*  Dermoid Sinus
     *  Demodectoc Mange
(Localized and Generalized)
  RIDGEBACK HEALTH

                                                            Demodectic Mange

                                                                                                    Race Foster, DVM 
                                                                                                 Drs. Foster & Smith, Inc.

Microscopic view of a demodectic mite Demodectic mange (also known as red mange, follicular mange, or puppy mange) is a skin disease, generally of young dogs, caused by the mite, Demodex canis. It may surprise you to know that demodectic mites of various species live on the bodies of virtually every adult dog and most human beings, without causing any harm or irritation. These small (0.25 mm) 'alligator-like' mites live inside of the hair follicles (i.e., the pore within the skin through which the hair shaft comes through), hence the name follicular mange. In humans, the mites usually are found in the skin, eyelids, and the creases of the nose.

Disease related to suppressed immune system

Whether or not Demodex causes harm to a dog depends on the animal's ability to keep the mite under control. Demodectic mange is not a disease of poorly kept or dirty kennels. It is generally a disease of young dogs that have inadequate or poorly developed immune systems or older dogs that are suffering from a depressed immune system.

What is the life cycle of Demodex canis?

The demodectic mite spends its entire life on the dog. Eggs are laid by a pregnant female, hatch, and then mature from larvae to nymphs to adults. The life cycle is believed to take 20-35 days.

How is Demodex canis transmitted?

The mites are transferred directly from the mother to the puppies within the first week of life. Transmission of the mites is by direct contact only. That is, the mother and puppy must be physically touching, as the parasite cannot survive off of the animal. This is important because it means the kennel or bedding area does not become contaminated, and therefore the environment need not be treated. Lesions, if present, usually appear first around the puppy's head, as this is the area most in contact with the mother. Virtually every mother carries and transfers mites to her puppies. Most puppies are immune to the mite's effects and display no clinical signs or lesions. A few are not immune and it is these that develop into full-blown cases of mange.

What are the signs of demodectic mange?

Individuals that are sensitive to the mange mites may develop a few (less than 5) isolated lesions (localized mange) or they may have generalized mange, in which case, there are more than 5 lesions involving the entire body or region of the body. Most lesions in either form develop after four months of age.

Early demodectic mange in a spaniel puppy The lesions and signs of demodectic mange usually involve hair loss, crusty, red skin and at times, a greasy or moist appearance. The mites prefer to live in the hair follicles, so in most cases, hair loss is the first noted sign. Usually, hair loss begins around the muzzle, eyes, and other areas on the head. In localized mange, a few circular crusty areas will be noted, most frequently around the muzzle. Most of these lesions will self heal as the puppies become older and develop their own immunity. Persistent lesions will need treatment that will be described later. In cases in which the whole body is involved (generalized mange), there will be areas of hair loss over the entire coat, including the head, neck, abdomen, legs, and feet. The skin along the head, side, and back will be crusty and oftentimes inflamed. It will often crack and ooze a clear fluid. Hair will be scant, but the skin itself will often be oily to the touch. Some animals can become quite ill and develop a fever, lose their appetite, and become lethargic. Patients with generalized demodectic mange need immediate vigorous treatment.

How is demodectic mange diagnosed?

performing a skin scraping on a dog Once Demodectic mange is suspected, it can usually be confirmed by a skin scraping or biopsy, in which case, the mites can be seen with the aid of a microscope. They are too small to be seen with the naked eye. The adults appear as tiny, alligator-like mites. Remember that these mites are present in every dog, so by themselves, they do not constitute a diagnosis of mange. The mite must be coupled with the lesions for a diagnosis of mange to be made.

How is demodectic mange treated?

The treatment of Demodectic mange is usually accomplished with lotions, dips, and shampoos. Fortunately, 90% of demodectic mange cases are localized, in which only a few small areas are involved and can often be treated topically. A treatment that has been successful for years has been a 1% rotenone ointment (Goodwinol ointment), or more recently, a 5% benzoyl peroxide gel applied daily. Bathing periodically with a benzoyl peroxide shampoo and feeding a high quality diet and a multivitamin with a fatty acid may also help some dogs. Most of these localized lesions will heal on their own and do not require overly aggressive treatment.

If a dog develops generalized demodicosis more aggressive treatment is usually required. Studies show that between 30% and 50% of dogs that develop the generalized form will recover on their own without treatment, but treatment is still always recommended for the generalized form. The treatment of choice continues to be Amitraz dips applied every two weeks. Amitraz is an organophosphate, and is generally available under the product name Mitaban. It is a prescription product and should be applied with care. Humans should always wear rubber gloves when applying it to their dog, and it should be applied in an area with adequate ventilation. It is recommended that longhaired dogs be clipped short, so that the dip can make good contact with the skin. Prior to dipping, the dog should be bathed with a benzoyl peroxide shampoo to help remove oil and cellular debris.

puppy with generalized demodicosis Most dogs with generalized demodicosis require between 4 and 14 dips. After the first three or four dips, a skin scraping should be performed to determine if the mites have been eliminated. Dips should continue until there have been no mites found on the skin scrapings taken after 2 successive treatments. Some dogs develop sedation or nausea when dipped, and toy breeds in particular are sensitive to amitraz. Half strength dips should be used on these sensitive animals.
Ivermectin should not be used in Collies and similar breeds.

Some dogs may not respond to this treatment, and the frequency of the dips may have to be increased or additional treatments may need to be instituted. Two other products, which though they are not licensed for the treatment of demodectic mange, are being widely used by veterinary dermatologists and general practitioners with some good results. One of these is ivermectin, which is the active ingredient in Heartgard, however, the concentration in Heartgard is not high enough to be effective against Demodex. Larger daily doses of liquid ivermectin must be given and should only be used under close veterinary supervision. Another drug, Milbemycin oxime (Interceptor), has also been given daily and been shown to be effective on up to 50% of the dogs that did not respond to Mitaban dips.

Dogs that have generalized demodicosis often have underlying skin infections, so antibiotics are often given for the first several weeks of treatment. In addition, we usually recommend the dog be put on a good multivitamin/ fatty acid supplement. Because Demodex flourishes on dogs with a suppressed immune system, it is wise to check for underlying causes of immune system disease, particularly if the animal is older when they develop the condition.

Prognosis and impact on breeding

Demodectic mange IS NOT an inherited condition, but the suppressed immune system that allows the puppy to be susceptible to the mites can be. Remember that all puppies receive the mites from their mother, but only a few have ineffective immune systems and develop the mange. This sensitivity can be passed genetically through generations. Individuals that have a history of demodectic mange, and their parents and siblings, should not be bred. Through careful breeding, most cases of generalized demodicosis could be eliminated.

Can I get Demodex from my dog?

The various species of Demodex mites tend to infest only one species of host animal, i.e., Demodex canis infests dogs, Demodex bovis infests cattle, and Demodex folliculorum infests humans.

Conclusion

In conclusion, a few important points should be repeated. The mites are transferred from the mother to offspring in the first few days of life. The first sign of hair loss usually does not occur until after four months of age. Demodectic mange is almost always curable or controllable with persistent treatment, except in rare cases with very immune suppressed individuals. The immune system condition that allows for the development of Demodectic mange can be an inherited condition, and breeding of these animals should not occur.
                                                                            WHAT IS COCCIDIA?
 

Coccidia are small protozoans(one-celled organisms) that multiply in the intestinal tracts of dogs, most commonly in puppies less than six months of age, in adult animals whose immune system is suppressed or in animals who are stressed in other ways (change in ownership, other disease present, stress, etc.).  In dogs, most coccidia are of the genus called ISOSPORA. Isospora canis and I. Ohioans are the species most often encountered in dogs. As a puppy ages it tends to develop a natural immunity to the effects of coccidia. As an adult it may carry coccidia in its intestines, shed the cyst in the feces, but experience no ill effects.

HOW ARE THE COCCIDIA TRANSMITTED?
Coccidia is carried from yard to yard by infected birds, droppings, feathers and flies. If one puppy has coccidia, usually all the puppies will, by fecal matter on the rectum and from stepping in another puppies fecal matter. A Puppy is not born with coccidia organisms in its intestines. However, once born, the puppy is frequently exposed to its mothers feces and if the mother is shedding the infective cysts in her feces, then the young puppies will likely ingest them and coccidia will develop within their intestines. Since young puppies usually those less than six months of age have no immunity to coccidia, the organisms reproduce in great numbers and parasitize the young puppies intestines. Oftentimes this has severe effects.

WHAT ARE THE SYMPTOMS OF COCCIDIA?
The primary sign of coccidia is diarrhea. The diarrhea usually has a foul smelling odor. The diarrhea may be mild to severe depending on the level of infection. Blood and mucous may also be present, especially in advanced cases. Severely affected animals may also vomit, lose their appetite, become dehydrated, and in some cases, if not treated, die from coccidia. Most infected puppies usually are in the four to twelve age group. The possibility of coccidia should always be considered when a loose stool or diarrhea is encountered in this age group. A microscopic fecal exam by a veterinarian will detect the cysts confirming a diagnosis.

WHAT ARE THE RISKS?
Although most cases of coccidia are very mild, it is not uncommon to see severe, bloody diarrhea resulting in dehydration and even death. Coccidia is most common to animals who are ill or infected with other parasites, bacteria or viruses. Coccidia is very contagious from the age group of four to twelve week age group in puppies. It should also be mentioned that STRESSplays a big role in the development of coccidia.  It is not uncommon for a seemingly healthy puppy to arrive at its new home and develop diarrhea several days later leading to a diagnosis of coccidia. Coccidia can surface during the stressful period of the puppy adjusting to a new home. Fortunately coccidia is treatable. Drugs such as sulfadimethoxine (Albon), trimethoprimsuladiazine (Tribrissen)and amprolium (Corid) have all been effective in the treatment and prevention of coddidia. and amprolium (Corid) have all been effective in the treatment and prevention of coddidia. Because these drugs DO NOT kill the organisms, but rather inhibit their reproduction capabilities, elimination of coccidia from the intestine is not rapid. By stopping the ability of the protozoa to reproduce, time allowed for the puppys own immunity to develop and remove the organisms. Drug treatments of five or more days are usually required. Puppies are no longer contagious after treatment for two days.
 

HOW IS COCCIDIA PREVENTED OR CONTROLLED?
Coccidia use to be thought of as a parasite that only came from unclean kennels. Now we know that it can be carried in by people, dogs and fleas as well. Adults dont always have symptoms and can be carriers of Coccidia. Because coccidia is spread by the feces of carrier animals, it is very important to practice strict sanitation. Clean puppy cages often and bath all pups and adults daily until gone. All fecal material should be removed. Housing needs to be such that the food and water cannot become contaminated with feces. Clean water should be provided at all times. Most disinfectants do not work well against coccidia. Incineration of the feces, steam cleaning, immersion in boiling water or a 10% ammonia solution are the best methods to kill coccidia. Coccidia can withstand freezing. Cockroaches and flies can mechanically carry coccidia from one place to another. Mice and other animals can ingest the coccidia and when killed and eaten by a cat, dog, for instance, can infect the cat or dog. Therefore, insect and rodent control are very important in preventing coccidia.  The coccidia species of dogs and cats do not infect humans.
*  Coccidia
              DERMOID SINUS
IN THE RHODESIAN RIDGEBACK
                       (A Review by a Veterinarian)
Taken from South African Rhodesian Ridgeback Club, Ridgeback Review
THE FORMATION AND SIGNIFICANCE OF DERMOID SINUSThe Rhodesian Ridgeback is a modern breed of dog that originated in the late nineteenth century, by the crossing of indigenous Hottentot dogs with various European breeds introduced into the Cape by the early settlers.The breed standard was established with the formation of the Rhodesian Ridgeback Club of Bulawayo in 1922.  The main characteristics of the breed is, as its name implies-a ridged back, which is formed in the haircoat along the top midline of the dog's back.  The ridge is formed by hair, which grows in the opposite direction to the hair of the surrounding coat.Breeders of Ridgebacks are aware of a well-known defect which occurs in the breed, the Ridgeback "Cyst" or as it is more correctly named in the scientific terminology, the Dermoid Sinus.  (Dermoid-arising from the skin, Sinus-a cavity or channel).Dermoid Sinuses are narrow tube-like structures, which are derived from a skin defect.  They penetrate from the skin surface to varying depths downward into the muscles and towards the spinal cord.  They are situated in the midline of the neck and croup, which is in front and behind the area occupied by the ridge (Fig 1).
                              Fig 1: Areas marked "X" indicate the sites at









                                which dermoid sinuses may develop

This is the only known congenital defect that occurs in the breed.  (Congenital means that the defect is formed before birth).  When considered as a defect in the dog family as a whole, Dermoid Sinuses occur only very rarely in dogs, other than Ridgebacks or Crossbred Ridgebacks.  It must therefore be obvious that it is an inherited defect which has become widespread in the "blood lines" of the breed as a result of the early selective breeding of the original stock from which the Ridgebacks of today have been produced.
The incidence of the defect throughout the breed is not known, as the recording of the numbers of Dermoid Sinus affected pups in litters has not been done on a scale large enough to enable a statistical analysis to be carried out.  In fact, the occurrence of Dermoid Sinus affected pups on the litters of breeders has been kept confidential, as most breeders feel that there is considerable stigma attached to dogs and bitches amongst whose offspring Dermoid Sinus affected puppies occur.At this point I would like to state that with the present situation of breeding with selected outstanding dogs and bitches, no breeder without a program of progeny testing can be sure that his "blood lines" is free from the hereditary Dermoid Sinus.  (The hereditary aspects of the condition will be dealt with in part two of this article).  Thus, every purchased Ridgeback may be considered a potential carrier of the condition.THE FORMATION OF DERMOID SINUSTo understand the way, in which a Dermoid Sinus is formed, it is necessary to have some idea of how the embryo develops from a single fertilized egg cell in the womb of the bitch.  Dermoid Sinus is a congenital defect that arises from a defect in the development of the embryo of a puppy.A fertilized egg resulting from a successful mating is a single simple cell.  From this cell a puppy consisting of millions of specilized cells, which constitute the tissues and organs, must me formed in 63 days.
Fig 2: Early stages of cell division.









A:  Single cell of fertilized eggB:  2 cell stage.C:  4 cell stage.D:  8 cell stage.E:  Multi-celled Spherical Mass, many cell divisions later.This process is accomplished by a rapid increase in the number of cell division.  The fertilized egg (a single cell) divides into two cells and subsequent divisions each double the previous number of cells, so that the numbers very rapidly increase.  In the ten successive divisions, 1042 cells are produced, and it can be seen that, by this means, the total number of cells is soon very large.The next stage is the organisation of the mass of cells produced to form a puppy.  The organisation process, which takes place for about the first three weeks of pregnancy, is called the embryonic development.  When the embryo is fully developed, a complete miniature puppy is formed which now becomes known as a foetus.  The next six weeks of pregnancy only results in the increase in size of the foetus to its normal birth size.Dermoid Sinuses arise from a defect in the development of the embryo.  Cell division gives rise to a spherical mass of cells.  The outer layer of these cells will eventually become the skin of the puppy.  Another part of the body also develops from this outer layer of cells.  This is the brain and the spinal cord, which runs from the head to the base of the tail.  The problem now is -how does the outer layer of cells give rise to the brain and the spinal cord?This is accomplished by the formation of a long groove over half the surface of the spherical mass of cells.  The groove deepens and then its outer edges close together giving rise to a tube-like structure.  This tube-like structure which is later to become the brain and spinal cord, sinks deeper below the surface layer and becomes detatched from it.  This process is shown in Figure 3.
Fig 3: Schematic Formation of Brain & Spinal Cord








A:  Formation of groove on surface of sphere of cells as seen from above groove.B:  Section through X-Y to show outer layer of cells folding inwards.C:  Deepening of the fold.
Fig 3: Continued









A:  Closing over of edges of the groove.B:  Closed.C:  Separation of outer layer (skin) from tubular structure (spinal cord).Dermoid Sinuses occur when small areas of attachment between the outer layer of cells (the skin) and the tubular structure (later to become the brain and the spinal cord) remain.In the puppy, this defective separation of the embryological tissues is present as a thin tubular attachment extending from the skin of the midline of the top surface of the dog to the deeper tissues below, and as deep as the spinal cord in some cases.The depth to which this tubular skin defect penetrates is the criterion used for the classification of four types of Dermoid Sinuses, shown in Figure 4 below.
Fig 4: Cross section through a dog's neck










TYPES OF DERMOID SINUSES
TYPE I:      Penetrates below the skin surface, its fatty tissue  overlying the neck muscles.TYPE II:     Penetrates into the muscles of the neck.TYPE III:    Penetrates to the supraspinous ligament, which runs over the top of the vertebrae.TYPE IV:    Penetrates to the spinal cord between the vertebrae.THE SIGNIFICANCE OF DERMOID SINUSThe detrimental effects of Dermoid Sinus are not just concerned with the fact that a visible anatomical defect is apparent in affected animals, but rather the complications which can arise as a result of a Dermoid Sinus becoming infected with bacteria.The narrow tube of skin which descends below the skin surface is lined with all the normal skin structures and of special significance are:  hair; sweat; and oil glands.The thin central cavity, which runs down the Dermoid Sinus, becomes filled in time with hair, skin oil and skin scales.  The contents usually become an ideal medium where bacteria, which are normally present on the skin, may grow.  They gain access to the material through the small pore-like opening at the point of attachment of the Dermoid Sinus on the skin surface.The accumulated skin secretion undergoes a process of putrefaction and the skin barrier of the Sinus walls breaks down and bacteria invade the tissues deep below the skin surface.  This usually results in the formation of an abscess, which eventually ruptures to the outside and drains as a chronically discharging purulent wound.Extensive surgical and medical treatment may be necessary to clear up such a complication and in some cases septic dermoid sinus may be unresponsive to treatment.If a Dermoid Sinus is recognized in a dog before it becomes septic, it can be removed surgically, with a good chance that no further complications will occurr.  In most cases, however, owners of animals are not aware of the presence of Dermoid Sinus and shortly thereafter septics almost always sets in.  Subsequently, the owners are obliged to obtain veterinary treatment to resolve the distressing complications.  This may be costly to the dog owner and embarrassing to the breeder when it is pointed out that he has sold a dog with a latent defect.DIAGNOSIS OF DERMOID SINUSIn the puppy, Dermoid Sinus can be detected by raising the skin in a longitudinal fold along the top midline in the area in which Dermoid Sinuses are known to occur (i.e. in front of and behind the ridge).  If the skin fold is raised with one hand and the skin allowed to slip back and forward between the thumb and forefinger of the other hand the presence of the Sinus can be felt as a thin cord-like structure between the two layers of skin (Fig 5 below).
Fig 5: Diagnosis of Dermoid Sinus









Feeling for presence of Dermoid Sinus by sliding longitudinal fold of skin between  the index finger and thumb.Raising the skin fold in this way tenses the tissues and a Dermoid Sinus will be pulled tautly between its skin attachment in the top midline and its attachment in the muscles below.The diagnosis can be confirmed by shaving the hair from the skin over the point at which the Dermoid Sinus is attached.  A small pore like opening in the skin from which a small tuft of hair protrudes is usually seen.  This is the opening of the Dermoid Sinus on the skin surface.The older the puppy, the thicker the Sinus will be and more easily it may be recognized.It must be realized, however, that the recognition of a Dermoid Sinus in puppies may not always be as easy a procedure as the above description may suggest.  If it is missed, a Dermoid Sinus may lie dormant for years before it comes to the notice of an owner by becoming septic.  If in doubt, the professional assistance of a Veterinarian should be obtained.