A Report on the Risk to NZ of Canine Heartworm (Dirofilaria immitis) and Quarantine Measures which could be considered Appropria

A Report on the Risk to New Zealand of Canine Heartworm (Dirofilaria immitis) and Quarantine Measures which could be considered Appropriate to reduce this Risk.

1. Summary

Environmental conditions in New Zealand are marginal for the transmission of Dirofilaria immitis although it would be possible for the parasite to become endemic but probably remain at a low prevalence. Known mosquito vectors are present and at least in some areas mosquito density is reasonably high. The temperature requirement for development of the infective larvae in mosquitoes would be the greatest limiting factor restricting establishment of this nematode. However, D. immitis is endemic in other areas around the world such as Melbourne, Australia and southern Canada which have not dissimilar summer temperatures to Auckland and Northland. D. immitis in these areas of Australia and Canada is usually at a low prevalence. If D. immitis was to become endemic in New Zealand it would only do so in Auckland or Northland because of temperature restrictions on larval development in mosquitoes. Establishment of D. immitis in New Zealand would be assisted by the long life expectancy of the parasite in dogs (up to about 5 years) which would allow periodic short-term warm temperature conditions to facilitate transmission. Given that approximately 1000 dogs annually come to New Zealand from Australia it could be expected that a small percentage are infected and would thus add to the pool of infected dogs from previous years. It is conceivable that as many as 50 or even more infected dogs may be present in New Zealand at any time. The slow onset of clinical signs or absence of clinical signs in dogs with few worms, combined with lack of awareness of the disease by practitioners in New Zealand, would mean many of these infected dogs are not diagnosed thus they continue as a source of microfilariae (first stage larvae).

Quarantine measures to reduce this risk would centre on imported dogs being shown to be free of circulating microfilariae, to be negative to an appropiate antigen-capture blood test and be treated on or soon after arrival with ivermectin or milbemycin oxime. The combination of these measures will still leave small "windows" where infected dogs may not be detected or be treated successfully.

2. Dirofilaria immitis

2.1 Introduction

There is no evidence that Dirofilaria immitis is endemic in New Zealand. A survey of 880 dogs in the Auckland and Whangarei areas in 1990 (sponsored by MSD AGVET) revealed no evidence of D. immitis infection in any dogs which had been continously resident in New Zealand. One dog had a suspicious serological test result but this animal had previously lived in Queensland, Australia. However D. immitis infections are periodically diagnosed in New Zealand in dogs imported from Australia. There are no import restrictions on dogs from Australia relating to D. immitis although at present approximately 1000 dogs travel to New Zealand from Australia annually.

2.2 Taxonomy

Dirofilaria immitis is a nematode of the Order Spirurida, Family Filariidae.

2.3 Life cycle

Adult D. immitis are normally found within the caudal pulmonary arteries of dogs and, less commonly, cats. Ferrets (Mustela putorius furo) are also susceptible (Miller and Merton, 1982). As the number of adult nematodes in an individual dog increases, they may also be found in the right ventricle and in very large infections they may also extend into the right atrium and possibly the vena cava (Calvert and Rawlings, 1983). This species is viviparous releasing fully formed microfilariae or first stage larvae into the circulation. These must be ingested by suitable mosquito intermediate hosts for development through to the infective third larval stage (L3) to occur. Over 60 species of mosquito have been identified as suitable intermediate hosts for D. immitis (Ludlam et al., 1970).

Development to the infective L3 takes 14-21 days but, as this is temperature dependent, it may be prolonged in cool temperatures (Dunsmore and Shaw, 1990). Minimum development times as short as seven (Konishi, 1989) or ten days (Christensen, 1977) have also been reported.

New definitive hosts are infected when the infective L3 leave the mosquito while it is ingesting a blood meal (McGreevy et al., 1974). Initial development of D. immitis occurs at the infection site. The moult from L3 to L4 occurs before day 3 post-infection (Kotani and Powers, 1982; Lichtenfels et al., 1985) although one study suggests it occurs from days 9 to 12 (Orihel, 1961). Some worms reach the dog's heart on days 70 to 85 with all worms arriving by days 90 to 120. The final moult to immature adults occurs about day 70 (reviewed by Abraham, 1988) although Lichtenfels et al.(1985) suggested it may occur as early as day 58. At this stage the nematodes are 2-4 cm in length. Mature male and female worms have mean lengths of 16 cm and 25 cm respectively. Microfilariae have been observed within female worms after 6 months (Taylor, 1960; Kotani and Powers, 1982; Orihel, 1961) with patent microfilaraemia observed by 7 - 9 months (Orihel, 1961; Kotani and Powers, 1982; Dunsmore and Shaw, 1990). The density of microfilariae in peripheral blood has been described as subperiodic with maximal number generally present late afternoon, early evening, but 5 to 20% still circulate even at minimum levels (reviewed by Abraham, 1988). They also exhibit seasonal fluctuations as well as daily (Sawyer, 1975).

2.4 Pathogenesis, Pathology and Clinical Signs

Adult heartworms damage the endothelial lining of the pulmonary arteries resulting in increased permeability to serum proteins and water leading to perivascular oedema. This is accompanied by the formation of characteristic villous proliferation of tissue within these arteries which progressively increase in size. Blood flow is obstructed and at least some flow is diverted to non-affected lobes of the lungs (reviewed by Rawlings and Calvert,1989).

Right-sided heart failure due to severe chronic heartworm disease is the result of protracted, elevated right ventricular afterload caused by pulmonary hypertension resulting from severe pulmonary arterial disease (Hribernik, 1989).

Clinical signs are usually related to the number of adult nematodes and the duration of the infection. Most heartworm infections are clinically inapparent for two or more years (Calvert and Rawlings, 1986). Small infections may continue to remain inapparent. With increasing severity a chronic cough will be noted together with some exercise intolerance, weight loss and the development of a dry, harsh coat. At this stage, radiography will detect some right ventricular enlargement and some pulmonary arterial changes. As clinical signs become more severe, the following may be seen: obvious weight loss, anorexia or cachexia, poor to nil exercise tolerance, polypnoea or dyspnoea with attempted exercise, syncope, haemoptysis, hepatomegaly, ascites and death (reviewed by Atwell, 1988a).

The most severe disease is seen after adult heartworms have died and their fragments have been swept into small pulmonary arteries (Rawlings and Calvert, 1989).

Some particular clinical syndromes may be seen occasionally. These include:

  1. Immune mediated occult disease - in this syndrome the dog's immune system destroys circulating microfilariae in the spleen, liver or lung and may result in severe, potentially fatal respiratory distress (Atwell, 1988b).
  2. Caval syndrome - a retrograde migration of adult worms into the vena cava occurs for unknown reasons. This mechanically obstructs blood flow, causes haemolysis due to mechanical trauma which may then induce disseminated intravascular coagulopathy. There are few treatment options and affected dogs frequently die (Hribernik, 1989).

As indicated above, heartworm disease is a potentially debilitating disease which may severely interfere with the quality of life of infected dogs and interfere with the physical capacity of working dogs and others. It may also cause death.

3. Suitable Mosquito Intermediate Hosts in New Zealand

Fourteen species of culicine mosquito are known to occur in New Zealand (Belkin, 1968). Of these, 11 are not known outside New Zealand. This culicine fauna of New Zealand has representatives of all the major phyletic lines although these indigenous species appear to have retained more primitive features than other living representatives of their phylads elsewhere. Three species have probably been introduced from external sources : Aedes australis (syn A. concolor), Culex quinquefasciatus (syn. C. fatigans) and Aedes notoscriptus. These three species are known overseas to be suitable intermediate hosts for D. immitis (reviewed by Russell, 1990) although there is only one early report of A. australis successfully transmitting D. immitis (Heydon unpublished cited by Woodhill, 1936). None of the indigenous species have been tested to see if they are suitable.

A. notoscriptus, as at 1968, was largely restricted to areas around sea ports (see Appendix 1) where it was probably introduced on ships (Graham, 1939; Belkin, 1968). It has now spread inland into rural areas aided by its utilisation of off-rim used tyres covering silage pits (Laird, 1990). In Australia, A. notoscriptus is found in all states, including Tasmania, (Lee et al., 1982) indicating its ability to survive in cool temperate areas. The extent, if any, that it has spread south in New Zealand has not been determined. It utilises a variety of still-water habitats including man-made containers as well as rot-holes in trees and ground pools (Belkin, 1968). It has been reported to be a frequent intruder into houses in Auckland but is essentially a sylvanspecies and is especially abundant in densely wooded gullies (Graham, 1939). It has been reported to feed on a variety of hosts, including man, horses, sheep, marsupials, poultry and dogs (reviewed by Lee et al., 1982). Graham (1929) in New Zealand indicated that it preferred to feed on cattle but will attack man. It would appear to have become increasingly adapted to domestic situations (Lee et al., 1982). A. notoscriptus was the second most common mosquito species isolated in the Northern Mosquito Survey of 1988-89 (Laird, 1990). In Australia, A. notoscriptus is the most readily infected of the six important vectors of D. immitis known there and is the species most likely to feed on dogs (Russell, 1990).

C. quinquefasciatus is a member of the Culex pipiens complex. C. quinquefasciatus is widespread throughout the tropics, subtropics and warm temperature regions of the world (Lee et al., 1982). For example, it is not permanently established in Melbourne, Victoria, but is believed to migrate into the area each summer (Lee et al., 1982). In New Zealand, as at 1968, C. quinquefasciatus appeared to be uncommon being largely confined to coastal areas around larger ports in the North Island (see Appendix 1) where it was probably introduced (Belkin, 1968). Laird (1990), however, found high concentrations of this species in Parnell, Auckland and in South Auckland and recorded it as the third most common species isolated in the Northern Mosquito Survey in 1988-89. Given the temperature restrictions for the species, it would not seem likely that it will greatly increase its range in a southerly direction in New Zealand, although there is one recorded isolation from Waitomo (Belkin, 1968) and another from Hamilton (Laird, 1990).

C. quinquefasciatus will breed in a wide range of non-saline standing water pools near human habitation (Van den Assem and Bonne-Wepster, 1964). Laird (1990) reported it to be utilising gully traps in and around Auckland. It is a domesticated species which mainly feeds at night on a variety of hosts including humans, poultry, other birds, horses, sheep, cattle, pigs and dogs (Lee et al., 1982). Preferred resting sites are the interior of buildings (Guinea, 1968).

Within the Auckland area, it could serve as an intermediate host for D. immitis, especially in these apparently focal areas of higher concentration but Russell (1990) only achieved an experimental infection rate of 6.5% for this species compared with 53.5% for A. notoscriptus indicating it was not a particularly important vector for D. immitis.

A. australis was not considered to be an important vector for D. immitis in Australia (Russell, 1990). This species only breeds in salt or brackish rock pools and in New Zealand is only distributed in the south of the South Island (Belkin, 1968). It has, however, been recorded from more temperate locations such as Sydney and Norfolk Island (Woodhill, 1936) suggesting it could become established in northern New Zealand. It was not recorded in the Northern Mosquito Survey, 1988-89 (Laird, 1990).

Culex pervigilans, an indigenous species of New Zealand, is the dominant, most common and widespread culicid in New Zealand (Belkin, 1968; Laird, 1990). There is a suggestion of some introgression of C. quinquefasciatus features in populations around Auckland (Belkin, 1968) suggesting the two species are closely related and may interbreed. It will utilise all types of ground water for larval development including both still and with a gentle flow (Graham, 1929). Its natural hosts appear to be birds and it has been reported that it does not seem to attack man very readily although most adult collections have been from indoors (Belkin, 1968). However, Laird (pers. comm.) suggested that this mosquito is a common biter of man and has also been observed at least once to bite a cat. Graham (1929, 1939) recorded it as sheltering in buildings over winter emerging to feed and breed during warm periods. Although no records exist to indicate if this mosquito feeds on dogs, it is possible that it will, at least occasionally, do so and due to its ubiquitous nature and similarity to C. quinquefasciatus, is perhaps another potential intermediate host for D. immitis.

3.1 Possible introduction of more mosquito species which are suitable as vectors for D. immitis

Aedes albopictus, which is a known intermediate host for D. immitis (Ludlam et al., 1970; Suenaga and Itoh, 1973), is not endemic in New Zealand. However, it has been intercepted in containers of used tyres from Japan on three recent occasions in 1993 : twice in Auckland and once in Christchurch (Laird, Calder, Thornton, Syme, Holder and Mogi, in press). Suenaga and Itoh (1973) have shown this is a suitable intermediate host in Nagasaki, Hokkaido, Japan, although Apperson et al., (1989) showed a local strain in North Carolina, USA, did not appear to be a suitable host. This species is a daytime feeder with a wide host range which includes dogs (Suenaga and Itoh, 1973).

Culex annulirostris is another known intermediate host of D. immitis which has been intercepted at least once on a ship in Auckland (Graham, 1939). This species is widely distributed in all states of Australia except Tasmania suggesting it could establish in New Zealand. It utilises various forms of groundwater for larval development (reviewed by Lee et al., 1982). In Australia it is an important vector of D. immitis (Russell, 1985).

The possibility of further suitable exotic mosquito species establishing in New Zealand is, therefore, a further argument for preventing D. immitis becoming established in New Zealand. If any became established they may have the ability to assist any focal endemic pockets of D. immitis to become more widespread. The introduction of exotic mosquito species would be assisted by the under-utilisation of larval habitats noted in New Zealand (Laird, 1990).

3.2 Survival of Mosquitos

At the cooler edge of their range, some mosquitos seek cool shelter after a blood meal and then hibernate over winter whereas others overwinter as larvae (Kettle, 1984). Hibernation of inseminated females is probably the commonest way of surviving winter (Kettle, 1984) and is the way most Culex species overwinter (Harwood and James, 1979). A. notoscriptus hibernates in both adult and larval forms in and around Auckland (Graham, 1939) whilst C. quinquefasciatus overwinters as larvae (Graham, 1939).

In general terms, females with ample food reserves may live 4 to 5 months particularly under conditions of hibernation but, during their period of greatest activity, female survival may average closer to 2 weeks (Harwood and James, 1979). Although a generalisation given the large number of mosquito species known (>1600), this does indicate that successful development of D. immitis may be restricted by the lifespan of adult female mosquitoes (only females take blood meals) particularly at cooler temperatures when development of D. immitis is slow. In one study the lifespan of A. notoscriptus averaged 37 days (range 2 to 104 days)(Laird, 1948).

Most female mosquitoes need a blood meal to develop a batch of eggs. Following oviposition, she will again seek a blood meal. They continue this cycle repeatedly (Kettle, 1984).

3.3 The Increased Geographical Distribution of D. immitis

This is a general phenomenon which has been observed around the world. The examples of North America and Australia are given below.

3.4 North America

In North America D. immitis is enzootic in an Atlantic and Gulf coastal zone stretching inland to the Mississippi river with the highest prevalence in the south east. The parasite is being recognised with increasing frequency along the western edge of this enzootic area (reviewed by Lok, 1988). There are also foci on the west coast of the USA including California where the prevalence has been observed to increase in the last 20 years (Lok, 1988) although it has been stable at about 1-2% during 1986-1988 (Wright and Boyce, 1989).

In Canada a series of veterinary practitioner surveys have been conducted since 1976. In that first year, 413 infected dogs were detected of which 19% had never left their home province. With increasing practitioner awareness more dogs were tested in subsequent years. The prevalence of infected dogs varied from 1-2% in 1979, 80, 81, 82, 83, 84 dropping to as low as 0.24% in 1988. However, by 1986 and 1988, 81% and 76% respectively of infected dogs had never left their home province indicating the parasite was firmly established although with a low prevalence. Three enzootic areas were apparent - one around Winnipeg in Manitoba, another around Montreal and the third in the southwest of Ontario. Most reported cases were from Ontario (Owen and Slocombe, 1986; 1987; Slocombe, 1978; 1990; Slocombe and McMillan, 1978; 1979; 1980; 1982; 1983; 1984; 1985; 1989).

3.5 Australia

D. immitis appears to be continuing to expand its range in Australia. In 1973 a survey of dogs in Sydney recorded a prevalence of 5% whilst in 1982-83 a prevalence of 12.6% was recorded in the same area. In 1992 a survey of dogs from council pounds in Sydney revealed a prevalence of 14.8% (Bidgood, 1992). Dogs from such pounds are usually young and Collins (pers.comm.) considers the prevalence in older, unprotected dogs in Sydney is probably about 30%. In cats the prevalence is very low with only two of 200 feral cats found to be infected (Kendall et al., 1991).

In 1946 in Melbourne, no evidence of D. immitis was noted in pound dogs whereas in 1982 a prevalence of 2.7% was recorded in similar dogs (reviewed by Lok, 1988) and in 1987 a prevalence of 6.5% was reported (Lording, 1988).

The apparent prevalence of heartworm in South Australia in 1988-91 was about 1% (Copland et al., 1992).

In Western Australia until the early 1980s, D. immitis was considered to be only endemic in the northern parts of the state and not in Perth (Edwards et al., 1989). A survey in the late 1980s found a prevalence of 2.8% in dogs which had not left the city (Edwards et al., 1989).

In Brisbane, Queensland, the prevalence in untreated dogs has increased from 10% in 1959 (Winter, 1959) to approximately 36% (Atwell and Carlisle, 1979; Welch et al., 1979). In Northern Queensland and in Darwin, Northern Territory, the prevalence in untreated dogs is approaching 90-100% (reviewed by Martin and Collins, 1985).

3.6 Key Epidemiological Factors which may Affect Establishment of D. immitis in New Zealand.

There are several key factors which affect the possibility of D. immitis establishing in New Zealand. They are:

1. Life expectancy of adult worms and microfilariae. Patent microfilaraemias have been observed 7½ years following a single infection (Newton, 1968). The life expectancy of microfilariae may be as long as 2½ years (Underwood and Harwood, 1939) although Dunsmore and Shaw (1990) indicate they only survive about 6 months.

Any infected dog moving permanently to New Zealand may be a potential source of microfilaria for many years. Even if treated with an adulticide, it may still pose a risk for a considerable time.

2. Slow onset of clinical signs. As noted above, clinical signs may not be apparent for two or more years although microfilariae may be in the circulation. Some dogs may never developovert clinical signs if their infections are small. Thus infected microfilaraemic dogs may live in New Zealand and never be diagnosed as such.

3. Absence of an effective immune response. There is only slight or no evidence of naturally acquired protective immunity in dogs (Grieve, 1992). As a consequence, in endemic areas dogs need to be treated prophylactically throughout life. There is little prospect for a vaccine in the near future although research is proceeding.

4. Occult infections. Absence of microfilariae may be due to (1) prepatent infection, (2) single-sex infection, (3) drug-induced or (4) immune-mediated factors. The incidence of occult infections has been variably quoted as 15% (Calvert and Rawlings, 1983), 10-67% (Calvert and Rawlings, 1986), 5-10% (reviewed by Wong et al., 1973) and 41% (Courtney et al., 1990). Occult infections will affect the sensitivity of diagnostic tests which rely on detecting microfilaria. However, unless the reason is that the infection is prepatent or drug-induced, these dogs probably present only a small risk for introducing the nematode into New Zealand.

5. Transplacental migration of microfilariae. Microfilariae are known to be able to cross the placenta but the L3 to adult stages are not capable of same (Calvert and Rawlings, 1983). Thus a patent infection may not be contracted from an infected dam. However, puppies less than six months of age may have a microfilaraemia although microfilaria counts are low and quickly disappear (Baldock, 1988). Antigen-capture assays may not detect these microfilaraemic pups as they usually utilise adult antigens. However, these young dogs would seem to be of negligible significance when considering the establishment of D. immitis in New Zealand.

6. Feline heartworm. Feline heartworm disease is consistently diagnosed in heartworm endemic areas but at a lower incidence than in dogs (Dillon, 1986). The cat is considered to be a relatively resistant host for D. immitis (Hribernik, 1989). Heartworm disease is more difficult to establish in cats than dogs (Donahoe, 1975; Fowler et al., 1972; Wong et al., 1983) with the percentage establishment of infective larvae substantially lower than in dogs (Donahoe, 1975). Worm burdens are lower than in dogs and their lifespan is shorter (probably less than two years) (Donahoe, 1975). More importantly, microfilaraemia is uncommon (fewer than 20% of cases) and is low or transient when present (Donohoe, 1975). Cats, therefore, represent only a small risk for the introduction of D. immitis to New Zealand.

7. Sex and breed difference of dogs. The ratio of infected male to female dogs has been found to be as high as 4:1 (Lewis and Losonsky, 1978). In addition, dogs that live outdoors are more at risk and large dogs appear more susceptible than small (Lewis and Losonsky, 1978; Wright and Boyce, 1990). These factors are of little relevance as dogs of all sizes and either sex may be infected and therefore would need to be considered equally in any quarantine regulations.

8. Number of larvae developing in a mosquito. On average, less than 10 infective larvae develop in a single mosquito and commonly only 1 to 5 are recovered, although higher numbers have been recorded in laboratory infections (Otto, 1969; Russell, 1985). Therefore, a single mosquito bite would usually result in only a small infection in a single dog. The likelihood of a single dog in New Zealand being infected on several occasions to get a large infection is small and probably restricted to dogs living with, or adjacent to, an infected dog in an area with a high mosquito density. Therefore it is likely that the initial infections with D. immitis in New Zealand will be small, may not become clinically apparent, and will thus remain undetected.

9. Dog density. D. immitis is more likely to be transmitted in an urban area where the dog density is high. In rural areas, dogs represent a smaller proportion of the available hosts on which mosquitoes can feed and the risk of transmission should be lower.

10. Mosquito dispersal. Mosquitoes may disperse up to 100 km but, in general, they rarely disperse very far. Aedes aegypti, for example, rarely disperses > 0.5 km, Anopheles gambiae rarely disperses >3 km but some such as Anopheles funestus may disperse up to 7 km (reviewed by Kettle, 1984).

While the limited dispersal of mosquitoes would restrict the spread of D. immitis from an initial focus, it would probably have little effect on the chance of an infected mosquito finding another dog, particularly in urban areas.

11. Temperature requirements for development - comparison of New Zealand regions with experimental studies. At 18°C development (in Aedes vexans) continued to the infective stage in a minimum of 27 days whilst at 26°C the time required reduced to a minimum of 14 days (Jankowski and Bickley, 1976). Similarly, complete parasite development was reported at 18.5°C, 22.5°C, 30.5°C and 34.5°C (in Aedes trivittatus) but at 14.5°C no development occurred although the nematodes survived and subsequently resumed development when the temperature was increased to 26.5°C (Christensen and Hollander, 1978). The optimum temperature for larval development was considered to be 22.5 to 26.5°C (Christensen and Hollander, 1978). In a separate study (in Anopheles quadrimaculatus) again no larval development was noted at 15.6°C but larvae survived and resumed development when the temperature was increased to 26.7°C moulting to L3 after 30 days. At 21.1°C development was slow and asynchronous (Kutz and Dobson, 1974).

No consideration would appear to have been made for daily fluctuations in temperatures and their effect on larval development especially around the lower temperature limit. Given the ability of larvae to survive at 14-15°C and resume development when temperatures rise, the effect of daily variation around the lower limit is probably to extend the time required to reach L3 rather than to prevent it.

The ability of D. immitis to remain viable in overwintering adults is unknown (Russell, 1989) but if it is not possible then transmission must be seasonal. A. notoscriptus is considered to be able to hibernate overwinter as an adult (Graham, 1939).

Examination of Appendix 2 shows that for areas north of and including Auckland, there are 3-4 months where mean temperatures are 18°C or above. For Gisborne and Napier this reduces to only two months. If seasonal transmission is to occur, the time available is limited particularly as development at these temperatures will be slow.

11. Temperature requirement for development - comparison with other known endemic areas. An alternative approach is to examine mean temperatures of known endemic areas around the world and compare these with New Zealand. Some of these are shown for North America, Japan and Australia in Appendix 2.

Sydney, Adelaide and Perth generally have warmer summer temperatures than the north of the North Island. Melbourne's summer temperatures are more similar to those of Auckland and Northland except the mean daily maximums are higher for Melbourne which presumably would assist larval development during the warmer daylight hours. Launceston, Tasmania, has similar mean temperatures to Tauranga and Gisborne but there are no reports of D. immitis being endemic in Tasmania (as yet!), suggesting these temperatures are unsuitable for larval development.

Mean daily summer temperatures for Winnipeg and Montreal, Canada, are similar to the north of the North Island except the mean daily maximums are higher. There have been no suggestions that D. immitis has become endemic in more northerly and hence cooler areas of Canada.

Nagasaki, Japan, has quite warm summer temperatures suggesting there may be as many as six months that are suitable for larval development.

It would seem, given the current state of knowledge, that temperatures in New Zealand are marginal for larval development of D. immitis. This would appear to be the most important limiting factor for the successful establishment of this nematode in New Zealand. This assumes that strains of this nematode will not evolve, e.g. in southern Australia, which can develop at cooler temperatures.

3.7 Diagnosis of Heartworm Infection

Diagnosis traditionally has relied on identification of microfilariae, usually by a concentration technique, where at least 1 ml of a dog's blood is examined. Any microfilariae found have to be distinguished, usually on size but also morphology and differential staining, from those of the closely-related nematode Dipetalonema reconditum.

Early serological techniques relied on detecting antibodies to D. immitis. However, these tests are unreliable and their accuracy varies tremendously (Atwell, 1988b). The diagnostic tests of choice are those which detect circulating parasite antigen (Atwell, 1988b). Appendix 3 summarises the sensitivity, specificity and accuracy of several commercially available diagnostic kits which detect circulating antigen (from Atwell, 1988b). These kits generally detect adult antigen and are not capable of detecting immature infections. As can be seen in Appendix 3b they also have difficulty detecting small infections.

4. Recommendation for Quarantine Measures to Prevent the Importation of D. immitis with Dogs from Australia

4.1 Adult dogs continuously resident in Australia

These dogs should have a negative serological test for circulating D. immitis antigen. Appendix 3 lists several such diagnostic test kits and their performance characteristics. The appropriate tests that may be used will probably change with time as new kits become available and others disappear. The availability of these in Australia would need to be reviewed periodically and gazetted accordingly. The antigen-capture diagnostic kits currently available in Australia are CiteR, DirocheckR, DiromailR and VetREDR. Blood from adult dogs (>6 months) should also be tested for the presence of microfilariae by an appropriate concentration technique. This need not be stated in detail, rather a stipulation that 1 or 2 mls of blood be examined by an appropriate filtration and staining technique or a Modified Knott's Procedure.

On arrival in New Zealand, dogs should be treated with either ivermectin at 0.006 mg/kg (Heartgard30, MSD Agvet) or milbemycin oxime at 0.5 mg/kg (Endovet, Ciba-Geigy). Both these anthelmintics are recommended to be used at these dose rates as once-a-month prophylactic treatments against immature D. immitis (see Appendix 4 for Technical Manuals for these products). Ivermectin (0.006 mg/kg) as a single treatment has also been shown to be effective at either 1.5 or 2 months post-infection (McCall et al., 1986; Paul et al., 1986; Ohishi et al., 1987). Milbemycin oxime (0.5 mg/Kg) has also been shown to be effective against slightly older larvae if given at both 60 days and again at 90 days post-infection (see Technical Manual Appendix 4). Unfortunately neither anthelmintic is effective against adult D.immitis. The efficacy of ivermectin (0.006 mg/Kg) against L3 D. immitis is lower than against later larval stages as a small number (5.7%) of adult worms developed in dogs treated 1 day after an experimental infection of 111-121 infective larvae whilst no adults were recovered in dogs treated at 30 or 60 days (Ohishi et al., 1987). Efficacy of milbemycin oxime against L3 D. immitis would not appear to have been determined.

A single treatment on arrival may allow a "window" between efficacy of either anthelmintic and detection by antigen-capture assay. A small "window" also exists with the reduced efficacy of ivermectin and possibly milbemycin oxime against L3 D. immitis. A follow-up blood test using an antigen-capture assay 5 to 6 months post-importation should detect most D. immitis which escaped initial detection or treatment on arrival but this would be difficult to enforce. A follow-up anthelmintic treatment one month after arrival would probably improve efficacy of both anthelmintics. Again, this follow-up option would be difficult to enforce. Another alternative would be to accept certified prophylactic treatments with the above products at monthly intervals for the 6 months preceding departure for New Zealand. However, most owners would probably not make enquiries about quarantine regulations in sufficient time to allow this option to be utilised.

4.2 Young Dogs

If less than 70 days of age, tests for circulating antigen will be of no use as they rely on the presence of adults. Similarly, no circulating microfilariae will be detected in dogs less than 6 months-of-age unless they represent a non-patent infection which is the result of microfilariae crossing the placenta from the dam. Young dogs should be treated on arrival as for older dogs in 1. above and similar alternatives to those in 1. above will also need to be considered. Ivermectin and milbemycin oxime are not recommended for use in dogs under 6 and 8 weeks weeks-of-age respectively.

4.3 Dogs visiting Australia temporarily

These dogs should be given monthly prophylactic treatment with either milbemycin oxime at 0.5 mg/kg (Endovet, Ciba-Geigy) or ivermectin at 0.006 mg/kg (Heartgard, MSD Agvet). If absent from New Zealand for less than one month, they should be treated on arrival back in New Zealand with either of these anthelmintics. If absent for more than one month, appropriate certification of monthly treatment will be required. If not, these dogs should be considered as for 1. The potential for a small "window" associated with decreased efficacy against L3s also exists with these dogs.

4.4 Declare Dirofilaria immitis as a Scheduled Disease

This will ensure that any foci of D. immitis infections that do develop will be controlled. Infected dogs can be treated and this would usually be in the best interests of the animal's health. Euthanasia is not a necessary course of action. Initially adult worms need to be killed using thiacetarsamide. The usual dose recommended is 2.2 mg/kg morning and night. However, the average worm kill at this dose rate was found to be 63% with only 40% of dogs being cleared of adult parasites. A 20% increased dose at each treatment increased efficacy to 94% but also increased the likelihood of adverse reactions. Dogs need to be monitored carefully during adulticide therapy with thiacetarsamide as toxic reactions may occur in up to 4% of dogs treated with the 2.2mg/kg regime (reviewed by Courtney, 1988). Additional supportive treatment such as cage rest and aspirin medication is recommended. New adulticides are being developed and should be available shortly. These should offer a higher efficacy and fewer side effects.

Adulticide treatment should be followed several weeks later with microfilaricidal treatment.

Dithiazanine iodide is the only licensed microfilaricide in the USA at a dose of 4.4 mg/kg/day for 7 days (Courtney, 1988) or 8.8 mg/kg/day for 7 days (Calvert and Rawlings, 1983). In Australia this product is not available and use is made of levamisole (11 mg/kg/day for up to 12 days) but side effects, especially vomiting, are common requiring therapy to be discontinued and reassessed (Calvert and Rawlings, 1983). The most effective microfilaricide is ivermectin (0.05 mg/kg) (Rawlings and Calvert, 1989) but this is an extralabel use not recommended by the manufacturers. Adverse reactions, especially in the Collie breed, may occur. In addition, all dogs may show shock-like clinical signs, which are not usually fatal, associated with the rapiddeath of large numbers of microfilariae following ivermectin treatment (Rawlings and Calvert, 1989).

Success of adulticide treatment can be monitored with antigen-capture diagnostic kits. Detection of a persistent microfilaraemia is also suggestive of the continued presence of adult nematodes.

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Appendices

Appendix 1: Distribution of Aedes notoscriptus and Culex quinquefasciatus at 1968 (from Belkin 1968)

Location Jan Feb Mar Apr May June July Aug Sept Oct Nov Dec
Kaitaia 19 (15-23.5) 20 (16-24) 19 (14.5-23) 17 (13-20.5) 15 (11.5-18) 13 (9.5-16) 11.5 (8-15) 12 (9-15.5) 13 (9-17) 14.5 (11-18) 16 (12.5-20) 18 (13.5-22)
Dargaville 18.5 (14-23) 19.5 (14.5-24.5) 18 (13-22.5) 16 (11-20.5) 14 (9.5-18) 12 (8-16) 10 (6-14.5) 11 (7-15.5) 12 (7.5-16.5) 14 (10-18.5) 15.5 (11-19.5) 17 (12.5-21.5)
Auckland 19 (15.5-23) 19.5 (16-23) 18.5 (15-22) 16.5 (13-20) 14 (11-17) 12 (9-15) 11 (8-14) 11.5 (8-14.5) 12.5 (9-16) 14.5 (11-17.5) 16 (12.5-19.5) 17.5 (14-21.5)
Tauranga 18.5 (8.5-18.5) 19 (14-24) 17.5 (12.5-17.5) 15 (10-20) 12.5 (8-17) 10 (5.5-14.5) 9.5 (4.5-14) 10 (5.5-14.5) 11.5 (7-16.5) 13.5 (9-18) 15 (10.5-20.5) 17 (12-22)
New Plymouth 17 (13-22) 17.5 (14-17.5) 16.5 (13-20.5) 14.5 (11-18) 12.5 (9-15.5) 10.5 (7-13.5) 9.5 (6-13) 10 (6.5-13.5) 11.5 (8-15) 12.5 (9-16) 14 (11-17.5) 15.5 (12-19)
Gisborne 18.5 (13-24.5) 19 (13.5-24.5) 17 (11.5-22.5) 15 (10-17) 12 (7-17) 10 (5-14.5) 9 (4.5-14) 10 (5-14.5) 11.5 (6.5-16.5) 13.5 (8-18.5) 15.5 (10-21) 17.5 (12-23)
Napier 19 (14-23.5) 19 (14.5-23.5) 17 (12.5-21.5) 15 (10.5-19.5) 12 (7.5-16) 9.5 (5-14) 8.5 (4-13) 9.5 (5.5-14) 11.5 (7-16) 14 (9-18) 16 (11-20.5) 17.5 (13-22)
Palmerston North 17 (12.5-22) 17.5 (12.5-22.5) 16 (11.5-20.5) 14 (9.5-18) 11 (7-14.5) 8.5 (4.5-12.5) 8 (4-11.5) 9 (5-13) 10.5 (6.5-14.5) 12.5 (8-16.5) 14 (10-18.5) 16 (11.5-20.5)
Wellington 16 (12.5-19.5) 16.5 (13-20) 15.5 (12-19) 13.5 (10.5-16.5) 11 (8-13.5) 8.5 (6-11.5) 8 (5.5- 10.5) 9 (6-10.5) 10 (7-13) 11.5 (8.5-15) 13.5 (10-17) 15 (11.5-18.5)
Westport 15.5 (11.5-19.5) 16 (12-20) 15 (11-19) 13 (9-17) 11 (7-14.5) 8.5 (5-12.5) 8 (4-12) 9 (5-13) 10 (6-14) 11.5 (8-15) 13 (9-16.5) 14.5 (10.5-18)
Nelson 17.5 (12.5-22) 17.5 (12.5-22) 16 (11-21) 13.5 (8.5-18) 10 (5.5-15) 7.5 (3-12.5) 7 (2-12) 8 (3.5-13) 10 (5.5-15) 12 (7.5-17) 14 (9-19) 16 (11-20)
Blenheim 17.5 (11.5-23) 18 (12-23.5) 16 (10-21.5) 13 (7.5-18.5) 10.5 (5-15.5) 7.5 (2.5-13) 7 (2-12.5) 8 (3-14) 10.5 (5-16) 12.5 (7.5-18) 14.5 (9-20) 16.5 (11-21.5)
Christchurch 16.5 (11.5-21.5) 16 (11.5-21) 14.5 (10-19) 12 (7.5-16.5) 9 (4-13.5) 6 (2-10.5) 6 (1.5-10) 7 (2.5-11.5) 9.5 (4.5-14) 12 (7-17) 13.5 (8-19) <15.5 (10.5-20.5)
Dunedin 15 (11-19) 15 (11-19) 13.5 (9.5-17.5) 11.5 (8-15) 9 (5.5-12.5) 6.5 (3.5-10.5) 6.5 (2.5-10) 7.5 (3.5-11) 9.5 (5-14) 11 (7-15.5) 13 (8.5-17) 14 (10-18)

Appendix 2a: Mean daily temperatures (mean daily minimum - mean daily maximum) as °C for various New Zealand centres (from Gerlach, 1974). The shaded area represents months with a mean temperature >18°C.

Location Jan Feb Mar May June July Aug Sept Oct Nov Dec
Brisbane 25 (17 to 35) 25 (17 to 34) 24 (16 to 33) 21 (12 to 31) 18 (8 to 28) 16 (6 to 25) 15 (4 to 24) 16 (5 to 27) 18 (8 to 30) 21 (11 to 33) 22 (14 to 34) 24 (16 to 36)
Sydney 22(14 to 35) 22 (14 to 33) 21 (13 to 32) 18 (10 to 28) 16 (7 to 23) 13 (5 to 21) 12(4 to 21) 13(5 to 23) 15 (7 to 28) 18 (9 to 32) 19 (11 to 33) 21 (12 to 35)
Melbourne 20 (9 to 39) 20 (9 to 38) 18 (7 to 35) 15 (5 to 29) 12 (3 to 23) 10 (1 to 18) 10 (1 to 17) 10 (1 to 21) 12 (2 to 24) 14 (3 to 29) 16 (6 to 33) 18 (8 to 37)
Adelaide 23 (11 to 42) 21 (11 to 41) 21 (9 to 38) 17 (8 to 32) 15 (6 to 26) 12 (3 to 20) 11 (3 to 19) 12 (3 to 23) 13 (4 to 27) 16 (5 to 33) 18 (7 to 37) 21 (9 to 41)
Perth 23 (12 to 39) 24 (12 to 39) 22 (11 to 37) 19 (8 to 33) 16 (7 to 27) 14 (5 to 23) 13 (4 to 20) 14 (4 to 23) 15 (6 to 26) 16 (7 to 29) 19 (9 to 35) 22 (11 to 38)
Launceston 18 18 16 13 10 8 8 8 10 12 15 16
Hobart 16 (7 to 23) 16 (8 to 32) 15 (6 to 31) 12 (4 to 24) 10 (2 to 21) 8 (1 to 16) 8 (0 to 16) 9 (1 to 18) 11 (2 to 22) 12 (2 to 26) 14 (4 to 30) 15 (6 to 31)
Winnipeg -18 (-38 to -1) -16 (-36 to 2) -8 (-29 to 8) 3 (-14 to 22) 11 (-5 to 29) 16 (2 to 32) 20 (6 to 33) 19 (3 to 33) 13 (-3 to 29) 6 (-9 to 22) -5 (-24 to 11) -13 (-34 to 3)
Montreal -10 (-27 to 6) -8 (-24 to 5) -2 (-19 to 9) 6 (-7 to 21) 13 (1 to 27) 19 (7 to 30) 21 (11 to 32) 20 (9 to 31) 15 (3 to 28) 9 (-3 to 22) 2 (-13 to 14) -6 (-23 to 7)
Nagasaki 6 (-3 to 17) 8 (-3 to 17) 10 (0 to 21) 15 (4 to 24) 18 (9 to 27) 22 (14 to 30) 26 (18 to 33) 27 (21 to 33) 24 (15 to 32) 19 (9 to 27) 14 (3 to 23) 9 (-1 to 19)

Appendix 2b: Mean daily temperatures (mean daily minimum to mean daily maximum) in °C for various locations where D. immitis is endemic (Rudloff, 1981). The shaded area represents months with a mean temperature >18°C.

  Sensitivity (%) Specificity (%) Accuracy (%)
aDifil II® 70 90 80
aDirochek® 33-90.3 84-99.1 58.5-94.8
aDirokit latex® 84.3-85.3 88.8-95.7 86.7-89.5
aDiromail® 78-100 96-100 92-100
aFilarochek® 67-97.3 85-98.2 78.5-97.7
bVetRED® 96.9-100 96.8 -

Appendix 3a: Results of Commercial Tests to Detect Antigen in Circulation

(a reviewed by from Atwell [1988b]; b Bundesen et al., 1990).

  Cite Heartworm ® Dirochek ®
Positive (%) Negative (%) Positive (%) Negative (%)
Heartworm absent 0 100 3.4 96.6
Heartworm present 83.3 16.7 85.6 14.4
patent infection 98 2 100 0
1 to 2 worms present 50 50 53.2 46.8
3 to 5 worms present 71 29 77.4 22.6
6 to 10 worms present 87.8 12.2 91.8 8.2
11 to 20 worms present 98.1 1.9 96.2 3.8
> 20 worms present 99.1 0.9 100 0

Appendix 3b: Comparison of two commercially available diagnostic kits to detect circulating antigen (Courtney et al., 1990)

  Sensitivity (%) Specificity (%) Accuracy (%)
Dirokit latex®
(Agen Biomedical Ltd.) 		82.9-85.3 95.7-100 87.7-89.5
Diromail®
(Agen Biomedical Ltd.) 		92.2 97.4 94.5
Dirochek®
(Synbiotics) 		92 99 95.4
Filarochek®
(Mallinckrodt) 		97.3 98.2 97.8

Appendix 3c: Sensitivity, Specificity and Accuracy from Technical Bulletins for some commercially available diagnostic kits to detect circulating antigen.

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