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I created this blog as an instrument of what I have encountered in the world of veterinary medicine as a proud vet student. Comments and suggestions are welcome here at;


Aina Meducci 2012


The following blog posts is not genuinely from my research but through readings and citation from trusted website. I do not own any of the copyright and therefore you may use it at your own risk


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Ectoparasite: Tick (Boophilus microplus) @ Rhipicephalus

My case study


See the lump?

see something here

and again


Id: Hay (has been given birth to a calf recently)
Species: Cattle
Age: About 2 and half years
Breed: Charlois
Sex: Female
Weight: About 600 kg
Nutrition: Feed on grass, free grazing
Previous treatment: Deworming

*No vaccination is given


General inspection

Overall inspection: Healthy
Temperament: Aggressive
Body condition: 5/9
Skin condition: Not smooth, lumps are found throughout the body. Ticks are found engorged on the skin

Ticks isolated from the cow's skin

*Other than that, other findings were consider normal

Physical examination

Temp: 39.1C (quite normal eh?)
Heart rate: 67 bpm
Respiratory rate: (umm..guess i missed this out lol)
Mucous membrane: Pink
TPR: <2second

Skin palpation reveals there were small lump on the skin and many ticks are found within the region. Other findings are normal

Samples taken:

Fecal sample (check on endoparasite)
Tick sample

Me preparing for fecal sample

When taking the fecal sample

A tick

Treatment given: 30 mL Ketasol (vitamin B) IM, Oxytetracyline 1mg/kg IM, Bayticol (cattle tickicide 20mL/cow) pour on method

Me giving Bayticol by pour on method
oh my! i look so fat :(


The next day, I did fecal egg count by using McMaster technique but the result is negative. Maybe it is due to deworming activity done by the farmer. I also checked on the tick and it is positively from the Boophilus species. Since we're not taking any blood sample, so we are not sure weather the cattle is infected with some blood parasite such as Babesiosis or anaplasmosis.

So I did some research to find out about Boophilus tick, of which something I have learnt in parasitology class from the previous semesters. Just for quick revision.

Boophilus females at various sizes

Rhipicephalus (Boophilus) microplus

R. microplus (formely known as Boophilus microplus) is a hard tick that can be found on many hosts including cattle, buffalo, horses, donkeys, goats, sheep, deer, pigs, dogs and some wild animals. Heavy tick burdens on animals can decrease production and damage hides. R. microplus can also transmit babesiosis (caused by the protozoal parasites Babesia bigemina and Babesia bovis) and anaplasmosis (caused by Anaplasma marginale). Under experimental conditions, this tick can transmit Babesia equi, the cause of equine piroplasmosis.

Species affected

R. microplus mainly infests cattle, deer and buffalo, but it can also be found on horses, goats, sheep, donkeys, dogs, pigs and some wild mammals.
Cattle are particularly vulnerable when they first encounter cattle ticks but develop a degree of resistance after repeated exposure. Bos indicus cattle (tropical breeds) and their crosses develop better resistance than do Bos taurus (British and European breeds). Horses, goats and sheep also suffer tick-worry but after a period of time they will develop strong resistance.

Life cycle

The cattle tick spends the parasitic stage of its life on the one host (one host tick). This stage takes approximately 21 days during which time the tick changes from a minute larvae to a nymph and finally an adult. Adult females feed slowly for about a week before rapidly filling with blood just prior to detachement. They then drop onto pasture, lay up to 3000 eggs and die. Eggs hatch to produce larvae which infest the pasture until picked up by a suitable host or they die. This non-parasitic stage can vary from approximately two months in summer to six to seven months over winter and is adversely affected by extremes in temperature and moisture levels. Males feed occasionally, but do not fill with blood. They wander over the beast for two months or more, mating with females.

Life cycle R.microplus

Pathology (general)

Ticks are primarily parasites of wild animals and only 10% of species feed on domestic animals, primarily sheep and cattle. The effect of ticks on host species can be divided into:

  • Cutaneous effects: Inflammation and infection
  • Systemic effects: Transmission of microorganism from another host, paralysis of the hist and bacteraemia resulting of the introduction of micro-organism

At the site of a tick focal dermal necrosis and haemorrhage occur, followed by an inflammatory response often involving eosinophils. Although a hypersensitivity reaction may be involved in the local response, the innate inflammatory response and dermal necrosis is sufficient to damage the hide. Tick bite wounds can become infected with staphylococcus bacteria causing local cutaneous abscesses or pyaemia. Heavy tick infestation can result in significant blood loss, reduced productivity, reduced weight gain and can cause restlessness. Tick bite lesions may also predispose animals to myiasis

Systemis effects: Vectors of disease.

Through their blood feeding habits, ticks are important as vectors of animal disease, transmitting a wide range of pathogenic viruses, rickettsia, bacteria and protozoa. In addition, many of the major diseases transmitted by ticks, such as tick-borne encephalitis, lyme disease, relapsing fever or Rocky Mountain spotted fever are pathogenic to humans. Wild and domestic animals are particularly important as reservoirs of the organisms causing these disease through animal/tick.human cycle of contact.

Ticks are effective vectors because;

  • They attach securely to their hosts, allowing them to be transferred to new habitats while on the host
  • The lengthy feeding period allows large numbers of pathogens to be ingested
  • While feeding the ticks often regurgitate, introducing pathogens to the host
  • Many species of tick are long lived
  • Females lay large numbers of eggs and therefore tick populations have rapid potential for increase
  • Of they fail to fond a host they can survive for lengthy periods without feeding
  • Ingested pathogens may be passed from larva to nymph and nymph to adult females to the next generation via ovaries
  • Non viraemic transmission may occur between co-feeding ticks

Identification of R.microplus

Rhipicephalus microplus is a member of the family Ixodidae (hard ticks). This tick was formerly known as Boophilus microplus; however, Boophilus has recently become a subgenus of the genus Rhipicephalus. Hard ticks have a dorsal shield (scutum) and their mouthparts (capitulum) protrude forward when they are seen from above. Boophilus ticks have a hexagonal basis capitulum. The spiracular plate is rounded or oval and the palps are very short, compressed, and ridged dorsally and laterally. Males have adanal shields and accessory shields. The anal groove is absent or indistinct in females, and faint in males. There are no festoons or ornamentation.

R. microplus adults have a short, straight capitulum. The legs are pale cream and there is a wide space between
first pair of legs and the snout. The body is oval to rectangular and the shield is oval and wider at the front. The
snout is short and straight. The nymphs of this species have an orange-brown scutum. The body is oval and wider at front. The body color is brown to blue-gray, with white at the front and sides. R. microplus larvae have a short, straight capitulum and a brown to cream body. Larvae have six legs instead of eight.

Boophilus microplus, male, body bottom


Boophilus microplus, female, body top


Two engorged adult female cattle ticks

Female (engorged ticks)

Tick control

In regions where this tick is endemic, control methods include acaricide treatment, pasture rotation, environmental modification, and integrated biologic and chemical control strategies. Acaricide resistance is common in the Boophilus subgenus of ticks. The use of resistant breeds is an important means of tick control in some countries. European (Bos taurus) breeds of cattle usually remain fairly susceptible to ixodid ticks, even after multiple exposure.

Ideally, the cattle should be removed from the infected pasture (although this is not always practical) and topical therapy is the used to reduce the tick population. The life cyle of the particular ticks involved will influence the application regime, with multiple-host ticks requiring prolonged insecticidal programmes, whereas control of one-host ticks may only require treatment for a few weeks of the year. Organophosphates and pyrethroids have been used to control tick populations. Resistannce of various topical insecticides is also an increasing problem.

The following compounds have been used in the control of ticks in cattle: Amitraz, chlorpyrifos, cypermectin, cyprothrin, deltamethrin, diazinon, dichlorvos, dioxathion, flumethrin, malathion, permethrin, phosmet, propetamhos and trichlorfon. These are available in various formulations including sprays, dip and slow-release ear tags. Systemic treatment with 200 ug/kg ivermectin every 2-4 weeks has also been shown to prevent tick engorgement and reproduction. Management measures include separation if cattle from infected pasture and cultivation of the infested land.

Sources: Cattle tick, Queensland Government, Rhipicipalus microplus, the center for food security and public health, Vet ectoparasite, biology, pathology, and control 2nd ed Blackwell science.

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Are we a human?

I was very much pissed off when somebody (i think) drooped 3 little poor kittens (about less than a month) nearby our hostel few weeks ago. All of them hasn't WEANED yet! poor creatures. As I were storming to get back in my room in one rainy Saturday night, I bumped into one of them, very skinny, whole body was wet, meowing for coldness. She stares at me with her beautiful bound eyes that ask for help. As a sense of responsible I took the kitty to my room, made a warm milk, and dried her off. She wasn't eaten for a few days and couldn't able to drink the milk at all.

I never gave up. I went to ask for a cat biscuit from someone and crushed it into tiny pieces and force feed the little kitten. After about 6-7 pieces of biscuit, I let her off outside. She suddenly poops with brownish, stringy diarrhoea. The next night, I found her on the toilet, looking very weak and couldnt able to get up. My friends took her and clean her up as she couldn't able to stand. After a while, she poops with the same watery brownish stringy diarrhoea. I was thinking that I will bring her to our faculty for at least give her fluid therapy to revive her strength. Next morning, I took her to our faculty and she poops again in my car. After I took her out to clean, this is what I found;

Three round worms in very small kitty

I took the worms and put it inside the formalin bottle. After a while, she was struggling to breath using her mouth and she is no longer sitting in sternal recumbency. It was an emergency and I took her immediately to vet. The vet says the kitty couldn't able to survive because she was too little and too weak and have to be euthanized. Her face turned blue and she close her eyes slowly. I have to let it happen, as I think that will be the best way for her.

The last time I saw her breathing is the last time her bound eyes look at me before rigor mortis starts to kick in..

RIP little kitty.

If only if we as human use only a piece sense of our responsibility, the poor kitty would be able to live, playing happily with her littermates. Please think before you ditch them.

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Horner's syndrome

I dropped into these words at last semester during my ophthalmology class. But it is then repeated in our neurological class. Seems to have interrelation on it right?


Horner's syndrome in a cat

Horner's Syndrome is a common neurological disorder of the eye and facial muscles, caused by dysfunction of the sympathetic nervous system. The condition usually occurs suddenly and without warning. The most common clinical signs of Horner's Syndrome are
  • Drooping of the eyelid on the affected side (ptosis)
  • The pupil of the affected eye will be constricted (miosis), or smaller than usual
  • The affected eye often appears sunken (enophthalmos)
  • The third eyelid of the affected eye may appear red and raised or protruded (conjunctival hyperemia)


Horner's syndrome is not a disease but a CONDITION!

What causes Horner's syndrome?

If the sympathetic nervous system that supplies the eyes is damaged or is malfunctioning, the parasympathetic system 'takes over', and the symptoms of Horner's Syndrome appear. The damage or malfunction can occur in the neck area, the ear area or the eye area. Damage may occur because of blunt force trauma such as that caused by an automobile accident or because of a bite wound from another animal.

Other problems that can cause damage or inflammation of the nerves in this area include diseases within the eye or in the retrobulbar (behind the eye) area, problems in the middle ear (otitis media), or tumors in the chest, neck or brain.In dogs, Horner's Syndrome is 'idiopathic', which means it has an unknown cause, in about half the cases. In cats, however, a cause is virtually always found, and idiopathic Horner's Syndrome is very rare. With many cats that develop Horner's Syndrome there is a recent history of trauma, particularly being hit by a car.

Nasopharyngeal polys removal in cats can also cause the development of Horner Syndrome due to nerve damage. It is usually temporary and does not effect cat's behavior.

Depending on the cat's recent history and other physical findings on examination, veterinarian may recommend a series of diagnostic tests to determine if there is an underlying cause. Initial tests will usually include a neurologic evaluation, an otoscopic examination (examination of the ears) and x-rays of the chest and neck area.

How can sympathetic damage occurs?

Chart showing Horner's Syndrome

The nerve carrying the tiny nerve fibers that provide sympathetic control to the eye have a long path. The damage may have occurred anywhere along this path.The nerves originate in the brain stem and travel down the spinal cord in the neck area exiting just inside the chest (at the level of the second thoracic vertebra). The nerves then form the cervical sympathetic trunk, a bundle of nerves that travels back up the neck, this time outside the spinal cord, to the middle ear (this area is shown in red).These nerves then connect to new nerves just below the ear. The new nerves continue their journey to the eye. The damage can occur in the neck area, the ear area or the eye area. Damage can occur in the form of trauma, tumor involvement, infarction (abnormal blood clot), middle ear infection, or diseases of the eye itself.


Localizing which area of the sympathetic nervous system is affected goes a long way in determining the nature of the damage as different areas of the system are prone to different types of injury. Certain eye drops can be used to stimulate different areas of the nervous system and determine if the lesion is in the first nerve segment or in the second nerve segment. Most injuries turn out to be in the second nerve segment.

With second nerve segment involvement: If ear infection is not obvious and disease of the eye beyond the Horner's syndrome itself is not obvious, then it is probably prudent to allow the syndrome to resolve on its own. This usually occurs within 6 to 8 weeks. Further diagnostics may be undertaken if new developments occur or if the syndrome persists beyond this time.

With first nerve segment involvement: Involvement of the first nerve segment indicates a problem in the chest or spinal cord and is more significant. Chest radiographs should be taken to rule out cancer spread to the chest (the only sign of this may be the Horner's syndrome). The front leg should be carefully checked for evidence of function loss as a tumor or protruding intervertebral disc could be exerting pressure on the spinal cord. Trauma to the neck as with a strong jerk from a collar or straining against a leash can also produce Horner's syndrome from this section of the nerve.

Generally more diagnostic work is needed for cases involving the first nerve segment as there is potential for more serious underlying causes. If the syndrome stemmed from pulling on the leash, it should resolve uneventfully, depending on how badly damaged the nerve is.


Most cases of Horner’s Syndrome will resolve spontaneously. It is important to treat any underlying disease. There are several diagnostic tests that will be performed to determine if there is an underlying cause in your pet. Symptomatic treatment usually involves phenylephrine drops placed in each eye every 12-24 hours to dilate the pupil. Other eye medications might be useful to avoid development of corneal ulcers from the exposed keratitis.


Prognosis and recovery rate

The prognosis depends on the underlying cause. Patients with chest trauma tend to have a quicker recovery rate (days to weeks) than patients with other lesions. If the underlying problem is Feline Dysautonomia, the prognosis is poor.

Sources: The pet health library; Wendy C brooks, Horner's syndrome in cat VCA Animal hospitals, Nasopharyngeal polyps in cats; ACVS Veterinary surgeon Karen Tobias

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An endocrine disease


Cushing's disease (hyperadrenocorticism) in dogs is a condition that results from the chronic overproduction of too much glucocorticoid in the body. In the normal dog, the pituitary gland produces a hormone called ACTH, which stimulates the adrenal gland to produce the glucocorticoid hormones necessary for the function of many systems in the body. If something goes wrong in the pituitary gland or adrenal gland and too much glucocorticoid is produced, then Cushing's disease develops.

Cushing's disease brought about by an adrenal tumor is commonly seen in the Toy Poodle, German Shepherd Dog, Dachshund, Labrador Retriever, and some Terrier breeds. The pituitary dependent form is commonly seen in the Poodle, Dachshund, Beagle, German Shepherd Dog, Boston Terrier, and Boxer.

A sex predilection for females is seen in some dogs with hyperadrenocorticism secondary to adrenal tumors. The most common clinical signs are polydipsia (PD), polyuria (PU), polyphagia, heat intolerance, lethargy, abdominal enlargement or “potbelly,” panting, obesity, muscle weakness, and recurrent urinary tract infections. Dermatologic manifestations are numerous and often include truncal alopecia, thin skin, phlebectasias, comedones, bruising, cutaneous hyperpigmentation, calcinosis cutis, pyoderma, dermal atrophy, secondary demodicosis, and seborrhea. Cutaneous mineralization (calcinosis cutis) is a characteristic although infrequent finding in dogs. Although mineral deposition may occur anywhere in the skin, the dorsal midline, ventral abdomen, and inguinal region are affected most frequently. 

For dogs ultimately diagnosed with Cushing's disease, hair loss was one of the most common reasons the owners first brought their dog in for evaluation.

Numerous mineral crystals are deposited along collagen and elastin fibers in the dermis and outer subcutis and may protrude through the atrophic and thinned epidermis. In less severe cases, the epidermis remains intact and appears irregularly elevated by the firm, opaque, white deposits of mineral. A narrow rim of hyperemia and foreign-body granulomatous inflammation often surrounds the areas of mineralization. The mineral deposits occur despite normal blood calcium and phosphorus levels probably because of the gluconeogenic and protein catabolic actions of cortisol. Mineralization may also occur in other tissues of the body, most frequently the airways and blood vessels.

Mineralization of skin

Increased Water Consumption and Urination: The most common symptom is increased consumption of water and the resultant increased urination (polyuria/polydipsia). The dogs drink between two and ten times the normal amount of water and the resultant increase in urination follows. This symptom is present in over 85% of all animals with Cushing's disease. Previously housebroken animals may begin to have accidents because their bladders fill quickly with the overproduction of urine.

Increase in Appetite: Increase in appetite (polyphagia) is another common clinical symptom that shows up in around 80% of the affected animals. Dogs may begin stealing food, getting into the garbage, begging continuously, and become very protective of their food. Despite having other symptoms, the owner may feel that the dog is okay because of his good appetite.

Abdominal Enlargement: Abdominal enlargement is a common symptom in up to 80% of the affected dogs. The potbellied appearance is a result of the shifting of fat to the abdominal area and a weakening and wasting of muscle mass in the abdomen.

Types of hyperadrenocorticism

1. Pituitary Dependant Hyperadrenocorticism

The most common cause of Cushing's disease is a microscopic, benign pituitary tumor (microadenoma) which oversecretes ACTH and ignores the adrenals' response. 50% of pituitary tumors are less than 3mm in diameter. The dog's pituitary keeps cranking out ACTH, causing the adrenals to keep cranking out cortisol, yet the pituitary does not respond to the elevated blood cortisol levels by stopping its release of ACTH. 85% of Cushing's cases are pituitary dependent. Dogs with pituitary dependent hyperadrenocorticism tend to have two very large adrenal glands, as both are constantly working to keep up production of excess cortisol.

Larger pituitary tumors (macroadenomas, over 1 centimeter in diameter) can place pressure on brain tissue and nerves, causing blindness, circling, seizures, or other neurological problems not directly related to hyperadrenocorticism. Some of these symptoms (e.g., incoordination) can resemble side-effects of medications used to treat Cushing's disease, further complicating diagnosis and treatment.

2. Adrenal-based Hyperadrenocorticism

Alternatively, there may be an adrenal tumor responsible for secreting too much cortisol. 50% of these are benign (adenomas), and 50% are malignant (adenocarcinomas) and are inclined to spread to the lungs and liver. Again, the interplay between pituitary and adrenal messages is lost, and the tumor keeps secreting too much cortisol irrespective of what the brain is telling it. 15% of Cushing's cases are adrenal-based. In these dogs, one adrenal gland tends to be extremely enlarged (due to the tumor and the overproduction of cortisol that goes with it), and the other tends to be extremely small (to try to compensate for the overactive larger one

Normal physiology of adrenal glands

3. Iatrogenic Hyperadrenocorticism

The third cause of Cushing's is one that we can create ourselves if we give a dog too much external glucocorticoid, especially for chronic conditions like allergies. We essentially do what the adrenal tumor would do by flooding the dog's body with an excess of corticosteroid. Although both the adrenals and pituitary will attempt to respond to our interference by cutting ACTH and cortisol secretion, if we continue to bombard the dog's body with too much glucocorticoid, symptoms of Cushing's disease will result. The reason dogs are given tapering doses or every-other-day doses of steroids like prednisone is to avoid this consequence. Dogs with this form of Cushing's tend to have two very small, atrophied adrenal glands. Nonetheless, if iatrogenic (veterinary-induced) hyperadrenocorticism develops, it is fully reversible. The external source of steroid is slowly withdrawn to allow the adrenals to "wake up" and resume functioning.


1. Urine Cortisol:Creatinine Ratio

In this test, the owner generally collects a urine sample at home (where the animal is not stressed). The sample is sent by the veterinarian to a special laboratory for testing. Most dogs with Cushing's disease have an abnormal result. However, there are other diseases that can also cause abnormal results. So if this test is abnormal, further diagnostic testing should be performed. 

2. Low dose dexamethasone test (LDDT)

The low-dose dexamethasone suppression (LDDS) test is the screening test of choice for hyperadrenocorticism in dogs. It is sensitive; only 5% of dogs with hyperadrenocorticism exhibit suppressed cortisol concentrations at 8 hr. In addition, 30% of dogs with PDH exhibit suppression at 3 or 4 hr followed by “escape” of suppression at 8 hr—this pattern is diagnostic for PDH. The major disadvantage of the LDDS test is the lack of specificity in dogs with nonadrenal illness (diabetes mellitus, chronic renal disease, liver disease); these dogs should be treated for the nonadrenal illness and stabilized before the LDDS test is performed.


•Obtain a baseline (0 hour) blood sample,
•Administer dexamethasone sodium phosphate (0.015 mg/kg) or aqueous dexamethasone (0.01 mg/kg) IV
•Obtain two additional blood samples four and eight hours later
•Serum cortisol concentrations are measured
•Dexamethasone -- exogenous steroid à provides negative feedback to the pituitary àsuppress the secretion of ACTH.
•Marked decrease in blood cortisol levels -- normal
•No decrease -- Cushing's disease (>90%)

2. ACTH test

This is another test that is commonly used in the diagnosis of Cushing's disease today. It will not distinguish between the two types of hyperadrenocorticism, but it may aid in the diagnosis in difficult cases. It is also used to evaluate the effectiveness of therapy. 

3. High dose dexamethasone test (HDDT)

Once a dog has been diagnosed as Cushing disease, this test can be used to differentiate between forms of Cushing's. Similar to the low dose dex test, a fasted dog has a baseline blood sample taken in the morning. The dog is then given a large dose of dexamethasone. Blood samples are taken 4 hours and 8 hours later. A dog with an adrenal tumor will not suppress at all. His adrenal tumor simply doesn't "care" about the level of blood cortisol; it keeps pumping out cortisol. A dog with a pituitary tumor still has some limited ability to respond to feedback and thus should respond to a high dose of dexamethasone with a suppressed cortisol level. Approximately 15%-20% of dogs with pituitary tumors will not suppress on a high dose dexa test; these dogs generally have large macroadenomas.


Treatment depends on the type of Cushing's disease, as well as on the overall health of the canine patient. As many dogs with Cushing's are elderly and may have concurrent health problems, treatment can be complicated. This is a serious illness for which there is no known cure. Dogs require life long treatment. Monitoring is required through periodic blood tests.

Cushing's is very rare in cats and is usually the result of insulin resistance in a cat with Diabetes Mellitus. Diagnosis is similar to the dog and treatment is usually surgical removal of the adrenal glands. Medical therapy is usually not effective in cats.

Mitotane (Lysodrane)
  • Selectively destroys glucocorticoids secreating cells in adrenal cortex 
  • Initial dose: 40-50mg/kg bid until both basal and post ACTH cortisol level are in ideal range. 
  • Maintain therapy with 50mg/kg/week 
  • Monitor the cortisol level by using ACTH test  If cortisol level is <1µg/dL, stop mitotane and administer prednisolone (0.1mg/kg)
Ketoconazole (oral antifungal)
  • Inhibits enzymes responsible for cortisol synthesis 
  • Administer 10-20 mg/kg q12h 
  • Monitor the cortisol level by using ACTH test 
  • Side effect: Vomitting, diarrhea, lethargy 

Trilostane is a newer treatment that is used to treat some dogs with Cushing's disease. It is more expensive, but may be an alternative treatment for dogs with adrenal tumors. As with Lysodren, the dog is reexamined repeatedly during the initial phase of treatment, and ACTH stimulation tests are performed. In many cases, after several months of therapy the dose needs to be increased.

**Cushing’ disease may predispose the animal with diabetes mellitus due to high glucose in the blood. If this occurs, treatment for diabetes should be initiated.


If Cushing's disease is caused by an adrenal tumor, the logical approach is to surgically remove the tumor and the affected adrenal gland. These tumors tend not to recur on the remaining adrenal gland. In theory, this can cure adrenal-based Cushing's disease, and prognosis is very good for dogs with benign adrenal tumors. Dogs may be treated with ketoconazole prior to surgery to try to minimize the symptoms of Cushing's disease, as one significant symptom of Cushing's is delayed wound healing. There are high risks associated with adrenalectomies, and given that patients are often elderly dogs, this may deter an owner from pursuing this treatment route. 50% of adrenal tumors are malignant and may have already metastasized to liver or lungs by the time they are discovered. Most owners opt for non-surgical treatment.


Guarded: The average life span with medical treatment is about 2 years, although longer survival is possible. Glucocorticoids reduce inflammation and suppress the immune system and predispose to other ailments such as Diabetes Mellitus, urinary tract infection, kidney disease, hypertension and pancreatitis.

Sources: Mercks Veterinary Manual 10th ed, http://www.kateconnick.com/library/cushingsdisease.html, Pet care suite 101: Cushing's disease in a dog

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Lymphatic system

It's been a while. I know. Cant get away with unnecessary things.


Before we start revising on LS, let us recall some of important related terms on this subject

Lymphadenopathy: Disease of lymph glands
Lymphangitis: Inflammation of lymph vessels
Splenomegaly: Splenic enlargement
Lymphocyte: Lymphatic cells
Tonsillectomy: Surgical removal of lymph node
Lymphoid: Lymph

Lymphatic anatomy and physiology

LS is composed of the tonsils, spleen, thymus, numerous glands, vessels, and cells that provide the body with immunity and destroy pathogens. LS also important for the constant transport of fluid (lymph) from the interstitial spaces to the general circulating blood


Tonsils are made up of lymphoid tissue but are not referred as lymph node. 2 tonsils are located in the throat (each side) near the base of the tongue. They are hidden within tonsillar crypts in the throat. Therefore during physical examination of a normal patient, tonsils may not be visible (unless a disease process is present to create tonsillitis).

Normal healthy tonsil
(couldnt found animal picture though)


Spleen is large, tongue-shaped organ located in the left craniodorsal abdominal cavity closely associated with the stomach and protected by the caudal rib cage. On the routine physical examination, the speen is not palpable unless splenomegaly exists. Spleen is very important for filtration of the blood It also serves as a very important storage area for red blood cells. During times of hemorrhage or increased need for greater oxygen transport in the body, the spleen will eject some of its stired blood back into circulation.


Thymus is a glandular lymphoid organ located in the mediastinum of the cranioventral thoracic cavity. Thymus is extremely important for maturation of specialized lymphocytes for the production of immunoglobulins (antibodies).The thymus is quite large in young, developing animals. As the animal age, the size and function of the thymus diminish. Consequently, the immune capabilities of a very young and of geriatric animals is compromised. The very young have not yet produced sufficient amounts of immunoglobulins, and geriatric animals no longer have the capacity to maintain sufficient antibody levels. This leaves these patients very susceptible to disease.

The location of the thymus gland differs in different animals. In mammals is located around the trachea at the level of the heart. Lying beneath the sternum (breastbone) and above the treachea (windpipe) and heart which is a small the two-lobed gland; each lobe is made up of LYMPHATIC tissue just behind the breastbone, and the soft, gelatinous tissue of the marrow deep within our long bones. In these primary lymphoid organs, lymphocytes grow and develop"In addition to the heart, the space between the lungs (mediastinum) contains the trachea, esophagus, thymus, large blood vessels, lymphatic vessels, and nerves. In newborn animal, the gland is small and grows with the animal until the onset of puberty then become small again.

Position of thymus

Lymph nodes and vessels

Lymph glands (lymph nodes) are located throughout the body. The peripheral lymph nodes that are clinically important for physical examinations in small animals are axillary lymph nodes, the precapular lymph nodes, the mandibular lymph nodes, the cervical lymph nodes, the popliteal lymph nodes and superficial inguinal lymph nodes. The mandibular, prescapular and popliteal lymph nodes should alwyas be palpated during PE of small animal patient. Retropharyngeal lymph nodes cannot be palpated. Lymph nodes are small, glandular structures that are partly responsible for the production of lymphocytes. Connected by network of lymphatic vessels, the lymph nodes are responsible for filtration of lymphatic fluid. Lymphatic fluid does not flow in response to pressure within lymphatic system. Lymphatic fluid is passively absorbed from the interstitium into the lymphatic vessels. One way valves keep the fluid flowing in one direction. Most pf the lymphatic fluid of the body wil enter the bloodstream via the thoracic duct. Generally, lymphatic fluid is transparent, colorless, watery substance.

Position of lymph nodes in a dog

Significant functions of LS

Excessive accumulation of interstitial fluid is clinically referred to as edema. If the lymphatic system is diseased in some way, it may not be able to accommodate the routine production and flow of the interstitial fluid. Absorption of fluid into the lymphatic vessels may be impaired because of obstruction. Many other mechanisms may contribute to edema formation. Some of those mechanisms include lymohatic disease, changes in osmotic pressure (hypoprotaenemia) changes in hydrostatic pressure and inflammation due to tissue trauma.

The edematous fluid serves to dilute cytotoxic agents as well as provide some protective cushioning of the area upon inflammation due to leaking of fluid from the vessles excessively into the interstitium.

Immunogenic responses

Source: Veterinary Medical terminology 2nd ed D.E Christenson saunders elsevier

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