Infectious Diseases Of Dairy Animals

Dairy animals are subject to numerous infections by different species of pathogenic microorganisms. All groups of microbes—bacteria, fungi, viruses, protozoa, and even algae—contain species that are pathogenic to dairy animals. The diseases caused by these organisms are tremendously costly to the dairy producer. Even if animals survive infection, the producer can suffer severe economic hardship in treatment costs, lost production of milk or calves, and disposal of infected milk or milk tainted by antibiotic residues. Quantitative data on the effects of bacterial infections on milk yield and milk composition are now available for several infectious diseases.

It is beyond the scope of this text to provide more than a general summary of the more important diseases and their causative agents. A listing of the more common bacterial diseases is provided in Table 8. For more detail, the reader is referred to veterinary texts, particularly the recent two-volume treatise of Coetzer et al. (1994).

A. Mastitis

Mastitis is an inflammation of the mammary gland that can affect virtually any mammalian species, but it is especially important in dairy animals because of their large udder sizes, high milk production rates, and extensive handling of teats. Mastitis remains the most costly disease of the dairy animal (DeGraves and Fetrow, 1993). Economic losses are well over $2 billion annually in the United States alone. Most of the economic losses associated with the disease result from the decrease in milk output and in the discard of milk from infected animals. When the costs associated with additional labor, veterinary fees, and therapeutic agents are added, the total represents 10-11% of the productive capacity of the dairy cattle industry.

Mastitis is classified as clinical or subclinical based on its severity, cause, and the characteristics of the exudate fluid; additional subclassifications can also be made (dePreez and Giesecke, 1994). Clinical mastitis is accompanied by macroscopic signs of disease in the animal (e.g., fever, swelling of the udders) and

Table 8 Major Bacterial Diseases of Cattle

Disease

Causative agent

Anthrax

Bacillus anthracis

Botulism

Clostridium botulinum

Bovine tuberculosis

Mycobacterium bovis

Brucellosis

Brucella abortus

Clostridial enterotoxemia

Clostridium perfringens types B, C, and D

Fusobacterium infections

Fusobacterium necrophorum

Gas gangrene

Clostridium chauvoei, C. novyi, C. septicum

Genital campylobacteriosis

Camplyobacter sp.

Haemophilus somnus complex

Haemophilus somnus

Leptospirosis

Leptospira pomona

Listeriosis

Listeria monocytogenes

Mastitis

Many agents (See Table 9)

Paratuberculosis

Mycobacterium paratuberculosis

Salmonellosis

Salmonella serovars

Tetanus

Clostridium tetani

in the milk. Clinical mastitis appears to cause similar reductions in yield in high-and low-yielding herds (Firat, 1993).

Subclinical mastitis can only be detected by laboratory methods, and is most commonly revealed by routine microscopic counts of somatic cells (>4 X 105 cells/mL, usually leukocytes) in the milk (Auldist and Hubble, 1998). If mastitis is caused by infection, the causative agent can be observed and often identified at the same time. Even subclinical mastitis is usually associated with a decrease in milk volume. In a recent review of the literature, Hortet and Seegers (1998) have calculated that each doubling of somatic cell count above 5 X 104 cells/mL reduces milk yield by 0.4 kg/day in primiparous cows and 0.6 kg/day in multiparous cows.

Mastitis may have any of several causes, chief among which are bacterial infections. Although the udder is constantly exposed to potential pathogens, development of mastitis requires both that the agent be sufficiently numerous and virulent and that the host be susceptible to infection. Susceptibility is a complex function of the animal and management practices, including milking technique. From an epidemiological standpoint, mastitis is regarded as contagious if it is transmitted from infected animals (i.e., almost exclusively by the milking process) or environmental if the pathogen's reservoir and the source of infection is the animal's environment. Numerous species of bacteria have been implicated in causing mastitis (Table 9), but the importance of individual species has changed with changes in dairy practice (Fox and Gay, 1993). Streptococcus aga-

Table 9 Causative Agents of Bovine Mastitis

Common agents:

Staphylococcus aureus

Streptococcus spp. (especially S. agalactiae, S. dysgalactiae, S. uberis) Coliform bacteria (especially Escherichia coli, Citrobacter freundii, Enterobacter spp., and Klebsiella spp.) Actinomyces pyogenes Less common agents: Listeria monocytogenes Pseudomonas aeruginosa Mycoplasma bovis

Corynebacterium bovis and C. diphtheriae

Nocardia spp. (especially N. asteroides)

Coagulase-negative Staphylococcus spp. (many species)

Bacillus cereus

Brucella abortus

Clostridium perfringens

Coxiella burnetii

Leptospira spp.

Mycobacterium bovis

Serratia marcesens

Prototheca zopfii (alga)

Source: duPreez and Giesecke, 1994.

lactiae was once the most common causative agent, but it has been displaced over the past few decades by Staphylococcus aureus. Several genera of the family Mollicutes (bacteria having very simple genomes and lacking a cell wall), including Mycoplasma spp., appear to have a growing involvement as causative agents of mastitis, as does Listeria monocytogenes.

Mastitic infection can occur via the blood or by trauma to the udder, but it far more commonly occurs via the streak canal of the teat. Although the arrangement of cells and folding of tissues within the teat provide considerable defense against invading pathogens, this defense weakens in cows with age or under conditions of high production. Infection, regardless of route, results in a suite of host responses. Among these are phagocytosis by polymorphonuclear neutrophils (Craven and Williams, 1985), production of antibodies which resist bacterial adherence to epithelial cells, and neutralization of toxins.

Infectious mastitis results in changes, which are often dramatic, in milk composition (du Preez and Giesecke, 1994; Hortet and Seegers, 1998). Fat content is reduced to below 3%, chloride is increased 1.5-fold, and lactose decreases substantially (often by 5-fold or more), because the pathogen uses this substrate for growth. Total protein content may show only slight changes, but the amount of casein may be reduced at the expense of protein from antibodies, somatic cells, and bacterial cells. In addition to its nutritional inferiority, mastitic milk is visually and organoleptically unappealing because of the presence of microbial polymers, the release of free fatty acids (as a result of lipase activity), and a reduced lactose and increased chloride content.

S. aureus, now the most common agent of clinical mastitis, is a grampositive nonmotile coccus that grows in characteristic aggregates resembling bunches of grapes. The virulence of S. aureus appears to result from a variety of characteristics, including production of extracellular polysaccharide (EPS) capsule, ability to involute into the epithelial cells, production of exotoxins (e.g., leukocidin and coagulase), and causation of tissue necrosis. Chronic mastitic infections are often characterized by bacterial growth in the form of adherent colonies embedded within a large EPS matrix (Brown et al., 1988). Most S. aureus isolates that have been recovered from mastitic milk show a characteristic ''diffuse colony morphology'' resulting from the constitutive or inducible production of the EPS capsule (Baselga et al., 1994). The specific EPS is normally determined by direct serotyping of capsular antigens. Although the EPS is apparently involved in adhesion of bacterial cells to ducts and alveoli in the mammary gland, it is not yet clear if the EPS is involved in the initial adhesion event or more firmly attaches the bacteria in place following initial adhesion of the cells to the mammary tissue. Regardless, these matrices provide the bacteria with resistance to antibiotic treatment (because of inaccessibility) and phagocytosis (because of the substantial size of the cellular complex).

Much has been written regarding the potential increase in mastitis that may arise from treatment of cows with bovine somatotropin (BST). Although BST treatments undoubtedly increase the prevalence of mastitis, there is considerable evidence (reviewed by Burton et al., 1994) that this effect is not the result of a reduced immunological capacity to resist infection, but instead is caused by extra stress placed on udders from increased milk volume. Thus, the enhanced levels of mastitis are similar to those observed in cows geared to high production by any of a number of feeding and management strategies regardless of exogenous BST supplementation.

B. Tuberculosis

Tuberculosis is a contagious, chronic disease resulting from infection by species of the genus Mycobacterium. Tuberculosis has been one of the most pervasive and destructive diseases of both humans and animals throughout all of recorded history, and Robert Koch's isolation in 1882 of M. tuberculosis (the main causative agent in humans) is one the greatest achievements of clinical microbiology.

Bovine tuberculosis is caused by M. bovis, an organism with an unusually wide host range that includes not only cattle but humans and other primates along with many domestic animals (e.g., dogs, cats, pigs, and goats) (O'Reilly and Daborn, 1995). Reservoirs of tuberculosis are also maintained in many wild animals, including bison (Bison bison) and elk (Cervus elaphus) in North America; badgers (Meles meles) in England; and opposum (Trichosurus velpecula) in New Zealand. These wild species represent a potential source of infection of domesticated ruminant animals, or they more commonly provide sufficient exposure to elicit positive tuberculin tests that complicate the undertaking of prophylactic measures to control the disease. In most nonbovine species, the infection is not self-maintaining; even in sheep and goats, the disease is rare.

M. bovis infections of humans through the drinking of milk from infected dairy cows was a serious public health problem early in the 20th century, and this spearheaded the impetus for compulsory disinfection of the U.S. public milk supply by pasteurization (Myers and Steele, 1969). These and other advances in sanitation, along with aggressive culling of infected animals, has largely controlled bovine tuberculosis in many parts of the world, but it remains an impending threat to dairy producers.

Bovine tuberculosis is normally spread among herds as a result of the introduction of infected cattle into noninfected herds. Infections are generally spread among animals by inhalation of aerosol microdroplets (2-5 |m diameter; small enough to reach the lung alveoli) released by infected animals when sneezing and coughing; however, transmission is also thought to be possible via feces and various body fluids that may contain the bacilli. The spread of the disease within a herd is largely governed by the susceptibility of its cows, which in turn depends on management conditions (e.g., stock density, the overall health of the herd, and control measures adopted by the producer) and by the relative number of young stock. Control measures are complicated by the generally chronic, subclin-ical nature of the disease. In most cases, the lesions are small in size and number and clinical signs are often not readily apparent. In clinical forms of the disease, the lymph nodes are the most common target, with the lungs being less often affected. Other organs are affected only rarely, and usually as a result of spread through the bloodstream; included among these are infections of the udder (discussed earlier as a form of mastitis). The pathogenesis of the disease has been recently reviewed by Neill et al. (1994).

As a genus, the mycobacteria are straight or slightly curved rods that lack motility and the ability to form endospores. Because of their high content of lipids, the cells do not stain readily by the Gram staining method, although electron microscopy reveals that the cell walls are clearly gram-positive. The lipids are responsible for the characteristic property of acid fastness (i.e., resistance to decolorization by an acid-alcohol mixture following initial staining by heated carbol fuchsin), a characteristic sufficiently rare among bacteria as to constitute

Table 10 Phenotypic Characteristics Differentiating Mycobacterium bovis from M. tuberculosis

Characteristic

M. bovis

M. tuberculosis

Primary host

Cattle

Human

Colony morphology

Moist, smooth, flat

Dry, wrinkled

Colony development

> 3 weeks

10-14 days

Nitrate reduction

Negative

Positive

Niacin production

Negative

Positive

Glycerol

Inhibits growth

Stimulates growth

Pyrazinamide

Resistant

Sensitive

Thiophene-2-carboxylic acid hydrazide

Sensitive

Resistant

strong preliminary evidence for a mycobacterial infection. The lipids are also responsible for the considerable resistance of the mycobacteria toward chemical agents, and this property is used to advantage in the isolation of mycobacteria from clinical samples. Tissues are ground in a saline solution and pretreated for 30 min or less with 1 M of NaOH or 2% HCl before neutralization, centrifugation (to concentrate the cells), and plating onto solid media.

The mycobacteria are notoriously slow growers in culture media, including the preferred rich diagnostic media such as Lowenstein-Jensen, Ogawa, Dubos, or Middlebrook 7H10 medium. Even in these media, growth is often not detected before 3 or 4 weeks of incubation at 37°C. Clinical and veterinary microbiologists should recognize that, in addition to host specificity, M. bovis and M. tuberculosis display several physiological differences (Table 10). The difficulty of culturing these organisms has led to attempts to develop alternate diagnostic tests, and evidence suggests that enzyme-linked immunosorbent assays (ELISAs), when used in combination with standard tuberculin tests, improve the diagnosis of infection (Gaborick et al., 1996).

Elimination of tuberculosis in infected herds is usually accomplished by either immediate slaughter of infected animals or by gradual isolation of infected animals until all of the remaining cattle are free of tuberculosis.

C. Paratuberculosis

Paratuberculosis (Johne's disease) is a chronic and infectious disease of the intestinal tract caused by Mycobacterium paratuberculosis (Huchzermeyer et al., 1994). The disease affects both domestic and wild ruminants, and it causes a severe diarrhea and debilitating weight loss. Infection normally occurs either con-genitally or via ingestion by young animals of feces from infected animals. Older animals may largely resist infection, because mycobacteria do not survive well in the fully developed rumen. In infected animals, the incubation period varies enormously, but clinical signs of the disease apparently require multiple exposures and are not normally manifested for 3-5 years. Even in totally infected herds, however, only a small percentage of the animals may display clinical signs, whereas the remaining, subclinically infected animals may or may not be actively shedding the agent in their feces. Subclinical infections result in approximately a 4% reduction in milk yields without significant changes in fat or protein content (Nordlund et al., 1996).

As a result of the low percentage of clinical cases in infected herds, the mortality rate within the herd is fairly low (Blood et al., 1989). The long incubation period and subclinical nature of the disease makes antibiotic therapy difficult and fairly ineffective in clinical cases. Vaccination is effective only in conjunction with a strong emphasis on animal hygiene, and must be used only in tuberculosis-free herds, because the vaccine interferes with serological or allergic tests. In humans, M. paratuberculosis is thought to cause Crohn's disease.

  1. paratuberculosis is a short, thin, gram-positive, acid-fast rod connected by intercellular filaments that give the organism an aggregated appearance under microscopic observation. Like the mycobacterial agents of bovine tuberculosis, M. paratuberculosis grows extremely slowly, even in the preferred Herrold's egg yolk medium, and requires exogenous mycobactin (a class of lipid-soluble cell wall components) for growth. Because of this slow growth, successful isolation of the bacterium requires that feces or intestinal tissue be macerated and exposed briefly to chemical agents (e.g., NaOH or various disinfectants) to eliminate other bacterial contaminants.
  2. Brucella Infections

Bacteria of the genus Brucella include several infectious disease agents, including Brucella abortus, which causes bovine brucellosis (contagious abortion) in cattle, bison, and other bovines; B. ovis, which causes epididimitis and orchitis in sheep; and B. melitensis, which causes abortion and orchitis in sheep and goats. B. abortus can also be transmitted to humans, in whom it causes undulant fever; this debilitating and often misdiagnosed disease (Latter, 1984) most often afflicts workers having extensive contact with cattle, but it has been reported in some cases to result from contamination of unpasteurized dairy products from infected animals (Bishop et al., 1994).

Members of the genus Brucella are gram-negative, nonmotile, nonsporulat-ing cells having a coccus or coccobacillus morphology. They are fairly fastidious in their growth requirements; most require for growth complex media containing serum and an atmosphere enriched to 5-10% carbon dioxide. One distinguishing feature of B. abortus is its use of erythritol, a four-carbon sugar alcohol, as an energy source. This substrate is abundant in the uterus of pregnant cows, stimulating the localization of the organism at that site.

Because the disease is often subclinical in nature, an extensive battery of tests is often employed to detect Brucella infections (Bishop et al., 1994). These include direct culture of the agent, detection of specific antibodies, and detection of allergic responses to the agent. Various inocula are used for direct culture, particularly uterine discharge, colostrum, or milk (from live animals); supramam-mary lymph nodes (from slaughtered animals); and lung, stomach, and liver (from aborted fetuses and full-term calves). The simplest test is the milk ring test in which killed Brucella cells are added to a fresh milk sample. If the milk is infected, a bluish ring will form around the cream line as the cream rises. Other tests involve the reaction of serum antibodies with antigens stained with Rose Bengal, the reaction of milkfat antibodies with stained B. abortus cells, or the complement fixation test, which is regarded as the most definitive of the antibody tests (Huber and Nicoletti, 1986). Recent application of the polymerase chain reaction to amplify species-specific repetitive DNA sequences shows promise for identifying infected animals and tracing outbreaks (Tcherneva et al., 1996).

Removal of infected stock is used to control outbreaks, but this strategy is complicated by the latency of the disease (Ter Huurne et al., 1993). Vaccination with avirulent strains of B. abortus is somewhat effective in controlling infection, particularly in heifers (Nicroletti, 1984; Al-Khalaf et al., 1992). Such vaccination enhances resistance to the disease but does not provide absolute immunity.

E. Enteropathogenic Escherichia coli

Several serotypes of E. coli, particularly O157:H7, cause severe intestinal illnesses in humans that can include bloody diarrhea and hemolytic uremic syndrome, and they are responsible for an estimated 400,000 infections and 250 deaths annually in the United States (Armstrong et al., 1996). E. coli O157:H7 has an unusually low infectious dose (as few as 10 cells), and it owes its potent virulence to a combination of its ability to invade gut mucosa, an outer membrane containing a lipid A endotoxin, and its production of a Shiga-like protein exotoxin (Bettleheim, 1996). E. coli infections usually result from consuming contaminated, inadequately prepared foods (e.g., undercooked meat, fruit juices, and vegetables).

Cattle are considered a major reservoir of E. coli O157:H7 (Bettleheim, 1996). The bacteria proliferate primarily in the hindgut and are shed in the feces where they may remain viable for months (Wang et al., 1996). Because of this, numerous quantitative studies have examined the prevalence of E. coli O157:H7 in cattle herds. Early work suggested that E. coli O157:H7 was fairly uncommon in dairy cows. A survey of 1131 dairy cattle and 659 calves in Ontario, Canada, for Shiga-like toxin-producing strains of E. coli (Wilson et al., 1992) revealed that ~10% of all cows and 25% of all calves were infected; in some herds, the infection rates were 60 and 100%, respectively. However, few of the 206 verotoxin-producing strains were serovars that had been isolated from humans, and none were serovar O157:H7. In contrast, although 5 of 60 dairy herds in Washington state had cows with fecal O157:H7 present, overall prevalence (only 10 of 3570 cows) was low (Hancock et al., 1994). More recent work, using more sensitive methods based on immunomagnetic beads (Chapman et al., 1994), reveals that O157:H7 is much more prevalent than previously suspected and may exceed 30% in dairy herds (Chapman et al., 1997; Mechie et al., 1997). Differences in O157:H7 strains both among and within herds have been noted at the genetic level using restriction endonuclease digestion profiles (Faith et al., 1996).

Because E. coli O157:H7 can successfully colonize human gut epithelia only if the bacteria can survive transit through the acidic gastric stomach, and because acid resistance is inducible, the preinfection environment may have a major role in the pathogenicity of E. coli O157:H7. There is strong evidence that diets high in concentrates, which promote low pH and high concentrations of volatile fatty acids in the bovine colon, result in fecal shedding of strain O157: H7 and other acid-resistant strains in their most virulent (i.e., acid-resistant) state (reviewed by Russell et al., 2000). Diez-Gonzalez et al. (1997) observed that feces from grain-fed animals contained higher densities of acid-resistant E. coli, and that these numbers decreased on a switch to a hay diet. Moreover, a recent study with beef cattle that naturally shed strain O157:H7 indicates that dietary management (particularly reducing the amount of grain feeding) can greatly reduce the prevalence of O157:H7 shedding (Keen et al., 1999).

F. Viral Diseases

Most of the major classes of viruses contain strains that are pathogenic to dairy animals (Table 11). The bovine leukemia virus is the most serious in the United States, where 10-30% of dairy herds may be infected. In tropical countries, rinderpest and hoof-and-mouth disease are probably the most serious viral infections of cattle. Unlike many bacterial infections of ruminant animals that can also be transmitted to humans, most viruses that infect ruminant animals have narrower host specificities and do not normally infect humans. Exceptions include the following: some of the Orthomyxoviridiae (influenza viruses) and Flaviviridae, which cause mild influenza-like diseases, and the parainfluenza type 3 virus, which causes a pneumonia-like condition. The more serious exceptions include the Bunyarviridae, causative agents of Rift Valley fever and Crimean-Congo hemorrhagic fever. The former is, in humans, a mild influenza with various and occasionally fatal complications, whereas the latter is a serious disease with a mortality rate in humans of approximately 30% (Swanepol, 1994).

Microbiology of the Dairy Animal Table 11 Viral Agents of Disease in Cattle

Viral family

Disease

Adenoviridae

Adenovirus infectiona

Bunyaviridae

Crimean-Congo hemorrhagic fever

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