Aug 9, 2005

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.

Jul 18, 2005

Avian Pox

AVIAN POX

Cause

Poxvirus, several strains.

Host

Variety of birds worldwide: upland gamebirds, songbirds, marine birds, parrot family, occasionally raptors, rarely waterfowl.

Transmission

Direct contact with infected birds, ingestion of food and water contaminated by sick birds or carcasses, or contact with contaminated surfaces such as bird feeders and perches. The virus enters through abraded skin. Insects, especially mosquitoes, may act as mechanical vectors.

Clinical/Field Signs

Avian pox can occur in two forms: cutaneous pox and diphtheritic or "wet" pox. In cutaneous pox (the most common form), wartlike growths occur around the eyes, beak or any unfeathered skin. This leads to difficulty seeing, breathing, feeding, or perching. In diphtheritic pox, the growths form in the mouth, throat, trachea and lungs resulting in difficulty breathing or swallowing. Birds with either type may appear weak and emaciated.

Lesions

Warty growths on unfeathered skin, sometimes in large clusters. Size and number of growths depend on the stage and severity of infection. Common sites include feet, legs, base of beak, and eye margins. Often emaciated due to inability to feed. In the diphtheritic form, there are raised, yellow plaques on the mucus membranes of the mouth and throat.

Wildlife Management Significance

The disease can be a significant mortality factor in some upland game bird (fall and winter), songbird (winter), and raptor populations. Birds can survive with supportive care, food and water, and protection from secondary infections. Warty scabs contain infectious viral material. Disease control recommendations are site specific, therefore contact the National Wildlife Health Center for assistance. Decontamination of bird feeders, birdbaths, transport cages and banding equipment with 10% bleach and water solution is recommended. In some situations, removing infected birds can be important to reduce the amount of virus available to vectors and noninfected bird populations. Vector control may be considered in affected areas.

Public Health Significance

There is no evidence of human risk.

Domestic Animal Significance

Poultry are susceptible and many are vaccinated against pox. The safety and effectiveness of this vaccine in wild birds is not currently known.

Contact the National Wildlife Health Center for additional information on this or any other wildlife health topic.

Jul 16, 2005

Not a good day

All 3 bunnies were dead this morning. Cause undetermined.
The Mockingbird passed away in the afternoon.
The only animal left is the little brown headed cowbird and he seems to be doing alright.

Jul 15, 2005

West Nile Virus Information

Frequently Asked Questions - West Nile Virus

Below are answers to frequently asked questions about the West Nile virus received by the Texas Department of Health (TDH). Answers to more than 50 frequently asked questions received by the national Centers for Disease Control and Prevention can be found at http://www.cdc.gov/ncidod/dvbid/westnile/q&a.htm
Q. Can dogs, cats and other pets get the West Nile virus?
A. Yes. But they rarely, if ever, get sick. No cases of West Nile disease have been confirmed in dogs and cats. The virus can infect many species of animals, but few actually get the disease. Most infections have been identified in birds, but West Nile virus has been shown to infect dogs, cats, horses, and domestic rabbits, as well as bats, chipmunks, skunks, and squirrels.
Q. Is there a vaccine for dogs and cats?
A. No.
Q. How many human cases have there been in the United States? How many deaths?
A. In 1999, 62 cases of severe disease, including 7 deaths, occurred in the New York area. In 2000, 21 cases were reported, including 2 deaths in the New York City area. In 2001, there were 66 human cases of severe disease and 9 deaths. No reliable estimates are available for the number of cases worldwide of West Nile encephalitis, the disease caused by the West Nile virus.
For the latest up-to-date information, go to http://www.cdc.gov/ncidod/dvbid/westnile/surv&control04Maps.htm.
Q. How many human cases have there been in Texas? How many deaths?
A. The first human death in Texas occurred on August 16th, 2002. For the latest up-to-date information on human cases in Texas, see the TDH West Nile Virus home page at http://www.tdh.state.tx.us/zoonosis/diseases/arboviral/westnile
More information about West Nile virus in Texas can be found at http://www.tdh.state.tx.us/zoonosis/diseases/arboviral/westnile.
Q. What is the risk of someone becoming infected with West Nile?
A. The risk is very low. Even in areas where the virus is circulating, very few mosquitoes are infected with the virus. Even if the mosquito is infected, less than 1% of people who get bitten and become infected will get severely ill. The chances you will become severely ill from any one mosquito bite are extremely small.
Q. Where in Texas has the virus been found?
A. For the most up-to-date information, go to http://www.tdh.state.tx.us/zoonosis/diseases/arboviral/westNile.
Q. Where does the virus live? Do birds or mosquitoes get it first?
A. Birds get it first. The virus is in their bloodstream. Mosquitoes become infected when they feed on infected birds. The infected mosquitoes can then transmit West Nile virus to humans and animals while biting to take blood. The virus is located in their salivary glands and, during blood feeding, the virus can be injected into the animal or human, where it can multiply, possibly causing illness in the animal or human.
Q. Is TDH doing spraying around the state to kill mosquitoes?
A. No. Vector control is up to the Mosquito Control Districts and local health departments.
Q. In addition to being infected by the West Nile virus, what else can cause bird "die-offs"?
A. Chemical spills, pesticides, drought, severe weather, and other diseases.
Q. What's an arbovirus?
A. Any of various RNA viruses which are the causative agents of encephalitis, yellow fever, and dengue and which are transmitted chiefly by arthropods, such as insects.
Q. What kind of laboratory tests are done to identify the West Nile virus?
A. Various tests can be done. The type of test will vary among mosquitoes, chickens, humans, and horses. The type of test also depends on the kind of samples available (blood serum, cerebrospinal fluid, brain tissue, etc.). Samples may be tested to find antibodies to West Nile virus, or there may be an attempt to isolate virus particles from the sample. Tests that can be done include Hemagglutination-Inhibition, IgM-Capture, Plaque-Reduction Neutralization, virus isolation, and PCR. More details are available in the Response Guide at http://www.tdh.state.tx.us/zoonosis/diseases/arboviral/westnile.
Q. Is there a human vaccine?
A. No, but several companies are working towards developing a vaccine.
Q. Can a human get the virus twice?
A. We don't think so. It is assumed that a person would develop a natural immunity to future infection by the virus, and that this immunity would be lifelong. However, this immunity may wane in later years.
Q. I've heard of " suspect cases," " positive cases," " confirmed cases," and " probable cases." What does it all mean?
A. Infections with West Nile virus may, or may not, produce illness. A few people who get ill may seek medical care. Those with severe enough disease that has the appearance of West Nile and similar viruses may have blood or spinal fluid sampled for testing.
Testing of samples has two main components:
  • Samples may be tested for antibodies to West Nile and other viruses. A positive result indicates that the patient may have been exposed to the virus, but does not prove that the virus is still in the patient.
  • Samples may also be tested to find the actual virus. This type of test is more difficult, takes much longer, and may not be successful. A negative test does not prove that the virus did not cause the illness.
Here are definitions of the terms you asked about:
Suspect: A patient with symptoms similar to West Nile might be considered a suspect by their physician. Since they would also be suspect for a multitude of others diseases with similar signs, they are not counted or reported by Texas.
Positive case: Many laboratories can test for West Nile and may find positive results. These results are often cross-reactions with other conditions and may not represent a true West Nile positive. Only those results that meet the case definitions for "Confirmed" or "Probable" will be reported as "cases."
Confirmed: A febrile illness associated with neurologic manifestations ranging from headache to aseptic meningitis or encephalitis, plus at least one of the following:
  • Isolation of WN virus from or demonstration of WN antigen or genomic sequences in tissue, blood, cerebrospinal fluid, or other body fluid;
  • Demonstration of IgM antibody to WN virus in cerebrospinal fluid by IgM-capture enzyme-linked immunoassay (EIA);
  • A > 4-fold serial change in plaque-reduction neutralizing test (PRNT) antibody titer to WN virus in paired, appropriately timed serum or cerebrospinal fluid samples;
  • Demonstration of both WN virus-specific IgM (by EIA) and IgG (screened by EIA or HI and confirmed by PRNT) antibody in a single serum specimen.
Probable case: Symptoms identical to that for a confirmed case plus one or more of the following:
  • Demonstration of serum IgM antibody against WN virus (by EIA);
  • Demonstration of an elevated titer of WN virus-specific IgG antibody in convalescent-phase serum (screened by EIA or hemagglutination inhibition (HI) and confirmed by PRNT).

Health Risks Associated with Wildlife as Pets

Many people have contact with wild animals and, especially if the animals are young, are tempted to take them home as pets. Baby animals are often cute, cuddly and responsive to attention. The temptation to remove them from their natural environment can be very strong, but before you try to make a pet out of a wild animal, please consider the following:

Most wild animals will not live very long in our normal household surroundings. Baby animals that do survive will undergo a drastic behavioral change as they become adults. They often become very aggressive and continually try to escape back to the out-of-doors. A tailor-made pet does not result from declawing, descenting, neutering or removing fangs from a wild animal. In addition, attempting to return such animals to the wild when their behavior becomes intolerable is actually a death sentence.

The dietary requirements of most wild animals are different from domestic pets. An improper diet can result in serious nutritional deficiencies such as rickets and other crippling conditions.

Most wild animals are normally most active at night. This perfectly normal behavior can be very disruptive to persons trying to sleep and attempts to change it may be very frustrating to the animal itself.

Many diseases which affect people can be carried even by healthy-looking wild animals. Rabies is one such disease and others include leptospirosis, tularemia and plague. Preventive vaccines against these diseases are not approved for use in wildlife.

Most wild animals are protected by various federal and state laws and permission from the proper authorities must be obtained before keeping a wild animal.

When you are tempted to take home a wild animal for a pet, ask yourself these questions:

* Is what I am doing legal?
* Am I willing to risk the health, and possibly the life, of myself and my family?
* Am I willing to risk destroying the animal?
* Am I willing to change my lifestyle to conform to the animal's natural and unalterable behavior?

If you cannot truthfully answer "yes" to each question, do not attempt to keep a wild animal as a pet.

Identified

The 2 unidentified birds are Brown-headed cowbirds.
One is not doing well, nor is the Mockingbird.
The other Chimney Swift died late yesterday afternoon.
Suspecting West Nile according to the symptoms.

Jul 14, 2005

Released today:

Released the 4 Sparrows and the Inca Dove this morning.

The 2 Chimney Swifts are not doing well, they stopped chattering and taking food.

1 of the 3 unidentified birds passed away 10 minutes ago. Metabolic bone disease.

Noon update: 1 of the Chimney swifts didn't make it, the other one is still refusing to eat...