Difference between revisions of "Dictyocaulosis - Cattle"

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==Clinical==
+
== Synonyms ==
 +
Husk, Hoose
 +
 
 +
<br>
 +
 
 +
== Introduction ==
  
 
*''Dictyocaulus viviparus'' causes [[Respiratory Parasitic Infections - Pathology#Dictyocaulus viviparus|parasitic bronchitis]]
 
*''Dictyocaulus viviparus'' causes [[Respiratory Parasitic Infections - Pathology#Dictyocaulus viviparus|parasitic bronchitis]]
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[[Image:Dictyocaulus viviparus.jpg|right|thumb|100px|<small><center>Dictyocaulus viviparus (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
[[Image:Dictyocaulus viviparus.jpg|right|thumb|100px|<small><center>Dictyocaulus viviparus (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
[[Image:Parasitic bronchitis.jpg|right|thumb|100px|<small><center>Parasitic bronchitis (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
[[Image:Parasitic bronchitis.jpg|right|thumb|100px|<small><center>Parasitic bronchitis (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
*Found in [[Tracheitis#Infectious causes of tracheitis|trachea]] and [[Bronchitis#Infectious causes of bronchitis or bronchiolitis|large bronchi]]
 
*Causes parasitic bronchitis, synonyms: bovine dictyocauliosis, husk, hoose
 
*Primary infection:
 
**Penetration phase (week 1)
 
***Larvae migrate to lungs, no clinical signs
 
**Prepatent phase (weeks 1-3)
 
***Development and migration of larvae -> [[Bronchitis#Bronchiolitis|bronchiolitis]] -> eosinophilic exudate -> air passage blocked -> alveolar collapse (distal to blockage) -> clinical signs (tachypnoea, coughing)
 
**Patent phase (weeks 4-8)
 
***Egg-producing mature worms
 
***[[Bronchitis|Bronchitis]] - due to mature worms
 
***[[Verminous Pneumonia|Parasitic pneumonia]] - due to aspiration of eggs and larvae -> cellular infiltration of [[Neutrophils|neutrophils]], macrophages, giant cells
 
**Postpatent phase (weeks 8-12)
 
***Majority of worms are expelled
 
***In 25% of cases clinical signs may reappear as a result of alveolar epithelialisation
 
***May be together with [[Pulmonary Emphysema|interstitial emphysema]] and [[Pulmonary Oedema|pulmonary oedema]], or secondary bacterial infection
 
*Reinfection syndrome:
 
**Immune cattle show clinical signs only if exposed to large numbers
 
**Pathogenesis - large numbers of larvae reach bronchioles where they are killed by immune response
 
**Pathology - parasite granulomata (grey-green, 5mm diameter, macrophages, giant cells, eosinophils) and eosinophilic plugs in bronchioles
 
<small>Above from RVC Parasitology study guide (2005-2006)</small>
 
*Preferentially in dorsocaudaland ventrocaudal regions
 
  
*Histologically
+
Dictyocaulus viviparous is the lung worm of cattle and is found in [[Tracheitis#Infectious causes of tracheitis|trachea]] and [[Bronchitis#Infectious causes of bronchitis or bronchiolitis|large bronchi]].
**Bronchial epithelium may show hyperplasia due to the chronic irritation
+
<br>
**Cross-sections of the parasites
+
It is a member of the trichostrongylodiea family and is responsible for parasitic bronchitis in cattle.
**Exudate contains many eosinophils
+
<br>
**Foci of necrosis in the rest of the lung tissue due to aspiration of eggs and larvae fromhese adults
+
The penetration phase lasts one week and occurs when the larvae migrate to lungs. There are no clinical signs.
**In mild infestations, the adults are normally expelled in two months - self cure
+
<br>
*Repeated infestation and secondary bacterial infection are common
+
Then the prepatent phase lasts 1- 3 weeks and is the development and migration of larvae leading to [[Bronchitis#Bronchiolitis|bronchiolitis]] and then eosinophilic exudate, causing the air passage to be blocked, resulting in alveolar collapse (distal to blockage). This is when clinical signs such as tachypnoea and coughing being to arise.
 +
<br>
 +
The patent phase then lasts around 4- 8 weeks and the mature worms produce eggs during this period. Signs of [Bronchitis|Bronchitis]] are seen due to mature worms and [Verminous pneumonia|Parasitic pneumonia]] is seen due to aspiration of eggs and larvae causing cellular infiltration of [[Neutrophils|neutrophils]], macrophages and giant cells.
 +
<br>
 +
Finally, the postpatent phase, which lasts around 8- 12 weeks is seen and here, the majority of worms are expelled. In 25% of cases clinical signs may reappear as a result of alveolar epithelialisation, which may occur together with [[Pulmonary Emphysema|interstitial emphysema]] and [[Pulmonary Oedema|pulmonary oedema]], or secondary bacterial infection.
 +
<br>
 +
Reinfection syndrome may occur if immune cattle are exposed to large numbers; only then will they show clinical signs.
 +
<br>
 +
The disease is carried form year to year by overwintering L3 on pasture, as well as carrier animals. Knowledge of the full epidemiology of the disease is not yet understood. Calves pick up the overwintered L3 on pasture and a patent infection occurs producing L1 on the pasture. These migrate from the dungpat via fungus (Pilobolus) and the rest of the calves then become infected. There may be multiple cycles in one year. Immunity however, is rapidly acquired.
 +
 
 +
 
 +
== Signalment ==
 +
The disease affects cattle. It is more severe in calves and can even cause death in these species. There are milder clinical signs in adult cattle. There are no sex or breed predilections to the disease.
 +
 
 +
<br>
 +
 
 +
== Clinical Signs ==
 +
Signs include coughing and tachypnoea. In calves it can causes weight loss and even death in severe cases. In adult cattle, infection will tend to cause reduced milk yields and mild respiratory signs.
 +
 
 +
 
 +
<br>
 +
 
 +
== Diagnosis ==
 +
History and season, as well as clinical signs are very indicative of the disease.
 +
<br>
 +
A faecal examination for '''larvae''' using the Baerman technique, should be performed. Sick and healthy cattle should be tested.
 +
<br>
 +
In adult cattle, a blood and milk ELISA can be used, however, this is of varying diagnostic quality.
 +
<br>
 +
Retrospective diagnosis can be achieved by assessing the response to anthelmintic treatment.
 +
<br>
 +
A post mortem can also be performed.  The '''Inderbitzen technique''' can be used, which is where worms are flushed out of the lungs by pumping water through the pulmonary arteries. The water and worms are collected over a sieve. Worms are counted and 200-300 are required to cause clinical disease. Upon post mortem, one may also see pulmonary oedema and emphysema, which is thought to be caused due to a hypersensitivity response to a massive invasion of lungworm larvae.
 +
 
 +
 
 +
<br>
 +
 
 +
== Treatment and Control ==
 +
If the animal is clinically affected, treatment with anthelmintic such as ivermectin can be used.
 +
<br>
 +
Control of the disease can be achieved by strategic anthelmintic dosing such as invermectin being given 3, 8 and 13 weeks post turnout. There are limitations to this, such as is larvae are encountered early e.g. in the first 2 weeks after turnout or late in the grazing season.
 +
<br>
 +
Vaccination, called 'Huskvac' is the control method of choice and prevents anthelmintic resistance aoccuring on farms. It should be given to first season calves that are reared indoors. The vaccine is oral and calves should be vaccinated 6 and 2 weeks prior to turnout. This results in the decreased clinical disease. The vaccine does not prevent infection completely, but reduces it enough to prevent clinical signs. Note; never mix vaccianted and unvaccinated animals.
 +
 
 +
<br>
  
*Two other types of lesion in lung tissue due to this worm have been reported:
+
== References ==
**Nodules (2-4mm in diameter) with greenish centres in the reinfection of an immune animal - the host mounting a successful defence and preventing larval migration
+
Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing.
**Pulmonary oedema and emphysema - thought to be a hypersensitivity response to a massive invasion of larvae in previously- sensitised animals - the gross and microscopic appearance is similar to that of [[Acute Bovine pulmonary Emphysema and Oedema|fog fever]]
+
<br>
 +
Fox, M and Jacobs, D. (2007) Parasitology Study Guide Part 2: Helminths, Royal Veterinary College.
 +
<br>
 +
Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses, Elsevier Health Sciences.
  
  
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[[Category:Bronchi and Bronchioles - Pathology]]
 
[[Category:Bronchi and Bronchioles - Pathology]]
 
[[Category:Respiratory Parasitic Infections]]
 
[[Category:Respiratory Parasitic Infections]]
[[Category:To Do - Clinical]]
+
[[Category:To Do - Review]]

Revision as of 14:41, 28 March 2011

Synonyms

Husk, Hoose


Introduction

Parasitic Bronchitis - Cattle

Dictyocaulus viviparus (Image sourced from Bristol Biomed Image Archive with permission)
Parasitic bronchitis (Image sourced from Bristol Biomed Image Archive with permission)

Dictyocaulus viviparous is the lung worm of cattle and is found in trachea and large bronchi.
It is a member of the trichostrongylodiea family and is responsible for parasitic bronchitis in cattle.
The penetration phase lasts one week and occurs when the larvae migrate to lungs. There are no clinical signs.
Then the prepatent phase lasts 1- 3 weeks and is the development and migration of larvae leading to bronchiolitis and then eosinophilic exudate, causing the air passage to be blocked, resulting in alveolar collapse (distal to blockage). This is when clinical signs such as tachypnoea and coughing being to arise.
The patent phase then lasts around 4- 8 weeks and the mature worms produce eggs during this period. Signs of [Bronchitis|Bronchitis]] are seen due to mature worms and [Verminous pneumonia|Parasitic pneumonia]] is seen due to aspiration of eggs and larvae causing cellular infiltration of neutrophils, macrophages and giant cells.
Finally, the postpatent phase, which lasts around 8- 12 weeks is seen and here, the majority of worms are expelled. In 25% of cases clinical signs may reappear as a result of alveolar epithelialisation, which may occur together with interstitial emphysema and pulmonary oedema, or secondary bacterial infection.
Reinfection syndrome may occur if immune cattle are exposed to large numbers; only then will they show clinical signs.
The disease is carried form year to year by overwintering L3 on pasture, as well as carrier animals. Knowledge of the full epidemiology of the disease is not yet understood. Calves pick up the overwintered L3 on pasture and a patent infection occurs producing L1 on the pasture. These migrate from the dungpat via fungus (Pilobolus) and the rest of the calves then become infected. There may be multiple cycles in one year. Immunity however, is rapidly acquired.


Signalment

The disease affects cattle. It is more severe in calves and can even cause death in these species. There are milder clinical signs in adult cattle. There are no sex or breed predilections to the disease.


Clinical Signs

Signs include coughing and tachypnoea. In calves it can causes weight loss and even death in severe cases. In adult cattle, infection will tend to cause reduced milk yields and mild respiratory signs.



Diagnosis

History and season, as well as clinical signs are very indicative of the disease.
A faecal examination for larvae using the Baerman technique, should be performed. Sick and healthy cattle should be tested.
In adult cattle, a blood and milk ELISA can be used, however, this is of varying diagnostic quality.
Retrospective diagnosis can be achieved by assessing the response to anthelmintic treatment.
A post mortem can also be performed. The Inderbitzen technique can be used, which is where worms are flushed out of the lungs by pumping water through the pulmonary arteries. The water and worms are collected over a sieve. Worms are counted and 200-300 are required to cause clinical disease. Upon post mortem, one may also see pulmonary oedema and emphysema, which is thought to be caused due to a hypersensitivity response to a massive invasion of lungworm larvae.



Treatment and Control

If the animal is clinically affected, treatment with anthelmintic such as ivermectin can be used.
Control of the disease can be achieved by strategic anthelmintic dosing such as invermectin being given 3, 8 and 13 weeks post turnout. There are limitations to this, such as is larvae are encountered early e.g. in the first 2 weeks after turnout or late in the grazing season.
Vaccination, called 'Huskvac' is the control method of choice and prevents anthelmintic resistance aoccuring on farms. It should be given to first season calves that are reared indoors. The vaccine is oral and calves should be vaccinated 6 and 2 weeks prior to turnout. This results in the decreased clinical disease. The vaccine does not prevent infection completely, but reduces it enough to prevent clinical signs. Note; never mix vaccianted and unvaccinated animals.


References

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing.
Fox, M and Jacobs, D. (2007) Parasitology Study Guide Part 2: Helminths, Royal Veterinary College.
Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses, Elsevier Health Sciences.