Fipronil termite treatment: pros and cons of a remedy

Review of a Fipronil Termite Treatment

Termites are well-organized insects, their life is really social. Every group of insects has special jobs to do for the whole colony.

More than that, termites are great helpers in the forest. As a small part of nature, they consume wood from fallen trees.

If there are no termites, it will take a great time for these trees to decompose. Termites and some other organisms also help to break down the timber really fast. As you see, their role in nature is great.

But if termites come to your yards and into houses, that’s a real disaster. Unfortunately, termites can see no difference between wood in the forest and in your house. So, they start ingesting wood and cellulose, turning any place into a remarkable mess.

There are some chemicals that help to cope with termites and some others destroying pests. One of such products is fipronil. Let’s see what is it, how and when you can use it and whether it is safe enough.

What is fipronil?

Fipronil is an insecticide that can be used to control various insects, about 12 species including termites.

The product’s main use is to control termites in different structures, but it is also used in baits in lawns in granule form.

Other insects that can be controlled with the help of fipronil are ants, beetles, cockroaches, fleas, ticks, mole crickets, thrips, rootworms, weevils and more.

It is a white powder that possesses a moldy odor.

This insecticide was firstly registered for use in the USA in 1996, quiet a young one.

How it works?

Termites and other insects are killed when they eat fipronil or get in contact with it. The main effect of the product is to disrupt the main functions of insects’ central nervous system. Some people are frightened with such effect and they wonder whether fipronil is safe for family members and pets.

Here you can learn more information about another effective termite control remedies: Bora-Care, Boric acid, Borate, Chlorpyrifos, Chlordane, Borax, Timbor, Termidor and Terminator.


While you are searching any info about fipronil you can find out that it is used in a number of products. There are granules for grass, gel baits, liquid products, spot-on-per products and even more. You can get that there are more than 50 products containing fipronil.

Fipronil is the main element in such brand products as Regent and Termidor. They are traditional ways of barrier treatment for termites.

The most popular product using fipronil is made by BASF. It is really widely used. This product was tested in a great number of countries in the world. It eliminates termites both by contact and ingestion.

The study of American scientists showed that termites were not only repelled by fipronil, they were also killed in the areas where insecticide was applied.

Check out the products of such giants as Bayer – Termite Killer Concentrate and Granules; and Spectracide – Termite Killer concentrate, sprayer, foam and Baiting stakes.

Fipronil termite treatment

The fipronil works and does its best to kill the termites.

Anyway, scientists inform all homeowners, that they should use it only with a pest control specialist.

The idea is that termites can live in a number of places in your house.

Only an expert can find out for sure where they can be. For homeowners that’s really difficult.

After you know the places where termites are, a professional should apply fipronil. To reach the best effect, this product should be placed in correct locations.

If in any way you are using fipronil independently, be very careful, follow instructions on label and try to avoid exposure. If exposure happens, you should follow the label instructions or First Aid instructions really carefully.

Here you can learn more information about effective treatment method called tenting (fumigation): dangers for termites, preparing for fumigation and cleaning after, how long does this procedure last?

How can I be exposed to fipronil?

A person using fipronil can be exposed to it in four different ways:

  • the chemical contacts your skin;
  • it contacts your eyes;
  • you breathe fipronil in;
  • you swallow it.

Contact with skin and eyes can happen while you are using fipronil. If you use fipronil for pets, to get rid of flea and ticks, they can be also exposed. You may swallow some product if you don’t wash your hands after using it.

To minimize the chances of exposure you should read the product label really carefully and follow what it says.

Brief exposure to fipronil is not really dangerous but it should better be avoided. Short contacts with skin can cause skin irritation. If a person eats fipronil, he can experience headache, vomiting, sweating, weaknesses and pains in stomach and so on. Signs of brief fipronil exposure do not last long, people start feeling better without special treatment.

How it changes the environment?

In the soil microorganisms break fipronil down into a number of small chemicals.

The sunlight is able to break it down on the surface.

So, fipronil is able to break down in soil, half of its amount goes away for about 125 days.

This process is called the “half-life” of the insecticide. The product sticks to soil rather tightly and doesn’t mix with water well.

Through the reaction with water, dip robin breaks down to a number of small chemicals. That’s why water starts being less acidic.

According to scientists’ research, fipronil is highly toxic to both freshwater and sea fish and invertebrates.

Other experiments showed that this chemical is toxic to some birds, but not to ducks. Different species react to it differently. So, it is highly toxic to bees, but not – to earthworms.

Useful articles

If you interested in more information of termites we recommend you to read the following articles:


Termites can be really dangerous and destroying. Homeowners should get rid of them by any appropriate method. Now you can decide whether fipronil termites control is what you need or not and are you going to use it.

Fipronil is one of the most popular pesticides because it works slowly and is undetectable. These qualities are great, because you can use it as termite bait or liquid.

When you use it as termite bait, you mix the poison with the cellulose termites like eating. Worker termites carry this poisoned food to the nest to share with others. During liquid treatment you apply poison to the soil near the house.

People should use fipronil really carefully, to minimize the harmful effect on nature. Do not forget to call for specialists when you decide to use it against annoying insects.


Fipronil is an insecticide of the phenylpyrazoles class and an active ingredient of one of the popular ectoparasiticide veterinary products, Frontline.

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Antiparasitic drugs


Clinical applications

Fipronil was discovered in 1987 and was developed initially for use in pest control in agriculture and public health. In dogs and cats, fipronil is available as a high-volume spray or a low-volume spot-on, with activity against ticks, fleas and ear mites. Hair shed from dogs for up to 2 weeks after topical treatment retains sufficient fipronil to kill dust mites ( Dermatophagoides spp) coming in contact. There is also some evidence that the speed of kill of ticks may be sufficient to reduce or prevent the transmission of a number of disease agents, including Ehrlichia canis, Borrelia burgdorferi and Anaplasma phagocytophilum.

Mechanism of action

Recent investigations suggest that the mechanism of action of fipronil is complex, involving multiple interactions of both parent fipronil and its oxidation product, fipronil sulfone, on GABA-gated and glutamate-gated chloride channels in the insect nervous system. Both fipronil and fipronil sulfone inhibit GABA receptors as well as desensitizing and nondesensitizing GluCls, though the activity of fipronil sulfone is much higher than fipronil for desensitizing GluCls. The net result of insect exposure to fipronil is blockade of inhibitory nerve transmission, resulting in hyperexcitability and death of susceptible parasites. GluCls have been observed only in invertebrates The binding affinities of fipronil and fipronil sulfone to mammalian GABA A receptors are much less than in arthropods (GABAA receptor binding IC50 human:insect of 135 and 17 respectively) with no binding to other types of mammalian GABA receptor, accounting (in combination with the low systemic bioavailability after dermal administration) for the selectivity of action. However, fipronil and its metabolites and degradation products are highly toxic to some species of fish.

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Fipronil is not thought to be significantly absorbed from topical sites of application but to translocate dermally, being confined to the lipids of hair follicles and sebaceous glands. From this reservoir, drug is released for many weeks, accounting for the sustained activity against fleas and ticks. On the basis of studies in humans, inadvertently ingested fipronil appears to be rapidly and well absorbed from the gastrointestinal tract, extensively metabolized to the sulfone and subject to significant enterohepatic recirculation. The elimination half-life is 7–8 h for fipronil but 7–8 d for fipronil sulfone.

Known drug interactions

It has been suggested, on the basis of a review of mechanisms of action, that prior exposure of arthropods to the organochlorine class of pesticides may predispose to resistance to fipronil . This hypothesis has not yet been tested, but resistance of fleas to fipronil has already been reported.

Piperonyl butoxide (by blocking oxidation of fipronil to its sulfone) appears to antagonize the antiparasitic action of fipronil.


Ramesh C. Gupta, Dejan Milatovic, in Biomarkers in Toxicology , 2014


Fipronil is an insecticide of the phenylpyrazoles class and an active ingredient of one of the popular ectoparasiticide veterinary products, Frontline. Frontline is commonly used on dogs and cats to kill fleas, and all stages of ticks (brown dog ticks, American dog ticks, lone star ticks) which may carry Lyme disease, and mites. Fipronil is also formulated as insect bait for roaches, ants, and termites; as a spray for pets; and as a granular form on turf and golf courses. The USEPA has determined fipronil to be safe for use on dogs and cats, with no harm to humans who handle these pets. Most of the time poisoning cases of fipronil occur in dogs and cats due to accidental ingestion of the product Frontline. In humans, poisoning is mainly due to accidental ingestions or suicidal attempt. In agriculture, fipronil is widely used for soil treatment, seed coating, and crop protection.

Mechanism of toxicity

The mechanism of action of fipronil is better understood in insects than it is in mammals. In insects, fipronil or its major metabolite (fipronil sulfone) noncompetitively binds to GABA A-gated chloride channels, thereby blocking the inhibitory action of GABAA in the CNS. This leads to hyperexcitation at low doses, and paralysis and death at higher doses. Fipronil exhibits a >500-fold selective toxicity to insects over mammals, primarily because of affinity differences in receptor binding between insect and mammalian receptors. In other words, fipronil binds more tightly to GABAA receptors in insects than in mammals. Fipronil is more selective at this receptor through the β3 subunit in insects than in mammals. This selectivity is less pronounced with fipronil metabolites (sulfone and desulfinyl). It needs to be emphasized that fipronil sulfone is rapidly formed in humans and experimental animals, and fipronil sulfone can persist much longer than fipronil; therefore the toxicological effects are also likely due to the sulfone metabolite. The toxicity of another metabolite, fipronil desulfinyl, is qualitatively similar to that of fipronil, but the dose-effect curve for neurotoxic effects appears to be steeper for fipronil desulfinyl. Also, fipronil desulfinyl appears to have a much greater affinity to bind to sites in the chloride ion channel of the rat brain GABA receptor. This finding appears to be consistent with the greater toxicity of fipronil desulfinyl in the CNS of mammals. Comparatively recently, Narahashi et al. (2010) has explained the mechanism of action of fipronil in detail in insects and mammals.

In laboratory animals, fipronil administration by the oral route can produce the signs of neurotoxicity, including convulsions, tremors, abnormal gait, and hunched posture. Similar signs can be produced following inhalation exposure. Poisoned dogs and cats usually show signs of tremors, convulsions, seizures, and death. Following dermal exposure, fipronil toxicity is more pronounced in rabbits than in rats and mice. Humans exposed to fipronil by ingestion may show symptoms of headache, tonic-clonic convulsions, seizures, paresthesia, pneumonia, and death.

Neurotoxic symptoms of fipronil poisoning in humans are typically associated with the antagonism of central GABA receptors.

It has been suggested that fipronil is a developmental neurotoxicant. In an in vitro study using differentiating N2a neuroblastoma cells, Sidiropoulou et al. (2011) demonstrated that fipronil caused severe disruption of the developmentally important ERK <½>-MAP kinase signal transduction pathway, as evidenced by significant reductions in the activation state of MAP kinase (MEK <½>), and particularly ERK <½>. These findings supported the contention that fipronil is a developmental neurotoxicant, and unrelated to GABA receptor inhibition. Recently, Roques et al. (2012) demonstrated that fipronil and fipronil sulfone induced thyroid disruption in rats. But, fipronil sulfone has greater potential than fipronil for thyroid disruption because it persists much longer in the organism than fipronil itself.


After topical application of Frontline™, fipronil spreads and sequesters in the lipids of the skin and hair follicles, and continues to be released onto the skin and coat, resulting in long-lasting residual activity against fleas and ticks. Jennings et al. (2002) reported the maximum concentration of fipronil on the canine hair coat 24 h after a single application of Frontline™ top spot. With a descending concentration trend, fipronil residue was detected on dog’s hair coat for a period of 30 days. Fipronil is metabolized to fipronil sulfone in the liver by cytochrome P450 ( Roques et al., 2012 ). Fipronil and its metabolites (primarily sulfone) can persist in the tissues, particularly in fat and fatty tissues, for one week after treatment. The long half-life (150–245 h) of fipronil in blood may reflect a slow release of metabolites from fat. Pharmacokinetic studies in rats suggest that fipronil excretes mainly in the feces (45–75%) and little in the urine (5–25%). Detection and confirmation of residue of fipronil and its metabolites is usually performed using GS-MS.

Detection of residue of fipronil or its metabolites in the body tissue, urine, feces, or on skin or hair can be used as biomarkers of fipronil exposure. Clinical signs and symptoms and pathological changes in liver are not specific, and are of little value in terms of toxicological biomarkers. For further details on toxicity of fipronil, readers are referred to Anadon and Gupta (2012) .

Neurophysiological Effects of Insecticides

31.3 Fipronil

Fipronil is a phenylpyrazole compound and was developed as a useful insecticide in the mid-1990s. It is effective against some insects such as the Colorado potato beetle and certain cotton pests that have become resistant to the existing insecticides. Fipronil is much more toxic to insects than to mammals, another advantage it has as an insecticide.

Fipronil has been found to block insect GABA receptor (Rdl). Wild-type Rdl of Drosophila was suppressed by TBPS, 4-n-proply-4′-ethynylbicycloorthobenzoate (EBOB), picrotoxinin, and fipronil ( Buckingham et al., 1994a ; Millar et al., 1994 ). Insect GABA receptors are different from vertebrate GABAA receptors in that they are not blocked by bicuculline ( Benson, 1988 ; Buckingham et al., 1994a ; ffrench-Constant et al., 1993 ; Millar et al., 1994 ; Sattelle et al., 1988 ), and are not potentiated by benzodiazepines and barbiturates ( Millar et al., 1994 ). The insensitivity to bicuculline is reminiscent of the GABAC receptor of vertebrates ( Qian and Dowling, 1993 ; Woodward et al., 1993 ).

Dieldrin-resistant Drosophila melanogaster and D. simulans were also resistant to fipronil but to a much lesser extent, and the [ 3 H]EBOB binding to these resistant strains was less inhibited by fipronil compared to susceptible strains ( Cole et al., 1995 ). Mutant Drosophila Rdl (A302S) expressed in Xenopus oocytes was also less sensitive to fipronil than wild-type receptors ( Hosie et al., 1995 ). Fipronil and desulfinyl derivative were more potent in houseflies than in mice as toxicants and in competing with [ 3 H]EBOB binding ( Hainzl and Casida, 1996 ). LD50 values of fipronil were 0.13 mg/kg and 41 mg/kg for housefly and mouse, respectively, and receptor IC50 values were 6.3 nM and 1010 nM for housefly and mouse, respectively.

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Fipronil block of GABAA receptors of rat DRG neurons has recently been analyzed in detail ( Ikeda et al., 1999 ). Fipronil suppressed the GABA-induced whole-cell currents reversibly with an IC50 of 1.66 ± 0.18 μM Preapplication of fipronil through the bath suppressed GABA-induced currents without channel activation. These results indicate that fipronil acts on the GABA receptors in the closed state. From co-application of fipronil and GABA, the IC50 value for the activated GABA receptor was estimated to be 1.12 ± 0.21 μM. The association rate and dissociation rate constants and the equilibrium dissociation constant of fipronil effect were estimated to be 673 ± 220 M −1 sec −1 , 0.018 ± 0.0035 sec −1 , and 27 μM for the resting GABA receptor, respectively, and 6600 ± 380 M −1 sec −1 , 0.11 ± 0.0054 sec −1 , and 17 μM for the activated GABA receptor, respectively. Thus, both the association and dissociation rate constants of fipronil for the activated GABA receptor are approximately ten times higher than those for the resting receptor, with a resultant lower Kd value for the activated receptor. Experiments with co-application of fipronil and picrotoxinin indicated that they did not compete for the same binding site. It is concluded that although fipronil binds to the GABAA receptor without activation, channel opening facilitates fipronil binding to and unbinding from the receptor.

Single-channel recording experiments using the GABAA receptor of rat DRG neurons have revealed that fipronil prolonged the closed time without much effect on open time and burst du ( Ikeda et al., 1999 ). Thus, fipronil reduces the frequency of channel opening, thereby suppressing the receptor activity.

Pesticide Use and Associated Morbidity and Mortality in Veterinary Medicine

7.9.6 Fipronil

Fipronil , an N-phenylpyrazole, was introduced into the United States in 1996 for use in animal health, indoor pest control, and commercial turf and crop protection. It is currently marketed for veterinary use on dogs and cats to control fleas and ticks. It is available as a spray (0.29%) and spot-on (9.7 % wt/wt) ( Hovda and Hooser, 2002 ). Fipronil is believed to act as a noncompetitive blocker of GABA-gated chloride channels.

Veterinary products containing fipronil have a low order of toxicity by dermal, oral, or inhalational exposure for dogs and cats. Fipronil exhibits greater selective toxicity to insects compared to mammals due to GABA receptor affinity differences ( Hainzl et al., 1998 ). However, intoxication can occur due to accidental ingestion or licking of the veterinary product ( Gupta, 2007a ). Application of the veterinary spot-on can cause skin irritation or hair loss at the site of application ( Gupta, 2007a ). There is some indication that dogs might be more sensitive to fipronil compared to cats. Off-label use of fipronil in young or small rabbits has been associated with anorexia, lethargy, convulsions, and death ( Webster, 1999 ).

Biotransformation of Individual Pesticides

Phenylpyrazole Insecticides—Fipronil

Fipronil (chemical name 5-amino-1-[2,6-dichloro-4-(trimethylmethyl)sulfinyl]-1 H-pyrazole-3-carbonitrile, CAS No. 120068-37-3) is a member of another relatively new class of pesticides, the phenylpyrazole insecticides. Fipronil is a widely used, broad-spectrum insecticide, with applications in crop production and in veterinary practice. Its mechanism of action involves binding to the GABA receptor. Metabolism in both surrogate animals and humans consists primarily of oxidation to the sulfone, the only metabolite produced in mice and by human liver microsomes ( Figure 9.6 ). In the latter case CYP3A4 and CYP2C19 are responsible for essentially all of the activity ( Tang et al., 2004 ).

Figure 9.6 . In vitro metabolism of fipronil.

Toxic Exposures

Peter M. Rabinowitz, . Lora E. Fleming, in Human-Animal Medicine , 2010

Pesticides With Low Relative Mammalian Toxicity

Fipronil is an N-phenylpyrazole compound that was introduced in 1996. When applied to a dog or cat, it spreads over the skin and accumulates in sweat glands, where it is slowly released over time. Skin absorption is thought to be minimal. It acts by blocking gamma-aminobutyric acid (GABA) receptors in insects, disrupting nervous system function. It appears to have less affinity for mammalian GABA receptors and is considered to have low acute toxicity. The major acute sign appears to be skin and eye irritation. In young rabbits, however, there have been anecdotal reports of anorexia, lethargy, seizures, and death. Fipronil is classified as a possible human carcinogen based on studies in rats showing an increase in thyroid tumors. 13

Imidacloprid is a chloronicotinyl nitroguanidine compound. It acts by blocking nicotinic acetylcholine receptors in the insect nervous system and, like fipronil, appears to have less affinity for mammalian receptors. It is capable of being absorbed through the skin but appears to have low acute toxicity. Animals fed significant amounts of imidacloprid over time have developed thyroid disturbances. It is classified as having evidence of noncarcinogenicity in human beings. 13

Spinosad is a macrolide insecticide derived from a naturally occurring actinomycete bacterium that activates nicotinic acetylcholine receptors by a novel mechanism. It also has effects on GABA receptor function that may contribute further to its insecticidal activity. It has a low mammalian toxicity. It requires topical application and spreads in the skin oils (requiring a day or two for distribution).

Metaflumizone is a semicarbazone insecticide derived from the pyrazolone sodium channel blocker insecticides discovered in the early 1970s. Metaflumizone has greatly improved mammalian safety over its ancestors.

Nitenpyram is a neonicotinoid chemical, interfering with nerve transmission in the flea but not the pet.

Luferuron is an insect growth regulator through chitin inhibition. Therefore lufenuron does not kill adult fleas.

Selamectin is a semisynthetic avermectin developed for use in dogs and cats. It treats a wide range of ectoparasites and endoparasites. It affects chloride channels in the nervous system of insects, producing paralysis, and has less effect on mammalian nerves. It is applied topically and absorbed systemically, where it acts in both the intestine and the skin glands to eliminate parasites. It is considered to have low toxicity in human beings, cats, and dogs. The major side effect is skin irritation.

Topical dermatological therapy

Antiparasitic agents

Antiparasitic agents such as pyrethrins, fipronil , selamectin, moxidectin, ivermectin or amitraz are indicated for mite infestations such as Otodectes cynotis. Recurrent clinical signs may be due to resistance of the mites. However, asymptomatic carrier animals are a potential source of reinfestation and all in-contact animals should be treated. Otodectes cynotis can be found on other body parts and whole-body treatments with effective miticidals may be needed to eliminate infection. Systemic therapy for ectoparasites is covered in Chapter 10 .

Adverse effects

Ototoxicity is of concern with most commercial otic preparations if the tympanum is ruptured and penetration into the middle ear is possible. In patients with chronic otitis externa it may be difficult to evaluate the tympanum even under general anesthesia. However, as antimicrobial topical treatment is the most effective medical therapy for an infected otitis externa (oral antimicrobials do not achieve the same concentrations in the ear canal), the risk of ototoxicity has to be balanced against the benefit of eliminating the infection. Fortunately, ototoxicity does not occur frequently in small animal practice.

Interactions with the Gamma-Aminobutyric Acid A-Receptor

96.3.3 Links between Polychlorocycloalkane and Recent Heterocyclics Apparently Acting at the Chloride Ionophore

Recently, arylpyrazoles, such as fipronil (27, Figure 96.11 ), and various 5-alkyl-2-arylpyrimidines (28) and 1,3-thiazines (29) ( Pulman et al., 1996 ), in which the planar heterocyclic ring replaces the spacers formed by the TBO and 1,3-dioxane and dithiane structures, have been added to the list of chloride ionophore blockers. Insecticidal activity was also found in triazoles (30, 31) ( Boddy et al., 1996 ; Von Keyserlingk and Willis, 1992 ) and pyrimidinones (32) ( Whittle et al., 1995 ) and a spirosultam (33) ( Bloomquist et al., 1993 ), demonstrating the diversity of structures that probably act at this site.

Cole et al. (1994) examined the inhibition of [ 3 H]-alpha-endosulfan binding in housefly head membranes by lindane and several cyclodienes and concluded that these insecticides are the only GABA-receptor ionophore blockers that consistently inhibit the binding in these membranes, not only of the earlier used ligands such as [ 35 S]-TBPS and [ 3 H]-EBOB, but also of [ 3 H]-alpha-endosulfan. However, a representative dithiane, EBOB, fipronil, and other pyrazoles were less effective in inhibiting [ 3 H]-alpha-endosulfan binding than the chlorinated insecticides, from which it appeared that the latter compete directly for the endosulfan site, whereas the others bind with different inhibition kinetics or at a site more closely coupled to the EBOB than to the endosulfan binding domain. Notably, the channel activator avermectin Ba did not inhibit endosulfan binding.

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An even more suitable ligand for the chlorinated insecticides is [ 3 H]-BIDN (34, Figure 96.12 ) ( Holyoke et al., 1994 ), a simple norbornene derivative, which has high insect and mammalian toxicity ( Kölbl et al., 1981 ; Middleton and Bingham, 1982 ). Several putative affinity probes for the binding site have also been described.

Figure 96.12 . Schematic representation of the GABAA-receptor of mammalian brain, showing five trans-membrane glycoprotein subunits, each with their four trans-membrane helices (M1-M4), of which the M2 segments (shown as cylinders, and black circles in the plan view) are believed to form the pore of the integral chloride ion channel ( MacDonald and Olsen, 1994 ). A modified subunit carrying cyclodiene resistance in Drosophila (Rdl) shows homology with the mammalian brain beta-subunit ( Ffrench-Constant et al., 1991 ).

When aryl pyrazoles synthesized as herbicides were found to be insecticidal, their convulsive activity was not immediately recognized to result from GABA-antagonism ( Klis et al., 1991 ). Cole et al. (1993) reported subsequently that several compounds, including fipronil (27, Figure 96.11 ) ( Colliot et al., 1992 ; Hatton et al., 1988 ), which has become a commercially successful insecticide, blocked the GABA-gated chloride ionophore with higher potency for a site in housefly than in mouse brain, offering the possibility of selective toxicity. Fipronil has relatively low acute mammalian toxicity ( Section 96.4.3 ). It inhibits [ 3 H]-EBOB binding to housefly head membranes and dieldrin-resistant flies show some resistance to it ( Cole et al., 1993 ; Colliot et al., 1992 ), providing a clue to its mode of action.

The cyclodiene insecticides and lindane were found to be potent displacers of [ 35 S]-TBPS binding to GABA-receptors in rat brain and inhibitors of GABA-dependent 36 Cl ion flux into rat brain microsacs, from which it was suggested that these PCCAs act as noncompetitive blockers of GABAA-receptors ( Abalis et al., 1985 ; Gant et al., 1987 ; Lawrence and Casida, 1984 ). Potency in these assays correlates with toxicity ( Casida et al., 1988 ), but TBPS is not a potent insecticide and [ 35 S]-TBPS is unsuitable as a radioligand for insect studies; it appears that the structural features required for binding at the housefly GABA-receptor are different from those for the mammalian one and [ 3 H]-EBOB, a highly potent insecticide, was ultimately designed as a superior ligand for insect binding studies ( Deng et al., 1991 ) and generally provides a good correlation between its displacement by PCCAs and their housefly toxicities. By use of this ligand, it was concluded that PCCA, PTX, dithiane-related compounds, and phenylpyrazoles all have the same mode of insecticidal action, a view supported by the up to 27-fold cross-resistance to EBOB shown by dieldrin-resistant houseflies ( Cole et al., 1993 ).

Moreover, the naturally occurring insecticide avermectin B1a and derived moxidectin ( Fisher, 1997 ), which behave as GABA-agonists, stimulating rather than inhibiting chloride ion influx, are potent noncompetitive inhibitors of EBOB binding. This implies that avermectin action involves the chloride ionophore but that it is bound at a site different from that involving EBOB and PCCA; nor, in contrast to EBOB, is there cross-resistance to dieldrin, so that the channel modification that confers dieldrin resistance does not apparently involve the avermectin binding site ( Deng et al., 1991 ). Based on ligand binding studies, Deng et al. (1993) proposed four partly associated sites in the housefly GABA chloride ionophore that are relevant to insecticidal action: site A, interacting with EBOB and its isosteres; B with TBPS and isosteres; C with phenylpyrazoles; and D with avermectins. Action at sites A and C gives similar signs of poisoning and cross-resistance to dieldrin; PCCA and some TBPS isosteres may act at both A and B. The avermectin site D is coupled in some way with A and C but not to the TBPS site B, which is also distinct from the phenylpyrazole site C. Thus, the redu-ced affinity for [ 3 H]-EBOB binding observed in dieldrin-resistant houseflies is due to its reduced affinity for the PCCA binding site, and the cross-resistance noted for TBOs, lindane, toxaphene, cyclodienes, dithianes, arylsilatranes (35, Figure 96.11 ), and PTX suggests that the structural modifications in the EBOB binding site are involved in resistance to all these insecticides ( Hawkinson and Casida, 1993 ) but fortunately do not confer resistance to avermectins, which have very high toxicity against agricultural and household insect pests, phytophagous mites, and plant and animal nematodes.

Toxicology and Human Environments

6.1 Chemicals of the agroecosystem

In studies using human hepatocytes and the HepG2 human liver cell line, 51 fipronil cytotoxicity was measured by adenylate kinase assays, as adenylate kinase is released into the medium from damaged cells. Caspase3/7 activity was also measured, which assesses caspase activity associated with apoptosis. Significantly elevated adenylate kinase levels were seen at 0.5 μM in HepG2 cells and 25 μM in human hepatocytes. Caspase3/7 activity was elevated at 0.1 and 25 μM. In studies of chlorpyrifos, exposure resulted in increased adenylate kinase activity in a dose-dependent manner which peaked at 50 μM in HepG2 cells and 12.5 μM in human hepatocytes. Caspase3/7 activity peaked at 12.5 μM in both cell types’ activity. Endosulfan exposure resulted in increased adenylate kinase activity at 50 μM in HepG2 cell and at 6.25 μM in human hepatocytes. Exposure to endosulfan increased caspase 3/7 levels in both cell types at the 1 μM dose, which peaked at 12.5 and 50 μM.

The cytotoxicity of the chloroacetanilide herbicide, alachlor, was demonstrated by Miranda and Meyer, 79 that of the fungicide, folpet, by Canal-Raffin et al., 80 and Liu et al. 81 showed that while both enantiomers of isocarbophos were cytotoxic to HepG2 cells, (−)-isocarbophos was twice as potent as (+)-isocarbophos.


Seppo Saari DVM, . Sven Nikander DVM, PhD, in Canine Parasites and Parasitic Diseases , 2019

Treatment and Prevention

Many ectoparasiticides have good effect against Cheyletiella , but there are few products registered for the purpose. Macrocyclic lactones, such as selamectin, moxidectin, and milbemycin oxime, are most commonly used. Fipronil and pyrethroids have a reported efficacy as well. Controlling Cheyletiella is difficult especially in kennels, where the mites seem to survive for long times when separated from their hosts. It is important to pay attention to the cleaning of the premises and see that all dogs in the kennel are treated with effective ectoparasite treatment for at least 6–8 weeks. Asymptomatic carriers have an important role in maintaining Cheyletiella infestations.

Cheyletiellosis Is a Zoonosis

When dealing with cheyletiellosis, the ability of the parasite to cause human infestations and severe dermatitis should always be kept in mind. It has been estimated in literature that the probability of Cheyletiella causing dermatitis symptoms in humans who deal with pets’ cheyletiellosis is 25%–80%. When the diagnosis of canine cheyletiellosis is made, the dog owner should be informed about the zoonotic character of the parasite. It is often difficult for the dog owner and the human dermatologist to discover the causality between a recently introduced puppy and simultaneously appearing dermatitis of the owner. The symptoms of cheyletiellosis in humans are most often seen on arms, feet, and the abdominal skin. The early stage is manifested by the appearance of macules (reddish spots), which quickly grow into papules (slightly elevated pimples) ( Fig. 9.37 ). Later the lesions may develop into blisters, pustules, or vesicles. Necrosis starting from the middle is typical of an old cheyletiellosis lesion. Regardless of the manifestation, the skin lesions caused by Cheyletiella are almost always severely pruritic. Since Cheyletiella is unable to complete its life cycle on the human skin, the infestation is self-limiting. If Cheyletiella are successfully eliminated from household dogs, the human skin lesions will disappear within a few weeks.

Fig. 9.37 . Cheyletiella is a zoonotic mite. The symptoms of cheyletiellosis in humans are most often seen on arms, feet and the abdominal skin. The early stage is manifested by the appearance of macules, reddish spots, which quickly grow into papules, slightly elevated pimples.

(Photo by Leena Saijonmaa-Koulumies, reproduced with permission.)

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