- Cotton-top tamarins are the only non-human primate that spontaneously develops colon cancer.
- Diagnostic and treatment options for a variety of cotton-top tamarin diseases are discussed.
The following is a detailed chapter describing some of the major clinical diseases found in cotton-top tamarins. Much of this information has been derived from studies of tamarins in research laboratories and is a valuable reference for managing cotton-top tamarins in zoos.
I. NORMAL REFERENCE VALUES
|Adult body weight (wild)
Adult body weight (captive)
|400-430 g (Savage et al., 1993)
Red blood cells
White blood cells
* Values are from The New England Regional Primate Research CenterClinical Chemistry
*Values are from The New England Regional Primate Research Center
II. EXAMINATION AND PROCEDURES
The health of all tamarins should be monitored on a daily basis by zoo keepers with follow up care by a veterinarian. The tamarins should undergo periodic physical examinations to facilitate early diagnosis and treatment of serious diseases. Periodic examinations and procedures should at least include the following:
History (abnormalities in health or behavior, changes in diet or environment, etc.)
Thorough physical examination (including dental exam, palpation for abdominal masses and pregnancy)
Tattooing/Transponder implant for identification
Tuberculosis testing (annually)
Depending on the environmental conditions and protocol of the individual institutions,
the following may be indicated:
Vaccinations (measles and rabies; based on the specific risk factors at each institution)
Prophylactic antiparasitic drugs (dependent on history of parasitic disease and risk factors)
Additional procedures that may be warranted depending on the specific situation are:
CBC, clinical chemistry
III. INFECTIOS DISEASES
Infectious diseases are common problems in callitrichids. A review of the most
common infectious diseases in callitrichids is presented, with special emphasis on the
diseases affecting cotton-top tamarins.
Tamarins are susceptible to infection by a large number of bacterial organisms. Significant clinical disease may occur secondary to concurrent viral or parasitic infection, prior debilitation, decreased immunity or the extensive use of antibiotics. The more significant pathogens are reviewed here. Readers are referred to Potkay (1992) for a detailed discussion of documented cases of infections in callitrichids.
Campylobacter is the most frequently isolated organism from nonhuman primates with diarrhea. C. coli is not considered pathogenic. C. jejuni is a common cause of diarrhea and enterocolitis in cotton-top tamarins. Campylobacter sp. are often isolated from asymptomatic animals (Paul-Murphy, 1993). This organism may be an enzootic and opportunistic infectious agent in many colonies. The fecal-oral route is the primary mode of transmission. The diseased state involves a secretary diarrhea. It is uncommon to find frank blood and mucus in the feces (Paul-Murphy, 1993). Soft mucoid feces are produced. Feces are fluid, yellowish and may contain occult blood in cases of greater severity (Russell, 1993). Whether diarrhea is due to the invasiveness of the organism or to the production of an enterotoxin is unclear. A cytotoxin may be involved in the pathogenesis of disease.
It is common to find gas-filled loops of bowel (Paul-Murphy, 1993). On histologic examination in macaques, there are no pathologic changes observed in the jejunum or ileum (Russell, 1993). There are changes associated with colitis observed 48-72 hours following infection. The lamina propria is moderately infiltrated with inflammatory cells, mainly neutrophils along with lymphocytes and plasma cells. There is neutrophilic infiltration between crypt epithelial cells and many neutrophils are found in gland lumens (crypt abscesses). In more serious cases, necrosis leads to flattening of the luminal epithelium and replacement with squamous cells. Dilated lymphatics containing mononuclear cell infiltrates are seen in the submucosa. The comma-shaped organisms may be observed in the lamina propria and on the surface epithelium. Goblet cells are lost from the luminal epithelium, cuboidal and flattened cells replace the columnar epithelium, and the lumen of the colon contains necrotic and degenerating epithelial cells and red blood cells (Russell, 1993).
It is difficult to distinguish diarrhea caused by Campylobacter from other bacterial causes. Animals with C. jejuni infection may show abdominal discomfort but do not have anorexia as seen with other enteric pathogens and signs are usually limited to a soft to fluid diarrhea (Russell, 1993). Early presumptive diagnosis of Campylobacter enteritis may be attempted through the identification of comma-shaped Gram-negative rods on Gram stained fecal smears (McClure et al., 1986). Definitive diagnosis requires isolation of the organism. Cultures should be made from fresh stool or a rectal swab. The presence of erythrocytes and leukocytes on fecal smears stained with methylene blue is highly variable. Blood chemistry findings are nonspecific. The leukocyte count may range from a normal leukocyte count to leukocytosis with a toxic left shift and the fibrinogen level is frequently increased (Paul-Murphy, 1993).
Administration of appropriate fluid and electrolyte replacement therapy is very important. Antimotility drugs interfere with intestinal motility and are contraindicated. Some antimicrobials which are successful in susceptible strains are aininoglycosides, clindamycin, chloramphenicol, furazolidine, erythromycin, ciprofloxacin and enrofloxacin. The current drug of choice for the treatment of Campylobacter enteritis is oral erythromycin but some resistant strains exist. Enrofloxacin is a suitable second choice for strains not sensitive to erythromycin. Antibiotic sensitivity tests are not routinely done but are indicated in those cases where animals do not respond to erythromycin or enrofloxacin (D. Lee-Parritz, pers. comm.).
Prognosis is good provided antibiotics, fluids and other supportive care are administered properly (D. Lee-Partitz, pers. comm.). Reinfection from the affected individuals' own feces or from feces of animals housed in the area can interfere with recovery.
This organism is generally an opportunistic pathogen infecting sick or debilitated animals (Richter, 1984). It is one of the more common bacteria currently associated with clinical disease in callitrichids. Clinical disease is usually associated with serotype 1 (Richter, 1984). Animals often present with acute death lacking prior clinical signs (D. Lee-Panitz, pers. comm.) The main manifestation of disease is lobar pneumonia. This organism may also cause septicemia and enteritis. Signs frequently observed are seizures, opisthotonos and abortion (D. Lee-Parritz, pers. comm.). Clinical signs may also include coughing, sneezing, dyspnea, nasal discharge, diarrhea, hypothennia, anorexia and lethargy.
Post mortem findings may include gaseous distension and congestion of the small intestine. The liver may be enlarged with diffuse yellow areas on the surface. Lesions show intense congestion and contain mono- and poly-morphonuclear leukocytes suggesting the cause of death to be septicemia (Potkay, 1992).
Isolation and identification of the organism can be made following culturing of samples from pharyngeal swabs or transtracheal lavage. Antibiotic sensitivity should be determined and appropriate therapy administered. Cephalosporins, chosen to penetrate into the meninges, may be an effective treatment (D. Lee-Parritz, pers. comm.). Supportive fluid and oxygen therapy may be necessary. Prognosis is generally poor with death occurring due to lobar pneumonia, meningitis or septicemia (D. Lee-Parritz, pers. comm.).
Salmonella sp.This organism is of special importance because of its zoonotic potential. Clinical disease in nonhuman primates is generally associated with the overall health of the population. Disease caused by Salmonella in New World monkeys is infrequently reported (Paul-Murphy, 1993). The fecal-oral route is the most common mode of transmission. Oral route infection may also occur when contaminated food items such as raw meat fed as a dietary supplement are consumed. Asymptomatic chronic carriers are common and may serve as sources of infection. Rodents and small birds may also be potential sources of infection. Insects have also been implicated as possible mechanical vectors. The potential for exposure may be high in zoos since the organism may be carried by a number of different species. Incidence appears to be higher in zoos than in primate research facilities (Paul-Murphy, 1993).
One manifestation of clinical disease seen with Salmonella in nonhuman primates is gastroenteritis. This disease is associated with a watery diarrhea due to net secretion of fluids throughout the intestinal tract following invasion of the mucosa by the organisms. Signs occur rapidly and may include anorexia, depression and fever. Dehydration can be severe. Sometimes stools may contain blood and mucus (Paul-Murphy, 1993).
There is congestion and edema in the ileum, cecum and colon. Superficial ulcerations and petechial hemorrhages may be found. The intestinal epithelium shows degeneration and desquarnation. Infiltration of the epithelium can occur with spread to the lymph nodes resulting in subsequent systentic infection. This organism sometimes causes fatal septicemias. Serositis and focal necrosis of the liver and lungs characterize fatal cases (Richter, 1984).
Isolation of the infectious agent is required for definitive diagnosis. Isolation may be difficult during the recovery phase of the illness. It is very difficult to isolate organisms from asymptomatic carriers which can present problems in terms of preventing the spread of the disease. Cultures should be made from fresh feces or rectal swabs. More mononuclear cells are found in fecal smears stained with methylene blue relative to the numbers found in cases of shigellosis. The percentage of mononuclear cells in the blood also tends to be higher in cases of salmonellosis when compared to shigellosis (Paul-Murphy, 1993).
Appropriate fluid and electrolyte replacement therapy are of primary importance. Antimotility drugs affect intestinal motility and are contraindicated.
Treatment with antibiotics is not indicated unless sepsis is evident (Richter, 1984) because of the risk of inducing a carrier state. Animals should be isolated and supportive therapy administered. The animal's own immune system is likely to resolve the disease (D. Lee-Parritz, pers. comm.) Resistance can pose a problem in the treatment of salmonellosis. Antibiotic sensitivity tests should be used to determine appropriate therapy. Some of the currently used drugs for the treatment of Salmonella gastroenteritis are cephalothin, cefazolin, trimethoprim-sulfamethoxazole, ciprofloxacin and norfloxacin. Many strains have shown resistance to arnpicillin, erythromycin, chloramphenicol, tetracycline, kanamycin and dihydrostreptomycin (Paul-Murphy, 1993). Reinoculation by the fecal-oral route from the animal's own feces or from the feces of animals housed together is a potential complication of successful treatment (Paul-Murphy, 1993).
According to Potkay (1992), this organism is an important pathogen in callitrichids and may be seen in concurrent infections with Salmonella. However, incidence of disease may be low to nonexistent (D. Lee-Parritz, pers. comm.) and there are few reports in New World primates (Paul-Murphy, 1993). Clinical disease is usually correlated with the overall health of the population. Transmission is mainly by the fecal-oral route. Isolation of this organism from the feces in callitrichids may occur without the presence of clinical disease (Richter, 1984).
Signs associated with clinical disease in nonhuman primates may occur abruptly and include watery stools containing blood and mucus, colitis, anorexia, depression, lethargy, fever, dehydration, abdominal discomfort, painful and ineffectual straining during defecation and death. Stools often have a characteristic odor (Paul-Murphy, 1993). Diarrhea is caused by invasion of the intestinal epithelium and subsequent intracellular multiplication in the submucosa or lamina propria. It is uncommon for this organism to invade beyond the lamina propria and enter the bloodstream. The site most affected is the colon where the luminal surface may be roughened. It may also be purulent or hemorrphagic. Shigella sp. can produce an exotoxin with both cytotoxic and enterotoxic effects. There is an acute inflammatory response of the intestinal tract which may result in the release of mediators that increase intestinal secretion and decrease absorption leading to fluid loss (Paul-Murphy, 1993).
Postmortem investigation may show petechia and erosions of the large intestine. Enlarged mesenteric lymph nodes are often associated with disease. Epithelial cell loss and infiltration of the lamina propria with polymorphonuclear leukocytes is seen. Crypt abscesses may occur (Paul-Murphy, 1993).
In order to obtain a definitive diagnosis, the organism must be isolated using fresh fecal specimens or rectal swabs. It may be difficult to isolate this organism during the recovery phase of the disease. Large numbers of polymorphonuclear leukocytes with many band forms are often found on examination of fecal smears stained with methylene blue. Blood chemistry tests may show a pronounced leukocytosis with a marked left shift and the presence of large numbers of toxic neutrophils and band forms. Fibrinogen levels are frequently elevated (Paul-Murphy, 1993).
Appropriate fluid and electrolyte replacement therapy are of the utmost importance. Antimotility drugs interfere with intestinal motility and are contraindicated. Antimicrobial resistance should be considered in implementing appropriate antimicrobial therapy. Shigella sp. have a strong potential for developing multiple resistance. Some effective antibiotics include ftimethoprim-sulfamethoxazole, arnpicillin, tetracyclines and fluoroquinolones. Many strains show resistance to ampicillin. Trimethoprim-sulfainethoxazole administered orally or parenterally is the recommended choice. For the initial treatment of dysentery, enrofloxacin may be a good option. Antibiotics may prove useful in decreasing the shedding period of this organism. Therapy may be complicated by reinfection from the animal's own feces and from the feces of infected individuals housed in the vicinity (Paul-Murphy, 1993).
This organism can be a cause of gastroenteritis in callitrichids. Infection may occur through contaminated food or water. There is increasing evidence that wild rodents may serve as a source of infection for nonhuman primates (McClure et al., 1986). Diarrhea which may contain blood is often observed. Pathologic findings include ulcerative enterocolitis of varying degrees and inflammation of the mesenteric lymph nodes. Necrosis of the spleen and liver are also common findings (McClure et al., 1986). Microscopic examination of imprint smears and lesion sections show numerous grain negative rods.
This disease is very uncommon in callitrichids and New World monkeys are relatively resistant. Mycobacterium tuberculosis may cause a slowly progressive respiratory disease. Disease may also involve visceral organs and the spinal column (Ott-Joslin, 1993). Transmission is through aerosolization and inhalation. Clinical signs are unreliable in indicating the extent of disease. Debilitation may only appear shortly prior to death.
Diagnosis is based on tuberculin hypersensitivity testing. Old tuberculin (1,500 units or 0. 1 ml) is injected intradermally into the upper eyelid and the area is subsequently examined at 24, 48 and 72 hour intervals for the presence of edema, induration or erythema. All nonhuman primates should be tested systematically on an annual basis and more frequently if warranted by the risk of exposure. On occasion, radiographs may aid in the diagnosis of well-developed cases by the identification of lesions. Euthanasia is generally the recommended procedure for positive individuals except in the case of extremely rare or valuable animals and clinicians should use appropriate judgment in determining mode of action. Regulations may vary and state or federal institutions should be consulted. Isoniazid is the common form of treatment for tuberculosis in humans and multiple agent therapy may be advised.
Pseudomonas is considered to be an important pathogen of callitrichids. Bronchopneumonia is the most common presentation. Debilitated animals are especially susceptible to disease caused by this organism. In callitrichid populations with enzootic infections, successful elimination of this organism is extremely difficult (Cicmanec, 1977; Deinhardt et al., 1967). Associated conditions include vegetative endocarditis, pericarditis, myocarditis, empyema and septicemia (Deinhardt et al., 1967).
Infraorbital abscesses commonly result from chronic dental disease or from sinus abscesses. Attempts should be made to determine the cause of infraorbital abscesses when they occur. The oral cavity should be examined for cracking, splitting and looseness of teeth, exposed pulp cavities, and periodontal disease. Radiographs may aid in diagnosis. The underlying cause should be appropriately addressed. Drainage and irrigation are important for successful treatment and should be implemented initially (D. Lee-Panitz, pers. comm.). Abscesses should be cultured and antibiotic sensitivity determined. Appropriate antibiotics should be administered systemically. These lesions may require long periods of time to heal (Richter, 1984).
Osteomyelitis may occur following puncture wounds and is frequently seen locally in bitten digits. Systemic antibiotics are recommended and it is important to be aware that healing may take long periods of time. Amputation of digits is often warranted.
Osteomyelitis may also occur on the tail tip following fecolith formation. Dermatitis, necrosis and exposure of the coccygeal vertebra occur subsequent to fecolith formation followed by osteomyelitis. The occurrence of fecolith formation may be prevented by increasing the distance between perches and the cage floor (Richter, 1984). In institutions with good husbandry practices, this problem should not occur.
Treatment involves bathing of the tail tip and local treatment with antibiotics. Systemic antibiotic use may be advisable. Wounds inflicted during fighting may lead to systemic osteomyelitis. Systemic antibiotics should be administered immediately. Repeated cultures should be made from infected sites and antibiotic sensitivity determined. Oral broad spectrum antibiotics such as cephalexin are the appropriate method of treatment pending receipt of sensitivity testing results (D. Lee-Parritz, pers. comm.). Radiography is useful in the diagnosis of osteomyelitis.
Little information is available concerning mycotic infections in callitrichids.
Candida sp. appears to be a normal inhabitant of the mucous membranes, genital tracts and skin of nonhuman primates (Migaki, 1986). Candidiasis occurs infrequently in debilitated animals or in animals which have received long-term antibiotic therapy. The most common agent is C. albicans. Manifestations in nonhuman primates include glossitis, usually seen as a thickened gray-white coat on the margins or tip of the tongue, esophagitis, and less frequently, gastritis. The creamy white plaque-like lesions form pseudomembranes and are due to heavy growth of the organism (Migaki, 1986). Ulcerations may be seen on the tongue or mouth. Signs often disappear if the underlying cause of debilitation is cured. Oral nystatin is generally effective in the treatment of gastrointestinal tract candidiasis in animals.
According to Wolff (1990), infections with these organisms seem to be rare in New World monkeys and Giardia sp. are not included in her description of the parasites of callitfichids.
While disease is infrequent, infections with Trypanosoma sp. are common. Most trypanosomes are not zoonotic. The only trypanosome known to be pathogenic in New World monkeys is T. cruzi which is also a significant human pathogen responsible for Chagas' disease. Caution should be exercised when working with feral animals and in endemic areas. The distribution of the organism is South and Central America and may occur in some areas of the southern and southwestern United States (Toft, 1986). Insect vectors from the family Reduviidae serve as the intermediate hosts.The trypanosomal form of the organism is found in the bloodstream. The leishmanial form is seen in cells of the skeletal muscle, cardiac muscle, reticuloendothelial system, as well as other tissues. When clinical disease does occur in New World primates, it is frequently associated with generalized edema and myocarditis. Other signs include anemia, splenomegaly, hepatomegaly and lymphadenitis. lestopathologic findings include the presence of pseudocysts in areas of the infected myocardium. These pseudocysts contain the organisms which have a central nucleus and a prominent kinetoplast shaped like a bar. The kinetoplast is diagnostic for this organism and helps in distinguishing it from Sarcocystis and Toxoplasma (Toft, 1986). With heavy infections in tamarins, monocytic infiltrations in the liver may be observed (Deinhardt et al., 1967).
Diagnosis is based on the identification of the organisms in thick and thin blood smears stained with Giemsa stain or by examination of organ smears or sections. Serological tests may also aid in diagnosis. There is no treatment available but attempts to control the insect vector may decrease the incidence.
According to Wolff (1990), natural infection in New World monkeys is uncommon but when it occurs the pathogenic effects tend to be relatively more severe than those seen in Old World monkeys. However, Richter (1984) states that E. histolytica appears to be fairly common in callitrichids. Several non-pathogenic Entamoeba sp. occur in New World monkeys so obtaining a definitive diagnosis of E. histolytica is important (Wolff, 1990). Cysts are infective and may be transmitted through ingestion of contaminated food, water, insects and fomites.
Ordinarily, the organism lives in the lumen of the intestinal tract causing no pathologic signs. It can become pathogenic when it enters the intestinal mucosa (Levine, 1970). The severity of clinical signs varies with the strain of organism, the nutritional and health status of the individual and the individual's gastrointestinal tract flora. When clinical disease occurs, it manifests as amebic dysentery. Clinical signs include severe diarrhea, dehydration, weakness, anorexia and vomiting. Diarrhea may or may not contain mucus and blood.
Post mortem examination shows colitis with necrosis and ulcerations. Histopathological findings include the presence of characteristic flask-shaped ulcers in the colon. Trophozoites may be seen around or in the ulcers (Toft, 1986).
Diagnosis is made by the identification of the organism in the feces. Fresh, wet mount, fecal preparations in a saline solution can be examined for the presence of motile trophozoites. Lugol's iodine may aid in the recognition of organisms. There is a non-pathogenic form of E. histolytica, as well, that has smaller trophozoites. The finding of erythrocytes within trophozoites is a method of diagnosing the pathogenic form because only the pathogenic type ingests red blood cells (Toft, 1986).
Metronidazole and paromomycin can be used for treatment of this disease (Wolff, 1990).
New World monkeys are highly sensitive to disease caused by this organism and death may ensue in 5-6 days (Wolff, 1990). Toxoplasma gondii is distributed around the world. Failure to identify seropositive callitrichids in the wild could be explained by their high susceptibility to the disease (Potkay, 1992) or possibly by their lack of exposure to infected rodents. The most likely form of transmission in captive animals is through ingestion of bradyzoites in animal tissues but infection may also occur following ingestion of sporulated oocysts which are shed by the definitive hosts belonging to the family Felidae or through transplacental transmission (Potkay, 1992). Insect vectors can aid in the spread of this organism by serving as transport hosts.
Signs associated with disease are nonspecific and may include decreased appetite progressing to anorexia, diarrhea, vomiting, weakness, sluggishness, depression, crouched posture, fever, cough, discharge from the nose and eyes, leukopenia, dyspnea, pale mucous membranes, abortion, coma and death.
Post mortem findings may include pulmonary edema, cardiomegaly, necrosis of the myocardium, hemorrhagic lymphadenopathy, enlargement and hyperplasia of the spleen, hepatic congestion and hepatocellular necrosis. Histopathological findings include interstitial and fibrinous pneumonia, focal myocarditis, focal hepatic necrosis, necrotic lymphadenitis, necrotic splenitis and intestinal lesions. Intracellular and/or extracellular tachyzoites are often seen in association with inflammatory lesions (Toft,1986).
Diagnosis is based on examination of histological sections and smear preparations for the identification of the parasites. Serological tests are available for identification of this organism. Monitoring of felid fecal samples for the presence of oocysts in a zoological setting may aid in the prevention of the spread to tamarins, however, oocysts are only shed for a very brief period of time, so their absence in the feces does not indicate absence of infection. Felid feces should be disposed of properly in order to avoid the possibility of sporulated oocysts contacting vectors and fomites (Flynn, 1973). Sulfadiazine, pyrimethamine and clindamycin have been used somewhat successfully to treat this disease in people and dogs (Wolff, 1990).
According to Wolff (1990), natural infection with this organism has not been found to occur naturally in callitrichids, but has been observed in colonies and may cause significant disease in immunocompromised individuals. Organisms are located in the bronchioles and alveoli. The main disease manifestation is interstitial pneumonia. Diagnosis is based on examination of pulmonary secretions and histological sections. Treatment of disease involves the use of trimethoprim and sulfa-methoxazole (Wolff, 1990).
Many nematode species occur in callitrichids. Some of the more significant pathogens are described here. For a detailed account of documented cases, see Potkay (1992).
Callitrichids may be infected by a number of pinworm species. However, morbidity is extremely low. Infection by the human pinworm Enterobius vermicularis may occur in captive populations of callitrichids (Wolff, 1990). To date, there do not appear to be any reports of infection with E. vermicularis in cotton-top tamarins. Humans may serve as sources of infection for primates who can then act as reservoirs and reinfect humans (Flynn, 1973). Organisms inhabit the large intestine. Irritation and perianal pruritis may occur resulting in self-mutilation, increased irritability and restlessness. Hemorrhagic enteritis and abdominal discomfort may be observed.
Diagnosis can be made by visualization of adults in the anal area. Celophane tape may be used in order to obtain eggs from the anus for identification. Pyrantel painoate can be used to treat pinworm infections (Wolff, 1990).
This spirurid nematode is a common parasite of the pancreas in callitrichids. This organism requires an intermediate arthropod host. Cockroaches may be capable of serving as intermediate hosts (Potkay, 1992). Acute chronic pancreatitis may result from infection (Wolff, 1990). Massive infections may be responsible for a wasting disease type syndrome in C. jacchus. Periductal fibrosis, proliferation of ducts and exocrine pancreatic atrophy may be observed (Potkay, 1992). Diagnosis is made at necropsy and it is often an incidental finding on histologic examination. It may be possible to diagnose infection through fecal flotation. There is no reported treatment but ivermectin may be effective (Wolff, 1990). Fenbendazole may also be a potential treatment.
Pterygodermatites nycticebi (Rictularia nycticebi)
This organism has been associated with morbidity and mortality in Leontopithecus rosalia (Montali et al., 1983). Cockroaches, crickets or other insects serve as intermediate hosts for this organism (Potkay, 1992). Clinical signs include watery diarrhea which may contain adult wom-is, anorexia, weakness, anemia, hypoproteinemia and leukopenia.
Post mortem findings have included the presence of numerous parasites in the gastrointestinal tract. Histologic exam demonstrated the anterior ends of the adult organisms embedded in the small intestinal mucosa. A necrotic pseudomembrane and clubbing of the small intestinal villi were also seen (Montali et al., 1983).
Diagnosis is generally based on the identification of eggs, worins or larvae in the feces. Prophylactic wonnings with ivermectin and mebendazole, as well as cockroach population control measures, can decrease the possibility of infection (Wolff, 1990).
Physaloptera dilatata can cause infection in callitrichids. The organism attaches to the gastric mucosa and can cause gastritis and hyperplastic gastric lesions with heavy infections (Wolff, 1990). Diagnosis is made by fecal Rotation. The use of high doses of mebendazole has proven effective in some Physaloptera species (Wolff, 1 990).
Infection with several species of filarial worins is a common occurrence in wild-caught callitrichids. Wild cotton-top tamarins have been observed with a filarial worm parasite belonging to the genus Mansonella. Typical of this parasite, the adult lives in the body cavity of the host and produces living microfilaria that circulate in the peripheral blood. They are not pathogenic (Savage, 1990).
Filarial worms inhabit the thoracic or abdominal cavities, or the subcutaneous tissues. Transmission occurs by way of blood sucking insects. However, there have not been any reports of clinical signs associated with infection (Potkay, 1992). Diagnosis is made by the identification of microfilariae in smears of the peripheral blood, or by demonstration of adults in subcutaneous tissue or in the peritoneal cavity on necropsy. According to Potkay (I 992), no treatments have been evaluated or reported.
Trematodes are often encountered in New World monkeys. Only some of the more important species are discussed here. For a synopsis of prior reports of trematode infections in callitrichids, see Potkay (1992).
This organism is a fairly common, moderately pathogenic fluke that resides in the bile duct. The mode of infection appears to be unknown. Mollusks serve as obligatory intermediate hosts. Generally, infection is asymptomatic, but various degrees of pathogenicity may be observed depending on the parasite level. Heavy infections can lead to an inflammatory reaction and thickening of the bile ducts, resulting in mechanical blockage. Fecal sedimentation may allow for identification of the characteristic eggs. Post mortem diagnosis can be made based on the presence of adult flukes in the bile duct. Praziquantel can be used to treat infection (Wolff, 1990).
Cestodes do not seem to be a serious cause of disease in callitrichids. Clinical disease or enteric pathology are rarely observed with tapeworm infections in nonhuman primates (Toft, 1986). Nonhuman primates may act as inter-mediate hosts developing larval forms in somatic tissues (Toft, 1986). The reader is referred to Potkay (1992) for a listing of reported cases of cestode infections in callitrichids.
Diphyllobothrium erinacci and Spirometra reptans
Infection is generally asymptomatic and the presence of spargana is usually an incidental finding at necropsy. Spargana are the pleurocercoid larval form of these organisms and the term for infection is sparganosis. Infection probably occurs following ingestion of crustacean intermediate hosts (Wolff, 1990).
Spargana may occur in just about any part of the body. They are usually found in subcutaneous, muscle and connective tissues as well as in the abdominal or pleural cavities. Inflammation and edema may occur following migration through the tissues or as a result of degeneration following the death of the organisms. Calcification of chronic lesions may occur allowing for radiographic visualization. Subcutaneous tissue nodules may be palpable in the live animal. There is no known treatment for infection but if necessary, organisms may be removed surgically (Wolff, 1990).
Prosthenorchis elegans and P. spirula
The acanthocephalans, thomy-headed wonns, are probably the most significant parasites of callitrichids. Insects, most commonly German cockroaches, serve as intermediate hosts. Infection with P. elegans is more common than with P. spirula (Potkay, 1992). These organisms frequently inhabit the distal ileum, cecum and proximal colon. Parasites are often found at the ileocecal valve (Richter, 1984). Toft (1986) lists several references and states that P. spirula generally inhabits the terminal ileum while P. elegans tends to be found in the cecum or colon.
The worm attaches its proboscis to the intestinal mucosa which results in pronounced inflammation, necrosis, fibrosis and the formation of nodules. The worms invade the intestinal walls leading to abscessation, peritonitis, and sepsis. Fatal peritonitis and septicemia can result when the intestinal wall is perforated.
There are no distinctive symptoms associated with infection (Potkay, 1992; Toft, 1986). Clinical signs of Prosthenorchis infection may include diarrhea, anorexia, cachexia, pain, depression, debilitation and death. Infection by secondary pathogens which are able to colonize the lesions produced by the parasites are usually responsible for fatal cases. The passage of bloody and scanty stools may be seen in severe cases. Mesenteric lymphadenitis and splenomegaly may be associated with infection (Potkay, 1992). Intussusception, mechanical blockage or rectal prolapse may occur with severe infections. Histologic findings include inflammation, mucosal ulcers, and granuloma and abscess formation in the intestinal wall (Toft, 1986).
Diagnosis is based on the demonstration of eggs in concentrated fecal samples and, less commonly, on the presence of worms. Fecal flotations are inadequate for the identification of eggs and direct smears or sedimentation methods must be employed (Toft, 1986). The presence of the characteristic thorny-headed worms found at necropsy are diagnostic. There appear to be no consistent and confirmed reports of successful drug therapy. Drugs like ivermectin have not been evaluated as potential treatments (Potkay, 1992). Worms may persist in healthy hosts so supportive nutrition and the administration of antibiotic therapy, when necessary, are important for preventing clinical disease (Richter, 1984). Surgical excision of worms may be an appropriate therapeutic approach. Cockroach control is an important aspect of preventing acanthocephalan infection.
Arthropods don't appear to be a serious cause of disease in callitrichids. As previously described, several insects may transmit viruses and parasites. See Potkay (1992) for a listing of reported cases of infection in calfitrichids.
Porocephalus clavatus nymphs are frequently found in Saguinus sp., although there do not appear to be any reports in S. oedipus to date (Potkay, 1992). The nymphs may be observed in a coiled "C" position, encapsulated in the peritoneal and thoracic cavities (Richter, 1984). Nymphs may be located within cysts in the lungs, liver and meninges, and beneath the parietal peritoneum and pleura (Potkay, 1992). Dead nymphs may result in chronic inflammation (Cosgrove et al., 1970). There have not been any reports of clinical signs and there are currently no treatments (Potkay, 1992).
Acariasis is seldom seen in callitrichids, even though they are parasitized by several species of mites (Potkay, 1992). Demodex sp. have been found on the skin and in the hair follicles and may cause dermatitis. Reported clinical signs in S. geoffroyi included cutaneous erythema, alopecia, and the formation of papules on the head, tail and limbs (Hickey et al., 1983). Focal inflammation and degeneration were observed in areas surrounding infected hair follicles. Diagnosis is made by the identification of the organisms following a deep skin scrape. Successful treatment in the above case involved the use of ronnel and rotenone ointment.
The Regional Reference Center for Simian Viruses of the Southwest Foundation for Research and Education located in San Antonio, Texas has been established for the investigation of nonhuman primate viruses and may be a useful resource for the identification of viral agents.
Herpesvirus tamarinus (Herpesvirus-T or Herpesvirus platyrrhinae)
Infection with this virus frequently results in a systemic fatal disease in callitrichids. The squirrel monkey (Saimiri sciureus) serves as the natural host for this organism. Infection is often latent in the natural host but may cause mild herpetic lingual ulcers and stomatitis. The virus is shed in oral secretions and oral lesions. Spread of the organism occurs through aerosols, direct contact or fomites. If the virus occurs in a susceptible monkey colony, it can reach epizootic levels by spreading rapidly, resulting in high mortality rates (Melendez, 1976).
Infection in tamarins is generally fatal. Common signs of disease include anorexia, weakness, depression, emaciation, rhinitis, conjunctivitis, sneezing, serous nasal discharge, ulcerative dermatitis, and vesicles and ulcers on the oral and labial surfaces. Hyperesthesia and pruritus with frequent scratching may be seen (Richter, 1984).
Post mortem findings include gastrointestinal tract ulcerations and hemorrhage, splenomegaly, bronchitis and focal pneumonia. Often hemorrhage and focal necrosis in the adrenal cortex and lymph nodes are seen. Gray-white focal necrosis of the liver and other organs may be found (Richter, 1984).
Intranuclear inclusion bodies are seen in neural, visceral and mesenchymal cells. The characteristic inclusion bodies are useful for differentiating this disease from other viral causes of hepatitis. Intranuclear inclusion bodies may be basophilic or eosinophilic. Multinucleated giant cells containing intranuclear inclusions may be found around areas of visceral necrosis or in mucosal cells. Histopathological findings include encephalitis, focal demyelination, proliferation of glial cells and neuronal degeneration. There is monocytic infiltration of the liver, spleen and lymph nodes (Richter, 1984).
Prevention involves avoiding contact with species that may be reservoirs for the virus which includes Saimiri, Ateles, Cebus, and Lagothrix. It is very important to house tamarins separately from these animals. There is a protective vaccine available for this disease. The vaccine is an attenuated variant of Herpesvirus T and is called T-SPV. This vaccine prevents disease in tamarins, with vaccinated animals demonstrating high levels of antibodies in 21 days following administration without showing any clinical signs of illness (Melendez, 1976).
Herpesvirus saimiri, Herpesvirus ateles and Epstein-Barr virus (EBV)
Experimental infection with these viruses can be oncogenic in S. oedipus. Following innoculation, they may lead to an aggressive neoplasm bearing a strong resemblance to lymphoma. It is important to keep tamarins at a safe distance from cebids in zoos because of the potential for infection. Callitrichids have been used extensively in the research of EBV. For a summarized account of experimental studies with these viruses in callitrichids, the reader is referred to Potkay (1992).
Human herpesvirus (Herpesvirus hominis or Herpes simplex)
There are no reports of natural infection with herpesvirus type 2 in callitrichids. Type 1 has been isolated from Saguinus sp. (Murphy et al., 1972). Experimental infection can lead to fatality so it is recommended to avoid contact between the tamarins and humans with active herpes fever blisters even though not much is known about the natural potential for pathogenicity.
CMV has been isolated from the salivary glands of S..fuscicollis without any signs of clinical disease (Nigida et al., 1979). The presence of this virus in nonhuman primates is usually an incidental finding at necropsy. In debilitated animals, it is important to be aware of the possibility of clinical disease as a result of latent viral infections (Richter, 1984).
Varicella virus (Chickenpox)
There do not appear to be any reported cases of natural infection with this organism in callitrichids.
Monkeypox resembles smallpox and is therefore a reportable disease (Ott, 1980). Although uncommon in humans, it is a zoonotic disease. HI titers to monkeypox have been identified in S. oedipus but the significance of this finding is unknown (Kalter et al., 1974). The disease can be fatal in marmosets (Ott-Joslin, 1993). Transmission occurs through direct contact with viral entry by way of skin abrasions or through the respiratory route (Ott, 1980; Ott-Joslin, 1993).
Ott-Joslin (1993) describes lesions in nonhuman primates as occurring on the hands, feet, hind limbs, buttocks, tongue, and the pharyngeal, laryngeal and tracheal mucosa. Lesions involve small papules which coalesce resulting in the formation of vesicles which develop reddish-brown crusts and slough after several days (Ott, 1980). Cellular proliferation, epidermal cell degeneration and necrosis, and eosinophilic intranuclear and intracytoplasmic inclusion bodies are seen on histological examination of lesions (Ott, 1980). Evaluation of lesions, histologic examination, and isolation of the viral agent are useful for diagnosing infection. Serology is not very useful in diagnosing the disease because antibodies are produced in low concentrations (Ott, 1980).
Disease caused by parainfluenza virus type I (Sendai strain) has been documented in callitrichids with various degrees of clinical sips and disease. Fever, nasal and ocular discharge, sneezing, coughing, tachypnea, dyspnea, conjunctivitis, piloerection, depression and weight loss are some of the clinical signs that have been observed (Murphy, et al., 1972; Flecknell et al., 1991). Pulmonary lesions may be seen at necropsy (Murphy et al., 1972).
Parainfluenza virus types 2 and 3 (HA-1 strain) have been isolated from Saguinus sp. without the presence of clinical signs (Murphy et al., 1972). Types 1 and 3 were isolated from the lungs of affected animals in an epidemic viral infection of a callitrichid population (Richter, 1984). Parainfluenza virus types 1 and 3 are frequent causes of childhood respiratory disease and care should be exercised in keeping infected individuals at an adequate distance from the tamarins (Richter, 1984).
Gastroenterocolitis caused by a paramyxovirus was described in a colony of S. oedipus (Fraser et al., 1978). This disease was associated with a high level of mortality. Clinical sips included inappetance, anorexia, diarrhea and dehydration. Post mortem findings included congestion and hemorrhage of the gastrointestinal tract. Colitis, gastritis, enteritis and cholangitis were seen. Epithelial syncytia with intranuclear inclusion bodies were associated with the colitis and cholangitis. In addition, intracytoplasmic inclusion bodies were observed in the bile duct syncytial cells.
Measles (rubeola) is a highly contagious virus which is spread through aerosolization, entering the host through respiratory or conjunctival mucosa. Fatal infection and clinical disease associated with high morbidity has been reported in S. oedipus (Levy and Mirkovic, 1971). This outbreak in a callitrichid colony resulted in 326 deaths. Clinical signs included lethargy, swollen eyelids, mucous nasal discharge, rhinorrhea, facial edema and maculopapular exanthema on the lips and skin. Death occurred within 8-18 hours following initial signs of disease. Yyule clinical signs and histopathology can aid in the diagnosis of rubeola, isolation of the virus, serology or immunocytochemistry are necessary for ruling out other paramyxoviruses and making a definitive diagnosis (Potkay, 1992; Lowenstine, 1993).
There were not any significant gross post mortem findings. The main histopathological finding observed at necropsy was interstitial pneumonia. Giant cells containing eosinophilic intranuclear inclusion bodies were observed. Large monocytes were seen in the lung parenchyma, some containing intranuclear inclusion bodies. Warthin-Finkeldey (W-K) type giant cells were present in the mesenteric lymph nodes, spleen, lungs and colonic lymphoid tissue. Animals surviving the infection were shown to have significant levels of hemagglutination inhibition antibody (HIA) against measles. Tamarins that were not exposed to the virus were negative for viral antibodies. See Lowenstine (1993) for an in depth discussion of measles virus infection in nonhuman primates.
Both human measles vaccine and human gamma globulin, which is generally high in rubeola antibodies, can be used prophylactically. Richter(1984)states that the use of inactivated vaccine and human IgG are recommended for use in callitrichid colonies. Vaccinating for measles does not appear to be standard protocol at zoological parks. However, clinicians in many laboratory institutions choose to vaccinate callitrichid colonies based on risk of exposure (D. Lee-Parritz, pers. comm.).
Clinicians should make an educated decision of whether or not to vaccinate tarnarins for measles based on the conditions at each individual institution. Effective protection is conferred by both killed and modified live vaccines (Lorenz & Albrecht, 1980). Ott (1 980), states that vaccination of marmosets with live vaccines is not recommended.
Callitrichid Hepatitis Virus (CHV)
This is a recently recognized, acute, fatal, epizootic disease of callitrichids. Epizootics have only occurred in zoos and wild animal parks and have not been seen in laboratory colonies (Montali, 1993). It has been determined that the agent responsible for this disease is an arenavirus which is closely related to lyrnphocytic choriomeningitis virus (Stephenson et al., 1991). Despite the fact that callitrichid hepatitis has not been associated with human disease, appropriate care should be exercised when working with infected monkeys (Montali, 1993). S. oedipus has been involved in prior outbreaks of this disease (Ramsay et al., 1989). It is thought that rodents serve as reservoirs of this organism (Ramsay & Montali, 1994; Ramsay et al., 1989). For this reason, the feeding of mice to tamarins should be avoided and attempts should be made to minimize contact with wild rodents. This disease is of serious concern due to the high incidence of sporadic outbreaks with extremely high morbidity and mortality.
Clinical signs may include anorexia, depression, lethargy, dyspnea and adipsia. Death often occurs without prior definitive signs. Mild lymphocytosis, and elevated levels of serum aspartate arninotransferase (AST), alkaline phosphatase and bilirubin are seen (Montali et al., 1989). These levels are indicative of hepatocyte injury and acute hepatitis.
Enlarged, sometimes mottled, yellow-tan livers are observed on post mortem examination (Montali, 1993). Congested lungs, splenomegaly, jaundice, subcutaneous and intramuscular hemorrhage, necrosis and inflammation in the spleen and lymph nodes, and pleuropericardial effusion which can be sanguinous may be seen. In some recent cases, nonsuppurative meningoencephalitis has also been observed (Montali, 1993). The liver seems to be the primary organ targeted and extrahepatic lesions tend not to be severe (Montali, 1993). All of these findings indicate that this disease is systen-iic but primarily hepatotropic (Ramsay & Montali, 1994).
Histopathologic findings in both natural and experimental infection include swollen and necrotic hepatocytes, and inflammation. Acidophilic bodies are found scattered throughout the hepatic lobules. These represent remnants of hepatocytes which underwent acidophilic degeneration (apoptosis) with the formation of acidophilic bodies (Montali et al., 1989; Montali, 1993). In some cases, fatty change may occur in the liver and lyinphoplasmacytic cellular infiltration may be present in the portal triads (Montali, 1993). Unlike with Herpesvirus T, there are no intranuclear inclusion bodies seen with this disease (Montali, 1993). Characteristic histological changes can aid in the diagnosis of this disease and definitive diagnosis can be made through serum and liver tissue immunoblot assay evaluation.
This disease is endemic in Central America, South America and Africa and is a potential cause of mortality among captive tamarins in these areas. Transmission is via Aedes sp. and Haemagogus sp. mosquito vectors. Mosquitos also act as reservoirs because once they are infected, they are infectious for the remainder of their lives. Generally this disease is of little concern in non-endemic areas. However, Aedes aegypti exists in the United States so this disease is potentially transmittable in this country (Ott, 1980).
S. oedipus is susceptible to rabies and there is evidence to suggest that they may contract the disease from modified live vaccines (Potkay, 1992). The form seen in monkeys is usually of the paralytic type so they generally bite only if they are agitated and transmission between monkeys and humans is very rare (Ott, 1980). The efficacy of killed vaccines are not known and human vaccines are not effective in nonhuman primates (Ott, 1980). However, INIRAB vaccine has been used successfully in a wide variety of species which suggests that it would probably be effective in nonhuman primates. Vaccination with killed vaccine is recommended for monkeys with high risk of exposure. Clinicians must evaluate the situation at individual institutions where tamarins are housed. Animals housed in open cages outdoors have more risk of being exposed. Possibly the greatest potential for transmission is from bats which are small enough to access open-bar cages. The prevalence of rabies in small rodents is extremely low so they most likely do not pose a risk.
There do not appear to be any significant reports of natural infections with retroviruses in callitrichids. The reader is referred to Potkay (1992) for a summarized account of numerous experimental studies in callitrichids. S. oedipus has been asymptomatically infected with simian immunodeficiency virus (SIV) (Miura, 1989). However, there are no reports of natural infection with this virus in callitrichids.
IV. OTHER DISEASES
Colitis and adenocarcinoma of the large bowel
Colon cancer is one of the most deadly forms of cancer in humans. Cotton-top tamarins are the only non-human primate known in which this type of tumor develops spontaneously. In captive populations of cotton-tops with good nutritional practices, this disease is the main cause of death. Other than those of the gastrointestinal system, the incidence of spontaneous malignant neoplasms in cotton-top tamarins is very low. Spontaneous colonic carcinoma occurs in about 35% of adult cotton-top tamarins in captivity and is most likely to occur in animals 5-10 years old (Clapp & Henke, 1993). Colitis and colon cancer either do not occur or are of relatively low incidence in natural populations of S. oedipus (Wood et al., 1989).
Since cotton-top tamarins spontaneously develop colonic adenocarcinoma they are considered an important model for the study of this disease. Colonic carcinoma has been reported at several different institutions in widespread geographical locations (Clapp, 1993). This suggests that environmental factors may not play a major role in the etiology of the disease, although they may exert some influence. A familial tendency is likely in some cases.
Tamarins with colitis are often responsive to treatment with sulphasalazine. Diarrhea usually resolves and the animal returns to its previous body weight. Histologic changes often persist. Treatment is frequently given for one or two months and the status of the animal is assessed by repeat colon biopsy. If severe changes persist, long-term therapy is warranted. The animal should undergo regular examination because neoplasia is highly likely in these animals, including palpation, biopsy, and contrast radiography when available. Campylobacter is often present in tainarins with colitis (D. Lee-Parritz, pers. comm.). However, the significance of Campylobacter is unknown at this time.
There is a strong link between colitis and colon cancer. The pattern frequently seen involves the development of idiopathic ulcerative colitis observed prior to and during the development of colon cancer. In S. oedipus, colon carcinoma develops either from preexisting adenomas or more commonly from flat epithelium (Clapp & Henke, 1993). S. oedipus colon cancer is considered to be multicentric in origin. Cancer probably originates in flat mucosal areas changed by chronic colitis at the crypt base in the reparative hyperplastic epithelium. Transformation of cells occurs, and the round, pleiomorphic, transformed cells invade the lamina propria where they form poorly defined colonies. Ulceration and erosion into the mucosal mass may occur resulting in a malignant ulcer. There is often a sciffhous fibrous connective tissue response to infiltrating neoplastic epithelial cells (J. Cooley, pers. comm). Metastasis occurs when malignant cells enter the lymphatics of the mucosa and travel to the lymph nodes (Lushbaugh et al., 1985). The neoplasm tends to metastasize to the regional lymph nodes, less commonly to the pancreas and lungs, and infrequently to the liver.
Cachexia is commonly associated with the occurrence of disease. Currently, when weight loss and chronic diarrhea occurs in this species, the most likely etiology is colitis and possibly colon cancer. Acute colitic episodes may be asyrnptomatic. In symptomatic cases, signs include loose stools, weight loss and lethargy.
Colonoscopy is useful in the evaluation and description of colitis. Colonoscopy and biopsy are required for definitive diagnosis of colitis or colon cancer. The proper procedure is well-documented (Clapp et al., 1993). A 5.0 mm fiberoptic pediatric bronchoscope adapted for use in this species is used with simultaneous video image display. Ulcers, nodules, hemorrhages and other abnormalities should be described and biopsy samples collected from these lesions. Biopsy specimens are fixed in 10 % neutral buffered formalin and histologic sections are prepared using routine techniques. Slides should be routinely stained with Periodic Acid Schiff (PAS) stain and hematoxylin and eosin. Histologic evaluation of colitis entails counting the number of inflammatory cells in the lamina propria and epithelium, and describing the changes in crypt morphology. Cases are considered chronic (inactive) when primarily mononuclear inflammatory cells are present. Polymorphonuclear leukocytes are indicative of more acute (active) cases (Clapp et al., 1993). Normal colons should not have elevated cellular infiltration of the lamina propria. Mstopathological changes may include the presence of branched and/or tortuous crypts and crypt atrophy.
Contrast radiography (barium enema) is helpful in the diagnosis of abdominal masses, especially in the ileocecal region beyond the reach of the endoscope. Colon cancers often appear as classic "apple-core" lesions. In an "apple-core" lesion, the bowel lumen is constricted because of an intramural mass. The mucosal surface is often ragged because of tumor gorwth. In a contrast radiograph, the barium column is contracted in the area of the tumor and has the appearance of an apple core (D. Lee-Parritz, pers. comm.).
Appropriate postmortem examination initially involves culturing of samples from both the ileum and colon and gross examination for plaque-like thickenings in colonic mucosa, irregular plaques on serosa, and enlarged mesenteric lymph nodes, followed by collection and fixation of tissue samples from all organs. The large and small intestines should be laid flat and opened to facilitate the evaluation of the entire intestinal tract. Following sampling for culture, the mesentery is cut adjacent to the intestine, the lumen is carefully opened, avoiding wiping or rubbing the mucosal surface, and the entire remaining intestine is immersed into fixative, usually 10 % neutral buffered fonnalin (J. Cooley, pers. comm). This is followed by collection and fixation of tissue samples from all organs.
Histopathological findings include effacement of normal colonic mucosal architecture and PAS+ mucin-producing cancer cells which may be located in the submucosal connective tissue and lymphatic spaces. Cancer extensions composed primarily of mucin and malignant cells are visualized with the PAS stain, extending into the tunica muscularis propria. Desmoplastic connective tissue is found around neoplastic cells. The characteristic colonic cancer cells are easily recognized in metastases seen in other organs (Lushbaugh et al., 1985).
Myelolipoma of adrenal origin has been identified in S. oedipus (Pearson et al., 1987; Stein et al., 1982). The myelolipomas seem to occur in aged individuals. The juxtarenal masses have not been considered to contribute seriously to clinical disease but may be associated with some loss of body condition. The finding may be incidental at necropsy.
Necropsy findings from one of the cases describe a dark red, well-encapsulated, spherical mass with some pale yellow areas. Histopathological findings included adipose tissue containing hemopoietic tissue that resembled bone marrow and included megakaryocytes. A thin rim of adrenal cortical cells and a connective tissue capsule were found in some peripheral areas of the mass (Pearson et al., 1987).
Although understanding has greatly improved over the years, the nutritional needs of callitrichids still remain poorly understood. For a list of references on current research in the area of callitrichid nutrition, the reader can consult Potkay (1 992).
Historically, hypoglycemia has been a problem in captive callitrichids and may be related to their high metabolic rates (Cicmanec, 1977). Early clinical signs included muscle tremors and unsteadiness. Fruits fed immediately following the onset were able to reverse early signs. For more serious cases, 20% dextrose administered through a stomach tube along with insulin given intraperitoneally were suggested. Alleviation or elimination of disease may be achieved by feeding sugar in small amounts of feed many times throughout the day and by ensuring provision of palatablefeed.
Tamarins require adequate vitamin C to avoid the onset of scurvy. Citrus fruits or alternative supplements are appropriate supplemental sources of vitamin C. However, citrus fruits may cause gastrointestinal distress so care should be exercised.
Vitamin D3deficiency used to be a widespread problem in callitrichid colonies resulting in osteodystrophia fibrosa (rickets and osteomalacia). Vitamin D3 is required by New World primates for normal bone metabolism. Vitamin D3 is more efficient at increasing calcium absorption than vitamin D2(Hunt et al., 1967). New World monkeys are unable to metabolize vitamin D2. Callitrichids have an even higher vitamin D requirement than cebids because of a decreased sensitivity of the 1, 25 OH-D receptor. Now that the need for D3 versus D2is understood, appropriate diets are usually formulated but it is important to be aware of the possibility of faulty diet preparation (Richter, 1984). Excessive feeding of insects should be avoided because these dietary components are high in phosphorous and feedings may exacerbate marginal vitamin D nutrition by inducing nutritional secondary hyperparathyroidism (D. Lee-Parritz, pers. comm.). The suggested daily dietary value is 500 IU D3/monkey/week to prevent hypovitaminosis D3 (Hunt et al., 1967).
See Potkay (1992) for a discussion of other vitamin deficiencies observed in callitrichids, both natural and experimentally induced.
Trauma caused by conspecifics
Physical conflicts between conspecifics may pose a serious health threat. Early detection of injuries is vital to prevent abscess formation, septicemia, osteomyelitis and fatality. Bacterial infection of wounds following fights in group-housed monkeys are common. Bacterial culturing, antibiotic sensitivity testing and treatment should be undertaken immediately but may not be necessary. Suturing of wounds is often successful if animals are consistently monitored to prevent premature removal of sutures. Systemic and local antibiotics should be administered in suitable cases.
Self-mutilation has been known to occur. This may involve biting or hair pulling. Self-inflicted alopecia can result. Attempts to increase the psychological well-being of the animals by providing a diverse environment with suitable climbing structures, nest-boxes and opportunities to hide from aggressive cage-mates is advised to minimize the incidence of self-induced trauma.Congenital
Congenital anomalies do not appear to be a common occurrence in cotton-top tamarins. Achondroplastic dwarfism, polydactyly, and syndactyly have been observed in a newborn male cotton-top tamarin. See Chalifoux (1993) for a description of the case.Miscellaneous
Diarrheal disease can be a very significant problem in captive tamarin populations. According to Richter (1984), it is the largest cause of morbidity in tamarin colonies. The cause in most of these cases goes undetermined. Some cases can be linked to bacterial or viral causes while in other cases nutrition, behavior or other unknowns may play a role. As previously discussed, chronic colitis has been linked in a causal relationship to colon cancer in cotton-top tamarins whereas other Saguinus species may have clinically similar colitis with the absence of colon cancer.
Signs include atony, megacolon and large quantities of feces. The feces often contain a large amount of mucus. Coprophagy may occur in cases of diarrhea (Richter, 1984).
On postmortem examination, the large intestine is often enlarged and filled with gas or ingesta. Histopathological findings include atrophy of crypts, inflammatory cell infiltration of the mucosa and hyperplasia of residual crypts. Supportive therapy is recommended for treatment of affected individuals. A slow recovery may occur in some cases, while in others death may result (Richter, 1984).
This disease, which is known by several names, is an extremely significant disease of poorly understood etiology. Since there may be many variable factors involved in each individual case, it probably should not be considered a disease in itself but rather a clinical syndrome. Potential causative factors may include stress, poor diet, heavy parasitism, chronic bacterial infection and colitis.
Marmoset wasting disease is clinically characterized by rapid and persistent weight loss with skeletal muscle atrophy especially seen in the legs. When a drop in body weight is seen, this disease should be considered. Anemia and hypoproteinemia with associated cervical or ventral edema commonly occur (Richter, 1984). Alopecia is often observed, especially on the tail. Weakness or paralysis of the hind legs, intermittent diarrhea and a wet or greasy appearance to the fur may be seen (Potkay, 1992). Affected animals are particularly prone to acute episodes of hypoglycemia with associated hypothermia. Rectal temperatures may drop as low as 300C and blood glucose levels may decrease to as low as 40 mg/dI. Attempts should be made to increase body temperature and blood glucose levels and to avoid the onset of Gram negative shock (Richter, 1984).
Post mortem findings include emaciation, muscle mass reduction and almost complete absence of body fat. Other possible findings include colon or other gastrointestinal or pancreatic lesions, Prosthenorchis, and Trichospirura. The nutritional and parasite control program should be carefully evaluated in colonies with a high incidence of marmoset wasting disease. Sporadic cases are likely the result of colitis or chronic metabolic illness (D. Lee-Parritz, pers. comm.).
It appears that most treatments have been geared towards altering feeding and nutrition in various ways. Treatment approaches should be tailored to the individual case based on possible etiologies and necessary supportive therapies. Efforts should be made through a problem oriented medical approach to narrow down the possibilities, and the original cause treated appropriately.
Intussusception occurs relatively frequently in callitrichids. What leads to intussusception is unclear but it probably involves increased gut motility following irritation due to inflammation from infection, parasites, toxins or other causes. The occurrence of intussusception and rectal prolapse are often associated.
Successful surgery in S. oedipus has been documented (Blampied & Allchurch, 1983). This involved a case where the ileum had passed through the ileocecal valve and telescoped into the anterior colon. Repeated episodes and treatment of rectal prolapse occurred prior to identification of intussusception and surgery. In a prior case, a cotton-top tamarin died following repeated episodes of rectal prolapse and replacement. Intussusception was found on necropsy (Blampied & Allchurch, 1983).
The most common location for intussusceptions are the terminal ileum. It is very uncommon for rectal prolapse to occur in the absence of intussusception, therefore rectal prolapse should be treated by laparotomy and cecocolopexy rather than simple reduction (Richter, 1984).
Acute shock is often seen with small intestine intussusception and this along with palpation can be used to aid in diagnosis. Intussusceptions are serious emergencies requiring immediate attention.
A retrospective study was carried out at the German Primate Center of all callitrichids, including a number of S. oedipus, necropsied beginning in 1973 (Brack, 1988). The study revealed that 91% of tamarins over 6 months old had spontaneous IgM-mediated mesangioproliferative glomerulonephropathy. Inflammatory renal lesions were found to be the most common organ lesions seen at necropsy. The disease is considered to be involved in about 20 % of all the callitrichid deaths at the German Primate Center. The destruction of increasing numbers of glomeruli influenced or resulted in the fatalities observed. Genetics appeared not to play a role in the occurrence of this disease.
There were no distinct clinical signs but up to 88% had continuous or transient hematuria and/or proteinuria, with urinary casts. Post mortem findings included mesangiosclerosis, proliferation and sclerosis of Bowman's capsule, intraglomerular adhesions, and glomerular sclerosis. IgM deposits were found in strong association with the mesangial lesions along with Clq, C3 and C4 which is suggestive of classical complement pathway involvement. This is similar to human IgM nephropathy. Nothing is known about the origin and nature of the antigen causing the mesangial IgM deposits and resulting lesions in callitrichids.
Inadvertant poisoning may occur and it is important to be careful of all substances that may come in contact with tamarin populations.
For brief restraint or phlebotomy, the injectable anesthetic, ketamine (10-20 mg/kg), is safe and effective for adult tamarins (D. Lee-Parritz, pers. comm.). A combination of ketamine (25 mg/kg) and midazolain Hcl (25 mg/kg) is effective for procedures that require the animal's body to be less rigid (Savage et al., 1993). Isoflurane is the anesthetic of choice for major surgical procedures. If gas anesthetics are not available, telazol or pentobarbitol may be used but neither provides good analgesia and pentobarbitol has a narrow therapeutic window (D. Lee-Panitz, pers. comm.). Pentobarbitol is a traditional method of anesthesia requiring minimal equipment and little expense but it is important to keep in mind that it does not provide good analgesia unless it is given at levels where it depresses respiratory reflexes (C. Sedgwick, pers. comm.).
VI. ALLOMETRIC SCALING
For safe and effective administration of injectable drugs, it is important to allometrically scale doses using specific minimum energy cost (SMEC) values. Theoretically, SMEC is the energy per unit of body size (kcal/kg) that an animal uses to maintain bodily functions at physiologic rest. SMEC = K(W kg0.75)/W kg = K(W kg-0.25) where K is 70 for placental mammals and W is the animal's weight in kilograms. MEC = K(W kg0.75) so SMEC is the MEC value divided by the animal's weight in kilograms. To determine the SMEC-dose of a drug, the dose rate (mg/kg) of the control animal is divided by the control animal's SMEC (C. Sedgwick, pers. comm.).
The proper doses of many drugs are unknown for tamarins so doses can be scaled using the standard human pediatric dose. Attempts should be made to accurately deten-nine the animal's weight in a triple beam balance prior to administration of the drug and the following procedure using the example of ceftriaxone in a 500 g cotton-top tamarin should be implemented to determine proper dosages.
According to the Physician's Desk Reference (1 995), the human pediatric daily dose rate is 100 mg/kg. Using a weight of 20 kg for a human child:
SMEC = K(W kg-0.25= 70(20 kg-0.25) = 33
SMEC-dose = dose rate/SMEC = 100/33 =3
For a 500 g cotton-top tamarin:
SWC = 70(0.5 kg-0.25) = 83.2
Scaled dose rate = SMEC x SMEC-dose = 83.2 x 3 = 250 mg/kg
Scaled dose = 250 mg/kg x 0.5 kg = 125 mg
To illustrate the importance of scaling based on body weight, using the extreme example of a 60 kg female gorilla, the scaled dose rate would be 75 mg/kg which is vastly different from that of the cotton-top tamarin. This is because smaller animals have a greater surface area to volume ratio. For a more in-depth discussion of scaling principles and strategies, see Sedgwick (1993).
This principle of scaling does not need to be adhered to in the administration of inhalant anesthetics. Inhalant anesthetics are effective at just about the same percent concentration independent of the size of the animal because smaller sized animals have a greater absorptive lung surface per unit of mass than larger animals. This is necessary due to their higher metabolic rates (C. Sedgwick, pers. conun.).