and volume increases the pressure in the lungs and air sacs and results in air from inside being pushed out to equalise the pressure. Expiration occurs as the air moves out of the lungs and air sacs.

Chickens actually require two respiratory cycles!

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(a flow diagram I made to try to understand how air travels through the respiratory system)

Similarities Differences
Both have air sacs Chicken’s air sacs are not inside the lungs, a sheep’s are
Air is drawn in and forced out of the lung due to change in pressure – by either movement of the body wall or by contraction of intercostal muscles There are very few blood vessels in air sacs so probably aren’t used in gas exchange like in sheep
They are both obligate nasal breathers but can breathe through their mouths and tend to do so when stressed There are no vocal cords, epiglottis or thyroid cartilages in a chicken like those that are found in sheep
Both produce mucus to catch bacteria and other foreign bodies – for protection Chickens don’t have a diaphragm, sheep do
Both have single cell layers in capillaries to allow for quick diffusion Chickens have very little elasticity in lungs like in sheep
Both have tracheas lined with epithelial cells A chicken lung is also much denser than a sheep’s
Both have closed circulatory systems Respiration in birds requires two respiratory cycles to move the air through the entire respiratory system. In mammals, only one respiratory cycle is necessary
When comparing birds and mammals of similar weight, birds have a slower respiratory rate
The respiratory system of birds is more efficient than that of mammals, transferring more oxygen with each breath
Holding a bird “too tight” can easily cause the bird to suffocate, with sheep this is harder to do


Respiratory Diseases in Sheep and Chickens

Sheep

Name Description Image Symptoms Treatment
Pasteurellosis  Causes septicaemia in young lambs, pneumonia in older sheep, and mastitis in ewes. It is a respiratory disease caused by M. haemolytica  Screen Shot 2017-01-27 at 20.18.10 Depression, lethargy, inappetance, increased respiratory rate, fever Oxytetracycline is the antibiotic used for pasteurellosis as there are few antibiotic resistant strains in sheep
Parasitic Chronic suppurative (pus formation) pneumonia/lung abscesses Very common in mature rams but are difficult to identify by inspection alone  Screen Shot 2017-01-27 at 20.45.05 Weight loss although appetite may appear normal, rectal temperature is often slightly elevated (up to 40.0°), higher respiratory rate, nasal discharge Penicillin is the antibiotic used for chronic respiratory disease 
Ovine pulmonary adenocarcinoma OPA is a contagious, viral, neoplastic disease of the lungs of sheep   Chronic weight loss, dyspnea, crackles, and copious amounts of serous nasal discharge from accumulated lung fluid in an adult sheep No specific treatment is available, affected sheep must be culled

 Chickens

Name Description Image  Symptoms Treatment
Gapeworm Caused by the worm “Syngamus trachea” -the adult worms live in the chicken’s tracheaChickens acquire the disease by eating infected earthworms/snails    Coughing, head-     shaking , ‘gaping’ mouth appearance Wormer such as Flubenvet or Solubenol
Infectious Laryngotracheitis   Herpesvirus causes significant inflammation of the upper airways, and can have a high mortality in chicken flocks   Gasping, coughing of mucus and blood, drop in egg production,sinusitis No definitive treatment (can only try to manage any secondary problems, such as secondary bacterial infections)
Infectious Bronchitis  Caused by a highly infectious virus (coronavirus)  Mortality rate is higher in young birdsThere are vaccines available which are given to chicks   Depression, gasping, coughing, tracheal rales (crackling), nasal discharge, drop in egg production/ producing soft-shelled eggsWhen the kidneys are affected – increased water intake and scouring No treatment (but if a secondary bacterial infection is suspected then antibiotics may help)

I found the similarities and differences between the two animals very interesting and will find out more about different animal families and their respiratory systems. The diseases were also interesting to so I could learn more about why each species is more susceptible to certain diseases than the other. If anyone has seen any respiratory diseases perhaps on work experience or out practising, I would love to know more about what you saw and how it was resolved! I once saw a horse with Chronic Obstructive Pulmonary Disease (COPD)!

Sol

References

http://www.shmoop.com/animal-movement/animal-respiration.html

http://jtd.amegroups.com/article/view/3377/html

http://allergenix.com.au/wp-content/uploads/2013/08/SheepModels.pdf

https://en.wikipedia.org/wiki/Obligate_nasal_breathing

http://www.poultryhub.org/physiology/body-systems/respiratory-system-thermoregulation/

http://www.s-cool.co.uk/a-level/biology/gas-exchange/revise-it/gas-exchange-in-humans

http://www.examstutor.com/biology/resources/studyroom/organs_and_systems/gas_exchange_in_mammals/ventilation_mammals.php?style=printable&PageTitleFull=2%20Ventilation%20in%20mammals

http://www.ehow.com/info_12289822_chickens-breathe-through-mouths.html

http://www.flytesofancy.co.uk/chickenhouses/Worming_Poultry.html

http://www.evolutionfarmvets.co.uk/respiratory-disease-chickens

http://www.thepoultrysite.com/diseaseinfo/83/infectious-laryngotracheitis-ilt/

http://www.infectious-bronchitis.com/signs-lesions-ib.asp

http://www.poultrymed.com/Poultrymed/Templates/showpage.asp?DBID=1&LNGID=1&TMID=103&FID=1519

http://www.nadis.org.uk/bulletins/respiratory-disease-in-adult-and-yearling-sheep.aspx?altTemplate=PDF

http://www.peteducation.com/article.cfm?c=15+1829&aid=2721

Marine Mammals – Killer Whales

Hi Readers,

After hearing the news that SeaWorld’s orca ‘Tilikum’, the whale that killed trainer Dawn Brancheau, has died I thought I’d blog about the controversial topic of keeping the orca’s in captivity. Having recently applied for work experience at an aquarium, working with sea mammals, I thought the topic would be very relevant.

I suppose the arguments for keeping these killer whales in captivity meant the animals could provide a rare opportunity to do crucial research, and the breeding program at SeaWorld does help with increasing killer whale numbers. The killer whale’s only predator is mankind. Although Orcas are not an endangered species, some local populations are considered threatened or endangered due to pollution, depletion of prey species, conflicts with fishing activities and vessels, habitat loss, and whaling.

However, “If SeaWorld didn’t exist, would our understanding of wild killer whales be significantly reduced? I think the answer to that is no, it would not,” says a veteran marine-mammal researcher who works at the National Oceanic and Atmospheric Administration. Furthermore, most animal right activists have said that releasing the orca’s into the wild now that SeaWorld has put an end to its breeding program would not be a wise idea. Most of the killer whales at SeaWorld have live there all their lives and would not survive without human help.

In my opinion, I think breeding programs to increase numbers of these beautiful creatures would be very beneficial, especially as it is our fault for reducing numbers – by whaling or oil spill contamination to their habitats. However, I do agree that the public should get to see these wonderful animals, especially if the money they use to buy a ticket can go towards breeding more of these magnificent creatures. On the other hand, getting them to do tricks and making them act outside of their normal behaviour, perhaps isn’t the way to do it. Unlike the orcas in the ocean, the killer whales in captivity need antibiotics, antifungals, and even antidepressants to maintain their health and well-being. I strongly disagree that this is okay…I believe any animals mental health is as important as ours.

A possibility for these animals could be moving to sea pens, this would allow the orca’s to be in a more natural habitat.

The Keiko example

 

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The killer whale featured in the 1993 film “Free Willy” is often cited in the debate over sea pens.

Keiko was captured off the coast of Iceland in 1979 and trained to perform at theme parks. Many years later, the orca was transported to a sea pen in Iceland in 1998 after spending several years at a Mexico City theme park. Keiko swam away during a short cavort outside of the pen while accompanied by caretakers on a ship. He later turned up in a deep inlet in Norway and was found playing with children and fishermen. The whale died a few months later of acute pneumonia.

SeaWorld trainers have said the experience showed that sea pens were not a safe environment for orcas. Others countered this view, saying the experience with Keiko taught experts how to build a better sea pen. If better pens can be made that will not allow the whales to get pneumonia, this case study proves that orca’s could survive if transferred from theme parks to sea pens.

I’d love to hear other people’s arguments for and against the captivity of any marine mammal, as well as the orca. Feel free to leave a reply!

Sol

References

http://www.takepart.com/feature/2016/06/14/killer-whales-new-life-after-seaworld

http://www.motherjones.com/environment/2014/12/seaworld-killer-whale-orca-science-blackfish

http://www.seaworldofhurt.com/features/seaworld-trainer-dawn-brancheau-death/

http://www.killer-whale.org/killer-whales-endangered/

http://wwf.panda.org/about_our_earth/teacher_resources/best_place_species/current_top_10/orca.cfm

http://www.latimes.com/business/la-fi-seaworld-sea-pens-20160317-htmlstory.html

http://www.bbc.co.uk/news/world-us-canada-38531967