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Saturday, May 11, 2013
Model Project on Angora rabbit rearing for wool production
Sunday, February 5, 2012
Mange in Sheep and Goats
| There are (5) types of the Mange in Sheep & Goat as given below. Sarcoptic Mange |
| Chorioptic Mange |
| Psoroptic Mange (Sheep Scab) |
| Demodectic Mange |
| Psorergatic Mange (Itch Mite, Australian Itch) |
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Tuesday, January 3, 2012
Abortion in Goats
See also management of reproduction: goats, Management of Reproduction: Goats.
Noninfectious causes of abortion in goats include plant toxins, such as broomweed or locoweed poisoning; dietary deficiencies of copper, selenium, vitamin A, or magnesium; and certain drugs such as estrogen, glucocorticoids, phenothiazine, carbon tetrachloride, or levamisole (in late gestation).
Major infectious causes of abortion in goats are chlamydophilosis, toxoplasmosis, leptospirosis, brucellosis, Coxiella burnetii , and listeriosis. Campylobacter causes abortions but is not nearly as important in does as in ewes.
Chlamydophilosis (Chlamydiosis, Enzootic Abortion):
Chlamydophila abortus (the agent of enzootic abortion of ewes) is the most common cause of abortion in goats in the USA. In naive herds, up to 60% of pregnant does can abort or give birth to stillborn or weak kids. Abortions can occur at any stage of pregnancy, but most are in the last month. Reproductive failure is usually the only sign of C abortus infection, but occasionally there is concurrent respiratory disease, polyarthritis, conjunctivitis, and retained placentas in the flock. Aborted lambs are usually fresh with no gross pathology. Placentitis is usually present and consists of reddish-brown exudate covering cotyledons and intercotyledonary areas. Microscopically, necrotizing vasculitis and neutrophilic inflammation are present in the placenta. Chlamydial organisms can be visualized in appropriately stained placental smears, but they cannot be differentiated from Coxiella burnetii . Fluorescent antibody or immunohistochemical staining, ELISA, PCR, or culture can be used to definitively identify C abortus . The placenta is the specimen of choice, but sometimes the diagnosis can be made by testing liver, lung, and spleen. During an outbreak, aborting does should be isolated and tetracyclines given orally or parentally. There is no chlamydial vaccine for goats, but the vaccine for sheep is relatively effective. Like sheep, goats that abort are immune. Sheep that abort due to C abortus remain infected for years, if not life, and shed the organism at the time of ovulation; whether or not this occurs in goats is not known. C abortus is zoonotic, occasionally causing serious disease in pregnant women.
Toxoplasmosis:
Toxoplasmosis is a common cause of abortion in goats in the USA, and toxoplasmal abortion in goats is similar to the syndrome in ewes (see above).
Leptospirosis:
The most common serovars of Leptospira interrogans involved in caprine abortion are grippotyphosa and pomona . While sheep are relatively resistant to leptospirosis, goats are susceptible, with abortions occurring at the time of leptospiremia. Some does have anemia, icterus, and hemoglobinemia; others are afebrile and are not icteric. Diagnosis is by serology or identification of Leptospira spp in the dam’s urine, the placenta, or fetal kidney. (See also Leptospirosis: Introduction.)
Brucellosis:
Brucella melitensis is the principal organism, with occasional abortions due to B abortus . Abortion may be accompanied by mastitis and lameness and is most common in the fourth month. The placenta is grossly normal, but does may develop chronic uterine lesions. Infection in adults is lifelong with organisms shed in the milk ( B melitensis is zoonotic but rare in the USA). In the USA, control is by test and slaughter. Tube agglutination and card tests can be used as screening tests. (See also Brucellosis in Large Animals: Introduction.)
Coxiella burnetii Infection:
Coxiella burnetii is increasingly recognized as an important cause of caprine abortion, especially in the western USA. Occasional outbreaks also occur in sheep. Late-term abortions, stillbirths, and weak lambs are the common presentations. Up to 50% of the flock may be involved. The placenta is covered by gray-brown exudate and the intercotyledonary areas are thickened. Microscopically, there is a necrotizing vasculitis in the placenta, and many chorionic epithelial cells are distended by small, coccobacillary organisms <1 mm in diameter. Infection involves only the placenta; without it, the diagnosis usually cannot be made. Diagnosis is by identification of C burnetii by immunologic staining methods or by isolation. Coxiella is zoonotic, causing Q fever in humans.
Listeriosis:
Listeria monocytogenes is a common pathogen in goats and causes sporadic abortions. There are no specific fetal lesions, and the fetus is often autolyzed. The doe usually shows no signs before abortion but may develop severe metritis after abortion. Diagnosis is by isolation from the placenta, abomasal contents, or uterine discharge. In the rare case of a herd outbreak, preventive treatment with tetracycline is recommended. (See also Listeriosis: Introduction.)
Noninfectious causes of abortion in goats include plant toxins, such as broomweed or locoweed poisoning; dietary deficiencies of copper, selenium, vitamin A, or magnesium; and certain drugs such as estrogen, glucocorticoids, phenothiazine, carbon tetrachloride, or levamisole (in late gestation).
Major infectious causes of abortion in goats are chlamydophilosis, toxoplasmosis, leptospirosis, brucellosis, Coxiella burnetii , and listeriosis. Campylobacter causes abortions but is not nearly as important in does as in ewes.
Chlamydophilosis (Chlamydiosis, Enzootic Abortion):
Chlamydophila abortus (the agent of enzootic abortion of ewes) is the most common cause of abortion in goats in the USA. In naive herds, up to 60% of pregnant does can abort or give birth to stillborn or weak kids. Abortions can occur at any stage of pregnancy, but most are in the last month. Reproductive failure is usually the only sign of C abortus infection, but occasionally there is concurrent respiratory disease, polyarthritis, conjunctivitis, and retained placentas in the flock. Aborted lambs are usually fresh with no gross pathology. Placentitis is usually present and consists of reddish-brown exudate covering cotyledons and intercotyledonary areas. Microscopically, necrotizing vasculitis and neutrophilic inflammation are present in the placenta. Chlamydial organisms can be visualized in appropriately stained placental smears, but they cannot be differentiated from Coxiella burnetii . Fluorescent antibody or immunohistochemical staining, ELISA, PCR, or culture can be used to definitively identify C abortus . The placenta is the specimen of choice, but sometimes the diagnosis can be made by testing liver, lung, and spleen. During an outbreak, aborting does should be isolated and tetracyclines given orally or parentally. There is no chlamydial vaccine for goats, but the vaccine for sheep is relatively effective. Like sheep, goats that abort are immune. Sheep that abort due to C abortus remain infected for years, if not life, and shed the organism at the time of ovulation; whether or not this occurs in goats is not known. C abortus is zoonotic, occasionally causing serious disease in pregnant women.
Toxoplasmosis:
Toxoplasmosis is a common cause of abortion in goats in the USA, and toxoplasmal abortion in goats is similar to the syndrome in ewes (see above).
Leptospirosis:
The most common serovars of Leptospira interrogans involved in caprine abortion are grippotyphosa and pomona . While sheep are relatively resistant to leptospirosis, goats are susceptible, with abortions occurring at the time of leptospiremia. Some does have anemia, icterus, and hemoglobinemia; others are afebrile and are not icteric. Diagnosis is by serology or identification of Leptospira spp in the dam’s urine, the placenta, or fetal kidney. (See also Leptospirosis: Introduction.)
Brucellosis:
Brucella melitensis is the principal organism, with occasional abortions due to B abortus . Abortion may be accompanied by mastitis and lameness and is most common in the fourth month. The placenta is grossly normal, but does may develop chronic uterine lesions. Infection in adults is lifelong with organisms shed in the milk ( B melitensis is zoonotic but rare in the USA). In the USA, control is by test and slaughter. Tube agglutination and card tests can be used as screening tests. (See also Brucellosis in Large Animals: Introduction.)
Coxiella burnetii Infection:
Coxiella burnetii is increasingly recognized as an important cause of caprine abortion, especially in the western USA. Occasional outbreaks also occur in sheep. Late-term abortions, stillbirths, and weak lambs are the common presentations. Up to 50% of the flock may be involved. The placenta is covered by gray-brown exudate and the intercotyledonary areas are thickened. Microscopically, there is a necrotizing vasculitis in the placenta, and many chorionic epithelial cells are distended by small, coccobacillary organisms <1 mm in diameter. Infection involves only the placenta; without it, the diagnosis usually cannot be made. Diagnosis is by identification of C burnetii by immunologic staining methods or by isolation. Coxiella is zoonotic, causing Q fever in humans.
Listeriosis:
Listeria monocytogenes is a common pathogen in goats and causes sporadic abortions. There are no specific fetal lesions, and the fetus is often autolyzed. The doe usually shows no signs before abortion but may develop severe metritis after abortion. Diagnosis is by isolation from the placenta, abomasal contents, or uterine discharge. In the rare case of a herd outbreak, preventive treatment with tetracycline is recommended. (See also Listeriosis: Introduction.)
Abortion in Sheep
Abortion in ewes, as in cows, is not always easily diagnosed. While many of the toxins that cause abortion in cows also cause problems in ewes, others such as Veratrum californicum and kale seem unique to the ewe. The major infectious agents causing abortions in sheep are Campylobacter , Chlamydophila , Toxoplasma , Listeria , Brucella , Salmonella , border disease virus, and Cache Valley virus.
Campylobacter spp Infection (Vibriosis):
Infection with Campylobacter fetus fetus and C jejuni results in abortions in late pregnancy or stillbirths. Ewes may develop metritis after expelling the fetus. Placentitis occurs with hemorrhagic necrotic cotyledons and edematous or leathery intercotyledonary areas. The fetus is usually autolyzed, with 40% having orange-yellow necrotic foci (1-2 cm diameter) in the liver. Diagnosis relies on finding Campylobacter organisms in darkfield or fluorescent antibody preparations from abomasal or placental smears or in uterine discharge. Identification of the species involved is important because in some areas C jejuni is as common as C fetus , and some vaccines do not include C jejuni . Strict hygiene is necessary to stop an outbreak. Use of tetracyclines may help prevent exposed ewes from aborting. The disease tends to be cyclical, with epizootics occurring every 4-5 yr; therefore, vaccination programs, which help prevent outbreaks, should be consistently practiced.
Enzootic Abortion of Ewes (EAE):
Chlamydophila abortus (Chlamydia psittaci serotype 1) is the cause of EAE, which is characterized by late term abortions, stillbirths, and weak lambs. C pecorum is the cause of chlamydial arthritis and conjunctivitis of sheep. Except for Australia and New Zealand, EAE occurs worldwide and is most important in intensively managed sheep. Abortions occur during the last 2-3 wk of gestation regardless of when infection occurs, and the fetuses are fresh with minimal autolysis. There is placentitis with necrotic, reddish brown cotyledons and thickened brown intercotyledonary areas covered by exudate. Chlamydial elementary bodies can be found by examination of appropriately stained smears of the placenta or vaginal discharge, but the organisms cannot be differentiated from Coxiella burnetii , which occasionally causes abortion in sheep. Definitive diagnosis is by identification of C abortus by ELISA, fluorescent antibody staining, PCR, or isolation. Ewes seldom abort more than once, but they remain persistently infected and shed C abortus from their reproductive tract for 2-3 days before and after ovulation. Rams can be infected and transmit the organism venereally. Control consists of isolating all affected ewes and lambs and treating in-contact ewes with long-acting oxytetracycline or oral tetracycline. C abortus bacterins are available and are effective in reducing abortions. In parts of Europe, a modified live vaccine is available for use.
C abortus is zoonotic but human cases are rare. All have involved pregnant women, who developed life-threatening illness. Only in a few cases in which the fetus was delivered by cesarean section did the infant survive. Pregnant women should not work with pregnant sheep, especially if abortions are occurring.
Border Disease:
Border disease occurs worldwide and is an important cause of embryonic and fetal deaths, weak lambs, and congenital abnormalities. It is caused by a pestivirus closely related to bovine viral diarrhea (BVD) virus and classical swine fever (hog cholera) virus. Abortion can occur at any stage of gestation. There are no clinical signs in the dam. Live infected fetuses usually are undersized, and they often have congenital tremors and an abnormally hairy coat (hairy shaker lambs). Diagnosis is by identification of border disease virus in the placenta or fetal tissues (kidneys, lungs, spleen, thyroid glands, abomasum) by fluorescent antibody staining, virus isolation, or demonstration of precolostral antibodies. There are no vaccines available. Inactivated BVD virus vaccines are sometimes used on sheep, but their effectiveness is unproved. (See also Border Disease .)
Cache Valley Virus:
Cache Valley virus is a mosquito-transmitted cause of infertility, abortions, stillbirths, and multiple congenital abnormalities in sheep. The virus is endemic in most parts of the USA, Canada, and Mexico. Often there are epizootics affecting sheep over a wide geographic area that can include several states. The most noticeable effects are stillborn lambs and the birth of live lambs with congenital abnormalities affecting the CNS and musculoskeletal system. Hydranencephaly, hydrocephalus, cerebral and cerebellar hypoplasia, arthrogryposis, scoliosis, torticollis, and hypoplasia of skeletal muscles are common. At the time of abortion or birth the virus is usually no longer viable, and diagnosis is by demonstration of antibodies in precolostral serum or body fluids. Vaccines are not available.
Toxoplasmosis:
If ewes become infected with Toxoplasma gondii early in gestation, resorption or mummification results; if ewes contract the disease late in gestation, abortions or perinatal deaths occur. Ewes do not usually appear sick. In an outbreak, there is usually a wide range in gestational age of aborted fetuses. In most cases there are no gross lesions, but in a few cases there are distinct small white foci, 1-3 mm in diameter, in some cotyledons. The fetal brain often has focal areas of nonsuppurative inflammation on histology. Fetal serology (indirect hemagglutination inhibition, latex agglutination, or fluorescent antibody) may also be used. Once infected, ewes are immune, so running unbred ewes with aborting ones may allow them to develop immunity. Preventing contamination of feed by cat feces may help reduce exposure. Toxoplasmosis is a zoonosis. (See also Toxoplasmosis: Introduction.)
Listeriosis:
Abortion caused by Listeria monocytogenes in ewes usually occurs in late gestation. There is some necrosis of cotyledons and the intercotyledonary areas, and the fetus is usually autolyzed. The fetal liver (and possibly lung) may have necrotic foci, 0.5-1 mm in diameter. Diagnosis is by culture. (See also Listeriosis: Introduction .)
Brucellosis:
The major importance of Brucella ovis is as a cause of epididymitis in rams, but it also causes late-term abortions, stillbirths, and birth of weak lambs. B melitensis is rare in the USA but causes abortion in areas where it is found. B abortus occasionally causes abortion in sheep. Brucella abortions occur late in gestation, resulting in placentitis with edema and necrosis of the cotyledons and thickened, leathery intercotyledonary areas. Many fetuses aborted due to B ovis are alive at the beginning of parturition, although fetuses can be mummified or autolyzed. Most fetuses aborted due to B melitensis or B abortus are autolytic. Culture of the placenta, abomasal contents, and the dam’s vaginal discharge are diagnostic. A vaccine for B melitensis is available in some countries. B melitensis and B abortus are zoonotic. (See also Brucellosis in Large Animals: Introduction.)
Salmonellosis:
Salmonella abortus ovis , S dublin , S typhimurium , and S arizona have caused abortions in sheep. S abortus ovis is endemic in England and Europe but has not been reported in the USA. The other serotypes occur worldwide. Most ewes are sick and febrile before aborting. There are no specific placental lesions, and the fetus is autolyzed. Diagnosis is by culture of placenta, fetus, or uterine discharge. See also Dentistry .
Other Causes of Abortion:
Bluetongue virus and Akabane virus (where present) cause abortion and congenital anomalies in sheep and are differential diagnoses for Cache Valley virus infection. Coxiella burnetii causes occasional abortion storms in sheep, with the clinical syndrome and fetal pathology being the same as for goats (see abortion in goats, Abortion in Goats). Neospora caninum has been reported to cause occasional abortions in sheep with the lesions resembling those of Toxoplasma gondii .
Campylobacter spp Infection (Vibriosis):
Infection with Campylobacter fetus fetus and C jejuni results in abortions in late pregnancy or stillbirths. Ewes may develop metritis after expelling the fetus. Placentitis occurs with hemorrhagic necrotic cotyledons and edematous or leathery intercotyledonary areas. The fetus is usually autolyzed, with 40% having orange-yellow necrotic foci (1-2 cm diameter) in the liver. Diagnosis relies on finding Campylobacter organisms in darkfield or fluorescent antibody preparations from abomasal or placental smears or in uterine discharge. Identification of the species involved is important because in some areas C jejuni is as common as C fetus , and some vaccines do not include C jejuni . Strict hygiene is necessary to stop an outbreak. Use of tetracyclines may help prevent exposed ewes from aborting. The disease tends to be cyclical, with epizootics occurring every 4-5 yr; therefore, vaccination programs, which help prevent outbreaks, should be consistently practiced.
Enzootic Abortion of Ewes (EAE):
Chlamydophila abortus (Chlamydia psittaci serotype 1) is the cause of EAE, which is characterized by late term abortions, stillbirths, and weak lambs. C pecorum is the cause of chlamydial arthritis and conjunctivitis of sheep. Except for Australia and New Zealand, EAE occurs worldwide and is most important in intensively managed sheep. Abortions occur during the last 2-3 wk of gestation regardless of when infection occurs, and the fetuses are fresh with minimal autolysis. There is placentitis with necrotic, reddish brown cotyledons and thickened brown intercotyledonary areas covered by exudate. Chlamydial elementary bodies can be found by examination of appropriately stained smears of the placenta or vaginal discharge, but the organisms cannot be differentiated from Coxiella burnetii , which occasionally causes abortion in sheep. Definitive diagnosis is by identification of C abortus by ELISA, fluorescent antibody staining, PCR, or isolation. Ewes seldom abort more than once, but they remain persistently infected and shed C abortus from their reproductive tract for 2-3 days before and after ovulation. Rams can be infected and transmit the organism venereally. Control consists of isolating all affected ewes and lambs and treating in-contact ewes with long-acting oxytetracycline or oral tetracycline. C abortus bacterins are available and are effective in reducing abortions. In parts of Europe, a modified live vaccine is available for use.
C abortus is zoonotic but human cases are rare. All have involved pregnant women, who developed life-threatening illness. Only in a few cases in which the fetus was delivered by cesarean section did the infant survive. Pregnant women should not work with pregnant sheep, especially if abortions are occurring.
Border Disease:
Border disease occurs worldwide and is an important cause of embryonic and fetal deaths, weak lambs, and congenital abnormalities. It is caused by a pestivirus closely related to bovine viral diarrhea (BVD) virus and classical swine fever (hog cholera) virus. Abortion can occur at any stage of gestation. There are no clinical signs in the dam. Live infected fetuses usually are undersized, and they often have congenital tremors and an abnormally hairy coat (hairy shaker lambs). Diagnosis is by identification of border disease virus in the placenta or fetal tissues (kidneys, lungs, spleen, thyroid glands, abomasum) by fluorescent antibody staining, virus isolation, or demonstration of precolostral antibodies. There are no vaccines available. Inactivated BVD virus vaccines are sometimes used on sheep, but their effectiveness is unproved. (See also Border Disease .)
Cache Valley Virus:
Cache Valley virus is a mosquito-transmitted cause of infertility, abortions, stillbirths, and multiple congenital abnormalities in sheep. The virus is endemic in most parts of the USA, Canada, and Mexico. Often there are epizootics affecting sheep over a wide geographic area that can include several states. The most noticeable effects are stillborn lambs and the birth of live lambs with congenital abnormalities affecting the CNS and musculoskeletal system. Hydranencephaly, hydrocephalus, cerebral and cerebellar hypoplasia, arthrogryposis, scoliosis, torticollis, and hypoplasia of skeletal muscles are common. At the time of abortion or birth the virus is usually no longer viable, and diagnosis is by demonstration of antibodies in precolostral serum or body fluids. Vaccines are not available.
Toxoplasmosis:
If ewes become infected with Toxoplasma gondii early in gestation, resorption or mummification results; if ewes contract the disease late in gestation, abortions or perinatal deaths occur. Ewes do not usually appear sick. In an outbreak, there is usually a wide range in gestational age of aborted fetuses. In most cases there are no gross lesions, but in a few cases there are distinct small white foci, 1-3 mm in diameter, in some cotyledons. The fetal brain often has focal areas of nonsuppurative inflammation on histology. Fetal serology (indirect hemagglutination inhibition, latex agglutination, or fluorescent antibody) may also be used. Once infected, ewes are immune, so running unbred ewes with aborting ones may allow them to develop immunity. Preventing contamination of feed by cat feces may help reduce exposure. Toxoplasmosis is a zoonosis. (See also Toxoplasmosis: Introduction.)
Listeriosis:
Abortion caused by Listeria monocytogenes in ewes usually occurs in late gestation. There is some necrosis of cotyledons and the intercotyledonary areas, and the fetus is usually autolyzed. The fetal liver (and possibly lung) may have necrotic foci, 0.5-1 mm in diameter. Diagnosis is by culture. (See also Listeriosis: Introduction .)
Brucellosis:
The major importance of Brucella ovis is as a cause of epididymitis in rams, but it also causes late-term abortions, stillbirths, and birth of weak lambs. B melitensis is rare in the USA but causes abortion in areas where it is found. B abortus occasionally causes abortion in sheep. Brucella abortions occur late in gestation, resulting in placentitis with edema and necrosis of the cotyledons and thickened, leathery intercotyledonary areas. Many fetuses aborted due to B ovis are alive at the beginning of parturition, although fetuses can be mummified or autolyzed. Most fetuses aborted due to B melitensis or B abortus are autolytic. Culture of the placenta, abomasal contents, and the dam’s vaginal discharge are diagnostic. A vaccine for B melitensis is available in some countries. B melitensis and B abortus are zoonotic. (See also Brucellosis in Large Animals: Introduction.)
Salmonellosis:
Salmonella abortus ovis , S dublin , S typhimurium , and S arizona have caused abortions in sheep. S abortus ovis is endemic in England and Europe but has not been reported in the USA. The other serotypes occur worldwide. Most ewes are sick and febrile before aborting. There are no specific placental lesions, and the fetus is autolyzed. Diagnosis is by culture of placenta, fetus, or uterine discharge. See also Dentistry .
Other Causes of Abortion:
Bluetongue virus and Akabane virus (where present) cause abortion and congenital anomalies in sheep and are differential diagnoses for Cache Valley virus infection. Coxiella burnetii causes occasional abortion storms in sheep, with the clinical syndrome and fetal pathology being the same as for goats (see abortion in goats, Abortion in Goats). Neospora caninum has been reported to cause occasional abortions in sheep with the lesions resembling those of Toxoplasma gondii .
Mycotic Pneumonia
Fungal infection of the lung results in an acute to chronic active, pyogranulomatous pneumonia.
Etiology:
Cryptococcus neoformans , Histoplasma capsulatum , Coccidioides immitis , Blastomyces dermatiditis , Pneumocystis carinii , Aspergillus spp , Candida spp, and other less common fungi have been identified as causative agents of mycotic pneumonia in domestic animals (see also fungal infections, Fungal Infections: Introduction). Often these agents are found in immunocompromised hosts, but can cause disease in healthy individuals as well. Infection is typically caused by inhalation of spores, which can lead to hemolymphatic dissemination. Pulmonary tissues and secretions are an excellent environment for these organisms. The source of most fungal infections is believed to be soil-related rather than horizontal transmission. Considering the high rate of exposure to these pathogens in certain environments, there are unresolved questions on the epidemiology of the condition, including individual susceptibility, pathogenicity of organisms, the immune response of the host, and concurrent disease. Blastomyces and Histoplasma are prevalent in the Mississippi and Ohio River valleys, whereas Coccidioides is found in the southwestern USA and northwestern Mexico. Cryptococcus is often associated with accumulation of pigeon excreta.
Clinical Findings :
Mycotic pneumonia is more commonly seen in small animals. Blastomyces infections typically occur in young, male, large-breed dogs. In cats, Cryptococcus has a predilection for the nasal cavity where it causes a granulomatous rhinitis and sinusitis. Acute, fulminant clinical presentations do occur but are rare, and the most common course of disease is chronic. A short, moist cough is characteristic. A thick, mucoid nasal discharge may be present. As the disease progresses, dyspnea, emaciation, and generalized weakness become increasingly evident. Respiration may become abdominal, resembling that of a diaphragmatic hernia ( Diaphragmatic Hernia: Introduction). On auscultation, harsh respiratory sounds are heard. In advanced cases, breath sounds are decreased or almost inaudible. Tracheobronchial lymphadenopathy can cause extrinsic airway compression. Neutrophilic leukocytosis or neutropenia with a left shift, nonregenerative anemia, and periodic fever can occur, possibly concurrent with bacterial infections. Radiography will show enlargement of tracheobronchial lymph nodes and variable, nodular to linear, interstitial infiltrates.
Lesions:
Multifocal to coalescing lesions of granulomatous to pyogranulomatous inflammation are present in the lungs. Abscess formation and cavitation may be seen in conjunction with yellow or gray areas of necrosis. Causative organisms are present within macrophages or areas of intense inflammation. Dissemination to multiple organ systems (eg, skin, eyes, peripheral lymph nodes, bones, CNS, male genitalia, oral cavity, nasal cavity) may occur.
Diagnosis:
A tentative diagnosis of mycotic pneumonia can be made if an animal with chronic respiratory disease exhibits the clinical signs described and does not respond to antibiotic therapy. Definitive diagnosis requires laboratory confirmation. Radiography may be useful. Serology can provide a presumptive diagnosis. Some antigens (eg, histoplasmin, blastomycin) have been developed and are an aid in diagnosis. Cytologic examinations of the sputum or exudates from sites of extrapulmonary inflammation may reveal the infective organism. The clinical diagnosis can be confirmed at necropsy by appropriate microbiology and histopathology. Special stains can be used to highlight the organisms.
Etiology:
Cryptococcus neoformans , Histoplasma capsulatum , Coccidioides immitis , Blastomyces dermatiditis , Pneumocystis carinii , Aspergillus spp , Candida spp, and other less common fungi have been identified as causative agents of mycotic pneumonia in domestic animals (see also fungal infections, Fungal Infections: Introduction). Often these agents are found in immunocompromised hosts, but can cause disease in healthy individuals as well. Infection is typically caused by inhalation of spores, which can lead to hemolymphatic dissemination. Pulmonary tissues and secretions are an excellent environment for these organisms. The source of most fungal infections is believed to be soil-related rather than horizontal transmission. Considering the high rate of exposure to these pathogens in certain environments, there are unresolved questions on the epidemiology of the condition, including individual susceptibility, pathogenicity of organisms, the immune response of the host, and concurrent disease. Blastomyces and Histoplasma are prevalent in the Mississippi and Ohio River valleys, whereas Coccidioides is found in the southwestern USA and northwestern Mexico. Cryptococcus is often associated with accumulation of pigeon excreta.
Clinical Findings :
Mycotic pneumonia is more commonly seen in small animals. Blastomyces infections typically occur in young, male, large-breed dogs. In cats, Cryptococcus has a predilection for the nasal cavity where it causes a granulomatous rhinitis and sinusitis. Acute, fulminant clinical presentations do occur but are rare, and the most common course of disease is chronic. A short, moist cough is characteristic. A thick, mucoid nasal discharge may be present. As the disease progresses, dyspnea, emaciation, and generalized weakness become increasingly evident. Respiration may become abdominal, resembling that of a diaphragmatic hernia ( Diaphragmatic Hernia: Introduction). On auscultation, harsh respiratory sounds are heard. In advanced cases, breath sounds are decreased or almost inaudible. Tracheobronchial lymphadenopathy can cause extrinsic airway compression. Neutrophilic leukocytosis or neutropenia with a left shift, nonregenerative anemia, and periodic fever can occur, possibly concurrent with bacterial infections. Radiography will show enlargement of tracheobronchial lymph nodes and variable, nodular to linear, interstitial infiltrates.
Lesions:
Multifocal to coalescing lesions of granulomatous to pyogranulomatous inflammation are present in the lungs. Abscess formation and cavitation may be seen in conjunction with yellow or gray areas of necrosis. Causative organisms are present within macrophages or areas of intense inflammation. Dissemination to multiple organ systems (eg, skin, eyes, peripheral lymph nodes, bones, CNS, male genitalia, oral cavity, nasal cavity) may occur.
Diagnosis:
A tentative diagnosis of mycotic pneumonia can be made if an animal with chronic respiratory disease exhibits the clinical signs described and does not respond to antibiotic therapy. Definitive diagnosis requires laboratory confirmation. Radiography may be useful. Serology can provide a presumptive diagnosis. Some antigens (eg, histoplasmin, blastomycin) have been developed and are an aid in diagnosis. Cytologic examinations of the sputum or exudates from sites of extrapulmonary inflammation may reveal the infective organism. The clinical diagnosis can be confirmed at necropsy by appropriate microbiology and histopathology. Special stains can be used to highlight the organisms.
Pharyngitis
Pharyngitis is an inflammation of the walls of the pharynx. It may accompany most upper airway viral and bacterial respiratory infections, eg, strangles in horses and distemper in dogs.
Functionally, the pharynx is divided into 2 components—the nasopharynx and the oropharynx. In most species, there is a common pharynx that is present at times other than deglutition. The unique caudal pharyngeal-laryngeal anatomy of horses shows complete separation of the pharynx into 2 components. (See also pharyngeal lymphoid hyperplasia, Pharyngeal Lymphoid Hyperplasia .)
Clinical Findings:
In general, animals with pharyngitis have a normal desire to eat and drink but may have difficulty swallowing. As a result of secondary peripharyngeal cellulitis and abscessation, some animals may present in an emergency situation (eg, a young foal with gross suppurative pharyngitis from strangles that is obstructing the pharynx and causing asphyxiation). The diagnosis in such cases is based on complete physical examination and radiographic and endoscopic evaluation of the throat, together with cultures of appropriate draining fluids and sites. In small animals, oral pain and resistance to having the mouth opened may indicate retropharyngeal abscessation and the presence of a penetrating foreign body or neoplasia of the mouth or tonsils.
Treatment:
The primary treatment is to identify and control or eliminate the predisposing factors. If pharyngitis has been caused by foreign bodies, removal of the offending object and effective surgical drainage accompanied by excision of necrotic tissue should be done under general anesthesia. In race training of horses, multiple therapies for pharyngeal lymphoid hyperplasia are used. Such therapies involve the use of intranasal sprays via catheters that may include a mixture of components (eg, fluorescein, dimethyl sulfoxide [DMSO], and local anesthetic and antimicrobial agents).
Calicivirus infections in cats may cause marked ulceration of the oropharyngeal mucosa, which is difficult to treat without a primary therapy for the virus. Supportive therapy may control secondary bacterial infection. It is important to maintain normal hydration and provide adequate nutrition, which may be accomplished by IV fluid therapy, feeding by pharyngostomy, or both.
Functionally, the pharynx is divided into 2 components—the nasopharynx and the oropharynx. In most species, there is a common pharynx that is present at times other than deglutition. The unique caudal pharyngeal-laryngeal anatomy of horses shows complete separation of the pharynx into 2 components. (See also pharyngeal lymphoid hyperplasia, Pharyngeal Lymphoid Hyperplasia .)
Clinical Findings:
In general, animals with pharyngitis have a normal desire to eat and drink but may have difficulty swallowing. As a result of secondary peripharyngeal cellulitis and abscessation, some animals may present in an emergency situation (eg, a young foal with gross suppurative pharyngitis from strangles that is obstructing the pharynx and causing asphyxiation). The diagnosis in such cases is based on complete physical examination and radiographic and endoscopic evaluation of the throat, together with cultures of appropriate draining fluids and sites. In small animals, oral pain and resistance to having the mouth opened may indicate retropharyngeal abscessation and the presence of a penetrating foreign body or neoplasia of the mouth or tonsils.
Treatment:
The primary treatment is to identify and control or eliminate the predisposing factors. If pharyngitis has been caused by foreign bodies, removal of the offending object and effective surgical drainage accompanied by excision of necrotic tissue should be done under general anesthesia. In race training of horses, multiple therapies for pharyngeal lymphoid hyperplasia are used. Such therapies involve the use of intranasal sprays via catheters that may include a mixture of components (eg, fluorescein, dimethyl sulfoxide [DMSO], and local anesthetic and antimicrobial agents).
Calicivirus infections in cats may cause marked ulceration of the oropharyngeal mucosa, which is difficult to treat without a primary therapy for the virus. Supportive therapy may control secondary bacterial infection. It is important to maintain normal hydration and provide adequate nutrition, which may be accomplished by IV fluid therapy, feeding by pharyngostomy, or both.
Aspiration Pneumonia: Introduction (Foreign-body pneumonia, Inhalation pneumonia, Gangrenous Pneumonia)
Aspiration pneumonia is a pulmonary infection characterized by inflammation and necrosis caused by inhalation of foreign material. The severity of the inflammatory response depends on the material aspirated, the type of bacteria aspirated, and the distribution of aspirated material in the lungs.
Etiology:
Faulty administration of medicines is a common cause of aspiration pneumonia. Liquids administered by drench or dose syringe should not be given faster than the animal can swallow. Drenching is particularly dangerous when the animal’s tongue is drawn out, when the head is held high, or when the animal is coughing or bellowing. Administration of liquids by nasal intubation is not without risk, and careful technique is especially necessary in debilitated animals.
Inhalation of irritant gases or smoke is an infrequent cause. Aspiration of vomitus or attempts by animals to eat or drink while partially choked can result in aspiration pneumonia as well. Disturbances of deglutition, as in anesthetized or comatose animals (eg, mature cattle under general anesthesia or cows in lateral recumbency), vagal paralysis, acute pharyngitis, abscesses or tumors of the pharyngeal region, esophageal diverticula, cleft palate, megaesophagus, or encephalitis, are frequent predisposing causes.
Cats are particularly susceptible to pneumonia caused by aspiration of tasteless products such as mineral oil. In sheep, poor dipping technique may cause aspiration of fluid. Calves and lambs may inhale inflammatory debris if affected with diphtheritic laryngitis. Inhalation of milk by pail-fed calves can cause an acute necrotizing pneumonia due to the diffuse distribution of foreign material. The muscles of deglutition may be affected in lambs with nutritional myopathy. Pigs fed fine particulate food in dry environments may inhale feed granules. Aspiration pneumonia in cattle following delayed treatment for milk fever is highly fatal. In dogs with myasthenia gravis, aspiration pneumonia is the leading cause of death.
Clinical Findings:
A clinical history suggesting recent foreign-body aspiration is of greatest diagnostic value. Horses may develop fevers of 104-105°F (40-40.5°C), which can drop back into the normal range in a few days. Pyrexia is also seen in cats, dogs, and less commonly in cattle. The patient presents with acute dyspnea, tachypnea, and tachycardia. Associated findings are cyanosis and bronchospasm. A sweetish, fetid breath characteristic of gangrene may be detected, the intensity of which increases with disease progression. This is often associated with a purulent nasal discharge that sometimes is tinged reddish brown or green. Occasionally, evidence of aspirated material (eg, oil droplets) can be seen in the nasal discharge or expectorated material. On auscultation, wheezing sounds, pleuritic friction rubs, and crackling sounds of subcutaneous emphysema may be heard. In cows that aspirate ruminal contents, toxemia is usually fatal within 1-2 days. Cattle and pigs recover more frequently than horses, but mortality is high in all species. Recovered animals often develop pulmonary abscesses. In outbreaks after dipping of sheep, losses occur from day 2 to day 7 and then decrease gradually.
Lesions:
The pneumonia is usually in the anteroventral parts of the lung; it may be unilateral or bilateral and centers on airways. In early stages, the lungs are markedly congested with areas of interlobular edema. Bronchi are hyperemic and full of froth. The pneumonic areas tend to be cone-shaped with the base toward the pleura. Suppuration and necrosis follow, the foci becoming soft or liquefied, reddish brown, and foul smelling. There usually is an acute fibrinous pleuritis, often with pleural exudate.
Prevention and Treatment:
Atropine sulfate helps to control salivation stimulated by general anesthetics (eg, thiobarbiturates). Use of an endotracheal tube with an inflatable cuff prevents fluid aspiration during surgery.
The animal should be kept quiet. A productive cough should not be suppressed. Broad-spectrum antibiotics should be used in animals known to have inhaled a foreign substance, whether it be a liquid or an irritant vapor, without waiting for signs of pneumonia to appear. Care and supportive treatment are the same as for infectious pneumonias. In small animals, oxygen therapy may be beneficial. Despite all treatments, prognosis is poor, and efforts must be directed at prevention.
Etiology:
Faulty administration of medicines is a common cause of aspiration pneumonia. Liquids administered by drench or dose syringe should not be given faster than the animal can swallow. Drenching is particularly dangerous when the animal’s tongue is drawn out, when the head is held high, or when the animal is coughing or bellowing. Administration of liquids by nasal intubation is not without risk, and careful technique is especially necessary in debilitated animals.
Inhalation of irritant gases or smoke is an infrequent cause. Aspiration of vomitus or attempts by animals to eat or drink while partially choked can result in aspiration pneumonia as well. Disturbances of deglutition, as in anesthetized or comatose animals (eg, mature cattle under general anesthesia or cows in lateral recumbency), vagal paralysis, acute pharyngitis, abscesses or tumors of the pharyngeal region, esophageal diverticula, cleft palate, megaesophagus, or encephalitis, are frequent predisposing causes.
Cats are particularly susceptible to pneumonia caused by aspiration of tasteless products such as mineral oil. In sheep, poor dipping technique may cause aspiration of fluid. Calves and lambs may inhale inflammatory debris if affected with diphtheritic laryngitis. Inhalation of milk by pail-fed calves can cause an acute necrotizing pneumonia due to the diffuse distribution of foreign material. The muscles of deglutition may be affected in lambs with nutritional myopathy. Pigs fed fine particulate food in dry environments may inhale feed granules. Aspiration pneumonia in cattle following delayed treatment for milk fever is highly fatal. In dogs with myasthenia gravis, aspiration pneumonia is the leading cause of death.
Clinical Findings:
A clinical history suggesting recent foreign-body aspiration is of greatest diagnostic value. Horses may develop fevers of 104-105°F (40-40.5°C), which can drop back into the normal range in a few days. Pyrexia is also seen in cats, dogs, and less commonly in cattle. The patient presents with acute dyspnea, tachypnea, and tachycardia. Associated findings are cyanosis and bronchospasm. A sweetish, fetid breath characteristic of gangrene may be detected, the intensity of which increases with disease progression. This is often associated with a purulent nasal discharge that sometimes is tinged reddish brown or green. Occasionally, evidence of aspirated material (eg, oil droplets) can be seen in the nasal discharge or expectorated material. On auscultation, wheezing sounds, pleuritic friction rubs, and crackling sounds of subcutaneous emphysema may be heard. In cows that aspirate ruminal contents, toxemia is usually fatal within 1-2 days. Cattle and pigs recover more frequently than horses, but mortality is high in all species. Recovered animals often develop pulmonary abscesses. In outbreaks after dipping of sheep, losses occur from day 2 to day 7 and then decrease gradually.
Lesions:
The pneumonia is usually in the anteroventral parts of the lung; it may be unilateral or bilateral and centers on airways. In early stages, the lungs are markedly congested with areas of interlobular edema. Bronchi are hyperemic and full of froth. The pneumonic areas tend to be cone-shaped with the base toward the pleura. Suppuration and necrosis follow, the foci becoming soft or liquefied, reddish brown, and foul smelling. There usually is an acute fibrinous pleuritis, often with pleural exudate.
Prevention and Treatment:
Atropine sulfate helps to control salivation stimulated by general anesthetics (eg, thiobarbiturates). Use of an endotracheal tube with an inflatable cuff prevents fluid aspiration during surgery.
The animal should be kept quiet. A productive cough should not be suppressed. Broad-spectrum antibiotics should be used in animals known to have inhaled a foreign substance, whether it be a liquid or an irritant vapor, without waiting for signs of pneumonia to appear. Care and supportive treatment are the same as for infectious pneumonias. In small animals, oxygen therapy may be beneficial. Despite all treatments, prognosis is poor, and efforts must be directed at prevention.
Sweating Sickness
Sweating sickness is an acute, febrile, tickborne toxicosis characterized mainly by a profuse, moist eczema and hyperemia of the skin and visible mucous membranes. It is essentially a disease of young calves, although adults are also susceptible. Sheep, pigs, goats, and a dog have been infected experimentally. It occurs in eastern, central, and southern Africa, and probably in Sri Lanka and southern India.
Etiology:
The cause is an epitheliotropic toxin produced by females of certain strains of Hyalomma truncatum . The toxin develops in the tick, not in the vertebrate host. The potential to produce toxin is retained by ticks for up to 20 generations, and possibly longer. Attempted experimental transmissions between affected and normal animals by contact or inoculations of blood have been unsuccessful.
Graded periods of infestation of a susceptible host by “infected” ticks have different effects on the host. A very short period has no effect; the animal remains susceptible. A period just long enough to produce a reaction may confer immunity, but if the exposure is >5 days, severe clinical signs and death may result. Recovery confers a durable immunity, which may last ≥4 yr. Other closely related forms of H truncatum toxicoses have been described.
Clinical Findings:
After an incubation period of 4-11 days, signs appear suddenly and include hyperthermia, anorexia, listlessness, watering of the eyes and nose, hyperemia of the visible mucous membranes, salivation, necrosis of the oral mucosa, and hyperesthesia. Later, the eyelids stick together. The skin feels hot, and a moist dermatitis soon develops, starting from the base of the ears, the axillae, groin, and perineum, and extending over the entire body. The hair becomes matted, and beads of moisture may be seen on it. The skin becomes extremely sensitive and emits a sour odor. Later, the hair and epidermis can be readily pulled off, exposing red, raw wounds. The tips of the ears and the tail may slough. Eventually, the skin becomes hard and cracked and predisposed to secondary infection or screwworm infestation. Affected animals are sensitive to handling, show pain when moving, and seek shade.
Often, the course is rapid, and death may occur within a few days. In less acute cases, the course is more protracted and recovery may occur. Mortality in affected calves is 30-70% under natural conditions. Morbidity in endemic areas is ~10%. The severity of infection is influenced by the number of ticks as well as by the length of time they remain on the host.
Lesions:
Emaciation, dehydration, diphtheroid stomatitis, pharyngitis, laryngitis, esophagitis, vaginitis or posthitis, edema and hyperemia of the lungs, atrophy of the spleen, and congestion of the liver, kidneys, and meninges are found in addition to the skin lesions.
Diagnosis:
For diagnosis, it is essential to determine the presence of the vector. Typically, there is a generalized hyperemia with subsequent desquamation of the superficial layers of the mucous membranes of the upper respiratory, GI, and external genital tracts, and profuse moist dermatitis followed by superficial desquamation of the skin.
Prevention and Treatment:
Control of tick infestation is the only effective preventive measure. Removal of ticks, symptomatic treatment, and good nursing care are indicated. Non-nephrotoxic antibiotics and anti-inflammatory agents are useful to combat secondary infection. Immune serum can be used to good effect as a specific treatment.
Etiology:
The cause is an epitheliotropic toxin produced by females of certain strains of Hyalomma truncatum . The toxin develops in the tick, not in the vertebrate host. The potential to produce toxin is retained by ticks for up to 20 generations, and possibly longer. Attempted experimental transmissions between affected and normal animals by contact or inoculations of blood have been unsuccessful.
Graded periods of infestation of a susceptible host by “infected” ticks have different effects on the host. A very short period has no effect; the animal remains susceptible. A period just long enough to produce a reaction may confer immunity, but if the exposure is >5 days, severe clinical signs and death may result. Recovery confers a durable immunity, which may last ≥4 yr. Other closely related forms of H truncatum toxicoses have been described.
Clinical Findings:
After an incubation period of 4-11 days, signs appear suddenly and include hyperthermia, anorexia, listlessness, watering of the eyes and nose, hyperemia of the visible mucous membranes, salivation, necrosis of the oral mucosa, and hyperesthesia. Later, the eyelids stick together. The skin feels hot, and a moist dermatitis soon develops, starting from the base of the ears, the axillae, groin, and perineum, and extending over the entire body. The hair becomes matted, and beads of moisture may be seen on it. The skin becomes extremely sensitive and emits a sour odor. Later, the hair and epidermis can be readily pulled off, exposing red, raw wounds. The tips of the ears and the tail may slough. Eventually, the skin becomes hard and cracked and predisposed to secondary infection or screwworm infestation. Affected animals are sensitive to handling, show pain when moving, and seek shade.
Often, the course is rapid, and death may occur within a few days. In less acute cases, the course is more protracted and recovery may occur. Mortality in affected calves is 30-70% under natural conditions. Morbidity in endemic areas is ~10%. The severity of infection is influenced by the number of ticks as well as by the length of time they remain on the host.
Lesions:
Emaciation, dehydration, diphtheroid stomatitis, pharyngitis, laryngitis, esophagitis, vaginitis or posthitis, edema and hyperemia of the lungs, atrophy of the spleen, and congestion of the liver, kidneys, and meninges are found in addition to the skin lesions.
Diagnosis:
For diagnosis, it is essential to determine the presence of the vector. Typically, there is a generalized hyperemia with subsequent desquamation of the superficial layers of the mucous membranes of the upper respiratory, GI, and external genital tracts, and profuse moist dermatitis followed by superficial desquamation of the skin.
Prevention and Treatment:
Control of tick infestation is the only effective preventive measure. Removal of ticks, symptomatic treatment, and good nursing care are indicated. Non-nephrotoxic antibiotics and anti-inflammatory agents are useful to combat secondary infection. Immune serum can be used to good effect as a specific treatment.
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