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in Domestic Chickens from Selected
*Armauer Hansen Research Institute, PO Box 1005, Addis Ababa, Ethiopia
Faculty of Veterinary Medicine, Addis Ababa University, P.O. Box 34, Debre Zeit, Ethiopia
Unit of Infectious Diseases, Department of Medicine, Karolinska Hospital, 171 76 B-2, Stockholm, Sweden
ΆCurrent address: The University of Tennessee, College of Veterinary Medicine, Department of Comparative Medicine, 2407 River Drive, Rm. A205, Knoxville, TN 37996-4543, USA
§International Livestock Research Institute, Animal Genetic Resources, PO Box 5689, Addis Ababa, Ethiopia
**Institute of Pathobiology, Addis Ababa University, PO Box 1176, Addis Ababa, Ethiopia
KEY WORDS: Avian mycobacteriosis,
Domestic poultry are important natural hosts of Mycobacterium avium (MAC), especially in the traditional poultry management system in the tropics. Qualitative and quantitative studies on a total of 95 chickens from three agro-climatic areas in Ethiopia were examined for avian mycobacteriosis through postmortem examinations and tissue staining (haematoxylin & eosin and acid-fast staining). The mycobacteria species were isolated and identified by using mycobacteriologic culture and experimental infection for virulence assessment. Five of the 95 examined chickens (5.3%) had gross tuberculous lesions in different visceral organs. On histopathologic examination, the lesions showed granuloma with typical Langhans giant cells in which acid-fast bacilli were shown by acid-fast stain. The culture on pyruvate-enriched Lowenstein-Jensen slants revealed growth of colonies on samples from 6 (6.3%) of the 95 chickens. Experimental infection with the strains from culture resulted in death of 10 (83.3%) of 12 inoculated chickens 56 to 110 days after inoculation, indicating that the isolates may be virulent strains of MAC. On postmortem examination, the experimentally infected chickens showed similar tuberculous lesions to natural infection that was confined at the site of injection, on the liver, spleen and (in two subjects) small intestine. The inoculated organisms were recovered from the respective organs. Therefore, this study showed that a virulent strain of MAC infects domestic chicken in Ethiopia.
Avian mycobacteriosis, formerly known as avian tuberculosis (AT), is a bacterial disease of birds caused by slow-growing nonchromogenic, intracellular acid-fast bacilli, Mycobacterium avium, and Mycobacterium intracellulare usually from the Mycobacterium avium complex (MAC) group1,2 and just recently by Mycobacterium genavense (M. genavense).3 Its occurrence has been reported from various parts of the world and in many species of animals, including domestic poultry,49, pet birds,3,6,8,10 wild, and zoologic birds,2,69,11 swine,1,4,6,7,10,11,13 cattle,1,4,8,14,15 and humans.1,6,8,13 In humans, M. avium is capable of inducing a progressive and disseminated type disease that is relatively refractory to treatment both in HIV/AIDS patients16,17 and in normal hosts.18 The significance of avian mycobacteriosis in domestic chickens has diminished in many countries as a result of the introduction of more intensive production systems2,19 that encompass better nutrition, shelter, and hygiene and management practices. However, it remains a problem in extensive (traditional) production systems under which chickens scavenge for survival in unhygienic environments. This predisposes them for various infections, including avian mycobacteriosis.20,21
Diagnosis of avian mycobacteriosis in chickens depends on demonstration of MAC in dead birds or detection of an immune response, cellular or humoral, in live birds.2,7,19 When clinical signs of the disease are seen in a flock or typical lesions of tuberculous are present at necropsy, demonstration of acid-fast bacilli in smears or histopathologic sections made from affected organs is regarded as sufficient for positive diagnosis.7,19
If acid-fast bacilli are not found, but typical signs or lesions are present in the birds, culture of the organisms on artificial media such as Lowenstein-Jensen, Stonebrink, and Middlebrook agar must be attempted.22,23 Experimental infection is one of the oldest and most frequently used methods. In addition to chicken, mice, guinea pigs, hamsters, and rabbits have been used for such challenge experiments.8,22 In tropical countries such as Ethiopia, where laboratory facilities such as molecular techniques or chromatography are limited, experimental infection of chickens should confirm the virulence of the isolated culture organism.
In our previous study, we showed a significant relationship of cestode coinfection with M. avium and a significant difference in prevalence of infection by altitude.24 The purpose of this study was to determine the prevalence of MAC, isolate and identify virulent strains of MAC from domestic chickens from three defined geographical areas in central Ethiopia.
MATERIALS AND METHODS
Study Area and Animals
A cross-sectional study was made on avian mycobacteriosis in 95 randomly selected indigenous breed chickens25 reared under extensive system from three selected agro-climatic regions at high (n = 29), middle (n = 30), and low (n = 36) altitudes in central Ethiopia. Debre Berhan (high altitude) is a cool wet region located at an altitude of 2,780 m above sea level with mean annual temperature range of 6.3˚C to 18.8˚C. Sebeta (mid altitude) is a warm and wet region located at an altitude of 2,240 m above sea level, with a mean annual temperature range 15˚C to 21˚C. Nazareth (low altitude) is a warm and dry region located at an altitude of 1,300 m above sea level, with mean annual temperature range of 15˚C to 28˚C.25
A randomly selected 95 indigenous breed chickens 26 (29, 30, and 36 from high, mid, and low altitudes, respectively) of both genders and age groups (young and adult) were used. Age of the chicken was determined using information from the owners supported by observation of the bursa, thymus, and vitteline glands.22
A structured questionnaire survey was performed in parallel with direct observations to 40 individuals, the 20 households (6 from high-, 6 mid-, and 8 from low altitudes) who were directly responsible for the care of chickens. The other 20 individuals interviewed were from village markets (who were selling their own chickens raised in their own backyards) in all of the three agro-climatic areas based on their willingness. During antemortem examination, physical parameters (live weight, carcass weight, thigh circumference, and breast dimension) were measured, and clinical signs considered to be indicative of avian mycobacteriosis were recorded before the chickens were killed. Just before necropsy, antemortem examination was made for any abnormalities and clinical signs of any disease.
For postmortem examinations, the chickens were killed and opened according to the procedures of Zander and Mallison.27 At necropsy, all internal organs were examined and any observed gross lesions were recorded on necropsy card. Tissues from organs showing pathologic gross lesions were collected in 10% buffered formalin. Furthermore, tissues from liver, spleen, and pieces of intestine at different segments were taken for histopathology regardless of the presence or absence of lesions and for the reason that they can be highly affected by the MAC group. 2 The tissues were dehydrated in alcohol, cleared in xylene, and embedded in paraffin and cut into thin sections of 4 to 5 ΅m. These were stained with haematoxylin & eosin and acid-fast stains for microscopic examination.28
Experimental Infection of MAC Strains
Strain virulence was assessed by experimental infection on 6- to 8-week-old dual-purpose type indigenous breed chickens (two chickens for each of the six isolates) according to the methods described by Matthews and Collins.29 Standard suspensions of each colonial growth were prepared. Each suspension was stored in liquid medium at 70˚C, and the viable count was assayed shortly before use. These suspensions were then adjusted by dilution to obtain the required dose for animal inoculation. The number of viable units of injected bacilli was 1.57 ₯ 1042.5 ₯ 106 CFU viable bacilli intramuscularly. At postmortem examination of the experimentally infected chickens, acid-fast smears were made from parenchymatous organs showing macroscopic granulomatous lesions.
The prevalence rate of avian mycobacteriosis is defined as the number of cultures that are positive from the total number of animals examined expressed in percent. Culture is considered here as the determinant of MAC as it showed the acid-fast bacilli definitively and used as gold standard.31 Postmortem examinations and special staining in histopathology were also used to further confirm cases. Altitude-, sex-, and age-dependent prevalence were compared and analyzed by the chi-square test (FREQ procedures of the Statistical Analysis System).32
The structured questionnaire survey (qualitative data) has revealed that the flock size in one household could range from 5 to 45. The poultry were kept along with other species of animals, especially herbivores; the highest association was seen with cattle (75%) and shoats (45%). The chickens were left to scavenge freely in their homestead, with occasional provision of limited amount of supplementary grains during harvest season. At night, the chickens mostly perched in trees or higher places behind the homesteads. However, in a few cases, they were confined in locally constructed wooden or metal cages on raised platforms, to prevent predators. Chickens were raised by farmers with low income and poor socioeconomic status as a sideline occupation to crop agriculture. The age at first lay ranged from 8 to 10 months. Hens were kept for longer periods as long as they laid eggs. Therefore, they usually lived their normal lifespan. Chicken droppings were cleaned from the settings at long intervals, implicating poor hygiene.
Gross Pathological Lesions
A total of five (5.3%) of the 95 examined chickens had typical tuberculous lesions on three visceral organs, bone marrow, and on the lightly feathered skin at the caudal part of the body. From the 6 culture positive chickens, 5 (83.3%), 5 (83.3%), 2 (33.3%), 1 (16.7%), and 1 (16.7%) had lesions in the small intestine, spleen, liver, bone marrow, and skin, respectively (Table 1). In all of the chickens that have manifested gross lesions, more than one type of organ was affected (Table 2). One chicken that was culture positive from the mid-altitude area did not show any type of gross lesions. Chickens from the mid- and low-agro-climatic areas showed grossly discernible lesions on the small intestine and spleen at all times. A slight difference was seen between the occurrence of gross lesions in chickens from mid and low areas. The adult age group had a higher occurrence of gross lesions than the young age group (Table 1).
The lesions were grayish-yellow to grayish-white, pin-point
to irregularly round, and few to innumerable nodules measuring up to
2 cm in diameter raised above the surface of the affected organs. Calcification
was not seen in the nodules. Organs such as the spleen and liver were
enlarged to about twice the
The five chickens with grossly discernible lesions on histopathologic H & E staining have shown the presence of granuloma characterized by caseonecrotic cores that were surrounded by a broad ring of palisading epithelioid cells, macrophages, multinucleate giant cells with a moderate mixture of heterophils, lymphocytes, and plasma cells. Parallel staining with Ziehl-Neelsen on another slide from the same specimen revealed acid-fast rods in the central necrotic part of the granuloma.
Of the 95 chickens sampled from all agro-climatic zones, a total of 6 (6.3%) chicken, 2 (2.1%) from mid and 4 (4.2%) from low altitudes, had colony growths on sodium pyruvate-enriched Lowenstein-Jensen (L-J) slants (Table 1). The smooth and transparent colony variants stained poorly with Ziehl-Neelsen staining. No growth was seen from samples of chickens from high altitude. The smooth and transparent colony variants have shown poor staining when smears were prepared and Ziehl-Neelsen staining was done.
Distribution of gross lesion in different organs in experimentally infected chickens is given in Table 3. Organized, tuberculous nodules, which ranged in size from small pinpoint to 8 mm in diameter and were further confirmed by direct smear microscopy showing acid-fast bacilli, were designated as positive findings for avian mycobacteriosis. Such gross milliary lesions were seen at the spot site of injection (breast muscles), on spleen, liver, and small intestine. Ten of the 12 inoculated chickens died between the intervals of 56 and 110 days after inoculation. However, two chickens, which were injected with the rough strain, survived until 140 days after infection. These were then killed, and pinpoint, barely visible lesions, which revealed infiltration of lymphocytes on histopathology, were seen on spleen and liver. The minimum and maximum survival period was 56 and 110 days, respectively.
The present study attempted to isolate and identify the possible etiologic agents of avian mycobacteriosis using culture, postmortem examinations, histopathologic techniques, and experimental infection for virulence assessment because no studies have been performed to determine the prevalence of avian mycobacteriosis of chickens in Ethiopia. Despite the paucity of information on avian mycobacteriosis of chickens in Ethiopia, sufficient evidence suggests that the disease is found at significant levels in domestic cattle. For example, MAC-like organisms were isolated on culture from dairy cattle in East Shoa, in central Ethiopia.33 The present study agreed with this, with the highest numbers of MAC isolation in chickens from the same area (ie, from Nazareth in East Shoa). Moreover, our questionnaire survey revealed a large association of chicken with other domestic animals, including cattle, sheep, and goats. However, no large associate was seen with pigs, and this study substantiates that. Pigs are not reared in most parts of Ethiopia because of religious and cultural taboos. Therefore, pigs had no importance in the epidemiology of MAC in Ethiopia, leaving cattle and other ruminants in second line for transmission. Similar observations were made by Mwalusanya et al.34 on the epidemiology for the spread of avian mycobacteriosis in chickens elsewhere in Africa where backyard chicken production is practiced under poor village management conditions.
The flock size, age at first lay, housing at night, and poor nutrition and management practices reported in our study is in agreement with reports from Tanzania34 and Ethiopia.35 These studies indicated that chickens are constantly exposed to overcrowding (which may lead to stress), unhygienic external environments, other domestic animals, and free-living birds that may serve as sources of infection. Overcrowding within a flock brings in stress, which in turn could affect the nature and number of lesions occurring. Subjecting chickens to various degrees of social stress after intravenous infection with M. avium has shown a strong association among stressors, the number of lesions with necrotic centers, and M. avium cells recovered, as was reported earlier.36
Some sex and age variation on the occurrence of avian mycobacteriosis was also recoded, with slightly higher occurrence in female and adult chickens than any other classes. Female chickens are allowed to live longer than their male counterparts because of the lack of culling practices. This gives bacilli a better chance to establish over a long period of time and to be shed in the external environment. Thus, older hens could act as a source of infection to other members in the flock and other domestic animals and also in contaminating the environment.
Because the feeding system forces chickens to scavenge, there is a strong probability that these scavenging chickens may also acquire the infection from the soil in a contaminated environment with the droppings of other infected chickens and other wild birds. The fact that all of the naturally infected chickens showed grossly discernible lesions exclusively in the small intestine and spleen in this study suggests that the probable route of infection is oral or per os. A similar observation was reported from experimentally infected domestic geese and ducks with M. avium-contaminated feed via an oral route.37 In another study in ring-necked pheasants and Hungarian partridges, transmission of M. avium complex bacilli from experimentally infected pheasant to poultry was successful after free contact between the two species. 38
In the present study, skin lesions were found on the lightly feathered caudal part of the chicken from the low altitude areas. A similar tuberculous lesion (15 mm in diameter) was reported on the skin of the caudal part of cloacae in a 2-year-old male carrier pigeon imported into Japan in 1994.39 The free-living pigeons in our study were one of the wild bird types that tend to mix up and feed with domestic chickens and might serve as a source of infection. The variation in size and number of lesions recorded in adult chickens could be caused by successive episodes of reinfection from previously established lesions. This is commonly seen in adult chickens.2
Isolation of MAC by culture could be considered the gold standard for the diagnosis of avian mycobacteriosis.42
Previously, a reduction of virulence8 was reported during subculturing at 37˚C, a temperature lower than the body temperature of poultry (42˚C). Hence, we used an incubation temperature of 42˚C in our study, to maintain the virulence of the isolates. Our culture results (total prevalence ranging from 2.1% to 6.3%) were comparable to a report by Schack-Steffenhagen and Seeger,42 who reported a total prevalence of 3.4% from liver of mature chickens imported into Germany from Holland and the United States, but could not show the micro-organisms from broilers in an intensive production system. The probable explanation for the failure of showing the bacilli could be ascribed to the broiler market-demand for a good quality of tender meat. Broiler birds are kept in production for a short period of time and are slaughtered at a relatively younger age, that is, long before the bacilli get established in the chicken.
The reason we obtained poor Ziehl-Neelsen staining from the smooth transparent colonies at the beginning was the apparently shorter duration of time for the hot carbol fuchsin on the slide. This improved after we increased the time to 10 minutes, according to OIE (World Organization for Animal Health) guidelines7 and hence improved the demonstration of acid-fast bacilli. It was difficult to decide whether the strains from the culture growth are M. intracellulare, M. paratuberculosis, or M. genavense,30 because all three are virulent serotypes capable of killing chickens. The problem in species identification of M. avium from other similar Mycobacteria species30 has many facets in developing countries, foremost, the lack of facilities. Furthermore, three M. avium serotypes are virulent, and infection with these can kill chickens. 2
The most affected organs in the experimentally infected chickens were site of injection, spleen, liver, and to a lesser extent, intestines. The cases that we have seen in the two experimentally infected chickens (C and D) showed barely visible pinpoint lesions, confirmed as infiltration of lymphocytes from the spleen. This might be an earlier reaction to the inoculation, before the lesion developed to a full tubercle size as a result of individual resistance. It could also be due to M. intracellulare strains considered to have lower virulence than M. avium to domestic chickens.29 In agreement with our report, Morita et al.39,43 showed that smooth and transparent colony variants cause many white tuberculous lesions in the liver, spleen, and lung of the inoculated chicken, and no macroscopic change was seen in birds inoculated with the rough and opaque variant. This was seen in our two chickens (C and D).
Thus far, latent MAC infection has been reported in humans. This infection is sub-clinical and therefore involves a long-term process (up to several years), thereby exposing the strains to unfavorable conditions for longer.8 Conversely, consistent virulence in MAC strains isolated from other domestic animals, including birds, may be caused by the short duration of the infection associated with a relatively short life expectancy of infected animals.
The major conclusions that we have drawn from this study are 1) that a virulent strain of MAC is present in local-bred chickens in central Ethiopia, especially in mid and low altitude areas; 2) that the distribution of lesions that were encountered in naturally infected chickens differed from that of experimentally infected chickens, which may be caused by differences in the route of infection; and 3) that poor management in traditional chicken-keeping systems is the major risk factor for avian mycobacteriosis.
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Correspondence: Dr. Markos Tibbo, International Livestock Research Institute, Animal Genetic Resources, PO Box 5689, Addis Ababa, Ethiopia; Fax 2511 461252; E-mail: email@example.com
Table 1. M. avium Complex Growth on Lowenstein-Jensen Media from the Three Selected Agro-climatic Zones
Number Lowenstein-Jensen Gross Histopathology
Factors examined media (%) Lesions (%) (%)
Overall 95 6 (6.3) 5 (5.3) 5 (5.3)
High 29 0 0 0
Mid 30 2 (2.1) 1 (1.1) 1 (1.1)
Low 36 4 (4.2) 4 (4.2) 4 (4.2)
Male 45 2(2.1) 1(1.1) 1 (1.1)
Female 50 4 (4.2) 4(4.2) 4(4.2)
Young 44 1(1.1) 1 (1.1) 1 (1.1)
Adult 51 5(5.3) 4(4.2) 4 (4.2)
*Altitude: high altitude, 2,780; mid altitude, 2,240; low altitude, 1,300 meters above sea level.
Table 2. Distribution of Gross Tuberculous Lesions in the Different Organs of Naturally Infected Chickens
Origin of chickens Distribution of gross lesions in different organs which bacilli
by altitude* aSI bL cSp dBM eSk were isolated
Mid altitude fP gA P A A Sp (Isolate 1)
Chicken No. 1 Sp (Isolate 2)
Chicken No. 2
Low altitude P A P A A Sp (Isolate 3)
Chicken No. 3 P P P A A Sp, L (Isolate 4)
Chicken No. 4 P P P P P Sp, L, SI (Isolate 5)
Chicken No. 5 P A P A A Sp (Isolate 6)
Chicken No. 5 5 2 5 1 1
aSI = Small Intestine; bL = Liver; cSp = Spleen; dBM = Bone Marrow; eSk = Skin; fP = Presence of tuberculous lesions in the respective organs; gA = Absence of tuberculous lesions in the respective organs *Altitude: high altitude, 2,780; mid altitude, 2,240; low altitude, 1,300 meters above sea level.
Table 3. Distribution of Gross Lesion in Different Organs of Experimentally Infected Chickens
Strains Experimentally Distribution of lesions Survival CFU
Locations isolated infected chickens a M b Sp c L d SI time (days) injected
Mid altitude Isolate 1 Chicken A A P P A 93 8x105
Chicken B A P P A 87 8x105
Isolate 2 Chicken C* A P A A 140 1.57x104
Chicken D * A P A A 140 1.57x104
Low altitude Isolate 3 Chicken E P P P A 99 5.5x105
Chicken F P P P A 83 5.5x105
Isolate 4 Chicken G P P P A 70 1.8x106
Chicken H P P P A 59 1.8x106
Isolate 5 Chicken I P P P P 68 2.5x106
Chicken J P P P P 56 2.5x106
Isolate 6 Chicken K A P P A 110 1.7x105
Chicken L A P P A 91 1.7x105
aM=injection spot at breast muscles; bSp=Spleen; cL=Liver; dSI=Small Intestine
Mid altitude, 2240 and Low altitude, 1300 m above sea level
*Chickens C & D were killed; all others died of the infection.
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