Preferred Scientific Name
- Klebsiella pneumoniae-induced mastitis
International Common Names
- English: Klebsiella pneumonia infections; mastitis; mastitis in cattle; mastitis in pigs; peracute coliform mastitis
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Klebsiella pneumoniae is one of a group of coliform bacteria (including Escherichia coli, Klebsiella oxytoca and Enterobacter aerogenes) that causes environmental mastitis.
Environmental mastitis is used to mean mastitis caused by bacteria that are transferred from the environment to the animal rather than from other infected quarters (Radostits et al., 1994).
As a result of control programmes for contagious mastitis pathogens in dairy cattle, mastitis caused by environmental pathogens is now the primary disease in well-managed dairy herds with low somatic cell count in bulk tank milk (Barkema et al., 1998).
Mastitis caused by K. pneumoniae can be particularly severe because of its poor response to conventionally applied antibiotic therapy and rapid progression to toxic shock and death (Sampimon et al., 2006).
Klebsiella spp. is a common cause of bovine mastitis (Podder et al., 2014). In many western countries, control programs for contagious mastitis have been in place for decades, resulting in a decrease in occurrence of Streptococcus agalactiae and Staphylococcus aureus mastitis and an increase in the relative impact of environmental mastitis pathogens. In some countries, Klebsiella spp. are appearing as important causes of mastitis (Munoz et al., 2007; Zadoks and Fitzpatrick, 2009).
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
Infections with coliform bacteria typically affect only one quarter, but cause clinical mastitis in up to 90% of cases and are usually associated with systemic disease (Nooyen, 2012).
Peracute coliform mastitis in the cow is a severe disease characterized by a sudden onset of agalactia and toxaemia. The cow may be normal at one milking and be acutely ill at the next. Complete anorexia, severe depression, shivering and trampling and a fever of 40 to 42°C are common. Within 6 to 8 h after the onset of signs the cow may be recumbent and unable to get up. The temperature may be normal or subnormal, and signs may superficially resemble parturient paresis (Radostits et al., 1994)
The affected quarter is usually swollen and warm but not remarkable. Coliform mastitis is not uncommonly missed on initial clinical examination. A discriminant analysis of clinical indicants revealed that only a history of previous mastitis in the affected quarter, muscle weakness, clear or white colour of milk, swelling of the udder, watery consistency of the milk, lack of previous mastitis in other quarters, lack of palpable udder abscesses and fever were significantly associated with coliform mastitis (White et al., 1986).
Chronic coliform mastitis is characterized by repeated episodes of subacute mastitis that cannot be readily clinically distinguished from other common causes of mastitis.
A clinical diagnosis of coliform mastitis is usually based on clinical signs, culture of coliform organisms from milk, and a high somatic cell count (Nooyen, 2012). However, in the peracute case, the milk sample may be negative because neutrophils have cleared the organisms (Radostits et al., 1994).
Streaking blood agar and MacConkey agar plates with 0.01 ml and 0.1 ml of milk, respectively, may aid in obtaining detectable growth and a definitive diagnosis. If the animal has already succumbed to the effects of endotoxaemia, bacteriology of chilled mammary tissue and regional lymph nodes along with histologic evaluation of formalin-fixed mammary tissue are diagnostic in confirming coliform mastitis (Nooyen, 2012).
For a number of mastitis pathogens, polymerase chain reaction (PCR)-based diagnostic techniques are being developed (O’Grady and Doherty, 2009). As it is expensive to do a separate PCR test for every possible mastitis pathogen, assays that can test for many bacterial targets in milk at the same time are promising (Koskinen, 2009; Burr et al., 2010; Cressier and Bissonnette, 2011; Ajitkumar et al., 2012).
|Cardiovascular Signs / Absent p waves||Sign|
|Cardiovascular Signs / Arrhythmia, irregular heart rate, pulse||Sign|
|Cardiovascular Signs / Atrial fibrillation||Sign|
|Cardiovascular Signs / Heart murmur||Sign|
|Cardiovascular Signs / Jugular pulse||Sign|
|Cardiovascular Signs / Palpable precordial thrill||Sign|
|Cardiovascular Signs / Peripheral venous distention, jugular distention||Sign|
|Cardiovascular Signs / Sinus tachycardia||Sign|
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Sign|
|Cardiovascular Signs / Ventricular premature beat, multifocal or unifocal||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Ascites, fluid abdomen||Sign|
|Digestive Signs / Decreased amount of stools, absent faeces, constipation||Sign|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Grinding teeth, bruxism, odontoprisis||Sign|
|Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Sign|
|General Signs / Generalized lameness or stiffness, limping||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Sign|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Kyphosis, arched back||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Reluctant to move, refusal to move||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Pain / Discomfort Signs / Pain on external abdominal pressure||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Sign|
|Respiratory Signs / Coughing, coughs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Skin / Integumentary Signs / Cold skin, cool ears, extremities||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
|Skin / Integumentary Signs / Skin edema||Sign|
|Urinary Signs / Haematuria, blood in urine||Sign|
|Urinary Signs / Proteinuria, protein in urine||Sign|
Klebsiella spp. enter via the teat canal and multiply rapidly within the udder, causing an acute symptomatology and loss of milk production. Susceptibility to the bacteria is greatest during the first two weeks of the dry period, due to ease of bacterial access through the teat canal at this time, the proliferation of bacteria in the skin of the teat, and deficient hygiene; and during the peripartum period, due to an increase in cortisol levels which has a negative effect on the inflammatory response and neutrophil function, a negative energetic balance, and oestrus (Herrera, 2009).
The primary host defense against coliform mastitis during lactation is the elimination of bacteria by neutrophils migrating into the gland in response to inflammation. Damage to the host is mediated by the release of endotoxin. Systemic signs of clinical mastitis include anorexia, fever, dehydration, and diarrhoea. Decreased milk production during clinical coliform mastitis results both directly and indirectly from the local and systemic effects of endotoxin (Hogan and Smith, 2003).
Coliform mastitis can result in bacteraemia and septicaemia as the blood-milk barrier is destroyed (Wenz, 2001). Septicaemia resulting from coliform mastitis is rare, but is often fatal when it occurs (Hogan and Smith, 2003).
Some cases of coliform mastitis may become chronic, but more than 50% of infections end within ten days (Nooyen, 2012).
Numerous capsular types of Klebsiella pneumonia are responsible for coliform mastitis in cattle (Braman et al., 1973). Genetic studies have shown a high level of diversity in K. pneumoniae genotypes within and between dairy herds (Paulin-Curlee et al., 2007, 2008).
Coliform mastitis is common in dairy cattle housed during the winter. It is uncommon in dairy cattle that are continuously in pasture (Radostits et al., 1994). Wet bedding, particularly sawdust and shavings, has been shown to promote the growth of coliform bacteria, especially Klebsiella spp. There is a strong association between rainfall and bedding populations and incidence of K. pneumoniae mastitis (Thomas et al., 1983).
For many years, wood-based bedding materials have been considered to be the most important source of intramammary infections due to Klebsiella spp. (Vecht et al., 1987; Sampimon et al., 2006) and prevention strategies include using inorganic bedding materials. However, several investigations have shown the presence and growth of Klebsiella in both organic and inorganic bedding materials (Hogan et al., 1989; Zdanowicz et al., 2004). In dairy farms, Klebsiella has frequently been isolated from milking machine equipment (Munoz et al., 2007), milking machine wash water (Silva and Costa, 2001) and drinking water (Nonnecke and Newbould, 1984; Munoz et al., 2007; Zadoks et al., 2011).
Faeces have been shown to be a source of environmental Klebsiella contamination (Munoz et al., 2006; Verbist et al., 2011). Zadoks et al. (2011) found the faecal shedding of Klebsiella spp. contributes to pathogen loads in the environment, including bedding, alleyways, and holding pens. Hygiene of alleyways and holding pens is an important component of Klebsiella control on dairy farms.
Mastitis caused by K. pneumoniae can be particularly severe due to its poor response to antibiotic therapy, rapid evolution to toxic shock, and death (Silva and Costa, 2001). Infection with Klebsiella spp. affects the profitability of dairy farmers due to discarded milk, costs of antibiotic treatment, and extra labour, death, or culling of infected animals and decreased fertility. Klebsiella spp. mastitis causes a considerable and often sustained decrease in milk production, with average losses of 7.6 kg/day shortly after infection and 5 kg/day in subsequent months (Gröhn et al., 2004).
As opportunistic pathogens, Klebsiella spp. can cause a variety of illnesses in humans, including pneumonia, urinary tract infections and septicaemia, in the immunocompromised or those with underlying conditions (Broberg et al., 2014).
Some K. pneumoniae strains produce enzymes called extended-spectrum beta-lactamases (ESBLs) and are resistant to many penicillin and cephalosporin antibiotics and often to other types of antibiotic. ESBL-producing K. pneumoniae have been detected on dairy farms, which could be a concern for both public and animal health (Ohnishi et al., 2012; Nóbrega et al., 2013; Timofte et al., 2014).
Most studies suggest that traditional antibiotics have only limited effects in treating K. pneumoniae mastitis (Erskine et al., 2002; Roberson et al., 2004; Ribeiro et al., 2008). However, Schukken et al. (2011) found that intramammary treatment of non-severe clinical mastitis with ceftiofur hydrochloride resulted in a significant increase in bacteriological cure compared with nontreated controls in animals infected with E. coli or Klebsiella spp.
Broad spectrum intravenous antimicrobials are given to severely affected cows to reduce the bacteraemia which may be present in up to 48% of coliform mastitis cases. Stripping of the affected quarter several times a day, in conjunction with oxytocin injections, has also been utilized to reduce the number of bacteria and endotoxin in the gland. Anti-inflammatory and fluid therapy may also be necessary to prevent shock and maintain overall hydration status (Nooyen, 2012).
The control and prevention of coliform mastitis is a challenge for dairy producers. Control measures that are applied for contagious mastitis pathogens are often ineffective in controlling mastitis caused by coliform bacteria. Because of the poor response to treatment, hygienic measures are the most appropriate control strategy for Klebsiella mastitis (Munoz et al., 2006). Vaccination has been reported to provide some protection against the risk of culling but does not affect the incidence or severity of clinical mastitis due to Klebsiella spp. (Wilson et al., 2007).
Since faecal shedding of Klebsiella spp. contributes to pathogen loads in the environment; hygiene of alleyways and holding pens is an important component of Klebsiella control on dairy farms (Zadoks et al., 2011). Important control measures include frequent changing of bedding, alley scraping, and strict cleaning of teats before milking.
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