Environmental Causes of Mastitis

Streptococcus uberis and Other Streptococcus spp.

(Non-agalactiae)

Aetiology.

S. uberis is ubiquitous throughout the farm environment because of faecal, salivary, and nasal contamination by cows harbouring the organism in their rumen, vagina, external genitalia, mouth, and skin of the teats and udder. Poor cleaning and preparation of the udder before milking predispose to mastitis caused by S. uberis as with other environmental pathogens. It is the most prevalent environmental Streptococcus sp. Associated with clinical mastitis. Most infections occur early in lactation or late in the dry period, although failure to use dry cow treatment may allow earlier infection during the dry period. Injuries to the teat or chapping of the teat skin encourage colonization of the skin by S. uberis and increase the risk of infection. There is an increased incidence of infection in the winter months. It is more common in older multiparous cows than in first- or second lactation animals.

Signs and Diagnosis.

Acute mastitis with swelling, oedema, and firmness of the affected quarter are nonspecific signs observed in those with S. uberis mastitis. Fever, malaise, and varying degrees of inappetence may be associated with mastitis. The secretion tends to have clots and flecks present and is more watery than normal, but the specificity of the clinical signs mandates bacteriologic culture for differentiation of S. uberis from other environmental streptococci. Subclinical cases are more common than clinical cases, especially in late lactation, and cause high SCCs and bacteria counts in the bulk tank milk.

Treatment.

Penicillin, cloxacillin, ampicillin, and cephalosporins are effective against most S. uberis infections. Erythromycin and pirlimycin are frequently used but have lower in vitro susceptibility. Tetracycline also is reported to work very well against S. uberis but not against other environmental streptococci. Clinical cures during lactation may be more difficult than during the dry period. For example, extended-duration intramammary treatment with ceftiofur (5 or 8 days of treatment instead of the standard 2-day treatment) may confer a significant increase in bacteriologic cure rates. Some environmental streptococci (non-agalactiae) are extremely resistant to antibiotics and require antibiotic sensitivity testing to best determine specific treatments. It appears that persistence of S. uberis mastitis in the face of antibiotic treatment is more often the result of antimicrobial resistance of the original strain than a result of reinfection with new ones, reinforcing the need for initial microbiologic testing to include susceptibility patterns in the face of an outbreak. Reinfection is common when cattle have teat or teat-end lesions that allow skin colonization by these organisms. It may be helpful in severe cases to combine systemic erythromycin or penicillin administration with intramammary treatment for a period of 3 to 5 days. Herds in which S. uberis and other environmental streptococci have been identified as causes of mastitis should have the environment of the cows evaluated, and if organic bedding is heavily contaminated switching to sand may be helpful, although it may also become contaminated with environmental organisms unless properly cleaned and/or replaced. Particular attention should be paid to the environment of the dry cows because infections are more common in the dry period. Milking procedures should gross appearance of the milk is too non-specific to allow an etiologic diagnosis to be made (Figure 8-42). Lack of also is reviewed because improper procedures may damage the teats and increase susceptibility. Routine dry cow antibiotic treatment should be used, and for herds with persistent problems, pre lactation therapy may decrease the infection rate. Teat dipping should routinely be used, but for environmental Streptococcus spp. infections, it may not be as important for control as dry cow therapy.

Arcanobacterium pyogenes

(Formerly 12.0pt;"> Corynebacterium & Actinomyces pyogenes)

Aetiology.

A. pyogenes causes “dry cow” or “summer” mastitis. Infection is extremely purulent, and abscessation of affected glands is common. Most, but not all, infections occur during the dry period, and the incidence of infection is increased during the dry period in unhygienic environments. Because A. pyogenes is a common skin organism of cattle, it is routinely isolated from abscesses and wounds in a variety of tissues. The organism may be spread by flies and fly bites of the teat end during summer months but can occur year-round in some operations. Teat injury may predispose to A. pyogenes and other gram-positive infections. Most infections begin after the udder has been dry for 2 weeks or more. Epidemics with up to 25% of the dry cows being affected are possible. A. pyogenes infection of the gland in heifer calves has been reported in England and in warm-weather zones of the United States. Affected calves were at pasture during the summer months and ranged in age from 5 to 22 months. The degree of damage to infected glands based on future productivity was not reported. Fly control reduced the further incidence of disease.

Signs.

Swelling of the infected quarter usually is acute and results in a very firm or hard, inflamed, painful gland or glands. Fever and inappetence may accompany acute infection. Cattle that are closely observed may have less severe and gradual inflammation of the infected gland. Therefore “acute” cases may in fact be well advanced when finally recognized and represent fulminant abscessation of a longer-standing, subacute or chronic infection. Cows having truly acute infections are febrile and have firm inflamed quarters and watery secretion with thick clots or rice-like clumps in the secretion. Cows with subacute or chronic infections do not appear ill systemically

but have extremely hard, greatly swollen glands with toothpaste-like or thick malodorous pus as the major secretion. Milking the affected quarter may be difficult because of the viscosity of the secretions. Abscesses may appear in chronic cases and are located anywhere in the gland. Such abscesses eventually drain percutaneously through the skin of the udder with typical discharge and odour associated with A. pyogenes. Most chronically infected glands are ruined by the infection. Dry cows with A. pyogenes occasionally may abort because of toxaemia and fever in acute cases. Occasionally A. pyogenes will be isolated from a recurrent or chronic case of mild

clinical mastitis in a cow with a history of coliform mastitis or mastitis caused by some other primary pathogen. The presumed pathogenesis in these cases is vascular damage, tissue infarction, and subsequent colonization of necrotic or compromised mammary tissue from pyogenic foci elsewhere in the body or via the teat.

Diagnosis.

Diagnosis is confirmed by culture of secretion from the quarter.

Treatment.

Although the prognosis is guarded, early recognition of A. pyogenic mastitis before abscessation offers the best opportunity for resolution. Before intramammary administration of antimicrobials, infected quarters must be milked out completely.

Penicillin also should be administered systemically (22,000 U/kg IM, twice daily) for a minimum of 1 week. Penicillin should be infused into the quarter once or twice daily using approved lactational intramammary products. Most cattle that improve require 7 to 14 days of antibiotic therapy. Cattle that do not improve eventually develop draining udder abscesses and cease lactating in the infected quarters.

Gradual softening of the infected quarter is the desired response. Other signs of improvement include the reduced size of the gland and more fluid secretion. Prevention of A. pyogenic mastitis revolves around the provision of clean, dry environments for nonlactating cows and heifers, frequent observation of dry cow’s udders for evidence of overt swelling or asymmetry, fly control, and aseptic administration of dry cow treatments. Although dry cow preparations certainly discourage A. pyogenes infections, careless administration of dry cow products may introduce A. pyogenes to the teat cistern.

Although protective against the introduction of some mastitis pathogens, dry cow formulations would be ineffective in conditions of overwhelming bacterial challenge Cure rates have been so low historically for A. pyogenes mastitis that practitioners have frequently elected to attempt to dry off the affected quarter or chemically sterilize it using solutions containing iodine, chlorhexidine, or formaldehyde. In some cases, attempted dry off or chemical sterilization meets with the identical outcome as the natural progression of the disease, namely, abscessation and spontaneous drainage from the skin of the affected quarter.

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Environmental Causes of Mastitis Streptococcus uberis and Other Streptococcus spp

Environmental Causes of Mastitis

Streptococcus uberis and Other Streptococcus spp.

(Non-agalactiae)

Signs and Diagnosis.

Treatment.

Arcanobacterium pyogenes

(Formerly 12.0pt;"> Corynebacterium & Actinomyces pyogenes)

Aetiology.

Signs.

Diagnosis.

Treatment.

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Environmental Causes of Mastitis Streptococcus uberis and Other Streptococcus spp

Environmental Causes of Mastitis

Streptococcus uberis and Other Streptococcus spp.

(Non-agalactiae)

Signs and Diagnosis.

Treatment.

Arcanobacterium pyogenes

(Formerly (adsbygoogle = window.adsbygoogle || []).push({}); 12.0pt;"> Corynebacterium & Actinomyces pyogenes)

Aetiology.

Signs.

Diagnosis.

Treatment.

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0 Comments

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(Formerly 12.0pt;"> Corynebacterium & Actinomyces pyogenes)