Trying to manage client expectations concerning performance attributes of flea control products and gaining and understanding of Integrated Flea Control requires: (1) an improvement in the clinicians investigation skills and understanding of difficult flea challenges, (2) that we gain an understanding of the biologic and epidemiologic factors responsible for persistent flea infestations, (3) that we achieve a better understanding of the client factors responsible for persistent flea infestations and (4) that we learn how to better manage client expectations of modern flea control products.
Trying to manage client expectations concerning performance attributes of flea control products and gaining and understanding of Integrated Flea Control requires: (1) an improvement in the clinicians investigation skills and understanding of difficult flea challenges, (2) that we gain an understanding of the biologic and epidemiologic factors responsible for persistent flea infestations, (3) that we achieve a better understanding of the client factors responsible for persistent flea infestations and (4) that we learn how to better manage client expectations of modern flea control products.
In order to provide clients with an understanding of realistic product expectations and factors responsible for persistent infestations, we must educate our pet owners on flea biology and the need for management of premise infestations. Finally we must be aware that the vast majority of complaints of product failure are due to lack of client education and unrealistic expectations. A global perspective is also important. Similar issues concerning flea control are seen worldwide. Almost always we are dealing with the same flea species (Ctenocephalides felis), we use the same products and pet owners often blame control failures on the products. In my experience the most common reasons clients perceive that flea products have failed are a lack of understanding of product performance attributes such as true speed of kill, duration of activity, and misconceptions concerning repellency. In addition most pet owners are poorly informed concerning flea biology and epidemiology.
When a flea infested pet is presented in the veterinary hospital there are 3 goals that must be achieved: (1) Relieving pet of its current discomfort (kill fleas currently residing on the pet(s)), (2) Eliminate the premise infestation (eliminate immature life stages and emerging fleas) and (3) Prevention (provide for long term flea control preventing recurrence of an infestation.)
1. Relieving the pet(s) of its current infestation is actually relatively easy. Several compounds will provide rapid and complete flea eliminations from pets.
• Imidacloprid: Dogs and Cats (monthly topical spot-on)
• Fipronil: Dogs and Cats (monthly topical spot-on or spray)
• Nitenpyram: Dogs and Cats (daily or as needed oral pill)
• Pyrethroids
• Sy: Dogs, (Various formulations) while some formulations are registered for use on cats, they frequently cause excessive salivation, anorexia and emesis. Caution: some pyrethroids such as permethrin may be lethal to cats.
• Selamectin: Dogs and Cats (monthly topical spot-on)
2. Elimination of Premise Infestation is now and has been the most difficult and time consuming part of flea control. Most pet owners are not aware that in order for a pet to have "Fleas" there must be eggs, larvae, pupae and emerging fleas somewhere in the premise. Many pet owners think that their pets acquired fleas directly from another flea infested dog or cat. Since the adult cat flea is essentially a permanent ectoparasites, metabolically dependent upon a constant host relationship, direct flea transfer between pets is a uncommon to rare occurrence.1 The difficult concept for many pet owners is that the fleas they see on their pets and in their homes came from flea eggs laid 3 to 8 weeks previously. Those initial few fleas came from flea eggs deposited by neighbor's pets, feral dogs and cats or possibly flea infested wild mammals. Those eggs deposited in the outdoor premises developed through to the adult stage and jumped on their dog or cat or even occasionally the pet owner. Most pet owners never see the first 2 to 3 fleas their pets acquire. What they are reacting to is the second or third generation. Those initial few fleas (trickle infestation), mate within a few hours and females start laying eggs within 24 hours and in a few days are producing up to 40 – 50 eggs/day.1 These fleas deposit their eggs into the haircoat of the pet with the eggs then fall out of the haircoat into the premises where they ultimately develop in a few weeks to the adult flea. By the time the pet owner reacts and take their pet(s) to the veterinarian there are already flea eggs, larvae, pupae and emerging fleas in the home and protected outdoor source points. Pet owners need to be educated to these biologic realities so that they understand where the fleas are coming from and why it may take several weeks to get complete flea elimination.
Historically we treated the flea infested premises through the application of insecticides and insect growth regulators onto the carpet, floors and the yard. This was done in an attempt to kill emerging fleas and prevent development of eggs and larvae. This was a difficult and time consuming process for most pet owners and ultimately often unsuccessful. Today we attempt to "break the flea life cycle" on the pet (at the host level) through the application or administration of products to the pets that stop flea reproduction.2 The over-riding concept of flea control today is to force fleas to "extinction" in a localized environment (home or yard) by preventing the flea population from reproducing. Currently this may be theoretically accomplished by 1). killing newly acquired fleas with a residual on-animal adulticide before they can initiate reproduction (24 hours) or 2) directly affecting the viability of the eggs (insect growth regulators or other ovicidal compounds).
The commonly used residual adulticidal flea compounds (fipronil, imidacloprid, selamectin, and pyrethroids) are contact insecticides. They do not kill instantaneously and while some pyrethroids such as permethrin, may have a rapid neurotoxic effective that may be perceived as "clinical repellency", the repellent and antifeeding effect against fleas may be poor and may even be non-existent if the fleas are pyrethroid resistant. Many pet owners mistakenly think that these pyrethroid products and others will either kill all newly fleas within seconds to minutes or completely repel them. While a few fleas may die within minutes, most will actually feed prior to dieing often many hours later.3 Therefore when they see a few fleas on their pets 1 to 3 weeks after treatment, they incorrectly assume the product is failing. Due to the contact neurotoxic action of these compounds newly acquired fleas often are not killed for several (18 – 48) hours. Close scrutiny of treated pets in an infested environment will almost always result in fleas being observed for up to 8 weeks and occasionally longer.
While these newer residual adulticides do not kill instantly they do kill most newly acquired fleas before egg production is initiated (24 hours).4,5 However, some level of flea survival and reproduction does occur prior to next application. This occurs 1) because the speed of flea kill slows during 3rd and 4th week after application due to decrease insecticide levels, 2) Pet owners may misapply the product resulting in under-dosing, 3) Frequent bathing or swimming can reduce insecticide levels and 4) Genetic variability of flea isolates resulting in differences in insecticide susceptibility.
Those factors that result in less than 100% residual flea kill and allow for limited egg production from surviving fleas have been recognized for almost a decade.3 This continued reproduction must be halted in order to prevent persistent flea infestations and selection for resistant fleas. Therefore the use of an integrated approach to flea control utilizing insect growth regulators that render flea eggs nonviable can add greatly to a flea control program. Eggs can be rendered nonviable by administration of topical or systemic IGRs. It was determined that treating cats with 210 mg/kg of methoprene prevented eggs from developing into normal adult fleas for at least 43 days.6 Research suggests that the ovicidal activity of topically applied IGRs such as methoprene or pyriproxyfen is due to exposure of the adults to IGRs7 with eggs being nonviable before even being laid. The use of topical or systemic IGRs provides for prolonged residual ovicidal activity, interrupting future flea development, even after residual activity of an insecticide is diminished.2,4,8-10
Control of premise life stages can be achieved without direct treatment of the premises through a combination of residual adulticidal activity (killing newly acquired fleas) and ovicidal activity (rendering eggs of surviving fleas nonviable). This well established concept of Integrated Flea Control2,11 is also termed "Breaking the life cycle at the host level" . This approach essentially turns the treated dog or cat into a "living flea vacuum". Over the next 3 to 8 weeks (occasionally longer) the flea eggs already in the premise develop into larvae, then into pupae and finally into adult fleas. As fleas emerge and jump on treated pets most are killed by the residual adulticide and if a few survive and lay eggs, those eggs are killed by the ovicidal activity. The population is driven to extinction through elimination of reproduction. This time period from treatment until control is achieved (elimination of all premises life stages) is called the "Development Window".11
Once the infestation is eliminated it is recommended to continue treatments essentially entering into a prevention program. Fleas produce disease through the consumption of blood, injection of salivary proteins and the transmission of infectious agents. Reactive treatments to kill fleas on pets are often to late to prevent infestation of the premises. Placing pets on a continuous long term preventive program will prevent recurrence of active infestations.
Case that incorporates common perceived control failure issues:
A young couple with a 9 month old baby brings in their 1 yr old mixed breed dog because it has fleas. Physical exam reveals several fleas on the dog and some alopecia over the tail head. The Veterinarian treats the dog with Frontline Plus and sends couple home with a six months supply of the product.
One week later the fleas are still in the home and on the on the dog so they take their dog to another Veterinarian. They tell the second Veterinarian that they are certain the fleas are resistant to the Frontline and that the other veterinarian had sold them a worthless product. They can not believe that the dog still has fleas and even worse since they stopped letting the dog into the babies room the baby has gotten bitten by fleas. The second Veterinarian runs a flea comb through the dog's hair coat and recovers 10 cat fleas. Due to their size none of the fleas appear to be fully engorged and none of the females appears to be actively reproducing.
This Veterinarian explains to the owner that none of these fleas has been on the pet more than a few hours and certainly less than 24 hrs, since it takes female cat fleas at least 24 hours to become reproductively active. The Veterinarian further explains that the product (or any product) is not a repellent and does not kill fleas instantly but is intended to kill newly acquired fleas within 24 to 48 hours. Actually it appears the product is working correctly.
The pet owner wants to know "Why are there more fleas now than a week ago?" The Veterinarian explains that the fleas on the dog and the fleas on the carpet came from fleas eggs laid 3 to 8 weeks ago. The pet owners react by saying "that is not possible because the dog did not have fleas then". The Veterinarian explains that most of the time (likely >90%) pet owners never see the first 2 to 3 fleas their pets acquire outdoors. The females then begin laying eggs within 24 hours and within a few days are laying 40 to 50 eggs a day. Fleas they are seeing now are actually the next generation. Therefore once you begin treatment you can expect to continue to see some fleas for a few weeks until all immature life stages have developed and fleas have emerged to be killed on the treated pet (Development Window).
The pet owners then ask "Why did the fleas get so bad in the bed room?" The Veterinarian explains that you removed the pet from the bedroom thinking incorrectly that the fleas were coming directly from the dog. The fleas on your dog do not jump off and on the dog. The fleas on the carpet in the bedroom came from pupae, which came from larvae, which came from eggs laid 3 to 8 weeks ago. Those are newly emerged unfed fleas that had never been on the dog. Fleas lay their eggs on the dog and then the eggs fall off into the carpet. Places pets spend most of the time are where most eggs and ultimately fleas will be found. The reason it has gotten worse is because the "living flea vacuum", the treated pet has been taken out of the room and all those emerging fleas are now feeding on the only remaining warm blooded hosts, you and the baby. Simply "let the dog back into the room". The product did not fail; the failure was simply a lack of client education by the first Veterinarian on the flea life cycle and performance attributes of the product.
Rust MK, Dryden MW. The biology, ecology and management of the cat flea. Ann Rev Entomol 1997; 42:451-473.
Dryden MW, Broce AB. Integrated flea control for the 21st Century. Comp Cont Ed Pract Vet 2002; 24:1 suppl. 36 – 39.
Dryden MW. Laboratory evaluations of topical flea control products. Proceedings British Veterinary Dermatology Study Group, April 1, 1998; Birmingham, United Kingdom.p14-17.
Dryden MW, Payne PA, Smith V, Mouzin L, Thompson L. Efficacy of selamectin and fipronil/(s)-methoprene against the adult cat flea, Ctenocephalides felis and flea eggs on cats. Am Assoc Vet Parasitol 47th Annual Meeting. July 13 – 16, 2002 Nashville TN. P36.
Payne PA, Dryden MW, Smith V, Ridley RK. Effect of 0.29% w/w fipronil spray on adult flea mortality and egg production of three different cat flea, Ctenocephalides felis (Bouche), strains infesting cats. Vet Parasitol 2001; 102(4):331-40.
Olsen A. 1985. Ovicidal effect on the cat flea, Ctenocephalides felis (Bouché), of treating fur of cats and dogs with methoprene. International Pest Control 1985; 27:1013.
Palma KG, Meola SM, Meola RW. Mode of Action of pyriproxyfen and methoprene on eggs of Ctenocephalides felis (Siphonaptera: Pulicidae). J Med Entomol 1993; 30:421-426.
Donahue WA, Young R. Evaluating a synergized pyrethrin/(S)-methoprene spray against feline flea infestations. Vet Med 1992; 87:999-1007.
Young DR, Jeannin PC, Boeckh A. Efficacy of fipronil/(S)-methoprene combination spot-on for dogs against shed eggs, emerging fleas and existing adult cat fleas (Ctenocephalides felis, Bouche). Vet Parasitol 2004; 10:397-407.
Blagburn BL, Vaughan JL, Lindsay DS, Tebbitt GL. Efficacy dosage titration of lufenuron against developmental stages of fleas (Ctenocephalides felis felis) in cats. Am J Vet.Res 1994; 55:98101.
Chin A, Lunn P, Dryden M. Persistent flea infestations in dogs and cats controlled with monthly topical applications of fipronil and methoprene. Aust Vet Pract 2005; 35(3) 89-96.
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