Dermatophilus

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Context/Importance

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The disease known as dermatophilosis is also known as: Senkobo disease in cattle, lumpy wool in sheep, streptothricosis, strawberry footrot, klontwol (Afrik.), ‘kirchi’ (Nigeria), giasin-gishu (Kenya), ‘drodro-boka’ (Madagascar), ‘savi’ (Tanzania), and ‘ambarr-madow’ (Somalia)

Dermatophilosis is an acute, subacute or chronic skin disease that affects a wide range of domestic and wild animal species as well as humans and is characterized by the development of an exudative epidermitis followed by scab formation, alopecia and thickening of the skin. The disease is caused by Dermatophilus congolensis, a facultatively anaerobic, Gram-positive actinomycete that produces motile zoospores that invade the skin. The morbidity and mortality rates of the disease vary depending on the season; it constitutes an important economic problem to livestock production, particularly during rainy seasons.

The disease was first reported in 1915 in the annual report of the Veterinary Department of the then Belgian Congo (now Democratic Republic of Congo) by Van Saceghem. Since then, it has been diagnosed in many tropical, subtropical and temperate parts of the world. When the disease was first reported, the causative agent was named as Dermatophilus congolensis and subsequently as Actinomyces dermatonomus, Actinomyces congolensis and Streptothrix bovis. It is now classified as Dermatophilus congolensis.

Dermatophilosis is of economic importance because it can cause great losses to the livestock and leather industries. These are mainly attributed to poor quality of hides and skin and to low meat production as affected animals may lose weight and become emaciated. Other losses are the result of decreased milk production, decreased working capacity of draught cattle, forced culling of infected animals before they reach market value, and death in severe cases.

Dermatophilosis affects a wide range of domestic and wild animals, including terrestrial and aquatic mammals. Occasional infections have been reported in many wild animal species, including white-tailed deer (Odocoileus virginianus),woodchuck (Marmota monax), striped skunk (Mephitis mephitis), racoon (Pryocyon lotor), giraffe (Giraffa camelopardalis) and antelope (Thomson's gazelle - Gazella thomsoni), chamois (Rupicapra sp.),zebra (Equus burchelli), small rodents and monkeys, polar bears (Tholarctos maritimus), snakes and lizards. Birds are highly resistant. The disease is known to occur in various species of African wildlife and its has been recorded in sable and roan antelope [1], African buffaloes, and zebras in the Kruger National Park, South Africa, and in Kafue lechwe in Zambia [2][3]

Epidemiology

The zoospores can remain dormant in the absence of any adequate stimulus, such as moisture, and, when in this state, are highly resistant to desiccation and may even remain viable after heating to 100 °C for up to 30 minutes. They lose their outer capsule and become motile by means of a tuft of flagella within 24 hours with the advent of warm, humid conditions, and can migrate from the moist scabs of the skin lesions that are induced by them. Motile zoospores are not very resistant to physical and chemical changes such as pH, osmotic changes and desiccation; these result in decreased viability after a few hours outside the scab lesions, but in a favourable substrate, such as the persistently moistened skin of a suitable host, they lose their motility, and germinate. In certain African countries, there is a close association between the presence of Amblyomma variegatum, and the occurrence of the disease [4][3]

Dermatophilosis has a worldwide distribution but it is most prevalent in humid, tropical, and subtropical regions. Predisposing factors such as rainfall, high humidity and ambient temperature, skin lesions (due to, for example, ectoparasites, thorns and other trauma), skin pigmentation, managemental practices, intercurrent diseases, malnutrition, stress and heredity, play an important role in the epidemiology and manifestations of the disease in the domesticated species. The effect of climate is, however, one of the most prominent epidemiological features of dermatophilosis. Another important feature is that animals in which the disease has regressed are often reinfected repeatedly in successive wet seasons[3].

Dermatophilosis is transmitted by direct or indirect contact. Close contact between animals, such as rubbing against each other, favours mechanical transfer of the organism. Indirect transference of the zoospores may occur mechanically through contact with plants, other objects or insects and arachnids harbouring the organism. The wetted skin and fleece, and particularly the wetted crusts of lesions, are attractive to flies, which promote the transmission of infection[3].

Prolonged wetting of the skin causes emulsification and disruption of the sebaceous film and maceration of the stratum corneum, rendering the skin susceptible to infection by D. congolensis[3].

The zoospores are found mostly in the scabs and dried exudate of the lesions, from which, if thorough wetting occurs, they are released in large numbers. As virtually no viable zoospores are detectable at the surface of scabs and exudate before they have been soaked, affected animals are probably not an important source of infection unless their lesions are wet. The number of viable zoospores in scabs decreases rapidly as scabs dry out, but small numbers may survive in them for several months[3].

Outbreaks of the disease may occur in both summer and winter. Under natural conditions, rain,misty weather, and dew are important in the release of zoospores. Severe wetting or saturation of the hair and skin for several days or weeks is often associated with a higher prevalence of dermatophilosis than is found in areas receiving a high but intermittent rainfall. During the rainy seasons, other predisposing factors, such as malnutrition, ectoparasites and intercurrent diseases, may also play a role in the epidemiology of the disease[3].

Higher serum levels of some minerals, such as zinc and iron, have been found in domesticated breeds resistant to dermatophilosis as compared to those in susceptible breeds, but the role that these minerals play in the resistance of susceptibility of animals to the disease is not clear. Decreased blood levels of ascorbic acid and cholesterol have also been reported[3].

Infestations with arthropods, especially the hard tick Amblyomma variegatum, have long been associated with an increased prevalence of dermatophilosis, the lesions occurring particularly in the most heavily infested areas of the body but there is no cogent explanation for this. It has been postulated that skin lesions due to delayed hypersensitivity as a result of repeated feeding of the ticks provide a portal of entry to D. congolensis and that the systemic effects on the immune system of the host of the immunomodulating factors, such as prostaglandin E2(PGE2), present in the saliva of ticks, predispose to the disease. The nymphal stage of A. variegatum has been experimentally incriminated in transmitting the organism. It has also been observed in herds subjected to tick control measures that the disease either does not occur, or its prevalence and severity are diminished[3].

Dermatophilus congolensis has been isolated from certain ticks such as Hyalomma asticum, A. variegatum and Boophilus microplus. Successful transmission of dermatophilosis has been achieved by feeding A. variegatum, collected from infected animals, on non-infected animals[3].

Biting and non-biting flies, such as Musca domestica, Lyperosia spp., Stomoxys calcitrans, tabanids, Glossina morsitans, Lucilia cuprina and Calliphoria spp., and mosquitoes have been implicated in the transmission and spread of dermatophilosis, although the actual role they play in its epidemiology is not very clear[3].

Other ectoparasites which can create a portal of entry for D. congolensis in animals, and which have been incriminated in the transmission of the disease, are Cochliomyia macelloma, lice, and mites such as Demodex spp. and Chorioptes spp.[3]

The establishment of the infection is facilitated by damage of the skin barrier by various mechanical injuries such as those caused by the feeding of ox-pecker birds (Buphagus spp.), shearing, branches of trees and spines of thorny bushes, and other sharp objects. It has been suggested that oral lesions observed in some animals may have been secondary to abrasions caused by browsing on thorny bushes[3].

In those cases of the disease, which are associated with mechanical injuries, serum and/or blood oozing from the lesions may attract flies and other insects carrying D. congolensis, as well as provide nutrient and a favourable environment for the establishment of the organism with consequent development of the disease[3].

Pathogenesis

Following infection, the zoospores reach susceptible sites of the skin by their own motility and a positive chemotactic response to carbon dioxide, which diffuses through the skin[3].

In contrast to dermatophytes, which are parasites of the stratum corneum, D. congolensis invades the living cell layers of the epidermis and the sheaths of the hair or wool follicles, in which extensive proliferation of the organism occurs; it does not invade the dermis or the hair or wool fibres. The organisms induce increased keratinization of the epidermis and an acute inflammation characterized by the accumulation of an exudate rich in neutrophils beneath the invaded part of the epidermis; the exudate separates the infected from the non-infected epidermis. The organisms do not penetrate the layer of the exudate, which apparently acts as a barrier to invasion of the uninfected layers of the epidermis. The new epidermis that forms underneath the exudate is invaded from the side, usually by filamentous organisms from adjacent follicle sheaths. The infected epidermis is then again separated from the uninfected epidermis by a layer of exudate, and so the process continues in cycles until a thick, laminated crust is formed, composed of alternating layers of para- and orthokeratotic hyperkeratosis and exudate. The new layers of epidermis are formed mainly as outgrowths from the sheaths of the follicles, and are also infected by bacterial filaments originating from these sites. The presence of the organismin the crusts acts as a source of infection to other animals and of re-infection in affected animals during rainy seasons[3].

The immunology of dermatophilosis is not well understood. Antigens of D. congolensis consist of exoantigens, which are mucoid, and of the hexosamine-galactose, xylose peptide type, and there is an immunological cross-reactivity of several strains of D.congolensis with respect to somatic agglutinogens, haemolysins and precipitinogens,but flagellar agglutinogen displays no strain variation. The antigenic structure of the organism hasbeen established as complex and appears to depend partly on the phase of the life-cycle. Crude antigenic products of D.congolensis strains have been separated into ‘exoantigens’ and ‘endoplasm’ antigens which are derived from the cytoplasmic contents of the whole cell[3].

Studies of the humoral immune response during natural and experimental infections of dermatophilosis in various hosts have established the presence of antibodies, which do not afford any protection against re-infection, nor do they have any influence on the course of the disease once it is established. However, successful immunization of cattle against D.congolensis infection by using a whole-cell antigen has been reported[3].

In Nigeria, experiences in the field and during the performanceof serological procedures for diagnostic purposes have shown that in dermatophilosis different levels and types of antibody occur in naturally infected cattle, which depend on the stage and severity of the disease. For instance, antibody to extracellular antigen is in abundance in the acute as well as the mild disease, while chronically infected animals show higher levels of antibody to whole-cell,cell wall, and cytoplasmic antigens. During the early stages of the disease,infected animals show higher antibody responses to whole-cell associated antigen than to extracellular antigens which indicate that the immune-competent cells of the host come in contact with the cell wall of D. congolensis before extracellular antigens have been produced[3].

It is thought that D. congolensis and certain poxviruses, such as orf virus in sheep and lumpy skin disease virus in cattle, may have a synergistic action, as it is often present in lesions caused by these viruses. Severe lesions similar to those observed infield cases of stawberry footrot have been induced in lambs infected with the orf virus and D. congolensis together, but not with either organism alone[3].

Clinical signs and pathology

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The lesions in wild animals are similar to those described in livestock.

The size, severity, and distribution of the lesions vary markedly among affected animals. Generally,in all the affected animal species, the disease is characterized by the appearance, in the areas affected, of an exudative to proliferative epidermitis with subsequent formation of scabs and crusts under which the hair or fleece tend to break or matt together. The matted hair or fleece may sometimes become detached, leaving raw areas. The detached hair or wool and crusts during the early stages of the disease to some extent resemble camel hair paint brushes; this stage is often referred to as the ‘paint brush stage’ of the disease. In the chronic stage, the scabs are dry and when removed, leave only a soft pinkish area because of the healing that has already occurred.

Severely affected animals become emaciated and the disease may terminate in death. On the other hand, mild cases may heal spontaneously under conditions such as the advent of the dry season, the feeding of high levels of concentrates, or the improvement of the general body condition by other means.

In equine animals, such as horses, donkeys and mules, the disease is known as ‘rain scald’ or ‘rain rot’, and lesions consist of irregular patches of matted hair or small, localized raised areas which are accumulations of sebum, or areas of alopecia. They occur particularly on the muzzle, especially around the nostrils, and on the ears, withers, back, croup, rump and tail. There is also a considerable amount of scurf on the affected part of thebody. Horses maintained under muddy conditions or on very wet pastures, may develop chronic lesions on the heels. This disease is known as ‘mud fever’.

Histopathologically, the most striking feature of the lesions of the uncomplicated disease is its superficial nature. Lesions are restricted mainly to the epidermis and upper layer of the dermis. Acute lesions are characterized by congestion and oedema of the dermis; degeneration,necrosis, parakeratosis and hyperkeratosis of the cells of the epidermis; accumulation of exudate on the surface of the skin; and infiltration of neutrophils and other inflammatory cells into the dermis and epidermis. Branching, septated, bacterial filaments or packets of parallel rows of coccoid zoospores up to eight rows thick are found in the exudate as well as the epidermis as far down as the stratum basale, but they do not usually invade the dermis. Organisms extend into the follicular sheaths for some distance, causing proliferation of the sheath cells. Wool and hair fibres are not invaded.

Roan and sable antelope

The skin lesions seen in these animals reflected a typical exudative dermatitis with the development of crusts. The size of the lesions varied from small nodules to large confluent patches where large areas of the skin were covered by dry exudate attached to the hair. These crusts may become cracked and then produce a purulent exudate due to secondary infections. During the early stages of the infection, the crusts are tightly adherent and their removal leaves a moist surface often containing small haemorrhages. Later on the crusts detach spontaneously. The early lesions occur on the forehead and around the eyes. Later on they appear on the dorsal aspect of the head, neck, thorax and the lumbar regions from where the lesions spread down the sides of the animals and onto the legs[1].

Diagnosis

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Dermatophilus congolensis 3 (Arrows) Zebra.jpg
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Dermatophilus congolense is classified in the family Dermatophilaceae, order Actinomycetales. It is a pleomorphic, aerobic and facultatively anaerobic, Gram-positive bacterium that produces zoospores. On germinating, the zoospores bud to produce a filament that is less than 1 µm wide, which later forms right-angled lateral branching. Initially transverse and then longitudinal septa develop in the filaments, giving rise to parallel rows of encapsulated coccoid cells, 1,5 µm in diameter (zoospores) of equal size that can either be single-stranded or up to eight rows wide.

All these structures are observed in smears made from lesions but they may appear fragmented as a result of the smear-making process (Fig 2, 3, and 4).

In cattle, ringworm lesions (which are usually characterized by circular skin lesions on the face or neck), mange (which is usually pruritic), subacute to chronic photodermatitis (which only affects the non-pigmented areas of the body), skin lesions associated with lumpy skin disease, pseudo-lumpy skin disease, and subacute to chronic sweating sickness may be confused with dermatophilosis. Similar differential diagnoses should be kept in mind in the various species of wildlife susceptible to the infection.

Control/Management

Roan and sable antelopes responded well to the administration of a mixture of penicillin and streptomycin supplemented by topical treatment containing copper sulphate and benzene hexachloride [1]

References

  1. 1.0 1.1 1.2 De Vos, V., & Imes, G. D. (1976). An outbreak of dermatophilosis in sable Hippotragus niger and roan Hippotragus equinus in the Kruger National Park. Koedoe - African Protected Area Conservation and Science, 19, 1-15.
  2. Siamudaala, V. M., Muma, J. B., Munang’andu, H. M., & Mulumba, M., 2005. Disease challenges concerning the utilization of the Kafue lechwe (Kobus leche kafuensis) in Zambia. Conservation and Development Interventions at the Wildlife/Livestock Interface, Implications for Wildlife, Livestock and Human Health, 11, 75-80.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 Coetzer, J. A. W. & Tustin, R. C., 2004. Infectious Diseases of Livestock with Special Reference to Southern Africa. Oxford University Press Southern Africa. 2nd Edition
  4. Sinclair, JM, 1920. Report of the Chief Veterinary Surgeon for the year 1920. Salisbury, South Rhodesia. 9pp