Johne’s disease

Hi Readers,

A couple of years ago I was lucky enough to hear Peter Orpin speak about Johne’s disease in a cattle vet-farmer meeting. I thought this week it would be a good idea to revisit the disease and its causes.

Cause of Johne’s

M. paratuberculosis bacteria embeds itself in the wall of the ileum (lower part of the small intestine). As an immune response, infected tissues attempt to regenerate healthy tissue which leads to visible thickening of the intestines. This prevents nutrient absorption, resulting in weight loss.

Late in the infection, antibodies are produced and found in the serum (blood plasma without the proteins used in blood clotting) of animals and indicates clinical signs of disease – death will follow soon after this.

When the microbe is excreted, it can contaminate the soil or water. Outside the host animal, the organism multiplies poorly—if at all—but it can survive over a year in the environment because of its resistance to heat, cold, and drying.

The primary cause of the spread of Johne‘s disease is contact with the faeces or saliva of an infected animal.

Symptoms

Because of the slow, progressive nature of the infection, signs of Johne’s disease may not show up until years after initial infection.

  • long-lasting diarrhoea
  • weight loss despite good appetite
  • Bottle jaw may also appear – fluid accumulation in the bottom jaw causing an abscess

Once clinical signs appear the animal will not recover and will continue to deteriorate.

There is no treatment for Johne’s but as always PREVENTION IS BETTER THAN CURE. It is much more cost effective to prevent than eradicate the disease once it has started spreading through the herd invisibly. The primary source of contamination is manure from an infected adult animal. It is very important to know the status of Johne’s in a herd when buying cattle as this is an easy way for Johne’s to enter a herd.

Vaccinating

A vaccine has previously been made available in the US to prevent the risk of Johne’s which uses a mixture of killed mycobacteria and oil. It can sometimes cause large lumps at the site of injection. Occasionally these lumps will become draining abscess-like lesions. Although the vaccine is given to calves less than 30 days old, the tissue reaction at the injection site may last for life.

Another vaccine is available made from live M. paratuberculosis (but not disease causing).

The efficacy of vaccines is controversial. Studies in the Netherlands have shown that herd owners who follow the recommended management changes to control Johne’s disease could be just as successful as those who vaccinate.

Has anybody ever seen this disease before when seeing practice? Let me know in the comments!

Sol

 

References

http://www.thecattlesite.com/diseaseinfo/173/johnes-disease/

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

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.

Screen Shot 2017-04-08 at 18.55.27

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

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.

Screen Shot 2017-01-28 at 07.42.48

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.

Screen Shot 2017-01-28 at 07.50.48

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.

Screen Shot 2017-01-28 at 07.45.21

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

Screen Shot 2017-01-28 at 07.47.11

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

Screen Shot 2017-01-24 at 19.06.54

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.

Screen Shot 2017-01-24 at 19.36.52

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!

Screen Shot 2017-01-28 at 11.15.41

(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