In the university veterinary hospital in UCD, we have also investigated a number of these herd problems.

There are several viral, bacterial and parasitic causes of respiratory disease in cows, including Infectious Bovine Rhinotracheitis (IBR), Respiratory Syncitial Virus (RSV), Parainfluenza 3 (PI3), Mannhaemia haemolytica, Pasteurella multocida, Mycoplasma bovis and Dictyocaulus viviparous (lungworm). This article describes the clinical presentation, pathology and diagnosis of reinfection hoose which we have found to be the one of the most common problems in affected herds.

Clinical Presentation

Time of the year – in the last three years, cows in affected herds have begun to cough from the month of April onwards. There is variation from year to year, depending on spring weather and grass growth. In 2013, coughing and milk drop was noted in herds from June onwards, with a peak during mid-July.

Grass v housed – this is invariably a disease of grazing cows and frequently recurs annually in severely affected herds following three to four weeks of spring grazing or two weeks following introduction to contaminated paddocks in the late spring or summer. There has been no evidence of coughing during the housing period on any of the farms investigated to date.

Clinical symptoms – in many herds, it is the younger cows that are first affected, but within a matter of weeks the majority of the milking herd is affected. In the early stages of disease, cows often have a raised temperature but this returns to normal as the disease becomes chronic or long-standing. The predominant symptoms are persistent coughing, increased respiratory rate and a sharp decline in milk yield (25%) that remains below normal for weeks and often for the rest of the lactation. Some of the severely affected cows develop secondary bacterial pneumonia and must also be treated with antibiotics and anti-inflammatories.

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Predisposing factors – as with most diseases, it is always worth looking for potential predisposing factors when large outbreaks occur. The common causes of immunosuppression have been found as risk factors during our investigations include negative energy balance (Figure 1), liver fluke/rumen fluke and the presence of persistently infected animals with BVD in the herd.

A very important risk factor for reinfection hoose is the overuse of anthelminthics in calves and replacement heifers, particularly the Ivermectin classes of wormers, resulting in the underexposure of calves to lungworm larvae with the resultant failure to develop a strong immunity.

Another risk factor is the grazing of calves on the same paddocks as the cows, as they will seed the pasture and multiply the numbers of infective larvae. Additionally, the introduction of in-calf heifers reared off-farm or bought in from farms of unknown lungworm status predisposes to outbreaks in adult cows due to inadequate acquired immunity.

Reinfection Hoose (Acute Larval Migration Syndrome)

When cattle are exposed to lungworm as young calves and yearlings, they develop immunity against disease, as occurs with other gutworms. They develop two types of immunity to lungworm: (i) immunity against maturation of the larvae in the lungs (which persists) and (ii) immunity to reinfection.

However, the immunity to reinfection by the parasite wanes relatively quickly, especially if animals have not been exposed to a significant burden of lungworm in early life. This can result in the situation where the immunity to reinfection among adult cows in the milking herd is low.

If this occurs on a farm with a high burden of lungworm larvae on the pasture, then significant disease can occur.

In reinfection hoose, the arrival of a large number of lungworm larvae at the small airways, after travelling from the intestines via blood or lymph, initiates a significant immune response within the lung that prevents the larvae from maturing to adults and finishing their natural life cycle.

It is this immune response, and the mucus and debris formed in the lower airways of the lung as a result of dead worm material, damaged host tissue and secondary bacterial infections, that leads to the persistent clinical signs of coughing, increased respiratory rate and effort and reduced milk production.

Difficulties with

Diagnosis

In lungworm infection in calves, the larvae mature to adults in the lungs and complete the life cycle with the production of eggs and the excretion of first stage larvae in the faeces.

This classic parasitic bronchitis can be diagnosed by finding lungworm larvae in faecal samples from affected calves. However, in reinfection syndrome, the larvae are prevented from maturing to adults by the immune response in the lungs and, therefore, there will not be larvae in the faeces.

As with faecal samples, the use of bulk milk ELISA testing or individual cow blood testing for lungworm antibodies is of limited use in the diagnosis of reinfection hoose, as these tests only detect antibodies against adult lungworm.

To reach a diagnosis requires the use of more challenging techniques such as bronchoalveolar lavage (lung-wash) to obtain samples of fluid and/or mucus directly from the lungs for cellular evaluation. The presence of a significant number of eosinophils is highly suggestive of reinfection hoose.

Treatment and

Prevention

In the face of an outbreak of coughing and milk drop, it is imperative that a veterinary investigation is carried out. If reinfection hoose is suspected, treatment consists of the use of wormers that are licensed for use in lactating cows.

This restricts farmers and vets to the use of eprinomectin (zero milk withdrawal) and albendazole (72-hour milk withdrawal).

It is unfortunate that the more efficacious anthelminthic, Levamisole, is not licensed for use in lactating dairy cows as it has been shown to combat the immune response in the lungs as well as kill the lungworm larvae, resulting in a quicker clinical response and a quicker and more consistent return towards normal milk production.

While eprinomectin has been shown to kill the larvae and lessen the coughing, cows often take up to two months to recover in terms of milk yield and many continue to milk poorly for the rest of the lactation due to the ongoing after-effects of the immune response.

Prevention is certainly better than cure. This can be accomplished by: (i) optimal anthelminthic therapy of calves and yearlings – specifically avoidance of over-dosing so that good immunity develops early in life; (ii) the grazing of cows on safe pastures where possible, as lungworm can overwinter on contaminated pastures, and avoiding grazing calves on milking cow pastures; and (iii) strategic use of anthelminthics to prevent the build-up of a significant parasite burden on grazing pasture – the use of eprinomectin in late spring/early summer and again during mid-summer may be required on some farms.

* Eoin Ryan is a UCD lecturer in Integrated Farm Animal Health and is a European specialist in bovine health management