First Quarter 2019 (Volume 1)  
Quarterly Update – Arkansas State Veterinarian’s Office – First Edition
My name is Randolph Chick (prefer “Randy”) and I have been privileged with the opportunity to serve the Arkansas veterinary profession and animal industry as the State Veterinarian, starting in October 2018. A resident of Washington County (when not in Little Rock), I have been involved in several aspects of the veterinary profession during my thirty-five year career. I graduated from both the University of Arkansas (Fayetteville) and the LSU School of Veterinary Medicine.

This missive is the first edition of an e-newsletter I hope will prove to be a welcome item in your Inbox. My proposal is to send some form of this communication to all Arkansas licensed veterinarians on a quarterly basis. I welcome any comments, suggestions or criticisms that would improve the content and valued reception of this effort. Please send any remarks to me at [email protected]                                                    
Some selected diseases to be highlighted in this edition :
 
Johne's Disease – Cattle and other species 
Johne's disease is a chronic enteritis of ruminants caused by Mycobacterium paratuberculosis . This bacteria embeds itself in the wall of the lower part of the small intestine known as the ileum. As an immune response, infected tissues attempt to regenerate healthy tissue which leads to visible thickening of the intestines. This prevents nutrient absorption, resulting in weight loss. Late in the infection, antibody production by the animal can be found in serum of animals and is an indicator that clinical signs of disease and death from the infection will soon follow.

M. paratuberculosis grows and multiplies inside the cells of an animal's immune system and are excreted in the feces, and to a lesser extent in milk and saliva. When the microbe is excreted, it can contaminate the soil or water. Outside the host animal, the organism multiplies poorly—if at all—but it can survive over a year in the environment because of its resistance to heat, cold, and drying.

The primary cause of the spread of Johne‘s disease is contact with the feces or saliva of an infected animal. Prenatal exposure may be a source of infection for calves. Becoming infected before birth is possible for a fetus if its mother is in the late stages of Johne’s disease. Another source of infection is milk from infected dams.

There are huge concerns in many beef and dairy herds across the world about the prevalence of Johne's disease. Because of the slow, progressive nature of the infection, signs of Johne’s disease may not show up until years after initial infection. When they finally do occur, the signs are long-lasting diarrhea and weight loss despite good appetite. Bottle jaw may also appear, which is fluid accumulation in the bottom jaw causing an abscess. Once clinical signs appear the animal will not recover and will continue to deteriorate. There is no treatment for Johne's disease.

Prevention is the most cost-effective way to manage Johne's disease. It is far less expensive to block introducing Johne's disease into a herd/flock than it is to control or eradicate the infection once it creeps in and invisibly starts to spread. Testing ill looking animals can confirm whether Johne's disease is present. If it is it may be more economical to cull infected animals, if not, the animal must be managed to ensure no young animals are exposed to their milk or manure.

Newborn animals must be protected from infection by being born and raised in a clean environment and fed milk and water free of M. paratuberculosis contamination. The primary source of contamination is manure from an infected adult animal. Producers are advised to purchase animals from a source herd free of Johne’s disease. Second best is to work with a producer who knows the level of Johne’s disease in his or her herd, follows good infection control practices, and then purchase test-negative animals from test-negative dams (fecal PCR).

Johne’s disease is a herd problem; knowing the test-status of numerous adults in the source herd will give you a much better sense of the risk of purchasing an infected animal than one test result you might get on the one animal you wish to buy. The efficacy of vaccines is controversial. Studies in The Netherlands have shown that herd owners who follow the recommended management changes to control Johne's disease will be as successful, if not more successful than those who use the vaccine.
Transmissible Gastro Enteritis (TGE) – Swine
TGE is a very important and highly infectious disease caused by a coronavirus. The virus is killed by sunlight within a few hours but will survive for long periods outside the pig in cold conditions. It is very susceptible to disinfectants particularly iodine-based, quaternary ammonia and peroxygen compounds.

Disease will persist in the farrowing houses over a period of 3 to 4 weeks until sows have developed sufficient immunity to protect the piglets . In herds of less than 300 sows the virus is usually self-eliminating provided there are good all-in, all-out procedures in farrowing houses and grower accommodation. In larger herds however the virus will persist in the growing herd because piglets at weaning, still under the influence of the maternal antibody, move into houses where the virus still persists. Once the lactogenic immunity in the sow's milk is no longer being taken, the pigs become infected, allowing the virus to multiply. The pigs then shed the virus, contaminating the weaner rooms and infecting pigs being weaned after them. TGE can become endemic in herds in a mild form with high morbidity but low mortality. This disease in the weaning and the growing pig is clinically indistinguishable from porcine epidemic diarrhea. In small grower-finisher units the virus is likely to disappear from the population. In large finishing units in which susceptible pigs are being brought in frequently, the virus is maintained indefinitely in the population by repeated infection of the newcomers.

Weaners & Growers- when the virus is introduced into a finishing herd for the first time there is rapidly spreading, vomiting and a watery diarrhea, eventually affecting almost all the animals. Disease disappears spontaneously over a three to five week period. Mortality is usually low. The main effect on the individual growing pig is dehydration which is resolved in about a week. Nevertheless the disease may increase the slaughter age by 5-10 days. Piglets- in the sucking piglet the disease is very severe; almost 100% mortality within 2 to 3 days in piglets under 7 days of age due to severe dehydration and electrolyte imbalance. There is no response to antibiotic therapy. The most striking feature is the wet and dirty hairy appearance of all the litter due to the profuse diarrhea. Sows - in acute outbreaks the most striking feature is the rapidity of spread of vomiting and diarrhea. Adult animals show varying degrees of feed intake and usually recover over a 5 to 7 day period. Causes / Contributing factors: the virus is shed in large numbers in the feces. Pig feces therefore are the major source of transmission either directly through the purchased carrier pig or indirectly through mechanical transmission. Poor pen hygiene associated with bad drainage. Poor hygiene procedures between pens; environmental contamination from one pen to another i.e. boots, brushes, shovels clothing etc. Feeder pipes and feed bins; this is a high risk source for the spread of enteric diseases. Dogs may shed the virus in their feces for 2 to 3 weeks. Birds and in particular starlings may transmit the disease. Contamination of feed. Continual use of buildings without all-in, all-out “breaks” may perpetuate disease. Continual purchase of naive weaners. Diagnosis: the clinical picture in acute disease is almost diagnostic. There are no other enteric diseases that spread so rapidly across all pigs. The ultimate diagnosis of TGE must be made in the laboratory from the intestine of a fresh dead pig using fluorescent antibody tests (FAT's). Isolation of the virus is also carried out. Porcine epidemic diarrhoea (PED) could give a similar picture but it would be less acute and with less mortality in sucking pigs. Diagnostics: clinical signs of PED closely resemble a Transmissible Gastro Enteritis (TGE) and Swine delta corona virus (SDCoV) outbreaks. While PED and TGE are caused by similar coronaviruses, cross immunity is not provided with infection of either virus. All three coronaviruses cause similar clinical symptoms early in the disease, making it impossible to identify without testing which specific virus is at the root of the infection on the farm. Laboratory testing is needed to identify the pathogen. Diagnostic tools used include PCR, ELISA, immunohistochemistry (IHC) and histopathology. Biosecurity is key in controlling swine coronaviruses as they spread indirectly through air, dust, feed, transport and people. Environmental testing with molecular tools helps audit the success of biosecurity measures, such as disinfecting transport trailers and barn facilities, and it enables producers to quickly get information about the actual situation on the farm. A PCR test is available for environmental and feed samples to simultaneous screen for all three swine coronaviruses: Porcine epidemic diarrhea virus (PEDV), Transmissible gastroenteritis virus (TGEV), Swine delta corona virus (SDCoV).
Scrapie – Goats & Sheep
Scrapie is a fatal, degenerative disease affecting the central nervous system of sheep and goats. It is among a number of diseases classified as transmissible spongiform encephalopathies (TSE). Infected flocks can experience significant production losses. Scrapie is the oldest known TSE, and under natural conditions only sheep and goats are known to be affected by scrapie. Once infected, the animal remains infected for life. Transmission of the classical scrapie agent is not completely understood, and apparently healthy sheep infected with the agent can transmit disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected.

Clinical signs of classical scrapie typically appear between two to five years after infection; therefore, infected animals rarely show clinical signs of infection before the age of 2 years, with the average age of clinical onset being 3-4 years. The prolonged incubation period, the subclinical nature of the infection during its early stages, and the fact that the only diagnostic tests currently available require brain or lymphoid tissue make detection of scrapie difficult. Sheep typically live one to six months after the onset of clinical signs, but some will die earlier or later. Duration of clinical signs may depend on the observational abilities of the producer. Some sheep may simply be found dead. Due to damage to the nervous system, affected animals often show behavior changes, such as nervousness or aggression, intense rubbing, and locomotor incoordination that progresses to recumbency and death. Other clinical signs may include tremors (especially of head and neck), head pressing or “star gazing,” significant weight loss with no decrease in appetite, wool pulling, and hyperesthesia. Additional signs in affected goats may include difficulty milking, premature kidding, and pica (eating or licking substances not normally eaten). Over a period of several years the number of infected animals increases while the age at onset of clinical signs decreases, making these flocks economically unviable. Animals sold from infected flocks spread scrapie to other flocks. Once an infected animal is detected, eradication of the disease from the flock or herd may consist of either selective depopulation of certain higher-risk exposed animals (e.g., only those that are genetically susceptible, heavily exposed, test positive or inconclusive, and/or showing clinical signs) or, less commonly, complete flock depopulation, as well as cleaning and disinfection of the premises. Approximately 30 percent of US sheep are genetically susceptible to scrapie. Susceptibility varies between flocks based on breed and whether genetic selection for resistance has been used. Owners of infected flocks are encouraged to restock with rams that are resistant (RR) and ewes of resistant or less susceptible genotypes (RR or QR). Researchers are still investigating the possibility of genetic resistance in goats, but have not yet identified a resistant genotype. Therefore, currently all goats are considered genetically susceptible.
Respiratory complex – Poultry
Respiratory infections in chicken and turkeys are seen worldwide but especially in temperate poultry-producing areas in winter months. A number of respiratory viruses (Infectious Bronchitis, Avian pneumovirus, Lentogenic Newcastle disease virus, among others - vaccine and field strains) and bacteria ( Ornithobacterium rhinotracheale , E. coli, etc. ) may be involved. Dust, ammonia and other gases, and other factors associated with poor ventilation, may act as predisposing factors. Morbidity is typically 10-20%, mortality 5- 10%. If condemned birds (at processing) are included mortality may be more than 10%.

Signs ; “snicking ” sound, head swelling, sneezing, conjunctivitis, nasal exudate, rattling noises on inspiration. Overall general malaise.

Post-mortem lesions - severe tracheitis with variable exudate (catarrhal to purulent), airsacculitis, p ericarditis.

Diagnosis - l esions, serology, response to environmental changes.
Differential includes many of concern, including Chronic Respiratory Disease (Mycoplasmosis – a Reportable Disease).

Given that many flocks are vaccinated it is necessary to establish normal serological response in vaccinated flocks in the absence of disease (some of which may, of course, be challenged by some of these pathogens). Treatment may include antimicrobial treatment of identified bacterial infections (VFD rules apply for all farm animal species, regardless of husbandry).

Prevention - effective ventilation (reduce ammonia), sanitation of drinking water and appropriately administered viral vaccines.
Exotic or Virulent Newcastle Disease  (END or VND) is a highly contagious viral disease impacting all birds; chickens are the most susceptible to the disease. There are few areas of the world that have not been affected by this disease. There are three very different forms of Newcastle Disease: mild (lentogenic), moderate (mesogenic) and virulent (velogenic or END or VND). Mild and moderate forms of Newcastle Disease may not cause birds to become sick, or can be controlled with different vaccination strategies. However, if combined with other disease agents or poor environmental conditions, it can become a significant disease problem. “Exotic” Newcastle Disease (or VND) is the very virulent form, which is a great concern to poultry producers because of the potential to cause illness and death, sometimes without any warning. It can also lead to possible trade restrictions. Strains of this virus are endemic in Asia, Africa and some North and South American countries. The U.S. and Canada have import restrictions, testing, and depopulation standards to reduce the risk of those strains. There have been cases of the disease in Arizona, California, Nevada and Texas; each incident was eradicated. When healthy birds come in direct contact with infected birds or their bodily fluids (feces or respiratory), the disease can move rapidly and infect entire flocks. Some wild birds, like cormorants, are highly susceptible and are known to carry and may spread the disease to domestic poultry if preventative measures are not in place. Respiratory issues, nervousness, tremors or paralysis, drops in egg production are signs; often only depression is noticed.

How is it diagnosed ?  Tracheal or cloacal swab samples or other tissues need to be collected from the birds and submitted to a certified laboratory for testing to identify and isolate the virus. It is zoonotic and people may become infected with Exotic Newcastle Disease; can cause conjunctivitis in humans , often in people who work closely with poultry and END is considered a mild risk to human health. Poultry products like meat and eggs are still safe to eat, and should always be cooked to safe temperatures.
Avian Influenza (AI) is a virus disease of poultry; can be of low pathogenicity (LPAI - causing mild disease), or of high pathogenicity (HPAI) causing severe disease and mortality. There are different strains of AI viruses: examples are H1N1 or H5N2. Some AI viruses can mutate and become HPAI viruses. Clinical signs; LPAI in chickens and turkeys resembles any other mild respiratory disease. In breeders, it can also cause a production drop, and birds may produce soft shelled eggs. With HPAI, the birds may become very quiet, not eat or drink, have diarrhea, and discolored combs and feet. Birds often die suddenly without any signs of disease. Natural carriers are wild birds, especially waterfowl (ducks and geese). Swine are sometimes infected with influenza viruses that may adapt to infect different mammals and birds, including humans. AI in poultry in our state is continuously monitored; broiler flocks are tested before processing and breeders and layers are tested several times during their production cycle. Occasionally, hobby and small production flocks are checked for the virus. An AI outbreak in commercial poultry could have disastrous consequences; steps would be taken for a rapid eradication of the virus from the area affected.

How can it be prevented?  Biosecurity is an excellent deterrent to nearly all diseases. Pestilence can travel in infected manure, on boots, via wild birds and other animals, etc. Sanitary measures and protective barriers/structures are important to prevent exposure. Surveillance and quick identification of sick animals reduces the risk of disease spread. 
Reportable Diseases of Domestic Animals (Arkansas and USDA)
It is the responsibility of the attending veterinarian (9 CFR 161.4(f), licensed and accredited in Arkansas) to forward information on Reportable Disease to the State Veterinarian’s office or the USDA-APHIS-VS office in Arkansas.
This requirement applies to all animals or diagnostic samples sent to Arkansas veterinary labs and especially any out-of-state diagnostic laboratories .

DO NOT depend on the diagnostic laboratory to perform this task!!!!­­­  

Arkansas State Veterinarian, AAD-ALPC (501) 823-1733
USDA APHIS-VS, AVIC (501) 725-7784

Please review the entire list of Reportable Diseases for Arkansas : https://www.aad.arkansas.gov/Websites/aad/files/Content/5937242/Reportable_Diseases_.pdf   

Entry Requirements/ CVI / Permit Issuance         

Entry Requirements
(origination of travel from any premise outside Arkansas borders into the state):

Certificates of Veterinary Inspection (CVI) – Arkansas accepts paper and most electronic forms of CVIs. Please consider adopting the use of electronic CVI if you do not use currently.

For Entry Permit Number assignments, please call (501) 225-1598 on Monday through Friday from 8:00 to 4:30 PM


Upcoming Arkansas Veterinary Continuing Education Opportunities (In State)
Food Animal Medicine Workshops – UA Cooperative Extension / ArVMA – varied locations https://www.uaex.edu/media-resources/news/september2018/09-21-2018-Ark-food-animal-vet-training.aspx  
            
Arkansas Veterinary Medical Association – Winter Meeting – Hot Springs, Arkansas – VERY SOON

Nearby Arkansas (selected webinars and conferences)

Mississippi VMA CE Webinars:

Missouri VMA CE Webinars: https://www.movma.org/page/introwebinars




Please forward any information you may run across concerning upcoming CE opportunities, especially webinars or conferences in surrounding states.