Corynebacterium renale group infections

M G COLLETT

GENERAL INTRODUCTION: IRREGULAR, NON-SPORING, GRAM-POSITIVE RODS

Introduction

The most important diseases caused by the Corynebacterium renale group (C. renale, C. pilosum and C. cystitidis) of bacteria are contagious bovine pyelonephritis (a specific infection of the urinary tract of cattle characterized by acute to chronic purulent cystitis, ureteritis and pyelonephritis), ulcerative posthitis in bulls and adult wethers, and vulvitis in ewes.

Contagious bovine pyelonephritis has been recognized in Europe for over a century, and has also been reported in the Middle East, Japan, the USA, South America, Africa and Australia. ^{12, 50, 54, 66, 68, 71} There have also been occasional reports of ovine pyelonephritis and cystitis.^{2, 31} Enzootic posthitis is an important disease in adult wethers in the high rainfall areas of Australia, where reports go back to the early 1900s.⁶⁴

The pathogenicity varies between C. renale, C. pilosum and C. cystitidis. Infection with either C. renale or C. pilosum causes pyelonephritis and cystitis in cows, while C. cystitidis infection causes a cystitis which is more severe and haemorrhagic than that caused by the former organisms.^{33, 36, 94, 95}

In sheep, reports of posthitis and vulvitis caused by bacteria of the C. renale group have come from South Africa, Nigeria, Australia (where the disease is very important), New Zealand and North America.^{7, 16, 20,69, 78, 79, 93} Oslington⁶⁴ from Australia classified urease-positive diphtheroids isolated from diseased and healthy prepuces as C. renale (49,6 per cent), C. pilosum ( 34,6 per cent) and C. cystitidis (6,9 per cent) with 9,1 per cent unclassified. Corynebacterium renale may be part of the normal flora of the female genital tract of sheep and goats,^{58, 59} and the organism has also been isolated from the accessory sex organs and epididymis of healthy rams.⁴⁴

In goats, ulcerative posthitis has been described in India⁵³ and in Angora wethers in Texas,⁷³ while a most unusual case of disseminated necrogranulomatous osteomyelitis (with pathological fractures), lymphadenitis, hepatitis and nephritis has been reported in a dairy goat in the USA.³

Bacteria of the C. renale group can cause pyelonephritis and cystitis in horses.^{12, 23} Corynebacterium pilosum has been isolated from the urine of an incontinent gelding.⁸⁶ In South Africa, Steyn in 1940⁸³ was the first to describe ‘pisgoed’, which he considered to be non-contagious. Corynebacterium renale has been isolated on rare occasions from the prepuce of normal bulls and from cases of chronic pyelonephritis in cows and enzootic posthitis and vulvitis in sheep at the Onderstepoort Veterinary Institute in South Africa.³⁰ The organism has also been isolated from cases of ulcerative balanoposthitis and vulvovaginitis, a readily transmissible venereal disease of Dorper sheep in South Africa. Mycoplasma mycoides mycoides LC has been shown to play a major aetiological role in this disease (see Ulcerative balanoposthitis and vulvovaginitis of sheep).⁸⁹

Aetiology

Bacteria of the C. renale group (C. renale, C. pilosum and C. cystitidis) are aerobic and facultatively anaerobic. Although originally all were classified as C. renale (see the introduction, Irregular, non-sporing, Gram-positive rods: Table 1), biochemical^{14, 40} and antigenic differences,⁹⁴ and differences in nutritional requirements³² between strains necessitated the designation of new species.⁹⁵ These bacteria are rather large (0,7 to 3,0 μm or more), non-motile, non-sporing, non-capsulating, irregularly staining Gram-positive rods, often with pointed ends and pili.¹⁴ A special selective medium for the isolation of urinary corynebacteria from samples contaminated with faeces or urine of cows has been developed.³⁵ On blood agar, the colonies are small, dewdrop-like, raised, opaque, yellow or ivory-coloured, and dull without haemolysis.^{60, 88} Colonies grown on agar can be pushed intact across the surface.⁶⁰ The bacteria hydrolyze urea more rapidly than most other urease- positive bacteria.¹¹

Epidemiology

In cattle herds where pyelonephritis occurs, prevalence rates are in the region of 0,5 to 1,5 per cent and up to a third of affected animals may die or have to be culled.⁵⁴

Corynebacterium renale and C. pilosum can be isolated from the vulvovaginal and penile mucosa of healthy cows and bulls, respectively. On the other hand, C. cystitidis has only been isolated from diseased cows, although it does occur in the prepuce of healthy bulls.^{36, 39, 94, 95} Some 10 to 20 per cent of animals may be carriers of the bacteria. ^{21, 61} Healthy cows may shed bacteria in their urine intermittently or regularly for seven months or longer.^{4, 33} The organisms can survive in moist paddock soil for two (C. renale and C. cystitidis) to seven months (C. pilosum).²⁸

Multiparous cows are mainly affected.⁵⁴ The disease often follows parturition, but pregnant animals may also be affected.^{4, 87} The disease is rare in heifers and bulls.^{4, 12, 61} In dairy herds, there is evidence that C. renale spreads from animal to animal along stanchion lines.⁶¹ The spray of urine from infected cows can probably directly contaminate the vulvas of animals standing in close proximity to them.³⁵ Venereal transmission is possible in cows.⁷² Careless use of catheters can also play a role in the spread of the disease.⁶⁶

Cold weather^{4, 37} and the stress associated with peak production⁵⁴ may predispose to the development of the disease. Pyelonephritis does not normally occur in association with post-parturient uterine diseases because of the aciduria in the latter.^{54, 66}

There are three important factors in the epidemiology of posthitis in adult wethers⁶⁴ and the first two also apply to bulls and rams. Firstly, a legume-rich high plane of nutrition, which causes an increase in urea in the urine; secondly, the presence of C. renale;^{10, 13, 68, 77, 78, 79} and, thirdly, low testosterone levels.⁷⁵ Affected bulls and wethers do not appear to develop immunity as recurrence after treatment is common.^{68, 76} Experimentally, steers can be infected with material from wethers and vice versa.^{77, 79} Morbidity rates in bulls can be as high as 100 per cent.⁶⁸

Posthitis occurs more frequently in adult wethers than in rams;^{57, 69, 79} 10 to 75 per cent of wethers can be affected with sheath rot.^{9, 65} Posthitis is particularly a problem where wethers are kept for many years for wool production — as with Merinos in South Africa and Australia—and to a lesser extent if wethers are slaughtered for meat at a young age — as in New Zealand.⁹³ In some areas, the prevalence of posthitis is so high that it is virtually impossible to maintain healthy flocks of wethers over the age of three years.⁶⁶ Venereal transmission has been reported in sheep.^{77, 79} Seasonal fluctuations in the incidence of the disease may be due to changes in protein intake associated with the stages of pasture growth, the legume content thereof, climatic factors or stocking rate;^{9, 56, 65, 76, 81, 91} to changes in the preputial tissues under the influence of androgens;⁵⁷ or to a variation in the prevalence of blowflies and other flies, which may be able to transfer infection mechanically.^{66, 79} In summer-rainfall areas, the incidence is highest in autumn and winter,^{9, 91} while in winterrainfall areas most cases occur in spring.^{81, 91}

Pathogenesis

Bacteria of the C. renale group have a predilection for the urinary tract because of their ability to metabolize large quantities of urea by means of the enzyme urease.^{4, 51} Consequently, the pH of the urine in affected animals is usually higher than normal.⁴

In cows, the vulva is the main portal of entry. Bacteria of the C. renale group adhere efficiently to superficial epithelial cells of the urinary tract of cattle;^{27, 29} adherence to the vulval epithelium is stronger than to superficial bladder epithelial cells and epithelial cells in urinary sediment.⁷⁰ Unlike most Gram-positive organisms, members of the C. renale group possess pili that promote attachment to, and colonization of, the mucosa of the urinary tract.^{24, 41, 42, 48, 67, 84} A high urinary pH promotes the attachment of piliated C. renale. ⁸⁴ Specific cell receptors⁷⁰ may be involved in the localization of the organisms, but the role of piliation in the pathogenesis of pyelonephritis²⁴ and in bacterial survival²⁸ appears equivocal. Piliated C. renale initiate infection, but once anti-pili antibodies are formed, phagocytosis of piliated organisms occurs more readily, leading to a population shift towards non-piliated organisms.^{25, 47}

After attachment to the epithelial cells of the vulva, the bacterial infection causes an ascending (retrograde) cystitis and pyelonephritis.^{12, 22, 27, 28, 52, 54, 55, 61, 74, 87} Neither humoral nor cell-mediated immunity appears to influence the ascent of organisms to the kidneys.⁶³ In the kidneys, the medulla is preferred to the cortex as a site for growth.⁵¹ The clinical signs of pyelonephritis are due mainly to the direct effects of bacterial multiplication.⁴

The preputial mucosa is probably the portal of entry in bulls, steers, rams and wethers. Ulceration of the prepuce probably results from chemical irritation when ammonia is produced following the hydrolization of urea by C. renale.^{13, 68, 71, 77, 78} Entire animals may be more resistant to infection because of the effect of testosterone on the development of preputial tissues.⁵⁷

Experimental models of C. renale pyelonephritis have been studied in mice,⁷⁴ rats⁴⁶ and goats.¹⁹

Clinical signs and pathology

Typically, cows with pyelonephritis show painful and frequent micturition. The urine is bloody or foetid, and contains neutrophils, mucus, blood, fibrin and colonies of large, Gram-positive, diphtheroid bacteria.^{4, 12, 50, 51, 67, 87} Its pH is raised (more than 8,5),^{4, 54} and the specific gravity is in the range of 1,008 to 1,021.^{54, 67} Haematuria may last for months after calving. Other clinical signs include anorexia, fever, loss of condition, a reduced milk yield, and, in severe cases, signs of colic manifested by the animal kicking at its abdomen, grinding its teeth, and restlessness.^{4, 33, 67} On rectal examination, the left kidney is usually enlarged and tender to touch and the ureters are thickened (up to 20 mm or more, in diameter).^{4, 12, 67, 87} The differentiation between cows with cystitis, where the ureters are not affected and systemic illness is absent, and those with pyelonephritis, where the ureters are thickened, can be aided by vaginal examination and palpation.⁶⁷

The course of the disease is usually several weeks to months and may terminate in signs of uraemia.⁶⁶

Serum creatinine and urea levels can be helpful with regard to prognosis,⁵⁴ as raised levels indicate that there is probably bilateral renal involvement.⁶⁷ A hyponatraemia is frequently observed in association with pyelonephritis because the sites of sodium reabsorption, the distal tubules and collecting ducts are progressively damaged.⁹⁰ Affected animals may have a hypoalbuminaemia and hyperglobulinaemia.⁶⁷

At necropsy, both kidneys are usually affected. They are severely enlarged, the calyces are distended, and little functional tissue remains. The pelves and ureters usually contain a brownish fluid made up of mucus, pus, fibrin, calculi and other debris.^{4, 33} The ureters are often grossly dilated, especially near the hilus, and show petechiation of the mucosa.⁴ The pelvic epithelium is thickened and contains petechiae. The infectious process extends from the pelvis to cause a slowly progressive and suppurative papillitis. This results in destruction of the medulla of each lobe and a radially arranged, tubulo-interstitial nephritis. Cortical fibrosis is eventually extensive and the capsule may be adherent in places because of the presence of subcortical abscesses.^{4, 12, 55, 74}

Histopathological changes in affected kidneys include foci of mixed leukocytic infiltrates, purulent foci in the medulla, the destruction of many tubules, and interstitial fibrosis. Gram-positive rods are present in inflamed areas and may also be detected within Bowman’s spaces.¹² The bladder mucosa is affected by varying degrees of pseudomembranous inflammation and haemorrhage.^{4, 12, 33, 74}

Corynebacterium renale causes ulcerative posthitis in bulls and, less commonly, in steers.^{68, 79} The prepuce swells and becomes tender, urination is painful (the affected animal may kick at its abdomen or flex its hind limbs) and urine and/or exudate may drain from the preputial orifice, which may even become occluded by scabs and swollen tissue.⁴⁵ Histopathologically, the lesions are characterized by acanthosis, para- and hyperkeratosis of the preputial mucosa, followed by the invasion of leukocytes and ulceration.⁶⁸ No micro-organisms are present in the preputial epithelium prior to ulceration.⁶⁸ In contrast to the situation in sheep, cows do not develop vulvitis.^{77, 79}

In adult wethers, and to a lesser extent in rams, illdefined, creamy-yellow areas of epidermal necrosis, on the external surface (often dorsally) near the orifice of the prepuce, develop into small (10 to 20 mm in diameter) ulcers (‘external ulceration’) which are covered by raised, thick and tenacious black scabs. These primary lesions are generally mild and unimportant but they may expand and coalesce with others to encircle, cover and occlude the preputial orifice,⁷⁶ resulting in the accumulation of urine and pus in the prepuce.

After a period of external ulceration, ulcers can then spread secondarily to the internal mucosa (‘internal ulceration’) of the prepuce and the glans and, if extensive and severe, eventual destruction of the urethral process follows (‘sheath rot’ or ‘pizzle rot’).^{9, 49, 56, 76, 79, 81, 91} The sheath becomes swollen and pendulous, aggregations of pus and necrotic debris accumulate inside the prepuce and the wool around the orifice becomes urine-stained. The animal becomes restless, kicks at its belly and urine starts to dribble.⁶⁶ The orifice may become occluded, urine fistulae may develop in the perineal area and blowfly maggots may proliferate in the associated wool and exudate. The ulcerated areas on the internal preputial mucosa are covered by tenacious brownish pus.¹⁶ Severely affected wethers die of post-renal uraemia.⁶⁶

In ewes, pyelonephritis and cystitis due to C. renale resembles the disease in cattle.^{2, 31} In flocks where posthitis is common, ewes may show vulvitis, but the lesions are usually transient and of little importance.⁷⁶ Initially, the vulval lips become reddened and then small, superficial yellow-brown crusty scabs develop on the apposed labial skin surfaces. The clitoris may enlarge and protrude from the vulval lips and become ulcerated. In some cases, swelling and ulceration may become more severe and flystrike may ensue. In severe cases, when healing takes place, some scarring may cause distortion of the vulva which may hinder natural mating and cause urine dribbling which could also predispose to flystrike.^{16, 82}

Equine pyelonephritis also resembles that in cattle.²³ The signs of colic, however, are usually more severe than in cattle, while urinary incontinence may occur and calcium carbonate crystals may be found in the exudate from the bladder.^{12, 86}

Diagnosis and differential diagnosis

The clinical signs, urinalysis, rectal and genital palpation findings and pathology are suggestive of corynebacterial cystitis and/or pyelonephritis in cows. It is important to culture the bacterium, either from urine in live animals or from the renal pelvis, ureter or bladder in dead animals,⁴ since other bacteria, such as Escherichia coli, can also cause pyelonephritis.⁶⁷ Concurrent infection with other organisms, such as streptococci, may also be encountered.¹²

Further aids to diagnosis include renal biopsy and diagnostic ultrasonography.^{17, 67} A serum antibody response occurs in cows with pyelonephritis and ureteritis but not in those with cystitis alone.^{33, 34} A fluorescent antibody test can also be used to differentiate between cystitis and pyelonephritis cases, since C. renale from cases of pyelonephritis are antibody-coated (IgG mainly; also IgA), whereas no antibody coating occurs in cases where the lower urinary tract (cystitis) is infected.^{1, 62}

Haematuria caused by corynebacterial pyelonephritis in cattle should be differentiated clinically from other causes of haematuria, such as bracken fern (Pteridium aquilinum) poisoning (‘enzootic haematuria’) and polypoid cystitis,⁹⁰ as well as ascending pyelonephritis caused by E. coli,⁶⁷ and pyaemic nephritis and renal abscesses resulting from Trueperella (Actinomyces) pyogenes infection.⁵⁰ Other causes of colic include traumatic reticulitis and acute intestinal conditions.⁶⁶

Other causes of posthitis in bulls include bovine herpesvirus I (infectious bovine balanoposthitis),^{43, 92} ureaplasma infection (causing granular vulvitis and ulcerative posthitis),²⁶ Strongyloides papillosus infestation,⁸ trauma in pendulous prepuces, urolithiasis and photosensitivity.⁴⁵

Escherichia coli and T. pyogenes can also cause pyelonephritis in sheep; such infections may ascend via the umbilicus and urachus in young lambs.

Diseases that should be differentiated from enzootic posthitis and vulvitis include ulcerative dermatosis (caused by an orf-like parapox virus) (see Orf), ulcerative balanoposthitis and vulvovaginitis [a more extensive, severe and often haemorrhagic disease caused by M. mycoides mycoides LC⁸⁹ (see Ulcerative balanoposthitis and vulvovaginitis of sheep), Australian genital mycoplasmosis (which is characterized by a granular vulvovaginitis)¹⁵ and obstructive urolithiasis.⁶⁶ Granular vulvitis in ewes can also be caused by several Ureaplasma spp.,^{5, 18} while experimental infection with bacteria of the Haemophilus/Histophilus group can also cause ovine vulvitis.⁶ There is no evidence that Fusobacterium necrophorum is involved in ovine posthitis.^{56, 89} In goats, a caprine herpesvirus can cause balanoposthitis.⁸⁵

Control

If bacteria of the C. renale group are cultured from healthy or clinically affected cattle, the infected animals should be isolated and not used for breeding because of the possibility of venereal spread.¹² In such herds, artificial insemination may control the spread of the disease.⁶⁶

Most affected cattle respond to injections of penicillin at doses sufficient to provide an adequate concentration in the urine for bacterial cure.⁶⁰ In early reports, total amounts of 10 000 000 IU were given at 1 to 2 000 000 IU per day.^{4, 51} Nowadays, daily treatments of 6 000 000 IU of penicillin G intramuscularly for six days have been reported as being successful,^{38, 54} although continuation of penicillin treatment for three weeks has been recommended.⁶⁷ The variable response to penicillin is probably related to the stage the disease process has reached at the time of treatment.⁴

Since C. renale prefers an alkaline medium for growth, response to parenteral penicillin can be enhanced by the acidification of urine by means of the oral administration of 110 g of sodium biphosphate (NaH₂PO₄.H₂O) per day for four days.⁸⁷

Bulls with posthitis can be treated with topical antiseptics, topical sulphonamide suspensions and/or solutions with drying agents, such as gentian violet. Affected animals should be kept in dry stalls or pens to prevent recontamination. ⁴⁵

In sheep, the prevalence of posthitis drops dramatically if affected animals are transferred from legume-rich pastures to natural grass or even to a diet of cereal hay or chaff.^{76, 91} Many cured animals will develop recurrent posthitis, however, if they are reintroduced to legume-rich pasture.⁸¹ External ulcers can easily be treated by dietary modification and/or the application of topical antiseptics, such as cetrimide, cupric sulphate, alcohol or chlorhexidine (‘Hibitane’).^{16, 65} Internal ulceration, on the other hand, is more difficult to cure, requiring topical antiseptics, as well as intramuscular procaine penicillin.^{65, 81} Bacteria of the C. renale group isolated from sheep with posthitis are sensitive in vitro to penicillin and bacitracin, less so to erythromycin, chlortetracycline, chloramphenicol, neomycin, oleandomycin and streptomycin, with only slight sensitivity to nitrofurantoin, novobiocin, oxytetracycline and polymyxin B.⁷⁸ Once the lesion has progressed to sheath rot, medical resolution is unlikely,⁷⁹ and surgery (a ventral longitudinal incision of the prepuce or a ‘V’ excision) should be considered, bearing in mind the possibility of flystrike.⁸¹

Prophylactic antiseptic treatment of the prepuce or vulva helps in the prevention of venereal transmission of posthitis and vulvitis.^{65, 79} Shearing and the removal of belly wool is also beneficial,⁷⁹ but the removal of wool around the preputial opening (‘ringing’) apparently has no beneficial effect.^{81, 91} ‘Pizzle-dropping’, a minor surgical procedure where the distal sheath is separated from the belly, is a useful prophylactic measure where adult wethers are to be kept for wool production.⁹³ Wethers drenched with the anthelmintic thiabendazole have a significantly lower prevalence of preputial ulceration, indicating that this drug also has antibacterial properties.⁸⁰ Slow-release subcutaneous testosterone propionate implants have been found to prevent posthitis in rams and wethers.^{57, 75, 91} For long-term prevention, implants need to be repeated every four to six months; this procedure has been successfully practised in Australia for the past three decades.⁶⁴ Other aspects to consider concerning prophylaxis include the feeding of cereal hay⁹¹ and circumcision.⁶⁵

Experiments using multivalent (C. renale, C. pilosum and C. cystitidis) and monovalent C. cystitidis vaccines have failed to induce protection against ovine enzootic posthitis in wethers.⁶⁴

References

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