Medullary trichomalacia in 6 German shepherd dogs

Abstract

Medullary trichomalacia is the name proposed for a hair shaft abnormality that was recognized in 6 German shepherd dogs. Affected dogs had multifocal areas of broken hairs, especially on the dorsolateral trunk. Microscopic examination of hair shafts revealed focal areas of loss of architecture, swelling, and apparent softening of the medulla, followed by longitudinal (lengthwise) splitting and breakage of the hair shaft. No cause could be found. Affected dogs were otherwise healthy, and apparent spontaneous recovery was the usual outcome. Relapses may occur.

Introduction

Hair shaft abnormalities are not commonly reported in dogs (1). Recognized entities include alopecia areata (1), anagen defluxion (1), trichorrhexis nodosa (1), trichoptilosis (2), congenital hypotrichosis (1), black hair follicle dysplasia (3), pattern baldness (1), color dilution alopecia (3,4), and various forms of follicular dysplasia (1,5). It is likely that hair shaft abnormalities are more common and numerous than the veterinary literature would indicate, because trichography is not routinely performed by many veterinarians. The purpose of this paper is to report a recently recognized acquired hair shaft abnormality in German shepherd dogs.

Materials and methods

Six German shepherd dogs were presented to the Centro Medico Veterinario (CMV) for evaluation of patchy areas of broken hairs over the dorsolateral aspect of the trunk, on the neck, or both (Table 1). Skin scrapings, trichography, fungal cultures, and flea combings were performed on all dogs. Trichography was performed as previously described (1). Briefly, a few hairs were plucked from lesions and from normal hair coat on all 6 affected dogs. In addition, hairs were plucked from a normal German shepherd dog. The plucked hairs were placed in mineral oil on glass slides, coverslipped, and examined under the microscope. Multiple 6-mm biopsy punch specimens were taken from 2 dogs (cases 5 and 6) and routinely processed for histopathological examination. One dog (case 5) was rebiopsied at a previously affected site after hair regrowth. Hairs from 1 dog (case 5) and a normal adult German shepherd dog were studied by light microscopy, scanning electron microscopy (SEM), and transmission electron microscopy (TEM).

Table 1.

Results

The dogs varied from 1 y to 7 y of age and included 4 females and 2 males (Table 1). Duration of lesions prior to examination at the CMV ranged from a few days to 1 y. The lesions were first noted between early spring (March) and late summer (September) in all dogs. Four of the 6 dogs (cases 3–6) were housed outdoors. None of the dogs were related.

The lesions were reported to occur suddenly, then either become static or gradually enlarge. The number of lesions per dog varied from 2 to 4, and all lesions were located on the dorsolateral aspect of the trunk, on the neck, or both (Table 1). The shoulder area was involved in all dogs, and in 2 dogs (cases 5 and 6) the lesions were bilaterally symmetric. Lesions were characterized by 10- to 15-cm diameter areas where hairs appeared broken off at differing lengths (Figure 1). Both primary and secondary hairs were affected, and affected hairs appeared dull and thicker than normal (Figure 2). Affected hairs appeared to be splitting longitudinally (lengthwise) at various sites along the shaft. The hairs did not epilate easily, but they were easily broken when manual traction was applied. The underlying skin was normal, the lesions were nonpruritic and nonpainful, and the dogs were otherwise healthy.

Figure 1. Areas of broken hairs over the left shoulder area.

Figure 2. Close-up of a lesion over the shoulder area. Hairs are broken off at different lengths and some hairs appear thicker than normal.

Four of the dogs had a previous history of either flea infestation (case 2), bacterial pyoderma (case 3), discoid lupus erythematosus and acral lick furunculosis (case 4), or multiple keratinous cysts (case 5). However, the distribution patterns of these previous dermatoses did not correlate with those of the current hair coat abnormality. Neither did the therapeutic protocols instituted for the previous dermatoses have any apparent relationship with the onset or progression of the current hair coat abnormality.

In 4 dogs (cases 3–6), it was possible to get detailed information concerning possible topical applications and injections in the affected areas during the previous 6 mo. Two dogs (cases 4 and 6) had never been shampooed, while 2 other dogs (cases 3 and 5) had been. In 1 dog (case 4), an insecticidal spot-on product (fenthion) had been applied to the shoulder, but this dog also had 2 patches of broken hairs on the back. In another dog (case 6), an annual vaccine (distemper-hepatitis- parvovirus infection) had been injected SC in the shoulder area, and 2 lesions had appeared 3 mo later. Case 5 had received 2 vaccinations (distemper-hepatitis-parvovirus infection and rabies), SC, in the shoulder area about 6 mo prior to the appearance of the lesions.

Skin scrapings and fungal cultures were negative for ectoparasites and dermatophytes, respectively. Flea combings revealed fleas in only 1 dog (case 2). Histopathological examination of skin biopsy specimens (cases 5 and 6) revealed telogenization (all hair follicles in telogen phase) and excessive trichilemmal keratinization of hair follicles, but no hair shaft abnormalities. Biopsy specimens from a previously affected, but now normal, area of case 5 showed no histologic abnormalities.

Light microscopic examination of affected hairs placed in mineral oil revealed segmental shaft abnormalities. The earliest abnormality appeared to be a change in medullary architecture. The affected medullary areas appeared paler and contained larger vacuoles than normal (Figure 3). These areas then lost all detail and became swollen and apparently soft (Figures 4 and 5). Longitudinal (lengthwise) splits developed within these areas (Figures 4 and 5). Shaft breakage occurred in these areas, resulting in the split shaft segments separating and taking on the appearance of spaghetti noodles (Figure 6). These changes were not found in normal hairs.

Figure 3. Early hair shaft abnormality. The affected medulla appears paler than normal and contains vacuoles that are larger (white arrow) than normal (black arrows) (1400× magnification; bar = 7.2 microns).

Figure 4. Further development of hair shaft abnormality. The affected medulla has lost architectural detail (small black arrow) and begun to split longitudinally (large black arrow) (350× magnification; bar = 28.6 microns).

Figure 5. Top hair shaft (arrow) shows extensive longitudinal splitting (350× magnification; bar = 28.6 microns).

Figure 6. Several hairs have broken. The longitudinally split shaft segments at the breaks have the appearance of spaghetti noodles (arrow) (350× magnification; bar = 28.6 microns).

Scanning electron microscopy of affected hairs revealed split ends and longitudinal fractures. In these areas, the cuticle was discontinuous and the cortical fibers were frayed and markedly disarrayed. In unaffected areas of the hair shaft, cuticular, cortical, and medullary anatomy appeared normal. Scanning electron microscopic examination of cross-sectioned abnormal medullary areas revealed vacuoles that were increased in number, more haphazardly arranged, and more variable in size and shape when compared with normal hairs (Figures 7A and 7B).

Figure 7. A) Cross section of normal hair shaft. The medullary vacuoles have an orderly arrangement resembling the face of a clock (SEM 1995× magnification; bar = 5.0 microns). B) Cross section of affected hair shaft. The medullary vacuoles are more haphazardly arranged and are more variable in size and shape (SEM 1995× magnification; bar = 5.0 microns).

Figure 7. A) Cross section of normal hair shaft. The medullary vacuoles have an orderly arrangement resembling the face of a clock (SEM 1995× magnification; bar = 5.0 microns). B) Cross section of affected hair shaft. The medullary vacuoles are more haphazardly arranged and are more variable in size and shape (SEM 1995× magnification; bar = 5.0 microns).

Transmission electron microscopy of affected hairs showed that the abnormal medullary areas contained a number of small, irregularly shaped vacuoles that apparently merged to form larger vacuoles. The larger vacuoles displayed a more irregular outline and were scattered throughout the medulla more haphazardly than those present in normal hairs. The interstitial areas between the vacuoles contained remnants of medullary cells, cell membrane remnants, cytokeratin filaments, and trichohyalin granules embedded in an amorphous substance (Figure 8A). In contrast, the interstitium of the medulla of normal hairs was occupied by a homogeneous substance containing only rare residual cell membranes (Figure 8B).

Figure 8. A) Affected hair shaft medulla. The interstitial area between vacuoles contains linear, lightly colored cell membrane remnants (black arrow head); rounded, darkly colored trichohyalin granules (long black arrow); and linear, dark black cytokeratin filaments (short black arrow) (TEM 45 500× magnification; bar = 0.22 microns). B) Normal hair shaft medulla. The interstitial area between vacuoles is homogeneous (TEM 45 500× magnification; bar = 0.22 microns).

Figure 8. A) Affected hair shaft medulla. The interstitial area between vacuoles contains linear, lightly colored cell membrane remnants (black arrow head); rounded, darkly colored trichohyalin granules (long black arrow); and linear, dark black cytokeratin filaments (short black arrow) (TEM 45 500× magnification; bar = 0.22 microns). B) Normal hair shaft medulla. The interstitial area between vacuoles is homogeneous (TEM 45 500× magnification; bar = 0.22 microns).

Only 1 dog (case 2) had received treatment for the hair coat abnormality prior to examination at the CMV (Table 2). After examination at the CMV, 4 dogs received treatment (Table 2): flea control for proven or suspected flea infestation (cases 2 and 4), enilconazole for suspected dermatophytosis (case 3), benzoyl peroxide or cephalexin for suspected bacterial infection (cases 4 and 6), and clipping of the lesions (cases 3 and 6).

Table 2.

The 2 dogs (cases 1 and 5) that received no treatment at the CMV recovered spontaneously after 3.5 mo and 10 mo of disease, respectively. Two dogs (cases 2 and 4) that received only therapeutic agents recovered after 4 mo and 15 mo of disease, respectively. Two dogs (cases 3 and 6) that received therapeutic agents and clipping of the lesions recovered after 2.5 mo and 5 mo of disease, respectively.

Follow-up information was available for 4 dogs (Table 2). Three dogs (cases 3, 4, and 6) remained normal for 2 y to 4 y following remission. One dog (case 5) developed lesions at the identical locations, during the same season, for the subsequent 2 y. At the time of each relapse, the lesions were clipped and normal hair regrew within about 2 mo.

Discussion

The hair shaft abnormality of German shepherd dogs reported herein is quite distinctive. We propose that this condition be called medullary trichomalacia. The earliest microscopic changes occur within the medulla of the hair shaft. A loss of anatomic detail is followed by swelling and apparent softening (malacia) of the affected medulla. The affected area of hair shaft then splits longitudinally (lengthwise) and eventually breaks. These microscopic changes are unique to medullary trichomalacia. Hence, definitive diagnosis of this disorder is achieved by trichography.

Trichography (the study of hairs and hair abnormalities) is a commonly performed laboratory procedure in veterinary and human dermatology (1,6,7). As was done in our study, hairs should always be sampled from normal as well as abnormal hair coat. Medullary trichomalacia has not, to the authors' knowledge, been previously reported in veterinary or human medicine. The authors routinely perform trichography on the majority of their canine dermatology patients and have not seen similar hair abnormalities.

Medullary trichomalacia affects middle-aged German shepherd dogs of either sex. The condition is characterized by the sudden onset of multiple areas of broken hairs, especially over the shoulder area. There is no pruritus, pain, or dermatitis associated with the hair coat abnormality, and the dogs are otherwise healthy.

The cause of medullary trichomalacia is unknown. We were unable to establish any clear associations with previous topical applications or injections. The exclusive onset of disease between early spring and late summer suggests possible seasonal environmental influences. The unique occurrence in German shepherd dogs suggests that genetic predisposition may be involved. However, none of the dogs were related, and the condition was tardive in onset.

Telogenization and excessive trichilemmal keratinization were present in skin biopsy specimens from 2 dogs. These 2 histopathological changes can be observed in skin biopsy specimens from dogs with endocrine, metabolic, or nutritional skin diseases (1). No assessment of hormonal or metabolic status was performed on any of the dogs. All of the dogs were otherwise healthy and were fed nutritionally complete commercial diets. The distribution of skin lesions, absence of other clinical abnormalities, and spontaneous resolution of lesions seen in these dogs is inconsistent with the course of untreated endocrine, metabolic, or nutritional skin diseases (1).

The early medullary abnormalities seen in affected hairs are not accompanied by evidence of cuticular or cortical abnormalities on light microscopic, SEM, or TEM examination. The altered vacuolization, cell membrane remnants, and free cytokeratin filaments and trichohyalin granules suggest an altered state of keratinization.

There is currently no effective treatment for medullary trichomalacia. All dogs (whether treated by topical applications or clipping, or with nothing at all) recovered completely after a period of 2.5 mo to 15 mo. Although most dogs remained normal after hair regrowth, 1 dog developed recurrent, seasonal disease for the subsequent 2 y. CVJ