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Sphynx Breeders & Fanciers Alliance
Preserve, Protect & Promote the Sphynx Breed

Got something to add to this page? Send it here: editor@sphynx-cat.org

Photo courtesy Sunshinesphynx Cattery

Health Texts

Follow the link to jump to each article!

1.  Feline Hip Dysplasia

2.  HCM & Fundraiser Information

3.  Ventricular Wall Thickness Measurements for HCM Screening

4.  Spasticity: How To Eliminate An Undesired Gene From a Breeding Program

5.  Congenital Deafness & BAER Testing Information

6.  Use of Lufenuron For Treating Fungal Infections

7.  Information & Dosages on Flagyl, Strongid-T, and Panacur

8.  Various Treatments & Dosages


Ringworm: How to treat it!

Ahh, the dreaded ringworm.  This fungus can be picked up anywhere:  daycare facilities (if you have small children), schools, playgrounds, shopping carts, doorknobs, clothing, other people's homes, and other pets!  Not only can this fungus affect our pets, but it can easily transfer to humans as well!  There are many old-fashioned techniques and methods to rid yourself of this fungus such as using bleach, antifungal creams designed for athlete's foot...However, there are much safer alternatives to controlling the spread and killing the spores in your home and for your pets.

This product, Health Guard Medicated Spray, which can be bought online here:

http://www.revivalanimal.com/store/p/2982-Health-Guard-Medicated-Spray-for-Kittens-Puppies.aspx

is a very inexpensive alternative with quick results!  This spray is excellent choice for Sphynx, as you can see the spots and treat them immediately.  You may also use another product:  Vibax laundry additive, that you can add to your washload for removing the spores from infected pet bedding and clothing.


Feline Hip Dysplasia

Article courtesy of FHDA

Hip Dysplasia is a disease that has been considered a canine-specific health issue occurring mostly in the larger breeds of dogs although occasionally seen in some smaller breeds.  This condition is also present in the general feline population and is seen in all types of body styles - from relatively small cats like the Siamese to the larger breeds like Persians and Maine Coon Cats.  This condition is also prevelent in the Devon Rex, which are in most, if not all, of today's Sphynx pedigrees.  To date, there has been limited knowledge and minimal awareness or public discussion of  this condition's impact on cats and those who love them.  It is becoming more evident that hip dysplasia does occur in cats and  warrants our attention.

The topic of feline hip dysplasia is one of many that should concern cat fanciers.  It in no way implies that feline hip dysplasia is the only health concern in cats.  While FHD occurs in the random-bred cat population where there is no control over which cats breed together, it also occurs in purebred cats.  In the case of purebreds, breeders are able to select which cats will breed. The greatest impact on reducing FHD can be made by breeders who choose to breed only cats that have been evaluated for the presence of hip dysplasia, and breed cats that have hips approved by OFA or rated in the "tighter" group by PennHIP.  Hopefully one day genetics research will lead to a screening test to further assist breeders in making these decisions.  There are many unanswered questions, but at the present time, treatment options are the same whether your dysplastic cat is pedigreed or not.

What is Feline Hip Dysplasia?

Hip dysplasia is an inherited trait involving multiple gene pairs - it is not congenital (meaning an animal is not born with it).  The condition develops over time from instability in the hip joint which results from an improper fit of the femoral head (ball-like structure) into the acetabulum (hip socket). This instability, called hip joint laxity, results in abnormal weight bearing within the hip joint.  From this, secondary changes and remodeling occur in an effort to stabilize the joint or avoid bone-on-bone contact.  When cartilage disintegrates, from abnormal wear, the femoral head and acetabulum rub together with every step causing pain and eventual osteoarthritis. 

1: Femur  2: Femoral Head (Ball-like Structure) 3: Acetabulum (hip socket)

    It has been suggested that cats with feline hip dysplasia (FHD) are not in pain.  Well, unless you can talk directly to your cat, and he can ANSWER you, how can you know for sure?  Cats are rather stoic creatures and it is speculated that they hide or mask their pain well.  Out in the wilds if a cat showed pain by limping or moving slowly, he would appear vulnerable and be an immediate target for predators.  Our domestic cats are still driven by natural instincts that tell them NOT to limp or not to move too slowly.  There may be a gradual decrease in certain movements or particular activities that cause pain.  For example, a cat in pain may not jump as high as usual, or it may move more and more slowly over time.  These may be symptoms that most people simply would not notice or would attribute to other things.  The gradual lack of movement may go undetected until one day - perhaps years from the onset of pain - the disease has progressed so that it becomes quite obvious with limping, not climbing, not jumping or the inability to go up stairs.  Even then, because onset has been so gradual and there was not a drastic change in behavior from one day to the next some people may still not realize there is a problem.Other symptoms that may indicate hip dysplasia include: continued dislike of being picked up, carried or being stretched as done at shows, yowling or grumbling when lifted or handled, a lack of motivation to move, stiffness, lameness, sensitivity to touch in the hindquarters, or even a popping sound coming from the back legs with each step.  Also seen as possibly associated with dysplastic felines: early rapid growth and weight gain and hips that are noticeably narrower than the shoulders (lean, narrow bodies as opposed to broad, sturdy bodies).  In addition, an association between medial patella luxation and hip dysplasia has been found. 
    These signs and symptoms don't always mean hip dysplasia, but if one or more are observed over time, consult your veterinarian.  X-rays may be indicated.  Since feline hip dysplasia is still relatively new to the veterinary community, be sure to mention FHD to your vet.  Some vets appreciate seeing information on new animal research so you might consider giving your vet the FHDA web site address.  http://users.netropolis.net/kazikat/FHD1a.htm 
    NOTE:  X-rays sent to OFA are evaluated by board-certified veterinary radiologists; you may wish to request that your vet go ahead and send the film to OFA for further evaluation.



HCM & Fundraiser Information

Hypertrophic Cardiomyopathy (HCM) is a cardiac disease that affects the heart muscle, causing an enlarged heart, and can occur in all cats.  It is not a Sphynx-specific disorder.  At this time, there is no test for HCM that is 100% accurate.  While using a cardiac ultrasound as a screen is helpful,  and should be strongly encouraged, breeders need a breed-specific DNA test in order to identify the disease is present.  While a negative ultrasound cannot guarantee a cat will never develop HCM, it can identify currently affected cats.  Of course, those cats should be spayed/neutered and treated.

The Winn Feline Foundation has made a recent breakthrough for the Maine Coons, and now those breeders have a DNA test.  Unfortunately, testing DNA must be done for each breed, as the DNA "markers" are different.  If all kittens were DNA tested, we as breeders could eliminate HCM from our beloved breed.    

ATTENTION!!!

Sphynx breeders & fanciers alike have joined together for a great cause:  to help find a cure for HCM in our beloved breed!  To donate: Simply go to the link below, and click DONATE TODAY. Then scroll down and enter whatever amount you wish to donate, click MEMORIAL DONATION, and then type in: HCM SPHYNX RESEARCH. Click ADD TO CART, then click CHECK OUT NOW. The prompts lead you to place your donation on a credit card.  Your donations are greatly appreciated!  Please note: Your donations ARE tax-deductable!

http://www.winnfelinehealth.org/donate.html

MORE THAN MONEY IS NEEDED!!
Have you been involved with HCM and one of your Sphynx, whether the outcome was good or bad? We need a copy of the cat's medical records. Dr. Kate Meurs will be collecting all available information relating to Sphynx and  HCM to include: PEDIGREES, MEDICAL RECORDS and/or AUTOPSY reports of HCM affected Sphynx cats, as well as those of Scanned CLEAR Cats. ALL INFORMATION WILL BE STRICTLY CONFIDENTIAL! Please forward, or have your vet forward the information to:

Kate Meurs, DVM
Washington State University – CVM
Department of Veterinary Clinical Science
Pullman, Washington 99164

Her email address is:
meurs@vetmed.wsu.edu

Her fax number is: 1-
509-335-0880  Please note - this is NOT a dedicated fax and you will have to use a cover sheet addressed to Dr. Meurs.

For more information regarding the Sphynx HCM Research Project, please follow this link:

http://www.sphynxbc.org/hcmresearch.htm



Ventricular Wall Thickness Measurements for HCM Screening

 
What are normal ventricular wall thickness measurements?  There is a chart listing norms and HCM ventricular wall thicknesses in an article:

Echocardiographic Assessment of Spontaneously Occurring Feline Hypertrophic Cardiomyopathy, An Animal Model of Human Disease

Philip R. Fox, DVM, MS; Si-Kwang Liu, DVM, PhD; Barry J. Maron, MD

From the Departments of Medicine and Pathology, The Animal Medical Center, Bobst Hospital and Caspary Research Institute for Veterinary Research (P.R.F., S.K.L.), New York, NY; and Minneapolis Heart Institute Foundation (B.J.M.), Minneapolis, Minn.

The full report can be viewed at:  http://circ.ahajournals.org/cgi/content/full/92/9/2645

Spasticity: How To Eliminate An Undesired Gene From a Breeding Program

How To Eliminate An Undesired Gene From a Breeding Program

by Gerard A. Scardino, MD

In recent years, a very serious neuromuscular condition, referred to as spasticity, has reared its ugly head as an autosomal recessively inherited condition that occurs in the Devon Rex.  And, because of their cross-breeing with the Sphynx, this condition is of much concern among Devon and Sphynx breeders.  This is principally due to the fact that, in many cases, it is lethal.  And, since it is an autosomal recessive problem, a carrier state also exists.  The task I think we have as reputable breeders is to institute intelligent, rational breeding procedures designed to eliminate this problem from our breeding stock.  During the course of this article, I will propose such a program which is based on general genetic principles for breeding out an undesired gene.  Since the gene that causes spasticity is an autosomal recessive gene, two copies of it must be present in order for the condition to exist.  If an individual only has one copy of the defective gene, then he is referred to as a carrier because he also has one normal copy of the corresponding normal allele of the same gene.  Since the gene is recessive, it is usually only discovered in breeding colonies when particular matings are done, usually between closely related individuals.

The first principle to remember in order to eliminate the problem from a breeding colony is that the affected animals, the spastics, or their parents, the carriers, should be eliminated from the breeding program.  The difficulty in this, however, lies in detecting which of the normal appearing cats carry the defective gene and thus are carriers of the condition.  In general, it is safe to assume that all offspring from known carriers are prime suspects.

In the case where an affected individual is available, that is, a spastic cat is available for breedings, it can be used in test matings with suspect individuals.  When such a suspect cat is mated to a suspected carrier, approximately half the progeny will be expected to have the condition.  Of course, it only takes one abnormal kitten out of such a mating to prove that the suspect carries the defective allele, i.e. only one defective kitten is necessary to prove that the suspect is a carrier.  A more difficult question to answer is how many normal kittens must be produced from such test matings before the breeder can be reasonably sure that the suspect is not a carrier.

To answer that question, one must recall that if the suspect is a carrier, the probability of the offsprings' recieving a normal gene from that parent is 1/2.  Thus, in the mating of the suspect catwith the spastic cat, the probability of producing a kitten with one normal allele is 1/2.  The probability of producing two kittens with one normal allele is 1/2 times 1/2, or 1/4.  The probability of producing three kittenswho have one normal allele is 1/2 times 1/2 times 1/2, or 1/8.  And, correspondingly, the probability of producing four kittens with one normal allele is 1/2 times 1/2 times 1/2 times 1/2, or 1/16.  We can, of course, go on with this progression and the confidence that the suspect is not a carrier increases with each normal kitten produced.  The point at which the breeder should stop is when the probabilities drop to an acceptably low level , that is, less than one percent.  Such a point will be reached when seven successive normal kittens have been produced.  In other words, the probability of getting seven kittens with one normal allele is 1/2 times 1/2 times 1/2 times 1/2 times 1/2 times 1/2 times 1/2, or 1/128 which equals 0.01, or one percent.  One must keep in mind, of course, that if just one affected spastic kitten is produced that wil lprove the suspect is a carrier and the test matings can stop at that point.  In a situation where an affected individual cat or a spastic cat is unavailable, then test matings must be made with carrier individuals, or heterozygous individuals; that is, those that have produced affected progeny.


Congenital Deafness & BAER Testing Information

Very little information is available documenting deafness in various cat breeds. Deafness can result from effects of the dominant white (W) gene. A dominant piebald or white-spotting gene (S) is also found in various cat breeds but there has been no report of deafness associated with its presence. Cats carrying the W gene are not always solid white, often having colored spots on their heads that may disappear with age. Unlike dogs with the merle gene, homozygous white cats do not have visual or reproductive defects, but they are more prone to the occurrence of blue irises and deafness, either unilateral or bilateral, and deafness occurrence increases with the number of blue eyes. Long-haired cats have a higher prevalence of blue eyes and deafness than short-haired cats. White cats carrying the underlying cs Siamese dilution pigment gene can have blue eyes without deafness, and it has been suggested that the presence of this gene explains why purebred white cats are less often deaf than mixed-breed white cats. Data supporting this is not available.

From studies of mixed-breed white cats (the W gene):

  • Out of 256 white cats from three studies, 12.1% were unilaterally deaf and 37.9% were bilaterally deaf, or a total of 50% were affected.
  • When cats that were the offspring of two white parents were examined, the prevalence of deafness (unilateral or bilateral) ranged from 52% to 96%.
  • When examined the effect of blue eye color on deafness, they found, respectively, a prevalence of deafness (unilateral and bilateral combined) of 85% and 64.9% in cats with two blue eyes, 40% and 39.1% in cats with one blue eye, and 16.7% and 22% in cats with no blue eyes.
  • Purebred white cats are said to have a lower prevalence of deafness than mixed-breed white cats, but supporting data are unavailable.

Pure cat breeds carrying the white (W) coat pigment gene and at risk for congenital deafness (no prevalence data available):

  • White
  • White Scottish Fold
  • European White
  • Norwegian Forest Cats
  • White Turkish Angora
  • Foreign White
  • White American Wirehair
  • White Cornish Rex
  • White American Shorthair
  • White Devon Rex
  • White Sphynx
  • White British Shorthair
  • White Manx
  • White Exotic Shorthair
  • White Persian
  • White Oriental Shorthair

It is obvious that much more research needs to be performed before deafness in cats is well understood.

What is the BAER test?

The hearing test known as the brainstem auditory evoked response (BAER) or brainstem auditory evoked potential (BAEP) detects electrical activity in the cochlea and auditory pathways in the brain in much the same way that an antenna detects radio or TV signals or an EKG detects electrical activity of the heart. The response waveform consists of a series of peaks numbered with Roman numerals: peak I is produced by the cochlea and later peaks are produced within the brain. The response from an ear that is deaf is an essentially flat line. Because the response amplitude is so small it is necessary to average the responses to multiple stimuli (clicks) to unmask them from the other unrelated electrical activity that is also present on the scalp (EEG, muscle activity, etc).

The response is collected with a special computer through extremely small electrodes placed under the skin of the scalp: one in front of each ear, one at the top of the head, and one between and behind the eyes. It is rare for a cat to show any evidence of pain from the placement of the electrodes - if anything the cat objects to the gentle restraint and the irritation of wires hanging in front of its face. The stimulus click produced by the computer is directed into the ear with a foam insert earphone. Each ear is tested individually, and the test usually is complete in 10-15 minutes. Sedation or anesthesia are usually not necessary unless the cat becomes extremely agitated, which can usually be avoided with patient and gentle handling. A printout of the test results, showing the actual recorded waveform, is provided at the end of the procedure.

BAER testing is required in Europe for Breeders of White & Van cats, and although it is not yet required elsewhere, it is strongly encouraged.  Here, you can find vets throughout the world that currently perform the BAER hearing test:  http://www.lsu.edu/deafness/baersite.htm


Use of Lufenuron For Treating Fungal Infections

Excerpts taken from article in JAVMA, Vol 217, No 10, November 15, 2000

Objective
To evaluate use of Luferuron for treating cutaneous fungal infections in dogs and cats.
Design
Retrospective Study
Procedure
Medical records were reviewed for dogs and cats that has been treated for dermatophytosis for other fungal infections by administration of lufenuron and 18 dogs and 42 cats that were not treated and served as a control group
Results
Dogs were treated once by oral administration of lufenuron tablets at doses ranging from 54.2 to 68.3 mg/kg (24.6 to 31.0 mg/lb of body weight. Samples of skin, scrapings, and hair were obtained daily from 14 dogs with dermatophytosis: mean duration from time of treatment to time of negative fungal culture results and resolution of gross lesions were 14.5 and 20.75 days, respectively. In all treated dogs, gross lesions resolved within approx 21 days. Cats were treated once by oral administration of lufenuron suspension in doses ranging from 51.2 to 266 mg/kg (23.3 to 120.9 mg/lb. Samples were obtained daily from 23 cats: mean durations from time of treatment to time of negative fungal culture results and resolution of gross lesions were 8.3 and 12 days, respectively. Time to resolution of lesions in most untreated control animals was approximately 90 days. Adverse effects of treatment were not detected.
Conclusions and clinical relevance. 
Results of this study suggests that lufenuron provided an effective, convenient and rapid method of treating fungal infections in dogs and cats. (J Am Vet Med Assoc 2000:217:1510-1513

Dermatophytes are classified on the basis of their morphologic characteristics and include morphologic characteristics and include Microsporum, Trichophyton, and Epidermophytonspp all of which are pathogentic for humans and animals. Three species, M canis, M gypseum and T mentagrophytes cause most clinical cases of dermatophytosis in dogs and cats.
Microsporum canis is the most common cause of ringworm and is transmitted from cats and dogs to humans. Spontaneous remission of dermatophytosis in companion animals often occurs within1 to 3 months, whereas treatment is undertaken to reduce transmission to other animals, including human, and eradicate the infection. Dermatomycoses that affect companion animals include nondermatophytic superficial fungal infections with organisms such as Aspergillue, Candica, Malassezia and trichosporon spp. Traditionally, fungal infections have been treated with griseofulvin and ketoconazole.
   Lufenuron is classified as an insect development inhibitor because of its ability to inhibit citin ( a poly-mer of n-acetylglucosamine) syntesis, polymerization, and deposition. It is used in veterinary medicine as a flea control treatment, administered orally once per month.
Results:
357 dogs and cats met study criteria, Sixty animals were untreated control and 297 animals with fungal infections had been treated with lufenuron. 71 were males, and 88 were females. 145 of these cats were mixed-breeds, 8 were Siamese, 7 were Persians, 1 was an Angora, and 1 was a Himalayan. Ages ranged from 2 to 128 months (mean, 16.2 + - 16 months) and body weight ranged from 0.55 to 5 kg {1.2 to 11 lb; mean 3.1 + - l.l kg (6.8 = - 2.4 lbs}). One hundred fifty-six cats were infected with M canis and 18 of these cats had generalized infection. Three cats were infected with T mentagrophytes. Lesions were located on the head and neck (n=136), limbs (10) trunk (7), and tail (6).
In these treated cats, hair started to regbrow after 5 or 6 days, and full growth was usually completed within 10 to 12 days. Mean clinical recovery time was 11.6 =m –  1.4 days. Of the 18 cats with generalized M canis infection, 14 recovered within 10 days, 2 recovered within 11 days, and 1 recovered within 14 days.  One2 month old Persian kitten did not recover, even after 20 days. Of the 23 cats examined individually on a daily basis by use of fungal culture, mycologic cure was detected within 7 to 14 days (mean, 8.3 =- 1.2 days), whereas clinical recovery was complete within 10 to 15 days (mean, 12 =- 1.8 days). In one cat, positive culture results were obtained again 35 days after treatment; a second treatment was admininstred, and negative culture results were obtained for the next 8 weeks. Three cats again developed clinical signs of infection several weeks after initial remission of clinical signs; M canis was cultured from the lesions, and the cats responded well to a second treatment of lufenuron.
Discussion
Results of the study reported here indicated that dermatophytosis persisted for 2 to 3 months in untreated animals, whereas dogs and cats that were treated with lufenuron has remission of clinical signs much more rapidly: approximately 10 to 15 days for cats and 16 to25 days for dogs. Furthermore, mean recovery times of dogs affected by superficial dermatomycoses were quite similar.
Evaluation of results of daily mycologic culture of specimens from 16 treated dogs and 23 treated cats permitted a comparison of mycologic cure and clinical recovery times in these animals. In all instances, culture results were negative before clinical signs had disappeared. Differences in duration between these 2 findings ranged from 1 to 19 days for dogs and 1 to 5 days for cats.
Lufenuron appeared not to have adverse effects. Kittens that weighed as little as 0.5 kg received an entire tube (133mg) of the drug equivalent to a dose of 266 mg/kg, which is considerably larger that that typically administered for flea control, with no apparent adverse effects. Nevertheless, approximately 5%of treated animals became reinfected including 1 dog and 1` cat that were monitored daily by use of fungal culture. Infections reappeared at 25 to35 days after treatment, respectively, and were successfully treated with a second dose of lufenuron. It is not known whether these animals has become reinfected by natural exposure or were latently infected despite treatment. Nevertheless, oral administration of lufenuron appears to be effective treatment for certain cutaneous fungal infections in dogs and cats.

For a complete reading of this article refer to JAVMA, Vol 217, No 10, November 15,2000



Information & Dosages on Flagyl, Strongid-T, and Panacur

Other than Flagyl these medications only help with diarrhea or loose stools when it is caused by parasites, or protozoa sensitive to the medicine.  Metronidazole does help with most diarrhea because it soothes the bowel, but that is only treating the symptom and not the cause.  It's also not recommended for kittens.  Another med to treat symptoms is Endosorb, but I don't always find that helps.  If the diarrhea is bacterial I find Biosol does a good job at curing that, usually almost immediately.

Metronidazole (Flagyl) is an antibiotic, antiprotozoal, and has anti-inflammatory effects in the bowel. It is used for protozoal infections such as giardia or entamoeba, and for bacterial infections.  It is also used for inflammatory bowel disease, colitis caused by other antibiotics, and diarrhea of undetermined cause.  It is tolerated better when given with food.  The dosage for treatment of giardia is 5-11 mg/lb orally twice a day for 10 days.  (Because giardia can be persistent I would give it for 10 days, stop for 5-7 days, then give it again for another 10 days)   Metronidazole causes birth defects and should not be given to pregnant animals.  It is also excreted in breast milk so should not be given to lactating females.  It should also not be given to kittens.  This is not the most effective medication for giardia.

Dosage for Strongid:  9 mg/lb once, then repeat in 7 days  (I always repeat the dose once again in 7 more days which is what my vet recommended)

Using the Strongid from Revival (Pyrantel Pamoate 250mg/5ml):  Give 0.2 ml per pound

Panacur: Efficiancy is increased when given with food.  Dosage is 23mg/lb  If treating worms give this dose for three days in a row.  If treating for giardia give this dose for 14 days, stop for one week, and repeat for 14 more days.
Using the Panacur granules from Revival:  Mix one packet with 10ml water.  Give 0.2 cc per pound


Various Treatments & Dosages

 Drug  Indication  Dose per lb.  Frequency
 Albendazole/Valbazen  Giardia  12 mg.  Twice per day x2 days
 
Amoxicillin / Amoxi
Drops, Biomox, Polymox
 Bacterial infections  5-10 mg  1-2x per day for 7 days
 Amoxicillin-potassium clavulanate/ Clavamox, Augmentin, Synulox

 Bacterial infections

 2.5-5 mg  1-2x per day for 7 days
 Ampicillin/Polycillan, Polyflex  Bacterial infections  10-15 mg  3x per day
 Azithromycin/Zithromax, Azitrocin  Bacterial/mycoplasmal infections  2.5 - 10 mg  1x per day to every other day
 Cefaclor/Ceclor  Bacterial infections  5-15 mg  2-3x per day
 Cefadroxil/Cefa-Drops, Cefa-Tabs, DuriCef  Bacterial infections  5-15 mg  2-3x per day
 Cefazolin/Ancef, Kefzol  Bacterial infections  5-15 mg  2-3x per day
 Cefpodoxime proxetil/Simplicef, Vantin  Bacterial infections  2-5mg  Once per day
 Cephalexin/Keflex  Bacterial infections  5-15 mg  2-3x per day
 Ciprofloxacin/Cipro  Bacterial infections  5 mg  2x per day
 Clarithromycin/Biaxin  Bacterial/mycoplasmal infections  2.5 mg  2x per day
 Clindamycin/Antirobe  Bacterial infections, especially in the mouth  5-10 mg Once per day 
 Clomipramine/Anafranil  Urine Spraying  0.1-0.25 mg  Once per day
 Doxycycline/Vibramycin  Bacterial and mycoplasma infections, chlamydia  3 mg  2x a day. MUST be given with water or as a suspension
 Enrofloxacin/Baytril  Bacterial infections 2 mg   Once a day. DO NOT exceed 2.3 mg/pound per day
 Erythromycin  Bacterial infections  2 -10 mg  3x per day
 Fenbendazole/Panacur  Roundworms, Giardia 23 mg   1x per day for 3 days
 Fipronil/Frontline Fleas, Mites   4 mg  Once a month. If using dog formulation, one drop (0.05ml) per pound
 Fluconazole/Diflucan  Fungal infections/ringworm  5 mg Every other day 
 Griseofulvin/Fulvicin Ringworm   7 mg microsized, 3.5 mg ultramicrosized  2x per day
 Imidacloprid/Advantage Fleas   5 mg  Once a month. If using dog formulation, one drop (0.05ml) per pound.
 Itraconazole/Sporonox Fungal infections/ringworm   5 mg Once per day 
 Ivermectin/Ivomec  Roundworms, mites  0.2-0.4 mg  Treat once. Repeat in 2-3 weeks. 0.05 ml of 0.27% solution per pound or 0.1 ml of 1% solution PER ADULT CAT
 L-Lysine  Herpes virus infections  250 mg PER CAT  2x per day
 Metoclopramide/Reglan  Anti-emetic  .1-.2 mg  3x per day
 Metronidazole/Flagyl Giardia, IBD   5-20 mg  Once to twice a day, given with food
 Orbifloxacin/Orbax  Bacterial infections  1-3.5 mg  once per day
 Penicillin/Penicillin G Procaine, Pen BP-48, Crystiben, Dual-Pen  Bacterial infections  10,000-20,000 IU  Every 4-48 hours, check label. Newborns: 0.05 ml at birth of 150,000 IU/ml Pen BP
 Ponazuril/Bayer Marquis Paste  Coccidia  10 mg  Given once, repeat in one week
 Praziquantel/Droncit Tapeworms   0.05 ml inj., 2.5 mg oral  Treat once
 Pyrantel Pamoate/Nemex 2, Strongid-T, Pyratabs, D-Worm, Evict  Roundworms  2.5 mg  Treat once. Repeat in two weeks
 Ronidazole/Tricho Plus  tritrichomonas intestinal parasites  15-25 mg  once or twice a day for two weeks
 Selamectin/Revolution Fleas, mites, roundworms  3 mg  Once a month. If using a dog formulation, one drop (0.05ml) per two pounds. CAUTION: this practice may increase the incidence of adverse reactions!
 Sulfadimethoxine/Albon Coccidia   12.5 mg, double first dose  once per day
 Terbinafine/Lamisil fungal infections,  ringworm  15-20 mg  once per day
 Tetracycline/Albaplex, Panamycin  Bacterial infections  10 mg  Two to three times a day. MUST be given with water or as a suspensi
 Toltrazuril/Baycox Coccidia   0.2 ml of 5% solution  Dose once; repeat in one week
 Trimethoprim/Sulfadiazine and Trimethoprim/Sulfamethoxazole/ Tribrissen, Septra, Bactrim  Bacterial infections  15 mg once per day 
 Tylosin/Tylan Bacterial infections   10-20 mg  2x per day


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