poop in the coop: what it tells you about backyard … it tells you about backyard chicken parasites...

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Poop in the Coop: What it Tells You about Backyard Chicken Parasites

Richard Gerhold, DVM, MS, PhD University of Tennessee

Knoxville, TN

Avian parasites consist of multiple species including helminthes, protozoa and arthropods. Included are some of the important parasites that may be found in various avian species. The likely hood of infection will depend if the birds are pet birds, captive collection, or backyard species. The listed parasites in this paper are not inclusive but give the major pathogenic producing parasites that may be encounter in veterinary medicine.

Toxoplasma gondii causes toxoplasmosis which is infectious for all birds. Cats are the definitive host and shed oocysts in their feces. Clinical signs in affected birds include incoordination, listlessness, seizures, and convulsions. Lesions can range from encephalitis, myocarditis, pneumonia, and splenomegaly. Infected birds can be diagnosed using the modified agglutination test Necropsy findings include histopath examination and PCR on affected tissues can identify T. gondii as well. Limiting cat access to yard is the most effective prevention and owners should be strongly encouraged to keep cats indoors.

Baylisascaris procyonis is a roundworm of raccoons and birds are infected by ingesting larvated eggs in the environment. Dogs can also serve as the definite host for B. procyonis and can shed eggs. The distribution of B. procyonis has been increasing recently. Larval migrans of B. procyonis can result in numerous neurological impairment clinical signs including encephalitis, circling, seizures, and death. Necropsy diagnostics include histopath examination and PCR. Limiting raccoon access to yard and making the areas unattractive to raccoons is the main way to prevent this disease.

Oxyspirura sp. roundworms which lead to eye worm infection have been reported in avian families. Affected birds generally have swollen conjunctiva and birds are observed scratching their eyes. The globe can be rendered non function from chronic inflammation. Infection in birds occurs by eating infected cockroaches so limiting arthropod ingestion is important. Ivermectin has been useful in treatment of eyeworms.

Avian trichomonosis is caused by Trichomonas gallinae which is a protozoal parasite that primarily affects columbids, birds of prey, turkeys and passerines. Clinical signs include swollen crop, listlessness, ruffled feathers, and often open mouthed breathing. Variable lesions can consist of caseous necrosis within the oral cavity and esophagus and less frequently the liver. The presence of the parasite does not indicate disease given the wide spectrum of virulence. Transmission of the parasite occurs by direct avian contact or via contaminated food and water. Gross lesions of trichomonosis are not pathognomonic. Other diseases including avian pox, candidiasis, aspergillosis, oral Capillaria spp. infection, and vitamin A deficiency can have similar gross findings. Testing to confirm infection is conducted by examining the oral swabs via wet mount by light microscopy to observe the undulating swimming motion. PCR testing is available as well. Successful treatments in early infections include metronidazole and carnidazole.

The thread-like nematode, Capillaria contorta can be found in the oral cavity and esophagus of numerous various avian species. The parasites are slender and long and may be difficult to see grossly. Lesions are similar to T. gallinae infection. Birds are infected by ingesting extremely environmentally resistant eggs and as such, treatment without prevention will not stop infection in a flock. Other capillarid spp. can be found in the gastrointestinal tract leading to weight loss.

Syngamus trachea often referred to as the gape worm often leads to open mouth breathing due to parasite infection of trachea. The parasites are red color and form a “Y” shape in the trachea. Variable clinical signs can include gaping and gasping, listlessness, and lethargy. Infected birds can be treated with benzimidazole antihelmentics.

Coccidiosis is an important disease in captive birds. Oocysts are shed in the host’s feces and following ingestion by another host, lead to cellular infection. Anticoccidial compounds fall into two categories including polyether ionophores and enzymatic reaction compounds. Ionophore compounds allow limited cycling of the coccidia in the bird which aids in producing immunity. Variable compounds are available and depending on previous compound use on a particular farm, experimentation may be needed to determine useable compound. Maxiban (narasin/nicarbazin) is toxic in turkeys. Live vaccines are available for use in the poultry industry; immunity develops rapidly after exposure, but needs reinfection to reinforce the developing protection.

The protozoa Histomonas meleagridis is the cause of blackhead and is considered the most important parasitic disease for wild turkeys and is an important cause of mortality for numerous game birds and domestic turkeys. Recently mortality has been seen in backyard chickens. Clinical signs include yellow diarrhea, weight loss, and ruffled feathers. Lesions include target shaped necrotic areas in the liver and ceca are markedly thickened with necrotic material. On fresh carcasses, histomonads can be observed via wet mounts of swabs from affected organs. Ring-neck pheasants are the natural host for H. meleagridis however chickens can serve as unapparent carrier for the parasites including the Heterakis nematode that is a vector for Histomonas. For this reason, turkeys, quail, grouse, or chukars cannot be raised in the same areas as chickens or pheasants. Nitrasone (Histostat7 Alpharma Inc. Clifton, New Jersey) has been used to prevent outbreaks; however, this drug is now banned,

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Ascardia spp are frequently reported in birds and can interfere with intestinal passage of food. Ascarids are relatively large and range from 3-6 cm in length in comparison to Heterakis spp. ranging from 0.5-1.0 cm.

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Worm in the Brain: Update on Meningeal Worm Infection in

Goats, Sheep, and Camelids Richard Gerhold, DVM, MS, PhD

University of Tennessee Knoxville, TN

Meningeal worm or brain worm infection in camelids, elk, moose, and sheep and goats is caused by the roundworm parasite, Parelaphostrongylus tenuis. Meningeal worm infection is one of the most common causes of neurological illness and death in camelids and treatment of chronic cases are often difficult and expensive. Infected animals present with a head tilt, arching of the neck, incoordination, difficulty getting up, and/or gradual weight loss. The parasite causes disease by migration of the worm through the brain or spinal cord of affected animals leading to internal trauma and inflammation. Currently, no live animal test is available and post-mortem testing is performed by microscopic examination of brain sections for evidence of the worm migration pathways. Aberrant migration of meningeal worm larvae through the neuropil and spinal cord of camelids, especially alpacas and llamas, causes severe clinical neurological disorders. Camelids are exposed to the intermediate larval stages of P. tenuis via the accidental ingestion of infected terrestrial slugs and snails. Many other domesticated species have also been proven to be susceptible to P. tenuis infection including sheep, horses, cattle, and bison. Infected animals present with a head tilt, arching of the neck, incoordination, difficulty getting up, and/or gradual weight loss. Treatment for camelids and ungulates with moderate to severe clinical disease is often expensive, but unrewarding, despite use of numerous anthelmintics and supportive. Parelaphostrongylus tenuis infection also has a huge impact on wildlife conservation.

The natural host of the metastrongylid parasite is the white-tailed deer, Odocoileus viginianus, which are unapparent carriers of the parasite. However, in other species of ungulates, like those listed above, the response to infection is quite different. The larvae emerge from accidentally ingested slugs and snails, and penetrate the host’s gastrointestinal track. From there, they migrate to and develop within the spinal cord for up to 1 month. The migrating P. tenuis larvae cause extensive central nervous system (CNS) damage and disabling neurologic disease. Lesions caused by P. tenuis migration are often difficult to identify, due to the fact that their histologic appearance varies so greatly. Currently, there is no commercially available antemortem test to confirm Parelaphostrongylus spp. infection in any species. Suspect cases of P. tenuis is often made in camelids following detection of cerebrospinal fluid (CSF) eosinophilic inflammation, combined with the clinical signs of head tilt, arching of the neck, incoordination, difficulty getting up, and/or gradual weight loss. A nested PCR can be used to detect P. tenuis from formalin fixed tissue which was successfully used for detection of Parelaphostrongylus spp. DNA in a Sika deer, horse, cattle, and guinea pig.

Prevention of parasite infection include minimizing deer populations through hunting, high fences to exclude deer, the use of livestock guardian dogs, and use of rock lined area on the outside of the fence. The use of molluscicides on the outer fence rocks can impede the entry of infected gastropods into pastures and minimize infection of P. tenuis into camelids and other animals. The use of injectable ivermectin has been used to prevent infection in P. tenuis infection; however, unintentional side effects could be selection of ivermectin-resistant Haemonchus contortus and other gastrointestinal nematodes.

Treatment for cases of meningeal worm include febendazole and anti-inflammatory drugs, particularly in early stage infections. As disease progresses, prognosis is less favorable and treatment may require a sling or further assistance given at a referral clinic.

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How to Identify and Treat Toxoplasma, Isopora, and Other Coccidial Infections


Knoxville, TN

Eimeria spp. have a direct life cycle and ingested sporulated oocyst reproduce in respective organs including liver, kidney, and mainly intestines. Through the process of multiple rounds of asexual reproduction will produce large number of merozoites. Following the last round of merizoite replication, the merizoites will differentiate into male and female stages to begin sexual reproduction. Once fertilization occurs feces. The processes of both asexual and sexual reproduction result in rupture of the infected cells and associated disease as a result of epithelial destruction.

The life cycle of Atoxoplasma, a coccidian parasite that infects birds, also has a direct life cycle with both asexual and sexual life stages. The asexual reproduction occurs in the intestines of infected birds and also in mononuclear phagocytes of the gut mucosa, resulting in infected mononuclear cells containing the merozoite that may stay in the gut or enter the blood to disseminate the parasite to other extraintestinal tissues such as the liver. Sexual reproduction occurs in the intestines and results in the excretion of oocysts in the feces.

Toxoplasma gondii and Isospora are different in that they have a direct life cycle but can utilize a paratenic host. The only definitive host for Toxoplasma is the cat. Thus, sexual reproduction (the formation of micro and macrogamonts) and shedding of oocysts occurs only the gastrointestinal tract of felids. Oocysts that are shed in the feces of cats will sporulate to become infective to nearly any warm-blooded vertebrate host. Any warm-blooded animal that consumes the oocyst may act as a paratenic host – i.e., the parasite can live in the tissues of the paratenic host but the parasite does not require growth or multiplication in the paratenic host in order to complete its life cycle. When the cat or paratenic host ingests the infective oocyst, the sporozoites are released and undergo massive asexual reproduction in the cells of the intestines and lymph nodes producing tachyzoites. These tachyzoites continue to multiply in other cells of the body (extraintestinal phase); destruction of infected cells is what results in disease and signs of disease will depend upon the organ infected (i.e., pneumonia if damage occurs in lungs, neurologic signs if damage occurs in brain). After the fast replicating tachyzoite stage, a slow replicating bradyzoite stage will begin in which the parasite forms cysts, containing the bradyzoites, in various tissues that can include the brain. The cysts will persist for the life of the animal. If a cat ingests a parentic host that has the encysted bradyzoites, the bradyzoites will enter the small intestinal epitheial cells and first undergo asexual reproduction and then the sexual reproductive life stage, shedding oocysts 3-10 days later. If the life cycle is direct, and the cat ingests sporulated oocysts (rather than the encysted bradyzoites of a paratenic host), it take 19-48 days to shed oocysts which suggests that the parasite can accomplish much of the required asexual reproductive stages in the process of forming bradyzoites in the paratenic host.

Isospora may undergo direct transmission or indirect transmission by use of a paratenic host. A rodent or bird may act as a paratenic host by ingesting the sporulated oocyst. In the paratenic host, the sporozoite is released from the oocyst and migrates to lymph nodes where it will encyst (monozoic cyst) and be infective to the carnivore that consumes the rodent. The host may consume the infected paratenic host or ingest the sporulated oocysts from the environment. There is no extraintestinal life cycle for this coccidian and both asexual and sexual reproduction occurs in the villar epithelium and nonsporulated oocysts are excreted in the feces. However, extraintestinal migration of the parasite may occur in the host after ingestion of the sporozoites in the host. Some sporozoites may enter the mesenteric lymph node (as also seen in the paratenic hosts) or may enter other extraintestinal tissues (spleen, liver) where they form cysts. Thus, monozoic cysts may form in both the definitive and paratenic hosts and remain for the life of the animal. In definitive hosts, the cyst may rupture and release sporozoites to reinfect the intestine.

The advantage of having an asexual life stage for these coccidian parasites is the ability for the parasite to rapidly and markedly increase the number of parasites from the ingestion of only a single sporozoite. Asexual reproduction allows the parasite to quickly and exponentially increase in a non-immune host. In theory one ingested oocyst can produce close to a 1million new oocysts in feces of naïve animal depending on age and available intestinal cells to infect.

Most (although not all) coccidian parasites undergo sexual reproduction in the gut. This is an important strategy for transmission because oocysts are therefore shed in the feces for a feco-oral transmission. Infection can result in clinical signs as a result of cellular destruction (the severity of disease seen is related to the degree of infection and cellular destruction). Diarrhea will increase the environmental contamination, which can aid in transmission especially in a captive environment. Although coccidiosis may cause morbidity and/or mortality, it would not be advantageous to the parasite to cause high degree of mortality thus the asexual reproduction ceases after a genetically predetermined number of cycles (which may vary per coccidian species).

Parasitic encystment (either as encysted bradyzoites in Toxoplasma or as monozoic cysts in the paratenic or definitive hosts for Isospora) is another strategy for the parasite for transmission or reinfection. The use of a paratenic host by Isospora and Toxoplasma is an advantageous because it increases the chance of exposure to the definitive host by “presenting” the parasite back to the definitive host. By infecting prey species (and affecting the prey species such that it is more susceptible to predation as is seen in Toxoplasma

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infection of rodents) the parasite increases its chances of returning to the felid host to complete the sexual stage of the life cycle. For wild felids with large home-ranges and solitary behavior, the ingestion of a paratenic host may be more likely than ingestion of infective oocysts directly.

Many, if not all, animals have been reported with one or more coccidian parasites, but infection does not typically cause disease in free-ranging wild animals in natural conditions. Clinical coccidiosis is seen in captive animals because transmission is enhanced by captive conditions. Because there is no requirement for an intermediate host, these parasites with a direct life cycle are easily transmitted in captive environments. Environmental contamination in a closed/confined space is much greater than over a natural habitat and the controlled temperature and humidity of captive animal holding can promote sporulation of the oocyst to its infective form. The oocysts can be destroyed by desiccation and direct sunlight but many commonly used disinfectants are not effective and thus a captive environment can be easily contaminated. Captive animals are also typically found at much higher density than wild animals, increasing the chance for shedding and exposure. In breeding or production facilities there are young animals that have not yet developed immunity to the parasite and are susceptible to infection clinical disease and likely to shed the parasite. Coccidian oocysts may be shed from asymptomatic animals as well (there have been reports of 30-50% prevalence in apparently healthy animals of a range of species) thus environmental contamination and risk for reinfection is high in a captive environment. Lastly, stress is a known factor in the development of clinical coccidiosis. “Winter coccidiosis” in cattle occurs likely due to the stress of extreme temperatures in combination with infection, while outbreaks of clinical coccidiosis have been seen after shipping (another stressful event) in other species. Sources of stress in captive animals can include high stocking density, poor nutrition, competition, and handling that could contribute to the development of clinical coccidiosis. While wild animals also have stressors, they do not have the added combination of high levels of environmental contamination, high stocking density, and intensive breeding or production.

The most pathogenic lesions in enteric coccidiosis occur as a result of the host cell rupture during the asexual propagation. Most coccidia develop in villus enterocytes but others may develop in crypt enterocytes or lamina propria. Rupture of the host cell at the end of merogony is associated with the release of schizonts (containing merozoites). Cell rupture also occurs when the oocyst is released after the sexual reproduction stage. Destruction of enterocytes or lamina propria results in diarrhea, dehydration, weight loss, and severe hemorrhage.

Antiprotozoal vaccines for animals include vaccines against coccidiosis for poultry, many of which are actually nonattenuated oocysts from various coccidian species. Anticoccidial treatment is often used at the time of vaccine administration. Interestingly, use of live coccidia vaccines in poultry houses can restore a drug-sensitive population of parasites to populations in which drug-resistant coccidia become prevalent. Live coccidiosis vaccines that incorporate attenuated oocysts and a nonliving subunit vaccine are also available.

Anticoccidial compounds generally fall into one of two categories. The first are polyether ionophores which disrupt the proper intra and extracellular concentrations of the various cations and leads to cellular dysfunction. The second group includes compounds that cause an enzymatic reaction. The various classes of anticoccidial compounds and their mechanism of action are listed below.

Polyether Ionophores fall into one of five categories including monovalent, monovalent glycosides, divalent, divalent glycosides, and divalent pyrole ethers. Their mode of actions is to form lipophilic complexes with alkali metal cations and to transport these ions across biological membranes. The end result is that the cell is unable to maintain the proper intra and extracellular concentrations of the various cations and leads to cellular dysfunction. A main way this occurs is by the Ionophores interfering with the K+/Na+ pump osmolarity. Ionophore drugs also allow some cycling of the coccidia in the bird which aids in producing immunity. Ionophores generally have lower rate of resistance development compared to the enzyme reaction drugs listed above and often allow some low level cycling of the coccidia in the host leading to host immunity. Anticoccidial drugs belonging to the polyether Ionophores include lasalocid, salinomycin, maduramicin, monensin, narasin, lonomycin, and semduramicin. Maxiban is toxic in turkeys and should not be used in this species, but is a safe drug for quail, pheasants and chickens

Enzyme or metabolic blocking anticoccidial compounds include sulfonamides are folate antagonists and their mechanism of action (MOA) occurs by competitive inhibitors of PABA in the dihydropteroate synethetase reaction to make folate. Normally, folate is reduced to tetrahydrofolate, using NADPH as a co-factor, and is used to create and methylate DNA. 2,4-diaminopyrimidines act in a similar fashion and block the reduction of folate to tetrahydrofolate. The combination of sulfonamides and 2,4-diaminopyrimidines is synergistic and is active on first and second generation schizonts and perhaps sexual stages as well. Amprolium is a thiamine antagonist and acts by competitively inhibiting the active transport of thiamine. Care must be taken not overdose animals on amprolium or secondary complications including polioencephalomalacia may develop due to lack of thiamine.

Coccidia are generally immunogenic and a single infection in an immunocompenent host will induce immunity to reinfection to some degree. However, exceptions to this generality have been noted. Immunity in coccidia occurs primarily as a result of the asexual replication, with the sexual stages contributing little additional protection. Immunity to a challenge inoculum is manifested as a reduction in clinical signs and reduced multiplication of the parasite. Circulating antibodies are effective at opsonization and cytopathological and enhancing the uptake of parasites of macrophages. The role of cell-mediated immunity has been shown to be the most important factor in host protection. Adoptive transfer of lymphocytes from Eimeria immunized animals to naïve animals leads

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to protection when challenged. It is assumed that the importance of cell mediated immunity is the same in all vertebrate hosts of coccidia.

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Ticks and Diseases They Cause in Pets- Ehrlichiosis, Anaplasmosis, Cytauxzoonosis, and More


Knoxville, TN Tick-borne diseases are extremely important and emerging diseases in the United States. The area in which you live will influence the diseases that are circulating in the environment. Although diseases such as Lyme disease has received a great deal of attention, other important diseases including ehrlichiosis, Rocky Mountain spotted fever, anaplasmosis and cytauxzoonosis have been emerging in various areas. A good travel history is imperative given various species of ticks and tick-borne diseases are more common in certain geographical areas. More information on tick-borne disease distribution can be found at http://www.capcvet.org/parasite-prevalence-maps/ Diagnosis of tick-borne diseases: Serology vs PCR Testing is warranted on animals with the aforementioned clinical signs. PCR testing (detection of pathogen DNA) is more sensitive than serology for detection of Rocky Mountain spotted fever and Anaplasma/Ehrlichia species during the acute phase of the disease, prior to the development of an antibody response. Therefore, if an animal presents with acute signs suggestive of tick-borne disease (i.e. fever, lethargy, thrombocytopenia, leukopenia, arthropathy, neurologic dysfunction), the best test for diagnosis is the PCR. Whole blood (EDTA) should be obtained for the test, prior to antibiotic administration.

Serology is useful for detection of chronic/persistent infections, during which the numbers of pathogens are lower or absent from circulation and cannot be detected as easily by PCR. This is particularly true for Lyme disease. This organism localizes in the tissues and is difficult to detect in the blood. It is important to note that antibodies to these tick-borne agents may persist for several months to years (especially for E. canis), so detection of antibodies does not distinguish current infection from previous exposure. Also, high seroprevalence to these agents has been documented in healthy dogs in endemic areas, such as the Southern USA, and most dogs exposed to Anaplasma or Ehrlichia species will not develop overt clinical disease. Therefore, PCR of skin or other tissues (not blood) and/or complete blood count is useful to determine if seropositive animals are currently infected and have clinical disease. Identification of ticks Tick bodies are divided into two primary sections including fused head and thorax and abdomen. All adult and nymphal forms have 4 pairs legs and no antennae and all larval forms have 3 pairs of legs. The importance of determining larvae vs other stages include to determine the likelihood of tick being infected with various pathogens. Unless transovarial transmission occurs, larvae are unlikely to be infected with pathogens, while nymphs and adults have higher likelihood include with pathogens in transstadial transmission. Whereas hard ticks have scutum, soft ticks do not have scutum. Ticks are great vectors due to their ability to be persistent blood-suckers which attach firmly & feed slowly, long life spans, may be geographically widespread, resistant to environmental conditions, high reproductive potential, and can pass infective agents through egg to next generation and/or through successive stages. Ticks bites in themselves can lead to wounds and Inflammation from salivary proteins. Secondary infection and disease can be due to toxicosis, local necrosis, and tick paralysis. Tick bites predispose animals to secondary attacks by myiasis-producing flies.

Soft tick have no scutum are soft, tough, leathery body, do not stay attached—instead take multiple small volumes of blood, and often feed at night.

Soft ticks include Otobius megnini (Spinose Ear Tick) transmits relapsing fever caused by a Borrelia spp. (different than Borrelia burgdorferi which causes Lyme Disease). Spinose ear ticks are more common in western states that are west of 100th meridian

Hard Ticks is largest family of ticks has a scutum (dorsal, hardened plate) that covers entire dorsum of males and forms an anterior shield in females. Hard ticks remain attached until engorged and then fall off to molt or lay eggs. General life cycle include:

Egg 6-legged larva 8-legged nymph 8-legged adult Oviposition (egg laying) occurs off of the host Nymphs and adults can be identified based on visual exam but often unable to distinguish larvae without microscopic

exam Nymphs and adults are more likely to harbor pathogens than larvae—this is why you need to be able to distinguish larvae (6 legs)

from nymphs/adults (8 legs). Tick species

All dermacentor spp. Ornate ticks with eyes Basis capitulum (mouth part) is rectangular if viewed from above and has stubby palps Resembles Rhipicephalus (both have11 festoons, small rectangular patterns on posterior abdomen)

http://www.capcvet.org/parasite-prevalence-maps/


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Dermacentor variabilis (American dog tick) Eastern half of U.S. and west coast, but rare in Central US Dogs, cats, humans, horses, cattle, fox, rodents, and other mammals Can cause tick paralysis in humans, dogs, etc. May take as little as 3 months, with favorable conditions, or up to 2 years Principal vector of Rickettsia rickettsia - Rocky Mountain Spotted Fever (RMSF) and others in Spotted Fever Group Infrequent vectors of tularemia, anaplasmosis, Babesia canis, Cytauxzoon felis

Rhipicephalus sanguineus (brown dog tick) Wide distribution Rhipicephalus ticks are similar in appearance to Dermacentor, except they have a hexagonal basis capitulum. All stages

parasitize on dogs and will attach to other animals, but usually not humans Can survive indoors for months to possibly years without a blood meal Domestic & kennel problem due to tropical nature of tick and because it cannot survival outdoors in North America Vectors Babesia canis voglei, tularemia, Ehrlichia canis, RMSF

Rhipicephalus (boophilus) annulatus (cattle fever tick) Southern U.S. & Mexico—spreading North into lower Texas Parasitize mainly on cattle; also deer, horses, donkeys, sheep, etc. in other countries, not U.S. and Mexico 1-host tick in U.S. and Mexico—re-emerging cases on US/Mexican border—large concern for USDA First demonstrated tick-borne disease Babesia bigemina (Texas cattle fever) VERY important disease to cattle industry—causes severe anemia and death in

cattle and is a reportable tick species! All amblyomma spp.

Ornate ticks Long mouth parts & commonly 11 festoons—allows one to differentiate from Ixodes spp which lack festoons

Amblyomma americanum (Lone Star Tick) Wide distribution, but mainly in southern U.S. Large silver spot at apex of scutum on females – hence name “lone star” All stages feed on wild & domestic animals, birds, & humans and is significant pest for humans & animals Can transmit Coxiella burnetii (Q-fever), tularemia, Ehrlichia chaffeensis, Ehrlichia ewingii, RMSF, Cytauxzoon felis

(cats) Vectors agent of Southern Tick Associated Rash Infection (STARI) in humans Cause of STARI is currently unknown—may actually be the host reaction to tick saliva—leads to swelling and pain at

bite region Amblyomma maculatum (Gulf Coast Tick)

Southeastern US in Gulf coast region, but has expanded range recently Ornate scutum – often confused with Dermacentor—examine mouth parts to differentiae Adults attack nearly all animals & humans and can transmit Hepatozoon americanum Hepatozoonosis—dog must eat

tick to be infected with Hepatozoon All Ixodes spp.

Inornate ticks and No festoons, has distinct anal groove anterolateral to anal orifice Used for identification in NON-ENGORGED tick but can’t see groove in engorged ticks—use mouth parts instead

Ixodes scapularis (Black-Legged Tick) Wide distribution, in East, South, and Midwest U.S. Highest populations in upper Midwest and New

England/midatlantic states Primary Lyme disease (Borrelia burgdorferi) vector in Eastern US and Midwest Vectors Babesia microti, Anaplasma phagocytophila

Ixodes pacificus (California Black-Legged Tick) Primary Lyme disease vector in the West Coast Tick-borne diseases

Tick paralysis Potentially fatal reaction to a paralyzing neuromuscular toxin secreted in the saliva of a female tick late in her feeding.

Cattle, sheep, horses, dogs, and humans seem to be most affected. Clinical signs include: headache, vomiting, general malaise, loss of motor function and reflexes, followed by paralysis

that starts in the lower body and spreads to the rest of the body

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Respiratory failure and death can result. Signs disappear rapidly when tick is removed, suggesting that the toxin is rapidly excreted or destroyed

Lyme borreliosis Agent: Borrelia burgdorferi Vector: Ixodes scapularis (Eastern and Midwestern US), Ixodes pacificus (Western US) Geographical distribution: New England and mid-Atlantic states, upper Mid-west, and Pacific coast. Animal health: Major cause of canine and equine disease, including endocarditis and joint pain. Most cases occur in the

spring and summer, during nymphal emergence, and in late fall and winter, during adult emergence. Human health: Acute and chronic diseases including joint pain, heart disease, and neurological disorders. Most cases

occur in the spring and summer, during nymphal emergence, and in late fall and winter, during adult emergence. Diagnoses: Lyme disease is diagnosed using serology tests, bacterial cultures, and/or PCR of tissue (NOT BLOOD).

Blood may be used for PCR in very acute cases, otherwise tissue biopsy is needed. Predictive value influences serological test interpretations—only treat animals with clinical signs suggestive of disease!!!

Rocky Mountain Spotted Fever Agent: Rickettsia rickettsia Sometimes placed in “Spotted Fever” disease group Vector: Dermacentor variabilis Geographical distribution: Eastern US mainly. Most frequently reported tick borne disease in the eastern US. Animal health: Recent evidence has shown that untreated RMSF may lead to death of the affected animal. Clinical signs include whole body pain and are painful on palpation.

Cytauxzoon felis Piroplasm of cats. Bobcats are reservoir host that is transmitted by Amblyomma americanum. Clinical signs: fever, dehydration, icterus, lymphadenomegaly, and hepatosplenomegaly. Treatment with atovaquone plus azithromycin. Diagnosis: PCR, blood smear (negative blood smear does not rule out infection) since early stage only see schizonts in macrophages. Prevention: Keep cats indoors!! Use preventative for tick infestation

Anaplasma phagocytophilum Intracellular rickettsia that causes human granulocytic anaplasmosis Infects granulocytes and leads to bleeding, fever, leukopenia, Clinical signs/symptoms may be worse with co-infection with Lyme or Babesia

Vectored by Ixodes scapularis so same geographical distribution as Lyme Disease. Can be transmitted by blood transfusion.

Diagnosis: clinical signs, PCR (acute cases), serology (chronic), CBC to look for leukopenia, Blood smear to look for morulae in granulocytes.

Don’t treat animals that are clinically normal but are only seropositive—potential false positive due to positive predictive value.

Treatment with doxycycline or minocycline Anaplasma platys

Intracellular rickettsia that causes infectious cyclic thrombocytopenia in dogs Common clinical signs include bleeding, due to cyclic thrombocytopenia…may be worse with co-infection with

Ehrlichia canis, which is transmitted by same tick. Transmitted by Rhipicephalus sanguineus –worldwide distribution Diagnosis: clinical signs, PCR (acute cases), serology (chronic). Don’t treat animals that are clinically normal but are

only seropositive—potential false positive due to positive predictive value. Treatment with doxycycline or minocycline

Ehrlichia canis Intracellular rickettsia that causes canine ehrlichosis Infects monocytes and leads to fever, anorexia, lethargy, thrombocytopenia, lymphadenopathy, edema, bone marrow

suppression. The acute stage is mainly due to a vasculitis. E. canis replicates in monocytes. The infected monocytes bind to vascular

endothelial cells and leads to a vasculitis Transmitted by Rhipicephalus sanguineus –worldwide distribution Diagnosis: clinical signs, PCR (acute cases), serology (chronic), CBC to look for leukopenia, Blood smear to look for

morulae in monocytes Don’t treat animals that are clinically normal but are only seropositive—potential false positive due to positive

predictive value. Treatment with doxycycline or minocycline

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Ticks and the Diseases they Cause in Pets and People: Lyme Borreliosis, Tick Paralysis, Rocky Mountain Spotted Fever


Knoxville, TN

Tick-borne diseases are extremely important and emerging diseases in the United States. The area in which you live will influence the diseases that are circulating in the environment. Although diseases such as Lyme disease has received a great deal of attention, other important diseases including ehrlichiosis, Rocky Mountain spotted fever, anaplasmosis and cytauxzoonosis have been emerging in various areas. A good travel history is imperative given various species of ticks and tick-borne diseases are more common in certain geographical areas. More information on tick-borne disease distribution can be found at http://www.capcvet.org/parasite-prevalence-maps/ Diagnosis of tick-borne diseases: Serology vs PCR Testing is warranted on animals with the aforementioned clinical signs. PCR testing (detection of pathogen DNA) is more sensitive than serology for detection of Rocky Mountain spotted fever and Anaplasma/Ehrlichia species during the acute phase of the disease, prior to the development of an antibody response. Therefore, if an animal presents with acute signs suggestive of tick-borne disease (i.e. fever, lethargy, thrombocytopenia, leukopenia, arthropathy, neurologic dysfunction), the best test for diagnosis is the PCR. Whole blood (EDTA) should be obtained for the test, prior to antibiotic administration.

Serology is useful for detection of chronic/persistent infections, during which the numbers of pathogens are lower or absent from circulation and cannot be detected as easily by PCR. This is particularly true for Lyme disease. This organism localizes in the tissues and is difficult to detect in the blood. It is important to note that antibodies to these tick-borne agents may persist for several months to years (especially for E. canis), so detection of antibodies does not distinguish current infection from previous exposure. Also, high seroprevalence to these agents has been documented in healthy dogs in endemic areas, such as the Southern USA, and most dogs exposed to Anaplasma or Ehrlichia species will not develop overt clinical disease. Therefore, PCR of skin or other tissues (not blood) and/or complete blood count is useful to determine if seropositive animals are currently infected and have clinical disease. Identification of ticks Tick bodies are divided into two primary sections including fused head and thorax and abdomen. All adult and nymphal forms have 4 pairs legs and no antennae and all larval forms have 3 pairs of legs. The importance of determining larvae vs other stages include to determine the likelihood of tick being infected with various pathogens. Unless transovarial transmission occurs, larvae are unlikely to be infected with pathogens, while nymphs and adults have higher likelihood include with pathogens in transstadial transmission. Whereas hard ticks have scutum, soft ticks do not have scutum. Ticks are great vectors due to their ability to be persistent blood-suckers which attach firmly & feed slowly, long life spans, may be geographically widespread, resistant to environmental conditions, high reproductive potential, and can pass infective agents through egg to next generation and/or through successive stages. Ticks bites in themselves can lead to wounds and Inflammation from salivary proteins. Secondary infection and disease can be due to toxicosis, local necrosis, and tick paralysis. Tick bites predispose animals to secondary attacks by myiasis-producing flies.

Soft tick have no scutum are soft, tough, leathery body, do not stay attached—instead take multiple small volumes of blood, and often feed at night.

Soft ticks include Otobius megnini (Spinose Ear Tick) transmits relapsing fever caused by a Borrelia spp. (different than Borrelia burgdorferi which causes Lyme Disease). Spinose ear ticks are more common in western states that are west of 100th meridian

Hard Ticks is largest family of ticks has a scutum (dorsal, hardened plate) that covers entire dorsum of males and forms an anterior shield in females. Hard ticks remain attached until engorged and then fall off to molt or lay eggs. General life cycle include:

Egg 6-legged larva 8-legged nymph 8-legged adult Oviposition (egg laying) occurs off of the host Nymphs and adults can be identified based on visual exam but often unable to distinguish larvae without microscopic

exam Nymphs and adults are more likely to harbor pathogens than larvae—this is why you need to be able to distinguish larvae (6 legs)

from nymphs/adults (8 legs). Tick species

All dermacentor spp. Ornate ticks with eyes Basis capitulum (mouth part) is rectangular if viewed from above and has stubby palps Resembles Rhipicephalus (both have11 festoons, small rectangular patterns on posterior abdomen)



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Dermacentor variabilis (American dog tick) Eastern half of U.S. and west coast, but rare in Central US Dogs, cats, humans, horses, cattle, fox, rodents, and other mammals Can cause tick paralysis in humans, dogs, etc. May take as little as 3 months, with favorable conditions, or up to 2 years Principal vector of Rickettsia rickettsia - Rocky Mountain Spotted Fever (RMSF) and others in Spotted Fever Group Infrequent vectors of tularemia, anaplasmosis, Babesia canis, Cytauxzoon felis

Rhipicephalus sanguineus (brown dog tick) Wide distribution Rhipicephalus ticks are similar in appearance to Dermacentor, except they have a hexagonal basis capitulum. All stages

parasitize on dogs and will attach to other animals, but usually not humans Can survive indoors for months to possibly years without a blood meal Domestic & kennel problem due to tropical nature of tick and because it cannot survival outdoors in North America Vectors Babesia canis voglei, tularemia, Ehrlichia canis, RMSF

Rhipicephalus (boophilus) annulatus (Cattle Fever Tick) Southern U.S. & Mexico—spreading North into lower Texas Parasitize mainly on cattle; also deer, horses, donkeys, sheep, etc. in other countries, not U.S. and Mexico 1-host tick in U.S. and Mexico—re-emerging cases on US/Mexican border—large concern for USDA First demonstrated tick-borne disease Babesia bigemina (Texas cattle fever) VERY important disease to cattle industry—causes severe anemia and death in

cattle and is a reportable tick species! All Amblyomma spp.

Ornate ticks Long mouth parts & commonly 11 festoons—allows one to differentiate from Ixodes spp which lack festoons

Amblyomma americanum (Lone Star Tick) Wide distribution, but mainly in southern U.S. Large silver spot at apex of scutum on females – hence name “lone star” All stages feed on wild & domestic animals, birds, & humans and is significant pest for humans & animals Can transmit Coxiella burnetii (Q-fever), tularemia, Ehrlichia chaffeensis, Ehrlichia ewingii, RMSF, Cytauxzoon felis

(cats) Vectors agent of Southern Tick Associated Rash Infection (STARI) in humans Cause of STARI is currently unknown—may actually be the host reaction to tick saliva—leads to swelling and pain at

bite region Amblyomma maculatum (Gulf Coast Tick)

Southeastern US in Gulf coast region, but has expanded range recently Ornate scutum – often confused with Dermacentor—examine mouth parts to differentiae Adults attack nearly all animals & humans and can transmit Hepatozoon americanum Hepatozoonosis—dog must eat

tick to be infected with Hepatozoon All Ixodes spp.

Inornate ticks and No festoons, has distinct anal groove anterolateral to anal orifice Used for identification in NON-ENGORGED tick but can’t see groove in engorged ticks—use mouth parts instead

Ixodes scapularis (Black-Legged Tick) Wide distribution, in East, South, and Midwest U.S. Highest populations in upper Midwest and New

England/midatlantic states Primary Lyme disease (Borrelia burgdorferi) vector in Eastern US and Midwest Vectors Babesia microti, Anaplasma phagocytophila

Ixodes pacificus (California Black-Legged Tick) Primary Lyme disease vector in the West Coast Tick-borne diseases

Tick paralysis Potentially fatal reaction to a paralyzing neuromuscular toxin secreted in the saliva of a female tick late in her feeding. Cattle, sheep, horses, dogs, and humans seem to be most affected.

Clinical signs include: headache, vomiting, general malaise, loss of motor function and reflexes, followed by paralysis that starts in the lower body and spreads to the rest of the body

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Lyme Borreliosis Agent: Borrelia burgdorferi Vector: Ixodes scapularis (Eastern and Midwestern US), Ixodes pacificus (Western US) Geographical distribution: New England and mid-Atlantic states, upper Mid-west, and Pacific coast. Animal health: Major cause of canine and equine disease, including endocarditis and joint pain. Most cases occur in the




Rocky Mountain Spotted Fever Agent: Rickettsia rickettsia Sometimes placed in “Spotted Fever” disease group Vector: Dermacentor variabilis Geographical distribution: Eastern US mainly. Most frequently reported tick borne disease in the eastern US. Animal

health: Recent evidence has shown that untreated RMSF may lead to death of the affected animal. Clinical signs include whole body pain and are painful on palpation.

Anaplasma phagocytophilum Intracellular rickettsia that causes human granulocytic anaplasmosis Infects granulocytes and leads to bleeding, fever, leukopenia, Clinical signs/symptoms may be worse with co-infection with Lyme or Babesia

Vectored by Ixodes scapularis so same geographical distribution as Lyme Disease. Can be transmitted by blood transfusion.

Diagnosis: clinical signs, PCR (acute cases), serology (chronic), CBC to look for leukopenia, Blood smear to look for morulae in granulocytes.

Don’t treat animals that are clinically normal but are only seropositive—potential false positive due to positive predictive value.

Treatment with doxycycline or minocycline

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Non Tick-Borne Diseases: Avian and Swice Influenza, Bartonellosis,

Leptospirosis, Rabies, and More Richard Gerhold, DVM, MS, PhD

University of Tennessee Knoxville, TN

Anthrax

Bacillus anthracis Ruminant reservoir Human: Reportable disease

Animals Sudden death Bloody discharge from orifices that DOES NOT CLOT Do not necropsy; burn carcass, send ear only to lab for confirmation of disease

Human 95% cutaneous Small, painless, red pruritic papules on skin that ulcerate; Tx w/ AB’s Inhalation FATAL URI with fever, shock and respiratory distress; death in 24h

Avian chlamydiosis

“Ornithosis/Psittacosis” Chlamydophila psittaci Bird reservoir Humans have flu like symptoms

o Fever, chills, headache, muscle aches, URI & LRI symptoms Reportable disease Birds are often subclinical

o Yellow-green diarrhea, conjunctivitis, nasal discharge, respiratory difficulty o Bacteria can persist in dander/heating/air ducts

Responds to antibiotics Avian and swine influenza

Normally not infective to humans Mutations/variations can occur that can lead to efficient transmission and binding to human cell receptors Wear PPE when dealing with avian and swine that are suffering from respiratory disease

Brucellosis Brucella abortus, B. melitensis, B. suis, B. canis Ruminants, horses, swine, dogs Human Reportable disease

Animal-to-animal or –to-human transmission Ingestion of materials contaminated with infected birth fluids. Coitus (pigs & dogs) HUMAN: Farmers moving placentas, etc. OR… Inoculation with the Strain 19 vaccine…OR…Consumption of

infected milk, or cleaning or eating infected feral swine Animals

Abortion Orchitis, Infertility

Cat scratch fever

Bartonella henselae Cats

o Cats have bacteria, asymptomatic

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o Fleas ingest, shed in flea feces Human

o Flea feces contaminate human wound o Lymphadenopathy

Self-limiting disease (2-3wks) or chronic malaise that can mimic Lyme disease Humans: Infection worse in immunocompromised people

o Local skin rxn & enlarged l.n. in area of bite o 1/3 of people will have fever, headache & malaise

PREVENTION = Flea control! Problem in nursing homes if animals are not well cared for

Gastointestinal disease

Campylobacter jejuni & C. coli o Birds & mammals (Chickens, cattle, pets)

Cryptosporidium sp. o Mammals, esp. cattle

Enteric Bacteria o Salmonella, E. coli

Wash hands! Keep things out of mouth! Most self- limiting diarrhea in humans if immunocompetent Food ingestion is common means of infection; direct contact possible

Leptospirosis

Leptospirosis is a zoonotic disease with a worldwide distribution and can potentially infect all mammals. Leptospirosis is an aerobic, gram negative spirochete bacterial infection caused by members of the genus Leptospira,

which contain around 220 distinct pathogenic serovars. o Common maintenance hosts of certain pathogenic Leptospiral serovars:

Dogs – Canicola Pigs, cattle, oppossums, and skunks – Pomona Raccoons and muskrats – Grippotyphosa Cattle – Hardjo Rats – Icterohaemorrhagiae Pigs and possibly mice and horses – Bratislava

Leptospirosis is typically transmitted by direct contact with the urine or other body fluids of infected animals or indirectly through contact with water or soil that has been contaminated with infected urine/body fluids.

An array of clinical effects have been reported, ranging from mild, subclinical infection to multiple organ failure and death.

Clinical signs of leptospirosis in wildlife have not been thoroughly documented, but it is believed that most infected wildlife are asymptomatic and serve as maintenance hosts for transmission of the organism to domestic animals and humans.

Clinical signs of leptospirosis in domestic animals and humans is species dependent but generally includes alterations in liver and kidney function. Infections in these incidental hosts can be asymptomatic or may result in kidney and/or liver failure, fever, jaundice, and death

Plague Yersinia pestis Two forms Bubonic and pneumonic Bubonic

o Rodents, lagomorphs o Spread through flea bites

Pneumonic o Cats, man o Spread through aerosol

Dogs are resistant but can carry the fleas Reportable disease in US

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Tx systemic abs Clinical signs in cats

Clinical signs vary depending on what form of plague is present. Plague should be suspected in any cat exhibiting a fever in an endemic region. Cats with bubonic plague typically have fever, dehydration, lethargy, weight loss, hyperesthesia, and lymphadenopathy. The submandibular, cervical, and retropharyngeal lymph nodes are usually involved if the cat acquires infection by ingestion of infected prey. Lymph nodes will enlarge, form abscesses, and may spontaneously drain. Toxoplasmosis Domestic and wild felids are the definitive host for the protozoan Toxoplasma gondii. The oocysts of Toxoplasma are extremely environmentally resistant and human and animal infections can occur months or possibly even years after the cat has excreted the oocysts. As such, cat feces-contaminated gardens, sandboxes, and other outdoor recreational areas may serve as a source of infection for humans and animals. In toxoplasmosis, infection occurs primarily by ingestion of sporulated oocyst in cat feces- contaminated soil or water or tissue cysts in undercooked or raw meat. Upon ingestion of tissue or environmental cysts, the parasites are released, penetrate the intestinal bilayer, and replicate rapidly inside host cells. Currently, toxoplasmosis is considered the third most frequently diagnosed food borne disease in the US and approximately 60 million US citizens are infected with the parasite. Higher frequency of T. gondii seroprevalence has been disclosed in free-roaming cats compared to pet cats, with the lowest seroprevalence in cats kept indoors.

Although the risk of infection of human infection through ingestion of oocysts has been less common than infection from ingestion of undercooked or raw meat, recent research suggests otherwise. A recently developed sporozoite specific antibody has been developed which allows for serological distinction between oocyst and tissue cyst infection given that sporozoites are only present in oocysts. Of 163 individuals in acute stage of toxoplasmosis infection 103 (63%) were positive for sporozoite-specific antibody indicating that the majority of human infection was due to oocyst infection from cat-feces contaminated environments. Clinically, Toxoplasma infections appear as abortions, and birth defects, as ocular diseases, neurological impairment leading to blindness, particularly hydrocephalus, in humans. Furthermore, toxoplasmosis is also a significant risk in individuals undergoing immuosuppressive therapy including transplant recipients. Toxoplasmosis is also a major cause of systemic infection and death for immunosuppressed (e.g., HIV/AIDS) patients. An increased of risk of neuro-inflammatory diseases including schizophrenia, autism, Alzheimers, and other has been suggested with T. gondii; more research is warranted to elucidate the neurological impacts of T.

gondii. Tick-borne diseases

Tick paralysis Potentially fatal reaction to a paralyzing neuromuscular toxin secreted in the saliva of a female tick late in her feeding. Cattle, sheep, horses, dogs, and humans seem to be most effected.

Clinical signs include: headache, vomiting, general malaise, loss of motor function and reflexes, followed by paralysis that starts in the lower body and spreads to the rest of the body


Lyme borreliosis

Agent: Borrelia burgdorferi Vector: Ixodes scapularis (Eastern and Midwestern US), Ixodes pacificus (Western US) Geographical distribution: New England and mid-Atlantic states, upper Mid-west, and Pacific coast. Animal health: Major cause of canine and equine disease, including endocarditis and joint pain. Most cases occur in the




Rocky Mountain Spotted Fever

Agent: Rickettsia rickettsia Sometimes placed in “Spotted Fever” disease group Vector: Dermacentor variabilis

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Geographical distribution: Eastern US mainly. Most frequently reported tick borne disease in the eastern US. Animal health: Recent evidence has shown that untreated RMSF may lead to death of the affected animal. Clinical signs include whole body pain and are painful on palpation. May see petechial and ecchymotic hemorrhages

Rabies Although rabies is detected most frequently in various wildlife populations in the U.S., multiple recent studies have disclosed that human exposure to rabies is primarily associated with domestic cats due to people being more likely to come in contact with cats. Rabies virus is transmitted via saliva from one host to another primarily via a bite from a rabid animal. Following a bite of a rabid animal and virus inoculation, the virus replicates in neurons and disseminates via the nervous system. Later in the infection the virus can be found in highly innervated organs including cornea, skin, and salivary glands Rabies leads to various neurological impairment symptoms and the disease is invariably fatal. 92% of actual human rabies infection has been associated with bat-associated rabies virus mainly due to bat bites not being noticed by humans. Only 1% of healthy bats and 11% of sick bats are found to be rabid. Effort should be made to make houses and areas unattractive to raccoons, skunks, and other rabies hosts. Visceral larval migrans Baylisascaris procyonis is a roundworm of raccoons and birds are infected by ingesting larvated eggs in the environment. Dogs, kinkajous, ringtailed coatis can also serve as the definite host for B. procyonis and can shed eggs. The distribution of B. procyonis has been increasing recently. Larval migrans of B. procyonis can result in numerous neurological impairment clinical signs including encephalitis, circling, seizures, and death. Necropsy diagnostics include histopath examination and PCR. Limiting raccoon access to yard and making the areas unattractive to raccoons is the main way to prevent this disease.

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