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BLOAT

Also known as choke or ruminal tympany, bloat refers to gas distension of the fore-stomachs (rumen and reticulum) of the cow. This condition is a very common encounter among herds in Kenya and occurs in two forms, either in the form of a persistent foam mixed with the ruminal contents called primary or frothy bloat, or in the form of free-gas separated from the ingesta called secondary or free-gas bloat.

Primary/frothy bloat

This form of bload is caused by the entrapment of the normal gases of fermentation in a stable foam. The coalescence of the small gas bubbles trapped in the igesta is inhibited and the pressure in the rumen increases because eructation does not occur. Certain plant substances such as Alfafa hay, legumes or vegetables (such as kale & turnips), and finely ground grain, have been shown to be primary foaming agents and initiate the process.

This kind of bloat is most common in animals grazing legume or legume-dominant pastures and it occurs when cattle are placed on lush pastures, particularly those dominated by rapidly growing leguminous plants in the vegetative and early bud stages, but can also be seen when high-quality hay is fed.

Free-gas/ Secondary bloat

This form of bload results from physical obstruction to eructation occuring from the esophageal region. Obstruction may be caused by a foreign body (eg, potatoe, avocado seed etc.), stenosis or pressure from an enlargement outside pressing on the oesophagus such as from tuberculous, lymphadenitis or bovine viral leukosis.

Other causes of free-gas bloat include: Obstruction of the cardia, interference with nerve functions/pathways involved in the eructation reflex such as vagus nerve, diaphragmatic hernia.

However, chronic ruminal tympany is relatively frequent in calves up to 6 months old without apparent cause; this form usually resolves on it’s own.

Signs of bloat

The following findings are seen on bloated cows:

Primary bloat

  1. Depressed milk yield
  2. Sudden distension of rumen
  3. Distension of left paralumbar fossa and abdomen
  4. Discomfort and animal may lie or stand frequently
  5. Belly kicking and rolling
  6. Frequent urination and defecation
  7. Protrusion of tongue and mouth breathing
  8. Vomiting may occur
  9. Dyspnea and grunting
  10. Respiration rate increases up to 60/min
  11. Rumen movements decrease and stops in severe cases
  12. If severity continues, animal collapses and dies

Secondary bloat

  1. Increased frequency and strength of rumination
  2. Tympanic resonance
  3. Distension of rumen and left paralumbar fossa.

Prevention

  • Avoid feeding or grazing high-risk plants such as legumes or clovers. If feeding is necessary, ensure a slow transition and always ill cattle with a high dry matter feed such as straw prior to grazing. Do not overfeed inely ground grain or other highly fermentable carbohydrates.
  • Continually administer an antifoaming agent during the risk period. This may be done by praying pastures with antifoaming agents – oils and fats or by adding antifoaming agent in feed or water.
  • Avoid feeding apples, potatoes, or feedstufs that can lodge in the esophagus and block eructation.
  • Prevent infections with bovine respiratory disease complex, bovine leukemia virus, and tuberculosis.

East Coast Fever (ECF)

East Coast fever (ECF) is a tick-transmitted protozoan disease of cattle characterized by high fever, dyspnea , lymphadenopathy and high mortalities. It affects cattle in East and Central Africa, particularly in Kenya, Uganda, Tanzania, Rwanda, Burundi and Malawi.

Etiology

The disease causing agent, Theileria parva is an apicomplex protozoan parasite. Classic East Coast Fever occurs in East Africa and is associated with T. parva transmitted from cattle to cattle by the brown ear tick, Rhipicephalus appendiculatus. ECF also occurs either as Corridor disease in eastern and southern Africa or as January disease in central Africa.

Occurrence

ECF affects mainly cattle but also buffalo, and occurs in countries in eastern, central, and southern Africa. Its occurrence is related to the distribution of the vector tick which has been recorded from large areas extending from southern Sudan in the north to western Zambia and eastern Zaire in the west, and to Mozambique and Zimbabwe in the south.

The disease is prevalent throughout the wetter areas favoring the development of the tick, but is absent from the wet highlands in the horn of Africa. It has been eradicated from southern Africa up to the Zambezi River. The endemic scenarios range from a stable situation with high prevalence of herd infection but low fatality rates (endemic stability), to a low prevalence/high fatality scenario (endemic instability).

Endemic stability develops in indigenous zebu cattle exposed to constant tick challenge as in wetter areas whereas endemic instability is seen with commercial production systems utilizing imported breeds or crossbreeds and in areas with a unimodal rainfall pattern that restricts tick activity. Epidemics occur when there is a breakdown in tick control especially during the rainy season or when susceptible animals are introduced into an endemic area.

Transmission

The vector of ECF is Rhipicephalus appendiculatus and in the field, the disease occurs only where this tick is found, save for Corridor disease which may be transmitted by R. zambeziensis. Other species of Rhipicephalus and Hyalomma spp. can transmit ECF experimentally, but they are not significant.

Economic Importance

ECF has a major impact on cattle production in eastern, central, and southern Africa. The disease is cause for death of large heads of cattle. Serious losses occur in exotic and indigenous cattle, mainly from reduced production of milk and meat due to morbidity and mortality, as well as from the heavy costs incurred in implementing effective tick control.

Clinical Signs

The first clinical signs of ECF in cattle appear 7 to 15 days following the attachment of infected ticks. These signs include:

  • Generalized lymphadenopathy involving superficial subcutaneous lymph nodes such as the parotid, prescapular and prefemoral lymph nodes.
  • One or 2 days later, there is fever, depression, anorexia, and a drop in milk in dairy animals. In later stages, there may be nasal and ocular discharges, dyspnea, generalized lymph node enlargeĀ­ ment, and splenomegaly. In severe cases, cliarrhea occurs, sometimes with dysentery; but usually only late in the course of the disease. Emaciation, weakness, and recumbency lead to death from asphyxia in 7-10 days.
  • Terminally, there is often a frothy nasal discharge. Occasional cases of brain involvement occur and are characterized by circling, hence ‘turning sickness’ or cerebral theileriosis.

Differential Diagnoses

  1. Corridor disease
  2. Mediterranean or tropical theileriosis
  3. Heartwater
  4. Trypanosomosis
  5. Babesiosis
  6. Anaplasmosis,
  7. Malignant catarrhal fever

Control

  • Vaccination-Animals are inoculated with a potentially lethal dose of infective sporozoite stabilate prepared from ticks and treated either simultaneously with a drug.
  • Vector control using acaricides-Organochlorides, organophosphorus , Synthetic pyrethroids and Amitraz, are applied in dips, spray races, or by hand spraying.

Always Contact your veterinarian whenever your identify abnormal behavior in your cows. Timely consultation and prompt treatment ultimately influences the prognosis.

Tick Paralysis

This is a condition that is characterized by lower motor neuron paralysis which come about as a result of bites by ticks of the species including Ixodes spp, Amblyomma spp. and Dermacentor spp. The biting ticks introduce salivary neurotoxins which lead to progressive motor paralysis, respiratory depression, and death in animals that have no immunity to the toxin.

The disease is usually found in Sheep, goats and cattle. However, other species such as dogs may be affected. The condition has also been reported in humans. All ages of animals potentially are at risk, and both sexes are equally affected.

The condition has multiple organs/system involvement affecting:

  • Musculoskeletal
  • Digestive
  • Cardiovascular
  • Respiratory
  • Nervous and
  • Hemolymphatic systems.

Clinical Signs

  1. In the initial stages of the disease, the animal is characterized with ataxia and weakness in hind limbs.
  2. As the disease progresses, the hind limns become paralyzed then ascending, flaccid tetraplegia which is symmetrical.
  3. Hypothermia of the affected limbs
  4. Inability to respond to stimuli in both superficial and deep tendons
  5. Dyspnea, dysphagia, inability to regurgitate cud normally, weak facial muscles.
  6. Nystagmus
  7. Death usually results from respiratory muscle paralysis.

Differential Diagnoses

  • Rabies
  • Botulism
  • Spinal cord compression
  • Trauma
  • Acute polyradiculoneuritis
  • Metabolic disorders
  • Myelopathy

Control And Prevention

  1. Timely removal of attached ticks. These can be manually removed or use suitable acaricides.
  2. External parasite sprays or dips can be used to control presence of ticks on animals. This has to done regularly for ultimate control.
  3. In addition, environmental control of ticks should be adopted to better control tick population in the animal environment.

Contact your veterinarian for supportive treatment and care. Do not give corticosteroids to animals with tick paralysis.