Botulism is caused by ingestion of preformed toxin produced by Clostridium botulinum. In mink, it is most often caused by ingestion of type C toxin.
Botulism may result in sporadic and heavy losses in unvaccinated mink that consume contaminated feed that has been improperly handled or stored. Vaccinated mink also may develop clinical signs of illness, although mortality is generally lower and animals may recover. Depending on the exposure level, some mink may die within a few hours to 24 hours following exposure to the toxin, whereas other mink may show varying extents of photophobia, hind end paresis, paralysis, recumbency, and dyspnea. Postmortem examination findings are usually nonspecific; death occurs from respiratory paralysis.
Historically, diagnosis was attempted using the mouse inoculation (lethality) assay; however, this assay is not reliable for diagnosis of botulinum toxicosis in mink and is increasingly being phased out by veterinary diagnostic laboratories for ethical reasons. Alternatively, diagnosis is confirmed by isolation of type C botulinum toxin from suspect feed samples or of bacteria or spores from GI samples, followed by culture and real-time PCR assay for Clostridium botulinum type C toxin genes. Differential diagnoses include rabies or other toxicoses, such as lead poisoning, although it would be unusual for either of these to affect large numbers of animals concurrently.
Suspect feed should be removed and sampled for testing, and stored feed or ingredients should also be tested for the toxin. Mink that recover do not develop immunity. Annual vaccination of kits (at 6–8 weeks) and breeders with vaccines containing type C botulism toxoid is recommended. Additionally, in some geographic areas, slaughter by-products fed to animals are acidified to pH 4.0 or heat-treated to minimize microbial growth. Feed should be frozen at –18°C if not fed immediately after preparation.
Hemorrhagic pneumonia is a highly contagious disease of mink caused by infection with Pseudomonas aeruginosa, a ubiquitous environmental bacterium.
Mink of all ages may be affected during an outbreak, and animals are more susceptible to infection during the stress of fall molt. Mortality may be high within a herd (≥20%), and mink are usually found dead with few prodromal signs. Gross lesions may include red oronasal discharge and red froth in the tracheobronchial tree, with severe hemorrhagic pneumonia and consolidation of one or more lobes.
Response to an outbreak involves immediate vaccination of the entire herd. A P aeruginosa bacterin is recommended as part of routine herd vaccination. Thorough cleaning and disinfection of pens and nest boxes should occur after an outbreak, including sanitization of waterers and water lines.
Escherichia coli also may cause hemorrhagic pneumonia in mink, and gross and clinical signs are indistinguishable from those caused by P aeruginosa. Histologic evaluation and bacterial culture and antimicrobial susceptibility testing are used to determine a definitive diagnosis and make appropriate antimicrobial recommendations, respectively. Infection with E coli most frequently occurs after exposure to contaminated water; however, feed components also may be contaminated, hence the need for appropriate on-farm hygiene and food handling practices. Intercurrent viral infections, such as those caused by influenza virus or parvovirus (Aleutian disease), may exacerbate bacterial infections.
Urinary tract infections (cystitis), commonly referred to as plum bladder disease, can cause serious losses in adult females in the spring during pregnancy and lactation and in heavy, rapidly growing males in the late summer and early fall. Fur on the ventral abdomen of affected mink may be stained in animals that dribble urine, leading to pelt downgrading or discarding; thus, this is both an important veterinary and economic consideration of farmed mink. The normal pH range for mink urine is 6.3–7.5; high-quality diets rich in animal proteins help to maintain a low urine pH. Infection with urease-producing bacteria, such as E coli, Pseudomonas spp, and Staphylococcus spp, can increase urine pH and precipitate crystallization of struvite (magnesium ammonium phosphate) uroliths. Several predisposing factors may underlie this disorder, including poor hygiene practices resulting in contamination of feed, cages, or nest boxes by opportunistic urease-producing bacteria; decreased access to water and decreased water intake during the winter or dehydration during hot periods in the summer; feeding a suboptimal diet (eg, dry pelleted rations or large quantities of plant-based, alkaline proteins are associated with increased urolithiasis); and genetic predisposition.
Apparently healthy mink may be found dead suddenly. Other animals with cystitis may strain and vocalize when trying to urinate (dysuria), dribble urine (commonly referred to as wet belly), or develop hematuria or rectal prolapse from constant straining. Males are particularly predisposed because of their long, narrow urethra, which can make passing uroliths difficult. A large, distended bladder can often be palpated clinically. Postmortem findings include acute hemorrhagic cystitis or pyelonephritis, usually associated with struvite calculi in the urinary bladder, kidneys, or urethra.
Bacteriologic culture of urine or tissue and antimicrobial susceptibility testing should be done for optimal antimicrobial selection; medication can be added to the feed. Good sanitation and hygiene practices help to reduce environmental contamination. Animals must have access to water at all times. When urolithiasis is chronic, there is some evidence that addition of urinary acidifiers may be beneficial. For example, 0.2% feed-grade ammonium chloride may be added to the feed from March to early June and from mid-July to October to reduce urine pH. Other common feed acidifiers include phosphoric acid, sodium bisulfate, and fish silage. Feed and urine pH should be monitored to keep urine pH between 6.0 and 6.6. Chronic use of some feed acidifiers may result in loss of food palatability with associated weight loss. Feed pH should not drop below 5.1.
Foot pad necrosis, also known as fur animal epidemic necrotic pyoderma (FENP) in the EU, is a serious, infectious skin condition affecting farmed mink, foxes, and finnraccoons. In mink, lesions are seen predominantly on the feet and head, characterized by hair loss, crusting, and hyperkeratosis with superficial to deep pyoderma, with or without ulceration. The etiology is likely multifactorial; however, it has been associated with infection with one or both of Arcanobacterium phocae and Staphylococcus delphini. Infection with other opportunistic agents may also be involved. Larger, heavier males may be affected more frequently, possibly due to initial mechanical abrasion of foot pads from cage floor bottoms permitting bacterial entry. No effective treatment has been developed. Producers should cull moderately to severely affected animals and wash and disinfect the cages in which these animals were housed. The pododermatitis and perioral crusting may appear superficially similar to distemper virus infection, a rapidly progressive and fatal disease in mink. Other clinical signs seen with distemper as well as histologic evaluation of lesions may be used for differential diagnosis. Ongoing cage maintenance is important to minimize mechanical abrasions, which may permit bacterial entry.
Mastitis occurs sporadically on mink farms and may be related to infection with one of several bacteria (eg, staphylococci, streptococci or E coli). Staphylococcal mastitis typically results in abscess formation in affected glands or in subclinical disease, with mild diarrhea in the dam’s kits. Infection with E coli tends to cause peracute, necrotizing mastitis and endotoxemia similar to that seen in dairy cattle. It is unclear whether preweaning diarrhea of kits (commonly referred to as sticky kit syndrome) occurs more often in litters from dams with mastitis. Predisposing factors to mastitis include poor nest box and cage sanitation, rough or sharp edges at the entrance of nest boxes, and bacterial contamination of feed. Prevention and treatment involve improving hygiene and management practices and treating affected females with appropriate antimicrobial agents based on culture and antimicrobial susceptibility testing.
Various bacterial diseases or conditions, including septicemia, pneumonia, pleuritis, enterocolitis, metritis, cellulitis, and abscesses, occur sporadically on mink farms. These diseases are associated with infection from a wide range of largely opportunistic gram-positive and gram-negative bacteria, including Proteus spp, Klebsiella spp, and Campylobacter spp, coliforms, streptococci, staphylococci, and Salmonella enterica serovars typically associated with poultry or pigs.
Indiscriminate use of antimicrobial agents on mink farms in North America and in the EU has resulted in moderately high antimicrobial resistance on farms. A key tenet of responsible antimicrobial stewardship is that treatment for bacterial diseases should be focused, supervised by the farm veterinarian, and based on culture and antimicrobial susceptibility testing. Depending on the number of animals affected, drugs may be administered to individual animals parenterally or administered to groups of animals in their feed or water. Drug dosages can be estimated on the basis of body weight; adult female mink average 0.9–1.4 kg, whereas males average 2.3–2.8 kg. Dosages recommended for cats can be used and adjusted for weight. Some sulfonamides (eg, sulfaquinoxaline and sulfamethazine) and streptomycin should not be used routinely in mink because of potential toxicity. Trimethoprim/sulfadiazine and sulfonamides should generally be avoided in pregnant mink because use may be associated with birth defects, fetal toxicity, and abortions.
Whenever possible, the most likely source of infection should be determined and eliminated. Enteritis often is caused by contaminated or spoiled feed and dirty nest boxes. Abscesses are often related to injury from wire or splintered wood in the pens, awns in hay or straw used for bedding, or spicules of bone in the feed. Past outbreaks of tularemia, anthrax, brucellosis, tuberculosis, and clostridial infections on mink farms have been caused by providing feed contaminated with tissue of animals that died from or are carriers of these infections. Careful selection of feed ingredients and disinfection of equipment and pens are important to prevent and control many potential pathogens. Animals found dead should not be used as mink feed.