The Diseases By Organ System

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The digestive system

Digestive disorders represent by far the most prevalent and chronic form of disease in captive giant pandas (Bush et al, 1985; Goltenboth, 1985a,b; Villares et al., 1985; Pan et al., 1991; Gual-Sil et al., 2000; F. Ollivet, unpublished data, pathology report, Paris Zoo). Gastrointestinal disease is the leading reported cause of death in captive pandas and also maybe so in free-ranging counterparts (Qiu & Mainka, 1993). Cubs often develop bouts of diarrhoea within the first month of life, particularly if hand reared on artificial milk replacer (I. K. Loeffler, unpublished observations). Cubs raised on milk replacer and recent weanlings often develop diarrhoea that can become a chronic condition. Episodes of abnormal stool, abdominal pain, passage of mucous faeces, vomiting and inappetance occur frequently, if not chronically, throughout the lives of many giant pandas ex situ.

Pathology of the oral cavity

A condition identified during the CBSG Biomedical Survey described as Stunted Development Syndrome (Zhang et al, 2000; see Chapters 4 and 15) is characterised by slow growth, small body size, ascites, infertility, general unthriftiness and chronic digestive problems. The individuals affected with this syndrome typically also have dental abnormalities characterised by severely worn, discoloured teeth, dentine exposure and enamel hypo- or dysplasia (Fig. 16.7; Plate XX). The cause of the dental abnormalities in these pandas is unknown, although possible aetiologies include pre- or neonatal exposure to canine distemper virus, malnutrition, fluorosis or early exposure to other infectious agents or toxins. Worn and broken dentition and open root canals are also a fairly common finding in giant pandas ten years old or older (Zhang et al., 2000; see Chapters 4 and 15).

Hypo Enamel Dysplasia
Figure 16.7. Giant pandas with Stunted Development Syndrome have dental abnormalities characterised by severely worn, stained teeth with dentine exposure (black arrow) and enamel hypo- or dysplasia (blue arrow). (See also Plate XX.)

An oropharyngeal fistula and sublingual abscess were diagnosed in a 28-year-old male giant panda (SB 121) at the Smithsonian's National Zoological Park (R. Montali, unpublished data, pathology report). The lesion appeared to be associated with a bamboo fragment which had migrated under the tongue. This animal was severely ill with chronic renal failure at the time and, despite two surgical treatments, the lesion failed to heal. Post-mortem examination revealed a fistulous pocket of abscessed material found caudolateral to the base of the tongue which was lined with fibrous connective tissue that extended into the oropharynx.

Gastrointestinal distress and faecal mucus excretion

Giant pandas are often observed to experience episodes of gastrointestinal discomfort, apathy and inappetance (particularly for bamboo) which are followed by faecal mucus excretion and then immediate relief. The frequency of these bouts of catarrhal colitis varies among institutions and individual animals. The male giant panda (SB 140) at Paris Zoo had a history of chronic abdominal pain with anorexia, groaning, faecal mucus and occasional vomiting from the age of 11 years. The condition was managed symptomatically with spasmolytic and demulcent therapy. This individual died at 27 years of age, and necropsy findings included chronic ulcerative and necrotising, suppurative colitis with local colonic perforations and chronic peritonitis (F. Ollivet, unpublished data, pathology report, Paris Zoo). To what extent the 16 years of intermittent colitis or the nonsteroidal antiinflammatory drug (NSAID) treatment the panda received for musculoskeletal pain toward life's end contributed to the colonic ulcers and perforations is not known.

Cytological examination of excreted mucus often reveals mild granulocytic inflammation, but does not point to obvious aetiologies (B. Rideout, unpublished observations). Mucus excretion and gastrointestinal pain may be associated with insufficient dietary bamboo. However, the association between mucus excretion and bamboo may be entirely coincidental, and other aetiological possibilities have not been fully explored. For example, pathogenic organisms have occasionally been cultured from mucous faeces (Goltenboth, 1985a; Villares et al, 1985; Gual-Sil et al, 2000), but not to an extent that could strengthen a causative association. Spore-forming, Gram-positive rods are also occasionally seen in smears of excreted mucus but likewise have not been correlated with clinical disease or mucoid stools (see Chapter 15).

Parasites

Frequent, unexplained episodes of gastrointestinal pain in the giant panda may be associated with parasites or (sometimes consequent) intestinal obstruction. Mortalities due to pancreatitis in the freeranging giant panda have been associated with parasite burdens and blockage of pancreatic ducts by ascarids (Qiu & Mainka, 1993). Although there was no reference to bile-duct obstruction in the latter citation, this could be an associated pathological finding. Baylisascaris schroederi is the only endoparasite that appears to be consistently recognised in the giant panda (Fig. 16.8). Larvae of this ascarid hatch in the intestine and penetrate the intestinal wall to enter the portal circulation to the liver and lungs where their migration may cause extensive inflammation and scarring. Eggs of this roundworm are notoriously difficult to observe upon faecal examination, probably because they are shed intermittently and because the high roughage content of the faeces interferes with routine laboratory detection. Pandas whose faecal examinations have produced repeated negative egg counts can suddenly vomit bundles of ascarids (D. Janssen, pers. comm.). Treatment of individuals (including those with possible false-negative results for B. schroederi eggs)

Baylisascaris Schroederi

Figure 16.8. Baylisascaris schroederi is a common intestinal nematode of the giant panda. The parasite has a life-cycle similar to other roundworms in which infective eggs are ingested by the host, the larvae hatch and penetrate the intestinal mucosa where they mature and return to the small intestine as adults 2.5 to 3 months later. Evidence of visceral larval migrans is often apparent upon necropsy.

Figure 16.8. Baylisascaris schroederi is a common intestinal nematode of the giant panda. The parasite has a life-cycle similar to other roundworms in which infective eggs are ingested by the host, the larvae hatch and penetrate the intestinal mucosa where they mature and return to the small intestine as adults 2.5 to 3 months later. Evidence of visceral larval migrans is often apparent upon necropsy.

with antiparasitic drugs may require multiple doses until the animal ceases to expel worms or shed eggs in faeces (Goltenboth, 1985a; Leclerc-Cassan, 1985; L. Spelman, unpublished observations, clinical records, Smithsonian's National Zoological Park). Yang (1998) provides one of the few descriptions of other intestinal parasites in the giant panda, including a hookworm (Ancylostoma caninum), another roundworm species (Toxocara selenactis) and a protozoan (Sarcocystis sp.).

The incidence of parasitism and its clinical significance to captive giant pandas is unknown. Analysis of haemograms during the CBSG Giant Panda Biomedical Survey (Zhang et al., 2000; see Chapters 4 and 15) frequently demonstrated an eosinophilia, which suggests parasitism or an allergic response. Protozoa such as Giardia, coccidia and Crypto-sporidia may cause subclinical disease that could become important in the context of other stressors. Ascarids may compromise nutritional status by directly interfering with nutrient absorption or by causing pathological changes to intestinal tissue. Hookworms cause mucosal haemorrhage or blood extraction that, in turn, may lead to anaemia and critical illness in young animals. Migrating larvae may cause extensive damage to hepatic or pulmonary parenchyma, which may be especially harmful to young, developing individuals. High parasite loads in females may be detrimental to a nursing mother (due to the high energy demand of lactation) as well as to her offspring because of the presumed lactational transmission of recrudescent larvae (as occurs with roundworms in the dog and cat). The impact of an endoparasitic infection on cub development is unknown but is an important topic for further investigation.

Enteritis and diarrhoea

Haemorrhagic enteritis and bacterial diarrhoeas occur relatively frequently in giant pandas and appear to be associated with a variety of potential aetiologies (Bush et al, 1985; Villares et al, 1985; del Campo et al., 1990a; Qiu & Mainka, 1993; Gual-Sil et al., 2000). Bacterial pathogens such as E. coli (del Campo et al, 1990a), haemolytic and nonhaemolytic Streptococcus, Salmonella (Villares et al., 1985; Gual-Sil et al., 2000) and Clostridium (Dammrich, 1985) have been implicated in various reports, although definitive diagnoses of the primary or underlying problems have not been made.

Faecal culture of an adult male giant panda (SB 187) at the Madrid Zoo who suffered frequent gastrointestinal disturbances demonstrated E. coli proliferation nearly every time he was ill (del Campo et al, 1990a). The predisposing factors of the recurrent infection remain unknown. Three endoscopies over four years revealed (at various times) pseudo-membranous colitis, haemorrhagic gastritis and oesophagitis (del Campo et al, 1990a). Madrid Zoo veterinarians performed an experimental oral inoculation on this panda with flora from normal faeces of another giant panda (SB 249) who also had suffered symptoms of gastrointestinal distress, but less frequently. The oral inoculations were combined with large quantities of lyophilised Lactobacillus, mucosal protectants, activated charcoal, dimethylpolisiloxane (another carminative) and spasmolytics, a combination that appeared somewhat effective. Dietary modifications included the removal of milk products and the reduction of roughage by feeding only stripped bamboo leaves (del Campo et al., 1990a).

It is worth noting that haemorrhagic enteritis in giant pandas in China has sometimes been diagnosed solely on the basis of a gross reddening of the intestine (B. Rideout, pers. obs.). Some of these cases could be misclassified and may in fact be due to shock-related congestion or intra-intestinal haemorrhage. The chronic enteritis experienced by many giant pandas poses the added risk of intestinal ulceration and megacolon (Fig. 16.9; Plate XXI).

Panda Organ System
Figure 16.9. (a) Chronic enteritis in a giant panda. Endoscopy demonstrating ulceration (arrow) of the intestine. (b) Megacolon found at necropsy. (See also Plate XXI.)

Some cases of acute hemorrhagic diarrhoea, although recurrent, resolve within a few days with no medical intervention (Bush et al., 1985; Goltenboth, 1985a). Clinical pathology in these cases indicates localisation of disease to the intestinal tract, and histopathological changes are limited to inflammatory cell infiltration in areas of sub-mucosal haemorrhage without evidence of infectious organisms (Bush et al, 1985). Other cases of haemorrhagic intestinal disease in this species have been severe and occasionally fatal. An adult female (SB 169) at Madrid Zoo died after an acute episode of haemorrhagic enteritis that lasted only 24 hours (Villares et al, 1985). Clinical signs included bloody faeces, abdominal pain, respiratory distress and progressive weakness. Necropsy revealed that the lesions were restricted to the small and large intestines. Mucosal surfaces were congested, and the wall of the large intestine was intermittently oedematous and friable. Histopathology indicated varying degrees of serosal and mucosal congestion, haemorrhage, necrosis, oedema and inflammatory cellular infiltration. Regional lymph nodes were similarly affected, but there was no evidence of mesenteric vascular occlusion. Villares et al. (1985) considered the lesions to be consistent with an acute toxicosis, allergic episode or thrombosis of a major mesenteric vessel, but not with a primary bacterial enteritis. The authors suggested that the giant panda died from toxic shock associated with an acute ischae-mic or anaphylactic intestinal necrosis.

Some reports describe enteritis as part of a multisystemic illness. A case from the Berlin Zoo involved a six-year-old female panda (SB 210) who died after an illness characterised by intestinal haemorrhage and severe central nervous system disturbance (Goltenboth, 1985b). The clinical course of illness progressed from what was believed to be enterotoxaemia with neurological signs to intestinal haemorrhage, sepsis, coagulopathy and hypovolaemic shock. Post-mortem examination revealed extensive oedema throughout the body (including the head) and a haemorrhagic diathesis along the full length of the intestinal tract (Dammrich, 1985). Histologically, the primary lesions affected the intestinal mucosa and lymphoreticular tissue and resembled those associated with enteropathogenic viral disease in the domestic cat and dog (Dammrich, 1985). This giant panda had been vaccinated against parvovirus annually for the preceding three years. Antibody titres were 1:256 and 1:480, the latter of which was higher than a typical vaccination titre in the cat or dog (Doammrich, 1985). Parvovirus, coronavirus and rotavirus could not be isolated from this individual's tissues, and efforts to detect other common canine and feline viruses by immunofluorescence also failed. An unidentified Clostridium sp. was isolated from the stomach and small intestine, which may or may not have been responsible for the signs of enterotoxaemia.

Viral diseases

Disease associated with parvovirus or other common canine and feline viruses in giant pandas is a largely unexplored issue in China. One report describes a survey for canine parvo-, corona-, adeno- and distemper virus in five captive and three recently rescued giant pandas at a Chinese breeding centre (Mainka et al., 1994). None of these animals had been vaccinated, and all had been in captivity either for some time or had been recently captured. The titres to coronavirus (in two captive individuals 1:160), distemper (one captive 1:50; one recently wild caught 1:30) and parvovirus (three captive 1:20, 1:320, 1:1280; two recently captured-individuals 1:160, 1:50) indicated prior exposure to these viruses. Seven (of seven) dogs and two (of three) cats surveyed in the study area had high parvovirus titres (1:250 to >1:10240). Positive titres to all viruses in all sampled dogs suggested that these pathogens were endemic. An outbreak of distemper that affected giant pandas and red pandas at one Chinese zoo has been described in the literature (Qiu & Mainka, 1993).

Vaccines approved for the giant panda are not currently available in China. Some zoos vaccinate with attenuated multivalent canine vaccines produced in China, but antibody titres have not been evaluated and vaccine efficacy is unknown. Some carnivores (ferret, red panda, maned wolf, African wild dog, kinkajou, grey and fennec fox and European mink) are highly sensitive to distemper virus, and vaccination with modified live (canine) product has resulted in clinical distemper and death (Montali et al., 1983). Anecdotal accounts of clinical cases in China suggest that giant pandas are susceptible to canine distemper virus, but the degree of vulnerability and epidemiology of the disease are unknown. Coronavirus particles have been observed in giant panda faeces, but a causative relationship between the virus and clinical signs has not been established (Pan et al., 1991; X. Xia, pers. comm.).

Vomiting

Frequent vomiting or regurgitation has been observed in some giant pandas who appear otherwise clinically normal (Zhang et al., 2000). One female (SB 297, born in captivity and classified as a Prime Breeder during the CBSG Biomedical Survey) regularly regurgitates and reingests her food while otherwise being in good health. This may be some form of stereotypical behaviour. Another young male (SB 394) described during the survey as robust and a proven breeder also had a history of postprandial vomiting.

Allergies

Food allergy was implicated in a case of generalised gastrointestinal illness in an adult female giant panda (SB 127) at the London Zoo (Knight et al., 1982). This individual presented with anorexia, polydip-sia, lethargy, ascites and progressive, severe weight loss. Following weeks of supportive therapy, the panda made a clinical recovery while maintaining a fluctuating eosinophilia that periodically rose to 40% of the total white cell count. She also had a peritoneal exudate with a specific gravity up to 2.4 g dl_1. The possibility of food allergens was considered, and, on the basis of a rising antibody titre to ovalbumin, chicken eggs were eliminated from the diet. The antibody titre to ovalbumin decreased over the next 14 months and the panda's clinical condition improved, although the undulating eosinophilia and low-grade peritonitis persisted. This individual also demonstrated antibody responses to monkey chow and wheat, but the titres fell after the acute illness episode without removal of these foodstuffs. Investigations into a separate cause for the persistent peritonitis and recurrent eosinophilia were initiated at the time the article was written, and preliminary findings localised a mass in the upper epigastric region.

A possible allergic reaction to soya-bean meal may have been responsible for acute joint pain in two giant pandas (SB 208 and 210) at the Berlin Zoo (Goltenboth, 1985a). The soya-bean meal ratio in the pandas' gruel had been doubled to encourage weight gain. Two days later, both individuals moved as though in great pain. The animals were treated with NSAIDs, and the soya-bean meal was omitted from the gruel. Both animals recovered fully within three days. Diagnostic evaluations were not reported.

Ascites

Abdominal fluid is a frequent, incidental observation in physical and post-mortem examinations of the giant panda (Zhang et al., 2000; see Chapters 4 and 15; R. Montali & B. Rideout, pers. obs.). In some individuals, ascites has been associated with a disease process, such as heart failure (R. Montali, unpublished data, pathology report, Smithsonian's National Zoological Park), chronic ulcerative colitis or peritonitis (F. Ollivet, unpublished data, pathology report, Paris Zoo) or as part of Stunted Development Syndrome (see Chapter 4). Giant pandas with chronic gastrointestinal disease often have ascites (Zhang et al, 2000; I. K. Loeffler, unpublished observations). In most cases, the aetiology is unclear. The condition does not appear to be associated consistently with clinical illness (e.g. cardiac or hepatic failure) or abnormal serum chemistry values (e.g. hypoproteinaemia) (Zhang et al, 2000; B. Rideout, pers. obs.).

The reproductive system

Most diseases of the reproductive tract of giant pandas are poorly described, and their impact on reproduction in males or females is unknown.

Embryonic mortality and abortion

Because it is currently impossible to distinguish pregnancy from pseu-dopregnancy in giant pandas (see Chapter 8), the incidence of embryonic death is difficult to assess. Anecdotal accounts of late-term abortion have been noted at two Chinese giant panda facilities but have not been investigated (I. K. Loeffler, unpublished observations).

Infectious diseases of the reproductive tract

A case of metritis and cervicitis was diagnosed in a 6.5-year-old female (SB 404) during the CBSG Biomedical Survey (Zhang et al., 2000). In the previous year, this individual had a sporadic urinary oestrogen profile, had been ill most of the year and was described during the survey as 'unhealthy'. Laparoscopy revealed ascites, and an ultrasound examination showed fluid in the uterus. A purulent vaginal discharge and suppurative cervicitis (diagnosed on cytology and biopsy) confirmed a diagnosis of endometrial infection. This panda was treated with antibiotics and conceived in the same season to produce a healthy cub that year (see Chapter 4).

Knight et al. (1985) reported a presumed Trichomonas infection of the vaginal vestibule (in an unspecified individual) that was treated with metronidazole (20 mg kg-1 orally; duration and outcome not reported). The same report indicated a laparoscopic finding of chronic endometrial hyperplasia, bilateral oviductal occlusion and diffuse peritonitis in another giant panda (SB 127) at the London Zoo. The authors described clearing the obstructions by catheterisation and oviductal lavage in two successive years, but did not report the panda's subsequent reproductive success.

Uterine lesions

Incidental observations of uterine lesions may indicate a potential cause of infertility in some giant pandas. A 22-year-old female (SB 112)

who died of heart failure at the Smithsonian's National Zoological Park was found at necropsy to have three leiomyomas distributed throughout the uterus (Fig. 16.10a; Plate XXII). Leiomyomas are benign tumours of smooth muscle cells that may (in high numbers) adversely affect fertility, particularly in older animals.

Testicular anomalies

A giant panda at the Smithsonian's National Zoological Park (SB 121) developed an enlarged testis at 25 years of age (see Fig. 16.10b). Testicular biopsy revealed a neoplasm that was confirmed postcastration to be a seminoma. Although vascular involvement was noted microscopically, there was no evidence of metastasis upon pathological examination at this male's death three years later. The testicular tumour in this giant panda resembled seminomas commonly observed in the domestic dog (R. Montali, unpublished data, pathology report, Smithsonian's National Zoological Park). Undescended testes or testicular hypoplasia (see Fig. 16.10c-f) were detected in three male giant pandas during the CBSG Biomedical Survey (see Chapter 7). One testis in a 14-year-old, wild-born male (SB 298) had hyperechoic foci at ultrasound that were believed to represent fibrosis or calcification (Zhang et al., 2000; see Chapter 4). He had successfully sired seven litters (11 total cubs) over the five years prior to the examination, and the lesions did not appear to interfere with his fertility.

The renal system

Clinical signs of renal dysfunction have been documented in young, adult and geriatric giant pandas. Aetiology and pathophysiology of uraemia in this species are usually undetermined (Knight et al., 1982; Nakazato et al., 1985; Li et al., 2001).

Renal failure in a young individual

Li et al. (2001) described a case of renal failure in an eight-month-old female (SB 484). She had been weaned a month prior to the onset of illness and was reported to have been less thrifty than her peers. The course of her six-month illness was marked with frequent vomiting,

Giant Panda Eyelid

Figure 16.10. (a) Leiomyoma (arrows) of the uterus in a 22-year-old giant panda. Leiomyomas are benign tumours of smooth muscle tissue and are common in Carnivora. (b) Seminoma (right) found incidentally in a 25-year-old individual. Both testes were surgically excised, and the neoplasm did not recur or metastasise. The top two items in the image depict the gross specimens, and the bottom two their cut surfaces. (c) Gross and (d) excised testes of an adult giant panda (SB 323) with unilateral testicular hypoplasia (arrows). The photograph in (c) was taken during the CBSG Biomedical Survey when the panda was 13 years old; he died one year later. Histopathology of a normal (e) versus hypoplastic (f) testis demonstrating the absence of germ cells in the seminiferous tubules of the latter. Arrows indicate the germ cell layer. (See also Plate XXII.)

Figure 16.10. (a) Leiomyoma (arrows) of the uterus in a 22-year-old giant panda. Leiomyomas are benign tumours of smooth muscle tissue and are common in Carnivora. (b) Seminoma (right) found incidentally in a 25-year-old individual. Both testes were surgically excised, and the neoplasm did not recur or metastasise. The top two items in the image depict the gross specimens, and the bottom two their cut surfaces. (c) Gross and (d) excised testes of an adult giant panda (SB 323) with unilateral testicular hypoplasia (arrows). The photograph in (c) was taken during the CBSG Biomedical Survey when the panda was 13 years old; he died one year later. Histopathology of a normal (e) versus hypoplastic (f) testis demonstrating the absence of germ cells in the seminiferous tubules of the latter. Arrows indicate the germ cell layer. (See also Plate XXII.)

diarrhoea, anorexia and abdominal discomfort. She was also pruritic and developed alopecia on the head and abdomen. Physical examination and blood analysis performed a month after illness onset revealed uraemia (blood urea nitrogen, BUN, >140 mg dl_1; normal is <15 mg dl-1), acidosis, anaemia and enlarged kidneys. Severe renal disease was confirmed by biopsy, ultrasonography and scintigraphy. Each kidney was twice normal size. Scintigraphy and urinalysis revealed reduced renal perfusion, hyposthenuria, glucosuria and proteinuria. A biopsy revealed renal tubular necrosis and mineralisation and renal tubule dilation. Although clinical signs improved gradually in response to allopathic and Chinese medicines, BUN and creatinine concentrations remained elevated, anaemia persisted, and she never recovered normal activity levels. SB 484 died six months after the initial uraemia diagnosis following an acute episode of haemorrhagic enteritis and anorexia. Necropsy revealed extensive kidney calcification, hepatomegaly and mucosal haemorrhage of the stomach and intestines. Further diagnostic tests were unavailable, and the aetiology of this young animal's renal failure remains undetermined. One possible consideration is the treatment of the initial diarrhoea with gentamicin, although the author reported that this drug was used frequently in giant pandas at this institution without complication.

Pyelonephritis and anaemia in an adult

Acute pyelonephritis occurred in a 14-year-old female giant panda (SB 112) at the Smithsonian's National Zoological Park four months after parturition (Bush et al., 1984). Her cub had died within a few hours of birth due to aspiration of infected amnionic fluid in utero (see 'Neonatal pathology',). SB 112 developed signs of acute renal failure with azotae-mia, haematuria and hyperphosphataemia. She also had a profound macrocytic, hyperchromic anaemia and hyperbilirubinaemia of unexplained origin, although the possibility of a haemolytic crisis was considered. Enterococcus sp., Klebsiella pneumoniae and E. coli were cultured from the urine and biopsied renal tissue, and Enterococcus was cultured from blood. The renal biopsy revealed neutrophils and proteinaceous casts within dilated proximal tubules (Fig. 16.11a; Plate XXIII). The medullary architecture was abnormal, with oedema and interstitial mononuclear inflammatory cells.

Figure 16.11. (a) Renal biopsy of a 14-year-old female giant panda with acute renal failure who was diagnosed with ascending coliform pyelonephritis. (Arrows designate neutrophils in the renal tubules.) (b) Renal cystic glomerular disease (arrows) in a 28-year-old male giant panda that died of chronic renal failure. (See also Plate XXIII.)

Figure 16.11. (a) Renal biopsy of a 14-year-old female giant panda with acute renal failure who was diagnosed with ascending coliform pyelonephritis. (Arrows designate neutrophils in the renal tubules.) (b) Renal cystic glomerular disease (arrows) in a 28-year-old male giant panda that died of chronic renal failure. (See also Plate XXIII.)

The severity of this female's anaemia warranted aggressive emergency therapy, which included a blood transfusion from her mate (SB 121). SB 112 responded to therapy with a return of clinical chemistry values to normal levels, and she became pregnant at her next oestrus the following spring. However, she may have retained a persistent, subclinical urogenital tract infection, which was offered as a possible explanation for the failure of all the live-born cubs produced in succeeding years to survive beyond a few days (see 'Neonatal pathology'.

Renal failure in a geriatric individual

The need to manage chronic renal failure is not uncommon in captive collections as good husbandry and veterinary care allow animals to live to ages that are unusual in the wild. The male giant panda SB 121 at the Smithsonian's National Zoological Park developed signs of renal failure at the age of 28 years. The clinical course of his six-month illness was characterised by azotaemia, anaemia and episodic epistaxis that was considered to be associated with renal hypertension. He was treated with fluids, erythropoietin (Epogen; Amgen, Thousand Oaks, CA; 10 IU kg-1 given subcutaneously at a tapering frequency), injectable iron supplementation (2 mg kg-1) and later amilodipine (a human antihypertensive drug; Pfizer, La Jolla, CA; 0.025-0.05 mg kg-1 orally once daily) (L. Spelman, unpublished observations, clinical records, Smithsonian's National Zoological Park). SB 121 had also been effectively treated for degenerative osteoarthritis for several years, but with the deterioration of his renal condition the arthritis became refractory to treatment. He was euthanised when advancing uraemia also became resistant to treatment (see Chapter 15; L. Spelman, unpublished observations, clinical records, Smithsonian's National Zoological Park).

At necropsy, both kidneys were enlarged, pale, scarred, mineralised and contained numerous cysts throughout the cortices and medul-lae (R. Montali, unpublished data, pathology report, Smithsonian's National Zoological Park; see Fig. 16.11b). Histologically, the kidneys showed diffuse cystic changes in the glomeruli, with tubular atrophy and interstitial fibrosis. Additionally, there was evidence of cardio-megaly and congestive heart failure (possibly hypertension induced) and uraemic metastatic calcifications of blood vessels and soft tissue. A macroaneurysm and thrombosis in the left retina were probably also associated with hypertension. Haemosiderosis in the lymph nodes, liver, spleen, adrenals and pancreas was consistent with anaemia secondary to end-stage renal failure. There was no evidence of the involvement of infectious agents. Despite SB 121's long-term treatment with NSAIDs to manage osteoarthritis, there was no evidence of renal papillary necrosis or other toxic changes. Cortical cysts are commonly seen in animals with end-stage kidneys.

Diabetes insipidus

An unusual case resembling diabetes insipidus in a subadult giant panda (SB 249) is reported in the literature (del Campo et al, 1990b). The three-year-old male was described as apathetic, inappetant and polydipsic (drinking up to 22l of water per day; normal is around 2.5l per day). Based on clinical signs and haematological analysis, diagnostic tests were undertaken for psychogenic polydipsia. A water deprivation test was discontinued after 12 hours due to a 4% loss in body weight. Urine osmolality revealed no significant variation in the 24 hours following initiation of water deprivation. Two injections of porcine vasopressin tannate (5 and 10 IU on consecutive days; source unspecified) and a few days of treatment with synthetic antidiuretic hormone (0.05 and then 0.09 mg kg-1 daily; source unspecified) resulted in no change in urine osmolality or water intake. Plasma concentrations of antidiuretic hormone were not detectable using standard laboratory assays. Treatment with chlorothiazide (0.2 mg kg-1; source unspecified) was initiated as a diagnostic indicator and then continued at 0.4 mg kg-1 every three days as a therapeutic measure. Like other saluretic drugs, chlorothiazide has paradoxical effects in patients with diabetes insipidus in that it actually reduces diuresis and polydipsia, and SB 249 responded accordingly.

However, this individual remained severely depressed and anorexic, particularly after the chlorothiazine treatments. Staff observed that the panda appeared nearly 'euphoric' after recovering from keta-mine hydrochloride anaesthesia (this male was tranquilised frequently for blood sampling and supportive therapy) and that he responded most positively to one particular keeper. Efforts then concentrated on the panda's psychological well-being. The keepers adopted a more positive attitude and were trained to brush the animal as a form of massage. Although water intake remained relatively high (about 6l daily), SB 249's weight and behaviour returned to normal over the course of a year. A behavioural and psychological evaluation would have been interesting, especially in light of this male's concomitant chronic gastrointestinal illness (see above). Regardless, this case illustrates the potentially profound influence of a giant panda's social environment on its health and well-being.

The neurological system

Seizure disorders in the giant panda have been reported occasionally (Hime, 1976; Keymer, 1976; Qiu & Mainka, 1993; I. K. Loeffler, collected anecdotal accounts), but aetiological or pathological origins have not been studied. Qiu & Mainka (1993) reported that five of 18 known neurological cases in the Chinese literature have been associated with: 1) a nasal sinus abscess with extension to the brain; 2) low blood levels of potassium and calcium; 3) adverse reaction to medication for tuberculosis; 4) a hormonal problem; or 5) heavy metal toxicosis (arsenic and mercury).

The details of the clinical course and diagnosis of these cases are unavailable. There has been no investigation into the incidence and pathology of microorganisms or other parasites that may affect the giant panda's central nervous system.

It is worth noting that five of six giant pandas maintained at the London Zoo over a 30-year span were reported to have had 'fits' (Keymer, 1976). In most cases, post-mortem examinations were not sufficiently detailed to establish a diagnosis or aetiology. The case of a 15-year-old female (SB 18) who died at the London Zoo following a five-month period of increasingly frequent seizures was carefully examined (Keymer, 1976). This individual had no histological lesions of the central nervous system or biochemical evidence for heavy metal toxicity or vitamin deficiency (Hime, 1976; Keymer, 1976). Histological changes in the brain were consistent with prolonged, repeated seizures, and no specific cause was identified.

The cardiac and respiratory systems

Cardiomyopathy (including dilated cardiomyopathy and endomyocar-dial fibrosis) has been found in some older giant pandas post-mortem (Keymer, 1976; Nakazato, 1985; R. Montali, unpublished data, pathology report, Smithsonian's National Zoological Park). The male at the Paris Zoo (SB 140), who died at 27 years of noncardiac causes (see 'The digestive system'), was found to have moderate, chronic endocarditis with dystrophic or senile valvular sclerosis, but no myocarditis (F. Ollivet, unpublished data, pathology report, Paris Zoo). SB 121, the 28-year-old giant panda who died at the Smithsonian's National Zoological Park of chronic renal failure (see 'The renal system'), had enlarged left heart chambers that were attributed to chronic hypertension and anaemia (R. Montali, unpublished data, pathology report).

Other cases are reported as having had no signs of cardiac insufficiency prior to sudden collapse. For example, the 15-year-old female (SB 18), who died with convulsions at the London Zoo (see 'The neurological system'), had a dilated right ventricle and evidence of aortic and heart valve fibrosis (Keymer, 1976). SB 112, the 22-year-old female at the Smithsonian's National Zoological Park, who died of sudden heart failure, had extensive cardiac fibrosis with an endomyocardial distribution observed in both ventricles (R. Montali, unpublished data)

Figure 16.12. Endocardial fibrosis in a 22-year-old female giant panda that died suddenly of cardiac arrhythmia. (a) Gross necropsy demonstrating fibrosis of endocardial tissue (arrow). (b) Histopathology of endocardial tissue. Fibrosis disrupts the course of electrical signalling through conducting fibres (arrow). (See also Plate XXIV.)

Figure 16.12. Endocardial fibrosis in a 22-year-old female giant panda that died suddenly of cardiac arrhythmia. (a) Gross necropsy demonstrating fibrosis of endocardial tissue (arrow). (b) Histopathology of endocardial tissue. Fibrosis disrupts the course of electrical signalling through conducting fibres (arrow). (See also Plate XXIV.)

(Fig. 16.12; Plate XXIV). The fibrosis appeared to entrap Purkinje fibres, particularly near the bundle of His and may have led to dysrhythmias and a heart block. Some pericardial and peritoneal effusions were present, but the histological appearance of the liver and lungs was inconsistent with long-standing congestive heart failure.

There is limited information on respiratory disease in giant pandas. One report describes pulmonary hyaline membrane disease in an 18-year-old female, SB 341, who apparently died of chronic pancreatic disease and respiratory failure (Chen & Pan, 1991). As already discussed, a leading cause of cub mortality is pneumonia, generally due to sepsis, failure of passive transfer and an immature or weak immune system. Pulmonary injury caused by migrating Baylisascaris larvae may also predispose young pandas to secondary bacterial pneumonia, although this has not yet been reported. There is one case (in the Chinese literature) oftuberculosis in the giant panda (see Qiu & Mainka, 1993 for a list of citations).

Skin

Alopecia and pruritus have been observed in giant pandas in association with renal failure (Li et al., 2001), stereotypical behaviours (Zhang et al., 2000) and ectoparasitism (Leclerc-Cassan, 1985). At the workshop on

Diagnostic and Clinical Pathology in Zoo and Wildlife Species (Beijing, June 2002), demodecosis was recognised as a significant skin disease in the giant panda. Periocular and generalised demodecosis were also observed during the CBSG Giant Panda Biomedical Survey, with one animal being severely affected with alopecia, erythema, pyoderma and skin lichenification (Zhang et al, 2000; see Chapters 4 and 15). References to Demodex in the giant panda also appear in the literature (Zhu, 1991). Although no data are available, we suspect that demodecosis in the giant panda is associated with a compromised immune status, as it is in the domestic dog.

A squamous cell carcinoma was observed in a 16-year-old male (SB 305) during the CBSG Biomedical Survey (Zhang et al., 2000; see also Chapters 4 and 15). The lesion was 50 cm in diameter and its pathology well advanced. It had been treated topically as a superficial skin infection for a chronic but unspecified period of time. The panda died four months after the survey examination.

The musculoskeletal system

Like most animals, the giant panda develops osteoarthritis with age. SB 121 of the Smithsonian's National Zoological Park began to show episodes of lameness by 11 years of age, particularly during the winter and breeding seasons. Progressive stiffness and lameness in the forelimbs and then in the rear limbs and back prompted the initiation oflong-term NSAID therapy (see Chapter 15; L. Spelman, unpublished observations, clinical records, Smithsonian's National Zoological Park). SB 121's osteo-arthritic pain was managed medically for 2.5 years until euthanasia due to renal failure. At necropsy, the articular surfaces of the left elbow were severely eroded, and the epicondyles of the ulna were marked by multiple exostoses; both carpal joints were similarly affected. Progressive osteoarthritis affected the thoracolumbar vertebrae.

Ocular system

Ocular changes described for the giant panda include conjunctivitis, corneal ulcers, cysts, retinal degeneration, neoplasms and lesions involving the whole eye that may have resulted from disease or trauma (Ashton, 1976; Hime, 1976; Lopez et al., 1996; Zhang et al., 2000; McLean et al., 2003; R. Montali, unpublished data, pathology report, Smithsonian's National Zoological Park). A recurrent case of keratoconjunctivitis in a young female (SB 18) at the London Zoo finally resolved with topical and injectable penicillin treatment (Hime, 1976). Upon this animal's death eight years later after a period of increasingly frequent seizures (see 'The neurological system'), cysts were identified histologically in the iris, retina and pars plana. This panda was also found to have bilateral retinal degeneration and lenticular sclerosis attributed to old age, but there was no evidence of cataract formation (Ashton, 1976).

A mass determined histopathologically to be a low-grade haem-angiosarcoma was removed from the outer ocular limbus of a 13-year-old male giant panda (SB 249) at Madrid Zoo (Lopez et al., 1996). The tumour appeared to be painless and was confined to the conjunctiva with no invasion of the underlying tissues. Haemangiosarcomas are not uncommon in a variety of species, and their development is potentially stimulated by sunlight (see citations in Lopez et al., 1996). It is not unusual for captive pandas to be exposed to ultraviolet radiation far in excess of levels in their native habitat of foggy, wet mountain forests. The panda in Madrid was moved to a more shaded enclosure, which is probably a good suggestion for all giant pandas housed in sunny areas.

A 14-year-old male (SB 298) examined during the CBSG Biomedical Survey in China had corneal and lenticular opacities in the left eye but without evidence of a cataract. The anterior chamber of the affected eye was distended, and the iris and pupil appeared abnormal. The lesions were suggestive of trauma, glaucoma or retrobulbar disease (Zhang et al, 2000). This male was noted for his aggressive behaviour, which may have been precipitated, at least in part, by the irritating ocular lesions or, alternatively, the trauma could have resulted from fighting with other pandas.

SB 121 at the Smithsonian's National Zoological Park had periodic episodes of bilateral ulcerative keratitis that began at 25 years of age and progressed markedly in the last two weeks of his life (R. Montali, unpublished data, pathology report). During the original bouts of keratitis, this male had positive titres against Herpesvirus canis (or another herpesvirus species that cross-reacted with H. canis; R. Montali, unpublished data). However, a direct relationship between herpesvirus and the ocular lesions could not be determined. Histologically, the ulcerated lesion showed superficial corneal inflammatory calcification associated with Gram-negative bacilli (McLean et al., 2003). Some of these changes were attributed to the panda's chronic renal failure and debilitated condition. Both retinas had small nodules of proliferated astrocytes, indicative of hamartomas and similar to the congenital lesions found in humans which arise from abnormal tissue development and maturation (McLean et al., 2003). Human hamartomas are usually associated with a multisystemic disease complex known as tuberous sclerosis (characterised by seizures, mental retardation, skin and eye lesions and neurobehavioural problems). SB 121 had none of the hallmarks of the human disease complex, and the hamartomas were believed to have arisen spontaneously, as they do occasionally in humans (McLean et al., 2003).

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  • juuso
    Can panda get the same diseases as humans?
    5 months ago

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