Mycobacterial Granulomas, Opportunistic Granulomas and Other Bacterial Diseases

UNIVERSITATEA DE ŞTIINŢELE VIEȚII
„REGELE MIHAI I AL ROMÂNIEI” DIN TIMIŞOARA
FACULTATEA DE MEDICINĂ VETERINARĂ
PROGRAMUL DE STUDIU LICENȚĂ
MYCOBACTERIAL GRANULOMAS,
OPPORTUNISTIC GRANULOMAS
AND OTHER BACTERIAL
DISEASES
TIMISOARA 2023
MYCOBACTERIAL AND OPPORTUNISTIC GRANULOMAS, AND OTHER BACTERIAL DISEASES
TABLE OF CONTENT
1. MYCOBACTERIAL GRANULOMAS ................................................................................................................ 2
2. TUBERCULOZA: MYCOBACTERIUM TUBERCULOSIS, MYCOBACTERIUM BOVIS,
MYCOBACTERIUM MICROTI ............................................................................................................................ 2
2.1. CLINICAL CHARACTERISTICS .......................................................................................................................... 2
2.2. DIAGNOSTIC ........................................................................................................................................................ 3
2.4. DIAGNOSTIC ........................................................................................................................................................ 3
2.5. CLINICAL MANAGEMENT OF TUBERCULOSIS ............................................................................................. 3
3. FELINE LEPROSY.............................................................................................................................................. 4
3.2. DIAGNOSTIC ........................................................................................................................................................ 5
3.3. MANAGEMENT CLINIC ..................................................................................................................................... 6
4. OPPORTUNISTIC GRANULOMAS................................................................................................................... 7
4.1. ACTINOMICOZA .................................................................................................................................................. 7
4.2. ACTINOBACILOZA ............................................................................................................................................. 8
4.3. NOCARDIOZA ...................................................................................................................................................... 9
5. BRUCELLOSIS ................................................................................................................................................. 10
6. LYME DISEASE ................................................................................................................................................ 11
7. AXILLARY TRICOMYCOSIS .......................................................................................................................... 12
8. PSEUDOPIODERMITE ................................................................................................................................... 13
8.1. PIODERMA CALUSULUI ................................................................................................................................... 13
8.1.1. Management clinic ....................................................................................................................................... 13
8.2. JUVENILE CELLULITE ...................................................................................................................................... 14
8.2.1. Cause and pathogenesis ................................................................................................................................ 14
8.2.2. Clinical characteristics .................................................................................................................................. 14
8.2.3. Diagnostic ..................................................................................................................................................... 15
8.2.4. Management clinic ....................................................................................................................................... 16
8.3. OTHER PYODERMA-LIKE DERMATOSIS....................................................................................................... 16
9. CUTANEOUS WOUND ..................................................................................................................................... 17
BIBLIOGRAPHY .................................................................................................................................................. 21
1
1. GRANULOAMELE MICOBACTERIENE
Chronic infection with mycobacteria is controlled by the formation of granulomas. Failure to
maintain granuloma leads to reactivation of the disease. Macrophages are the dominant cell type in
granulomas, but CD4+ T cells are the primary organizers of granuloma structure and function. Recent
work indicates an unrecognized role for nonspecific T cells in maintaining granuloma function in the
chronic phase of infection. In addition, it became clear that mycobacteria and host T cells collaborate
in the formation of granulomas. A better understanding of how nonspecific T cells contribute to
granuloma formation, as well as how bacteria and T cells maintain a harmonious relationship over the
host's lifetime, will facilitate the development of new strategies for treating mycobacterial disease.
2. TUBERCULOZA: MYCOBACTERIUM TUBERCULOSIS,

MYCOBACTERIUM BOVIS, MYCOBACTERIUM MICROTI
The incidence of "true" tuberculosis (TB) in dogs and cats has decreased in parallel with the
decrease in tuberculosis in humans and cattle, but may become more prevalent due to changes in the
epidemiology of human tuberculosis. Animals that live where there are a large number of people
(restaurants or public places), have close contact with an infected owner (for example, sleep in the
room with the sick person), live on a farm with tuberous cattle or are fed a variety of unprocessed
meat or unpasteurized milk from endemic disease areas have an increased risk of infection. Although
dogs and cats are susceptible to both M. tuberculosis and M. bovis, there appears to be a higher
incidence of M. bovis infection in cats. The predominant lesions in small animals are respiratory and
digestive, but there may be localized skin lesions. In cats, the signs can be insidious, and since
diagnostic tests were unreliable until recently, epidemiological data have doubtful validity.
M. microti causes TB in voles, wood mice and sharks, and in cats most likely from altercations
with voles; it can also infect humans and larger mammals, especially domesticated llamas in Europe.
[10]]
2.1. CLINICAL FEATURES
Skin lesions comprise single or multiple ulcers, abscesses, plaques and nodules. Nodules may
be in the skin or adherent to subcutaneous tissues. It discharges thick pus, yellow to green, with an
unpleasant odor. Lesions are most common on the head, neck and limbs. Patients usually seem sick;
have anorexia, weight loss, fever and localized or generalized lymphadenopathy.
2
2.2. DIAGNOSIS
The diagnosis is made by history, physical examination, X-ray, cytological evaluation,

including Ziehl Neelsen staining (ZN) for acid-rapid bacilli (AFB), biopsy, culture, bacille
CalmetteGuérin (BCG) or purified protein derivative test (PPD) (in dogs), serological testing or
lymphocytic blastogenesis test (in cats).
Biopsy samples may show nodular to diffuse dermatitis due to pyogranulomatous

inflammation (with necrosis and caseation), rare multinucleated and mineralized histiocytic giant
cells, and little to many AFBs. Smears or biopsy do not differentiate between true TB and other
mycobacterial granulomas. Injection of cultures into guinea pigs causes death in 6 to 8 weeks, but not
if the body is nontuberculous. BCG or PPD (250 tuberculin units/0.1 ml) preparations for humans can
be used to test dogs for TB.
Intradermal injection (0.1 ml of PPD or 0.1 to 0.2 ml of BCG) is best performed on the inner
surface of the pinna and read every 48 to 72 hours (not earlier). The erythema that reabsorbs at that
time is a negative test result. Severe erythema with central necrosis progressing to ulceration at 10 to
14 days is significant. Ulceration after 18 to 21 days can occur in normal dogs. This test is not reliable
in cats. [15]]
Affected animals may show signs of respiratory and/or gastrointestinal diseases, generalised
lymphadenopathy or nodular skin disease with regional lymphadenopathy.
2.4. DIAGNOSIS
Because organisms tend to be numerous, they can be visible and aspirated mass, white blood
cells in peripheral blood and bone marrow and in various tissues. In specimens stained with Wright or
Diff-Quik spots, the body is rod-shaped, refractile. Acid-fast spots are necessary to positively highlight
the body. Differentiation of this organism from other mycobacterial species requires culture or
polymerase chain reaction (PCR).
2.5. CLINICAL MANAGEMENT OF TUBERCULOSIS
Dogs and cats with TB caused by M. tuberculosis and M. bovis can be point sources of
infection for humans and other animals and should be destroyed. M. microti was investigated in the
3
1940s for its potential as a human tuberculosis vaccine, and although rare human infections have been
described, it poses little risk to humans.
Since M. avium is abundant in the environment, treatment of infected animals is reasonable,

provided that all persons in contact are immunologically normal and excellent hygiene is practiced.
Most details about MAC TB treatment are found for the cat. For maximum efficacy and to prevent
resistance development, initial intercurrent use of three antimicrobials for a period of 2 months is
recommended, followed by a follow-up phase of two for a further 6 months.
Current practice involves initial combinations with rifampin (10-20 mg/kg once daily), a
fluoroquinolone and clarithromycin (5-10 mg/kg every 12 hours) or azithromycin (7-15 mg/kg once
daily) and a continuation period using rifampin and either a fluoroquinolone or
clarithromycin/azithromycin. Among fluoroquinolones, lack of efficacy of older agents including
ciprofloxacin and enrofloxacin is reported and should not be used in MAC. In infections
Marbofloxacin (2.75 mg/kg once daily) is still quite useful. New generation fluoroquinolones such as
moxifloxacin and pradofloxacin are likely to be much more effective.
Other potentially useful drugs include clofazimines (4-8 mg/kg once daily) and doxycycline
(10 mg/kg every 24 hours). Again, two or three of these alternative medicines should be used
simultaneously. Liver function should be monitored during treatment with rifampin. The course of
treatment is long and should be continued for a long time after the resolution of all clinical signs of
the disease.
3. FELINE LEPROSY
Feline leprosy is a granulomatous, nodular, cutaneous infection of cats with acid-fast bacilli that are
difficult or impossible to cultivate. Molecular methods are now available to help identify organisms
associated with these infections, and the nature of feline leprosy has become much clearer. Two forms
are recognized: a syndrome in young adult cats caused by infection with the rat eprose bacillus, M.
lepraemurium, and syndromes in older cats associated with Mycobacterium visibile (in the United
States) and a new unnamed mycobacterial species (in Australia and New Zealand). Recently, infection
with the new species, Mycobacterium sp. Tarwin strain, which causes diseases with characteristics of
both syndromes, was reported in a localized area in rural Victoria, Australia. [8]]
4
M. lepraemurium is the cause of murine leprosy, and feline infection with this organism is
thought to result from the bites of infected rodents. Infection is usually seen in adult males younger
than 5 years of age, but can occur in older cats that have an increased susceptibility due to concomitant
disease or genetic makeup. The initial lesion is a focal mass comprising a subcutaneous granuloma.
Additional lesions develop and can be up to 4 cm in diameter. Growth can be quite rapid, with
a spread to surrounding areas, including regional lymph nodes. The lesions tend to remain localized
initially, but may, in some cases, become widespread. There may be ulceration of larger masses and
the formation of abscesses or fistulas that show no signs of healing. Lesions are mainly found on the
head and limbs, sometimes with small lesions on the nose, lips and tongue. They are painless and there
is generally no systemic disease. The disease has been reported in New Zealand, Australia, Britain,
France, Italy, the Netherlands, the United States and Canada. Usually, clinical disease has a long
incubation period, with recognition of the disease in winter after exposure in summer.
[20]
In Australia, cats older than 9 years have been shown to develop generalised nodular disease.
The disease develops slowly over months to years, and nodules do not ulcerate. Analysis of 16S rRNA
amplicons from lesions in several cases showed the greatest nucleotide identity with M. leprae,
Mycobacterium haemophilum and Mycobacterium malmoense. A very slow-growing mycobacterial
species was isolated from a single case. This appears to be a new mycobacterial species. In western
parts of Canada and the United States, a different syndrome described as "feline multisystem
granulomatous mycobacteriosis" associated with diffuse skin disease and widespread dissemination
to internal organs and caused by M. visibile has been described.
Recently, infection with Mycobacterium sp. Tarwin strain has been described in Victoria,
Australia, causing diseases with features of both of the above syndromes. Both young and old cats are
affected by lepromatous lesions on the head and limbs, suggestive of traumatic pathogenesis. The
disease follows an indolent and progressive course. [7]
3.2. DIAGNOSIS
The diagnosis is confirmed on the basis of history, physical findings and detection of acid-fast
bacilli in smears prepared from needle aspiration, crushed preparations of biopsy samples and
5
histological sections (modification of ZN or Fite-Faraco). Such preparations contain AFB easily

demonstrably surrounded by variable granulomatous to pyogranulomatous inflammation. In Diff-
Quik-stained smears, mycobacteria can be recognized as bacilli with negative staining in macrophages
and giant cells. Tissue homogenizers should also be presented to culture to identify slow-growing
species, including M. avium complex, M. genavense and tuberculosis-causing species (M. bovis, M.
microti), which can cause identical clinical presentations, and eliminate tuberculosis M. If positive,
such cultures can then be used to determine susceptibility in vitro. Since causative organisms are
fastidious, culture is usually negative, and identification requires PCR amplification and nucleotide
sequencing of gene fragments from fresh, frozen, freeze-dried tissue specimens; This has the added
benefit of providing quick results. Formalin fixed tissues are sometimes suitable for PCR studies, as
long as the fixative is in contact only with the tissue specimen for less than 24 hours.
Histopathological examination may reveal two types of reactions. One is the tuberculoid
response with caseous necrosis and relatively few organisms (paucibacillary), with AFB often only in
areas of necrosis. These epithelioid granulomas are usually surrounded by areas of lymphocytes,
which are usually aggregated around vessels. The second type of reaction (lepromatous leprosy) is a
granuloma composed of solid sheets of large foamy macrophages containing a large number of AFB
(multibacillary disease). The organisms are grouped into globes in a parallel stacking arrangement.
Multinucleated giant histiocytic cells often contain bacilli, and lymphocytes and plasma cells can
surround the vessels. Many polymorphonuclear leukocytes may be present and make the lesion
resemble a pyogranuloma. The lepromatous reaction generally indicates a weak immune response of
the host.
Differential diagnostic considerations include TB; granulomas due to opportunistic

mycobacteria or foreign organisms; mycotic infections such as kerion, mycetoma, and
pheohiphomycosis; chronic bacterial infection; and neoplasms such as mast cell tumors, carcinomas,
and lympherreticular tumors. [3]
3.3. CLINICAL MANAGEMENT
Wide surgical excision is the treatment of choice when there is early diagnosis and lesions are
localized. Surgery must be combined with antimicrobial therapy that begins before surgery and
provides effective tissue levels during and after surgery to ensure first-line healing. Combination
therapy involving two or three antimicrobials is considered to be the most effective.
6
Clofazimine (up to 10 mg/kg once daily orally; typically 25-50 mg every 1 to 2 days) has the
best reported success rate for M. lepraemurium infections. This combined agent with clarithromycin
(62.5 mg twice daily) or rifampin (10-15 mg/kg once daily) has been recommended as optimal therapy
for feline leprosy caused by Australia's new mycobacterial species. The choice of drugs should take
into account side effects in individual cats. Treatment should be for several months and at least 2
months after resolution of the lesion. The lesions have been reported to resolve spontaneously in some
cats with true murine leprosy.
4. OPPORTUNISTIC GRANULOMAS
4.1. ACTINOMYCOSIS
Actinomycosis is a rare pyogranulomatous or suppurative disease of many species caused by

Actinomyces organisms. Actinomyces odontolyticus, Actinomyces viscosus, Actinomyces meyeri,
Actinomyces hordeovulneris , Actinomyces bowdenii and Actinomyces canis have been suggested
as causes. They are gram-positive, non-acid-fast, catalase-positive, filamentous anaerobic rods, which
are commensal opportunistic inhabitants of the oral cavity and intestine. Infection arises from trauma
and contamination of penetrating wounds, especially those involving foreign bodies. Hunting or field
dogs in hot climates are most commonly affected. It takes months to 2 years for signs to develop after
injury; However, organisms can be found in the exudate within 2 weeks. The typical clinical lesion is
a subcutaneous swelling or abscess of the head or neck, thoracic, paralumbar or abdominal region.
The lesion is usually delicate and may or may not have drainage routes. Paralumbar lesions are usually
a direct extension of retroperitoneal involvement. Other forms include osteomyelitis and empyema.
Drainage pathways (similar to mycetoma) can discharge a thick yellowish-gray or thin hemorrhagic
melting exudate that may or may not contain yellow sulfur granules. [12]]
Figure 3.1. Actinomicoza felinã [https://commons.wikimedia.org/wiki/File:Feline_Actinomycosis.JPG].
7
Figure 3.2. Actinomicoza felinã [https://commons.wikimedia.org/wiki/File:Feline_Actinomycosis.JPG].
The diagnosis is made by anaerobic culture (may require 2-4 weeks), direct smears, fine-needle
aspiration and biopsy using special spots (Gram, Brown-Brenn or Gomori methenamine silver). No
method is completely reliable, and cytological study seems to be the most effective. Histopathological
examination reveals nodular to diffuse dermatitis, panniculitis, or both due to suppurative or
pyogranulomatous inflammation. Tissue grains (sulfur granules) are present in about 50% of cases.
The granules are basophilic and often have an eosinophilic periphery (HoeppliSplendore material).
Gram-positive, non-acid-fast, filamentous, occasionally beaded organisms are found in granules, but
are not easily visible in common H&E preparations. Actinomycosis must be differentiated from
nocardiosis, a disease to which it closely resembles. The most successful treatment involves surgical
excision, plus a long course of antibiotics. High-dose penicillins (e.g., penicillin, amoxicillin,
oxacillin) are the optimal empirical treatment of choice. Other medications that may be effective
include clindamycin, erythromycin, cephalosporins, chloramphenicol, and tetracycline. Treatment
should continue for at least 1 month after complete remission and usually lasts 3 to 4 months. [28]]
4.2. ACTINOBACILLOSIS
Actinobacillosis is a rare disease of several animal species caused by Actinobacillus lignieresii.

It resembles actinomycosis in many of its cutaneous manifestations, but the causative organism is a
gram-negative aerobic coccobacillus that does not survive long outside the host animal. Clinical
lesions are bites, wounds or lesions around the face and mouth. The infection develops over weeks to
months, and its course is long. Clinical features include single or multiple abscesses with thick walls
of the head, mouth, neck and limbs. They discharge a thick, white to odorless green pus with soft
yellow granules.
Diagnosis is based on aerobic cultures of pus, direct smears or biopsy of affected tissues.
Histopathological examination reveals diffuse nodular dermatitis, panniculitis, or both due to
8
suppurative or pyogranulomatous inflammation. Tissue grains (sulfur granules) are usually present.
The berries are basophilic, surrounded by eosinophilic material Hoeppli-Splendors. Special stains
(Gram or Brown-Brenn) are required to demonstrate Gram-negative organisms. Clinical management
includes surgical removal or drainage and curettage. Sodium iodide (40 mg/kg (dog), 20 mg/kg (cat)
orally every 12 hours) and high doses of streptomycin or sulfonamides have been suggested for
therapy. The body is sensitive to tetracycline and chloramphenicol.
4.3. NOCARDIOSIS
Nocardiosis is a rare disease characterized by pyogranulomatous and suppurative infection of

the skin or lungs by widespread dissemination and caused by Nocardia spp. In recent times, the
spectrum of this genus has expanded, and some species have changed. The cells of the organisms
involved include the Nocardia asteroid complex, composed of types I-VI and including Nocardia
nova (type III) and Nocardia farcinica (type V), Nocardia brasiliensis and Nocardia otitidiscaviarum
(formerly Nocardia caviae), which are common soil saprophytes that cause infection through wound
contamination, inhalation and ingestion, especially in animals immunocompromised. Nocardia are
gram-positive filamentous aerobes that branch. With the exception of N. brasiliensis, their
geographical distribution is worldwide.
N. nova has been isolated in pure culture from cats with skin swelling and drainage routes and
appears to be the main species affecting cats. [11]]
Clinical features are indistinguishable from those seen in actinomycosis and include cellulitis,
ulcerated nodules and abscesses that often develop draining sinuses. Lesions usually occur in areas of
injury, especially on the limbs and legs, and are often accompanied by lymphadenopathy. Cats often
have lesions on the ventral abdomen that resemble panniculitis or opportunistic mycobacterial
infection. Piotrax may be present, along with other systemic signs such as weakness, anorexia, fever,
depression and dyspnoea, and neurological signs may be present. Hypercalcemia may be present and
affect the kidney function of the animal.
9
Figure 3.3. Inguinal region during hospitalization (October 2015), [Polina Vishkautsan, 2020]
The diagnosis is made by direct smear by fine needle aspiration, aerobic culture and biopsy.
Histopathological study reveals nodular to diffuse dermatitis, panniculitis, or both, with or without
tissue grains. Special stains (Gram and Brown-Brenn) are needed to demonstrate organisms. Nocardia
spp. can be distinguished from Actinomyces spp. since they are partially acid-fast (with modified Fite-
Faraco stain) and usually branch at right angles.
Clinical management includes surgical drainage of infected tissues, but antibacterial therapy is
mandatory. Nocardial organisms exhibit variable sensitivity to antibiotics, and the correlation between
in vivo and in vitro results varies. [14]] For example, in a number of feline cases in Australia, N. nova
was susceptible to clarithromycin, erythromycin, amikacin, trimethoprimsulfamethoxazole,
cefotaxim, imipenem and minocycline, while N. farcinica was resistant to clarithromycin and
erythromycin. Where possible, susceptibility data should be obtained on a case-by-case basis. If the
body cannot be isolated, drugs that may be empirically effective include drugs, potentiated
sulfonamides, erythromycin, clarithromycin, cephalosporins, chloramphenicol, tetracyclines and
various parenteral drugs. Treatment should be continued for at least 1 month after clinical remission.
Early vigorous treatment when lesions are localized improves the likelihood of healing. [19]]
5. BRUCELLOSIS
Brucellosis is a systemic bacterial infection caused by Brucella canis. Despite widespread
dissemination in the body, systemic signs of the disease are rare, as are skin lesions. Brucellosis can
produce secondary scrotal dermatitis resulting from licking the skin. Some cases can lead to necrosis
of the testicle, with severe inflammation of the entire scrotum and draining ulcers. B. canis was
isolated from exudate. B. canis was also isolated from a 15-month-old female laboratory beagle with
chronic exudative lesions that resembled aclal lick dermatitis. Over a period of 16 months, the extent
10
of painful lesions developed on the legs. [26]] The lesions were hyperemic, edematous and
granulomatous, with an irregular pitted surface. A blood-purulent exudate was present, and regional
lymph nodes were enlarged. Histological examination revealed dermal, subcutaneous and tendinous
edema, pronounced lymphoid nodules, a prominent infiltration of macrophages, plasma cells and
scattered lymphocytes and neutrophils. Enlarged lymph nodes were characterized by sinusoid
histiocytosis and umbilical cord medullary plasmacytosis. These findings are typical for tissue
response to brucella infection. The diagnosis is supported by the results of serological examination
and confirmed on culture. [2]
Figura 4.1. Brucella la microscop, [Carolyn R. Gold, 2015]
Treatment of canine brucellosis should not be carried out lightly, as the infection can spread to
humans and is not easy to eradicate in the dog. Affected dogs should be removed from breeding
programmes and neutered if possible. Although the body shows in vitro sensitivity to tetracyclines,
chloramphenicol, aminoglycosides, spectinomycin, rifampin, ampicillin, sulfonamides and
quinolones are common when a particular drug is used individually for a single course of treatment.
The highest success rate requires the use of multiple drugs. Synergism between tetracyclines and
fluoroquinolones and aminoglycosides and sulfonamides have been demonstrated.
6. LYME
Lyme borreliosis is a complex multisystem disorder caused by the spirochete Borrelia
burgdorferi. The body is transmitted by hard-shelled ticks of the genus Ixodes. Other ticks, flies, fleas
and mosquitoes have been found to house the body, but the vector status of these arthropods and
insects is uncertain. In all species, the predominant sign of Lyme borreliosis is polyarthropathic. In
humans, an expanding feature of the annular macula or papule (erythema chronicum migrans)
develops within 1 to 2 weeks at the site of the tick bite. Although lesions of chronic erythema migrans
11
have been reported in dogs, no histological studies have been conducted to confirm this diagnosis. In
experimental dogs, erythema was not observed. Undoubtedly, such lesions appear, but they are hidden
by the hair cape. Because Lyme borreliosis is a systemic immune complex disorder, skin lesions other
than erythema chronicum migrans might occur but are apparently rare. In a report of 110 seropositive
dogs, 4 had hives skin lesions, rashes or wet dermatitis. Another investigator reported recurrent
tetracycline-responsive lesions of pyotraumatic dermatitis in seropositive dogs. The diagnosis of Lyme
borreliosis is corroborated by a serological study, which can confirm exposure to B. burgdorferi, but
cannot prove the disease. Seropositive dogs with clinical abnormalities considered from Lyme disease
are generally treated with doxycycline (10 mg/kg once daily for 1 month). Early treatment is essential
to prevent irreversible changes to joints. [16]]
7. AXILLARY TRICHOMYCOSIS
Trichomycosis axillaris is a bacterial infection of human hair shafts. It mainly involves axillary
and pubic hair. A similar infection with Corynebacterium spp. has been reported in a beagle. The
animal had diffuse, irregular, uneven alopecia, which affected the neck and flank regions. There was
no dermatitis. In the areas involved, some hairs were broken, and some hairs displayed small hard
nodules. Masses of bacteria enveloped the hair in those locations. The nodules developed on the
inoculated hair and eventually involved the entire hair. Inoculation of normal hair from other dogs
produced no alopecia and no bacterial growth. This is not a fungal disease, despite its name, nor have
fungal elements been seen or isolated on culture. This is an unusual and inconsistent disorder that
should easily respond to hair cutting and frequent use of antibacterial shampoos.
Figure 6.1. (a) Medium strength enlargement of plucked axillary hairs, (b) High strength enlargement of plucked
axillary hairs, [Hong Kong J. Dermatol. Venereol, 2019]
12
8. PSEUDOPYODERMA
8.1. PYODERMA OF THE CALLUS
Calus dermatitis is a secondary infection of a callus subjected to repeated trauma or soaked

without mandatory changes in the environment. The callus is the initial response to trauma. The
continued trauma, and the proliferative reaction of the skin that follows, produce cracks in the callus
that lead to a folding dermatitis. Additional trauma causes epidermal breakdown, ulceration of
pressure points and fistulas. Injuries are most common on the joints of the rooster and elbow of giant
breeds such as Great Danes, St. Bernards, Newfoundlands and Irish wolfhounds. Sternal calluses on
the chest of dachshunds, setters, pointers, boxers and Doberman pinschers can also become ulcerated
and secondary infections. Often there is no specific bacterial flora involved in this infection, although
staphylococci can be isolated. Pressure point granulomas, which contain loose hairs, may develop.
Ulcerated or fistulated lesions can be deeply infected, and exudative cytological examination should
be performed in all cases. The surface must be cleaned and the lesion firmly squeezed out before
sample collection. In many cases, pieces of hair shafts appear on the surface. Pyogranulomatous
inflammation is common.
8.1.1. Clinical management

Special attention should be paid to alleviating trauma so that tissue can heal. This can be
achieved through the use of beds with water, special bedding, pads for different parts of the body or a
combination of these measures. In severe cases, surgical excision of the callus may be indicated. This
is a major surgery with a difficult postoperative course, and the reader refers to soft tissue surgery
texts for treatment details.
Mild surface inflammation and folding dermatitis can be relieved by daily jacuzzi baths in warm water.
Distal lesions may be subject to soaking in a bucket. In the case of imbedded hair trees, a slightly
hypertonic solution of magnesium sulfate (Epsom salts) (30 ml/L or 2 tablespoons/qt of warm water)
may be beneficial. In uninfected lesions, hydrotherapy is usually sufficient to cause healing. When
this is not possible, topical application of an antibiotic cream or preparation H, a preparation for human
hemorrhoids containing live yeast extract and shark liver oil, may be beneficial. Infected lesions
require a prolonged course of antibiotics. Six weeks or more of treatment is usually required. Because
the infected tissue will not return to its normal state with antibiotic treatment, the client is unable to
determine when the infection is resolved. Cytological examinations should be carried out every two
13
weeks. When there is no sign of infection, treatment should be continued for another 7 to 14 days.
Relapses are prevented through management changes. [17]]
Figure 7.1. Pyoderma la un caine atopic, [Tait Jennie, 2021]
8.2. JUVENILE CELLULITIS
Juvenile cellulitis (juvenile pyoderma, puppy strangulation, juvenile sterile granulomatous

dermatitis and lymphadenitis) is an uncommon granulomatous and pustular disorder of the face,
pinnae and submandibular lymph nodes, usually chicken. [9]
8.2.1. Cause and pathogenesis
The cause and pathogenesis are unknown. Heritability is supported by an increased occurrence
in certain breeds and family histories of the disease. Special stains and electron microscopic
examination of tissues do not reveal microorganisms, and cultures are negative. Attempts to transmit
the disease with the tissues of the lesions were unsuccessful. The appearance of sterile granulomas
and pustules that respond dramatically to glucocorticoids suggests an underlying immune dysfunction.
Responses of blastogenic lymphocytes to phytomitogens are suppressed in combination with a serum
suppressive factor. The age of onset and the frequent occurrence of vaccinations before onset have
also made vaccine reactions a cause for concern. What would be the trigger to the disease, is apparently
self-limiting; Dogs can resolve spontaneously over 1 to 3 months. [24]]
8.2.2. Clinical features

Puppies are usually affected between the ages of 3 weeks and 4 months, and one or more
puppies in a litter may have this condition. Several reports have been reported of dogs with older onset
14
of age and typical injuries and findings. Although numerous breeds have experienced the disorder,
golden retrievers, dachshunds and Gordon settlers appear to be predisposed. Other breeds such as the
English Cocker Spaniel, Labrador Retriever and Lhasa apso may be predisposed, but better studies
are needed to validate the breed's observations, as many breeds have been affected. No sexual
predilection was reported. [23]] The initial abnormality observed by most owners is an acutely swollen
face, especially the eyelids, lips and muzzle. Physical examination at this time reveals striking
submandibular lymphadenopathy. In some cases, lesions may be limited to swollen lymph nodes,
while other dogs in the affected litter have concomitant classic skin lesions. Within 24 to 48 hours,
papules and pustules develop rapidly. The affected areas are edematous, and lesions usually progress
to fistulation, leakage and crusting. Lesions are most common on the lips, muzzle, chin, bridge of the
nose and periocular area. Otitis externa is common, and pinnae are frequently thickened and
edematous. Puppies occasionally have concomitant sterile pyogranulomatous panniculitis with firm
to fluctuating subcutaneous nodules, which may be painful or fistulated. These nodules occur mainly
on the trunk or in the preputial or perianal areas. The affected skin is usually painful, but not itchy.
Some dogs may be lethargic and depressed, but the lack of marked anorexia and pyrexia is a
distinguishing feature from severe pyoderma secondary to generalized demodicosis and sterile nodular
panniculitis.
Older dogs have more systemic signs and tend to be pyrexic. Lameness, arthritis, and paresis
may be observed. In one case, paresis was associated with sterile inflammation of the cerebrospinal
fluid. Two Shetland shepherd puppies with panniculitis had neurological signs consistent with spinal
cord injuries. One case was reported with juvenile cellulitis 2 weeks after hypertrophic osteodystrophy
was diagnosed. [29]]
8.2.3. Diagnosis
In very early cases, the differential diagnosis is angioedema. However, angioedema is not
accompanied by marked regional lymphadenopathy or systemic diseases. After the appearance of
dramatic inflammatory lesions, differential diagnosis includes staphylococcal dermatitis, demodicosis
and adverse skin reaction of the drug. Cytological examination of papulopustular lesions reveals
pyogranulomatous inflammation without micro-organisms, unless a secondary infected ulcerated area
is taken. Carefully made cultures are negative. Biopsies of early lesions reveal several discrete or
confluent granulomas and pyogranulomas consisting of clusters of large epithelioid macrophages with
15
neutrophil cores of variable size. The sebaceous glands and epitrichial sweat glands can be erased. In
subsequent severe lesions, suppurative changes in the superficial dermis in and around the hair
follicles, ruptures and in the underlying panicle are predominant. [9]
8.2.4. Clinical management

Early and aggressive therapy is indicated because scarring can be severe. High doses of
glucocorticoids are the treatment of choice. Oral prednisone or prednisolone (2 mg/kg once daily) is
given until the disease is inactive (usually within 14-28 days). Dogs with intercurrent truncated
panniculitis may require a longer course of treatment to resolve all lesions. Some dogs respond much
better to oral dexamethasone (0.2 mg/kg once daily). If there is cytological or clinical evidence of
secondary bacterial infection, bactericidal antibiotics (cephalexin, cefadroxil, amoxicillin clavulanate)
should be administered simultaneously. Cyclosporine with prednisone was also effective.
Interestingly, griseofulvin 14.2 to 34 mg/kg every 12 hours was reported effective within 3 weeks of
treatment in 6 out of 6 cases. [24]] The authors speculated that this was due to the drug's
immunomodulatory effect. Topical therapy, especially wet soaking with aluminum acetate or
magnesium sulfate, is helpful, but chickens often find unwanted apprehension and pain, and the
struggle and stress associated with topical therapy become counterproductive. Relapses are less
common. [25]]
Figure 7.2. Juvenile cellulitis in dogs, papular with pustules and wet exudate on the muzzle and periocular region
of the puppy,
[https://materiale.pvgazeta.info/revista-44/caini-anticelulita-juvenili-juvenil-piodermite.html]
8.3. OTHER PYODERMA-LIKE DERMATOSIS
a. Acne
b. Intertrigo
16
c. Linear IgA pustular dermatosis

d. Sterile panniculitis
e. Pemphigus erythematosus
f. Pemphigus foliaceus
g. Sterile eosinophilic pustulosis
h. Sterile pyogranuloma syndrome
i. Subcornish pustular dermatosis
j. Eosinophilic facial folliculitis and furunculosis
9. CUTANEOUS WOUND
The skin forms a protective barrier without which life would be impossible. This defense has
three components: physical, chemical, and microbial. Hair forms the first physical line of defense to
prevent pathogens from coming into contact with the skin and minimize external physical or chemical
insults to the skin. Hair can harbor microorganisms. The stratum corneum forms the basic physical
barrier of defense. Its thick, tightly packed keratinized cells are permeated by an emulsion of sebum,
sweat, and epidermal lipids that is concentrated in the outer layers of keratin, where it functions as a
physical barrier. In addition to its physical properties, the emulsion provides a chemical barrier to
potential pathogens. The water-soluble substances in the emulsion include inorganic salts and proteins
that inhibit microorganisms. Sodium chloride and antiviral glycoprotein interferons, albumin,
transferrin, complement, glucocorticoids and immunoglobulins are in emulsion. [18]] The surface
lipids of the skin are not constant in quantity or composition, and sebum is constantly broken down
by the resident flora into free fatty acids, some of which kill bacteria and fungi. In normal dog skin,
IgG and IgM are found in the interstitial spaces in the dermis, dermal blood vessels and hair papillae;
IgM is found in the BMZ of the epidermis, hair follicles and sebaceous glands; IgA is found in
epitrichial sweat glands (suggesting that it functions as a cutaneous secretory immunoglobulin); and
C3 is found in the stratum corneum and dermal interstitial spaces. In cats, IgM was detected at the
BMZ of the nasal plane. [13]] The polymeric immunoglobulin receptor, the secretory component, is
expressed and synthesized by keratinocytes and secretory and ductal epithelium of sweat glands. This
receptor can interact with IgA and IgM; This interaction may be a mechanism to protect the skin from
microbial agents and foreign antigens. Antimicrobial peptides (AMPs), including catelicidins and β-
defensins are small cationic peptides that participate in innate immunity against a wide variety of
pathogens. AMPs have been found in the epidermis, hair follicles, and sebaceous glands of healthy
17
dogs and cats. [27]] There is a relationship between the acidity of the skin surface ('acid mantle') and
its antimicrobial activity. The buffering ability of the skin surface against external and internal
acidifying and alkalizing effects depends on several buffering systems, including lactic acid in sweat,
ammonia in sweat, and amino acids. In general, inflammation causes the pH of the skin surface to
shift from acidic or neutral to alkaline. The pH of the skin surface is usually measured by a glass
electrode technique (pH meter). [5]] The single factor with the greatest influence on the skin flora is
the degree of hydration of the stratum corneum. Increasing the amount of water on the surface of the
skin (increase in ambient temperature, increase in relative humidity or occlusion) increases the number
of microorganisms enormously. In general, moist or greasy areas of skin support the largest
populations of microorganisms. In addition to effects on microflora, epidermal water content appears
to be important in regulating epidermal growth, keratinization, and permeability. Skin hydration
studies are usually performed with an evaporimeter and/or corneometer. [6] The balance between
keratin and water is essential for keratinized tissues to perform their role correctly. The stratum
corneum can increase its thickness by over 100% by taking up water. By comparison, hairs can only
increase their thickness by about 15%. This difference can be explained by the relatively low
concentration of cystine in the stratum corneum compared to that of hairs. Transepidermal water loss
(TEWL) is the evaporation of water vapor from the surface of the skin and reflects the integrity of the
stratum corneum. A characteristic of healthy skin is that the relationship between TEWL and hydration
(water retention capacity) remains directly proportional. In pathological skin, the correlation between
TEWL and the water content stratum corneum shows an inverse relationship due to the barrier function
of damaged skin or changes in keratinization (increased tewl, decreased hydration). In dogs, basic skin
hydration was different in different places and lower in dry skin than normal skin. In normal
Newfoundlands, the relative moisture of the coat was about 50% in the chest wall, and lateral thigh,
and about 70% below the tail and on the ventral neck. No differences in relative humidity were
observed with different coat colors or between males and females, but relative humidity under the tail
and on the ventral neck increased with age. In dogs subjected to artificial heat or bright sun, the average
skin temperature rose from around 35°C to around 39°C and the water content of the coat almost
doubled. [4] The normal microflora of the skin also contributes to the skin's defenses. Bacteria, and
occasionally yeasts and filamentous fungi, are located on the surface of the skin, in the superficial
layers of the epidermis (especially in the intercellular spaces of the stratum corneum) and in the
infundibulum of the hair follicles. The flora can change with different skin environments, which
include factors such as pH, salinity, humidity, albumin level, and fatty acid levels. The close
18
relationship between host and microorganisms allows bacteria to occupy microbial niches and inhibit
colonization by invading organisms. Interactions between cutaneous microbes can be classified as
follows. [22]]
One-sided and reciprocal antagonism ("interference"). Production of growing conditions by

one organism that are unfavorable for another. Proposed mechanisms include nutrient intake,
generation of unfavorable redox potential or pH, occupation of tissue receptors or production of
inhibitors (enzymes, antibiotics or bacteriocins).
Mutual enhancement ("synergism"). Nutrients (amino acids) made available by the actions of
one organism can allow "cross-feeding" by others. A possible example of this phenomenon is the
frequent finding of increased populations of S. pseudintermedius and M. pachydermatis in the skin of
lesions.
Neutral association Keratinocytes synthesize various antimicrobial peptides (catelicidine and

βdefensins) that form a barrier to innate protection of the host against microbial pathogens (bacteria,
fungi, viruses, protozoa). These peptides appear to function in regulating cell proliferation,
extracellular matrix production, and cellular immune responses.
It is believed that some organisms live and multiply on the skin, forming a permanent
population; These organisms are known as residents and can be reduced in number, but not eliminated
by frostbite methods. Resident skin biotas are not evenly spread over the surface, but are aggregated
into microcolonies of various sizes. Other microorganisms, called transient, are just contaminants
acquired from the environment and can be removed by simple hygiene measures. A third class of
organisms whose behavior falls between that of residents and passers-by were called nomads. These
organisms are able to colonize and reproduce for short periods of time and can take advantage of
changes in the microenvironment of the skin surface. Thus, they become frequently established and
proliferate on the surface of the skin even deeper. Most studies on the normal microbial biota of cat
and dog skin have been strictly qualitative. The skin is a highly effective environmental sampler,
providing a temporary refuge and pathway station for all kinds of organisms. Thus, only repeated
quantitative studies allow the researcher to reliably distinguish between resident and transient bacteria.
It is still controversial about which microorganisms are truly resident on canine and feline skin, since
most studies have been short-term and have failed to describe the dynamic situation.
19
In cats, most studies indicate that Micrococcus spp., coagulase-negative staphylococci, α-

hemolytic streptococci and Acinetobacter spp. They are normal skin residents. Of coagulase-negative
staphylococci, Staphylococcus simulans have been isolated most frequently and is likely a normal
resident. [1] Staphylococcus capitis, Staphylococcus epidermidis, Staphylococcus haemolyticus,
Staphylococcus hominis, Staphylococcus sciuri, and Staphylococcus warneri have been isolated
primarily from household cats, as opposed to catty cats , suggesting that cats acquire these staph
species through human contact. Among coagulase-positive staphylococci, S. aureus and S.
pseudintermedius were isolated more frequently from household cats than from catty cats. Cats may
also be asymptomatic carriers of dermatophyte Microsporum canis. In dogs, most studies indicate
that Micrococcus spp., coagulase-negative staphylococci, α-hemolytic streptococci and Acinetobacter
spp. They are normal skin residents.
Coagulase-negative (Staphylococcus schleiferi schleiferi) and coagulase-positive staphylococci (S.
epidermidis, Staphylococcus xylosus, Staphylococcus schleiferi coagulans and S. pseudintermedius)
are regularly isolated from the skin and hair cape of normal dogs, and there are no significant
quantitative or qualitative differences in staphylococci of skin and hair or between staphylococci
species and the body. The, nasal and oral mucocutaneous regions are also important sites of transport
S. pseudintermedius. S. pseudintermedius is a resident of the mucosa and is spread to the skin and
haircoat by grooming work. Propionibacterium acnes can also be found on the skin surface and in
dog hair follicles in sufficient numbers to be considered part of the normal canine biota. In addition,
it is well known that many saprophytic fungi – including M. pachydermatis, Alternaria spp.,
Aspergillus spp., and Penicillium spp. – can be grown from the skin and hair of normal dogs and cats.
[21]]
Studies in normal dogs have shown the following: the largest population sites for Micrococcus
spp. and coagulase-negative staphylococci were on the surface of the skin, and these organisms could
be considered residents; Clostridium spp.were present on the surface of the skin and hair follicles,
and could be considered residents ; and gram-negative aerobics were present on the surface of the
skin, in hair follicles and in greater numbers on proximal hair shafts, indicating that they may be
residents. Interestingly, S. pseudintermedius was present in greater numbers on distal than proximal
hair shafts, but the organism was also present in greater numbers in the hair follicle than on the surface
of the skin. This suggests the possibility of two populations of S. pseudintermedius.
20
BIBLIOGRAPHY
Books, articles from specialized magazines

1. Abraham, JL, Morris, DO, Griffeth, GC, et al., 2007, Surveillance of healthy cats and cats with
inflammatory skin disease for colonization of the skin by methicillin-resistant coagulase- positive
staphylococci and Staphylococcus schleiferi ssp. schleiferi. Vet Dermatol.
2. Baldi, PC, et al., 1997, Diagnosis of canine brucellosis by detection of serum antibodies against and
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Vet J.
4. Chesney, CJ., 1997, The microclimate of the canine coat: The effects of heating on coat and skin
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5. Chikakane, K, Takahashi, H., 1995, Measurement of skin pH and its significance in cutaneous
disases. Clin Dermatol.
6. Elsner, P, et al., 1994, Bioengineering of the Skin: Water and the Stratum Corneum. Boca Raton, FL:
CRC Press.
7. Foley, JE, et al, 2005, Clinical, pathological and molecular characterization of feline leprosy
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8. Fyfe, JA, et al., 2008, Molecular Characterization of a novel fastidious Mycobacterium causing
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Blackwell Publications.
11. Hirsh, DC, Jang, SS., 1999, Antimicrobial susceptibility of Nocardia nova isolated from five cats
with nocardiosis. J Am Vet Med Assoc.
12. Hoyles, L, et al., 2000, Actinomyces canis sp. nov., isolated from dogs. Int Syst Evol Microbiology.
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15. Kramer, TT., 1978, Immunity to bacterial infections. Vet Clin North Am Small Anim Pract.
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diagnosis, treatment, and prevention. J Vet Intern Med.
17. Lloyd D., 2013, Bacterial skin diseases. In: Miller WH, Griffin CE, Campbell KL, eds. Muller &
Kirk’s Small Animal Dermatology. 7th edition. St. Louis, MO: Elsevier.
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Vet Science.
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cases. Aust Vet J.
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24. Park, C, Yoo, JH, Kim, HJ, et al., 2010, Combination of cyclosporin A and prednisolone for juvenile
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defensins in dogs with atopic dermatitis. Mol Immunol.
28. Welsh, O, et al., 1987, Amikacin alone and in combination with trimethoprim-sulfamethoxazole in
the treatment of actinomycotic mycetoma. J Am Acad Dermatol.
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Australian shepherd puppy. Can Vet J..
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1. *** https://commons.wikimedia.org/wiki/File:Feline_Actinomycosis.JPG , File: Feline
Actinomycosis.JPG, accesat 20.05.2023.
2. https://materiale.pvgazeta.info/revista-44/caini-anticelulita-juvenili-juvenil-piodermite.html,
Pvgazeta materials. Info Juvenile anti-cellulite dogs (juvenile pyoderma), veterinarian, accessed
20.05.2023.
3. https://microbe-canvas.com/diseases/actinomycosis/ , Actinomycosis, accessed 2023-05-19.
4. *** https://www.akc.org/expert-advice/health/brucellosis-dog-breeders-shouldnt-skip-testingforthis-
dangerous-disease/ , Brucellosis: Dog Breeders Shouldn’t Skip Testing for This Dangerous Disease,
American Kennel Club, accesat 21.05.023.
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https://medcomhk.com/hkdvb/details.asp?id=897&show=1234, Answers to Dermato-venereological
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Dermatologists., accesat 20.05.2023.
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https://bioone.org/journals/journal-of-feline-medicine-and-surgery-open-
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24

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Mycobacterial Granulomas, Opportunistic Granulomas and Other Bacterial Diseases

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UNIVERSITATEA DE ŞTIINŢELE VIEȚII

„REGELE MIHAI I AL ROMÂNIEI” DIN TIMIŞOARA

FACULTATEA DE MEDICINĂ VETERINARĂ

PROGRAMUL DE STUDIU LICENȚĂ

2. TUBERCULOZA: MYCOBACTERIUM TUBERCULOSIS,

2.1. CLINICAL FEATURES

The diagnosis is made by history, physical examination, X-ray, cytological evaluation,

Biopsy samples may show nodular to diffuse dermatitis due to pyogranulomatous

2.3. CLINICAL FEATURES

2.5. CLINICAL MANAGEMENT OF TUBERCULOSIS

Since M. avium is abundant in the environment, treatment of infected animals is reasonable,

3.1. CLINICAL FEATURES

histological sections (modification of ZN or Fite-Faraco). Such preparations contain AFB easily

Differential diagnostic considerations include TB; granulomas due to opportunistic

3.3. CLINICAL MANAGEMENT

Actinomycosis is a rare pyogranulomatous or suppurative disease of many species caused by

Figure 3.1. Actinomicoza felinã [https://commons.wikimedia.org/wiki/File:Feline_Actinomycosis.JPG].

Figure 3.2. Actinomicoza felinã [https://commons.wikimedia.org/wiki/File:Feline_Actinomycosis.JPG].

Actinobacillosis is a rare disease of several animal species caused by Actinobacillus lignieresii.

Nocardiosis is a rare disease characterized by pyogranulomatous and suppurative infection of

Figura 4.1. Brucella la microscop, [Carolyn R. Gold, 2015]

Calus dermatitis is a secondary infection of a callus subjected to repeated trauma or soaked

8.1.1. Clinical management

Figure 7.1. Pyoderma la un caine atopic, [Tait Jennie, 2021]

8.2. JUVENILE CELLULITIS

Juvenile cellulitis (juvenile pyoderma, puppy strangulation, juvenile sterile granulomatous

8.2.1. Cause and pathogenesis

8.2.2. Clinical features

8.2.4. Clinical management

8.3. OTHER PYODERMA-LIKE DERMATOSIS

c. Linear IgA pustular dermatosis

One-sided and reciprocal antagonism ("interference"). Production of growing conditions by

Neutral association Keratinocytes synthesize various antimicrobial peptides (catelicidine and

In cats, most studies indicate that Micrococcus spp., coagulase-negative staphylococci, α-

Books, articles from specialized magazines

Web site- uri

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