Squirrel Baby

The local Sheriff brought me this lil fellow yesterday:










He was cold and dehydrated and emaciated, but I sat with him all night
and kept feeding him electrolytes and just switched over to milk replacer.
Looks like he is coming around.

Great Horned Owl

Toxoplasmosis in Cats

Unfortunately all kittens came down with the same symptoms and didn't not survive.
Toxoplasmosis was the only disease that I could find that fit all the symptoms, so for my own reference:

Toxoplasmosis in Cats

Toxoplasmosis, a disease of cats and other mammalian species, is caused by a parasitic protozoan, Toxoplasma gondii. Protozoa are single-celled organisms that are among the simplest creatures in the animal kingdom. Although infection with Toxoplasma is fairly common, actual disease caused by the parasite is relatively rare.

The Life Cycle of Toxoplasma
Cats, domestic and wild, are the definitive host (host in which the adult, or sexually mature stage, of the parasite is produced) and are the parasite's primary reservoir of infection. Domestic cats are important in transmission of Toxoplasma to other animals and human beings, which become involved only as intermediate hosts of the parasite. Consumption of raw meat tissues is another important means of transmission.

Cats acquire Toxoplasma infection by eating any of the three infective stages of the parasite: cyst, oocyst, or tachyzoite. Following ingestion of cysts in infected prey (rodents or birds), the intraintestinal infection cycle begins. This cycle occurs only in members of the cat family. The organisms multiply in the wall of the small intestine and produce oocysts, which are then excreted in great numbers in the feces for two to three weeks. Within five days the shed oocysts may sporulate, becoming infectious to other animals and to humans. Sporulated oocysts are highly resistant to environmental conditions and can survive in moist shaded soil or sand for many months.

During the intraintestinal infection cycle in the cat, some Toxoplasma organisms released from the ingested cysts penetrate more deeply into the wall of the intestine and multiply as tachyzoite forms. Very soon these forms spread out from the intestine to other body sites, starting the extraintestinal infection cycle. Eventually the cat's immune system restrains this stage of the organism, which then enters a dormant or "resting" stage by forming cysts in muscles and brain. Most cysts probably remain dormant for the life of the host. The extraintestinal infection cycle occurs not only in cats but also in the intermediate hosts (including humans).

Most healthy exposed cats shed oocysts during acute infection with Toxoplasma, but will not shed them after the acute infection. Even in those few cats that do re-excrete oocysts after another exposure to Toxoplasma, the number of oocysts shed is smaller and may even be insufficient to transmit the parasite effectively.

Ingestion of tissue cysts in infected prey or in other raw meat is probably the most common route by which cats are exposed to Toxoplasma. Congenital infection (transmission from mother to fetus) occurs in sheep, goats, and humans, but is much less common in cats.

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Signs
Most cats show no clinical signs of infection with Toxoplasma. Occasionally, however, clinical disease—toxoplasmosis—occurs, kittens and young adult cats being more often affected than older animals. Lethargy, depression, loss of appetite, and fever are typical early nonspecific signs. Pneumonia, manifested by respiratory distress of gradually increasing severity, is the outstanding sign in many cats. Hepatitis (inflammation of the liver) may cause vomiting, diarrhea, prostration, and jaundice (yellowing of the mucous membranes). Inflammation of the pancreas and enlargement of lymph nodes also occur. Toxoplasmosis can also affect the eyes and central nervous system, producing inflammation of the retina or anterior ocular chamber, abnormal pupil size and responsiveness to light, blindness, incoordination, heightened sensitivity to touch, personality changes, circling, head pressing, twitching of the ears, difficulty in chewing and swallowing food, seizures, and loss of control over urination and defecation.

In some cases, coinfection with feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV) may predispose a cat to develop toxoplasmosis.

Diagnosis
Toxoplasmosis may be strongly suspected by the history, signs of illness, and the results of supportive laboratory tests. A presumptive diagnosis may be made by demonstration of a fourfold or greater increase in antibody titers to Toxoplasma (indicating a recent infection) over a three- or four-week period in a cat showing signs suggestive of toxoplasmosis. A definitive diagnosis requires either microscopic examination of tissues or tissue impression smears for distinctive pathologic changes and the presence of tachyzoites or inoculation of suspect material into laboratory mice.

The presence of significant antibody levels in a healthy cat suggests that the cat has been previously infected and now is most likely immune and not excreting oocysts. The absence of antibody in a healthy cat suggests that the cat is susceptible to infection and thus would shed oocysts for one to two weeks following exposure.

Treatment and Prevention
The two drugs that are most often used—pyrimethamine and sulfadiazine—act together to inhibit Toxoplasma reproduction. Treatment must be started as soon as possible after diagnosis and continued for several days after signs have disappeared. In acute illness, treatment is sometimes started on the basis of a high antibody titer in the first test. If clinical improvement is not seen within two to three days, the diagnosis of toxoplasmosis should be questioned.

Pyrimethamine may be unpalatable or toxic to some cats, even if given in small amounts. Recently, the antibiotic clindamycin has been reported to be effective in treating feline toxoplasmosis, with few side-effects observed.

No vaccine is as yet available to prevent either Toxoplasma infection or toxoplasmosis in cats, humans, or other species. Research in this area is in progress.

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Toxoplasma and Human Health
Although the incidence of toxoplasmosis among humans probably has not changed significantly over the years, awareness and concern about the disease have increased within the medical and veterinary communities. It has been estimated that 30 to 50 percent of the world's human population has been infected with Toxoplasma and harbors the clinically inapparent cyst form. This encysted form is important because, if given the opportunity, it can produce disease in immunocompromised patients. For this reason veterinarians are often called on to clarify the role that cats play in the transmission of Toxoplasma to humans.

Contact with oocyst-contaminated soil is probably the major means by which many different species—rodents, ground-feeding birds, sheep, goats, pigs, and cattle, as well as humans living in developing countries—are exposed to Toxoplasma. In the industrialized nations most transmission to humans is probably due to eating undercooked infected meat, particularly lamb and pork (in many areas of the world, approximately 10 percent of lamb and 25 percent of pork products contain Toxoplasma cysts). The organism may also on occasion be present in some unpasteurized dairy products, such as goat's milk.

Congenital infection is of greatest concern in humans. About one-third to one-half of human infants born to mothers who have acquired Toxoplasma during that pregnancy are infected. In general, Toxoplasma infection of the fetus is least common (but disease is most severe) if the maternal infection occurs during the first trimester of pregnancy. Fetal infection is most common (but disease is least severe, often without symptoms) if the maternal infection occurs during the third trimester. The vast majority of women infected during pregnancy have no symptoms of the infection themselves.

It has been estimated that Toxoplasma is responsible for over three thousand human congenital infections in the United States each year, most of which are symptomless. Among symptomatic individuals, symptoms may be present at birth, or may first appear weeks, months, or even years later (the majority of clinical cases appearing at puberty, for example, are the result of congenital, rather than recent, infection). Ocular and central-nervous-system disturbances, deafness, fever, jaundice, rash, and respiratory disease, in varying combinations, are among the more common clinical manifestations in these patients. In immunocompromised persons—those undergoing immunosuppressive therapy (e.g., for cancer or organ transplantation) or those with an immunosuppressive disease such as AIDS—enlargement of the lymph nodes, ocular and central nervous-system disturbances, respiratory disease, and heart disease are among the more characteristic symptoms. In these patients—especially those with AIDS—relapses of the disease are common, and the mortality rate is high.

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Minimizing Exposure
Tissue cysts can be destroyed by thoroughly cooking meat to an internal temperature of 70°C (158°F) for at least 15 to 30 minutes. Freezing and thawing, salting, smoking, or pickling will not reliably destroy cysts in meat. Restricting the access of pet cats to rodents and birds and offering them only cooked meat, commercially prepared cat food, and pasteurized dairy products should prevent most transmission. (Nor should humans eat uncooked meat or unpasteurized dairy products.) Scavenging can be discouraged by placing secure lids on all garbage cans.

Because excreted oocysts are highly resistant to environmental conditions and millions may be present in a single stool, contamination of garden soil, flower beds, children's sandboxes, cats' litter boxes, and other areas of loose, moist soil where cats defecate may be extensive. Under such conditions transmission of oocyts to humans can be minimized by the following measures:

• Avoid contact with potentially contaminated soil, or wear rubber gloves during contact, and follow by washing hands vigorously and thoroughly with soap and water.

• Cover children's sandboxes to prevent contamination by cats.

• Dispose of feces from litter boxes daily or every other day to remove oocysts before they sporulate and become infective.

• Disinfect potentially contaminated litter boxes with scalding water or with dry-heat sterilization (55°C, 131°F).

• Chemical disinfection does not reliably destroy oocysts.

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Specific Recommendations for Pregnant Women
A pregnant woman (or one who contemplates pregnancy) can minimize exposure to Toxoplasma by taking the following measures:

• Exclude rare or undercooked meat and unpasteurized dairy products from the diet.

• Test household cats for antibodies to Toxoplasma. Assuming that a cat is healthy, a positive antibody test indicates that the animal is most probably immune and not excreting oocysts and thus would be an unlikely source of infection. A healthy antibody-negative cat is most probably susceptible to infection and would shed oocysts for one to two weeks after exposure to Toxoplasma. If possible, the cat should be tested before the woman becomes pregnant.

• Have herself tested for antibodies, preferably before becoming pregnant. A positive test would indicate past infection that will not be transmitted to the fetus. The presence of antibodies also lessens the likelihood that congenital transmission would occur should she be exposed again to the parasite during pregnancy. An antibody-negative woman would thus be at greater risk of transmitting Toxoplasma to the fetus should she become infected during pregnancy.

• Protect cats from infection (or reinfection) by preventing access to birds, rodents, uncooked meat, and unpasteurized dairy products.

• Avoid handling litter boxes. Even if a cat is antibody-positive and hence most likely immune, there exists a potential for reshedding of oocysts (although in much smaller numbers than during the initial infection). For safety, litter boxes should be changed daily or every other day by another person to eliminate any potential for accidental infection.

• Avoid handling free-roaming cats, because the fur or paws could be contaminated with oocysts, which might be transmitted by hand-to-mouth contact. Any cat allowed indoors should be kept off the bed, pillows, blankets, or other furnishings the woman uses.

• Avoid handling any cat showing signs of illness.

• Wear rubber gloves if working with garden soil. Uncooked vegetables, whether grown in a home garden or supplied commercially, should be washed thoroughly before ingestion, in case they have been contaminated by cat feces.

• Make a habit of vigorously and thoroughly washing hands with soap and water after contact with soil, cats, unpasteurized dairy products, or uncooked meat or vegetables.

August 16th

4 orphaned kittens were in need of fostercare, so I jumped in as I do often for the Erath County Humane Society when the wildlife lets up for the year. The above kitten is named Freakles for obvious reasons!



Her brother Foggy.



Their sister Patches who suffers from hypoglycemia.



This adult inca dove has a broken wing.



And these little darlings I am babysitting for a fellow opossum lover. My own 2 cripped opossums are doing great.

New Mockingbird

Mockingbird, 4 weeks old. Arrived crusted with catfood from the good intented attempt by a birdlover to save the bird. Nose and eyes were crusted over, bird was not able to see. After 3 sessions with cottonswabs and water, we got most of it off.
However, due to the wrong diet for a full week, the first signs of Metabolic Bone Disease are showing. Hopefully it's early enough!

Mockingbird has a great appetite and bowel movement is normal again and he gained back strength.

Avian Diseases Reference

GASTROINTESTINAL DISEASES OF BIRDS

James K Morrisey, DVM, DABVP (Avian)

Diseases of the Oral Cavity

The oropharynx is a common site for a variety of lesions in birds. A thorough examination of the oral cavity is usually not possible in the awake parrot, however, a quick visual examination can be performed and the pet sedated if lesions are noted. Other species such as raptors, passerines, and columbiformes are more easily examined while awake. Clinical signs associated with oropharyngeal diseases vary, but may include halitosis, anorexia, inappetance, dysphagia, rubbing of the beak, or gaping.

Plaques or granulomas are a clinical sign common with several diseases including bacterial infections, yeast infections, hypovitaminosis A, parasitic diseases, and viral diseases. Cytology and culture of the lesion will help to determine the cause. Cytological samples may be collected by rubbing a sterile cotton-tipped applicator along the lesion and then rubbing the sample on a clean slide. Several slides should be made because special stains such as acid fast or periodic acid Schiff may be required. Bacterial infections of the oropharynx can be caused by a variety of bacteria, including Staphylococcus sp., Klebsiella sp., and other Gram negative bacteria. These bacteria may cause granulomas or a generalized stomatitis. The bacterial overgrowth may be caused by underlying immunosuppressive diseases or may be secondary to damage to the oral mucosa by irritants, rough food items, or the accumulation of food caused by beak deformities. Treatment should be with systemic antibiotics based on culture and sensitivity results. Topical treatment may be performed by placing an antiseptic solution such as chlorhexidine (1ml in 30ml of water) in the water supply or by gently flushing the oral cavity. Granulomas can also be caused by Mycobacteriosis. Mycobacterium avium is the most commonly isolated species from oral lesions.¹ Other species such as M. genovense and M. tuberculosis have been identified, therefore culture and sensitivity of mycobacterial organisms is recommended. Mycobacteriosis more commonly affects the lower GIT and will be discussed later.

Candidiasis can cause whitish oral plaques within the oral cavity. Candida albicans is a frequently cultured organism. The infection may be primary or secondary to other systemic or oropharyngeal disease or long-term antibiotic use (especially in young birds). This disease may be called thrush, especially by falconers. Cytology of the lesion reveals the darkly staining budding yeast cells. Treatment may be topical with chlorhexidine or nystatin (300,000 IU/kg PO BID) for mild infections. More severe infections may require systemic antifungal drugs such as ketoconazole (10-30mg/kg PO BID) or fluconazole (20mg/kg PO q 48hr).²

Vitamin A deficiency can result in squamous metaplasia of the epithelial lining of the oral cavity resulting in the formation of plaques or granulomas. In addition to these lesions, the choana may be wider than normal and the papillae blunted. Cytology of these lesions will often reveal only scant normal Gram positive bacteria although. the granulomas may be secondarily infected. Biopsy of the lesion will differential primary versus secondary infections. A dietary history will assist in the diagnosis. Treatment is with dietary modification. Vitamin A may be given parentally (30,000 IU/kg weekly) for one or two doses if indicated. It should be noted that the choana and choanal papillae may remain abnormal even after successful treatment.

A variety of parasitic diseases may cause oral lesions in psittacines. Capillaria sp. can cause lesions in the oral cavity, esophagus, and ingluvies.³ Typical lesions include inflammatory masses in the oral cavity, hemorrhagic inflammation of the commisure of the beak, and a dipththeritic membrane in the oral cavity. The thread-like nematodes can be found in the inflammatory material. This disease is rare in domestically raised species. Treatment is with ivermectin (0.2mg/kg SQ q 2wk). Trichomoniasis is common in raptors and columbiformes but has also been reported in psittacines including budgerigars, cockatiels, and Amazon parrots.⁴ Lesions consist of white or yellow plaques or nodules in the oropharynx. The organism can be visualized with microscopic examination of a wet mount sample. Treatment is with metronidazole (25mg/kg PO BID for 7 days).

The diphtheroid form of pox viral infections can also cause oral lesions ranging from exudative lesions to caseous plaques when secondary infections occur. The virus requires damage to the epithelium to gain entry into the site. Affected birds may have concurrent involvement of the unfeathered skin around the eyes and beak. The dry form of pox is more common in raptors and these birds may show only the lesions at the mucocutaneous junction. Diagnosis is by histologic examination of lesions. Intracytoplasmic inclusion bodies or Bollinger bodies are characteristic of a pox infection. Treatment is with supportive care, such as antibiotics or anti-yeast medications for secondary infections. The prognosis is guarded in severely affected animals. Isolation of the affected animal is important to prevent transmission by the actively shedding lesions.

Traumatic injuries to the tongue are common in psittacines because of the tongue is often used as a tactile organ. Like mammals, the tongue is very vascular and may bleed extensively when injured. Chemical and heat burns, lacerations, and other injuries can occur. Treatment is similar to other species. If sutures are placed in the tongue the beak may need to be wired closed to prevent the bird from removing the sutures. If this is performed, a pharyngostomy tube should be placed. Foreign bodies such as wood, plastic or pieces of toys can also cause oral lesions in psittacines. Carnivorous birds may develop oral lesions from chasing or attacking their prey.

Neoplastic diseases of the oral cavity are less common but can occur in psittacines. Papillomas are the most commonly encountered oral neoplasia and may involve the oropharyngeal, choanal or laryngeal regions.⁵ Squamous cell carcinomas are the second most common oral neoplasia and may involve the oral cavity and tongue. These tumors produce ulcerative and painful lesions and are often associated with inappetence. Other oral neoplasias include fibrohistiosarcoma and fibrosarcomas.

Diseases of the Esophagus and Crop

Many of the diseases that affect the oral cavity also affect the esophagus and crop such as candidiasis, bacterial infections, trichomoniasis, and capillariasis. Clinical signs of crop disorders include regurgitation, inappetence, anorexia, and delayed crop emptying. The term sour crop or crop stasis are often used as diseases but are only clinical signs of several disease states. In addition to the aforementioned causes, crop stasis can occur with any metabolic or systemic disease, as well as esophageal or gastric foreign bodies. Crop stasis is more often a problem with neonatal birds, but can affect adults as well. The normal flora of the psittacine crop should include a few Gram positive bacteria and rare yeast. Bacterial overgrowth of Gram positive or negative organisms can occur as a primary problem or secondary to crop stasis. Diagnosis is based on cytology of crop aspirate or crop swab and culture and sensitivity. The bacterial overgrowth should be treated with crop flushes using an antiseptic solution and broad-spectrum antibiotics (until results of culture and sensitivity are available). The presence of any underlying diseases should be determined and treated.

Candidiasis is a common infection of the crop, especially in young birds. It can be a primary or secondary disorder and often occurs concurrently with bacterial infections or occurs secondarily to treating a bacterial infection. Diagnosis is based on the presence of budding yeast spores in cytological samples of the crop. The presence of the psuedohyphae indicates an invasive infection. In chronic or advanced cases a thickened crop may be palpable during physical examination. Treatment may include crop flushes, oral nystatin or other antifungals. Systemic antifungals should be used in invasive or systemic disease. Delayed crop emptying has been associated with thyroid disorders, such as goiter and thyroid adenocarcinomas. Secondary bacterial or fungal infections may occur in these situations. Definitive diagnosis of thyroid disease may require radiographs or surgical or post-mortem examination of the thyroid glands.

Non-infectious diseases of the crop and esophagus include crop fistulas, traumatic injuries of the crop, foreign bodies, and neoplastic diseases. Crop fistulas typically form because the crop wall is damaged by hot foods such as feeding formulas, table food, and hot beverages. Microwaved food is often implicated because food is heated unevenly and focal hot spots may develop. This disease is more common in neonatal birds being hand fed, but can occur at any age. When the crop wall is burned it becomes necrotic. The overlying skin is very tightly adhered to the crop and may be damaged with the initial insult or may be damaged after the crop wall has become necrotic. In either case a fistulous tract develops at the site of tissue necrosis through the crop wall and the skin causing leakage of food items onto the birds feathers. Surgical treatment is recommended and should not be attempted until all damaged tissue has formed a fistula. Attempting to treat the crop before all the damaged tissue has become apparent may result in dehiscence or subcutaneous deposition of food. The surgery involves separating the crop from the skin at the fistula and then closing the crop and skin separately. The crop is closed with a two layer inverting pattern while the skin is closed routinely. Small, frequent meals are recommended for two to three weeks after surgery to avoid stretching the crop.

Traumatic injuries to the crop can occur secondary to tube feeding, bite wounds, or foreign bodies and are treated similarly to crop fistulas. If there has been subcutaneous food deposition and abscess formation the prognosis is guarded and may require primary closure of the crop while allowing the skin to close by second intention. Foreign bodies such as whole seeds, nuts, wood, metal, and pieces of toys are typically located in the crop. this disease is most common in young psittacines, piscivorous birds, and scavengers. Diagnosis is based on palpation, history, and radiographs. The objects may be removed manually or through an ingluviotomy.

Neoplastic lesions of the thoracic esophagus and crop include squamous cell carcinoma, adenocarcinomas, leiomyosarcoma, and fibrosarcoma.⁵ Clinical signs include dysphagia, regurgitation, preference for soft foods, anorexia, and inappetance. Suspected diagnosis can be obtained with normal and contrast radiography or fluoroscopy of the area. Definitive diagnosis requires a biopsy which can be obtained through the mouth or an ingluviotomy incision using flexible or rigid endoscopy. The author has seen an invasive mucormycosis infection that resembled neoplastic disease, so biopsy is essential. Treatment of esophageal masses, once severe clinical signs begin, is unrewarding.

Diseases of the Proventriculus and Ventriculus

There are a variety of disease that can affect the avian stomachs, although differentiation of these diseases can be difficult. Clinical signs depend on the etiology, but may include regurgitation, weight loss, inappetence, or a change in appetite. Proventricular dilatation is a suspected viral disease which is thought to be caused by either an 80nm enveloped virus ⁶, or a corona-like virus.⁷ This disease attacks the myenteric and central nervous systems causing a lymphoplasmacytic neuritis with resultant dysfunction of the nerves. More than 50 species of psittacines and several species of non-psittacines have been infected. Clinical signs include weight loss despite a ravenous appetite, delayed crop and proventricular emptying, and passage of undigested food in the droppings. Radiographs will often reveal a dilated, food-filled proventriculus and ventriculus, although there may be no radiographic signs in birds that are mildly affected or have the CNS form of the disease. An enlarged proventriculus on radiographs is not diagnostic for this disease as it may be normal (post-prandial, or young animal) or caused by other GIT disease such as foreign bodies, enteritis, or metabolic disease. Fluoroscopy can be helpful in the diagnosis by demonstrating poor contractility in the proventriculus, isthmus, and ventriculus. Typically, closure of the isthmus is not seen in cases of PDD. The intestines are usually hypomotile as well, but may be hypermotile in some cases. Definitive diagnosis is based on finding lymphoplasmacytic ganglioneuritis on biopsy of the crop or proventriculus. Biopsy of the crop has a 70% success rate if a medium to large blood vessel is included in the biopsy.⁶ Scanning electron microscopy and serology have been used in the diagnosis, but are not commercially available, as yet. Treatment is supportive with soft, easily digested foods, and may extend the life of affected birds for more than a year.

Megabacteriosis is a disease of the proventriculus and ventriculus that has experienced a recent burst of interest because it has been debated whether it is a fungus or bacteria. Megabacteria is a 20-50 m m long rod-shaped organism that has characteristics of both fungal and bacterial elements. It is gram and PAS positive that is not damaged by antibiotics, but does show sensitivity to antifungals. It has a eukaryotic nucleus, characteristic of fungus, but does not have membrane-bound organelles within the cytoplasm like a bacteria. Transmission electronmicroscopy has shown an extensive intracellular membrane network but organelles without DNA, making it non-fungal in nature. Obviously more research is necessary to attempt to classify this organism. There is also some disagreement as to whether it is a primary or secondary problem or normal flora.^8-10 This organism has been associated with a syndrome called ‘going light’ I small psittacines and passerines, which is characterized by high morbidity and low mortality with clinical signs such as weight loss, anorexia, and passing whole seeds in the feces. Similar signs have been observed in other psittacines along with apathy, regurgitation, and dark green to black feces. A dilated proventriculus may also be seen radiographically. Diagnosis is based on demonstration of the organism in fecal samples or in the wall of the proventriculus. The organism has been associated with thickening of the proventricular wall and the koilin layer of the ventriculus because of the raised pH caused by loss of hydrochloric acid production. Treatment may be as simple as acidification of the water with acetic or citric acid, oral supplementation with Lactobacillus organisms or oral antifungals such as nystatin or amphotericin B. Significant economic loss in aviaries associated with the infection with the microsporidian parasite Encephalitozoon hellem has been reported in budgerigars associated with megabacteriosis.¹¹

Bacterial proventriculitis can be a primary problem or secondary to overgrowth of opportunistic pathogens. Because this disease usually affects the intestines, as well it will be discussed later. Candida albicans can invade the wall of the proventriculus and gizzard causing maldigestion/malabsorption signs. Diagnosis and treatment is similar to other forms of candidiasis. Parasitic diseases of the proventriculus and ventriculus is rare in psittacines, but occurs frequently in other species.

Proventricular and ventricular foreign bodies such as wood, metal, plastic, and other materials occur in psittacines and other species, especially ratites and waterfowl. Neonatal parrots may ingest bedding materials and toys or whole, unshelled peanuts and other seeds. These materials can cause proventricular impactions and stasis resulting in regurgitation and anorexia. Diagnosis is based on history, radiographs, and endoscopy or exploratory surgery. Medical treatment may be instituted and may be successful and includes flushing the proventriculus and ventriculus via stomach tube, laxative, and endoscopy. Ulcerative lesions may occur because of the foreign body or stress.

Neoplastic diseases of the proventriculus and ventriculus have been reported in many species.^3,8 These tumors can occur in either structure or in the isthmus. The types of tumors reported include adenocarcinomsa, carcinomas, and leiomyosarcomas. Grey-cheeked parakeets seem to have a high incidence of occurrence. Clinical signs include weight loss, anorexia, melena, and maldigestion.

Diseases of the Intestines

Diarrhea is the most consistent finding in birds with disorders of the intestinal tract, although other signs such as weight loss, anorexia maldigestion, melena, and voluminous droppings can occur. Bacterial enteritis is the most common cause of diarrhea in pet birds. Gram negative bacteria, such as Escherichia coli, Klebsiella, Salmonella, and Enterobacter spp. are most often implicated in psittacines and passerines. Other important bacteria include Clostridium, Campylobacter, and Mycobacterium spp.. Poor sanitation, poor food quality, stress, age, and concurrent diseases are predisposing factors. Diagnosis is based on fecal culture and cytology and treatment should be based on sensitivity results. Clostridium perfringens can cause a necrotic enteritis and foul-smelling feces in psittacines and is often found concurrently with E. coli infections. Clostridium tertium has been reported as a cause of megacolon and chronic, foul-smelling diarrhea in a cockatoo.¹² The sporulated bacteria of Clostridium spp. resembles a safety pin and can be seen on fecal gram stains. Definitive diagnosis is based on anaerobic culture. Campylobacter jejuni can be found in psittacines, especially neonates, and can cause lethargy, anorexia, diarrhea, and emaciation.

Mycobacteriosis is typically a disease of the GIT in birds, unlike mammals. M. avium, M. bovis and M. avium-intracellulare are the most commonly implicated species.^3,8 Transmission is through the fecal-oral route and tubercles form throughout the GIT. Clinical signs include weight loss, despite a good appetite and diarrhea. Radiographs may reveal thickened bowel loops and hepatomegaly. Leukocytosis, monocytosis, elevated liver enzymes, and beta and gammaglobulinopathies often occur on routine blood work. Grey cheeked parrots and other members of the Brotogeris genus are very susceptible. Definitive diagnosis requires an intestinal biopsy, although a positive liver biopsy with thickened bowel loops is highly suggestive. Acid fast testing of the feces is unreliable as the organism is shed intermittently. It is important to culture the organism because of the zoonotic potential, although this may take several weeks and specialized growth media. Human clinicopathologic laboratories are good sources for this specialized equipment. Treatment is not recommended because of the potential of producing antibiotic resistant strains that may become serious human hazards.

Protozoal parasitic infections, such as giardiasis, cryptosporidiosis, and coccidiosis, have been reported in psittacines, but are much more common in other species, especially waterfowl and other wild birds. Giardiasis is probably the most common of these disease in parrots and occurs more frequently in the smaller species. Clinical signs may be inapparent, or the birds may show a failure to thrive, weight loss, and diarrhea. Feather picking has been associated with giardiasis in cockatiels. Diagnosis is by direct fecal examination, trichrome staining of feces, or ELISA testing. Treatment is with antiprotozoals such as metronidazole or carnidazole. Fenbendazole may also be effective; however, possible fatal reactions may occur. Resistance and reinfection is possible. Cryptosporidiosis is uncommon in psittacines but can cause mild to severe clinical signs in some birds. Diagnosis is based on microscopic examination of feces or histopathologic samples.

Lead toxicosis, although primarily a neurologic condition, an cause GIT signs such as stasis, regurgitation, and melena. Diagnosis is based on history, the presence of other supportive signs, and blood lead levels. Treatment includes the use of chelating agents, laxatives and magnesium sulfate (to protect the GIT and bind any lead still present), and supportive care. Ileus can also occur with inflammatory disorders such as peritonitis and enteritis, foreign bodies, intussusception, and parasitic diseases. These birds are in a potentially critical situation because of fluid pooling and resulting dehydration and should be treated accordingly.

Diseases of the Cloaca

Diseases of the GIT portion of the cloaca include cloacitis, cloacal prolapse, and papillomatosis. Cloacitis or ‘vent gleet’ in domestic fowl occurs sporadically in females during times of reproductive activity. A variety of bacteria have been isolated and treatment consists of cleaning the area and applying local and systemic antibiotics. Prolapse of the cloacal tissue may be caused by conditions such as chronic egg-laying, egg binding, constipation, toxemia, nutritional disorders and may be associated with behavioral disorders (usually sexual) and idiopathic straining. The presence of pink, glistening tissue outside the vent is diagnostic. The tissue may be edematous or hemorrhagic because of trauma and exposure. The prolapsed tissue may be of GI, reproductive, or cloacal origin. Treatment can be difficult and consists of identifying the exposed tissue and manually replacing it. A horizontal mattress suture on each side of the vent can be used to temporarily reduce the prolapse. Recurrent prolapse requires surgical, behavioral, and nutritional intervention. Surgical treatment options include cloacopexy and cloacoplasty.

Cloacal papillomas are irregular, cobblestone appearing mucosal lesions. These papillomas are the most commonly reported cloacal mass in pet birds and occur predominantly in South American species, such as macaws and Amazon parrots. A variety of causes have been implicated, including a new herpesvirus and papillomavirus.^13,14 Lesions may b associated with blood droppings, tenesmus, foul smelling feces, and flatulence. The application of vinegar is supposed to help identify papillomatous material, however, biopsy is required for definitive diagnosis. Treatment options include surgical removal, mucosal stripping, chemical cautery, cryosurgery, and laser surgery. Lesions may resolve spontaneously but can often recur.