出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/02/05 20:10:25」(JST)
Dirofilaria immitis | |
---|---|
Scientific classification | |
Kingdom: | Animalia |
Subkingdom: | Eumetazoa |
(unranked): | Bilateria |
Superphylum: | Platyzoa |
Phylum: | Nematoda |
Class: | Secernentea |
Subclass: | Spiruria |
Order: | Spirurida |
Family: | Onchocercidae |
Genus: | Dirofilaria |
Species: | D. immitis |
Binomial name | |
Dirofilaria immitis (Leidy, 1856) |
Dirofilaria immitis, the heartworm or dog heartworm, is a parasitic roundworm that is spread from host to host through the bites of mosquitoes. The heartworm is a type of filaria, a small thread-like worm, that causes filariasis. The definitive host is the dog, but it can also infect cats, wolves, coyotes, foxes and other animals, such as ferrets, sea lions and even, under very rare circumstances, humans.[1] The parasite is commonly called "heartworm"; however, adults often reside in the pulmonary arterial system (lung arteries) as well as the heart, and a major effect on the health for the animal is a manifestation of damage to the lung vessels and tissues.[2] Occasionally, adult heartworms migrate to the right heart and even the great veins in heavy infections. Heartworm infection may result in serious disease for the host, with death typically as the result of congestive heart failure.
Although at one time confined to the southern United States, heartworm has now spread to nearly all locations where its vector, the mosquito, is found. Transmission of the parasite occurs in all of the United States (cases have even been reported in Alaska), and the warmer regions of Canada. The highest infection rates are found within 150 miles of the coast from Texas to New Jersey, and along the Mississippi River and its major tributaries.[3] It has also been found in South America,[4] southern Europe,[5][6] Southeast Asia,[7] the Middle East,[8] Australia, Korea, and Japan.[3][9]
Heartworms go throughout several life stages before they become adults infecting the pulmonary artery of the host animal. The worms require the mosquito as an intermediate stage to complete their life cycles. The rate of development in the mosquito is temperature-dependent, requiring about two weeks of temperature at or above 27°C (80°F). Below a threshold temperature of 14°C (57°F), development cannot occur, and the cycle will be halted.[10] As a result, transmission is limited to warm months, and duration of the transmission season varies geographically. The period between the initial infection when the dog is bitten by a mosquito and the maturation of the worms into adults living in the heart takes six to seven months in dogs and is known as the "prepatent period".
After infection, the third-stage larval heartworms (L3) deposited by the mosquito grow for a week or two and molt to the fourth larval stage (L4) under the skin at the site of the mosquito bite. Then, they migrate to the muscles of the chest and abdomen, and 45 to 60 days after infection, molt to the fifth stage (L5, immature adult). Between 75 and 120 days after infection, these immature heartworms then enter the bloodstream and are carried through the heart to reside in the pulmonary artery. Over the next three to four months, they increase greatly in size. The female adult worm is about 30 cm in length, and the male is about 23 cm, with a coiled tail.[11] By seven months after infection, the adult worms have mated and the females begin giving birth to live young, called microfilariae.
The microfilariae circulate in the bloodstream for as long as two years, waiting for the next stage in their life cycles in the gut of a bloodsucking mosquito. When ingested by a mosquito, the microfilariae undergo a series of molts to the infective third larval stage, and then migrate to the salivary glands of the mosquito, where they wait to infect another host. The incubation period required to reach the stage where the microfilariae become transmittable to another host can be as little as two weeks or as long as six weeks, depending on the warmth of the climate, and the larval life cycle ceases entirely if the ambient temperature drops below 14°C (57°F).
Hosts of Dirofilaria immitis include:[1]
Dogs show no indication of heartworm infection during the six-month prepatent period prior to the worms' maturation, and current diagnostic tests for the presence of microfilariae or antigens cannot detect prepatent infections. Rarely, migrating heartworm larvae get "lost" and end up in unusual sites, such as the eye, brain, or an artery in the leg, which results in unusual symptoms such as blindness, seizures and lameness. But normally, until the larvae mature and congregate inside the heart, they produce no symptoms or signs of illness.
Many dogs will show little or no sign of infection even after the worms become adults. These animals usually have only a light infection and live a fairly sedentary lifestyle. However, active dogs and those with heavier infections may show the classic signs of heartworm disease. Early signs include a cough, especially on exercise and early exhaustion upon exercise. In the most advanced cases where many adult worms have built up in the heart without treatment, signs progress to severe weight loss, fainting, coughing up blood and, finally, congestive heart failure.
Wolbachia pipientis is an intracellular bacterium that is an endosymbiont of Dirofilaria immitis. All heartworms are thought to be infected with Wolbachia to some degree. Research indicates the inflammation occurring at the die-off of adult heartworms or larvae is in part due to the release of Wolbachia bacteria or protein into the tissues. This may be particularly significant in cats, in which the disease seems to be more related to larval death than living adult heartworms (see below). Treating heartworm-positive animals with an antibiotic such as doxycycline to remove Wolbachia may prove to be beneficial, but further studies are necessary.[13]
Three methods can be used for the diagnosis:
Microfilarial detection was accomplished most commonly in the past by the microscopic identification of microfilariae on a direct blood smear, above the buffy coat in a microhematocrit tube (or capillary tube), using the modified Knott test, or after millipore filtration. The accuracy of these tests, typically used for routine screening or diagnosis of heartworm infection, is improved by multiple testing. The modified Knott test and millipore filtration are more sensitive because they concentrate microfilariae, improving the chance of diagnosis.[2] The direct smear technique allows examination of larval motion, helping in the distinction of Dirofilaria immitis from Acanthocheilonema reconditum. This distinction is important because the presence of the latter parasite does not require expensive and potentially harmful therapy. However, the potential for amicrofilaremic infections is 5-67%. The number of circulating microfilariae does not correlate with the number of adult heartworms, so is not an indicator of disease severity.[2]
Antigen testing, in most practices, has supplanted or supplemented microfilarial detection. Combining the microfilaria and adult antigen test is most useful in dogs receiving diethylcarbamazine or no preventative (as macrolides as for example ivermectin or moxidectin typically render the dog amicrofilaremic). Up to 1% of infected dogs are microfilaria-positive and antigen-negative.[2] Immunodiagnostics (ELISA, lateral flow immunoassay, rapid immunomigration techniques) to detect heartworm antigen in the host's blood are now regularly used. The weakness of these tests is they only detect the antigens released from the adult female worm's reproductive tract, so will produce negative results during the first five to eight months of infection.[2] The specificity of these tests is close to 100%, and the sensitivity is more than 80%.[14] A recent study demonstrated a sensitivity of only 64% for infections of only one female worm, but improved with increasing female worm burden (85%, 88%, and 89% for two, three and four female worms, respectively). Specificity in this study was 97%.[2] False-negative test results can be due to low worm counts, immature infections and all male infections.
X-rays are used to evaluate the severity of the heartworm infection and develop a prognosis for the animal. Typically the changes observed are enlargement of the main pulmonary artery, the right side of the heart, and the pulmonary arteries in the lobes of the lung. Inflammation of the lung tissue is also often observed.[15]
If an animal is diagnosed with heartworms, treatment may be indicated. Before the worms can be treated, however, the dog must be evaluated for heart, liver, and kidney function to evaluate the risks of treatment. Usually, the adult worms are killed with an arsenic-based compound. The currently approved drug in the US, melarsomine, is marketed under the brand name Immiticide.[16] It has a greater efficacy and fewer side effects than previously used drug (thiacetarsamide sodium, sold as Caparsolate) which makes it a safer alternative for dogs with late-stage infections.
After treatment, the dog must rest (restricted exercise) for several weeks so as to give its body sufficient time to absorb the dead worms without ill effect. Otherwise, when the dog is under exertion, dead worms may break loose and travel to the lungs, potentially causing respiratory failure and death. According to the American Heartworm Society, use of aspirin in dogs infected with heartworms is no longer recommended due to a lack of evidence of clinical benefit and may be contraindicated. It had previously been recommended for its effects on platelet adhesion and reduction of vascular damage caused by the heartworms.
The course of treatment is not completed until several weeks later, when the microfilariae are dealt with in a separate course of treatment. Once heartworm tests are negative, the treatment is considered a success.
Surgical removal of the adult heartworms as a treatment also may be indicated, especially in advanced cases with substantial heart involvement.[17]
Long-term monthly administration of ivermectin year-round at three times the dose normally used for heartworm prevention (see "Prevention") will eventually kill adult heartworms. However, this is not the treatment of choice for removal of adult heartworms for two reasons. First, this treatment is not as effective as melarsamine. More importantly, adult heartworms do not begin to die until 18 months of treatment have elapsed, which is not acceptable for dogs with high-volume infections. Long-term treatment over a year with doxycycline daily and Heartguard Plus has been shown to be effective in early heartworm patients which are asymptomatic.
Prevention of heartworm infection can be obtained through a number of veterinary drugs. The drugs approved for use in the US are ivermectin (sold under the brand names Heartgard, Iverhart, and several other generic versions), milbemycin (Interceptor Flavor Tabs and Sentinel Flavor Tabs) and moxidectin (ProHeart) administered as pills or chewable tablets. Moxidectin is also available in both a six-month and 12-month, sustained-release injection, ProHeart 6 or ProHeart 12, administered by veterinarians. The injectable form of moxidectin was taken off the market in the United States due to safety concerns in 2004, but the FDA returned a newly formulated ProHeart 6 to the market in 2008. ProHeart 6 remains on the market in many other countries, including Canada and Japan. Its sister product, ProHeart 12, is used extensively in Australia and Asia as a 12-month injectable preventive. Topical treatments are available, as well. Advantage Multi (imidacloprid + moxidectin) Topical Solution, uses moxidectin for control and prevention of roundworms, hookworms, heartworms, and whipworms, as well as imidacloprid to kill adult fleas. Selamectin (Revolution) is a topical preventive likewise administered monthly; it also controls fleas, ticks, and mites.
Preventive drugs are highly effective, and when regularly administered, will protect more than 99% of dogs and cats from heartworm. Most compromises in protection result from failure to properly administer the drugs during seasonal transmission periods.[10] In regions where the temperature is consistently above 14°C (57°F) year-round, a continuous prevention schedule is recommended.
Lapses of up to four months between doses of ivermectin-based products still provides 95% protection from adult worms. This period is called the reach-back effect.[18] Annual heartworm testing is highly recommended for pet owners who choose to use minimal dosing schedules.
Heartworm prevention for cats is available as ivermectin (Heartgard for Cats), milbemycin (Interceptor), or the topical selamectin (Revolution for Cats) and Advantage Multi (imidacloprid + moxidectin) topical solution.
While dogs are a natural host for D. immitis, cats are an atypical host. Because of this, differences between canine and feline heartworm diseases are significant. The majority of heartworm larvae do not survive in cats, so unlike in dogs, a typical infection in cats is two to five worms. The lifespan of heartworms is considerably shorter in cats, only two to three years, and most infections in cats do not have circulating microfilariae. Cats are also more likely to have aberrant migration of heartworm larvae, resulting in infections in the brain or body cavities.[19]
The infection rate in cats is 1-5% of that in dogs in endemic areas.[20] Both indoor and outdoor cats are infected. The mosquito vector is known to enter homes.[21]
The vascular disease in cats that occurs when the L5 larvae invade the pulmonary arteries is more severe than in dogs. A syndrome related to this inflammatory reaction has been identified in cats: heartworm-associated respiratory disease (HARD). HARD can occur three to four months after the initial infection, and is caused by the presence of the L5 larvae in the vessels. The subsequent inflammation of the pulmonary vasculature and lungs can be easily misdiagnosed as feline asthma or allergic bronchitis.[22]
Obstruction of pulmonary arteries due to emboli from dying worms is more likely to be fatal in cats than dogs because of less collateral circulation and fewer vessels.[23]
Acute heartworm disease in cats can result in shock, vomiting, diarrhea, fainting, and sudden death. Chronic infection can cause loss of appetite, weight loss, lethargy, exercise intolerance, coughing, and difficulty breathing. The signs of HARD can persist even after complete elimination of the heartworm infection.[22]
Diagnosis of heartworm infection in cats is problematic. Like in dogs, a positive ELISA test for heartworm antigen is a very strong indication of infection. However, the likelihood of a positive antigen test depends on the number of adult female worms present. If there are only male worms, the test will be negative. Even with female worms, an antigen test will usually only become positive seven to eight months after infection. Therefore, a cat may have significant clinical signs long before the development of a positive test. HARD can be found in cats that never develop adult heartworms and therefore never have a positive antigen test.
An antibody test is also available for feline heartworm infection. It will be positive in the event of exposure to D. immitis, so a cat that has successfully eliminated an infection may still be positive for up to three months. The antibody test is more sensitive than the antigen test, but it does not provide direct evidence of adult infection.[24] It can, however, be considered specific for diagnosing previous larval infections, and therefore fairly specific for HARD.
X-rays of the chest of a heartworm-infected cat may show an increased width of the pulmonary arteries and focal or diffuse opacities in the lungs. Echocardiography is a fairly sensitive test in cats. Adult heartworms appear as double-lined hyperechoic structures within the heart or pulmonary arteries.[25]
Arsenic compounds have been used for heartworm adulticide treatment in cats, as well as dogs, but seem more likely to cause pulmonary reactions. A significant number of cats develop pulmonary embolisms a few days after treatment. The effects of melarsomine are poorly studied in cats. Due to a lack of studies showing a clear benefit of treatment and the short lifespan of heartworms in cats, adulticide therapy is not recommended, and no drugs are approved in the US for use in cats.[23]
Treatment typically consists of putting the cat on a monthly heartworm preventive and a short-term corticosteroid.[19] Surgery has also been used successfully to remove adult worms. Three drugs are approved for use in cats in the US: ivermectin, milbemycin, and selamectin. The prognosis for feline heartworm disease is guarded.
The dog heartworm is of negligible public health risk, because it is unusual for humans to become infected. Additionally, human infections usually are of little or no consequence, although rarely an infected human may show signs of respiratory disease. In most cases, however, the heartworm dies shortly after arriving in the human lung, and a nodule, known as a granuloma, forms around the dead worm as it is being killed and absorbed. If an infected person happens to have a chest X-ray following granuloma formation, the nodule may be large enough to resemble lung cancer on the X-ray and require a biopsy for a pathologic assessment. This may well be the most significant medical consequence of human infection by the dog heartworm.
At one time, the dog heartworm was thought to infect the human eye, with most cases reported from the southeastern United States. However, these cases are now thought to be caused by a closely related parasite of raccoons, Dirofilaria tenuis. Several hundred cases of subcutaneous infections in humans have been reported in Europe, but these are almost always caused by another closely related parasite, Dirofilaria repens, rather than the dog heartworm.
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リンク元 | 「蠕虫」「糸状虫症」「イヌ糸状虫」 |
関連記事 | 「Dirofilaria」 |
蠕虫類 | 病原体名 | 病名 | 感染経路 | 寄生部位 | 症状 | 診断 | 治療 | |
線虫類 | Ancylostoma duodenale | ズビニ鉤虫 | 鈎虫症/十二指腸虫症 | F型幼虫経口感染、経皮 | 空腸上部 | 皮膚炎、若菜病、貧血 | 飽和食塩水浮遊法、遠心沈降法 | pyrantel pamoate、鉄剤 |
Necator americanus | アメリカ鉤虫 | |||||||
Strongyloides stercoralis | 糞線虫 | 糞線虫症 | F型幼虫経皮感染 | 小腸上部 | Loffler症候群 | 糞便塗沫、普通寒天平板培養による R型、F型幼虫の検出 |
thiabendazole, ivermectin | |
Enterobius vermicularis | 蟯虫 | 蟯虫症 | 虫卵経口感染 | 盲腸~大腸 | 夜間の掻痒、不眠、情緒不安定 | 肛囲検査法「柿の種」 | pyrantel pamoate | |
Ascaris lumbricoides | 回虫 | 回虫症 | 虫卵経口感染 | 小腸孵化→門脈→ 肺発育→食道嚥下→小腸 |
Loffler症候群。急性腹痛 | 糞便虫の虫卵の証明 | pyrantel pamoate | |
Toxocara canis | イヌ回虫 | 幼虫移行症 | 生後1-2ヶ月の感染犬の 糞から経口感染 |
なし | 幼虫移行症→失明 | 免疫診断 | 治療法無し? | |
Wuchereria bancrofti | バンクロフト糸状虫 | フィラリア症/糸状虫症 | アカイエカ | リンパ系 | 急性期:リンパ肝炎、リンパ腺炎を伴う熱発作(filarial fever) 慢性期:乳糜尿、リンパ管瘤、陰嚢水腫、象皮病 |
急性期:夜間のmicrofilariaの検出 慢性期:特有の症状を考慮 |
diethylcarbamazine & ivermectin | |
Brugia malayi | マレー糸状虫 | |||||||
Dirofilaria immitis | イヌ糸状虫 | アカイエカ | なし | 幼虫移行症→肺血管閉塞→胸部X線画像銭形陰影 | ||||
Gnathostoma spinigerum | 有棘顎口虫 | 顎口虫症 | ドジョウ、雷魚、ヘビの生食 | 消化管壁貫通→皮下移動による腫瘤や線状皮膚炎 | 移動性腫瘤、皮膚爬行疹 雷魚やドジョウの生殖の問診 免疫血清診断 |
なし | ||
Gnathostoma hispidum | 剛棘顎口虫 | |||||||
Gnathostoma doloresi | ドロレス顎口虫 | |||||||
Gnathostoma nipponicum | 日本顎口虫 | |||||||
Anisakis simplex, larva | アニキサス幼虫 | アニサキス症 (1)胃アニサキス症、 (2)腸アニサキス症、 (3)異所性アニサキス症 |
経口感染 終宿主:クジラ、イルカ。 中間宿主:オキアミ。 待機宿主:サバ、ニシン、アジ、タラなど |
胃や腸 | (1)急激な上腹部痛"胃けいれん" (2)腹痛、急性虫垂炎、イレウス様。劇症型と緩和型がある (3)腹腔内の炎症性肉芽腫 |
胃内視鏡検査 | 内視鏡による虫体摘出 | |
Pseudoterranova decipiens | ||||||||
Trichinella spiralis | 旋毛虫 | 旋毛虫症 | 経口感染 豚肉、クマ肉の生食 |
(1)成虫侵襲期:下痢、腹痛 (2)幼虫筋肉移行期:顔面浮腫、心筋障害など (3)幼虫被嚢期:全身浮腫、衰弱 |
急性期:ステロイド 殺虫:mebendazole | |||
鞭虫症 | 盲腸 | 慢性下痢、腹痛、異食症、貧血 | セロファン重層塗沫法、 ホルマリンエーテル法 |
mebendazole | ||||
Spirurin nematode larva | 旋尾線虫 | 旋尾線虫幼虫 | ホタルイカの生食 | なし | 皮膚爬行疹、イレウス様症状 | 予防:-30℃24時間。 生食には-30℃4日間以上 |
摘出 | |
吸虫類 | Shistosoma japonicum | 日本住血吸虫 | 日本住血吸虫症 | 糞便虫の虫卵→ミラシジウム→ ミヤイリガイ体内でセルカリア→ 人畜の皮膚より浸入→循環系→ 門脈に寄生 |
門脈 | (1)潜伏期:侵入部の掻痒性皮膚炎。肺移行期:咳、発熱 (2)急性期:虫卵の門脈系寄生、産卵。住血吸虫性赤痢。 (3)慢性期:虫卵の肝、脳などの塞栓。肝硬変。脾腫、腹水 |
糞便虫の虫卵の検出。 直腸粘膜層掻爬法、 肝穿刺による組織内虫卵の検出。 補助診断として免疫血清学的検査。 |
praziquantel |
Paragonimus westermani | ウェステルマン肺吸虫 | 肺吸虫症/肺ジストマ症 | 経口感染 淡水産のカニ、イノシシ肉の生食 |
肺 | 痰、咳、胸痛、時に喀血 | 痰や便の虫卵検査、 胸部写真、 断層写真で明らかな虫嚢。 免疫学血清検査 |
||
Paragonimus miyazakii | 宮崎肺吸虫 | 肺 | 気胸、胸水貯留、膿胸、好酸球増加 | praziquantel | ||||
Clonorchis sinensis | 肝吸虫 | 肝吸虫症/肝ジストマ症 | 経口感染 虫卵→(マメタニシ:セルカリア)→ セルカリア→(魚:メタセルカリア)→ 摂取→(ヒト:成虫)→虫卵 |
胆管 | 胆汁流出障害による肝障害→肝硬変 | 糞便、胆汁(十二指腸ゾンデ法)。 肝吸虫卵の検出。CT像。エコー検査。 |
praziquantel | |
横川吸虫症 | 淡水魚(アユ、フナ、ウグイ、シラウオ)の生食 | 小腸粘膜 | 下痢、腹痛 | 糞便虫の虫卵 | praziquantel | |||
条虫類 | Taeniarhynchus saginatus | 無鉤条虫 | 腸管条虫症 | 経口感染。中間宿主:ウシ | 小腸 | 無症状。下痢。 広節裂頭条虫感染では悪性貧血。 |
糞便虫の虫卵と体節により診断 | praziquantel。 有鉤条虫の場合はガストログラフィン。 有鉤条虫の駆虫の際、 虫体を破壊しない →虫体の融解による嚢虫症 |
Taenia solium | 有鉤条虫 | 経口感染。中間宿主:ブタ | ||||||
Diphyllobothrium latum | 広節裂頭条虫 | 経口感染。中間宿主:サケ、マス | ||||||
日本海裂頭条虫 | 経口感染。中間宿主:サケ | |||||||
腸管外条虫症 | ||||||||
有鉤嚢虫症 | 有鉤条虫の虫卵の経口摂取 | 皮下、筋肉内 脳、脊髄、眼球 |
皮下、筋肉内:小指頭大の無症状腫瘤 脳、脊髄、眼球:Jacksonてんかん。痙性麻痺など |
皮下の虫嚢 | 外科的摘出。 成虫寄生がなければ、praziquantel, albendazole + ステロイド | |||
Echinococcus granulosus | 単包虫 | 包虫症/ エキノコックス症 (単包虫症) |
終宿主:イヌ、キツネなど。 中間宿主:ヒト、ブタ、野ネズミなど。 終宿主の糞便虫の虫卵を中間宿主が接種して発症 |
肝、肺、まれに脳、腎、筋肉 | 肝寄生:肝部疼痛、満腹、時に黄疸、下肢浮腫 肺寄生:胸部圧迫感、胸痛、咳、血痰、時に喀血 |
肝や肺の嚢胞形成から疑う。 早期に診断に皮内反応→ CT、エコー→ 生検。免疫血清学的診断法 |
外科的切除。 albendazoleの長期投与 | |
Echinococcus multilocularis | 多包虫 | 包虫症/ エキノコックス症 (多包虫症) |
イヌ糸状虫、ヌ糸状虫属、ディロフィラリア属、Dirofilaria属
.