Merck and the Merck Veterinary Manual
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Related Conditions & Diseases
Some examples of serious conditions that may result in nausea or vomiting include concussions , meningitis infection of the membrane linings of the brain , intestinal blockage, appendicitis , and brain tumors. Another concern is dehydration.
Adults have a lower risk of becoming dehydrated, because they can usually detect the symptoms of dehydration such as increased thirst and dry lips or mouth. But young children have a greater risk of becoming dehydrated, especially if they also have diarrhea , because they often are unable to communicate symptoms of dehydration. Adults caring for sick children need to be aware of these visible signs of dehydration: In infants, also watch for decreased urination and a sunken fontanelle soft spot on top of the baby's head.
Recurrent vomiting in pregnancy can lead to a serious condition called hyperemesis gravidarum in which the mother may develop fluid and mineral imbalances that can endanger her life or that of her unborn child. Rarely, excessive vomiting can tear the lining of the esophagus , also known as a Mallory-Weiss tear. If the esophagus is ruptured, this is called Boerhaave's syndrome, and is a medical emergency.
Continued Is Vomiting Harmful? If the nausea lasts for more than a few days or if there is a possibility of being pregnant If home treatment is not working, dehydration is present, or a known injury has occurred such as head injury or infection that may be causing the vomiting Adults should consult a doctor if vomiting occurs for more than one day, diarrhea and vomiting last more than 24 hours, or there are signs of dehydration.
Take an infant or child under six years to the doctor if vomiting lasts more than a few hours, diarrhea is present, signs of dehydration occur, there is a fever, or if the child hasn't urinated for hours. Take a child over age six years to the doctor if vomiting lasts one day, diarrhea combined with vomiting lasts for more than 24 hours, there are any signs of dehydration, there is a fever higher than degrees, or the child hasn't urinated for six hours. You should seek immediate medical care if any of the following situations occur with vomiting: There is blood in the vomit bright red or "coffee grounds" in appearance Severe headache or stiff neck Lethargy, confusion, or a decreased alertness Severe abdominal pain Diarrhea Rapid breathing or pulse.
Continued How Is Vomiting Treated? Treatment for vomiting regardless of age or cause includes: Drinking gradually larger amounts of clear liquids Avoiding solid food until the vomiting episode has passed If vomiting and diarrhea last more than 24 hours, an oral rehydrating solution such as Pedialyte should be used to prevent and treat dehydration.
Pregnant women experiencing morning sickness can eat some crackers before getting out of bed or eat a high protein snack before going to bed lean meat or cheese. Vomiting associated with cancer treatments can often be treated with another type of drug therapy. There are also prescription and nonprescription drugs that can be used to control vomiting associated with pregnancy, motion sickness, and some forms of dizziness. However, consult with a doctor before using any of these treatments.
MG can be spread to offspring through the egg. Most commercial breeding flocks, however, are MG-free. Introduction of infected replacement birds can introduce the disease to MG-negative flocks. MG can also be spread by using MG-contaminated equipment. Outbreaks of MG can be controlled with the use of antibiotics. Erythromycin, tylosin, spectinomycin, and lincomycin all exhibit anti-mycoplasma activity and have given good results.
Administration of most of these antibiotics can be by feed, water or injection. These are effective in reducing clinical disease. However, birds remain carriers for life. Eradication is the best control of mycoplasma disease.
The National Poultry Improvement Plan monitors all participating chicken and turkey breeder flocks. Birds infected with the synovitis form show lameness, followed by lethargy, reluctance to move, swollen joints, stilted gait, loss of weight, and formation of breast blisters. Birds infected with the respiratory form exhibit respiratory distress.
Greenish diarrhea is common in dying birds see Table 1. Clinically, the disease in indistinguishable from MG. MS is transmitted from infected breeder to progeny via the egg. Within a flock, MS is spread by direct contact with infected birds as well as through airborne particles over short distances. Recovery is slow for both respiratory and synovitis forms. Several antibiotics are variably effective. The most effective are tylosin, erthromycin, spectinomycin, lincomycin, and chlorotectracycline.
These antibiotics can be given by injection while some can be administered in the feed or drinking water. These treatments are most effective when the antibiotics are injected. Eradication is the best and only sure control. Do not use breeder replacements from flocks that have had MS. MM affects turkeys of all ages, although poults are affected more severely than mature turkeys.
Recently, MM has been shown to infect pigeon, quail and peafowl. A drop-off in production and hatchability can be expected in breeder flocks. There can be very high mortality in young poults. Unthriftiness, respiratory distress, stunting, crooked neck with deformity of cervical vertebrae, and leg deformation are common in young birds see Table 1. Egg transmission is low in the early breeding period, but rises as the the age of the flock increases.
Infections can be introduced into a flock by contaminated equipment, shoes, and clothing of workers and visitors. Several antibiotics have been effective including tylosin, erythromycin, spectinomycin, and linco-spectinomycin. The best preventive measure is to keep MM-free breeders.
The MM-free status of breeders can be confirmed by periodic blood tests through the National Poultry Improvement Plan. When the source of the disease is the hatchery, the disease is called brooder pneumonia. In older birds, the disease is called aspergillosis. All birds domestic poultry, pigeons, canary and zoo bird species , animals, humans, and plants are susceptible. Aspergillosis occurs as an acute disease of young birds and a chronic disease in mature birds.
Young birds have trouble breathing and gasp for air. Characteristically, there are no rales or respiratory sounds associated with aspergillosis. Occasionally there is paralysis or convulsions caused by the fungal toxin. Mortality in young birds averages 5—20 percent, but may be as high as 50 percent. Mature birds also have respiratory distress, reduced feed consumption, and may have a bluish and dark color of the skin cyanosis. Nervous disorders, such as twisted necks, may occur in a few birds see Table 1.
Mortality in mature birds is usually less than 5 percent. Aspergillosis is caused by a fungus. The fungus grows well at room temperature and higher. All litter and nest materials peat moss, peanut hulls, sawdust, peat, bark, straw have been known to have been contaminated with aspergillus.
Feed and water should be suspect when attempting to identify the source of contamination. There is no cure for infected birds. The litter can be sprayed lightly with an oil-base germicide to control dust and air movement of fungal spores. It is important to thoroughly clean and disinfect the brooding area between broods. Use only clean litter, preferably soft wood shavings. Do not use sawdust, litter high in bark content, or shavings that have been wet.
Chickens between 12 to 25 weeks of age are most commonly clinically affected. Occasionally pheasants, quail, game fowl and turkeys can be infected. Marek's disease is a type of avian cancer. Tumors in nerves cause lameness and paralysis. Tumors can occur in the eyes and cause irregularly shaped pupils and blindness.
Tumors of the liver, kidney, spleen, gonads, pancreas, proventriculus, lungs, muscles, and skin can cause incoordination, unthriftiness, paleness, weak labored breathing, and enlarged feather follicles. In terminal stages, the birds are emaciated with pale, scaly combs and greenish diarrhea see Table 2. Marek's disease is very similar to Lymphoid Leukosis, but Marek's usually occurs in chickens 12 to 25 weeks of age and Lymphoid Leukosis usually starts at 16 weeks of age.
The Marek's virus is transmitted by air within the poultry house. It is in the feather dander, chicken house dust, feces and saliva. Infected birds carry the virus in their blood for life and are a source of infection for susceptible birds. Chicks can be vaccinated at the hatchery. While the vaccination prevents tumor formation, it does not prevent infection by the virus.
Although primarily a disease of chickens, lymphoid leukosis can infect turkeys, guinea fowl, pheasants, and doves, but not on a large scale. The virus involved has a long incubation period 4 months or longer. As a result, clinical signs are not noticeable until the birds are 16 weeks or older.
Affected birds become progressively weaker and emaciated. There is regression of the comb. The abdomen becomes enlarged. Greenish diarrhea develops in terminal stages see Table 2. The virus is transmitted through the egg to offspring. Within a flock, it is spread by bird-to-bird contact and by contact with contaminated environments. The virus is not spread by air. Infected chicken are carriers for life.
The virus is present in the yolk and egg white of eggs from infected hens. Most national and international layer breeders have eradicated lymphoid leukosis from their flocks. Most commercial chicks are lymphoid-leukosis negative because they are hatched from LL-free breeders. The disease is still common in broiler breeder flocks.
In affected chickens greater than 3 weeks of age, there is usually a rapid onset of the disease with a sudden drop in feed and water consumption, watery droppings leading to soiling of feathers around the vent, and vent pecking.
Chicks are listless and sit in a hunched position. Chickens infected when less than 3 weeks of age do not develop clinical disease, but become severely and permanently immunosuppressed see Table 2. The virus is spread by bird-to-bird contact, as well as by contact with contaminated people and equipment. The virus is shed in the bird droppings and can be spread by air on dust particles. Dead birds are a source of the virus and should be incinerated. There is no specific treatment. Antibiotics, sulfonamides, and nitrofurans have little or no effect.
Vitamin-electrolyte therapy is helpful. High levels of tetracyclines are contraindicated because they tie up calcium, thereby producing rickets. Surviving chicks remain unthrifty and more susceptible to secondary infections because of immunosuppression. This disease should not be confused with St. Chickens are used as sentinels test animals in SLE suspect areas, such as southern Florida.
While SLE is also carried by mosquitos, that is where the similarities between the two encephalitis diseases end. Chickens do not get SLE. Refer to Factsheet VM71 St. Equine encephalitis is a contagious disease of birds especially pheasants , mammals especially horses , and people.
Birds are the major source of the virus. Two forms affect birds: The clinical signs are identical and include reduced feed consumption, staggering, and paralysis. Surviving birds may be blind, have muscle paralysis, and have difficulty holding their head up. Damage to the bird's nervous system varies with species. In pheasants, there is pronounced leg paralysis, twisting of the neck, and tremors. Chukar partridges and turkeys show drowsiness, paralysis, weakness, and death see Table 2.
Infected mosquitoes are the primary source of the virus. The Culiseta melanuria mosquito is the primary transmitter of the virus to poultry. Other mosquito species transmit the disease too, but feed mostly on other animals. Cannibalism of sick or dead birds by penmates is a major source of transmission within pens. Remove the source of infection by establishing mosquito control: This removes cover and resting areas for mosquitos.
Eliminate mosquito breeding areas. Fog areas with malathion. It is possible to immunize birds, especially pheasants, with the vaccine prepared for horses. The recommended dose is one-tenth of a horse dose per bird. The disease is most prevalent in chickens less than 6 weeks of age. Pheasants, corturnix quail, and turkeys are natural hosts as well, but less susceptible than chickens.
Ducklings, young pigeons, and guinea fowl can be experimentally infected. Signs commonly appear during the first week of life and between the second and third weeks. Affected chicks may first show a dull expression of the eyes, followed by progressive incoordination, sitting on hocks, tremors of the head and neck, and finally paralysis or prostration.
Affected chicks are inactive. Some may refuse to walk or will walk on their hocks. In advanced cases, many chicks will lie with both feet out to one side prostrate and die. All stages dullness, tremors, prostration can usually be seen in an affected flock. Feed and water consumption decreases and the birds lose weight.
In adult birds, a transitory drop 5—20 percent in egg production may be the only clinical sign present. However, in breeding flocks, a corresponding decrease in hatchability is also noted as the virus is egg- transmitted until hens develop immunity. Chickens which survive the clinical disease may develop cataracts later in life see Table 2.
The virus can be transmitted through the egg from infected hen to chick, accounting for disease during the first week of life. The disease can also be spread through a flock by direct contact of susceptible hatchlings with infected birds, accounting for the disease at 2—3 weeks of age. Indirect spread can occur through fecal contamination of feed and water.
Recovered birds are immune and do not spread the virus. There is no treatment for outbreaks. Infected birds should be removed, killed and incinerated.
Recovered chicks are unthrifty. The natural hosts for EDS virus are ducks and geese, but EDS has become a major cause of reduced egg production in chickens in many parts of the world. No illness has been observed in ducks or geese. Chickens of all ages and breeds are susceptible. The disease is most severe in broiler-breeders and brown-egg layer strains.
There are no reliable signs other than the effects on egg production and egg quality. Healthy-appearing hens start laying thin-shelled and shell-less eggs.
Once established, the condition results in a failure to achieve egg production targets. Transient diarrhea and dullness occur prior to egg shell changes.
Fertility and hatchability are not affected see Table 2. It is believed that the syndrome was first introduced into chickens from contaminated vaccine.
Vertical transmission occurs from infected breeders to chicks. Newly hatched chicks excrete the virus in the feces. Several serotypes of the reovirus have been identified. Some localize in the joints tenosynovitis while others target respiratory or intestinal tissues septicemic form see Table 2. The principal sign of tenosynovitis is lameness with swelling of the tendon sheaths of the shank and area extending above the hock see Table 2.
Affected birds are lame, sit on their hocks, and are reluctant to move. Rupture of the tendon can occur in older roaster birds, resulting in permanent lameness of the affected leg.
If more than two joints are affected, the entire carcass will be condemned. Infection can also play a part in broiler stunting, the result of malabsorption syndrome. In chicks, malabsorption due to viral enteritis is called "helicopter disease" because feathering is affected. Wing feathers protrude at various angles. A reovirus is believed to play only a secondary role in this syndrome. In commercial layer flocks, increased mortality may be the first sign of the septicemia form see Table 2.
Egg production will decrease by about two to three times the mortality rate. For example, a mortality rate of 5 percent will be accompanied by a 10—15 percent drop in egg production. In the septicemic form, joint involvement is present but less pronounced. Affected birds become cyanotic blue and dehydrated. The tips of the comb turn purplish. The entire comb darkens as the disease progresses see Table 2.
The infection spreads rapidly through broiler flocks, but less rapidly in caged layers. Spread is by respiratory and digestive tract routes. The virus is shed in the feces. There is no satisfactory treatment available. With hens, tetracycline, molasses, and oyster shell therapy is helpful. Domestic fowl of all species primarily turkeys and chickens , game birds especially pheasants and ducks , cage birds, wild birds, and birds in zoological collections and aviaries are susceptible.
Fowl cholera usually strikes birds older than 6 weeks of age. In acute outbreaks, dead birds may be the first sign. Fever, reduced feed consumption, mucoid discharge from the mouth, ruffled feathers, diarrhea, and labored breathing may be seen. As the disease progresses birds lose weight, become lame from joint infections, and develop rattling noises from exudate in air passages. As fowl cholera becomes chronic, chickens develop abscessed wattles and swollen joints and foot pads.
Caseous exudate may form in the sinuses around the eyes. Turkeys may have twisted necks see Table 3. Multiple means of transmission have been demonstrated. Flock additions, free-flying birds, infected premises, predators, and rodents are all possibilities. A flock can be medicated with a sulfa drug sulfonamides, especially sulfadimethoxine, sulfaquinonxalene, sulfamethazine, and sulfaquinoxalene or vaccinated, or both, to stop mortality associated with an outbreak.
It must be noted, however, that sulfa drugs are not FDA approved for use in pullets older than 14 weeks or for commercial laying hens. Sulfa drugs leave residues in meat and eggs. Antibiotics can be used, but require higher levels and long term medication to stop the outbreak.
On fowl cholera endemic farms, vaccination is advisable. Do not vaccinate for fowl cholera unless you have a problem on the farm. Rodent control is essential to prevent future outbreaks. Affected chicks may have external navel infection, large unabsorbed yolk sacs, peritonitis with fetid odor, exudates adhering to the navel, edema of the skin of ventral body area, septicemia and dehydration see Table 3. Infection occurs at the time of hatching or shortly thereafter, before navels are healed.
Chicks from dirty hatching eggs or eggs with poor quality shells, or newly hatched chicks placed in dirty holding boxes, are most susceptible. Eggs that explode in the hatching tray contaminate other eggs in the tray and increase the incidence.
There is no specific treatment for omphalitis. Most affected birds die in the first few days of life. Unaffected birds need no medication. Control is by prevention through effective hatchery sanitation, hatchery procedures, breeder flock surveillance, and proper preincubation handling of eggs. Mushy chicks should be culled from the hatch and destroyed. If chick mortality exceeds 3 percent, the breeder flocks and egg handling and hatching procedures should be reviewed.
Chickens and turkeys are most susceptible, although other species of birds can become infected. Pullorum has never been a problem in commercially grown game birds such as pheasant, chukar partridge, and quail. Infection in mammals is rare. Death of infected chicks or poults begins at 5—7 days of age and peaks in another 4—5 days.
Clinical signs including huddling, droopiness, diarrhea, weakness, pasted vent, gasping, and chalk-white feces, sometimes stained with green bile. Affected birds are unthrifty and stunted because they do not eat see Table 3. Survivors become asymptomatic carriers with localized infection in the ovary. Pullorum is spread primarily through the egg, from hen to chick. It can spread further by contaminated incubators, hatchers, chick boxes, houses, equipment, poultry by-product feedstuffs, and carrier birds.
Treatment is for flock salvage only. Several sulfonamides, antibiotics, and antibacterials are effective in reducing mortality, but none eradicates the disease from the flock. Pullorum eradication is required by law. Eradication requires destroying the entire flock. As part of the National Poultry Improvement Program, breeder replacement flocks are tested before onset of production to assure pullorum-free status.
This mandatory law includes chickens, turkeys, show birds, waterfowl, game birds, and guinea fowl. In Florida, a negative pullorum test or certification that the bird originated from a pullorum-free flock is required for admission for exhibit at shows and fairs.
Such requirements have been beneficial in locating pullorum-infected flocks of hobby chickens. Rapidly growing young birds, especially chickens and turkeys weeks of age, are most susceptible.
Necrotic enteritis is a disease associated with domestication and is unlikely to threaten wild bird populations. Necrotic enteritis is primarily a disease of broilers, roasters and turkeys.
Ulcerative enteritis, on the other hand, commonly affects pullets and quail. Initially there is a reduction in feed consumption as well as dark, often blood-stained, feces.
Infected chickens will have diarrhea. Chronically affected birds become emaciated. The bird, intestines, and feces emit a fetid odor see Table 3. Necrotic enteritis does not spread directly from bird to bird. Bacteria are ingested along with infected soil, feces, or other infected materials. The bacteria then grow in the intestinal tract. Infection commonly occurs in crowded flocks, immuno-suppressed flocks, and flocks maintained in poor sanitary conditions. The clostridia bacteria involved in necrotic enteritis is sensitive to the antibiotics bacitracin, neomycin, and tetracycline.
However, antibiotics such as penicillin, streptomycin, and novobiocin are also effective. Bacitracin is the most commonly used drug for control of necrotic enteritis. As with all drugs, legality and withdrawal time requirements must be observed. Prevention should be directed toward sanitation, husbandry, and management. Captive quail are extremely susceptible and must be maintained on wire-bottom pens or on preventive medications. Chickens, turkeys, partridges, grouse, and other species are occasionally clinically affected.
In quail, the disease is acute with high mortality. In chickens, signs are less dramatic. Acute signs are extreme depression and reduction in feed consumption. Affected birds sit humped with eyes closed. Other signs included emaciation, watery droppings streaked with urates, and dull ruffled feathers see Table 3. Accumulated mortality will reach 50 percent if the flock is not treated. Birds become infected by direct contact with carrier birds, infected droppings or contaminated pens, feed and water.
Bacteria are passed in the droppings of sick and carrier birds. Infection can be spread mechanically on shoes, feed bags, equipment, and from contamination by rodents and pets.