Abstract

Kiwi (Apteryx sp.) numbers in the wild are declining. Their unique biology makes them susceptible to introduced predators. Incubating eggs removed from the wild, raising the chicks, and then releasing them back into the wild are being used on an experimental basis to overcome the effects of high neonatal mortality. The conservation status, biology, and the veterinary care of kiwi are discussed in this paper.

Introduction

There are at least four species of kiwi: the brown kiwi (Apteryx mantelli) in the north island and at Okarito in the south island, the tokoeka (Apteryx australis) in the southern south island and on Stewart island, the great spotted kiwi (Apteryx haastii) in the northern south island, and the little spotted kiwi (Apteryx owenii) now restricted to Kapiti Island and several offshore islands.¹

Due to the declining wild population, The Kiwi Recovery Program was launched in 1991 with the aim of “maintaining and, where possible, enhancing the current abundance, distribution and genetic diversity of Kiwi.”² Kiwi have been held in captivity since 1932 and the first captive breeding occurred in 1945.³ As of January 1998, the international studbook shows there are 80 kiwi held in captivity in 15 institutes in New Zealand and 34 held in 13 institutes overseas.⁴

Conservation Status

Reasons for Decline

The range and numbers of kiwi have been reduced since humans arrived in New Zealand, but particularly over the last 100 years. The reasons for the decline include forest clearance, which has reduced available habitat and produced fragmented populations. However, the most important factor is the introduction of predators. Possums damage eggs, mustelids and feral cats kill young chicks, and dogs and ferrets can kill adults. Up to 95% of all chicks are being killed within the first 2 months of life in some areas.⁵

Operation Nest-Egg

This has been established as an experiment to allow the hatchlings to grow to a weight where they can defend themselves in the wild. Eggs are removed from wild kiwi nests and incubated in artificial incubators. Ten institutes have been involved with varying success.⁵ Chicks are given earthworms within the first week and then are encouraged to eat the artificial diet. Birds are held in captivity for up to 5 months or until 1000 g, and then released. None of the released birds over 1000 g have succumbed to cats or stoats, but some of the birds have died due to other predators (e.g., dogs and ferrets). The plan is to change some of the release procedures and sites to improve success.

Biology

Flightless and with only vestigial wings remaining, kiwi occupy a secretive, nocturnal niche feeding on leaf litter and soil invertebrates, and fallen fruits. Adults will live on average 20 years in the wild but may live up to 40 years.

They have several unusual physical features. They have small eyes, but still have good night vision. They hear well and have an excellent sense of smell; the nostrils being uniquely placed at the tip of the long bill. The feathers are very simple, with a single rachis and unlinked barbs, and hang like hairs. Wings are vestigial and they have no tail. Legs are short and very powerful, and the feet have four toes with claws, which are used for fighting and digging. They also have paired functional ovaries, a remnant of a diaphragm, and a body temperature and metabolic rate which is lower than most birds.

Females are larger and heavier than males. The female lays one to two eggs, 2–4 weeks apart, which are very large and comprise up to 15–20% of the body weight of the female (approximately 375–450 g). The eggs have a very long incubation period (80–85 days). Each chick hatches fully feathered and first leaves the nest after 1 week, when it will feed unaccompanied. In the first seven days, a steady weight loss is normal. The chick will remain in the area until the next breeding season when it will disperse.

Common Health Problems

Trauma

Aggressive exchanges between birds have often resulted in the death of one of the birds. Trauma to the bill tip has been seen in captive kiwi. Repair is very difficult, due to the narrow fragile nature of the bill. Despite attempts at repair, the bill tip often becomes ischemic. Some birds have been known to adapt. Birds that have been caught in traps are sometimes brought to a captive facility. Often the leg is irreparable, and amputation is indicated. Birds will often adapt, but amputees only survive for short periods.

Embryonic Mortalities

Embryonic mortalities are commonly seen in kiwi eggs that have been incubated artificially. The standard procedure for incubation is not fully understood. Bacterial contamination is seen and abnormalities in yolk sac internalization are commonly seen in eggs subjected to high incubation temperatures. Incubation length should be 80 days plus. Chick and embryo deformities have been seen and these include crossed or bent bills, curled toes, and anophthalmia.⁶

Ventricular Foreign Bodies

Ingestion of foreign bodies has been a common cause of death in adult kiwi. Small nails, pieces of metal, and soft materials can be found in the substrate and are readily ingested, leading to perforation of the stomach wall and leakage of ventricular fluids into the coelomic cavity. This can often lead to peritonitis and death. Surgical removal by way of a proventriculotomy and treatment with broad-spectrum antibiotics has been successful. It is important when changing the substrate to check for foreign bodies. A metal detector can be helpful for identifying metal in the substrate.

Egg Related Peritonitis

Egg related peritonitis is a common cause of mortality in breeding females.⁷ Death has occurred within several days of laying in some birds. Considering the enormous size of the egg, it is not surprising egg peritonitis does occur commonly. Treatment consists of long-term antibiotics, supportive care, and possibly peritoneal lavage. It is important at all times to gently examine breeding females, especially immediately prior to egg laying, and to ensure the birds are not overweight.

Yolk Sac Retention and Infection

One of the common problems encountered in the first 3 weeks of life is retention of the yolk sac, with or without infection. Normally, the yolk should be absorbed within the first 2 weeks in most birds, but in certain instances yolk digestion and absorption slows or ceases.⁸ Clinical signs include continued weight loss beyond normal weight loss in the first 10 days, failure to eat, weakness, depression, dyspnea, abdominal distention, and often the inability to stand correctly.⁹ The retained yolk sac is often 20–40% of the body weight of the chick.⁸ Diagnosis is based on the symptoms and a doughy mass on abdominal palpation. Radiography reveals an enlarged mass. The etiology is not clearly understood, but includes sub optimal incubation conditions, excessive handling, systemic disease, or infection of the sac. Infection has been associated with E. coli, Proteus sp., and Streptococcus sp.⁹ Treatment consists of surgical removal, with enteral nutritional supportive care and broad-spectrum antibiotics.⁹

Cryptococcosis

This disease has been seen only once in the veterinary field in New Zealand. It was seen in a 22-year-old female North Island brown kiwi, Apteryx australis mantelli.¹⁰ No gross abnormalities were seen on necropsy. Several of the organs showed a multifocal to diffuse inflammatory reaction associated with cryptococcal organisms. The organism cultured from liver samples was Cryptococcus neoformans var gattii. It is thought that birds are not very susceptible to cryptococcus species because of their high body temperatures. It does not grow readily above 40°C. However, kiwi have a much lower body temperature (around 37.5°C). Cryptococcus will grow readily under these conditions. This organism is generally associated with two species of Australian gum trees, Eucalyptus camuldalensis and E. tereticornis.¹¹ Neither of these two species was found in the kiwi enclosure substrate. It is believed that this species of cryptococcus can be associated with other species of gum.¹²

Aspergillosis

Aspergillosis has been the cause of death several times in adult kiwi. Birds usually show weight loss, whilst still maintaining a reasonable appetite. Terminally they show dyspnea and marked depression. Characteristic fungal plaques are seen on air sacs and granulomata are seen in the lungs and throughout the coelomic cavity.

Coccidiosis

Coccidiosis has been seen in many kiwi. The disease is seen in the first 2 years of life, but most commonly in the first 6 months. The disease is associated with diarrhea, severe dysentery and melena, inappetence, dehydration, and weakness. Birds soon die if not treated. On histologic examination, a massive colonization of the intestinal mucosa associated with coccidial life-forms is seen.¹³ Evidence of various life-forms has also been seen in the renal pelvis in a 1-month-old kiwi and in the liver parenchyma, in the bile ductules, and in the pancreas of other kiwi.¹⁴ An inflammatory reaction was seen at each site. The etiology is presumed, at this stage, to be an Eimeria sp. Diagnosis is based on clinical signs and the presence of large numbers of oocysts on fecal flotation. The condition has been successfully treated with toltrazuril (Baycox, Bayer Ltd., New Zealand) at 7–10 mg/kg for 2 days. Supportive care is also required. The area where kiwis live should be ‘spelled’ wherever possible. Removal of all of the substrate to a depth of 30 cm and replacement with fresh leaf litter should be considered at least yearly. Regular fecal flotation should be performed on juveniles (e.g., every 3–4 weeks until 18 months of age). If oocysts are detected, they should then be treated and the substrate changed, or the bird removed from that area. Much is still to be discovered about the epidemiology, pathogenesis, and etiology of this condition and its presence in the wild is being evaluated.

Visceral Gout

Visceral gout has been seen on several occasions in chicks within 4 months of hatching. There have been no reports of this condition in adults. Chicks are usually found dead. Possible causes of gout include excessive protein in the diet coupled with high levels of calcium, vitamin D₃, and dehydration.¹⁵ Visceral gout was associated with congenital ureteral obstruction in one neonate.

Suspect Biotin/Pantothenic Acid Deficiency

Within 3 weeks of developing generalized skin lesions, several adult kiwis had died despite treatment. The lesions resembled seborrheic dermatitis. Exudative encrustations were seen on the head, around the mouth and ears and, later, on the feet.⁷ Histologically there was a marked hyperkeratosis with exfoliating sheets and inflammatory crusts associated with mixed bacteria and micro abscesses.⁷ The history indicated that the vitamin supplementation had been absent from the diet for only 3 weeks. Treatment with B vitamins quickly and successfully reversed the signs. Other birds died before a diagnosis was made. Similar conditions have been reported in other captive institutes. The condition most closely resembles biotin or pantothenic acid deficiency, which is seen in domestic chickens.¹⁶

Miscellaneous Health Problems

Generalized steatitis has been seen adult kiwis possibly associated with vitamin E deficiency. Adult birds have been found dead with significant hemorrhage in the coelomic cavity associated with hepatic lipidosis. Pneumoconiosis is seen commonly as an incidental finding in kiwi.¹⁷ It is thought to be associated with the inhalation of fine dust particles through the distally placed nostrils.

Coagulative necrosis of the lung, liver, and thymus, associated with tachyzoites, were seen in a juvenile little spotted kiwi. This was thought to be due to toxoplasmosis, but this has not yet been confirmed. Generalized avian tuberculosis has been seen in an adult kiwi. Miliary white nodules were seen throughout the liver, on the serosal surface of the spleen, gizzard, and the intestinal tract. Tetramisole toxicity and death has occurred when birds had been wormed with the anthelmintic, Aviverm™. The dose rate was not known. It is therefore not known whether it is a species related or a dose related sensitivity to the drug. Fenbendazole and ivermectin at standard dose rates are safe to use. The nematodes Cyrnea aptericis are found in the gizzard and Heterakis gracilicauda in the large intestine. Normally these nematodes cause little pathology, except when found in high numbers.

Literature Cited

1.  Baker A.J., C.H. Daugherty, R. Colbourne, and J.L. McLennan. 1995. Flightless brown kiwis of New Zealand possess extremely subdivided population structure and cryptic species like small mammals. Proc. Natl. Acad. Sci. 92: 8254–8258.

2.  Butler D., and J.L. McLennan. 1991. Kiwi Recovery Plan. DOC Threatened Species Rec. Plan Ser. No 2 Department of Conservation, PO Box 10420, Wellington.

3.  Billing, T. 1998. Captive management resources. In: Proceedings of the New Zealand Captive Management Advisory Group Meeting—Kiwi Recovery and the Contribution of Captive Management. In preparation.

4.  Wilcken, J. 1998. Population analysis: The captive population of North Island brown kiwi. ASMP, Sydney.

5.  Colbourne, R. 1998. Operation nest egg. In: Proceedings of the New Zealand Captive Management Advisory Group Meeting—Kiwi Recovery and the Contribution of Captive Management. In preparation.

6.  Bassett, S. 1998. Kiwi embryo mortality. In: Proceedings of the New Zealand Captive Management Advisory Group Meeting—Kiwi Recovery and the Contribution of Captive Management. In preparation.

7.  Boardman, W.S.J. 1995. Causes of mortality in North Island brown kiwis at Auckland Zoo 1960–1994. Kokako 2:1:11–13.

8.  Flammer K., and S.L. Clubb. 1994. Neonatology. In: Ritchie B., G. Harrison, and L. Harrison (eds) Avian Medicine: Principles and Application. Lake Worth, Wingers Publishing Inc 820.

9.  Cambre, R.C. 1992. Indications and technique for the surgical removal of the avian yolk sac. J. Zoo Wildl. Med. 23:55–61.

10.  Allan, F.I., A.J. Woodgyer, and M.A. Lintott. 1995. Cryptococcosis in a North Island brown kiwi (Apteryx australis mantelli) in New Zealand. J. Med. Vet. Mycology 33:305–309.

11.  Ellis, D.H., and T.J. Pfeiffer. 1990. Natural habitats of Cryptococcus neoformans var gattii. J. Clin. Micro. 28:1642–1644.

12.  Pfeiffer, T.J., and D.H. Ellis. 1992. Environmental isolation of Cryptococcus neoformans var gattii from Eucalyptus .tereticornis. J. Med. Vet. Mycology 30:407–408.

13.  Boardman, W.S.J, W.J. Hartley, A. Julian, K. McSporran, and B. Smits. Suspect coccidial infections in the North Island brown kiwi in New Zealand. In preparation.

14.  Thompson, E.J., and I.G.A. Wright. 1978. Coccidiosis in kiwis. NZVJ 26:167.

15.  Minsky, L. and M.L. Petrak. 1982. Miscellaneous and Metabolic Diseases. In: Petrak, M.L. (ed) Diseases of Cage and Aviary Birds. Lea and Febiger, Philadelphia, 638–645.

16.  Austic R.E. and M.L. Scott. (1991) Nutritional Diseases. In: Calnek BW (ed). Diseases of Poultry. 9th ed, Ames, Iowa, Iowa State University Press 51–58.

17.  Smith, B.L., W.S.H. Poole, and D. Martinovich. 1973. Pneumoconiosis in the captive New Zealand kiwi. Vet. Path. 10:94–101.