Dirofilaria immitis

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Dirofilaria immitis (Leidy, 1856) Railliet & Henry, 1911

Figures 4-52 through 4-56)

ETYMOLOGY:Diro = dread + filaria = thread along with immitis = ????????

SYNONYMS:Filaria sanguinis Cobbold, 1869; Dirofilarialouisianensis Faust, Thomas, and Jones, 1941.

HISTORY: Heartworm has long been known as a disease of the canine host. Otto (1974) reviewed the history of cases that have been reported in cats from 1921 onwards, and at that time lists 12 cases from cts in the United States, and he suggests that the relative common occurrence of the worm in cats mitigated against it being considered an abnormal host for this parasite. In recent years, it has become more and more obvious that if the prevalence in dogs is an area is fairly high, there is a good chance that some percentage of cats will also be infected. The cat may be relatively commonly infected with this parasite, but the inability of the cat to support large numbers of worms or patent infections would argue that in the biology of this parasite, the dog and other canids are the hosts of true importance for maintaining infectious foci around the world.

GEOGRAPHIC LOCATION: Otto (1974) cites cases in cats from the United States with cases in Hawaii, Brazil, the Philippines, Tahiti, New Guinea, Indonesia, China, and Japan. Since the time of this report additional cases have been described from the United States and from around the world, e.g., Italy (Venco et al., 1999), Australia (Kendall et al., 1991), Taiwan (Fei and Mo, 1997), India (Patnaik, 1989), Japan (Roncalli et al., 1998), and Brazil (Labarthe et al., 1997)

LOCATION IN HOST: In the cat the worms have usually been recovered from the right ventrical and pulmonary artery. In cats, there is also a tendency for the worms to appear in ectopic sites. There have been several cases reported where heartworms have been recovered from the brains of cats at necropsy (Ader 1979, Cusick et al., 1976, Doahoe and Holzinger, 1974, and Fukushima et al., 1984, Lindquist and Winters, 1981).

PARASITE IDENTIFICATION: The adult worms are relatively easy to identify due to their size and location in the host. The long white worms are very easily recognized when removed from the cat either surgically or at necropsy. Unfortunately relative to diagnosis, cats tend not to have circulating microfilariae (Fig 4-52.), thus, it is difficult to verify infections by examination of the blood. However, recently developed antigen detection kits make it possible to detect infections in cats as long as there are female worms present (Atkins, 1999). The antigen which circulates in the blood of the host is a uterine antigen produced by female worms, thus, if only male worms are present, there will be no circulating antigen.

LIFE CYCLE: The life cycle in the cat fairly well mimics that which occurs in the dog; however, cats tend not to support anywhere near the same number of worms and are significantly refractory to infection (Zanotti and Kaplan, 1989). Cats experimentally infected with Dirofilariaimmitis third –stage larvae (Figs. 4-53 & 4-54) appear to develop detectable levels of circulating antigen slightly later than would be expected in dogs (Mansour et al., 1995). Cats typically support only one to three adult worms, although under various experimental conditions cats can harbor greater worm burdens (Stewart et al., 1992).

CLINICAL PRESENTATION AND PATHOGENESIS: Cats with a more typical presentation of heartworm infection will present with signs of respiratory or gastrointestinal disease. Such signs will include dypsnea, coughing, systolic murmur, vomiting, anorexia, dysphagia, diarrhea, or syncope (Malik et al, 1998). These would be the signs expected in those animals with a chronic infection. In cats with acute onset disease, signs will be associated with the worms in either the cardiovascular system or ectopic sites. When associated with the cardiovascular system, signs may be associated with pulmonary artery obstruction, pneumothorax, or chylothorax (Birchard and Bilbrey, 1990; Smith et al., 1998). When worms enter ectopic locations such as the skin (Dillon et al., 1987) or the brain (Figs. 4-55 & 4-46), the signs associated with the infection will be related to the organ system damaged by the migrating worms. Radiography and echocardiography are both useful tools in the diagnosis of feline heartworm disease (Venco et al., 1998).

TREATMENT: Currently the recommendation is typically that cats be treated with symptomatic therapy because adulticide therapy using thiacetarsamid or melasormine are considered to put the cat at risk for sudden death (Atkins, 1999; Malik et al., 1998). Surgical removal of heartworms from the right atrium of cats using catheter bearing basket-type retrieval forceps is also successful, especially when the worms are visualized during removal with ultrasonography (Borgarelli et al., 1997).

EPIZOOTIOLOGY: The episootiology of feline heartworm disease seems to mimic that of dogs. It may be that other species of mosquitos different than those typically biting dogs are more important in the transmission of the infection to cats (Borgarelli et al., 1997)), however, more work needs to be done in this area.

HAZARDS TO OTHER ANIMALS: The heartworms in a cat would only be infectious to another host through transmission by the mosquito intermediate host. The fact that cats seldom are microfilaremic would suggest that they play very little role in serving as reservoirs for this infection.

HAZARD TO HUMANS: Infections in humans do occasionally occur due to canine heartworm, but people have to get bitten by a heartworm infected mosquito to become infected. The fact that the worms in cats are poor producers of microfilariae would indicate that the infection of cats provides little risk to owners.

CONTROL/PREVENTION: Prevention of heartworm infection in cats can now easily be introduced by the monthly administration of several products, ivermectin and selamectin, that are capable of preventing this infection in cats.


Ader P. 1979. Heartworm (Dirofilaria immitis) in the brain of a cat- review and case report. Calif Vet, Nov pp 23-25.

Atkins C. 1999. The diagnosis of feline heartworm infection. JAAHA 35:185-187.

Birchard SJ, Bilbrey SA. 1990. Chylothorax associated with dirofilariasis in a cat. JAVMA 197:507-509.

Borgarelli M, Venco L, Piga PM, Bonino F, Ryan WG. 1997. Surgical removal of heartworms from the right atrium of a cat. JAVMA 211:68-69.

Cusick PK, Todd KS, Blake JA, Daly WR. 1976. Dirofilaria immitis in the brain and heart of a cat from Massachusetts. JAAHA 12:490-491.

Dillon AR, Brawner WR, Grieve RB, Buxton-Smith B, Schultz RD. 1987. The chronic effects of experimental Dirofilaria immitis infection in cats. Seminars Vet Med Surg (Small Anim) 2:72-77.

Donahoe JMR, Holzinger EA. 1974. Dirofilaria immitis in the brains of a dog and a cat. JAVMA 164:518-519.

Fei CYand Mo KM. 1997. Survey for endoparasitic zoonoses in stray dogs and cats in Taipei city. J Chin Soc Vet Sci 23:26-33.

Fukushima K, Hutsell D, Patton S, Patton CS. 1984. Aberrant dirofilariasis in a cat. JAVMA 184:199-201.

Kendall K, Collins GH, Pope SE. 1991. Dirofilaria immitis in cats from inner Sydney. Aust Vet J 68:356-357.

Labarthe N, Lúcia Serrão, Melo YF, de Oliveira SJ, Lourenço-de-Oliveira. 1998. Mosquito frequency and feeding habits in an enzootic canine dirofilariasis area in Niterói, state of Rio de Janeiro, Brazil. Mem Inst Oswald Cruz 93:145-154.

Lindquist WD, Winters KD. 1981. Cerebral feline dirofilariasis. Fel Pract 11:37-40.

Malik R, Church DB, Eade IG, 1998. Syncope in a cat. Aust Vet J 76:465-471.

Mansour AE, McCall JW, McTier TL, Supakorndej N, Ricketts R. 1995. Epidemiology of feline dirofilariasis. Infections induced by simulated natural exposure to Aedesaegypti experimentally infected with heartworms. Proc Heartworm Sympos ‘95, Auburn, Alabama. pp. 87-95.

Otto GF. 1974. Occurrence of the heartworm in unusual locations and in unusual hosts. Proc Heartworm Sympos pp 6-13.

Patnaik MM. 1989. On filarial nematodes in domestic animals in Orissa. Ind Vet J 66:573-574.

Railliet A, Henry A. 1911a. Sur une filaire péritonéale des porcins. Bull Soc Pathol Exot 4:386-389.

Railliet A, Henry A. 1911b. Remarques au sujet des deux notes de MM. Bauche et Bernard. Bull Soc Pathol Exot 4:485-488.

Roncalli RA, Yamane Y, Nagata T. 1998. Prevalence of Dirofilaria immitis in cats in Japan. Vet Parasitol 75:81-89.

Smith JW, Scott-Moncrieff C, Rivers BJ. 1998. Pneumothorax secondary to Dirofilariaimmitis infection in two cats. JAVMA 213:91-93.

StewartVA, Hepler DI, Grieve RB. 1992. Efficacy of milbemycin oxime in chemoprophylaxis of dirofilariasis in cats. Am J Vet Res 53:2274-2277.

Venco L, Morini S, Pedemonte F, Sola LB. 1999. Cardio pulmonary filariosis in the cat.Obiettivie Documenti Veterinari 20:39 46.

Venco L, Calzolari D, Mazzocchi D, Morini S, Genchi C. 1998. The use of echocardiography as a diagnostic tool for the detection of feline heartworm (Dirofilariaimmitis) infections. Feline Pract 26:6-9.

Zanotti S, Kaplan P. 1989. Feline dirofilariasis. Comp SA 11:1005-1018.


Figure 4-52. Dirofilariaimmitis. Microfilaria from dog blood as view with differential interfence contrast in a Knott’s preparation. Note that the width of the microfilaria at midbody is wider than a red blood cell ghost. Cats usually have very few circulating microfilariae.

Figure 4-53.Dirofilariaimmitis. Infective third-stage larva emerging from the proboscis of a mosquito.

Figure 4-54.Dirofilariaimmitis. Infective third-stage larva; it can be seen that this stage has a fully formed intestinal tract.

Figure 4-55.Dirofilariaimmitis. Damage to the brain of a cat by the ectopic migration of an adult worm.

Figure 4-56.Dirofilariaimmitis. Same lesion as the previous figure showing the extent of the damage.

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